StellarWords

Marvel.Conceive.Advance (My Fresh, New Blog)

2007-10-10T09:17:00.000-07:00

In the spirit of marvel and march, I created a new blog this autumn. It will be home to all further writing, research, and musings!

*http://www.meagangwhite.com/ *

Many thanks to the faithful reader who pointed out my need to redirect:)

Best,
MGW

Science is BeautyWords

2007-08-24T14:13:00.000-07:00

Did you know that science is beauty?

This image illustrates evolving dynamical patterns formed during the spreading of a surface-active substance, or surfactant, over a thin liquid film on a silicon wafer. The usually slow spreading process was highly accelerated.

Never regard your study as a duty, but as the enviable opportunity to learn to know the liberating influence of beauty in the realm of the spirit for your own personal joy and to the profit of the community to which your later work belongs. * A Einsten *

.MGW.

The West is Burning

2007-08-08T15:52:00.000-07:00

The West is Burning: Exploring AIR’s U.S. Wildfire Model

This summer, much of the western United States is in flames. Wildfires spurred by above-normal spring and summer temperatures and one of the worst droughts in decades have charred more than 4.5 million acres across the 11 western states. Between July 16th and 19th alone, 1000 new blazes ignited, prompting fire officials to raise the nation’s fire preparedness level to 5, its absolute highest.

The rise in singed acreage is largely due to bone-dry conditions, exacerbated by the Forest Service's policy of quickly halting fires that threaten residential areas. This policy permits accumulation of dry brush—perfect fire fuel. The most common cause of wildfires today, however, is human activity, including illegal campfires in heavily vegetated areas. The latter was the source of one of the summer’s most costly blazes, which occurred in late June near South Lake Tahoe, California. Dubbed the “Angora Fire,” the event destroyed 329 buildings and ravaged 3,100 acres. The U.S. Forest Service had initially hoped to contain it within a week, but what began as a small brushfire soon intensified into a full blown inferno. It raged for more than ten days, destroying nearly every structure in its path, before crews finally contained it. At the time, AIR estimated that total insured losses from the fire would likely exceed $150 million.

The Angora Fire highlights a worrisome trend: while the frequency of U.S. wildfires has remained relatively constant over the past several decades, wildfire-driven losses have significantly increased. Since 1980, wildfires in the U.S. have been responsible for insured property losses exceeding $10 billion.

This increase in losses is driven by the increase in the number and value of exposed properties in a high-risk construction area known as the wildland/urban interface (WUI)—a buffer zone where human development intersects dense woodland vegetation. Fire here can move readily between structural fuel and vegetation fuel, facilitating unusually rapid spread. Well over half of California wildfires occur in WUI zones.

Meanwhile, Americans continue to move in, building well-equipped first and second homes, particularly in the fire-prone West. Contractors in the WUI aren’t shirking from building opportunities either; between 1990 and 2000, the rate of construction on WUI-designated land exceeded that of non-WUI areas by a factor of three. The rush to build results in a convergence of risk factors: an unprecedented accumulation of fuels in areas of increasing population and property. This trend is similar to the one seen on coasts where Americans have an undaunted inclination to build vacation houses on hurricane-prone beaches.

Complicating risks for residents in fire-prone zones is the unpredictable nature of the wildfire peril; a sudden ignition can result in either a moderate blaze or a catastrophic event depending on atmospheric conditions, topography, and moisture content of local vegetation. Furthermore, fires can drive losses disproportionate to their size. For example, the 2003 Cedar fire was the largest in California history, destroying more than 270,000 acres. But it caused just $1.2 billion in insured losses, making it far less devastating than the $3.1 billion Oakland Hills fire in 1991, which scorched less than one percent of the acreage but ranks as the most expensive fire event in U.S. history.

According to the National Interagency Coordination Center (NICC), many tens of thousands of fires occur each year. And the risk of catastrophe property losses is increasing as population growth in the WUI continues apace. To help insurers more accurately quantify potential losses and support underwriting guidelines, AIR released its US wildfire model in 2006.

The AIR Wildfire Model for California

The AIR wildfire model utilizes a fire spread algorithm to simulate how a blaze will spread once it is ignited, as well as extensive maps outlining wildfire history to aid in predicting where fires will start. Historical data was pooled from, among others, two complementary sources: the California Department of Forestry and Fire Prevention (DCFFP) and the U.S. Forest Service (USFS).

In addition to historical information, the model is shaped by five key factors—the features governing wildfire frequency and severity. These are 1) ignition number and location, 2) vegetation, 3) weather conditions, 4) topography, and 5) fire suppression activities.

Ignition

Ignition can result from natural causes, like dry lightning—the source of most of this season’s wildfires—or human activity, such as the illegal campfire that spurred July’s Angora blaze. As previously mentioned, the vast majority of loss-causing wildfires occur in areas designated as WUI. WUI zones were originally designated as such by a 2001 U.S. Department of Agriculture and U.S. Department of the Interior report on communities at risk from fire. WUI boundaries are not well defined, however, and continue to change as the population disperses.

The maps below show the locations of historical California wildfires. The leftmost map shows California Department of Forestry and Fire Prevention (CDFFP) data overlaid on California WUI areas, shown in green. The CDFFP data consists of locations of fires larger than 300 acres from 1900 to the present, and fires larger than 20 acres from 1905. The center map adds the U.S. Forest Service (USFS) data for fires exceeding one acre, and the rightmost map shows all USFS-reported fires, regardless of size. The USFS data only covers fires reported from 1986-1995.

Vegetation (Fuel)

Fuel, another model parameter, is classified into different types of wildland vegetation, including coniferous trees, grass, and chaparral. Each burns at a unique rate and generates flames of different intensities. Grass, for example, does not hold moisture particularly well and can dry out even in a short drought, quickly transforming into ideal tinder through which flames can zoom.

In forests, fire spread rates are more complex. Forest fires may be fairly slow to spread depending on the undergrowth, but they can also be exceedingly difficult for fire-fighters to access and put out. Additionally, if forest fires manage to spread vertically into the canopy, they may become full-fledged crown fires, which move at incredible rates through treetops and can be virtually uncontrollable.

Weather Conditions

Wildfires in California are highly seasonal due to variation in temperature and precipitation within the year. During the six months from May through October, the average maximum temperature rises considerably. During the same time, little or no rain falls. This lack of precipitation removes moisture from vegetation until it reaches a very dry state, which in turn increases both the probability that wildfires will occur, and the rate at which they spread.

Seasonal winds represent another influential weather component. They can quickly revitalize a blaze, depending on their speed and direction. The Cedar fire of 2003 provides an excellent demonstration; its early growth was driven primarily by the presence of strong Santa Ana gusts—hot, dry easterly winds unique to California. Fortunately, Santa Anas are often short-lived. In the case of the Cedar fire, they were soon replaced with westerly winds from the Pacific Ocean, and this reversed the fire’s direction. The AIR U.S. wildfire model allows for such shifts. It incorporates historical data on average hourly wind speed and direction from NOAA Cooperative Observation Program (COOP) weather stations.

Scientists understand how fuel and weather affect a fire once it is ignited, but understanding just how it will spread so as to predict its final footprint is still a challenge. Fortunately, scientists have a considerable amount of data on fire size, location, and shape, as well less extensive data on wildfire duration and associated wind speeds. The model inputs these variables in the fire spread algorithm, which successively refines the initial approximation that on flat ground, and in uniform fuels, a fire will spread in an elliptical pattern. Wind speed and direction, along with local slope, are the major determinants of the ellipse’s shape. Vegetation factors in, too; as was noted above, fire spreads faster in some fuels than others, and if a sufficiently large region of non-fuels is encountered by a moving blaze, spread is halted accordingly.

Topography

Topography also affects how fire spreads. Fire travels upslope more readily than it does on level ground because flame advancing at an upward angle encounters a larger cross-sectional area of fuel than flame on level or downward sloping ground, feeding its growth. Additionally, trees and grasses immediately upslope from a smoldering fire are preheated by sweltering winds. These winds rob fuels of their moisture, turning them into perfect tinderboxes. The AIR model incorporates topographic data from the U.S. Geological Survey (USGS). These data are used to magnify fire spread when flames are traveling up-slope and to reduce it if a fire site is on level or downward sloping ground.

Fire suppression

The fifth and final parameter contributing to the overall wildfire picture is fire suppression—the suite of tactical techniques used by firefighters to halt expanding flame. These include clearing underbrush, airdropping fire retardants, and building fire breaks, or gaps in vegetation.

Decisions regarding where and when to deploy firefighting resources are influenced by fuel conditions and weather forecasts. Officials review information on how a fire is developing, too, and where it is headed in order to identify potential locations at which to fight a particular blaze. In unpopulated areas, wildfires are often allowed to burn out. This eliminates fuel buildup. In areas closer to human habitation, however, fire policies are aimed at extinguishing fires as quickly as possible. AIR’s fire spread algorithm approximates human decision-making with respect to fire suppression based on such trends.

Damage Estimation

Using a synthesis of the factors outlined above, AIR scientists are able to simulate a wildfire’s perimeter—the area a fire could ultimately affect. A complementary analysis predicts the intensity with which the fire will impact points in the perimeter’s interior. Predictor variables (flame length, fire spread rate, heat per unit area, etc.) are computed using the USFS wildfire simulation program, FlamMap, as well as topographical and road access data provided by the ISO FireLine tool. Combinations of these variables are analyzed in order to determine how they compare to historical fire pictures described in damage reports. In this way, a point-intensity index with a value between zero and one can be derived.

This value is further refined using AIR damage functions, which produce estimates of fire-driven loss by incorporating the structural characteristics of specific properties, including vulnerability of different roofing and siding materials. Since people continue to populate fire-prone woodland spaces, engineers have identified construction materials that are fire-resistant. Unfortunately, many homes today still have wood siding and either wood or asphalt shingle roofs, both of which are highly susceptible to ignition.

In addition to building materials, AIR damage functions also account for set-back distances—cleared space separating a home from the surrounding vegetation. A post-disaster survey conducted by AIR investigators revealed that most of the fire-ravaged homes in the Angora blaze did not have these cleared spaces. Of the homes that did survive with minimal damage, complete or partial setbacks were in place.

Conclusion

The 2007 wildfire season is shaping up to be one of the most destructive in recent memory, threatening homes, power lines, and communication towers across the western U.S. The AIR wildfire model helps to quantify the risk driven by such catastrophic events.

.MGW.

YourVisionWords

2007-07-19T20:17:00.000-07:00

Vision.

Mine's constantly evolving—always finding its sparkle-eye spirit in adventure, its muscle in mountain.

My vision for long life is inspired by short bursts of Milky Way bright on clear October nights and the sound of humans listening. It wears wonder. My vision plays hard and rarely comes in too soon. It sweats after newly-thought thoughts and lets their novelty grease its lining. It finds momentum in the pure, honest motion of running.

I want the freedom to learn for the rest of my life.

* * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * *

Recently, I prompted a dear friend to describe his vision. The prompt made its way to other friends—to mentors and dreaming minds.

Below: my humble prompt, and beyond, the beginnings of wonder in words I hope to continually capture.

Send me your vision: MeaganGWhite@gmail.com

*Prompt*

He'd learned a lot there in just two years, under crimson tides and Cambridge skies; Boston's yards had been good teachers. Its labs were informative, too, as was the every day company. And something else had been particularly edifying—something not at all crimson. It was a distant vision of superlative calm. He'd shaped it in still moments when energy was high, and when he had to describe this vision in words, he opted just to smile and say, I could best sum up this vision o' mine by describing a structure I'd build.

"It'd be a pretty sweet structure, too," he'd say, and then he'd proceed to describe it. People nearby couldn't wait to be captivated. The description went something like this:

A Corporate Structure

The description started metaphorically, with the bricks and mortar of biotech.

“We've only just begun to see what is possible in that realm,” he said. He was convinced that biotechnology could resolve a host of global issues—from energy crises to dilemmas in medicine. “I think it will change the world.”

The scholar depicted biotech’s impact in the form of a corporate structure. Part of the structure’s elegance was grounded in the assortment of builders; not only would his own immediate knowledge of science be utilized, but so would the savvy of eccentric thinkers in semi-distant fields. Leaders like Steve Jobs and Howard Hughes would be called upon to contribute.

Ultimately, his biotech construction would house innovative energy and medical solutions for the masses and more who entered its doors...

A Salmon Head in Gelatin

You start with the foundation: a six-inch thick slab of orange jello, with chunks of mandarin orange for structural stability. Any shape you wish. But just before the gelatin's gelafied, stick a thin layer of cotton balls over the top. Stretch out each ball before placing it in the gelatin, so small bits of orange show through the top.

Cuz calm, really, is all about aesthetic.

Last comes the garnish, the flourish: the fish. One, solitary saffron salmon head placed in the very center of the masterpiece.

"I don't do buildings"

I don't build buildings, but rather, construct dreams. Painstakingly, meticulously, in the vision of their creator. There is honor in continuing a dream a la Sagrada Familia, but it is perhaps more noble to think for oneself, reinventing mistakes and reveling in errors as though you were the first to commit them, and the last to learn from them.

A Tree House

This tree house would span dozens of the most majestic trees as they stood sentinel around a crystalline mountain lake, stashed away, inaccessible to those who wouldn't appreciate and float in it, thinking of bouncing bubbles and butterflies (a little Zarathustra for you).

The lower branches of the trees would be bare, supporting only our floating house. The canopy would strategically part, illuminating airborne epiphanies and squirrels as they resonated joy throughout the air. The branches would sway in the slow breeze and torrents of time, making bridges for friends to cross, and coves for family to sleep...

The summers would be green and gold under the foliage, the winters blue and white among the skeletal remains.

During the fall we would starve, as who could remember to eat with such color and awe-inspiring death enveloping us? And during the spring we would cry, overwhelmed at the beauty of budding leaves, and blinking infant-eyes.

The bedrooms would grow at our whims. Instead of a rug I would have thigh high ferns, which would part as I walked around contemplating life. A massive hardwood desk would arise with it's back to the lake, a mossy chair cushioning my ass. A leafy canopy would darken my bed at night, giving only slightly, letting the Milky Way float down as I watched it sleep.

In the morning shafts of light would use laser capture techniques to juggle specks of dust, and as we focused in on the thousand dust particles no doubt could reach us, and any feat would become probable.

This house would stand as an open invitation to those who will it. An open forum for life. No one would stay for long, because those who know how to love such things know that there is unfulfilled life outside this ring of trees, but the lake and its shade would be there, and I would prune its branches as needed. And fertilize it... with my poop.

A Simple Rowboat

The sweetness of the structure lies in its stark simplicity. A simple rowboat of light maple and soft pine, the lines of the wood merge swan-like at the bow. As she rests on the water, she hovers on each crest of the wave, never more than a quarter inch beneath the surface. The oars lie propped and parallel on the seat, big enough only for one.

Smooth and as elegant, almost more so than the boat herself, the oars beckon to be taken and pulled. Despite the wind that so often batters the sea, the vessel an image of complete and total serenity and the oars remain motionless.

To the uninformed, the structure is a well-crafted boat. She is measured flawlessly, varnished perfectly, designed brilliantly. She is indisputably seaworthy. To those who know, she is an oasis and an escape. Sleek, and alive, each stroke of the oars brings the owner of the boat further into the horizon.

The oars push the boat to unimaginable speeds driving away the careless thoughts that clutter the everyday mind. The product of a still moment with high energy, the small boat closes the distance to the vision of superlative calm, a vision of azure and navy with cool borders.

A Structure in Flux

it isn't the kind of structure one man could build, or the type of structure that you could understand by looking at it for a moment in time.

This was a building wrapped in it's own history. From the very first date when the location was chosen those first pioneers could never have imagined what it looks like on this day.

From humble beginings it was a dirt hut. It was a convenient central location for the intersection of two river and a view of the mountains; a natural crossroads. Travelers from many lands would cross paths there to echange ideas.

As feat trod in and out so did hands help to expand the walls and support the roof. Over time the meeting place grew with every new idea brought in. At certain times individuals sheaperded renovating activities and at other times groups placed their stamp.

But each generation left their own improvements. New materials enabled further increases in architectural capability, but the core utility remained the same. It was a house of ideas built to incubate and hatch eggs of thought, and itself a reflection of the ever improving capability if it's inhabitants.

Truly a structure in flux. Though solid - always changing identity. A building not of brick and mortar, but supported by the cumulative thoughts and voices of those who had found shelter there. It was a forum for expression not just inside, but by it's very existence- symbol and example, standing for free expression within and without.

So when you see the high vaulted ceilings, know that the mural pays tribute to the great minds that once looked to that same point in wonder. See the cascading wall of water and reflect in the pool at it's base- though the fountain remains itself, there is never a moment when it is at rest.

Recognize that the green roof is an homage to the original mud hut and a testimony to the cyclical nature of thought; when ancient technology finds its way to the cutting edge. From the solar/geothermal internal temperature control system recognize that this building is connected to the earth, finding it's own equilibrium from natural ebb and flow. This is not just a structure build on the earth, but out of it and into it.

A house of innovation for innovation and built by it. A monument of human achievement but gracious through and through for the gifts of the natural world. A secular house of god, and shrine to aspirations of wisdom.

A bookshelf

It would be a bookshelf full of favorites and all the world's time to read. Beside the bookshelf, a hammock, and below the hammock, the wildest wildflowers reaching up to a slow, gold sunset.

No talking.

to be continued...and many thanks to those who have contributed :)

Predicting Hurricanes In a Warming World Words

2007-06-14T20:19:00.000-07:00

Predicting Hurricane Risk in a Warming World

*This article highlights one catastrophe modeling firm's approach to predicting hurricane risk in the face of global warming.*

In recent years, devastating hurricane events like Andrew and Katrina have increased media attention on higher hurricane activity due to climatological factors, including global warming. The catastrophe modeling community is aware of the buzz, and while some among it question the influence of climate change, others believe the warming trend signals a new regime—one that calls for similarly radical changes to hurricane modeling methodology.

From AIR’s perspective, the debate is not whether climate factors have an influence on hurricanes; scientists tend to concede that they do. If there is any debate at all, it is on how to provide insurance companies concerned with deriving reliable results from catastrophe models with the latest science, particularly that of the influence of elevated sea-surface temperatures (SSTs) in the Atlantic.

The Atlantic basin has been in an active phase since 1995. This phase is characterized by above long-term average hurricane activity. Some scientists, like those at the National Oceanic and Atmospheric Administration, associate this with the warm phase of the Atlantic Multidecadal Oscillation (AMO), a climate signal measuring the change in North Atlantic SSTs. The AMO is just one of several measures of Atlantic sea-surface temperature anomalies, but other measures indicate warming trends now, too.

At AIR, climate scientists have been monitoring the relationship between global warming and Atlantic hurricane frequency since the early 1990s. They stay abreast of the latest scientific literature on the AMO and other climate signals, evaluate related findings, and conduct research of their own. In 2005, AIR meteorologists undertook new and extensive analyses of the link between elevated SSTs in the Atlantic and landfall frequency and location—a research effort that is still ongoing. The result was a near-term hurricane catalog released in April 2006.

Unlike AIR’s standard catalog, based on over a century’s worth of hurricane data and more than 20 years of research and development, the near-term version relies solely on hurricane statistics from 2004 and 2005—seasons of notable Atlantic intensity. But despite general consensus as to the impact of warming seas in these years, standard use of a near-term catalog inspired by recent storm trends remains controversial. That’s largely because researchers have not yet translated their finding regarding a jump in Atlantic hurricane intensity into information useful to insurance companies—a percentage increase in foreseeable insured hurricane losses on land.

To date, the primary focus of investigation has been on basinwide storms, leaving landfall trends unexplored. If hurricane risk is to be assessed with a high degree of confidence, however, the relationship between hurricane activity in the Atlantic, landfall activity, and regional insured losses will require significant additional investigation. AIR meteorological teams are making great strides on this front.

Meanwhile, in the face of uncertainty around the near-term view—the methodology of which is currently undergoing rigorous review by peers—AIR maintains that a short-term model offers a valuable perspective from which to manage hurricane risk. The issue then becomes how to offer this untested model to insurance companies.

When it was first released in 2006, AIR made the scientific judgment to keep the near-term catalog separate from its standard version. By doing so, it did not impose a new model with high uncertainty on its clients, but instead allowed them to choose for themselves just how they wanted to use the model’s new information in their decision making processes.

This year, AIR will make the same provision—offering the near-term catalog as a supplement to its long-term model, rather than a replacement. Interestingly enough, the long-term model is scrutinized, too. It has occasionally been characterized as “backward looking” because it incorporates data from 100+ years, but this judgment requires inspection. The purpose of using historical data is not to reproduce the past, but to better estimate what may happen in the future. Along those lines, AIR’s standard catalog provides clients with scenarios that could happen in upcoming storm seasons even though they have not happened before—scenarios that include both more intense storms and years with more landfalls than have been historically seen. Ideally, nothing should happen that the model does not account for, and the AIR model for U.S. hurricanes has performed very well in this regard.

.MGW.

9/11 Animation EngineeringWords

2007-06-13T10:38:00.000-07:00

Most Americans think they know what brought down the World Trade Center on September 11, 2001, but civil engineers aren't so sure. They're still seeking answers--answers that could save lives in future attacks--and the search continues with the help of a state-of-the-art animated visualization created by researchers at Purdue University.

Investigators at Purdue's Rosen Center for Advanced Computing have created an animation they say reveals more information than could be conveyed through a scientific simulation alone.

While a scientific simulation shows details essential to an engineer--the structural damage caused by a plane tearing through several stories of the World Trade Center within a half-second--it doesn't deliver details useful to a layperson, such as flames and smoke. In the animation, these details are clearly rendered, and that's important.

A damage picture that lacks them is scientifically inaccurate.

When a plane hits a building, it moves through the structure like flaming lava; the kinetic energy of the fuel associated with the moving aircraft causes a significant portion of damage. Thorough examination of the 9/11 attack on the World Trade Center revealed that the weight of the 10,000 gallons of fuel--more than the impact of the crash--caused the building's collapse. In fact, if it hadn't been for the fuel-driven fire, the structural damage to the WTC's north tower might haven been much less, comparable to that seen had the crashing aircraft been filled with water.

Purdue's animation detailing the impact of fire is the latest in a series of post-9/11 projects by the university team. The team's goal is to identify the structural damage that occurs when an airplane collides with a building, and ultimately, to prepare builders to design structures that will stand up to anything--even terror.

.MGW.

View o' the Charles

2007-06-06T19:03:00.000-07:00

Charles River

.MGW.

Tides Need Moon Words

2007-05-17T18:11:00.001-07:00

--Tides Need Moon--

Tides need moon for motion,
Waves want wind to be.
Politicians make decisions;
They need currency.

Shoots need sun to shoot up.
Roots reach but need earth.
Laissez-faire needs freedom,
As do I--for mirth!

I call for salty looseness
Of Gibraltar gales and hues,
And repartee, and severance
From small and tiny views.

.MGW.

Chinese Typhoon Words

2007-05-17T14:38:00.000-07:00

Modeling Typhoon Risk in China

Nowhere else in the world are typhoons more frequent than off China’s coast, in the Northwest Pacific basin.

The word typhoon stems from the Chinese JuFeng which originated in 5th century Chinese literature to mean “scary wind.” While typhoons in China certainly cause significant wind damage, the torrential rainfalls that accompany many typhoons also cause considerable damage from flooding. At work these days, I'm writing articles that provide an overview of China’s typhoon hazard, as well as the vulnerability of the Chinese building stock to typhoon-induced wind and flood.

.MGW.

Old Complications Rising Words

2007-05-04T22:20:00.000-07:00

Old Complications on the Rise:
Anesthesiologists, Are we as good as we think?

[Will post in full after published in Anesthesiology News]

Despite vast improvements in surgical and anesthetic practice, a new trio of studies makes it appear that anesthesiology may have a ways to go. Advances in technology have seemingly contributed to increases in old anesthesia-related complications. At least, that's what these findings—highlighted by three abstracts presented in March at the International Anesthesia Research Society's (IARS) 81rst Congress—would initially suggest.

The abstracts, each based on a database of more than 37,000,000 patients assembled by the Agency for Healthcare Research and Quality (AHRQ), discussed rising trends in three areas: postoperative respiratory failure (PORF), anesthetic complications, and postoperative septic shock (POSS). The first complication, PORF, actually doubled from 1994 to 2003, increasing from two to four percent.

“We would not have anticipated an increase in PORF, let alone one so pronounced,” said this study’s lead author, Mark Nunnally, MD, an anesthesiologist at The University of Chicago, where all three studies were based. “Our effort now is directed at uncovering as much as we can about why this finding exists in a database this size.”

Recent investigations have associated increased PORF with age; patients over 45 are more susceptible. Other contributing factors have included patient incomes below $25,000, care from non-metropolitan hospitals, and use of Medicare or Medicaid versus private insurance.

As anesthesiologists consider why PORF and other old complications are getting worse, one point seems clear: surgical and anesthetic techniques are not to blame...

.MGW.

26.2 Words

2007-04-23T16:02:00.000-07:00

In your element
you can be
as fierce
and as fast
as your will can see...

.mgw.

Wrinkles in TimeWords

2007-03-08T06:08:00.000-08:00

Wrinkles in Time in the OR:
A Call for Synchronized Clocks

Wrinkles in timekeeping can cost hospitals big bucks. Lawsuits and compliance issues are just two problems stemming from imprecise timestamps—a consequence of nurses, anesthesiologists, and other healthcare providers recording times from unsynchronized clocks.

“I’ve been in many medical institutions where all the clocks are different,” said anesthesiologist Michael Jopling, MD, Chairman of Anesthesiology at Mount Carmel St. Ann's Hospital in Columbus, Ohio, and President of the Society of Technology in Anesthesia (STA). “This is very frustrating. It creates a big problem for record keeping.”

But even synchronization of clocks—including those in computers and physiological monitors, as well as clocks on walls—wouldn’t iron every last wrinkle in the hospital timekeeping dilemma. There’s yet another fold.

This March, thanks to the Energy Policy Act of 2005, Daylight Saving Time (DST) will begin three weeks early—a move meant to reduce energy consumption. Unfortunately, the time change has unintended consequences. Devices with clocks not programmed to make the DST transition could supply incorrect timestamps for weeks.

Now, specialists at Geisinger Medical Center in Danville, Pennsylvania are teaming up to tackle both problems—starting with synchronization. Anesthesiologist Mark Poler, MD, is spearheading the movement. He has been instrumental in encouraging Geisinger to replace independent time pieces with those that are specially synchronized.

The devices, known as Primex radio-synchronized clocks, have base stations that acquire time from Global Positioning System (GPS) satellites in orbit. The base stations are positioned throughout the hospital and use a radio transmission on a licensed frequency to rebroadcast time to clocks equipped with special receivers.

Dr. Poler’s interest in bringing Primex clocks to Geisinger was spurred by troublesome trends he’s noticed in the operating room (OR). “People keep time by their wrist watches,” he said. “Others take times from clocks on the walls that don’t run at the same speed because nobody’s bothered to set them.”

This lack of synchronization means that a patient leaving the OR at 10:12 in the morning could magically arrive in the recovery room at 10:05am—a mysterious step back in time.

To further confuse matters, Dr. Poler explained that computers used to record the duration of medical procedures have clocks in them which may or may not be synchronized to each other either, let alone to clocks on the wall. This is also the case for physiological monitors that measure heart rate and blood pressure and .often do not have network ports or software to facilitate synchronization to a reference standard.

But what really got him thinking about the synchronization problem was a financial concern: the realization risk that Geisinger was overcharging Medicare due to erroneous calculations of elapsed time from unsynchronized clocks.

Determination of elapsed time in the OR affects billing; errors can have major financial consequences. In particular, underestimating time results in less time billed and lost hospital revenue, and overestimating chargeable time is a compliance issue punishable as fraud. All medical institutions walk a fine line between justifying charges based on time of rendered services versus taking great care not to overcharge.
.
While reviewing the record books at Geisinger, Dr. Poler observed that certain short procedures occurring over midnight and lasting only 15 minutes were instead logged at 15 45 minutes and 23 hours. This happened because timekeeping operating room management software was unable to handle the transition to a new date at midnight. Subsequently, checks and procedures had to be put in place for the billing process.

Meanwhile, mistakes like these—which are due in part to lack of clock synching—could lead to billing thousands of additional dollars in one hospital.

“When hospitals bill time to Medicare or insurance companies, they do not want to bill for time that didn’t actually occur,” said Dr. Jopling. “This is a compliance issue, and it’s grounds for huge penalties.” Mistakes in timekeeping have lead to thousands of additional dollars being billed in one hospital.

Needless to say, compliance with medical regulations is a critical motivation, which Geisinger has actively pursued, for synchronizing clocks. A second major impetus is avoiding lawsuits.

“It’s interesting—the clock rarely causes problems for the actual patient, but discrepancies in timekeeping can provide a field day for lawyers who misinterpret records,” said Michael O’Reilly, MD, an anesthesiologist at The University of Michigan Health System in Ann Arbor.

Dr. O’Reilly explained that healthcare workers trying to reconstruct an operating room event for the medical record book write a timeline. “When the timeline reflects gaps or inconsistencies,” he said, “people can be sued.”

Random elements in timekeeping can be misconstrued as incompetence on the part of the physician. “If you’re talking about delivering a baby by emergency C-section,” said Dr. Poler, “and the delivery actually happened in 5 minutes, but according to the clocks it was 13, and then the baby isn’t born perfectly, the attorney could say the surgeons were slow and inept.” In fact, the procedure actually happened efficiently and there was nothing the surgeons could have done to make that baby’s outcome good.

Dr. Poler believes the cost of synchronizing clocks at hospitals could be trivial compared to the money hospitals save in lawsuits.

Meanwhile, it’s possible that the money Congress hoped to save in oil consumption by initiating the Energy of Act of 2005 could be paid to technology specialists called to update timekeeping devices, including devices at hospitals.

“The change in the dates for Daylight Saving Time is extremely sticky and has the potential to deliver some of the chaos that was predicted for Y2K,” said Robert Murcek, Director of Network Infrastructure and Support at Geisinger.

Employees unaware of the new legislation might not know the correct weekend to make the time change. In hospitals, this means that lab computers could be updated while OR clocks are forgotten, or vice versa. Time stamps could be misplaced by an hour on blood pressures and heart rates. Billing departments could charge for an extra hour of operating room care. The list goes on and on.

“The real consequence of the time change,” said Dr. Poler, “is that people must be aware that it will occur and that the clocks they have are either going to handle it correctly or not at all—and they probably all won’t do the same thing.” At the last Daylight Saving Time change, most Primex clocks made the expected adjustment. However some did not “fall back,” demonstrating that the system is not foolproof. Dr. Poler said that pairs of analog clocks within a foot of each other have been reported to show a one hour time difference. Meanwhile, digital clocks that lose the synchronization signal at a time change simply start to display dashes.

He is hopeful that the Primex clocks will handle the transition to the early DST, as the clock makers have promised.

Dave Thewlis, Executive Director of Calconnect—an IT consortium of calendaring and scheduling systems, vendors, and customers which is working towards interoperability between different systems—says the time change doesn’t have to be a headache if people prepare.

Most software vendors are publishing notices telling their customers whether or not there’s a problem with their individual programs. “My advice is to check with your software vendor about updates,” said Thewlis. “If an update has to happen, make sure it happens prior to March 11th—the first day of the new Daylight Saving Time. If a program doesn’t need an update, get it in writing. The last thing you’d want to do is have someone say you don’t have anything to worry about when you really do need to update the software, especially in the medical profession.”

Administrators at Geisinger are already checking with software vendors, according to Mr. Murcek, to ensure that applications receive necessary updates.

Meanwhile, all this watching of the clock is a headache for physicians. “We spend a lot of time doing clerical timekeeping work and we want to reduce that,” said Dr. Jopling. “We’d rather be engaged with the patient.”

This may be possible someday. There is talk of employing a tracking device that would instantaneously record everything from when a patient receives a drug to when he enters the recovery room. Until then, though, each tick of the clock must be carefully recorded.

“We’re really coming into a transition period right now,” said Dr. Jopling. “Some hospitals have a computerized, paperless process and others are more paper-based, but as we start to move forward, one thing’s for sure: we need all of our medical devices to be synchronized.”

.MGW.

CoverWords

2007-02-23T11:20:00.000-08:00

Bottom left cover of February's "Anesthesiology News": Surge in Coated Stents Raising Issues For Anesthesiologists.

(that's me...wheee!)

.MGW.

Weaker than EuclideanWords

2007-02-08T10:09:00.000-08:00

I'm helping a grad student at UCSB draft a letter to "Nature" that will highlight exciting elements of 3 years of research he undertook in the Virtual Reality Lab while an undergrad at Brown University. His research seeks to understand the geometry underlying cognitive maps. In other words, he wants to know what kind of math humans use to navigate the world.

Previous studies say it's standard metric geometry, but he's not so sure...

Introduction only:

To understand how we as humans navigate our surroundings—to find detours, for example, or simply to walk next door—many researchers have first tried to understand how we represent the world mentally, in our heads. Researchers have sought to do this since 1948, when the term “cognitive map” was first introduced.

To date, every study assumes that humans impose a metric structure on mental representations of space. In other words, in order to navigate, we depend on knowledge of distances and directions between learned places along a one-dimensional route or in a two-dimensional environment. This outwardly logical assumption advocating metric structure is grounded in a series of experiments which shaped the constraints of cognitive maps, starting with visual tests performed by Shephard & Metzler in 1971.

Shephard and Metzler asked individuals to look at two shapes and decide as quickly as possible whether the two were the same. If the shapes were in the same view point, participants could identify matches within a second. When shapes were rotated at different angles, however, participants took noticeably longer to identify sameness.

A similar experiment by Bundensen, Larsen, & Farrel in 1981 using rectangles sized at different ratios gave concurring results; participants took longer to identify sameness the greater the scale adjustment—up or down—of the rectangle.

Together, these two studies seemed to imply that when we perceive an object in the world, we do it so accurately that we then have an almost physical copy, or map, in our brains. This was further affirmed by Kosslyn, Ball, & Reiser in 1978. They found that participants asked to memorize a map and then mentally scan from different target locations took longer to scan from objects the further apart they had been.

In 1976, Chedru localized where in the brain spatial maps exist by studying patients with spatial neglect—a condition in which an individual’s visual field is bisected by a vertical line. Chedru concluded that perception of space is dependent on location in the visual field, further laying the groundwork for our understanding of constraints on a cognitive map. His findings also indicated that processes related to spatial perception occur in the parietal lobe.

Studies by Taylor & Tversky in 1992 revealed that humans can learn a new environment equally well independent of their method of learning. The researchers taught participants the layout of a park using one of two methods—verbal description of a route navigation, or verbal description of a survey view. Participants then had to say whether statements about the layout of the park were true or false and they had uniform success despite different learning methods.

Learning our surroundings does seem to benefit from some physical input. Presson and Montello (1994) and Resier (1989) asked participants to imagine walking from home to point A, and then to point B. They then had to indicate the direction from point B back to home again, and they were consistently incorrect.

In a different experiment, when participants actually walked the route—from home to A, and A to B—the physical action of walking greatly improved their ability to indicate the direction from B to home.

The researchers doing this experiment concluded that we live in a physical world such that without physical inputs, we cannot construct an accurate mental representation of space (Klatzky, Loomis, Beall, Chance & Golledge).

Despite the number of studies pointing to metric structure as the basis of wayfinding ability, it is possible that cognitive maps are based on a less stringent geometry and in turn, have a less defined shape. The apparently metric behavior associated with navigation could in fact be accounted for by adaptive strategies based on topological geometry, which relies not on knowledge of distances and directions between learned places but on knowledge of environmental features—places, junctions, and landmarks.

This latter notion dissociates spatial knowledge from Euclidean geometry and opens the forum to progressively weaker geometries, which preserve fewer of the properties that remain invariant in metric structure. A cognitive map based on constraints of such geometries might only preserve ordinal structure, such as the adjacency relationships among neighborhoods, or relationships between places based on interlinking paths. Shortcuts and detours could be derived from knowledge of the connectivity or neighborhood structure together with visible landmarks.

The recent development of ambulatory virtual environments makes it possible to study the spatial knowledge used during actual navigation and in particular, to analyze the hypothesis that a geometry other than Euclidean facilitates human wayfinding...

.MGW.

CancerStemCellNicheWords

2007-01-16T14:02:00.000-08:00

--Sacking the Cancer Stem Cell Neighborhood--

[This article was posted on "Science Magazine's" website today, to coincide with the embargoed release of a paper from "Cancer Cell."]

Scientists have found the Achilles heel of a special class of cells that jump starts tumor growth. According to a new study, targeting the niche where they live is the key to destroying these previously invincible cells. This insight paves the way for more effective cancer therapy.

Until recently, researchers believed that all cells in a tumor were pretty much the same. But in the early 1990s, a team at the University of Toronto found some interesting characters hanging out in a population of leukemia cells: instead of rapidly dividing like their companions, about one in every million leukemia cells was capable of maintaining itself in a culture dish without differentiating and then initiating tumor growth when transplanted. These were indications that the cell was likely a stem cell.

Since then, researchers have discovered similar stem cells—including those behind acute myeloma leukemia, two brain cancers, and breast cancer—but no drug to date has successfully eliminated CSCs, which infinitely renew themselves and generate cells to replenish the tumor even after the bulk of it has been eliminated by chemotherapy or radiation. CSCs can do this in part because they grow at a sluggish rate, rendering them insensitive to conventional therapies designed to target rapidly dividing cells.

Now, researchers lead by neurobiologist Richard Gilbertson at St. Jude Children's Research Hospital in Memphis, Tennessee, have found a way to target cancer stem cells independently from the bulk of the tumor. They did so by looking for similarities between these stem cells and non-cancerous neural stem cells. Neural stem cells—immature cell masses that give rise to more specialized cells that form nerve tissue—are concentrated in blood vessel-rich regions called "vascular niches." These regions are lined with endothelial cells, which secrete chemical signals that promote stem cell survival. Gilbertson's team inferred that cancer stem cells might require a similar niche.

Sure enough, after examining a large cohort of human brain tumors, the researchers found that cancer stem cells were frequently located close to capillaries—the body's tiniest blood vessels. When the researchers injected human brain tumor cells called medulloblastomas together with endothelial cells in mice, the animals sprouted larger tumors than mice receiving tumor cells alone, the team reports today in Cancer Cell. This experiment further supports the role of endothelial cells and the vascular niche in providing signals that promote tumor growth.

Additionally, in tumor-bearing mice, drugs used to deplete blood vessels caused a significant drop in CSCs and subsequently inhibited tumor growth. The same vessel-killing drugs hardly effected the survival of cells in rest of the tumor, confirming that CSCs require a vascular niche.

"This study is an excellent example of bringing stem cell insight to cancer," says Richard Wechsler-Reya, a cancer biologist at Duke University Medical Center in Durham, North Carolina. "I think this is going to be the beginning of a really popular approach to treating cancer stem cells."

.MGW.

Gotta See About a MountainWords

2007-01-12T14:58:00.000-08:00

[Fiction]

Manhattan smelled of snow the morning I decided to leave it---not for eternity though, just for the weekend. The weather was right for skiing.

And without thinking about the work I'd miss or the stories needing my time, I threw my warmest fleece in a backpack, grabbed the pod, and sat down at my MAC: "Dear Editor and colleagues, I'll talk to you next week. Gotta see about a mountain, Meagan."

That morning, as New York highways turned into New Hampshire roads, the wintery sky above my car was as resistant to categorization as any sunrise scene I'd ever known. Gray clouds--fat and stoic--formed castles in the air, while whiter, wispy things lingered oddly outside their gates. Together these fat and small clouds barely veiled a pink sun, and I looked at it often and in spurts--a routine I kept up all the way to New Hampshire.

The cloud castle gates had closed on the sun when my car finally stopped. I wasn't in a parking lot though. And I wasn't at a ski resort. I had stopped at a footpath leading to a mountain named by no map. Just a mountain somewhere. I'd seen it from a distance once and thought it might want to be visited by someone willing to climb.

Snow made my climb especially quiet that dark afternoon; no sounds but my own deep breaths and the occasional hawk. The hawks were watching me but I was watching the view, and the way the mountain slope was slipping into a misty depth with my each upward step.

It was a steep mountain, that's for certain, but I hoped it would slip steeper still on the opposite face. When I got there and threw down my pack, I was glad to see just that. It was peace enough for the moment--hunting and finding a great decline. So I enjoyed it, but not by skiing down on the skis I'd brought. Instead, I opened my backpack and took out a book.

Like the mountaintop, this book had no name. Its pages weren't filled and there was no preface. There was no author either--not until the pink sun peeked out from cloud castle gates and blinded all wild eyes on the mountaintop. That's when I was moved to pen something--fast and strong--on those very blank pages. I authored the book, writing something so raw and true it might have been just like a hawk's pulse in flight.

I felt easy...

Before too long, I grabbed the book and my pack and flew down the mountain on a slope skiied only by wintering deer. And perhaps it was the wind's kiss or the birds closely watching, but I had never felt so alive.

.MGW.

Scientist As RebelWords

2007-01-11T20:52:00.000-08:00

Freeman Dyson may be short in stature--or so he seemed when I met him last year--but his accomplishments are undeniably tall. A former member of England's Royal Air Force, a longtime physics professor at Princeton, and a distinguished scientist with a bent for elegant mathematics, this Brit also has a way with words; he is lovely writer.

In Dyson's newest book, The Scientist as Rebel, the seasoned physicist speaks to the nature of scientists throughout the ages. "From Galileo to today's amateur astronomers, scientists have been rebels," he writes. They are free spirits, like artists and poets, casting off the restrictions their cultures impose. In their hunt for Nature's truths, they are guided as much by imagination as by reason, and their brightest theories have the uniqueness and beauty of great works of art.

Dyson affirms that the best way to understand science is by understanding those who practice it. He tells stories of scientists at work, and looks with a skeptical eye at fashionable scientific trends.

Dyson also reflects on broader philosophical issues--the limits of reductionism, the morality of nuclear bombing, the preservation of the environment...

This charming scientist offers a fresh and eloquent perspective on today's topics of scientific debate, as well as a narrative that highlights the finer linings of some of the greatest minds of all time.

.MGW.

InterestAndStrengthWords

2007-01-08T14:58:00.000-08:00

“Love many things, for therein lies the true strength, and whosoever loves much performs much, and can accomplish much, and what is done in love is done well.” --Vincent Van Gogh

"A large volume of adventures may be grasped within this little span of life, by him who interests his heart in everything." --Laurence Sterne

I aspire.

.MGW.

WildernessWords

2007-01-08T12:36:00.000-08:00

Caledonia-my home sweet home

"In wilderness lies the preservation of the world." HD Thoreau

Anti-CancerWords

2007-01-03T13:17:00.000-08:00

In the pipeline...

Researchers at Hopkins have created a hybrid molecule that causes cancer cells to self-destruct. The recipe: a sugar + a fatty acid called butyrate.

Butyrate slows the spread ofcancer cells, which scientists have known for 20 years. Unfortunately, attempts to use this molecule as a general drug for tumors haven't worked well because of the need for exceedingly high doses.

To get around the dosage problem, scientists have tried to make butyrate more potent by modifying it or joining it to other compounds. Results have been disappointing though; there are toxic side effects associated with partner molecules.

Now, Gopalan Sampathkumar, a postdoctoral fellow in JHU's Department of Biomedical Engineering, has found that when butyrate is matched with just the right sugar, the resultant hybrid molecule acts like a cancer-killing weapon, wiping out every cancer cell in its immediate path within about 15 days.

This is not the first time scientists have tried combining butyrate with sugars, but the sugars used previously just eased the delivery process, helping the hybrid molecule get into the cancer cell. Sampathkumar was more selective. He chose a sugar called cetyl-D-mannosamine, or ManNAc, which acts like ammunition in the cancer-killing process. It helps enzymes to resume the normal assembly of sugar molecules, which often goes awry when cancer occurs.

Meanwhile, the butyrate half of the hybrid molecule corrects aberrant gene expression. The result is a double attack, triggering just what the doctors ordered: cancer cell suicide.

More to come after I talk with the docs. This hasn't yet been tested in humans or animals and I'd like to know what the prospects are for this cancer-killing strategy in our generation.

.MGW.

Arcos De La FronteraWords

2006-12-29T17:36:00.000-08:00

-Arcos de La Frontera: Red Puppet in a White City-

[This is an archived piece. I wrote it after a particularly lively trip during my travels in Spain.]

I had never ridden a mule, and the man had no teeth. I think that’s what made it so easy; we were both unsure. But he smiled at me, a visitor, as I mounted that mule, and I thought I could not soon be higher than this—on a mule’s back on a hilltop whose skirts were sheer rock.

This hilltop, a fine point of defense, had drawn Moors to Arcos, but it had not drawn me. I had come to Spain’s most dramatically perched pueblo—a pueblo blanco—because I wanted to walk narrow streets of a town too old to wake up. I wanted to see its cobblestones and its whitewashed homes, and know who lived inside.

This toothless man did not, though I was lucky to meet him. He lived below, where sheer rock plunged to dirt. The dirt, like the hilltop, had tempted the Moors; it was fertile and rich, and I could tell from one green glimpse that it was the dirt’s fruit that had fattened the mule.

He was most certainly fat, and I was uncomfortable. But I smiled despite it, with all of my teeth, and held tight as the man pulled his beast through the streets. In Arcos, the streets are strikingly narrow. Lined with small elegant homes and wrought ironed gates, they are not meant for creatures so fat.

As my feet brushed white plaster, I wondered why nobleman had not wanted streets sufficiently wide for grand carts and carriages. Perhaps they’d been happy to walk.

Men like the man who pulled me that day could have walked four by four; unlike his mule, he was thin as the gates. I watched him amble—lovely, light steps—and the only sound in the town was mule hoof on street.

Now he didn’t know me and I didn’t know him but my backpack probably explained a lot, and my eagerness, too. And I’m certain my Spanish—blunt and not sweet—had helped earn me free passage that day. But I was content to be thought a traveler. Afterall, I was just that, and maybe, I thought, maybe he knew who lived behind these white walls, where I could sit and bite olives.

Olives are Arcos and oranges are, too. Their scents haunt the air; I couldn’t stop smelling. But I stopped when he stopped. The man pulling me stopped in the middle of town and reached into a bag on his old leather belt. He pulled out a thing which I would not think men tote—a puppet, tiny and brown, but a little bit red. Red where someone had painted his shirt.

And then, as bulls do, the children came out. They came out of white doors to see that red puppet. The square held them there; a square lined with benches and guarded by trees, but not olive trees. These were orange trees. But not the oranges you eat. These oranges were stored in barrels on ships and then made into marmalade, and they were also good for tossing. My senora had explained that. And I guessed that these children tossed them often and happily, and probably off of the hilltop.

The oranges were pale though, compared to the puppet. The children knew what he could do, and they watched the thin man and I watched him, too, as he made his puppet walk. He hadn’t bothered to tie up his mule, and I sat on its back—fat and heaving—and wondered if the man was a farmer or just a minstrel that made children laugh.

I laughed, but not too much, because my eyes looked away. I looked at the children and their bronzed skin. Their simple eyes wide and bright, very bright. I thought they must play hard and sleep well at night. Most of them were thin, like the man, though their laughter was fat. It echoed off white walls ‘til one mother called: que te vengas!

It was six o’clock.

I think I got lucky that day; I dismounted my mule and received an invite to eat olives inside white doors. I don’t think I’ve ever known olives so good—an old taste that lingers. Old like Arcos and fat like the mule. And full like the children, who laughed at the table and questioned my speech. I told them everything about my home. They wanted to know this, for they’d never seen it. I will never forget seeing theirs.

.MGW.

FDA PanelWords

2006-12-20T12:01:00.000-08:00

--Drug-Eluting Stents Not Safe for All...Yet--

[This piece is a continuation of an investigation I'm doing for Anesthesiology News in light of the FDA panel that convened earlier this month.]

A man who underwent hip surgery seven weeks after receiving a drug-eluting stent experienced a heart attack within 12 hours of his hip procedure, according to a study published last month in the Journal of Clinical Anesthesia.

Presumably, the heart attack was a result of discontinuing Plavix®—the anti-clotting medication required after placement of a drug-eluting stent.

Providing adequate surgical care for patients with drug-eluting stents is a big issue,” said the study’s lead author, Mayo Clinic anesthesiologist Michael Brown.

This issue surfaces amidst general controversy over drug-eluting stents. Earlier this month, the FDA convened a two-day panel in Gaithersburg, Maryland, to evaluate the safety of these devices, which now prop open the arteries of 3 million Americans.

Unlike conventional stents, drug-eluting stents ooze chemicals designed to battle restenosis, or renarrowing. But the chemicals they spew not only prevent the growth of artery-clogging cells, they also inhibit cells that would naturally fight clotting.

This means that patients with drug-eluting stents suffer suppressed anti-clotting systems and should stay on medications like Plavix for several months to a year.

According to Roger Moore, vice president of the American Association of Anesthesiologists, people on anti-clotting medication present unique challenges for anesthesiologists. That’s because anti-clotting drugs reduce the tendency to clot at the expense of bleeding—a risk inherently high during surgery. As such, patients on medications like Plavix are often recommended to discontinue their regimens before surgery.

But without Plavix, clotting risks skyrocket, and clotting—unlike restenosis—is linked to heart attacks, and even death.

The FDA panel in Gaithersburg sought to determine how likely drug-eluting stents are to cause long-term blood clots, and what should be done. While the American Heart Association recommends at least 3 to 6 months of Plavix treatment following drug-eluting stent placement, the optimal duration of this medication has not yet been established. The Gaithersburg panel meeting marked the first time the FDA sought the help of anesthesiologists and surgeons to inform such guidelines.

During the trial, presentations by doctors and stent manufacturers and data from numerous studies verified that drug-eluting stents increase clotting—both for approved patients, as well as for those who are “off-label.” Despite clotting risks, however, the panel concluded that drug-eluting stents are safe, as long as they’re used in conjunction with anti-clotting medication and in the intended population.

But—as evidenced by Michael Brown’s study—drug-coated stents cause problems even within the FDA-approved group when people who have them undergo surgery.

“The fact of the matter is that more and more people will be getting drug-eluting stents,” said Richard Shemin, a cardiac surgeon who was present on the FDA panel, “and surgeons and anesthesiologists are going to have to learn how to take care of people who have them.”

The most obvious strategy, according to Dr. Moore, is to postpone surgical procedures during the 6 month window directly after stenting.”

If surgery is emergent, however, a preoperative cardiology consultation is the next best approach.

“Communication between the surgical team and the cardiologist who placed the stent is vital,” said Sanjay Kaul, Director of the Vascular Physiology and Thrombosis Research Laboratory at Cedars-Sinai Medical Center in Los Angeles. His medical center has formed a Plavix Taskforce Committee to encourage interdisciplinary discussion.

“The problem now is that too often these conversations don’t take place,”
said Thomas Slater, an interventional cardiologist at NYU’s Tisch Hospital in Manhattan. He emphasized the need for anesthesiologists to consult with a patient’s cardiologist to understand the trade-off between the risk of stent thrombosis, or clotting, versus the risk of surgical bleeding.

“Anesthesiologists should learn why and when the stent was placed, how big it was, and how long the patient has been on anti-clotting medication,” said Dr. Slater. The risk of stent thrombosis is contingent upon these factors, as well as others such as presentation of the initial acute coronary syndrome, vessel lesions, bifurcation stenting, and an underdeployed stent.

In patients for whom the clotting risk is low, discontinuing Plavix to avoid excessive bleeding is less of a concern. For patients at an increased risk, however, remaining on anti-clotting medication during surgery should be a definite consideration.

And there are other ways anesthesiologists and surgeons can make the operating room safer for patients with drug-eluting stents.

For example, while stenting may have successfully opened significant obstructions in a patient’s major coronary arteries, obstructions could still exist in coronary arteries in the periphery. “This needs to be considered in approaches to anesthetic management,” said Dr. Moore.

He said that anesthesiologists operating on patients with drug-eluting stents should also avoid anesthetic techniques that could increase bleeding in areas already sensitized to it by Plavix. Additionally, anesthesiologists should monitor a patient’s cardiac status since any patient with a stent has previously had cardiac disease, which the stent may not have cured.

Finally, a study published this month in the Canadian Journal of Anesthesia discusses the potential for new anti-clotting medications—drugs with predictably short onsets and offsets of anti-clotting action. A patient on such a drug could stop the long-acting antiplatelet agent and switch to the short-acting, reversible one before surgery, to minimize bleeding. The short-acting agent could even be continued throughout the surgical procedure if the bleeding incurred was not excessive.

“Ultimately, drug-eluting stents are still great devices as long as patients who have them are well-managed in a surgical setting,” said Dr. Shemin. “With time and experience, as well as the willingness of specialists to communicate, we’ll know better how to do that.”

.MGW.

Making "Safe" Stents SaferWords

2006-12-17T07:04:00.000-08:00

--The key to making “safe” drug-eluting stents safer--

When it comes to tackling matters of the diseased heart, like clogged arteries, drug-eluting stents have rapidly become standard procedure. After hitting the market in 2003, these medical devices now prop open the arteries of 3 million Americans.

Earlier this month, however, the FDA convened a panel to evaluate their safety. These metal tubes—which ooze tissue-killing chemicals into arteries—do an extraordinary job of fighting the re-clogging associated with conventional stents, but they have also been linked to clotting, a phenomenon that can lead to heart attacks, and even death.

Clotting occurs more readily with drug-eluting stents because chemicals in the stent coating are nonselective; they inhibit the growth of harmful artery-clogging cells, as well as growth of cells that would fight clotting naturally.

Despite ties to clotting, the FDA panel concluded on December 8th that drug-eluting stents are safe, as long as they’re used in conjunction with anti-clotting medication, and in the intended population. But risks still loom; even within this approved group, drug-coated stents are causing quite a stir for a particular set of people—those who undergo noncardiac surgeries shortly after stenting.

“Surgery appears to carry a greater risk for these patients than we saw in patients with bare metal stents,” said Deepak Bhatt, Director of the Interventional Cardiology Fellowship at the Cleveland Clinic in Ohio.

That’s because Plavix—the anti-clotting medication required after drug-eluting stent placement—increases bleeding. And since the risk for bleeding is naturally higher during surgery, patients on Plavix should stop taking it before an operation. Without this medication though, the likelihood of harmful clotting skyrockets.

Herein lies the trade-off for people with drug-eluting stents who undergo surgery: stay on Plavix and bleed, or discontinue it, and clot.

According to Richard Shemin, a cardiac surgeon present on this month’s FDA panel, “the fact of the matter remains that more and more patients are getting drug-eluting stents, so surgeons and anesthesiologists are going to have learn how to take care of [complications in] people who have them.”

This becomes especially apparent in light of studies like one published last month in The Journal of Clinical Anesthesia, which reports that a man who underwent hip surgery seven weeks after receiving a drug-eluting stent experienced a heart attack within 12 hours of his hip procedure, presumably due to the clots that formed as a result of discontinuing Plavix.

“This is a big issue,” said the study’s lead author, Mayo Clinic anesthesiologist Michael Brown. “People outside the cardiology realm don't really appreciate the difference between a conventional bare-metal stent and a drug-eluting one, let alone the problems associated with a drug-eluting stent during an operation.”

The good news for patients with drug-eluting stents is that there are ways for physicians to improve safety in the operating room.

“The most obvious strategy,” said Richard Moore, Vice President of the American Society of Anesthesiologists, “is to postpone surgical procedures during the 6 month window directly after stenting. That’s when the patient is undergoing the most intense anti-clotting therapy.”

If surgery is emergent, however, a preoperative cardiology consultation is the next best approach.

“Communication between the surgical team and the cardiologist who placed the stent is vital,” said Sanjay Kaul, Director of the Vascular Physiology and Thrombosis Research Laboratory at Cedars-Sinai Medical Center in Los Angeles. “The problem now is that too often, these conversations don’t take place.”

Dr. Kaul says that anesthesiologists need to consult cardiologists before stopping Plavix.

“They should confer with the cardiologist to understand why the stent was placed, when it was placed, how big it was, and how long the patient has been on anti-clotting medication.” This information helps determine a patient’s clotting risk. For some, it’s relatively low. For others, it’s higher, and remaining on anti-clotting medication during surgery should be a definite consideration, despite chances of bleeding.

Dr. Moore says that anesthesiologists operating on patients with drug-eluting stents should also avoid techniques that could increase bleeding in areas already sensitized to it by Plavix. Additionally, anesthesiologists should monitor a patient’s cardiac status since any patient with a stent has previously had cardiac disease, which the stent may not have cured.

“Ultimately, drug-eluting stents are still good devices as long as patients who have them are well-managed in a surgical setting,” said Dr. Shemin. “With time and experience, as well as the willingness of specialists to communicate, we’ll know better how to do that.”

.MGW.

Drug-Eluting StentWords

2006-12-08T06:02:00.000-08:00

--Drug-Eluting Stent Controversy: No Clear-Cut Answer--

Drug-eluting stents, called by some the biggest breakthrough for interventional cardiology in 25 years, have been the source of recent controversy. These devices appear to pose a higher risk of blood clots, which can lead to heart attacks, than conventional bare-metal stents. An FDA panel convened last week in Gaithersburg, Maryland, to evaluate this risk.

Drug-eluting stents ooze medicine that prevents arteries from growing scar tissue and ultimately, from renarrowing--a problem commonly associated with conventional stents. When drug-eluting stents hit the market in 2003, they were highly endorsed by cardiologists and have been widely used ever since, inhabiting the arteries of 3 million Americans.

Now, it seems these drug-spewing stents are more likely to cause blood clots--a risk considered more severe than the renarrowing associated with stents of old. This risk can be minimized, however, when patients remain on anti-clotting medications, like Plavix and aspirin. But this medication is very expensive and induces bleeding during prolonged use.

And there is yet another problem associated with drug-eluting stents; patients who have them and later undergo surgery must be taken off of their anti-clotting medication so as to minimize chances of perioperative bleeding. But discontinuing anti-clotting medication invites risk of late stent thrombosis (clotting).

Thus, the trade-off: patients with drug-eluting stents who undergo surgery can either stay on their anti-clotting meds and endure complications associated with bleeding, or discontiue them entirely, risking clot formation that could lead to heart attacks.

I'm speaking with cardiologists across the nation, and anasthesiologists, too, to see how they will resolve the issue of drug-eluting stent safety. More to come. And it will start with George Vetrovec in Virginia.

.MGW.

Pièce de résistance Words

2006-10-23T15:28:00.003-07:00

--Pièce de résistance--

Ages and days have passed since I've updated this blog, but I have been writing, and writing more than ever. Unfortunately, my best energy is devoted to work I can't blog: the science of Joan Massaguè, Marcel van den Brink, Michel Sadelain, and beyond. These physician-scientists are making strong strides on all fronts--performing allogeneic bone marrow transplants, identifying the genes that underly metastasis, engineering red blood cells to deliver proteins...

You can read more about their work in journals like Nature and Cell, but not here! And they're doing this fabulous work in MSK's new research building (pictured above). It's an Upper East Side gem--23 floors of the best kept scientific secrets in the world.

In other news, I've been working on some longer pieces. They cover topics ranging from Basques to beauty, and they light me up and extract my deepest parts. Meanwhile, travel writing has captivated me, too; I like to recall Spain and write about its rhythm. (I am no Michener, but I aspire.)

So I'll post these pieces soon, and other ones, too. There could be a pièce de résistance among them! If one strikes you as such, please read it twice:-)

Happy writing!

.MGW.

TwoWildWords

2006-07-18T19:38:00.000-07:00

--Two Wild--

Grace,
man-i-fest in the midnight,
Seals stares of ravens who
spot
Slits between your skin and my skin
Recede as the cold night turns hot.

Strength,
ev-i-dent in the morning,
Feeds hunt of hungered who
sense
Muscle and sinew in man flesh
Exposed at companion’s expense.

Poise,
vis-i-ble in the daylight,
Locks stance of hunters who
know
Union of two wild creatures
Shall never shatter by bow.

Light,
obv-i-ous still in sundown,
Lingers on watering
pools
And fires the innermost lining
Of twilight’s most auspicious fools.

.MGW.

GammaRayWords

2006-06-17T14:40:00.000-07:00

Explosions in Space

Gamma-ray bursts don't loiter, and neither can the people who hunt them. That's why astronomer Andy Fruchter has set his cell phone to ring every time one of these massive explosions - packed with the energy of a trillion suns - occurs in outer space. Since the 1960s, when scientists scanning the sky for elicit nuclear tests first witnessed these powerful explosions and misconstrued them for Russian bombs, the origin of gamma-ray bursts (GRBs) has been a mystery. But Fruchter's recent attention to cosmic detail has filled in one of the gaps: he and his team have identified the types of galaxies where these bursts occur in a study published in Nature on May 10.

A GRB, best-described as a flash of very high-energy radiation, can be triggered by the collapse of a massive star. It is always accompanied by a supernova - another type of explosion resulting from the death of a star - and a GRB will be followed by a supernova instants later in a powerful succession of blows. However, although one might expect the two events to form in similar environments, images from the Hubble Telescope collected by Fruchter and other astronomers from the Space Telescope Science Institute in Baltimore show that they don't. In fact, the presence of a supernova doesn't always indicate that a GRB has occurred.

This is where it gets tricky. Although a GRB is a lot brighter than a supernova, and is observed first, it is actually produced by the supernova, which is typically of much higher energy. Sometimes the collapse of a star will only result in a supernova: for a GRB to occur as well requires the right conditions.

Fruchter observed long-duration GRBs (those lasting more than 2 seconds) and noticed that if a supernova occurred in a massive - and older - galaxy, this supernova would not have an associated GRB. He attributes this to the high metallicity characteristic of older galaxies, where metal ions have had years to accumulate, and suggests that GRBs can only be produced by supernovae in galaxies with low metal levels.

Metallicity inhibits GRBS in two ways. First, metal ions in the atmosphere absorb emissions, or the gas jets, constituting a GRB, and this smothers the burst. Second, the magnetic field generated by the metal ions opposes and slows the rapid spin needed to generate a GRB. "Some supernovae would like to produce GRBs," explains Fruchter, "but they can't."

Luckily, these are the supernovae seen in massive, metal-rich, evolved galaxies, like ours. If a GRB were to occur in our Milky Way galaxy, it could destroy the ozone, start fires on Earth, cause mutations and even mass extinctions. So Fruchter says that one of the results of this study is: "Relax!" It is very unlikely that our galaxy will host such an explosion and the closest star where one could occur is about 150,000 light years away.

This reassuring conclusion has been reached after painstakingly capturing images of GRBs with the Hubble Telescope for the past 10 years. "There are well over 3000 gamma- ray bursts known," Fruchter explains, "but only 40 or so for which we have a good image." But the next time an image is captured, the astronomers won't be so much wondering if it's close to home. Instead, they will be using it to study star formation in the early universe. Since GRBs are very bright, they are visible in areas where stars have formed, whereas these areas are normally not observable using telescopes available today.

.MGW.

CentralParkWords

2006-06-13T19:57:00.000-07:00

Central Park has energy
That’s city-colored green.

It’s drinkable in sunset drops
With skyscraper-gold sheen.

I felt it blow my hair tonight
And slowly make me wish

To swim—sans ropa—for the world
In lake depths off of 5th.

.MGW.

MadisonAveWords

2006-05-29T06:35:00.000-07:00

--Madison Ave--

Beautiful are:

Your blue eyes;
Two blinking seas of focus.

And
Truth.

Beautiful are:

Your strong steps;
Might lives in your stride.

And
Grace.

Exquisite are:

Your ideas;
They mingled with my mine on Madison Ave.
So that now,
I have

A memory

Of notions yours and notions mine
Stitched in New York winter time
‘Neath city lights—

December nights.

Some things stand out oh-so-bright!

I love to hear you think.

.MGW.

QuixoticWords

2006-05-18T20:27:00.000-07:00

--Quixotic--

Quixotic mind and starry-eye,
Idealistic will, romantic sigh;
Propose your color,
amber-gold,
Propose it to the morn.

Buoyant pulse, inventive tongue,
Naïve voice, refined and young;
Cast your shade,
a glowing pink,
Cast it to the noon.

Idyllic step, and tranquil soul,
Fiery heart, design meek-bold;
Let fly your hue,
a riotous red,
Let fly it in the night.

Churn cool stars and fuel hot flames,
Incite visions, enter games.
Don this blush,
a dappled burst,
Don it all your days.

.MGW.

LibertadWords

2006-05-10T10:16:00.000-07:00

--Libertad--

More freedom swims in the fastest mile
Than floats in the longest year.
When minds confine bold wings and choice
I find my free will here:

On gravel roads and ocean sands
And mountain paths long lost.
Recall do I my strength and voice;
This memory’s free of cost—

Unless you count the June sweat
And the muscles screaming slow.
And the out-of-breath and
Up-the-hill that lets you know you know

just

who

you are.

.MGW.

NYTimesWords

2006-05-08T06:36:00.000-07:00

--> Dangling Particles
[Or, Why science writing is tough.]

Click:

.MGW.

ElegyWords

2006-05-07T20:34:00.000-07:00

Lengthy, but lovely to ponder:

"The First Duino Elegy"
by Rainer Maria Rilke

Who, though I cry aloud,
would hear me in the angel orders?
And should my plea ascend,
were I gathered to the glory
of some incandescent heart,
my own faint flame of being
would fail for the glare.
Beauty is as close to terror
as we can well endure.
Angels would not condescend
to damn our meagre souls.
That is why they awe
and why they terrify us so.
Every angel is terrible!
And so I constrain myself and
swallow the deep, dark music
of my own impassioned plea.
Oh, to whom can we turn
in the hour of need?
Neither angel nor man.
Even animals know that we
are not at home here.
We see so little of what
is clearly visible to them.
For us there is only
a tree on a hillside,
which we can memorize, or
yesterday's sidewalks, or
a habit which discovered us,
found us comfortable and moved in.
O and night...the night!
Wind of the infinite
blowing away all faces.
Within our solitude appears
a nearly lovely god
or goddess, all the
heart is ever apt to meet.
Lovers fare no better,
concealing, by their love,
each other's destiny.
Do you still not understand?
Pour your emptiness
into the breeze-
the birds may soar
more swiftly for it.

Yes, springtime needed you!
The very stars, row on row,
sparkled for your attention.
From bygone days a wave rolled
or a violin yielded itself as you
wandered by some open window.
These were your instructions.
But what could you do-
distracted, as you were,
by all of that significance?-
as though each signpost
pointed on beyond itself
towards something higher yet:
a mere prelude to The Beloved!
(Where would you find room to
keep such a one, in amongst
those vast, weird thoughts,
always coming and going,
often spending the night?)
Sing, in your lovelorn
longing, of the losers.
Make their dark fame glisten.
Sing of those whom you are
nearly moved to envy in the
purity of their despair:
hearts more loving in their pain
than many never broken.
Sing again-and yet again-
your altogether insufficient
praise of them.
The hero lives!
His ruin is but a pretext
to be born again.
Depleted Nature calls her lovers
back into her bosom, as though
she had not strength to fashion them anew.
Have you yet sung the bold grief
of Gaspara Stampa so poignently
that another girl, likewise spurned in love,
might be moved to similar transcending passion?
Is it not time these ancient seeds of pain
put forth a flower?...time that, lovingly,
we free ourselves from lovers?...
time we fit ourselves, quivering
like an arrow to its bowstring,
enduring tension with the prospect
of flight exceeding the limits of
the feathered shaft, the string,
the very bow which looses it?
Nowhere may we remain.

Voices, Voices!
Hear, my heart,
as only the holy hear,
lifted from Earth by
celestial command but
taking no notice, so
perfect is their listening.
You could not bear to hear
the voice of God.
Not that, no...
but perhaps attend
the ceaseless murmer of
silence: the vespers
of the untimely dead,
borne upon the wind...
the whispers of the
children who haunted
that cathedral in Naples-
the church in Rome...
the injunction discovered
on a tombstone last year at
Santa Maria Formosa.
All they ask:
"Weep no more for us!
Your tears muddy the
path of our ascent."

Strange to be no more of Earth.
To quit half learned habits.
To view roses and their kind
no more in human terms.
To be no more a babe in arms
that ever fear to drop you.
To leave the name you are
known by like a child leaves
a broken toy.
Strange to desire nothing.
Strange to watch the
known world dissolve.
Death is very difficult.
Lost time is painfully
reconstructed until the
struggle yields some
slight glimmer of eternity.
The living are mistaken
in their distinctions-
angels often do not know
whether they walk among
the quick or the dead.
So 'tis said.
The storm of eternity roars;
all voices drown in its thunder.

Children who have gone do not require us.
Weaned, they need no mother's breast.
Our joys and sorrows don't concern them.
But we, for whom the mysteries are golden,
still unsolved, our very sustenance-
can we exist without them?
Grief is our spirit's fodder.
Remember the Lament for Linos: how
the first shaft of song shot through
barren air carving a sudden vacuum
in the astonished space where
godlike youth forever vanished,
leaving only a melody, which is
our sole comfort and enchantment.

.MGW.

WildTypeWords

2006-05-07T06:02:00.000-07:00

Wild-Type

“Wild-type,” she told him.
He didn’t understand.
He poured the wine and smiled at her
And reached out for her hand.

Her hand was tan and sun-kissed
From running on the beach.
Her skin was cool and lovely,
From sailing on dusk sea.

“The classic form of something,
As in nature it occurs.”
He laughed a bit and clamped his hand
Much harder upon hers.

“You know, like horses racing?
Or breezes full of hawk?
Like dancing in the thunder, or
Scaling steepest rock?”

The hawks he knew had cell phones;
His breezes were fast cars,
And when the thunder bellowed,
Inside, he watched the stars.

“Wild-type,” she told him.
“Come WITH me, see it real.”
The night was navy-blue and crickets
Clicked like roulette wheels.

A field is where she took him.
Orange lilies lay in wait.
An owl or two observed the pair;
A shadow watched their date.

“Dance with me?” she asked him.
“A wild-eyed, graceful waltz?”
He quipped: “No music have we.
How to keep the pulse?”

“The music’s in the moonlight.
Its metronome’s ideal!
The orchestra is whisper-led;
The dancefloor is grass-teal.”

He hesitated briefly,
And then he took her waist.
They danced in fields to rhythms
Wild-type, and perfect paced.

.MGW.

NinWords

2006-05-07T06:01:00.000-07:00

My very favorite thought:

We do not grow absolutely, chronologically. We grow sometimes in one dimension, and not in another; unevenly. We grow partially. We are relative. We are mature in one realm, childish in another. The past, present, and future mingle and pull us backward, forward, or fix us in the present. We are made up of layers, cells, constellations.
-- Anais Nin

.MGW.

BareWords

2006-05-06T22:05:00.000-07:00

--Bare Bronze--

Bare bronze shoulder.
Dress bright white.
Breezy brown hair.
Night so right…

Night so right for
Fire-fly kisses,
Sand dune smiles,
And high-tide wishes.

Bare bronze shoulder.
Eyes bright blue.
Easy laughter.
Me and you…

Me and you and
Moonlight swimming
Long, light talks
And slow, deep listening.

Bare bronze shoulders.
Hearts bright thrilled.
Summer joined and
Souls fulfilled.

.MGW.

MustWords

2006-05-04T12:34:00.000-07:00

[An adaptation of John Mosefield's "Sea-Fever"]

I must go down to the seas again
For the call of the running tide
Is a wild call and clear call
That may not be denied.

I’ll sail down to the seas again
To that wild-hearted life
To the whale’s way and the gull’s way
Where the wind’s a whetted knife.

And I’ll wear summer stars in evening eyes
Drink sea breezes with lime
And cherish every sun-kissed step
Of a wave-licked summertime.

.MGW.

JuxtaposeWords

2006-05-04T09:44:00.000-07:00

Madame, all stories, if continued far enough, end in death, and he is no true-story teller who would keep that from you.

--Ernest Hemingway

All goes onward and outward, nothing collapses, and to die is different from what any one supposed, and luckier.

--Walt Whitman, "Leaves of Grass"

.MGW.

DubiousWords

2006-04-30T19:39:00.000-07:00

Dubious Benefits: Cochlear Implants in Question

In the basement of a medical building in Baltimore, Maryland, neuroscientist David Ryugo is keeping 12 congenitally deaf cats happy. It’s costing him $70,000 a year. Meanwhile, 250 miles south in a lab at Duke University, electrical engineer Leslie Collins persists in the same mission she’s had for the past 20 years: to carry many frequencies within few wires. At the University of Iowa, chief of Head and Neck Surgery Bruce Gantz is teaching surgeons how to rescue hair cells in the inner ear. And across the world in Australia, Rob Shepherd serves as acting director at a facility that’s home to “Australia’s finest scientists and research staff.” These four scientists share one mission: to make cochlear implants better. Money, effort, and energy have funneled into this goal for years—a goal driven by a view rooted deeply in the medical field, and epitomized in a statement made in 1853 by Prosper Meniere:

“The deaf believe that they are our equals in all respects. We should be generous and not destroy that illusion. But whatever they believe, deafness is an infirmity and we should repair it whether the person who has is it is disturbed by it or not.”

Meniere, a leader at Paris’s school for deaf youth, believed as Ryugo, Collins, Gantz, and Shepherd do after him, that speech could and should be a deaf person’s primary mode of communication. This view is shared by surgeons, speech therapists, and often the parents of deaf children. These people stand behind cochlear implants; they may mold their careers out of them.

Meanwhile, critics like deaf spokesman Harlan Lane question cochlear implants. These devices, they say, make deafness seem like a disability, when in truth, as Lane asserts, deafness is a culture. In his book, The Mask of Benevolence, Lane counters that the only reason Prosper Meniere, and the doctors and scientists after him, called repairing deafness a duty was because of fear: physicians wanted to keep their hands in the ear. But they knew then, as now, that many deaf people were not frustrated by being deaf, nor did the deaf see not hearing as a problem. Rather, they had grown accustomed to it. They embraced and were fully functional in their deaf culture—a world not easily understood by the hearing and speaking people outside it, but nonetheless, a world defined by its own, organic language and by distinct habits and views found nowhere else. Deaf people “speak” with their hands, incorporating flowing and fast gestures and colorful facial expressions into every second of their conversation. They are intelligent, driven individuals, as evidenced by the number of students earning higher degrees at Gallaudet, America’s premier deaf university, in Washington, D.C. They can function in the world at large, holding jobs and raising familes.

By keeping their hands in the ear, then, and by advocating implants, Lane believes that physicians and scientists are threatening this deaf way of life, especially for deaf children with hearing parents who see implants as the norm. Cochlear implants may mean the end of deaf culture, Lane asserts. The New York Times Book Review called Lane’s attack on implants, The Mask of Benevolence, “a tightly reasoned… persuasive and gracefully angry book.” Gracefully angry was just what he was during our February interview when I phoned him in his Boston office. Amidst the thousands of dollars and brightest of minds being dedicated to cochlear implants though, I needed to determine exactly what might keep someone from advocating them, exactly how these devices threatened the deaf way of life, and whether cochlear implants and deaf culture could co-exist.

In Lane’s mind, deaf culture and cochlear implants cannot co-exist. Beyond simply threatening cultural deafness by diminshing the need to sign, implants pose certain physical risks. “Once a child undergoes implant surgery,” he said, “the child is an implant patient for life.” Unlike other medical devices, such as implantable lenses for vision correction, for example, which can be removed if the eye changes, cochlear implants are permanent. What’s more, they completely destroy the inner ear. The surgery to implant them ruins any residual hearing a patient might harbor, erasing hopes that he will ever again hear on his own. This is an indisputable, biological fact, one with which everyone would agree. It is why some parents are hesitant to implant apparently deaf infants; they have no idea how much hearing their child might retain, but with the implant—the “heroic medicine,” as Lane calls it—all potential to hear naturally, however small, is lost.

Other physical risks of surgery remain clear and present, too, as they would for any procedure. A slip of the physician’s hand in the sensitive middle ear region, where drilling persists, has occasionally caused paralysis of regions of the face. The vestibular nerve, part of the auditory nervous system, has also been hurt in surgery, leading to long-term disruption of the patients’ sense of balance. Another risk associated with implants has been meningitis, a potentially fatal infection of the fluid near the brain. In 2003, the New England Journal of Medicine reported that the incidence of this infection was 30 times higher in implanted children than in those without implants. The FDA and the Center for Disease Control linked this incidence of meningitis to positioners, the small rubber wedges that enabled surgeons to more carefully position the devices deep within the inner ear. These wedges often harbored infection-causing bacteria, but fortunately, positioner-bound implants were only manufactured by one company—Advanced Bionics—and the FDA banned surgeons from using these models in 2002.

But physical risks like nerve damage and menigitis are just the tip of the iceberg. Psychological troubles created by implants, critics say, are far worse. Critics point out an irony inherent to these devices: meant to permit hearing and speech, they may actually leave children languageless for years. That’s because parents who spend $40,000 for an implant want their deaf child to be like them—to not merely hear, but to speak, and this speaking does not include signing. Many parents who pay for implants don’t encourage their child to sign at all in fact, Lane argued, and may even scold them for attempting it. Thus, for a period in their young lives, these children cannot sign, nor are they yet adept at understanding speech with an implant. And because parents develop hopes that the implant will make their child “normal,” they don’t take time to learn sign language themselves either.

To get feedback from the implant-friendly side and balance my query, I spoke with Dr. Lauri Rush, director of the Mental Health Center at Gallaudet University, and mother of a three-year old deaf girl with cochlear implants. Dr. Rush could not have disagreed more with Lane’s arguments on langaugelessness. Her three-year old daughter, implanted just a year ago, can sign very well, which both Dr. Rush and her husband have encouraged, but her daughter also speaks, and signing is not taking away from her ability to excel at it. The Rushes have enrolled their child in speech therapy courses, where she works with a trained audiologist to improve her listening and speaking skills.

And rather than leaving the girl languageless, Dr. Rush said that implants are doing just the opposite for her child: “I wasn’t worried about my daughter growing up deaf because I know lots of successful deaf people here at Gallaudet,” she said, “but I was worried that she wouldn’t understand written language very well, which is a common problem for deaf people. And I wanted her to be able to read, and now with the implant, she can hear better and so she can read pretty well, too.” Rush said her daughter is reading up to 30 words at this point, an accomplishment for any three-year old.

Surgeons who perform implant surgeries advocate this route of training in spoken language, rather than sign language, for their patients. Lane says this is a problem because research shows that throughout schooling or life, the typical implanted child will rely on some form of sign language. And since developmental milestones exist for signing, just as they do for spoken language, a child prevented by parents from practicing it will never master it. He will not master it, either, if he practices it too late, which occurs when parents wait to permit sign language until they find that their child is making little progress with an implant.

This delayed opportunity to master a language—whether signed or spoken—could, Lane argues, prevent a child from fluently exchanging messages with and learning about the world around him. It could delay the normal growth of the child’s intellect, in other words. Implant critics would say this occurs too often in implanted children, for neither their implants nor their hands permit full communication, and they are forced to straddle two languages ineffectively. Lauri Rush’s experience shows that this doesn’t have to be the case. She has shown that a child can effectively communicate with both sign language and cochlear implants and that having her daughter sign has not taken away from the child’s ability to be successful with her implant.

Rush’s willingness to learn sign language as a parent and to encourage it for her implanted daughter is unique, Lane says. It is not to be expected in a family that commits time, emotion, and money to the implant process. This conflict of interest is not apparent in families where both the child and parents are deaf, however, and so rarely do “deaf of deaf” children experience a delay in language mastery; even if they do undergo implant surgery, their deaf parents encourage them to sign from an early age, arming them with language from the get-go. And now, according to Rush, three “deaf of deaf” students have been implanted at the deaf elementary school near Gallaudet University. These students’ deaf parents chose to implant their children, just as Rush, a hearing mother, chooses to sign with her daughter. Implants for “deaf of deaf” are a rare occurrence, and this step reflects the beginning of an acceptance of cochlear implants in the deaf community.

Critics like Lane still worry. They feel that cochlear implants impinge upon identity. “A partially successful implant,” he explained, “may be worse [for a child’s identity] than none at all.” Implants, he says, can deny deaf children a clear sense of self. Once a child undergoes surgery, his ability to develop as a deaf person is hindered by the family’s commitment to the implant process—the intensive training for speech and hearing, the auditory benefit the implant provides, its visual appearance, and by the possible delay in acquiring sign language.

That the child will be able to develop as a hearing person either, though, is unlikely. Deaf children—even those with implants—are different from hearing children; though they gain hearing, many never lose their connection to the deaf world, or their inclination to sign. They typically grow up in schools with other deaf children, all of whom have habits—gestures, facial expressions, tendencies to touch—unlike those of hearing people. And when deaf people with implants go to get jobs, employers are often hesitant to consider them; though their hearing might be reasonable or even good, the implanted deaf still can’t always speak perfectly. An employer given the chance to hire either a hearing person or a deaf person with implants would likely choose the former, if for no other reason than his fear of the unknown, even if both were equally qualified.

Thus, a deaf person with implants will feel alienation from his new group, the hearing world, since he will not always be fully accepted or comfortable there. Simultaneously, he will maintain enough loyalty to his original group, the deaf community, that things said and done to discredit them will likely offend him. As such, an implanted child may slip between two potential sets of friends. “[He will] tend to be culturally homeless,” writes Dr. J. William Evans at the University of California Center on Psychosocial and Linguistic Aspects of Deafness, “belonging to neither the deaf nor the hearing communities.” Here again, Rush disagrees. Her daughter goes to school with deaf children who have implants, and with deaf children who do not. “They all play together,” she said. “And the older deaf students here at Gallaudet are becoming more accepting, too. I’ve heard them say that they realize their peers with implants still have difficulties. They still face problems hearing, despite the technology. They’re still deaf.” At Gallaudet at least, it seems that the deaf are realizing the limitations of cochlear implants and instead of categorizing their implanted peers as sell-outs, they are respecting their decision.

Lane says that psychological troubles associated with implants are faced not just by the children wearing them; some difficulties associated with cochlear implants are unique to the parents. An implant that does not live up to expectations may cause Mom and Dad to suffer a second cycle of regret and acceptance, just like the one suffered upon learning their child was deaf. Rush acknowledged experiencing a grieving period, which lasted several weeks, after her own daughter was identified—not diagnosed—as being deaf. But she has not grieved since because the implant has been a success. Stresses related to implants do sometimes mount as parents struggle to teach initial speech skills. While specialists initiate much of this teaching, the majority must progess at home. Rush did not deny this hurdle, but when she cannot understand her daughter’s speech, the two of them sign and communicate perfectly. Another stress Lane proposed might be the money involved in purchasing and maintaing an implant. Raising enough funds for the many medical and paramedical services an implanted child requires strains relationships, and while most third-party health insurance plans provide some benefits, a good part of the follow-up care and the training has to come from parents’ personal savings. “I’ve seen them hold raffles, sell ice cream, appeal to the generosity of neighbors and relatives,” said Lane. “Anything to get enough money to pay for this process.” But the process, Rush would say of her experience, has been completely worth the price.

Above all, though, Lane feels that hearing parents of deaf children with implants face obstacles on a social plane. Their plight is much like that of white couples who adopt a black child. Again, this wasn’t the case for Lauri Rush, who found little opposition from the deaf community when she asked various faculty and friends at Gallaudet how they felt about her decision to implant her daughter. “Only two people responded negatively,” she recalled.

Rush’s experience may not speak for the deaf world at large, but it provides hope that families who embrace implants can maintain respect for deaf culture, a respect which appeases the deaf, and that these families will perpetuate the deaf world’s strongest custom—sign language—despite taking a step associating them with the hearing world. Yet, Lane still believes that the option implants provide is an option that breeds intolerance. Parents who choose not to use implants for their children are often asked why they would deny their young ones the chance to hear, instead of being acknolwedged for the efforts to embrace deaf culture.

Truthfully, Lane was moderately convincing on the other end of the phone; his laundry list of explanations for why one might avoid an implant was, if not “tightly reasoned,” at least reasonable to me. Yet because Lauri Rush has so successfully fostered co-existence of implants and sign language under one roof, and because she has taken little heat from the deaf community for her decision, I won’t buy Lane’s accusations that cochlear implants disable deaf culture.

Furthermore, before Lane hung up, he gave me one more reason to doubt him, and this reason was science-based. He said that no evidence exists to date that implant surgery must be done within a certain time period in a young child’s life in order for the child to reap maximum benefits. Implanted early or late, at 1 year or 3, he said, the child will benefit the same; he won’t acquire language at a faster or more thorough rate, regardless, and he’ll probably rely on signing at some point anyway. In other words, implants could never be guaranteed to provide great hearing. Lane based this claim on the notion that scientists have not yet identified an exact critical period—or window of time in which cochlear implants must expose children’s developing brains to spoken-language input. Scholars have argued for years that such a period exists. Already, cochlear implants inserted at early and late stages of childhood are helping deaf youths to better hear language, so that they can speak and read it more clearly, but the arrival of an implant during such a specific window of time would likely ensure that the child receiving the implant could function—hearing and speaking—with little or no problem, meaning that the surgery, the training, the stress, the money, and all the other investments would provide a certain and strong return. But Lane was quick to point out that the scientific literature has failed to provide clear boundaries as to when such a hypothesized critical period might begin and end.

I didn’t tell Lane about David K. Ryugo and his research with congenitally deaf cats. I wonder how he might have responded, to know that in the basement of Traylor Hall at The Johns Hopkins Medical School, the critical period is, for the first time, beginning to be defined and understood.

BirthdayWords

2006-04-26T08:10:00.000-07:00

-Enlightened You, on the Eve of your Birthday-

There’s a pulse that prevails now in evenings—
A pulse that’s so beautiful blue,
A pulse long as Niles and strong as the sea.
A pulse that reminds me of you.

You have in your mind eye’s a vision
To shape of your life something grand
And I know that you will. And I watch as you are
Becoming a brilliant-bold man.

I watch as you tackle cold science;
Equations and rigid-hard fact.
I observe how you, too, absorb Hegel,
No passion is there that you lack…

For you give your whole mind to your studies;
Initiative is what you take.
You rarely sojourn, but enlightened, press on;
Your will shall prove tricky to shake.

And I think, as a loving observer,
Who watches from Baltimore’s bay,
That you feel, my dear Mark, that you’re solo,
That parts of your climb will be gray.

But alone you are not in your efforts
To coalesce science and thought.
You stand beside strong men before you,
Who’s paths were not easily wrought.

You stand beside Plato and Caeser.
You sit next to leaders and kings.
And you rest beside men who aspired
To do, with their lives, noble things.

Tis true that their roads were brief thorny,
And maybe they, too, met loud fools,
But in their walks, pressing and forward,
Their minds became sharpest of tools.

Let the horns of your mind lead you onward.
I know you’ll achieve the unique;
Because that’s who you are, Mark— original.
I excitedly await your peak.

Happy Birthday!

.MGW.

IfWords

2006-04-19T21:26:00.000-07:00

"If" by Rudyard Kipling

[an excerpt from my favorite poem]

If you can fill the unforgiving minute
With sixty seconds' worth of distance run,
Yours is the Earth and everything that's in it,
And--which is more--you'll be a Man, my son!

.MGW.

Thesis Words

2006-04-10T13:15:00.000-07:00

Woo! April 10th, 2006, and the Master's thesis is done! It's about 40+ pages-- a bit too long to blog, but feel free to inquire within if you might like to read some/all. Here's the lay of the land, as far as sections:

· Dubious Benefits: Cochlear Implants in Question
· Defining the Critical Period: Cochlear Implants Restore Auditory Nerve
· From Impulse to Instrument: How Cochlear Implants Came to Be
· Fine Tuning: Improving Music by Adding Pitch
· Hybrid Implants: Better Hearing on the Horizon
· Twice As Good: Bilateral Implants for Adrean Mangiardi
· BAHA in Baltimore: How John Niparko Inserts Bone Anchored Hearing Aids

I owe many thanks to Hopkins neuroscientist David K. Ryugo. I surely would not have always known quite where to turn without him!

.MGW.

YoroParkWords

2006-04-09T09:13:00.000-07:00

Opened in October 1995, the Site of Reversible Destiny - Yoro Park - is an "experience park" conceived on the theme of encountering the unexpected. Strange angles, steep slopes, bold images... Keeping your balance there may be a challenge. Keeping your mind engaged should prove everything but.

http://www.yoro-park.com/e/rev/

.MGW.

HybridWords

2006-04-06T09:19:00.002-07:00

--Hybrid Implants on the Horizon: Shorter Electrodes are Helping More Hear--

In a research lab in Iowa, otolaryngologist Bob Gantz is destroying the cochlea. His cochlea-crushing moves aren’t hindering hearing, however, but helping it. That’s because “the ear,” as Gantz explained “is a forgiving organ,” a fact which scientists too worried about ruining its inner microstructure have not previously understood. They fear that snaking electrodes of cochlear implants into the cochlea destroys whatever hair cells still live there, causing complete hearing loss. Gantz, on the other hand, has dared to poke short electrodes into the cochlear space, and he’s shown that he can obliterate its outermost parts without disturbing the function of the hair cells deeper within the ear. This insight has allowed the University of Iowa scientist to develop a promising new cochlear implant, called the hybrid implant, which combines short electrodes with a familiar device—the hearing aid. Gantz’s invention blends the best of bionics with acoustic hearing to benefit a unique population who could not be helped by implant or hearing aid alone: people with high frequency hearing loss.

Hearing loss depends directly upon the health of hair cells in the cochlea. These microscopic cells, housed along the snail-shaped inner ear, pick up vibrations and convert them into electrical impulses that the brain recognizes as sound. Hairs in the deepest part of the cochlea pick up low-frequency sounds, such as music. Hairs at the cochlea’s entrance pick up high-frequency sounds, including speech. People who are profoundly deaf, like those who wear cochlear implants, can hear neither high nor low-frequency sounds on their own because the majority of their hair cells are damaged.

But complete hearing loss, affecting all the hair cells, isn’t the only type. With age-related hearing problems, for example, or with hearing loss suffered by Iraqi soldiers exposed to relentless gun fire and bomb blasts, not all hearing wanes. Rather, these people tend to lose high-frequency hearing first, meaning their inner hair cells are still intact. While most vowels are in the low frequency range, most consonants are high frequency sound bites, and as such, get distorted or lost for such patients. As specific consonants disappear, individuals can no longer discriminate a “g” from a “t,” for example. And since consonants are the milestones of speech, breaking up words which would otherwise be streams of squishy vowels, people with high-frequency hearing loss have great difficulty with speech understanding. They lose more and more words, until they’re unable to make sense of entire sentences.

For this group, whose only problem is detecting high-frequency sounds, a regular implant is a problem. Its far-reaching electrodes destroy hair cells deep within the ear, eliminating any ability to hear low-frequency information naturally. And even though the implant does step in and provide low-frequency hearing, it is a shackle compared to the cochlea, which, lined with thousands of hair cells, does a far better job of allowing people to hear low-frequency tidbits like music or the pitches in voice that distinguish one speaker from another. Thus, preservation of normal hearing is often preferable to the rougher sound estimates of a surgical implant for patients with residual heairng. But so far, there’s been no way to address patients in this middle ground—to allow them to enjoy the richness of sound through the low cochlear zones that are still working, while compensating for the high-frequency dead zones. These people have had to trudge through life not with implants but with hearing aids, which don’t clarify sound, but simply amplify it. And hearing aids turn up the volume for all sounds, not just speech. “But you could use the hearing aid to make the sound as loud as you like,” Gantz explained “and if you filter those consonants out, the sound still doesn’t make sense as words.” This has made for a disgruntled population of hearing-impaired patients—those who get nervous and depressed at social funtions because they cannot make out words, especially amidst heavy background noise.

Now, Gantz has the solution: make the electrode shorter, so it substitutes only for the hearing that’s already lost. Pair the short implant with a regular hearing aid to amplify the remaining low-frequency hearing, and people with high-frequency hearing loss just might hear again more like they did years earlier.

This resolution seems simple. But the idea to use shorter electrodes to selectively help hearing would certainly not have evolved so soon had Gantz not been willing to take a chance. “Electrodes were seen as risky. Once you start pushing them into the first turn in the inner ear,” Gantz explained, “there is a tendency for these wires to ride right into the sensitive scala media (a fluid-filled sack within the cochlea), meaning you disrupt the hairs cells attached to it and lose all residual hearing.” But Gantz believed that with calculated intrusion, hair cells in the depths of the ear would forgive a little interference. His courgae to explore this notion—to pry and poke in the cochlea—was fueled by observations of the work of a man who had dared to do it with cats, continents away in Australia.

At the Bionic Ear Institute in Melbourne, Robert Shepherd had been testing the fortitude of hair cells since the early 90’s. “I came across Shepherd’s work in a literature search,” Gantz said. “Before I knew about it, I had the concept myself that you could damage some hair cells and the rest would be okay, but I knew I was going to have to do animal studies before I could take this to patients.” Gantz found that Shepherd had already done such studies—the first of their kind—in cats. The Australian’s work involved winding electrodes into the ears of hearing kittens, whose hair cells were fully in tact. “I contacted Shepherd,” Gantz said, “and he told me about the kitten study. Basically, where he put the electrodes, the hair cells were a little bit damaged, but when he went deeper into the cochlea, the hair cells were still okay.”

Shepherd’s promising results in animals were a springboard for Gantz’s eventual work in humans. The Iowa physcian used the Australian scientist’s data “to convince the FDA that there was a possibility we could actually do human studies.” Gantz’s efforts were especially important in light of changing candidacy for cochlear implantation. “Hearing specialists were and are continuing to implant not merely the profoundly deaf, but also deaf people with more and more residual hearing,” he said. “But as you implant these patients, you hurt their remaining low frequency hearing—their music perception, or their ability to distinguish voices.”

By targetting only high-frequency hearing then, Gantz was hoping to avoid this. Ideally, his efforts would help not just a select group of patients, like older folks or Iraqi soldiers with specific high-frequency hearing loss, but also cochlear implant candidates who retained some low-frequency hearing and could benefit by keeping it. “Residual ability to hear is often better than what the implant provides,” Gantz emphasized. In everyday life, problems associated with relying on implant-generated low-frequency hearing are manifest at parties, business meetings, large events, anywhere where more than one voice—differentiated by a slight change in a low-frequency pitch—is presented to a patient. “Patients with cochlear implants always complain that they can’t hear speech in noise,” Gantz said. That’s because the implant doesn’t provide them enough pitch options to distinguish one voice from the next. In a crowd of talkers, many voices may resonate at the same pitch, leaving implant users clueless and frustrated. Hopkins neuroscientist David Ryugo also frequently hears this complaint. “People with hearing problems in noisy places get pretty depressed,” he said. “They might just go sit alone at a table somewhere to get away from the noise or to have a one-on-one conversation.” The physician in Gantz wanted to use his shortened electrode to stop this, to help patients who were going to get implants anyway to keep the best of what they had—their residual ability to detect sound. The scientist in Gantz was ready to explore every possible means of cochlear manipulation to make this a reality. “It’s really a balancing act,” he said, “of where the implant is better versus trying to save the residual hearing.”

In the late 90’s, Gantz began experimenting with act of balancing. He tested with a short electrode which extended only 6millimeters into the cochlea, compared to the standard 24. Gantz’s first test group was a population of subjects with little residual hearing. “I think the 1st group of 6mm subjects had only 10-15% word understanding,” he recalled. By doing trials in these patients, whose hearing abilities were nearly as bad as the profoundly deaf who regularly received full-spectrum implants, Gantz reduced risk. If he were to destroy their residual hearing, they hadn’t started with much anyway. Furthermore, in case his patients did lose this low-frequency ability, which would require them to receive full-spectrum implants, Gantz’s team had prepared a special secondary back-up electrode that could be inserted at the standard distance of 24mm into the ear, right beside the shortened version. His bases were covered.

But Gantz didn’t have to use the back-up. His study was a success. “The most important thing that we learned using the 6mm device,” Gantz said excitedly, “was that we could keep the hair cells of the inner ear alive when we used a short electrode! We knew because we preserved our patients’ voice discrimination just the way it had been for them before their operation.” This was the first time that hair cell plasticity had been demonstrated in humans. “Unfortunately,” Gantz explained, “we did not publish our results since we were trying to get enough data to submit to a high impact journal like Science or Nature. Both publications thought this study was too focused and needed to go to a journal with a speciality.” So Gantz’s work did not see print until 2003. He did present the concept, however, at the 10th anniversary of the National Institute of Deafness in October of 1998.

So far, about 60 patients have received the hybrid implant, manufactured by Cochlear Corporation. About 10 have had it for more than a year. “The device is still in clinical trials but initial results have wowed us,” Gantz said. He’s referring to patients’ ability to understand words. “We have a special test for word understanding,” Gantz explained. “And it’s the most difficult test we can do. We test with words that are monosyllabic.” Gantz explained that when you hear a word in the context of a sentence, “you get a lot of info from the context and you could guess at the words you don’t hear.” But when you hear a monosyllabic word alone, not only is there no emphasis on one syallable or the other, but there’s no context. A patient who can understand such words demonstrates that the hybrid is truly clarifying consonants. And it appears that it is: a year after the surgery, hybrid implant recipients are understanding an average of 70 percent of the words in standard hearing tests—up from 25 percent before the operation when they may have relied soley on hearing aids.

And the combination of bionic and acoustic not only beats a hearing aid, but a regular implant, too, which permits patients to understand just 50% of the words thrown at them in a hearing test. Gantz said that it will be important for some full-spectrum implant wearers to make the transition to hybrids. “Right now,” Gantz said, “a lot of people with 10-15% residual hearing are getting regular implants. They’re going to lose significant low-frequency hearing that way.”

While hybrid implants have proven successful in trials, they’ve not yet been approved by the FDA. Meanwhile, Gantz continues to receive funding from Cochlear Corporation. The Australia-based implant manufacturer waits in the wings for Gantz’s device to be market-ready. “The hybrid implant is a potential cash cow,” Ryugo said of Cochlear’s willingness to get involved. And in Gantz’s lab, “we’re all wondering when the hybrid’s going to be released for general use,” he said. When it is, the Iowa physician’s next concern is that other surgeons will understand how to implant the device. “There are certain surgical strategies you need to make the hybrid work,” he emphasized. “You have to know the anatomy, to get the electrode in there without hurting the critical hair cells. This role may be limited to technical surgerons,” he said, “not general ENT [ear, nose, and throat] doctors. And we’ll need to have people practice this a lot in labs.” In a phone interview, Gantz joked that he wished he could use larger surfaces, like pig ears, or even those of elephants, to practice this difficult surgery.

Gantz emphasized other ways in which inserting a hybrid would be unlike surgery for a normal cochlear implant. Mostly, it comes down to the cochleostomy—or opening of the cochlea—which is considered the most important intracochlear surgery moment. “We do things a little differently at that stage than Niparko does, for example” Gantz said, referring to the surgical style of reknown cochlear implant specialist and Hopkins physician, John Niparko. Though Niparko’s surgery involves a longer electrode, it is still the same width as the electrode of the hybrid, “and so he makes a hole in the cochlea, just like we do, that is 5 millimeters in diameter,” Gantz explained. “But during the cochleostomy, I take extra precaution. I’m very careful not to penetrate into the cochlea.” Gantz uses a sharp, diamond burr and small hooks to open up the snail-shaped organ. “Then I slide the electrtode in gently, in a minute or two,” he said. Gantz explained that so far, trials reveal that surgeons who pay attention to these details are doing quite well.

Beyond surgery, Gantz is also concerned that audiologists will understand how to instruct people in adjusting to hearing with the hybrid, once it is firmly implanted. “At Iowa, we’ve been implanting these on a trial basis for seven years, so our audiologists know how to help patients. But we’ve got to think about how to train other people to explain how to use this device effectively because it’s not easy to use.” After receiving the implant, most patients are pretty excited. “They haven’t heard this well in a long time since they have been struggling so long with hearing aids,” Gantz explained, “and all of a sudden they just say, wow! This is great.” But there are a lot of variables that factor into continued success. “Audiologists have to have a lot of experience with the programming.” Gantz mandates that specialists train and remind his patients that their brains will have to adjust to decoding electronically generated sound. Many people require extensive training to reap full benefits, and some describe an echo effect for a few weeks, as if they were hearing from two different places, until they become accustomed to the hybrid. “It’s not like turning on a lightbulb,” Gantz reiterated. “It may take six months to a year for patients’s brains to register what’s going on.”

But the wait and the training are worthwhile. Several trial patients have had the implant for 4 years now, and Gantz reported that even after that period, they are not at a stagnant place in their adjustment, but are continuing to distinguish more and more words. “It’s really retraining the brain, adapting to this thing,” Gantz said. “It’s like a learning new foreign language.” And he continues to have ideas about how to make his hybrids better. Cutting out all the high-frequencies in the hearing aid, so that the implant alone can cover them, is one strategy. “But most audiologists,” he said, “why would they wanna do that?” It appears that for as much success as his hybrids are likely to have, they will likely face opposition, too.

In the end, hybrid implants work precisely because they don’t go the extra mile, or millimeter. Rather they are a “short” version of their full-spectrum ancestors, the original electrode, combined with the familiar hearing aid. They act on a distinct part of the cochlea and they leave the rest alone, and in doing so, they provide a service that neither an implant or hearing aid could render. Most importanlty for Gantz though, he says the patients who have received his hybrids are happy, and they are no longer avoiding social situations for fear they can’t converse.

.MGW.

SevilleWords

2006-03-27T18:51:00.000-08:00

Semana Santa in Seville: "A blend of the sacred and profane."

-New York Times, 3/26/06

"I have long believed that any man interested in either the mystic or romantic aspects of life must sooner or later define his attititue concerning Spain."
- James Michener, Iberia

Te echo de menos, Sevilla.

.MGW.

ThoreauWords

2006-03-24T14:16:00.000-08:00

A quick, sweet line. Mighty fine:

"Be true to your work, your word, and your friend." --HDT

I aspire.

.MGW.

SynergisticAntiTumorWords

2006-03-23T10:14:00.000-08:00

--Betting on a Winner—Combination Biotherapies for Cancer--

"The beauty of this approach is that replication is constrained in CIK cells and rapid in tumor targets."
Chris Contag, Stanford University

Treating cancer may soon be a matter of finding the best horse and the best jockey for the job. Researchers have saddled a cancer-killing virus on the back of a tumor-targeting immune cell in one of the most powerful attempts yet to win the race against cancer. Their result illustrates the potential for improved cancer treatment through targeted biological therapies.

Most current cancer treatments, like chemotherapy, are unable to distinguish healthy cells from cancerous ones. They end up killing hair cells or cells that line the gut. Other therapies, like immune cell-based cancer treatments that are primed against certain tumor molecues, don't often generate a sufficiently strong anti-tumor response because they are not effective against a variety of tumor cells. A new wave of cancer treatments, however, could skirt these issues. These treatments, known targeted biological therapies, build on known methods of combining cancer-killing viruses with immune cells, which move unhindered through the body, delivering their viral cargo to tumors while leaving nearby healthy cells alone. However, even though these targeted therapies hold much promise, their use has been limited. Injection of engineered viruses into the bloodstream can be inefficient because these viruses may leave their immune host too soon and be eliminated by an immune response or infect noncancerous cells, so that only a small fraction of them is delivered to any given tumor.

Now virologists at Stanford University led by Steve Thorne have found a way to deliver sufficient amounts of cancer-killing virus straight to tumor cells. At present, the immune cytokine-induced killer (CIK) cells and the vaccinia virus are the "best in class." CIKs cells, unlike other types of immune cells, target a variety of tumors. They are also capable of carrying their viral cargo deep into tumor tissue, where it can't harm surrounding healthy cells.

Meanwhile, the vaccinia virus, which has had a long history as a vaccine for smallpox, is perfectly suited for cell destruction, and the Stanford team’s move to place it in CIKs has restricted its replication to tumors. That’s because, like other viruses, vaccinia can replicate in an immune cell host, but as Thorne found when he infected CIK cells with the virus, its replication in this immune cell is delayed. The vaccinia virus completes its life cycle in stages in the CIK host, saving a rapid burst of replication until 48 or 72 hours after infection, compared to 4-8 hours in other cell types. Since it remains hidden in the CIK cell until interaction with the tumor cells, it is more potent.

Targeting is also more efficient with this super duo; as reported in the March 24th issue of Science, 48 hours after Thorne injected the virus-infected CIK cells into mice, he detected very little virus in any other organ besides the tumor, and the virus was replicating deep inside it. When the virus was delivered alone, on the other hand, it did not burrow far enough into the tumor to be effective. To prove that neither individual CIK nor vaccinia would have been as effective as the combined effort, Thorne injected each as single therapies. While only 1 out of 8 total mice survived longer when treated with just CIK or just the virus, survival was significantly increased for 6 out of 8 mice with the combined therapy.

"This is an excellent example of how combination cancer therapies can have additive effects," says Inder Verma, a geneticist at The Salk Institute in La Jolla, Calfornia. "I think this is the way of future cancer treatments."

.MGW.

Omega-3Words

2006-03-23T10:10:00.000-08:00

Omega 3: The “Heart Friendly” Fat?

[also appearing on NPR's site, in light of a Nature Biotech study on genetically engineered omega-3 fatty acids]

Bacon doesn’t have a very good reputation when it comes to a healthy diet. But now, scientists are aiming to make bringing home the bacon – and some other fatty meats – a little healthier. In the current issue of the journal Nature Biotechnology, a team of scientists report they’ve genetically engineered pigs to produce higher levels of omega-3 fatty acids – a kind of fat believed to reduce the risk of heart disease.

What is omega 3 fat?

Omega-3 fatty acids are a kind of polyunsaturated fat found in certain kinds of fish and plants. Your body doesn’t make omega 3, so you have to eat it. Omega 3 comes in three forms, known as DHA, EPA, and ALA. Scientists have been most interested in the potentially beneficial effects of combinations of DHA and EPA. In general, the standard American diet is thought to contain too little omega 3 fat, relative to another type called omega 6.

Why is omega 3 believed to be “heart friendly”?

Several decades ago, researchers noticed that people living in the Arctic who had diets rich in omega 3 also had low rates of heart disease. Since then, several large studies have found more evidence of a link, according to the American Heart Association. Studies have also suggested that people at risk for coronary heart disease benefit from consuming omega-3. One prominent theory is that the fat reduces the inflammation of tissues that is linked to heart disease.

What foods contain this “good” fat?

Fatty fish like mackerel, lake trout, herring, sardines, albacore tuna and salmon are high omega-3s. Tofu and oils made from canola, walnut and flaxseed are also good sources. You can also buy omega 3 supplements.
It isn’t clear how much omega 3 you need to ingest to get benefits, according to the Heart Association, although it recommends eating two fatty fish meals a week. It also warns that ingesting too much of an omega 3 supplement can lead to health problems, such as excessive bleeding.

Are scientists trying to engineer other animals to produce omega 3?

Yes. In 2004, researchers at Massachusetts’s General Hospital reported engineering a worm gene that successfully produced levels of omega 3 when transferred to mice. And scientists are investigating other methods for engineering larger animals, such as cows and chickens, so they can make meat, eggs, and milk rich in omega-3.

.MGW.

StringTheoryWords

2006-03-19T17:32:00.000-08:00

--The Strings--
[2 one of my favorite authors]

The strings that stretch between our minds comprise my own string theory:
The world is made of souls and saints and visions to love dearly,
But while I give and receive hues from those I know and knew,
The symmetry of boldest shade is often strung to you.

It’s not something I can explain, nor do I know its source.
I know it thrills me day to day and keeps me on high course.
It keeps your image in my mind; your words in its recessess,
And every whisp and whim of you it in my mind impresses.

You encompass spans of space, though you are not near.
You exert a force on me when miles split our sphere.
I am charged electric at the thought that someday soon
A rendezvous of time yours-mine will rest us 'neath one moon.

As quantum strings have tension, much like regular strings of twine,
I feel it's fundamental to the strings' path, yours to mine.
String theory is in larval stage, unable to be tested,
Just as I believe that our best strings will have yet to be bested
!

.MGW.

OtolaryngologyWords

2006-03-18T08:52:00.000-08:00

From Impulse to Instrument: Cochlear Implants Come to Be

[beginning only!]

Modern cochlear implants were born in the 1950’s, but the first electrical experiments to improve hearing actually began over 200 years before that, in picturesque Como, Italy, when Count Alessandro Volta put 2 metal rods in his head and used his own invention, the electric battery, to pass a current between his ears. As electricity surged into his skull,Volta heard a noise like a “thick, boiling soup.” He was trying to understand the relationship between tissue and metals, and the electric current that was produced when they touched, and in doing so,Volta had shown that stimulating the auditory system with an electrical impulse could create perception of sound. Volta had done so, however, by stimulating the wrong part of the auditory system, the cochlea. Prior to 1950 in fact, all attempts to create hearing with current made this mistake; instead of bypassing the nonfunctional organ, they electrically stimulated the cochlea, or whatever was left of it, by acting on a few, remaining, intact cochlear hair cells.

In 1950, however, the French hit a nerve. While attempting to help a deaf man whose inner ear was riddled with tumors, French otolaryngologist Charles Eyriès teamed up with a biophysicist named André Djourno. Djourno had had extensive experience in stimulating nerves with metal wires, and Eyries was eager to try this kind of neural stimulation in the ear of his patient. During the operation, the two decided to implant a wire-wrapped iron rod under the skin and close to the remaining end of the deaf man’s acoustic nerve. They connected the rod to a circuit and the patient reported hearing sounds like "roulette wheels and crickets.” Together, the otolaryngologist and the biophysicist had proved a connection between neural, not cochlear, stimulation and perception of sound that would lay the framework for formation of modern implants. But Eyries and Djourno did not pursue implant research further. Instead, an otologist a continent away in California picked up where the French team left off.

In 1957, a patient rushed to the Los Angeles office of Dr. William House bearing a newspaper article that claimed a once totally deaf patient in France could now hear due to an electrical device— the device implanted by Dijourno and Eyries. House became interested in restoring hearing with electricty and after translating their paper from French to English, attempted to make similar mechanisms himself. He implanted them into three patients in 1961, but the devices worked only briefly before being hampered by technical barriers. The electronics of the process had eluded House. Also, the insulating material he had used to cover the metal in these makeshift implants was being rejected by the patient’s body. Neurophysiologists rejected House’s ideas, too; he was treading on their cochlear turf, which bread hostility, and they were also skeptical of his method since they thought electrical currents near the deafened cochlea would destroy remaining nerve tissue.

In 1969, however, the outlook for House’s work into hearing restoration improved. That year, an innovative engineer named Jack Urban became interested in the idea of cochlear implants, and he offered House help. As House explained in his memoir, My Perspective, each of these men brought important skills to the table: “My orientation was the selection of the patients and the surgical approach for implants,” House said, “and Jack applied his genius for electronics to the problems we faced.” They tried many different systems of stimulating the cochlea. Over time, though, House and Urban actually had most success with a method in which they put precisely the same signal into the electrode, rather than trying to sort sound by frequency before it reached that point. The electrode would do resolving and sifting of frequencies in sound, before presenting them to the acoustic nerve. In 1969, while fitting their deaf patients with models using this technique, House and Urban were excited to see that they responded, that they perceived the sensation of sound. They would walk out of House’s laboratory moments after surgery and point to objects—like birds—whose sounds they could actually hear. The otologist-engineer team had created the first successful, wearable cochlear implant. It used a single electrode and was designed mostly to aid lip-reading and House was adamant about Urban’s contribution to this milestone: “I firmly believe that without Jack, cochlear implants would have taken many more years to develop. Many of us owe him an unpayable debt of gratitude.”
But even though House’s patients were hearing, skepticism lingered. For those who had not actually seen the patients, the belief that cochlear implants had limited potential was common. Neurophysiologists, like Harvard’s prominent Nelson Kiang, felt that a single-electrode device could not really produce hearing, but only a kind of buzzing. “Dr. Kiang felt strongly,” House explained in his memoir, “that if an electric field was generated around the neural tissue in the inner ear, the nerve fibers would all fire, go into a refractory state, and then fire again repeatedly for as long as the stimulation lasted.” But those House had implanted proved otherwise; they had heard more than a buzzing caused by wires in the head. They’d heard something caused by the outside, like the sound made by the chirping birds, which only a functional implant could have permitted. With his patients’ stories to buoy him, House requested to present his preliminary anecdotal findings at a national meeting. “I was turned down on the basis that reporters would be [there],” House wrote, “and that their reports of the implant would cause otologists to have to contend with a flood of patients with unrealistic expectations.” Finally, however, in 1973, The American Otological Society’s Saint Louis meeting held a session on cochlear implants.

After that, the pace of progress quickened, mostly due to Australian researcher Graeme Clark. He sought to take implants, then single-electrode devices, to the next level and toyed with the idea of putting multiple electrodes inside. This move to more electrodes would provide more “notes” for deaf ears, and make their perception of sound closer to that of a normal person’s. Clark’s experiments were successful, and in 1978, a resident of Melbourne named Rod Saunders become the first person in the world to receive a multi-electrode cochlear implant...

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TransformationWords

2006-03-17T18:06:00.000-08:00

Getting More Bang for our Bite: Fast Transforming Strawberries Pave Way for Vitamin-Packed Fruit

The food pyramid is a guideline, not a lost monument in Egypt. But it
would seem so from the way people discount it, eating ridiculously low amounts of fruits and vegetables for example, especially in the West. Now, a superfast method of introducing DNA into strawberries could compensate for this by helping scientists to identify key genes, like those involved in antioxidiant production, so as to pack more nutrition into each berry, however few, that humans bite.

Strawberries, like all fruits, provide compounds that are essential to life. They are a major source of
phytochemicals, which reduce cancer risk, and they also happen to be an especially important source of vitamin C. Strawberries actually provide more of this vitamin than an orange would.

But even though strawberries pack a lot of nutritional punch, scientists say these fleshy, red fruits could be engineered to produce even more. That would be an important step towards improving human health since strawberries are widely consumed; in the list of the world’s economically important crops, their family—the Rosaceae family—ranks third.

Until now, however, though scientists have been able to engineer foods like corn and soybeans, they haven’t been able to touch the genome of the commercial strawberry. Its cumbersome size—8 sets of chromosomes— and lengthy life cycle have made this fruit more difficult to transform than others. Transformation, a process which introduces foreign DNA into a genome, must occur for scientists to identify genes and understand their functions. All previous attempts at transformation in strawberries have failed though. And since scientists can’t identify which strawberry genes do what, they surely haven’t been able to engineer them.

This month, however, molecular biologists at Virginia Polytechnic Institute in Blacksburg, Virginia, report the development of a method of transformation that’s both fast and thorough, transforming 95% of berries involved and doing it relatively quickly, in just 4 months. “This method introduces DNA into lots of strawberries extremely effciently so that we get a large crop of mutants,” said lead investigator Vladimir Shulaev.

Shulaev and his colleagues achieved this efficiency for two reasons. First, they used a simpler berry. All strawberries have 7 basic chromosomes in common and vary only in number of chromosome sets. While the commercial strawberry, Fragaria ananassa, has 8 sets, the species Shulaev selected, known as the Alpine strawberry, has only two. It also has a shorter reproductive cycle: 14 to 15 weeks. “The trick, which is new, was to find a variety of berry that could be easily transformed, “ said Janet Slovin, an expert on plant development at the United States Department of Agriculture. “Shulaev did that.”

His team also took painstaking steps to improve the transformation process, to yield as many mutant berries as quickly as possible, in other words. To guarantee rapid infection, they used a more aggressive strain of Agrobacterium, the cellular shuttle that introduces foreign DNA into the strawberry genome. They also ensured that very few non-transformed plants slipped through the selection process by using a fierce antibiotc known as hygromycin. In transforming any given species—whether a fruit, vegetable, or slug—the foreign DNA used often confers antiobiotic resistance. That way, selection for successful transformants simply boils down to which individuals surive in the presence of an antibiotic.

“This method’s efficiency is crucial for generating the large numbers of mutants we need to study the function of strawberry genes,” said Slovin, “and it’s a major step in developing a system that will allow scientists to identify commercially important genes, like those that convey health benefits.” Shulaev and his colleagues have paved the way for making a better berry.

Journal Reference: Planta DOI 10.1007/s000425-005-0170-3

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Wild2Words

2006-03-13T19:41:00.000-08:00

Our eyes have been on comets since Aristotle's time; he called them "stars with hair." And now, with the end of space probe Stardust's seven-year mission to Comet Wild 2, scientists are getting their first hands-on look at one of these ancient bodies.

I wrote a light piece on this for NPR's website. You can check it out here, if you like!

http://www.npr.org/templates/story/story.php?storyId=5260829

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FineTuningWords

2006-03-10T06:38:00.002-08:00

Fine-Tuning: Improving Music by Adding Pitch

On March 7th, the New York Times published a sunny review of cochlear implants. The article— Risks Fall, Hopes Rise for Hearing Implants— boasted decreased woes and rising effectiveness for cochlear implant users. Times’ science writer Nicholas Wade said that the story of cochlear implants in the past 20 years “has been an increasing, even surprising, success.” Reconfigured implant models have meant that far fewer patients are contracting meningitis, an infection previously prevalent in implant wearers. In fact, according to a study begun in September, 2002, only 1 out of 3,436 implanted children has had this infection. That’s because manufacters have redesigned implants with smarter seals that minimalize bacterial growth near the brain. Meanwhile, the devices are helping children as young as 1 to develop normal language by the time they are 3 or 4, something never before seen in profoundly deaf youth. Yet amid accolades for implants, those who use them, including 11,000 Americans under the age of 18, are not entirely content with their products. One complaint in particular still lingers: the wonders of Beethoven, Bach, and the Beatles elude implant users. This group can perceive many sounds, including speech, but they cannot clearly hear music.

Music is an especially rich form of sound. In general, sound is introduced into air by a vibrating object, like a guitar string, for example. The vibrating object disturbs the air, or any other medium through which it moves, causing the particles of that medium to move back and forth at a particular frequency. This frequency, when perceived by the brain, is called pitch. Like other sounds, music is composed of pitch, which might be compared to a note, and it is also composed of temporal information, the change in a pitch’s volume over time. Unlike speech, however, music appreciation relies more heavily on the former—on pitch. The range of pitches needed to convey musical sounds is far wider than the range needed to convey frequencies in the human voice. And it is this range that is so severely compromised in implant users, making their music listening experience less colorful.

To grasp what an implant patient might hear, try to imagine your favorite song played entirely with a single note, so that the song changes merely based on that note’s volume. Or, equally unpleasant, consider a song played with only eight notes, when it requires hundreds more. While people who hear normally can perceive pitches numbering into the thousands, people with implants are limited to little more than 20. Their “rainbow” of sound is reduced. It’s as if they were seeing portratis of sunsets painted in yellow and black when such natural wonders would normally require oranges and auburns, golds and yellows, and even hues of red, to be truly appreciated.

These scenarios are analagous to those faced by implant users, and they occur for one reason: people with these devices can only hear as many notes as they have electrodes. Electrodes are the means through which cochlear implants resolve frequencies from the air into information that the brain recognizes as sound. Each electrode—a wire capable of receiving electrical stimuli like that delivered by the speech processer— responds to a set of frequencies yet conveys only a single pitch to the brain. To date, the only way to increase the number of pitches that implants can convey is to increase the number of electrodes.

But unlike the microscopic hair cells that perform a simliar role in a functional ear, electrodes— which signal the hearing nerves and send sounds to the brain—cannot be present in infitnite numbers. Even the most advanced implant available today, Cochlear’s Nucleus Freedom 22, has but 22 of them. That’s because there isn’t much room within the the depths of the inner ear, where the electrode spray nestles, curled about the cochlea like wiry fingers, and any increase in electrode number would require reducing the space between these individual “fingers”. This reduction in space prevents electrodes from stimulating independent sets of nerves. If there are 25 nerves spread along a certain segment of the cochlea, for example, and only two electrodes, electrode 1 can stimulate nerves 1-10 while electrode 2 stimulates 11-20; the implant will register two clear notes. If 2 more electrodes are added however, so that there are 4 wires within the same small cochlear space, the nerve populations being stimulated by those electrodes will likely overlap: electrode 1 might stimulate nerves 1-10, 2 might stimulate 5-14, 3 would stimulate 11-20, and so on, in an overlapping sequence. Since the nerve sets are triggered by more than one signal, they are more frequently active, and so they must also recover from activation more often. This recovery period—known as refractory mode—is a time when nerves are less responsive to stimuli, muddling their ability to send sound to the brain.

A simple solution might seem to be to not use neighboring electrodes, but rather to use 1 and 3 instead of 1 and 2, for example, in hopes of hitting different nerve sets and generating two distinct pitches. However, this assumes that you know which nerves an electrode stimulates, and scientists do not yet know the electrode to nerve pattern.

Since increasing electrode number to improve hearing is not an option, then, implant recipients have had to rely on only 22 separate pitch perceptions to convey music. There are infinitely more than 22 notes in the spectrum of music. A piano, for example, has 88 keys, each representing a different note. And so the cochlear implant seem like a straitjacket; after hearing a sound, the device is forced to choose the pitch that comes closest to that sound’s actual pitch. With only 22 pitches to choose from, though, rarely do the chosen and actual pitches match.

Just when it would seem that electrodes would doom the lives of the deaf to a dim world of 22 notes, however, scientists are proving otherwise. Another way—not yet tried— exists to provide more pitch options, and Leslie Collins, an electrical engineer at Duke University, is being funded by both the NIH and implant manufacturer Cochlear Corporation to study this alternative. “It’s called fine-tuning,” she said, “and a lot of people don’t think it will work, but we do.”

Fine-tuning works not by increasing the number of electrodes, but rather, by increasing the number of available frequencies within each electrode. Right now, implants are designed to allow deaf people to hear speech, but fine tuning will manipulate the available electrodes in the existing versions so that the implants can respond to a broader range of frequencies—frequencies beyond those prominent in the human voice—allowing people to more clearly hear music.

That is not to say that cochlear implants perform a small feat by making 22 notes known to the brain. This process does permit language understanding, and it does so by stimulating electrodes in a fashion that mimicks the way the frequency of a pitch stimulates the cochlea. For each pitch that occurs, a different location within the cochlea resonates. Low pitches affect parts of the cochlea deep within the ear. High pitches stimulate parts father out. In an implant, this is analagous to specific pitches vibrating specific electrodes. Pitches vibrate certain electrodes based on work done by the speech processor, where all the software is located, which sifts through the frequencies that make up a sound and then stimulates electrodes accordingly.

But for each pitch that occurs, something else that effects hearing happens, too. In the hearing ear, not only is a certain location of the cochlea stimulated, but it is stimulated at a pulse, so many beats per second, corresponding to the frequencies in the pitch. This means that for normal listeners, stimulation is a function of both pulse and location. Implants do not take advantage of the method of pulse to affect sound, however. Instead, they use one common rate.

A few years ago, in 2002, biomedical engineer Fan-Gang Zeng at University of California at Irvine experimented with pulse. He used cochlear implants to define the relative contribution of location codes versus pulse codes in pitch perception. Because the two codes vary together as the frequency of sound varies, their relative contribution to pitch has been a topic of continuous debate for over 100 years. It still remains unsettled, however, and cochlear implants provide the perfect opportunity for understanding pitch components because, with them, location can be studied independently of pulse, and vice versa. That’s what Zeng did. He isolated pulse and tested its affect on pitch by changing the stimulus frequency—and using multiple frequencies— on a single electrode pair. He performed tests in people with implants and found that they could detect differences in pitch for frequencies up to roughly 300Hz. These results suggested that 300Hz is the upper boundary of the pulse code for pitch perception. Collins, inspired by Zeng’s initial look into fine-tuning, is investigating whether pulse rate can be added to gain even more benefit, so that ultimately, implant wearers will have more than 22 options.

“Electrodes offer people one pitch. Just one pitch per electrode.” Collins said, “But we want to offer them 2, 4, or even 8, or maybe more than that someday, all within one wire.”

Collins’ goal is to determine the optimal number of frequencies to add to a single electrode to improve music perception. “By designing each channel such that it provides multiple pitch sensations,” Collins said, “we will allow the implant to provide a more accurate pitch estimate. ” With a cochlear implant however, there’s never a guarantee that a frequency vibrating a certain electrode will register a certain note. “Even with rate there to help, you can never assume that kind of accuracy,” Collins said. Furthermore, even with pulse, today’s implant users can only discern frequencies of up to 300 Hz.

Applying pulse does increase pitch options though. “In one electrode, you get a different pitch out of the model for every rate used, up to about 500 pulses per second. You get fine-tuning.” At 50 pp, you may have a C, and then as you increase rate you will get some progression of notes. “You cannot claim you will get c# then d then d# etc,” said Collins “because you cannot necessarily tell 50 pps from 51 pps and so you cannot micromanage the process. There are some discrete rates that you can tell apart— maybe 50, 60, 70, 90, 110, 150 etc—and each of those rates on the same electrode will have a different pitch.” Changing pulses per second doesn’t change the location of the nerve that is stimulated by the electrode. Rather, the same set of nerves is stimulated but it fires at different rate. When it does so, the brain recognizes a new note, depending on pulse.

Collins and her colleagues are not physically working with implants, but with models, and so the frequencies they’re considering are not technically added to electrodes. Instead, they are processed in “channels,” electrical abstractions which exist within the acoustic models on computers in Duke’s labs. Collins’ models process speech in the same manner as a cochlear implant would. However, instead of stimulating the electrodes of an implant user, the speech sound bites processed by these models are presented acoustically to normal-hearing listeners, sitting in labs. “The research lives and dies by the people that are willing to sit here and listen and participate in these sometimes excruciatingly boring experiments,” Collins said. Those people assess quality of speech emering from the computers They assess sounds an implant might convey in a quiet environment, and those from a noisy environment.

In the typical model—one lacking pulse stimulus—one electrode might be selected to represent hundreds of frequencies. The lowest-frequency electrode, for example, might represent 250-350 Hz, and it would be stimulated in an identical manner, in terms of location and pulse, for any frequency within that range. It’s like a cell phone ringing the same ring every number dialing it beginning in “123”. Adding pulse is like adding a caller ID system, however; the phone rings differently for each incoming number, and the phone owner distinguishes these different sounds. When pulse is added, the “ring” changes. If a tone of 250 Hz occurrs, no longer is the pitch percept the same as it would be at 350Hz. Rather, 250 Hz would be associated with a lower pulse rate which would act to lower the pitch percept, “fine-tuning” the sound of the note. And if a tone of 350 Hz occurred, the pulse rate would be increased accordingly.

Collins used pulse models to test 3 levels of frequency tuning. She sought to determine the minimal amount of tuning necessary, or the minimum amount of frequencies to provide, to substantially improve hearing in implant patients.. Collins was surprised to discover that minimal tuning—just 2 frequencies per channel, compared to the standard of 1— was all that was necessary for normal-hearing subjects to notice significant improvement.

Tests are still on-going. Neither Collins nor Zeng have sold their ideas yet, nor have they been implemented in the marketplace. But Cochlear Corporation is funding both of their work, and its website boasts fine-tuning as one of its newest initiatives.

Collins admitted that the idea to focus her lab’s research specifically on improving music listening wasn’t her idea: “I have a couple of students who are extremely enthusiastic about applying this research into fine-tuning to music perception. They are essentially the driving force behind the music work – we had originally been continuing to work in speech but one student in particular is a musician and has an incredible drive to provide better music quality to implant subjects.”
She’s very excited about the implications—and some of the results gathered so far—of her research in fine-tuning, however. “I always tell a story about my Ph.D. research where I was testing out a hypothesis that if I changed the way people’s speech processors were tuned, that I could make them understand speech better. We had done a ton of experiments trying to get the basic data, then we had started to bring in the subjects to test their speech recognition based on what we had measured experimentally. We measured people’s speech recognition using their standard speech processing algorithm, then reprogrammed their speech processor based on the data and the hypothesis. I turned on the new processor for one of the subjects, and before I could even get one subject into the sound proof booth to measure his speech recognition, he turned to me and with this amazing light in his eyes said “Oh my gosh, this sounds so much better!” When we measured his ability to understand sentences, his recognition had gone up by something like 50%. I was basically hooked from that day forward.” Collins has been studying improving sound for implant patients ever since. “The most exciting thing for me,” she said, “is thinking that you might actually be able to help these folks understand speech and appreciate music just a little better.”

Meanwhile, Collins is aware that some patients could be receptive to this new technology, but others may not be. They’ve found variability between patients in their studies at Duke. “No one knows what it is based on,” she said. “My sense with implant subjects is that it is always variable – some do great already, and you can’t help them. Some do very poorly already, and you can’t help them. This is probably going to be the most effective for the middle of the road people, although it may improve the ‘quality’ of speech and music even for those that are already doing well. I guess we will just have to wait and see.”

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ThymusWords

2006-03-06T19:31:00.000-08:00

Two Thymuses Are Better Than One

By Meagan White
ScienceNOW Daily News
2 March 2006

Mice have a trick up their sleeve--or rather in their neck: a second thymus. The original thymus, nestled under the breastbone, churns out infection-fighting T cells. Now scientists have found that, at least in mice, this additional thymus has the same function. The finding raises the prospect of a confounding factor in immunological studies in mice, and perhaps humans.

In the early 1960s, Jacques Miller, the so-called "father of the thymus," noticed that when he removed the multilobed organ from mouse chests, the animals retained some of their immune functions. This suggested to him that mice had thymus tissue elsewhere in their bodies. Just a few years later, Lloyd Law and colleagues at the National Institutes of Health in Bethesda, Maryland, proved Miller right, finding an extra, single-lobed thymus concealed below cervical muscles in the lower necks of mice. No one bothered to see whether this extra thymus actually worked, however, because scientists believed it was too small to have any immune benefits.

Now, immunologist Hans-Reimer Rodewald and his colleagues at the University of Ulm in Germany, have discovered that in certain strains of mice, the second thymus is as good as the first. While studying immune disorders in BALB/c mice, a strain deficient in T cell production, the researchers stumbled across the cervical thymus. To prove that this structure was indeed an extra thymus, the team genetically modified the mice to express fluorescent molecules in thymus tissue. Sure enough, the spare thymus lit up.

But did it work? Rodewald's team decided to graft the spare thymus into immunodeficient mice. When the researchers inoculated the rodents with hepatitis B particles, the mice mounted the same type and strength of immune response seen in healthy animals. That means a second thymus organ could contribute to the health of a mouse in other experimental settings, such as after surgery that removes the thymus, the team reports online today in Science. And that may explain why, in some studies, researchers have continued to find T cells in mice, even after the thymus had been excised, says Rodewald.

Cervical thymus tissue has been observed in some humans as well, but scientists had assumed that this too had no function. Daniel Littman, immunologist at New York University School of Medicine, speculates that it might: "During cardiac surgery in children, the thymus is often removed, and yet there is no known detrimental effect on the immune system," he says. "This is obviously something that will need to be evaluated."

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WoolacombeWords

2006-03-06T19:07:00.000-08:00

"Live in the sunshine, swim the sea, drink the wild air..."
-Emerson

"They say the sea is cold,
but the sea contains
the hottest blood of all,
and the wildest, the most urgent."
-DH Lawrence

Woolacombe, England.

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HeartbeatWords

2006-03-01T19:14:00.000-08:00

~Beautiful Adversary~
2MDL

If it can beat me, I will win.
And that means you win, too.
It must beat us both and well
For me to dance with you.

It must faster push my pulse
Than it's been pushed before.
Must race me fast in evening dark;
My loss will make me sure.

And when it leaves me trembling-hot
Near wind-blown field or sea
I'll shudder-smile in moonlight rays;
I'll know it's meant to be.

Poise of one who speeds my heart
To paces beyond norm
Is soul I'll share my heart with now-
In thrill of heartbeat storm.

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CoalesceWords

2006-03-01T08:00:00.000-08:00

“After a certain high level of technical skill is achieved, science and art tend to coalesce in esthetics, plasticity, and form. The greatest scientists are always artists as well.” -- Albert E

I aspire.

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Twice as Good: Bilateral Implants for Adrean Mangiardi

2006-02-23T20:15:00.000-08:00

--Twice as Good: Bilateral Cochlear Implants for Adrean Mangiardi --

{caveat: not yet edited!}

The first device ever to replace a human sense received its stamp of approval in 1984. That year, cochlear implants were marketed as safe – as more than “experimental” – by the FDA. Today, the largest population of cochlear implant users found in one place congregates in Rochester, New York, at the world’s first and largest technological college for deaf students: The National Technolgical Institue for the Deaf.

This institute, better known as NTID, is home to over 11,000 deaf staff, students, and faculty, and of these, 180 can hear birds chirp better and footsteps advance faster than their deaf peers because they have chosen to get a cochlear implant. Now, three of these 180 implant users have taken yet another step; they’ve gone on to do something that’s practically unprecedented, even in the relatively young field of cochlear implants: they’ve gotten implant #2.

“Getting bilateral implants,” said Karen Black, director of communications at NTID, “is the newest of the new in cochlear implant technology.” This is impressive in a field whose modern history spans less than 25 years. True, a researcher named Volta put metal rods in his ears over 200 years ago, in 1790, but his attempts to stimulate hearing with electricity were not successful. And in 1961, when clinician William House performed the first modern implant surgery, much to the dismay of the neurophysiologists who wished he’d “keep [his] hands out of [their] cochlea,” scientists were skeptical. They doubted that the single electrode mechanism of an implant could cause anything beyond a buzz in the ear. As such, it wasn’t until about 20 years ago, with the FDA’s official accolade, that the cochlear implant was taken seriously by both the scientific and medical community. After this, research and advancements progressed rapidly.

But all study was directed at one effort: making sound perception and language acquisition better with a single implant. One implant for creatures with two ears. Great strides were indeed made; most notable was Graeme Clark’s 1985 invention of an implant that, unlike William House’s, used multiple electrodes. Clark’s was the first device in history that permitted even severely deaf people to understand speech. Previously, scientists had thought that providing quality speech understanding, even with the benefit of more than one electrode, was impossible since the inner ear requires 10-20,000 neurons to do so. Clark proved them wrong.

But amidst his and other advances, questions loomed in yet another place: the deaf population. To get an implant, or not to, many wondered. Getting even one was questionable, especially since benefits seemed variable from patient to patient. Today however, three students at NITD, including 25 year-old film major Adrean Mangiardi, have moved beyond wanting one implant and are happily sporting two. “My life is way better now,” Adrean says of his bilaterally-implanted days. He underwent a second surgery that was both painful and costly (implants are 40,000$ a piece). And I sought him out to learn why.

* * * * *

Adrean Mangiardi is technologically-savy. He studies film-making at Rochester Institute for Technology, supported by NITD, where he can maneuver video equipment with finesse. He also understands the in’s and out’s of the physics behind the bypass filters in his cochlear implants, in case he needs to troubleshoot. My interview with him – the self-proclaimed “brave man who’s desire to listen doesn’t stop [him], even though the idea of bilateral cochlear implants is fresh” -- was done via email, from my MAC to his.

The 25-year old Pennsylvania native, deaf since age __, got his first cochlear implant ten years ago, when he was 15. “Before I had the first one,” Adrean said, “I was losing my hearing each day. But I had a disgusted look on my face whenever I saw wire [from an implant] on somebody else’s body. I hated being deaf though and wished to be normal like everybody else.”

Adrean said that it was his mom who finally motivated him to go through with the first surgery. “One day she and I were driving to the mall and she started begging me to get the first implant,” he said. Adrean doesn’t recollect why; he had been able to communicate reasonably well with both of his hearing parents. He was actually surprised at his mother’s request. “I sighed and thought, why she would ask me that, knowing I didn’t want it?”

After the incident in the car though, he felt himself thinking about his mother’s words a lot more than usual. “From that moment on, I wondered what would it be like to wear the implant,” Adrean wrote. “I made a decision to go for it.” It is clear that his parents had a lot to do with this decison. “My parents know what’s best for me so I thank them for trying to help me out.” The second implant, however, which Adrean got just last year, was an idea that was completely his own.

“I noticed that wearing one cochlear implant was the standard way, but I’m not a standard guy,” Adrean said. “I seek rare possibility and make it happen for me.” He said his interest in film was one reason he decided to double up. “I cannot wait to work in the professional moviemaking business. Having bilateral implants will help me achieve my goal in filmmaking.”

Adrean also expressed that even though his single implant aided him greatly – letting him hear doors squeak and birds squawk as he’d never heard them before – he still had trouble localizing sound in large groups. He couldn’t pick out one voice amidst many, in other words, as he might need to do in a party situation, or in any large group scenario. “I wanted the second implant because I thought it could improve my life on a daily basis with my friends, too.”

His friends, in fact, were surprised by Adrean’s impulse. “One time, I was at a party at my friend’s apartment,” he recounted, “and I met a couple of girls who only wear one implant. I explained my plan of getting the second one and they were shocked.” When Adrean asked them what the “big deal” was if he only wanted to hear well, the girls explained that they wouldn’t want to go through that surgery again for anything.

“It was the surgery that scared them away,” he said. Adrean looked past it though. “I knew that it would be painful, but cochlear implant lasts forever, at least I hope, and I am the evidence that wearing two implants is a good way to improve your listening ability.” When he bumped into the skeptical girls a second time, outfitted with not one, but two implants, they asked him a billion questions about his new bilateral experience. “I think one day,” he said, “they will plan to get another one.”

But the road to bilateral victory wasn’t greased. There were other skeptics, besides Adrean’s friends, and there were uncertainties. Adrean’s physician didn’t actually know if the second implant – a $40,000 investment – would benefit they boy at all. “The doctor said that it might not help one bit or it might help a lot,” Adrean said. “But, what does he know? He’s not using it. He’s a doctor who can put things into our head and that’s it.” Adrean continued to express – in his written response – that with his second implant, and with some experience since the surgery, he is doing a lot better now than he had been when wearing just one. “Way better.”

There were mild side effects, however. After all, 2 implants is a lot of titanium and platinum for a brain accustomed to interacting with only bone. “I know that I didn’t get dizzy from the first implant,” he said, “but after I got the second one, I was dizzy for a few months because my inner balance was tampered with.” This dizziness is supposed to happen –a product of the ________ in the brain. But with Adrean’s second surgery, it lasted longer. “I didn’t know that the symptom would last that long,” Adrean said, “and I stumbled more than usual in the first few months after surgery and my eyes wouldn’t stay still when I tried to look at a something.” A year later, Adrean says that he is fine. The dizziness is gone and his vision is focused. “I’m very happy about that,” he confided. “I thought those problems would be permanent.”

And day to day, his life is richer. The biggest noticeable difference though, Adrean said, is not his ability to excel in filmmaking, or to distinguish a voice from across the room in a crowded party. “It is the birds. There a lot of noticeable differences now that I have two implants, but birds are one thing that I never heard before when I was a kid. Now, I hear them everywhere and it is so cool. I wish to film the life in a rain forest because there I will hear bird sound that I never heard before.”

Adrean also explained that though he’d been using his first implant for 10 years, and that had worked well enough, having a second one “gave me a boost to hear certain decibels, especially higher ones, that I couldn’t reach before.”

Oddly enough, there are ways in which having two implants, versus one, limits Adrean. “With one implant, I can wear a hat. I can’t with two because the hat would be pinching my head together. It’s not a good feeling.”

Regardless of any difficulty in donning a hat, Adrean says that the best way to explain the difference between having one implant and having two is that his life was fine before, “but now my life is improving everyday.” He’s especially happy with his ability to localize sound and no longer feels frustrated in large groups. He’s no longer overwhelmed by noise because he can now extract individual sounds better from it. He sees himself as a leader, too. “I hope that others will follow and understand the possibility of having a better chance of hearing things with two cochlear implants.”

I asked Adrean one last question: You’re surrounded by efforts to improve hearing at NTID, so what do you see as the next big break-through in hearing technology? His answer kindled my imagination. “I once had a dream that there would be a cochlear transplant,” he had typed. “There’s a liver transplant, a heart transplant, a kidney transplant, and so on. Why not a cochlear transplant, too? I seek for something natural as possible instead of something electric and artificial.”

There is nothing artificial about Adrean Mangiardi, or his drive to accomplish what he seeks. We may see his films. We may find him in rainforests. Either way, he will clearly hear – and be worthy of – our accolades.

.MGW.

ExcerptWords

2006-02-23T18:23:00.000-08:00

A lovely excerpt -- about runners and love -- from a Sharon Olds' poem:

They are like great runners:
they know they are alone
with the road surface, the cold, the wind,
the fit of their shoes,
their overall cardio-vascular health--
just factors,
like the partner in the bed,
and not the truth,
which is the
single body
alone in the universe
against its own best time.

.MGW.

VitalSignsWords

2006-02-22T21:07:00.000-08:00

"Vital Signs"

http://www.jhu.edu/~jhumag/0206web/wholly2.html#vitals

Appeared in Hopkins Magazine's February issue

.MGW.

Talpid2Words

2006-02-21T19:05:00.000-08:00

--Mutant Chickens Grow Teeth--

By Meagan White
ScienceNOW Daily News
21 February 2006

Warning: Mutant chickens may bite. Researchers have identified a genetic mutation that creates incipient teeth in bird embryos. The discovery provides a modern day glimpse of a feature that hasn't been seen in avians for millions of years.

Birds lost their choppers 70 million to 80 million years ago. That's what made an experiment in 1980 so surprising: After scientists grafted oral tissue from mice onto a chicken's gums, the birds grew round, mouselike teeth. But because avians and mammals are not closely related, scientists doubted whether the experiment proved that birds had truly retained a genetic vestige of their forbearers' bite.

Now a group of developmental biologists has found a strain of birds that don't need outside help to grow teeth. While investigating a gene mutation known to affect organ development in chickens, Matthew Harris of the Max Planck Institute in Tübingen, Germany, noticed sharp protrusions on the jaw of a 16-day-old embryo. Scientists had never suspected a connection between tooth formation and the gene--known as talpid2--because embryos with the mutation rarely survive past 12 days. Further investigation by Harris and colleague John Fallon at the University of Wisconsin, Madison, indicated that the teeth were conical and saber-shaped, resembling those of an alligator or crocodile.

To see how tooth formation in these chickens compares to that of other animals, the team looked at the expression pattern of a gene called sonic hedgehog (shh), which is essential for tooth production in vertebrates. In normal chicks, shh was expressed in a region analogous to the sides of the gums, but in alligators and talpid2 mutants, shh appeared in the center of the gums. The mutant version of talpid2 thus appears to turn shh on in the right place for growing teeth. Over time, changes in the gene may have disrupted this ability, resulting in tooth loss, the researchers report 21 February in Current Biology.

The finding is a great example of how altering the location of gene expression can cause changes in body types over time, says biologist Scott Gilbert of Swarthmore College near Philadelphia, Pennsylvania. "The real wow here," adds Paul Sharpe, a biochemist at the Department of Craniofacial Development at Kings College London, "is that these guys essentially show a glimpse of what the teeth probably looked like in the first birds."

.MGW.

BAHA.Words

2006-02-01T15:12:00.001-08:00

-- BAHA in Baltimore: How John Niparko Inserts a Bone-Anchored Hearing Aid --

“It’s not pretty,” Dr. John Niparko declared, smiling and plucking purple gloves from his fingers after a successful surgery. “There’s a lot more blood here when I do it than you would typically see in a BAHA procedure. But I get the job done.”

Niparko – famous worldwide for his cochlear implant work, including implantation of Heather Whitestone, America’s first deaf beauty queen – is head of the Listening Center at The Johns Hopkins Medical School. The Baltimore physician performs about 10 bone anchored hearing aid (BAHA) surgeries a year. And even though, as Niparko said, the BAHA procedure has been considered “simple enough to be pulled off in the office,” it is indeed complex.

This hidden complexity has left room for the reknown Hopkins surgeon to customize the way he approches insertion of bone anchored hearing aids. Niparko inserts them differently than most otolaryngologists across the nation, which has yielded him greater success, as measured by the fact that only 5% of his patients return for replacements.

“That’s a tremendously low rate,” said Steve Hazard, manager of CochlearTM, one of only three companies to make cochlear implants and other hearing devices. Hazard had come all the way from Colorado, Cochlear’s headquarters, to photograph the surgery in Baltimore the day that I observed. At each step of the way, Hazard took pictures of Niparko’s signature moves for a much-needed medical manual that his company will distribute to surgeons around the world.

“In a BAHA surgery, it all comes down to detail,” explained Dr. Marc Eisen, the young doctor who had worked alongside Niparko to perform his very first BAHA procedure the February morning that I visted the Hopkins Outpatient Center. “There is this feeling out there among other surgeons that the BAHA procedure is simple,” he continued. “This is because there are really no vital structures -- like facial nerves -- put at risk. Also, the steps sound simple: raise up the skin, thin the skin, drill a pilot hole, place the device, and place the thinned skin down over it. And in the short-term, these steps work well.”

Niparko doesn’t just think short-term, however. “What I learned working with him,” Eisen said, “is that for long-term success of a bone anchored hearing aid, three details matter: the size of the skin flap, its thinness, and the angle at which you place the part of the hearing aid that’s outside the head. These details are not well described in the BAHA literature.”

Bone anchored hearing aids work through bone conduction, one of two ways – the second being air – that sound is conducted to the inner ear. The cochlea, the part of the inner ear which receives the sound and converts it to the electrical signals that the brain can understand, is still functional in BAHA recipients, unlike in cochlear implant patients, for example. Therefore, the job of a BAHA is simply to get the sound to the cochlea, and it does so by enhancing the already naturally occurring transmission of sound to the bone.

Bone anchored hearing aids benefit people who cannot wear traditional air conduction hearing aids – placed in the outer ear – due to outer or middle ear deformities. People with microtia, a disease in which the outer ear is either severely deformed or entirely absent, as well as patients with chronic ear infections, inflammation, and astresia – the absence of the ear canal – are good candidates.

And as far as which hearing device – air or bone – improves hearing to a greater extent, “there is no clear cut winner,” Eisen said. However, the advantages of the BAHA are several-fold in the right situation. In cases of a patient with severe, unilateral deafness, for example, a conventional hearing aid offers little benefit, but the BAHA, explained Eisen, “seems to route the sound to the good ear, giving the patient some benefit of binaural (two-ear) hearing.”

Hearing via a bone anchored device involves a three-part system. A small box called a processor is attached to a screw that is drilled into the skull, behind the ear. The screw attaches to the third part of the hearing aid, a titanium implant. Both the implant and the screw must be inserted surgically, as I watched Niparko and Eisen do. And while the implant is lodged below the skin flap, the screw – meant to stay completely in the bone – is drilled into the skull afterwards. At 3 or 4 millimeters deep, the screw is not at risk of penetrating to the other side of the bone or piercing the dura, the fibrous coat which protects the brain. “This would be a sure route for meningitis,” Eisen explained.

Over time – about three months after the surgery – the titanium implant naturally integrates with the skull bone in a special process known as osseointegration. During this process, the implant bonds with the surrounding bone tissue, making a direct structural and functional connection. This lets vibrations from the sound processor be transmitted via the bone to the cochlea, on the other skull’s other side. The long term success of Baha rehabilitation is based on titanium’s unique ability to integrate with tissue and on the fact that an active bond between tissue and implant is created at the molecular level, such that the implant is not only accepted but also incorporated within the bone.

After successful osseointegration, the final part, the sound processor is attached to the screw. At this point, sound vibrations can be picked up from the air and travel through the screw to the implant, which vibrates. This initiates vibrations within the skull and inner ear, and these vibrations stimulate the nerve fibers of the cochlea directly, allowing hearing.

Patients who receive BAHAS are typically happy. Few of them, studies site, prefer their old hearing aids, and the majority report increased comfort and function. This wasn’t always the case for bone conduction hearing aids, however; “If you simply saw the old ones,” Eisen explained, “you would immediately have your answer as to why people found them uncomfortable. They weren’t implants, but headbands that held the hearing aid tightly against the skull someplace. They were also cumbersome and noticeable.”

Unlike the old bone conduction hearing aids, BAHAs do require surgery, but it is typically a short, minimally invasive procedure, lasting not much more than 30 minutes. As I observed in February though, Niparko takes his time, performing a BAHA in an hour, from start to finish.

“This process should take about 15 minutes – in and out,” joked a young resident in the operating room as he pulled on his face mask moments before the surgery. But he was wrong; Niparko – a tall, lean man with a careful eye – takes longer than average, and this is just one aspect of his BAHA surgery strategy that strays from the norm.

For starters, the size of skin flap made at the initial incision is larger -- that of an orange versus a ping pong ball – when Niparko is at the helm. “I don’t mind taking time to make the larger cut,” Niparko explained to Hazard, as the man watched, and took shot after shot.

Incision size is crucial; sufficient subcutaneous tissue – or fat – needs to be removed from under and around the skin flaps so that once the screw is drilled into the skull, it is less likely to be disrupted by creeping tissue. This tissue, though only millimeters in thickness, often grows back and pushes the screw out of line.

On the day of the surgery, Niparko spent calculated time using a pick to pull thin lumps of yellow, fatty tissue from under perimeter skin flaps of his large incision. After pulling an especially wide tissue lump from the patient’s head, Niparko plucked a ruler from the pocket of his green standard-issued Hopkins scrubs: “4 inches!” he said, commenting on its diameter. The tissue was so large that when the nurse dropped it in on a steel table nearby, it made a thud loud enough for me – on the other side of the room – to clearly hear.

Beyond incision size, the second detail Niparko focuses on is the angle of processor attachment. “I’ve never heard a better insight into the success of this surgery,” Hazard commented, after hearing Niparko explain his emphasis on a drilling the screw, perfectly straight, into the skull to avoid complications with the processor. Apparently, it does not function as well when it touches skin – when it’s angled up or down because of bad screw alignment, in other words. That’s because if the processor touches flesh, its vibrations are dampened, making the transfer of those vibrations – from processor to screw to implant – less efficient. “Remember,” Eisen reminded me later, “it is all about physics. No electrical stimulation like a cochlear implant.”

Eisen explained that surgeons do not use a device to measure the angle at which they enter the skull. “We just have our line of sight to guide us. This is why it’s important for the surgeon to anchor his arms.” As Eisen drilled the screw 4 millimeters deep into patient’s skull that day, Niparko loomed over him and lectured on angles. “Don’t let it be anything but 90 degrees,” he said. Meanwhile, Hazard watched closely, seemingly amazed at what I found to be a simple idea.

Niparko then did something which captivated all in the room. To determine how well the screw was affixed to the skull, he bent low to the patient’s head and hit the screw with a small metal pole. He listened carefully to the pitch generated. “A sharper ring should mean more solid fixation,” Eisen later explained. Niparko was dissatisfied with the high pitched ring that chirped quickly in the silent room, and he instructed Eisen to turn the screw again. To make it tighter.

Then Niparko tapped, listened, and -- still dissatisfied -- asked Eisen for yet another twist of the screw. After the final turn of screw into skull, Niparko was happy with the high pitch ting generated from careful insertion.

“Niparko’s strategy is great,” Hazard said. “Especially because he cuts a large flap when making the incision. Larger than most and large enough so that the tissue around the BAHA implant doesn’t become an issue and push the implant out of line. This takes more time and most surgeons won’t do it. They cut small flaps. Or they do a dermatrome. But Niparko doesn’t care. He’s takes his time and makes a big cut.”

By paying attention to tissue removal and drilling angle, then, Niparko has customized the BAHA surgery. His signature moves have yielded him success about which the world will hear with the coming of Hazard’s manual. Surely, Niparko’s patients will hear of it, too.

.MGW.

SIDS.Words

2006-01-31T10:21:00.000-08:00

--Common cardiac gene linked to sudden infant death in African Americans--

(Shorter version appearing on ScienceNOW, Wednesday, February 1)

Infants with 2 copies of a common variant in a gene associated with irregular heartbeat are 24 times more likely to experience sudden death, a new study shows.

The variant, considered common because it is present in over 10% of African Americans, does not cause sudden infant death syndrome (SIDS) on its own, nor is it a problem when present in one copy. However, a double dose of the defect seems to make infants more vulnerable to environmental stresses that are typically associated with SIDS and that healthy children can easily tolerate.

"The common polymorphism alone does not cause SIDS," said Steven Goldstein, M.D., Ph.D., professor and chairman of pediatrics at the University of Chicago and director of the study. "Our findings suggest, however, that it renders infants vulnerable to environmental challenges -- such as a long pause in respiration -- that are tolerated by children without the mutation."

"The hope," he added, "is that findings like this may one day allow us to intervene. We might screen to identify children at high risk and teach parents how to lessen the likelihood of secondary challenges. We have already begun to evaluate drugs that may mitigate the risk."

SIDS is the sudden and unexpected death of a child with no detectable lethal disorder. It is the leading cause of infant mortality in the United States among infants between one month and one year of age. While research suggests that environmental factors – like sleeping on the stomach or exposure to second-hand smoke – are partly to blame, the fact that African Americans are three times more likely than Caucasians, and six times more likely than Hispanics or Asians to experience sudden death, suggests an important role for genetics, too.

Particular genetic variation tends to run in ethnic groups. Yet no previous work has specifcally examined a group of African American SIDS victims to understand how genetic variation might contribute to SIDS in this cohort. “That’s what is different about this study,” said Alfred George, M.D., chief of the Division of Genetic Medicine at Vanderbilt University School of Medicine.

Goldstein and colleagues at the University of Chicago studied genes in the heart tissue of 133 African American infants diagnosed, after autopsy, with SIDS. Goldstein’s search focused on abnormalities in one gene in particular: SCN5A, which codes for a sodium ion channel in the heart and in which rare SIDS-related mutations had previously been found. His team indentified genetic variants in SCN5A, observing that one variant in particular, Y1103, was 24 times more frequent in two alleles in SIDS victims than it was in healthy individuals. Goldstein had no idea how a double dose of Y1103 increased risk of SIDS, however, since it did not appear to hinder ion channel operation – or interrupt heartbeat -- under normal conditions.

SIDS is not purely genetic, though, and Goldstein decided to consider environmental triggers, too. It is known that sudden death occurs in settings of interrupted breathing, common in infants who sleep on their stomachs. Interrupted breathing deprives cells of oxygen and causes a slight increase in acid levels in the blood.

Goldstein simulated this acidic environment in culture, and then compared cells with the Y1103 mutation against normal cells. The cells with the abnormal channels misbehaved in acidic conditions; they could not regulate sodium ion levels, a difficulty which leads to changes known to increase the risk for abnormal heart rhythms and sudden death. The Chicago team speculates online February in the Journal of Clinical Investigation that, in the setting of impaired breathing, SIDS occurs more readily when an individual carries two copies of Y1103.

“This study doesn’t imply that Y1103 is the only genetic factor in SIDS,” George explained. “However, it supports the idea that genetic variation coupled with a specific environmental stressor, like acidosis, may trigger sudden death. The study emphasizes the need to determine the true incidence of genetic causes of sudden death in infants. Once that’s done, a decision can be made as to the rationale and cost effectiveness of general population screening for these genetic factors.”

According to Debra E. Weese-Mayer, M.D, professor of pediatrics at Rush University's Center for SIDS Research in Chicago, “the study is a major step forward in terms of the sophisticated kind of analsyis that should be expected as additional cardiac rhythm genes are considered in SIDS.”

.MGW.

NewSiteWords

2006-01-22T17:36:00.000-08:00

A new site has been made! It contains links to the articles I publish at Science Magazine's website.

If interested, you can also type the following into your browser!

http://www.kalin-bg.com/meagan-white/

.MGW.

CD8+T-cellWords

2006-01-15T17:06:00.000-08:00

-- Mouse study suggests a risk of serious side effects with peptide
vaccines --

(To be published on ScienceNOW, "Science" magazine's website, on Thursday, January 19th)

T-cells – crucial players in the body's defense against viruses -- have good memories, but that could mean bad luck for vaccine recipients. According to a new study, vaccinating mice with peptides that mimic viruses to which the mice have already been exposed can be harmful. That’s because peptides trick the mouse’s T cells into making toxic antiviral compounds that – when present in large numbers – not only kill viruses, but also cause host symptome ranging from mild harm to death. These negative effects, say researchers at The Scripps Research Institute, are due to activation of too many T cells at one time. The study has implications for improving design of peptide vaccines for humans.

Peptide vaccines are new members in today’s arsenal of vaccination tools. The peptides – or proteins -- used in these vaccines bolster the immune system because they are identical to short sequences of virus proteins called epitopes. T cells learn to recognize epitopes, in different viruses, so that when next exposed to them, the T cells activate, attacking the epitopes and preventing infection in the host. Epitope injection in peptide vaccines also poses a risk, however; unlike DNA-based vaccines, for example, where proteins have to be processed before epitopes are in the proper form to activate T cells, peptide vaccines can activate T cells immediately. In naïve mice – those not previously exposed to a certain virus – immediate activation is necessary to prevent infection. But what happens if a recipient of a peptide vaccine already has a large number of T cells specific for the viral epitope being injected? That would make for quite a lot of T’s, both the old epitope-specific ones and the newly recruited ones, responding to peptide injection. And while tons of T cells tackling the trouble sounds like it would be beneficial, it’s not.

Researchers at Scripps Research Institute have determined how particular T cells, known as CD8+ cells, respond to peptide vaccines. At the Department of Neuropharmacology, J. Lindsay Whitton and colleagues, whose results will be published next month in The Journal of Clinical Investigation, infected mice with lymphocytic choriomeningitis virus, or LCMV. Eight days later, Whitton vaccinated these mice either with a peptide representing the LCMV epitope, or with saline alone. The saline-injected mice displayed no negative side effects, but the peptide-injected mice developed several shocklike symptoms, including hypothermia, and died within 24 hours of injection. (Whitton and his colleagues identified TNF – tumor necrosis factor – as the molecule responsible for the temperature drop and the lethal effects in these mice. The TNF, they discovered, was produced by the CD8+ T cells in response to the LCMV peptide.) Thus, peptide injection in a naive individual does not activate large numbers of T cells, since the T cells present have not yet seen the virus, nor had a chance to congregate in epitope-specific pools. However, this same peptide injection activats numerous T cells – thereby harming the host -- in an individual who has been previously exposed to the virus. Whitton was careful to explain that “this study is a cautionary flag for peptide vaccines, and not an indication to abandon ship.”

Matthias von Herrath, head of the Immune Regulation Lab at La Jolla’s Institute for Allergy and Immunology agrees, saying that peptide vaccines are useful, “as long as we ensure that they cannot cause synchronous activation of pre-existing T cells.”

Mark Larche, Ph. D. and Senior Research Fellow at the Imperial College of London’s Department of Clinical Immunology, also corroborates on the potential for peptide vaccines. He attributes their negative side effects to dosage issues. “The message of this study is that yes, you will have problems with the wrong -- too high -- dose of peptides, but that does not mean peptides will not be good vaccine components. Peptide vaccines offer the ultimate in specificity. It’s just that great attention must be paid to defining doses so as not to cause activation of huge numbers of T cells.”

Larche has done work similar to Whitton’s in asthma patients, administering synthetic peptides that elicit T cell responses. “We have spent a lot of time working out the dose relationships,” he explained, “and you can avoid negative side effects with peptide vaccines while still achieving immunological tolerance, by delivering low doses. The correct dose-finding studies in humans should make this effect less of an issue. Essentially, you want to induce an immune response with these vaccines, but you don't want to induce a response so great that the antiviral effects, like TNF, end up killing the subject. Everything in moderation...just like everything else in life.”

.MGW.

UpdateWords

2006-01-12T12:56:00.000-08:00

Hark! A blog update?!

Great Scott... nearly a month has passed since the last.

And an update is most assuredly due. Yes-- this is true. (Thank you to those who've acknowledged. I appreciate your interest!)

I admit I've been remiss in updating my blog. But it's not been bare of new beef for no reason. Nooo. Rather, I've not been writing science here because I've been thinking science, elsewhere, for this semester. (Although... you can look for an article at the end of next week on a new mouse study, done at Scripps Research Institute, that suggests risk of serious side effects associated with peptide vaccines. MmmmmT cells.)

But, I've not been blogging science for the past month because I'm:

1) reading lots of it.

I'm preparing to do my Master's thesis this semester, and that will entail some good background work. Some interviews at the Medical School. Some serious time with the books. *Topic to be disclosed at a later date!

2) Teaching an interdisciplinary intersession course at Hopkins: "Digital Storytelling: Narrating your Personal History."

This course requires students to write narratives -- which will be turned into documentaries -- about influential familiy members. I am working with the students to develop narratives that convey a theme, or a point, if you will, for a broader audience. Narratives that leave the reader with a better understanding of some difficult life tenet.

The digital media department is working with the students, too. The science writing link? I will learn the art of podcastin'. And as a communicator of science, any new means of media that I can grasp especially well will position me better.

Bring on the podcasts!

* * *

This semester, I'll be interning at NPR in DC, working with Anna Vigran at Science Desk. Radio broadcast. Another form of communication.

My blog should still be changing though; I'll be taking psychopharmacology and Rise of Modern Science here at Hopkins, both of which will provide good fodder for my inquiring mind. For articles!

I'll also intern with David Grimm, writing 350-400 word pieces for Science Magazine's online site, ScienceNOW. These should come out bi-monthly. And be onnnnn the blog.

Lastly, thesis work will give me lots to think about~ to write! And really truly, I aspire to just research & write science as it strikes me -- the science of everything around me.

Thank you again, for stopping to glimpse. Happy 2006! May biology, physics...chemistry, nanotechnology... space and the sea!... stars, vessels, and memes... provide us with new excitement -- new discovery -- each and every day.

Best,

MGW

HopkinsMagWords

2005-12-07T13:36:00.000-08:00

This is yet another version - incorporating outside sources now - of the piece I'd done on Dr. David Ryugo and his work with cochlear implants at the Med School. Hopkins Magazine asked me to write this for their February issue. So... here it is! Ryugo once more:

*side note: I had wanted to call this piece, "The Sound in the Furry: Cochlear Implants Preserve Auditory Nerve Structure in Deaf Cats"... but I'm not so sure what Faulkner would think. wink, wink.*

--Cochlear Implants Restore Auditory Nerve in Deaf Cats--

Some children born deaf may never hear again, but not if David Ryugo’s cats have anything to do with it. With the help of a rare collection of deaf felines, he and fellow scientists at the Johns Hopkins Center for Hearing and Balance have discovered why medicine’s most advanced hearing restoration devices – cochlear implants – benefit only 80% of the deaf children who have them.

Ryugo, a Ph.D. and professor of otolaryngology at Hopkins Medical School, used cochlear implants to electrically stimulate the nerves responsible for hearing in young, deaf cats. He did this over a three month period, and his results, published in Science on December 2nd, point to a link between introduced nerve activity, and the structure – abnormal or not – of the auditory nerve ending. Moreover, his work explains something that scientists haven’t understood for the last 4 decades: how cochlear implants actually work. “It has just been assumed that the auditory system functions normally when an implant is inserted,” Ryugo explained. “The reasoning has been something like this: if a car runs out of gas, it stops. Put gas in, and the car runs again.”

His work has filled in the gaps, though, illustrating exactly how the “gas” – or cochlear implants – jumpstart the hearing process. In his cats, all of which regained hearing after electrical stimulation, cochlear implants functioned for one reason: they preserved the normal structure at the end of the auditory nerve. Nerve endings permit communication between neurons in the auditory pathway and must be intact to send sound, as electrical waves, to the brain. When intact, they exhibit distinct structural characteristics which allow for the release and capture of chemicals called neurotransmitters. This process – occurring at the end of a healthy auditory nerve - permits sound to reach the brain. In other words, it permits hearing.

In a deaf ear, nerve endings are abnormal; they cannot convert sound vibrations into the electrical impulses that hit the auditory nerve, causing the brain to register sound. Like the deaf cats in Ryugo’s study, deaf children have inner ear damage which prevents them from generating electrical signals. Thus, as has been assumed, the cochlear implant generates them instead.

Now though, Ryugo’s research suggests that in this process, implants do one more thing: they preserve the auditory nerve ending. Nerve endings exhibit a certain plasticity, and as such, Ryugo says that implants are capable of preserving their structure (and thereby restoring hearing), if and only if they are inserted in a timely fashion-- before the nerve ending withers away.

Before evaluating the nerve endings of his deaf cats, inserted with implants, Ryugo made sure that they could hear. “The cats exhibited certain behavior responses that alerted us to the fact that they were responding to sounds in their environment,” Ryugo said. He had trained each implanted cat that a particular sound -- a rhythmic cadence, finger-snapping, or hand clap, for example -- signaled a special food treat. Different sounds signaled different treats (tuna, roast beef, sardines) to the different cats, he explained, “and voila! They would come to these sounds the same way a hearing cat comes when you shake its food box. We knew they could hear.”

Graduate student Erika Kretzmer compared nerve tissue from the inner ears of three groups: deaf cats with implants, deaf cats without them, and normal hearing cats. She discovered that deaf cats that had received cochlear implant stimulation actually maintained the nerve connections critical to hearing. “There wasn’t a significant difference between nerve endings of normal hearing cats and implanted cats,” Ryugo said.

In the deaf cats without implants, however, nerve connections were withered. “Their nerve endings were disrupted,” explained Ryugo. Instead of being characteristically branched and elaborate, “they were stubby and truncated, like trees growing on the edge of a windy cliff.” This image also describes nerve structure in deaf children.

For many reasons – including an appreciation of Deaf culture - not every parent of a deaf child considers cochlear implantation. But for those who do, understanding the trade-off between waiting and acting is important. Each year, 3 out of 1000 children in the United States are born unable to hear. The success of implantation in any of these children, Ryugo says, depends upon the progression of abnormalities at the auditory nerve ending. If children born deaf are left untreated for too long, the ends of their nerves may start to wither. (Ryugo observed this in his cats.) Eventually, this withering abnormality may become irreversible, meaning that implants will be powerless to preserve the normal nerve ending.

By illustrating how cochlear implants impact physical abnormalities in cats, Ryugo’s research is helping to define the “window of opportunity” for cochlear implantation in humans, who probably benefit in the same way; the auditory systems of both species are nearly identical, and “the cochlear implants used to stimulate our cats were the same technology that was developed for deaf children,” Ryugo said,”only smaller.” Ultimately, this work will give insight to doctors debating how long they can wait to perform risky implant surgery.

"There is an optimal time window for inserting implants,” Ryugo said. Doctors are sometimes hesitant to do it at young stages, though, because once implants are inserted, a patient loses all changes of regaining hearing on their own. Futhermore, “it is always difficult to know the age at which a child is strong enough to endure the surgical process,” Ryugo explained. “But what we think this study tells parents of deaf children is that if cochlear implants are being considered, the earlier they're done, the better.”

The study provides more evidence to support the current recommendation of many hearing specialists that cochlear implants be installed by age 2. “In Europe,” Ryugo said, “they’re even putting implants in kids at 12 months now.” The chairman of the Neurobiology and Anatomy department t the University of Utah School of Medicine, Thomas Parks, confirms the significance of Ryugo’s work as a call for advanced implantation. “This study provides additional strong evidence that early intervention with cochlear implants in children is essential. It prevents deterioration of neuronal circuits that are thought to be vital for both normal speech perception and sound localization, perhaps the two most serious problems for youth with severe hearing loss.”

According to Dr. Robert Shepherd, director of The Bionic Ear Institute in Melbourne, Australia, “the work of Dr. Ryugo and his colleagues is very significant because it shows for the first time, that when neural activity is re-introduced to the auditory nerve via a cochlear implant, changes at nerve ending structures vital to the auditory pathway can be at least partially reversed.” Ryugo’s work has important implications for understanding neural function in the pathological sense, and, as Shepherd explained, “it also suggests that the central auditory pathway is capable of plastic change after an implant’s in there.”

Shepherd, who is familiar with Ryugo’s work, recalled earlier studies in which the Hopkins otolaryngologist showed that nerve ending structures undergo change following deafness. “It was hypothesized that these changes were a result of a lack of neural activity in the deafened auditory nerve,” Shepherd said, “and this new work supports that hypothesis, too.”

Ryugo’s research is also interesting because, until now, there’s never been a good group of animal models to use for studying the effects of cochlear implants in the deaf. “We’re the only ones in the country with a colony of congenitally deaf cats,” Ryugo explained. The cochlear implants were unique, too; Advanced Bionics specially miniaturized the implants just for his study.

In the future, Ryugo wants to further define the “window of opportunity” for cochlear implantation by using his cats to perform time-course studies which will elucidate specific stages of development in the auditory nerve ending. “This could help doctors really pinpoint how much leeway they have, when thinking about surgery in children,” he said. Already, though, his work has sounded a call which is resonating – loud and true -- among hearing specialists worldwide: when it comes to implants in deaf children, the younger the better. And though until today, the window of opportunity for cochlear implantation has been unknown, and as such, closed for some 20% of deaf children, Ryugo’s work ensures that someday, physicians armed with knowledge of the auditory nerve ending will never again have to shut this window on deaf ears.

.MGW.

SiblingDonorWords

2005-12-07T04:09:00.000-08:00

A (science) book recommendation -

For the writing course I teach, I based the third essay assignment on Jodi Picoult's novel, My Sister's Keeper.

It's been a big hit. The students love it. Librarians are lauding it, including the science librarians here at JHU.

Here's what Picoult says about what inspired her book, which illustrates struggles of life in a family where one child has been cloned - as a spare parts donor - for another:

"Today's political and scientific battles over cloning and DNA and gene replacement therapy led me to think about some of what the future might hold, on a personal level, for people —and thus the story of Anna and Kate was born. In a way, I think of this book as Sophie's Choice for the new millennium. If you use one of your children to save the life of another, are you being a good mother… or a very bad one?"

A good winter read.

.MGW.

FierceGraceWords

2005-12-04T19:20:00.000-08:00

Someone told me I remind them of this photo:

"Fierce Grace" -- by Tony Stromberg

How cool... I love!

Because it reminds me of a poem I wrote(below);
Because it reminds me of what I want to be.....

~Primitive Elegant~

Primitive-elegant.
Exists such a glow?
One wild as wolf tracks,
One gentle as snow…

Can the same swift steps that race ‘neath the moon
Waltz, graceful-light, to the violin’s tune?
Does snow-pearl skin, unaccustomed to earth
Blaze like skin bronzed after riverside mirth?

And how do they join,
Fair-mannered & fierce?
Can such distinct spirits
Share one gorgeous sphere?...

So that when coalesced,
They’d sing songs of merge,
With lines painting Venice,
but still praising birds.

On pine-lined paths I forge crystal dreams;
My pulse pushes fast at silk-sand-woven seams.
I’ll race you, bear-lightning.
I’ll pace you, harp-song.
Primitve elegant?
It’s here lived,
all along.

.MGW.

PotentialThesisWords

2005-12-04T15:27:00.000-08:00

The Science Writing Thesis begins next semester.... 40 pages of beautiful science.

I'm not sure what I want to write about yet -- and I don't have to be -- but here are some ideas I'm toying with... in the form of an un-edited, unsolicited proposal that I'd submitted to my advisor, Ann Finkbeiner.

Feel free to take a peek! Again, all ramblings and ideas, at this point.

In general, I’m very interested in topics that are highly integrative… between science and law for example, or science and business. I realize that with thorough research and exploration, any topic (ie: Thesis Idea #1, below) becomes integrative.

However, I did think it might be gangbusters to pursue a thesis (ie: Thesis Idea #2, also below) that was integrative and controversial right from the get-go.

So I have two ideas. The first one – work with Dr. Ryugo, otolaryngologist at Hopkins Med School - is straightforward:

--Thesis Idea #1--
I’m looking into three new angles of his research with cochlear implants. Ryugo’s excited:

(1) embedding cochlear implants with chemicals. The "Big Pharma"/ biotech connection. Steroids, growth factors, etc.

(2) bilateral cochlear implants, and how they could be used to help better decipher sounds from within "noisy" backgrounds. “Anyone can pick an airhorn out of a gymnasium? We want to know how the brain tones down all the extra crap and picks a piccolo out of a symphony,” Ryugo said. This entails position, location, and spectrum analysis of sound. Refining hearing with 2, versus 1, implant.

This becomes relevant in cases where deaf people in rooms with overwhelming background noise become depressed because they cannot distinguish sounds. Ryugo wants to make cochlear implants more “brain-like,” so that they can do this, and distinguish sound signals on a more refined level.

(3) developmental stages of the endbulb. If Ryugo can track these – if he can define them in humans – they’ll know exactly how long physicians can wait to insert implants in children, and still see a benefit. It’s been done in rats, mice, and cats already…

Of a thesis based on his work, Ryugo said: “The 3 topics would all be interesting--each would require a broad introduction to your topic involving themes such as (1) neurotrophic and growth factors as well as steriods; (2) the idea of auditory streams, signal extraction from noise, and sound localization; (3) development, deafness, and animal models.”

--Thesis Idea #2--
Intersection of Science and Law:
Faulty science in courtroom presentation of science-based medical evidence & expertise.

I have a Gettysburg College connection here – a forensics investigator, biology major, and Gburg grad (1972) named Linda Jankowski, now working as the head of The Central Laboratory of the New Jersey State Police Forensic Science Bureau in Trenton.

Issues/Concerns
+ Difficulty qualifing “expert” scientific witnesses
+ Divergence between legal uses and interpretations of science-based medical evidence and the uses and interpretation of that evidence by

a) the medical and health care researchers who produce it.
b) the practitioners and health plans that use it in making clinical decisions and policies.

Background:
The courts have long had difficulty knowing how to deal with scientific evidence, because judges (and lawyers) are not trained to evaluate its validity. That has led to some cases where verdicts have been reached that are considered by the scientific community to be based on faulty science.
So the Supreme Court (and other courts) have tried to establish standards for determining when scientific evidence is admissible. The Supreme Court has heard at least two cases on the issue that try to come up with approaches to improve the quality of evidence admitted as scientific. The consensus remains though: scientists don’t see the problem is solved.

One case of interest: the Woodward case. It’s famous because doctors testified to entirely different conclusions about the meaning of the medical evidence involved. The AMA, out of embarrassment, convened some sort of panel to try to determine how that could happen. Looking into this…

And there are many examples of problematic cases: cases where juries accepted the idea that a person's cancer was caused by things that the scientific community doesn't believe cause cancer, cases where forensic evidence was admitted that the scientific community would consider unreliable (including eyewitness testimony, fiber and hair analysis, some kinds of fingerprints evidence, silicon breasts, etc.), and so forth.

I have to choose an area to concentrate on, some sort of scientific evidence that I’m particularly interested in. At first, though, as Michele Cotton advised, I’d need to get a sample of what’s out there.

So far, I’ve talked to two sources about this idea, which is in its egg stages. And Jankowski would be a third. Here I could have the beginnings of a Hopkins angle (Ryugo), a legal angle (Michele Cotton), and a lab angle (Linda Jankowski).

1) David Ryugo – yes, the cochlear implant chap! – said that he’d be glad to discuss this topic with me and that “it is potentially treacherous (wooohoooo! Get out the bullshit detector!) because there are ‘professional’ medical witnesses who claim to be experts and sell their expertise to law firms. It is a very lucrative past time and Hopkins docs are restricted in how much they can do.”

I would be interested – as one angle of this work - in talking to the “Hopkins docs” to learn about what evidence they feel justifies their practice and treatment decisions. And how this has changed over time.

2) Michele Cotton, formerly a poverty lawyer in NY. Left Harvard Expository Writing Program last year to teach here at Hopkins, where she is now.

3) Linda Jankowski, heads the DNA lab for the New Jersey State Police. Recently (last spring) profiled in the Gburg Alumni Magazine for a case in which the New Jersey state prosecutor had a problem: two different suspects in two separate rape cases were about to go to trial, and yet the modus operandi of both appeared to be the same. There was question as to whether only one of the suspects had committed the two crimes, and whether one defendant was innocent.

Jankowski headed this investigation. Undoubtedly, both suspects could have gone to trial (but they didn’t, based on her analysis of the evidence). Also, if the victims had identified the suspects, they most likely would have been found guilty and sent to prison. But with DNA testing in Jankowski’s lab, a different scenario unfolded...
The prosecutor asked for a DNA analysis. The evidence established that only one individual was responsible for both rapes – annnnnd, it was neither of the two men who’d been held supsect.

This is a typical tale, but I’d be interested in going to her lab, and asking Jankowski about the complications she encounters in evaluating evidence.

Not all evidence in her lab relates to DNA. They conduct analyses in four different areas - drugs, toxicology, criminalistics, and DNA.   They work on evidence related to determining the identity of seized drugs, or measuring blood alcohol levels… scientific technicians sift through trace evidence like hairs, fibers, and paint chips. Criminalistics also includes identifying blood or semen, which is then sent on to the DNA lab.

Other Institutions to consult:
+ IOM: Institutue of Medicine
+ AHRQ: Agency for Healthcare Research and Quality

Buzzwords/Issues to Address:
+ evidence-based medicine (EBM) … what kind of evidence?
Hair fibers, DNA, testimony from doctors, from psychologists, etc
+ what type of evidence is most flawed?/least reliable?
+ judicial practices that increase familiarity with, and therefore promote greater reliance on, the use of science-based medical evidence by the courts.
+ judicial rulings on and interpretations of scientific evidence and expert testimony
+ policy issues relating to the application of evidence-based medical findings
+ impact of recent Supreme Court decisions regarding the role of the judge in qualifying expert witnesses.
+ impact of recent Supreme Court decisions regarding the role of the judge in screening scientific and technical evidence for presentation to juries.
+ determining what physicians take to be evidence that justifies their practices and treatment decisions. (How has this changed over time?)
+ How can those involved in developing the evidence base for medical practice most effectively present this information in legal settings?
+ credibility of evidence from: population studies and controlled clinical trials.

.MGW.

CochlearWords

2005-11-30T19:07:00.000-08:00

-- Cochlear Implants Maintain Nerve Health in Deaf Cats --

Scientists from the Johns Hopkins University Center for Hearing and Balance have discovered why cochlear implants – devices intended to restore hearing –benefit some deaf children, but not others.

David Ryugo, P.h.D. and lead investigator of the study, used cochlear implants to electrically stimulate the nerves responsible for hearing in young, deaf cats. His results point to a link between introduced nerve activity, and the structure – abnormal or not – of the auditory nerve ending. Cochlear implants function to promote hearing, according to his study, because they preserve normal structure at the end of the auditory nerve.

Deaf humans probably benefit from implants in the same way that Ryugo’s cats did. Both species have similar auditory systems, and “the cochlear implants used in these cats are the same technology that was developed for deaf children,” he said. ”but smaller.”

Until now, scientists have not understood how cochlear implants work. “It has just been assumed that the auditory system functions normally when an implant is inserted,” Ryugo explained. “The reasoning has been something like this: if a car runs out of gas, it stops. Put gas in, and the car runs again.” Ryugo’s work is filling in the gaps, though, illustrating exactly how the “gas” – or cochlear implants – jumpstart the hearing process in congenitally deaf children.

Each year, 3 out of 1000 children in the United States are born unable to hear. Not every parent of a deaf child considers cochlear implantation, but for those who do, understanding the trade-off between waiting and acting is important. The success of implantation, according to Ryugo’s study, depends upon how far nerve ending abnormalites can advance. If children born deaf are left untreated for too long, their nerve endings start to wither. Eventually, this withering abnormality may become irreversible; implants can’t restore the nerve.

“Younger is clearly better, as far as treatment with cochlear implants goes,” explained Ryugo. “In Europe, they’re even putting implants in kids at 12 months,” Ryugo said, “but it is always difficult to know the age at which a child is strong enough to endure the surgical process, and to know how much leeway doctors have when deciding how long they can wait to perform surgery.” Ryugo’s work will help define the “window of opportunity” for cochlear implantation though, by illustrating how these devices impact physical abnormalities in the nerve ending of a deaf ear.

In his study, published in Science on December 2nd, young deaf cats with implants responded to sounds in their environment. “They exhibited certain behavior responses that alerted us to the fact that they were hearing,” Ryugo said. He had trained each implanted cat that a particular sound -- a rhythmic cadence, finger-snapping, or hand clap, for example -- signaled a special food treat. Different sounds signaled different treats (tuna, roast beef, sardines) to the different cats, he explained, “and voila! They would come to these sounds the same way a hearing cat comes when you shake its food box. We knew they could hear.”

Ryugo’s graduate student Erika Kretzmer compared nerve tissue from the inner ears of three groups: deaf cats with implants, deaf cats without them, and normal hearing cats. She discovered that deaf cats that had received cochlear implant stimulation actually maintained the nerve connections critical to hearing.

“There wasn’t a significant difference between nerve endings of normal hearing cats and implanted cats,” Ryugo said.

In the deaf cats without implants, however, nerve connections were withered. “Their nerve endings were disrupted,” explained Ryugo. “They were stubby and truncated, like trees growing on the edge of a windy cliff.”

Nerve endings promote communication between neurons in the auditory pathway. They exhibit structural characteristics which advance the release and capture of chemicals called neurotransmitters. This process permits sound to reach the brain. It permits hearing.

Until now, there’s never been a good group of animal models to use for studying the effects of cochlear implants in the deaf. “We’re the only ones in the country with a colony of congenitally deaf cats,” Ryugo explained. The cochlear implants were unique, too; Advanced Bionics specially miniaturized the implants just for his study.

Cochlear implants work by performing an essential step in the hearing process: they convert sound vibrations into electrical impulses that hit the auditory nerve, and then travel to the brain. A deaf child has inner ear damage that prevents him from generating these electrical signals, however. So the cochlear implant does it for him. Ryugo’s research suggests that implants are only capable of preserving auditory nerve structure if inserted in a timely fashion, before the nerve ending withers away.

In the future, Ryugo wants to further define the “window of opportunity” for cochlear implantation by performing time-course studies to elucidate exactly how nerve endings in the ear develop.

The researchers were funded by The Emma Liepmann Endowment Fund, and grants from the NIH and the Advanced Bionics Corporation. Authors on the paper are David Ryuogo, Erika Kretzmer, his graduate student, and John Niparko, all at Johns Hopkins School of Medicine.

.MGW.

MoxifloxacinWords

2005-11-22T17:48:00.000-08:00

---Chaisson's Changes: Bringing Bayer (and beyond) to TB---

What worked for Grandpa may work for a lot of us, but it won’t work for Richard Chaisson. As principal investigator of CREATE, the Consortium to Respond Effectively to the AIDS-Tuberculosis Epidemic, he’s spent the past five years fighting to reduce tuberculosis – killer of 1 person every 15 seconds --throughout the world. But Chaisson’s been fighting a stagnant system. There has been no new tuberculosis medication for 40 years. “People working on TB don’t ever change,” he explained. “They don’t believe in change.”

Yet, change has come. It’s come on the shoulders of giants like the Bill and Melinda Gates Foundation, who funded CREATE in 2004, and, more recently, it’s come from Bayer Pharmaceuticals. The drug manufacturer has agreed to take an unusual step and give its most promising antibiotic –moxifloxacin- to TB patients in developing nations. Ultimately, the driving force behind these efforts, including Bayer’s decision to join in the fight against TB, has been Chaisson himself, the same man who claims that at one point, “tuberculosis was just a hobby.”

Today, Chaisson directs the Johns Hopkins Center for Tuberculosis Research, but his interest in infectious diseases was born in the early 1980s, with HIV. At that time, Chaisson was doing his medical residency at an AIDS clinic in San Francisco. “It was a perfect time to be studying infectious diseases” he said, “ because all of sudden- woah! AIDS just popped up.”

Something else popped up, too. A link between HIV, the newest invader on the immune scene, and TB, an epidemic of ancient proportions. Chaisson observed that many patients had both diseases. “AIDS patients were especially vulnerable to TB since their immune systems had already been compromised by the HIV virus,” he explained. “There was a huge overlap between TB and AIDS, yet research in the area was severely neglected.”

Now, neglect is the last thing that HIV/TB studies suffer, with Chaisson at the helm. Most recently, he persuaded Bayer to permit their best-selling, patented antibiotic to be tested against tuberculosis. Bayer makes about $500 million a year from this drug, moxifloxacin, and would stand to lose a lot of money by establishing a market in poor countries. In fact, when Chaisson first approached Bayer about using moxifloxacin, “they weren’t interested at all,” he said. But that soon changed.

With the formula for moxifloxacin in hand, courtesy of a Physician’s Desk Reference, Chaisson went to the Food and Drug Administration and applied for an IND, or Investigational New Drug application. An IND is required to gain FDA approval when studying new indications of a drug, as Chaisson would be doing by testing “moxi” against TB, versus pneumonia or sinusitis, for example. Bayer got wind of Chaisson’s effort, and changed their tune.

“When Bayer discovered that the studies were going to happen,” he explained, “they decided that they needed to be part of the process. So, they joined forces with those of us studying the drug through the TB Alliance.”

Chaisson explained that while academic researchers would have continued to study the drug with or without Bayer, the Global Alliance would only study the drug if Bayer joined in, so that the drug could be made available at an affordable price if it proved effective. “The Alliance really did something of great value with Bayer's cooperation and support,” he said.

Now, Bayer is actively engaged in the trials, which involve thousands of patients in eight nations, including Brazil, Zambia, Uganda and Spain. They are donating the drug and the placebo, overseeing the toxicity reporting, and will ask the FDA for approval after the studies are done. According to Chaisson, “now that Bayer is part of a partnership with the TB Alliance and others, including our group at Johns Hopkins, it doesn’t have to invest as much or risk as much as it would have otherwise.”

The partnership between Bayer and the TB Alliance was formed on October 18th. The trial will study the potential of moxifloxacin to shorten standard treatment time from 6 months to 4. It’s already been shown to do this in mice. If the antibiotic shortens TB treatment in humans, Bayer will make millions of doses and sell them, at reduced prices, to poor countries.

This effort is well worth it. TB infects one in three people in the world, killing 5,000 people a day. It has emerged as the leading killer of HIV-positive people, too, and many doctors believe that HIV cannot successfully be fought without also fighting tuberculosis. Chaisson’s energy is relentless, and it seems that in targeting TB years ago in San Francisco, he could not have directed it to a more worthwhile pursuit.

.MGW.

IntercessionWords

2005-11-21T16:52:00.000-08:00

What the roommie and I will be up to over intercession... the written meets the digital -->

"Hi Meagan and Virginia,

We are delighted that you have agreed to teach a section each of expository writing to our Student Success Series group here at Hopkins. The course is called 'Digital Storytelling: Recording Personal History.'

I think you're going to have fun.

--Best, Rosemary Varner-Gaskins"

ohhhexcited. ScreenWords. words on the screen... mix it up, Media.

.MGW.

SchistosomeWords

2005-11-21T15:07:00.000-08:00

-- Fighting "The Quiet Plague": Cedarwood Oil Disrupts Osmoregulation in Schistosome Parasites --

Lathering up with topical creams before each swim may no longer be necessary to prevent schistosomiasis, a water-borne parasitic infection also known as “the quiet plague.” Researchers at The Johns Hopkins Bloomberg School of Public Health recently showed that they could reduce the ability of schistosome parasites to infect their hosts by killing the larvae in their watery homes. A mix of red cedarwood oil and surfactant, sprayed on the surface of ponds or lakes, gets the job done.

Schistosomiasis affects 200 million people in 74 countries. It is the most socio-economically devastating parasitic disease, after malaria. In their larval stage, the parasites that cause this disease are released into the water by infected, aquatic snails. The parasites then localize at water surfaces, waiting to contact and penetrate host skin. There are topical creams to prevent infection, but the idea of covering all surface skin each time water immersion is contemplated is not a viable option for the public at large.

Instead of treating the skin, Johns Hopkins researchers, including microbiologist Clive Shiff and his post-doc Dr. Jean Naples, have developed a method to reduce infection by treating schistosome-infested waters. Their strategy is unique because it exploits the parasite’s normal host-seeking behavior. Typically, lipids (fats) on the skin alert schistosome parasites waiting in water surfaces to the fact that they’ve made human contact. They then begin the process of host invasion, shedding their outer coat, known as the glycocalyx. Without this coat the parasites cannot osmoregulate, and if they remain in an aqueous environment instead of penetrating the host, they will absorb too much water, swell, and die.

Shiff and his colleagues observed that the same effect occurred when they exposed parasites to the unsaturated fatty acids of red cedarwood oil, a food and fragance additive approved by the FDA. Sure enough, the glycocalyxes of these parasites broke down, visible with a microscopic analysis, and the parasites died within minutes. Shiff knew that the parasites’ ability to infect was compromised; while mice tails exposed to untreated, schistosome-infested water were infected with an average of 12 parasites, only 1 parasite was detected in a mouse tail infected with schistosomes previously exposed to cedarwood oil. A surfactant known as Tween 80 was also mixed with the oil in test tubes, to enhance oil dispersal on the water surface. The oil-surfactant combination was up to 99.2% effective in reducing schistosome’s ability to infect the mice. Large-scale tests still need to be done in nature, in lakes and ponds, but there are at least two factors that already point to feasibility of using red cedarwood oil to reduce schistosome infection: 1) this oil is biodegradable, and 2) due to its specific gravity, it floats in water in close to the same water compartment that schistosomes occupy, while waiting to encounter a host. This means that only the water surface – not the entire volume – would need to be treated for effective attack. Shiff’s work was published in the American Journal of Tropical Medicine and Hygiene.

According to Dr. Peter Neal, a urologist studying schistosomiasis infection at Marshfield Clinic-Indianhead Center in Rice Lake, Wisconsin, “this paper presents a novel method of exploiting the specialized behavior of the parasites with a readily available, non-toxic, stable, and seemingly easy to use substance. If the in vitro results are borne out in field tests, the use of red cedarwood oil extracts mixed with a surfactant could promise to diminish the suffering and health care costs associated with this common parasite. This organism potentially affects one billion people worldwide. A simple method of control is therefore highly desirable."

.MGW.

FreemanDysonWords

2005-11-18T16:06:00.000-08:00

Okay. This is not an article. This is an articulation. Of pure excitation!!!!

Today--- I shook hands with FREEMAN DYSON!

Yes, at the Space Telescope Science Institute at Hopkins, where he spoke. AHHHHH!

Dyson is quite possibly the most charmingly, disarming scientist I've ever met. Even when discussing nuclear bombs.

LOTS to say about him... and little time to update this blog. But! If looking for a stellar read, scope "Disturbing the Universe." A masterpiece of his. Freeman Dyson -- a brilliant scientist, an innovator of his time -- has a way with words.

Interesting tidbit about Dyson-- he was a member of the JASONS, a group of 40 scientists who met each summer after 1959 to consider defense related problems for the Pentagon.

As the Vietnam War escalated in spring 1966, a Pentagon official close to President Johnson was heard by scientist Freeman Dyson to say, "It might be a good idea to toss in a nuke from time to time, just to keep the other side guessing."

This comment apalled several of the JASONS, Dyson included, and it spurred their study to systematically explore the utility of tactical nuclear weapons in the Vietnam War. The study looked at the effects of using nuclear weapons against a variety of targets, as well as the likely political effects of a nuclear campaign.

The conclusions drawn by the JASONS (about whom my advisor, Ann Finkbeiner, will soon release a book!) might be relevant today, given the possible conflicts faced by the United States. They also become relevant considering that the Bush administration has expressed willingness to use nuclear weapons against "rogue states."

More soon! much in the pipeline... Richard Chaisson/TB/Bayer. Ryugo & his congential felines. Perhaps some Schisto work... woah, Nelly!

-MGW-

StudentEssayWords

2005-11-18T15:39:00.001-08:00

This semester, I am teaching a science-based/laced expository writing class at Hopkins. It's called "Reprogenetics and the American Family," and recently, I assigned a book to my students: My Sister's Keeper, by Jodi Picoult.

This book is a fictional account relating to issues that can stem from using one child as a genetic donor for a sibling in the same family. Anna, the novel's main character, was born with one purpose in mind - to be a donor for her older sister Kate, who was diagnosed with terminal leukemia at age 2. In the book, thirteen-year old Anna sues her parents for the rights to her own body - at the risk of losing her sister. The ensuing battle, both within the family and within the courtroom, shakes the concept of family to the very core, and calls into question the term "good parenting."

For all other essays this semester, I've had guided prompts- instructing the students, more or less, on how to enter an argument, develop a thesis, and convey a novel thought. This time around, with My Sister's Keeper, students had free reign. I asked them to touch on the debate about quality versus sanctity of life, and to incorporate outside sources -especially court cases- but every other element of this paper was to be theirs.

Here, I'd like to share a bit of sophomore Lindsay Brown's paper... specifcally, her introduction and the poem she wrote, to preceed it. Lindsay is pre-med. She's also an eloquent writer. Take a peek!

“Ode to a Peaceful Day”

I lie here in your bed of steel,
My arms are straight and taut,
You say you feel and understand,
So, why do you tighten my knot?

The doctor says my heart is weak,
My lungs can barely breathe,
I gasp and moan from pains I feel,
Oh, if only I could leave!

The tube is long, my throat is sore,
My lips are chapped and dry,
I want to talk so I can tell,
But no tears will fill my eye.

It hisses and purrs about my head,
The “machine of life” they say,
My time has come to see the sky,
So let me have my way.

My body’s weak, I want to sleep,
My eyelids feel like lead,
But peace evades my restless soul,
While I remain in this bed.

I hear the angels at my door,
I’m ready to move on,
The tubes and plugs are all removed,
My spirit fades away with the dawn.

*

“Sometimes I hate myself,” Anna murmurs.
“Sometimes,” I tell her, “I hate myself too.”
This surprises her. She looks at me, and then again at the sky again.
“They’re up there. The stars. Even when you can’t see them.”
-Picoult

*

The service-station boy, in his white uniform, seemed uneasy until the bill was paid. He said, “You people sure have got nerve.”
Tom looked up from the map. “What you mean?”
“Well, crossin’ in a jalopy like this.”
“You been acrost?”
“Sure, plenty, but not in no wreck like this.”
Tom said, “If we broke down maybe somebody’d give us a han’.”
“Well, maybe. But folks are kind of scared to stop at night. I’d hate to be doing it. Takes more nerve than I’ve got."
Tom grinned. “It don’t take no never to do somepin when there ain’t nothin’ else you can do. Well, thanks. We’ll move on.”
-Steinbeck, Grapes of Wrath

*

In literature, martyrs only come in one size or shape. Anna’s jalopy is a courtroom. Her wreck is her age. Like Tom, she doesn’t waiver, she had no other choice. John Steinbeck’s message in the Grapes of Wrath is no different than Jodi Picoult’s in My Sister’s Keeper. Authors, however, would never let a reader think such an absurdity could possibly be true, and disguise this truth with interplay of words and contexts.
Anna, perhaps in less obvious ways that Sara, clearly stands out as a martyr in Jodi Picoult’s, My Sister’s Keeper. Her going to court, in effect, to end her sister’s life is an ultimate act of love and devotion and a concrete reaction to her sister’s illness and subsequent desire to die. Campbell on the other hand acts as a martyr in leaving Julia. However unfounded his perceived notions about his own illness may have been, he acts, seemingly quite contrarily, to give Julia life. The irony is that in the end, it is Anna who gives Kate life and Campbell who takes a great deal of Julia’s away. Each act of sacrifice is marked by a distinct period of alienation and sadness, but save by this path of darkness may dawn and a period of great quality and sanctity of life be reached.
What happens when martyrdom jumps out of the pages of classics and into the modern world, and is palpable in a U.S. courtroom? How are service station boys, in the form of jury members, able to comprehend and judge the actions of a martyr and, most importantly, at what point the destruction of a period of alienation and sadness is not worth the final rewards?

.MGW.

SynapseWords

2005-11-10T13:56:00.000-08:00

In the works... here's a preview...

Based on personal interviews with:
Dr. David Ryugo, Professor of Otolaryngology & Neuroscience at Johns Hopkins Medical School.
His manuscript - "Restoration of Auditory Nerve Synapse in Cats by Cochlear Implants"- is being sent to Science Magazine on November 8th, and should be published within a month or so after that.

Dr. David Ryugo has a very special collection of cats. He recently took me to the lower levels of Traylor Hall, at Hopkins Medical School, where he keeps them... a dozen or so furry white felines which cost him hundreds of thousands of dollars to purchase, and which are all congenitally deaf (deaf from birth). They are the only such population in the world, and they are perfect animal models for studying deafness.

In deaf humans, cochlear implants have restored hearing for many, but not all recipients. Dr. Ryugo wanted to know why... He performed tests to better comprehend synaptic plasticity in the auditory nerve, which is vital in understanding the beneficial effects of cochlear implants in congenitally deaf children. Dr Ryugo seeks to identify the latest stage at which implants could be placed in deaf children, so that they could still obtain some benefit. (If cochlear implants are inserted too late- if parents are hesitant, in other words- these instruments may not work at all to improve hearing.)

Previously, the clinical consensus as to why cochlear implants worked for some patients but not others was that language development prior to deafness lead to the best outcomes. Among congenitally deaf children, the younger the age of implant activation, the better the aural language results. These clinical experiences imply that uncorrected congenital deafness introduces irreversible abnormalities in the developing central nervous system. In mammalian models of congenital deafness, the synaptic structure of auditory nerve endings is abnormal. Ryugo wondered if the status of auditory nerve synapses represented an important link to the success or failure of cochlear implants.

He studied defects in the auditory nerve... specifically, he studied myelinated auditory never fibers called the endbulbs of Held. They transmit signals from the auditory nerve fiber to the postsynaptic cell with a high degree of fidelity. Congenitally deaf animals exhibit endbulbs with marked reduction in branching. Moreover, they contain fewer synaptic vesicles. These structural abnormalities have been associated with transmission irregularities at the synapse of endbulbs that may underlie loss of temporal resolution in the midbrain in neonatally deafened cats.

Ryugo stimulated deaf cats via a 6-channel cochlear implant and found that their endbulb synapses resembled those from normal hearing cats, after 3 to 6 months. I'm just brushing over the results here- until I write my article- but Ryugo hypothesizes that the changes observed after cochlear implantation at this crucial synapse enable the development of integrative and cognitive brain functions reflected in aural and oral communication in deaf children...

Beyond this angle, Dr. Ryugo is also interested in studying how chemicals could be imbedded in cochlear implants, to improve hearing. A pharmacological approach to improving deafness.

Side-note: Dr. Ryugo is one of the most enthusiastic people I've ever met. If you find yourself in Baltimore, look him (and his cats) up. A true delight.

-MGW-

Post-ReadingWords

2005-11-09T17:00:00.000-08:00

On November 7th, I read several pieces of my work aloud for the Writing Seminars Department. (All grad students do this. It's fun!!)

One piece I read was about the Kalenjins- an African tribe that lives on a plateau 7,000 feet above the sea, in northwest Kenya. They make up only .0005% of the world's population, but win 40% of its top distance events.

They are "the superstars of marathon running." The long distance elite.

I explained the biology behind why. Their "runaway" success is definitely linked to genetics, and to three factors in particular: abnormally high levels of the enzyme resposible for lactate turnover and breakdown, the right genes for high altitude survival, and an overwhelming proportion of slow twitch fibers in their skeletal muscle mass.

I don't have my piece posted, nor do I have the personal account of my love o' running here (which I read aloud, too... oohhfun!). But, I do have a bit of sweet feedback- an email from a poet... A tribute to running. And to science writers.

"Hey there, great reading on Monday night. I'm so impressed with the science writers this year. Good stuff. Anyway, my Dad's friend Deneen owns the shop 5K in Fells Point, and he thinks she would probably really like to read your stuff on running... I never knew that running could be such a dance, a religion, a spirit... a life mantra! I think if everybody ran, the world would be a better place... as you made it sound. Good science. Good energy. Thanks, T"

LifeWords

2005-11-08T18:23:00.000-08:00

Not-so-long-ago, these lines sparkled in an email, in my inbox...

"There are plenty of people in this world who might "work" but why should relationships have a different
standard. If nothing else, the relationship should be a higher standard. Everyday you work hard to reach your goals, to reach your expectations...demand nothing less in other people. They need to complement and complete your endeavors, your inspirations, your life."

-one of my favorite authors ;-)

.MGW.

Published(!)Words

2005-11-04T15:07:00.000-08:00

I sold a clip to ScienceNOW this week! My first published story.
ScienceNOW is Science magazine's online news source.

You can see the article under my Links, if you'd like!
-->"My First Published Piece (ScienceNOW)"

You can visit ScienceNOW's homepage, too...
--> "New Alzheimer's Target Identified" --Meagan White (Nov.4)

I wrote this piece based on interviews I'd done with neurologist Katrin Andreasson at Johns Hopkins Medical School, and with pharmacologists at Vanderbilt University. Their paper was published on November 2nd, in the Journal of Neuroscience.

Essentially, by deleting a receptor in the brain, they've identified a new target -downstream in the cyclooxygenase pathway- for Alzheimer's therapeutics... and this could lead to drugs that are much safer than NSAIDs, those typically prescribed.

According to Vanderbilt University pharmacologist Oliver Boutaud, an expert on the COX pathway, "this study is a milestone in the search for new therapeutic targets for Alzheimer's."

beautifulSCIENCE. write on...

.MGW.

Skip-a-BeatWords

2005-10-31T16:36:00.000-08:00

--Nature of Love--

First the stars in the skies
Fell into our eyes,
and twinkled in wide iris pools.

Then the grass on the ground
Laughed in wind, pulled us down
And we rolled in its fingers like fools.

When the sea’s salt-sweet breeze
Hid and sought near our knees
You took my hand, pulled me to waves.

And as tides rushed o’er us
I fast learned to trust
Night-capped deep that encircled our blaze.

Oh, lightning and flame
Would be dull, would be tame!
Compared to the fire we spark…

When we roll on the floor
In the grass by the shore…
And let skip-a-beats light up the dark.

.MGW.

JAK/STATWords

2005-10-28T15:21:00.000-07:00

--Somatic control of germline sexual development is mediated by the JAK/STAT pathway--

One of the world’s most important migrations ends in a place marked by no map: the gonad. This organ makes sperm and eggs, but it cannot perform this task- inherent to the success of sexual reproduction- unless germ cells first migrate to the gonad tissue, to receive the signals that will dictate their destiny as male or female. Despite the gonad’s role in shaping the sexual identity of germ cells, however, little is known about the molecular mechanisms underlaying this process. “For years, there has been this dance between somatic gonad cells and germ cells,” explained Johns Hopkins biology professor Mark Van Doren, “but we haven’t been able to identify the elements involved.”

Last July, however, Nature published a study in whichVan Doren and his colleagues identified one element- a “switch” for sexual identity. They demonstrated that in Drosophila, the JAK/STAT pathway- a cellular signaling route- mediates a critical signal from the male somatic gonad that is required for male germ cell development. In other words, no active JAK/STAT, no potential for a germ cell to become sperm.

Van Doren observed that STAT92E, a protein marker for JAK/STAT activity, was only expressed in male germ cells. This was the first tip that the pathway might play a unique role in male development. To confirm that presence of the STAT protein was due to JAK/STAT activation, however, Van Doren expressed a JAK inhibitor in his Drosophila. As expected, STAT92E expression was lost in the male germ cells. Interestingly, the presence of active JAK enabled germ cells – both male and female - to gain STAT protein expression. Female germ cells would normally not express STAT92E at all, leading Van Doren to his first conclusion:“The JAK/STAT pathway’s activity is necessary and sufficient for expression of STAT92E,” a protein seen in males.

But the JAK/STAT pathway is itself dependent on environmental factors for activation, as Van Doren observed. The pathway only “turned on” in germ cells that had completed their migration to the gonad. And just as contact with the gonad affected germ cell development, Van Doren found that sex of the gonad was influential, too. Normally female (XX) germ cells present in a masculinzed soma expressed the STAT92E protein characteristic of male germline development. Female germ cells also behaved uncharacteristcially in the presence of the JAK/STAT ligand, a binding molecule unique to the pathway. Typically, this molecule is expressed only in male gonads, reflecting that JAK/STAT activity (and all its components) is specific to males. When the ligand was expressed in female tissue, however, the female germ cells produced STAT like males would.

Male germ cell proliferation was also observed to be regulated by JAK/STAT acitivation, via the male gonad. Proliferation is specific to male germ cells during their early growth stages, but it was missing in male germ cells that lacked the somatic gonad. Additionally, female cells in a masculinzed soma proliferated early, as males would. This latter case could be problematic in an organism:“the sex of germ cells and the sex of the soma have to jive in order for sexual development to continue,” Van Doren explained. This understanding may provide rational for studies of drugs to help infertile couples.

Signals from the somatic gonad through JAK/STAT don’t act alone to influence malenss. Autonomous cues, like the male germline marker-1 (mgm-1), also play a part. On the whole, though, Van Doren’s study indicates that male germ cel development is first and foremost dependent upon non-autonomous cues via the JAK/STAT pathway. “But this isn’t the only pathway affecting the sex of germ cells,” Van Doren was careful to explain. And in the future, he hopes to identify additional somatic signals and germ cell autonomous cues that contribute to sexual development of the germline- the only means a species has to pass genetic cargo from one generation, to the next.

.MGW.

SmartWords

2005-10-23T11:42:00.000-07:00

Intelligence-enhancing drugs?

In the 1970s, psychologist Corneliu Giurgea stated that "Man is not going to wait passively for millions of years before evolution offers him a better brain."

Michael S. Gazzaniga, director of the Center for Cognitive Neuroscience at Dartmouth College, recently claimed that "if we are smart enough to invent technology that increases brain capacity, we should use that advantage."

Where does such technology stand today?

Geneticists have recently isolated a gene on chromosome 6 that they believe is involved in intelligence... Neuroscientists are gaining clearer understanding of which neurochemicals are involved in learning and memory, important components of cognitive function. And, according to Gazzaniga, many "smart" drugs that improve intelligence, learning, memory, and recall are in clinical trials right now.

To gain a better sense of how intelligence-enhancing drugs work (or don't), and to understand what role they might play in society, I've been talking to a neuroscientist (Dr. Solomon Snyder), a pharmacologist (Dr. Craig Hendrix), and a geneticist (Dr. Georg Ehret) from various institutes at JHU's Med School...

Could we/ should we be smarter on drugs?

Upcoming... upcoming...in the works!

.MGW.

PictureWords

2005-10-16T16:45:00.000-07:00

A picture's worth a thousand WORDsss. xoxoxo MGW

MarathonWords

2005-10-15T12:53:00.000-07:00

Post-Marathon, I reflect!

[ Baltimore Marathon
Completed 10.15.05
3hrs, 53min, 10sec
115th/886 Females ]

Soon, ohhh soooo soon, I am going to craft a lucious exposé on distance running.

For running is rich.

It is
pain
pride
endorphins
vision
you me
him her
doubt
assurance
courage
summit

fast faster
live longer
love-you-in-the-shower-later

relief challenge
mind body
soul sweat
race pace
hours minutes
wild steady
ancient present
city trail
sun wind
solo team
hills highs
hearts muscles.
Running is beautiful.

My exposé is on its way!
I hope to address running science, too- the science of Kenyans, endoprhins, pacing and pulsing, sweating and salt. The science of winners. The science of drive.

Finished in 3:53! and what a small sliver of time to dedicate to something which has so greatly enriched my life...

If I've run with you before, much love to you. And if I've not, that still-same love, and hopes of striding together soon!

Yes,
In your element,
you can be
as fierce and as fast
as your will can see...

.MGW.

GammaRayBurstWords

2005-10-14T14:14:00.000-07:00

Gamma ray bursts don’t loiter, and neither can the people who hunt them. That’s why astronomer Andy Fruchter’s cell phone rings every time one of these cosmic bursts – packed with the energy of a trillion suns – explodes in outer space. Though the origin of gamma ray bursts (GRBs) has eluded understanding since the 1960s, when scientists scanning the sky for elicit nuclear tests first witnessed these powerful explosions and miscontrued them for Russian bombs, Fruchter’s recent attention to cosmic detail has filled in a gap in the GRB mystery: what kinds of galaxies these massive explosions occur in.

Along with other astronomers from the Space Telescope Science Institute in Baltimore, Fruchter collected Hubble Telescope images which prove that long gamma ray bursts only occur in“scruffy environs.” This means there will be no mass exctinction of humans from cosmic GRBs anytime soon; our home galaxy, highly-evolved and metal-rich, is anything but scruffy. More importantly, though, Fruchter’s work co-localizes the occurrence of GRBs with supernovae, a second type of extremely energetic explosion.

Gamma ray bursts and supernovae occur at almost the same moment in time, in a quick and powerful one-two blow. Both result from the collapse of a massive star, with supernovae preceeding GRBs on the celestial timeline. “One would expect the two events to form in similar environments, too” Fruchter explains. But his Hubble images show that they don’t. In fact, the presence of a supernova doesn’t always indicate that a GRB will follow. To understand why the two aren’t always co-localized, Fruchter and his colleagues compared the locations – or, the galaxies- where GRBs and supernovae go off. They found that GRBs require a different set of characteristics from their host galaxies. The two explosions live in every different environments.

Though all GRBs are probably formed in supernovae, not all supernovae produce GRBs. Fruchter observed that if a supernova occurs in a massive galaxy, one which is aged, this supernova will not go on to produce a burst. He attributes this to the high metallicity characteristic of older galaxies, where metal ions have had years to accumulate, and suggests that GRBs can only be produced by supernovae in galaxies with low metal levels. Metallicity inhibits GRBS in two ways. First, metal ions in the atmosphere absorb emissions, or the gas jets constituting a GRB, and this smothers the burst. Second, the magnetic field generated by the metal ions opposes and slows the rapid spin needed to generate a GRB.

“Some supernova would like to produce GRBs,” explained Fruchter, “but they can’t.” These are the supernova seen in massive, metal-rich, evolved galaxies, like ours. Fruchter joked that “one of the conclusions of this study is ‘Relax!’ ” But even though we don’t have to worry about GRBs going off in our galaxy, we can still observe these massive explosions from Earth.

NASA employs a special spacecraft, known as Swift, to capture GRB images. They are difficult to capture, though. GRBs last only a few seconds – minutes at most- and occur randomly from all directions in the sky. To find them, the Swift spacecraft scans the sky. Its telescopes are designed to automatically detect the first flash of an explosion and then target that event as quickly as possible- usually in under a minute. It approximates GRB positions so that other telescopes, like the Hubble, can follow up and obtain pictures of the afterglow. Fruchter emphasized the difficulty of capturing such images. “There are well over 1000 gamma ray bursts known,” he explained, “but only 40 or so for which we have a good image.”

While charting these explosions has been difficult, Fruchter knows how to increase his odds. “My cell phone makes a really obnoxious noise, that I can’t ignore, if a gamma ray burst goes off” he laughed, pulling his phone from his pocket. Fruchter has followed the call of GRBs, elucidating their origins, and now we are all one step closer to understanding they mysteries surrounding these majestic explosions.

.MGW.

EP2Words

2005-10-12T08:08:00.000-07:00

Deleting EP2 Could Be Good For You
-Hopkins Study Finds Deleting EP2 Receptor Reduces Symptoms of Alzheimer’s in Mice-

Scientists at Johns Hopkins recently discovered that deleting a single receptor in the brain reduces symptoms in mice with the equivalent of Alzheimer’s disease. The discovery might lead to development of anti-inflammatory therapies safer than those currently used in Alzheimer’s prevention, the researchers say.

Alzheimer’s disease is a gradually worsening condition that impairs older people’s ability to carry out daily tasks, eventually stealing all ability to function. Though scientists associate certain changes in brain tissue with the disease (i.e. plaque build-up and nerve cell inflammation), they still don’t know what causes it, nor is there a cure.

Research suggests that drugs like ibuprofen and naproxen prevent symptoms of Alzheimer's. Unfortunately, chronic use of these drugs, non-steroidal anti-inflammatories known as NSAIDs, can cause side effects like gastric ulcers and intestinal bleeding. Additionally, COX-2 inhibitors, a specific type of NSAID, can cause serious cardiovascular problems. Last December, the U.S. Food and Drug Administration withdrew the COX-2 inhibitor Vioxx from the market and issued a health advisory for those COX-2 inhibitors remaining on shelves.

This new work, however, suggests that Alzheimer’s symptoms could be prevented, without incurring negative side effects of NSAID use, by blocking a prostaglandin receptor known as EP2. The findings are described in a recent issue of the Journal of Neuroscience

“This is just the beginning of a model for treating Alzheimer’s,” emphasized Johns Hopkins neurologist Katrin Andreasson, “but the identification of downstream prostaglandin pathways that function in Alzheimer’s disease should assist in development of anti-inflammatory therapies that are more selective than NSAIDs.”

In general, NSAIDs work by inhibiting the cellular pathway that promotes inflammation, a hallmark of Alzheimer’s disease. “They inhibit the formation of the mother of all prostaglandins, molecules that cause swelling” Andreasson explained, and they do this by first inhibiting activity of the enzymes COX-1 and COX-2.

But because inhibiting COX enzymes has lead to health problems, Andreasson’s group studied downstream components of the COX pathway in their search for treatment. Earlier work in the field suggested an important role for one such component, the prostaglandin PGE2. Levels of this prostaglandin, which has EP2 as its receptor, are elevated in patients with probable Alzheimer’s This observation suggested that PGE2-EP2 signaling may function in Alzheimer’s development, and so the researchers developed a mouse that would be insensitive to PGE2’s effects by EP2, its receptor.

“The EP2 receptor,” explained Andreasson, “provides a novel and selective target for development of therapies in Alzheimer’s. There are no EP2 antagonists available now.”

Dr. Richard Breyer of Vanderbilt University knocked out EP2 in a population of mice. He found that their brains exhibited less inflammation and plaque build-up than did brains of mice with the EP2 gene intact.

Inflammation was measured by observing brain levels of free radicals, harmful oxygen species that disrupt neurons. Free radicals are generated indirectly by EP2; as Andreasson explained, “EP2 activation elicits an innate immune response in supporting cells in the brain,” and part of this immune response is free radical production. The study showed that mice without EP2 had significantly lower levels of free radicals in their brains, correlating to reduced inflammation.

The researchers also assayed plaque deposition, a second hallmark of Alzheimer’s. Since free radicals boost activity of the enzyme that breaks plaque precursor protein into the smaller proteins forming plaques, the presence of free radicals (like those generated in EP2-PGE2 signaling) causes plaque build-up. The study found that deleting EP2 reduced this phenomenon up in mice.

Since EP2 deletion reduced symptoms of Alzheimer’s without interfering with COX activity, blocking it might help prevent Alzheimer's disease, while simultaneously avoiding health risks associated with NSAID use. “This work may be the mechanism by which NSAIDs prevent Alzheimer’s,” said Andreason.

She admits that there’s still more work to do, however. “We are looking at the function of other prostaglandin receptors in the Alzheimer’s mouse model.”

The researchers are also curious about the exact mechanism- direct or indirect- by which EP2 activation leads to plaques. “We are still trying to figure out exactly how the EP2 receptor promotes increased oxidative stress associated with free radicals,” Andreasson said. “We’re trying to figure out whether we can target those pathways therapeutically, too.”

The researchers were funded by the American Federation for Aging Research and the Nancy and Buster Alvord Endowment. Authors on the paper are Andreasson, Xibin Liang, Qian Wang, Tracey Hand and Liejun Wu of Johns Hopkins; Thomas Montine of the University of Washington, Seattle; and Breyer, Vanderbilit University.

.MGW.

SchizophrenicWords: DISC1 Gene

2005-10-10T21:27:00.000-07:00

-Transgenic Mice Provide New Insight into Schizophrenia-

Akira Sawa has been messing with mice, and now they’re schizophrenic. Recently, the Johns Hopkins neuroscientist elimated expression of the DISC-1 gene in rodents, and he showed this to delay neuronal development. Sawa’s population of transgenic mice exhibits the same delayed neuronal migration seen in another group: schizophrenic humans.

Sawa hopes to use his transgenic models to better understand development of schizophrenia – a disease with no known cure. “There are no clear cut biological markers for the disease,” he explained, and as such, both environmental and genetic factors have been implicated in causing it.

While some researchers point to the delayed onset of schizophrenia (manifest at ages 15 to 30) as a sign that environmental factors are to blame, Sawa joins those who ascribe a larger role to genetic predisposition. “There are several candidate genes for schizophrenic susceptibility,” he said, and though he acknowledges that environmental factors (psychological stress in childhood, viral infection in the womb) have a role in schizophrenic development, Sawa’s take is that the disorder actually starts before birth, as the brain develops.

To prove this, Sawa sought to link genetics to poor neuronal migration- a hallmark of schizophrenia. In his study, he focused on manipulation of one gene in the candidate list: DISC-1. Why this gene? “There are a lot of false positives in these studies,” Sawa explained, in reference to the list of genes implicated in the disorder, and “90% of these are junk,” he said. However, Sawa selected DISC-1 because, unlike the other candidate genes, it was not a known gene with a known function. Additionally, “only DISC-1 has a clear-disease associated mutation.”

Furthermore, previous studies link a truncated DISC-1 gene to familial history of schizophrenia. In his experiment, Sawa had no power to truncate DISC-1, but he was able to observe what happened when something went wrong with the gene by eliminating its expression all together. To do this, he introduced Ribonucleic Acid Interference (RNAi) into mouse embryos. RNAi targets a specific gene and silences its expression by preventing protein synthesis. Sawa used electric current to open channels and insert the RNAi targetting DISC-1 into the heads of mice developing in the womb. At this stage, neuronal abnormalities could be observed in the mouse brains.

In normal brain development, neurons migrate from inside the chambers of the brain to its outer cortex at a certain rate. This process was significantly delayed in the transgenic mice, however, reflecting poor neuronal migration. This is what Sawa had hoped to see. A biological marker had been established in DISC-1.

Sawa’s mice models provide means for pharamaceutical companies to test new therapies, based on biological markers. Sawa stipulates that this just the beginning of understanding schizophrenia, though; more biomarkers must be found in people before schizophrenia can be cured. Sawa explained that with stem cells harvested from humans, more biomarkers will be able to be pinpointed. It’s good to know that these markers can be tested in the the minds of mice so that someday soon, the minds of men will be less plagued by disease. Sawa’s messing with mice may yet yield a masterpiece in the treatment of schizophrenia.

.MGW.

ScienceOfLoveWords

2005-10-03T18:03:00.000-07:00

~On Shores of Amygdala~

Amygdala – a fine hotel
On Dopamine’s high coast.
All guests who come return again,
But pairs return the most.

Receptionist, she greets the guests,
Releasing to each pair
A garden key, a telling hint:
“Blooms oxytocin there.”

Amygdala – a fine hotel,
On shores of highest height.
Below its cliffs the waves do kiss,
And hearts swell, all the night.

.MGW. ;-)

TransplantWords

2005-10-02T12:34:00.000-07:00

--One Man, Six Organs: Georgetown Transplant Patient Goes Home--

Greg Marshall is “dying for a sausage.” His digestive organs stopped working 2 years ago, and ever since, the 43 year old New York native has been fed intravenously. But solid foods will soon again be in his diet; on August 25th, Marshall underwent a rare 14-hour transplant surgery at Georgetown University Hospital. Last month, just three weeks after the operation, he walked out with a functional digestive tract. And six new organs.

"It's exceptional that we're able to take six organs and replace them and actually make them work," said Thomas Fishbein, head surgeon for Marshall’s transplant surgery.

Marshall had received a liver, kidney, pancreas, stomach, small bowel, and colon. Only 20 such transplants have been performed in the United States, according to the United Network for Organ Sharing. And not all of these transplants involved six organs. Because the intestine includes the small bowel, the colon, and the stomach, other surgeries categorized as “liver-kidney-pancreas and intestine” transplants may have only involved replacement of 1 or 2 of these three intestinal organs. In Marshall's case, all three were replaced. Doctors also replaced many of his immune cells in an effort to prevent his body from rejecting the transplants.

And today, several weeks later, he’s feeling just fine. “He’s got that twinkle back in his eye,” his wife told reporters. Before the transplant, Marshall had suffered from Gardner Syndrome, a rare immune disorder caused by a defect in the APC (adenomatous polyposis coli) gene. In America, only one person in one million is diagnosed with Gardner Syndrome each year. Characterized by abnormal production of polyps and tumors in the intestine, it ultimately results in organ failure, and makes digestion nearly impossible. Furthermore, it is inherited in an autosomal dominant pattern; if Mom has it, there’s a 50% chance that you will, too. In fact, Marshall’s mother does have the disease, and so does his sister. But neither of them had ever experienced a complete immune shutdown, like Marshall had before the surgery, when he was confined to the couch by his intravenous feeding tube.

In hopes of ending Marshall’s battle, Dr. Fishbein replaced his intestinal organs (stomach, small bowel, colon), and he also replaced his liver, kidney, and pancreas. Marshall needed replacements for these last three organs due to scarring left over from a 1997 operation. That year, his stomach had protruded oddly from his lean frame, and curious doctors located a basketball-sized tumor in his abdomen. Removing it meant that he’d need a bowel transplant, but Marshall’s body rejected the organ, resulting in so much scarring in his digestive system that his other organs began to stop working, too.

After that, Marshall waited several years for a new set of organs. In multiple organ transplants, patients can be given organs from multiple donors, but doctors at Georgetown prefer that all organs come from one donor. “When we get to these sort of numbers more than four... five, six organ transplants in a single setting, it works much better if we are able to have the organs attached to one another," Dr. Fishbein explained. Naturally, the number of available donors is low.

“I didn’t believe it was ever going to happen,” Marshall said. Then, last August, doctors phoned to inform him that a donor with six compatible organs had indeed become available. Marshall would be getting a multiple-organ transplant the following day.

“I was happy for us, but sad for the people who had lost someone,” said Marshall’s 16 year old son, Brandon, referring to the donor’s family. Brandon also acknowledged how lucky his father is; many people “are still waiting for organs.” The telephone call was clearly a relief for the family. For a year, the intravenous line that fed him had limited Marshall’s movements. He’d rarely been able to leave the couch, and he’s never gotten to play with his 18 month old granddaughter. “I’m looking forward to spending time with her,” Marshall says now, after the surgery.

For the time being, he’s staying in a hotel near Georgetown University Hospital so that his progress can be monitored. Because of careful precautions (i.e. organs from just one donor, replacement of immune cells), there is little chance that Marshall’s body will reject the transplanted organs. However, it is always a possibility, and rejection usually occurs within the first three months. According to his family though, Marshall is “in good spirits” and among other things, he looks forward to soon eating his first real meal.

.MGW.

RudyardWords

2005-09-30T18:36:00.000-07:00

"Words are, of course, the most powerful drugs used by mankind."
-Rudyard Kipling

I would concur.

And I recently asked a friend of mine how he felt about Kipling's quote. A full-fledged challenge/response hit my inbox not long after:

"So I was sitting at work reading about B-cell activation, differentiation, and proliferation, and I thought of another side of the words v. drugs argument. This is purely logistical, and somewhat argumentitive, but here goes: Words are the most powerful drug effecting society not just because of their long lasting/profound effects on people, but also because so many more people take in words than take in drugs.

So here's what we'll do: You keep on taking in words, and I'll starting taking in equal amounts of drugs, say one dose per conversation you have in a given day, and we'll see who's life is effected more. I started this morning, so you'll need to catch up catch up."

.MGW.

Quake&GenderWords

2005-09-27T09:58:00.000-07:00

--Seize the Opportunity to Further Seismic Understanding: Earthquake Insight from Recent Study--

In 1960, the Earth rang, its crust shaken by the free oscillations of the world’s largest earthquake. One hundred twenty-three years of accumulated stress had come to call at a fault zone in south-central Chile, stirring the Earth and shocking seismologists; this giant quake had been early. Or had it?

The last known earthquake along the Chilean fault had struck in 1837, one hundred twenty-three years prior to 1960. Because an earthquake’s magnitude is generally thought to relate to the number of years between its occurrence and that of its predecessor, seismologists observing this span were perplexed. Sure, 123 years might sound like plenty of time for giant quake-causing stress to build in Earth’s outer layer, but historic record shows that typically, several centuries are required to build the type of energy this Chilean giant had rleased. One hundred plus years could hardly account for the energy with which this 1960 quake- literally off the Richter scale - had subducted the Nazca plate below its easterly neighbor (the South American plate), nor could this stunted span explain why associated tsunamis, or earthquake-generated waves, had soaked not only Chile, but Hawaii, Japan, and the Philippines, too.

Indeed, according to history, seismologists of 1960 should have felt safe assuring local south-central Chileans that a massive quake would not manifest itself there in the mid-twentieth century. But such a quake had. Futhermore, the entire timeline of quake activity at this fault zone confused seismologists; after the first documented earthquake there, observed by Spanish conquistadors in 1575, the zone was twice more shaken before 1960: in 1737, and again, exactly one-hundred years later, in 1837. So how to correlate this 1960 giant with such an earthquake history, showing a predecessor only a century or so before?

To explain this seismic mystery, Marco Cisternas, a Chilean researcher from the Pontificia Universidad Catolica de Valparaiso, joined ranks with a University of Washington geologist, Brian Atwater. As outlined in September 15th's "Nature," the two scientists and their colleagues sought to understand the 1960 earthquake based on physical evidence: shoreline changes in the stratigraphic record - in the sand and soil deposits produced by tsunamis.

At an estuary near the fault zone, Cisternas and Atwater investigated shoreline changes. Residents who witnessed the 1960 quake confirmed that the giant had indeed changed their shore: the green forest thriving there before, for example, was defoliated after the quake as a result of the tides that routinely flooded the subsided region following 1960. By contrast, nautical records depict leafy trees in this area after 1837. Why hadn’t 1837’s earthquake destroyed forests, too?

Examination of tsunami-generated sand deposition in this estuarine region provided further insight. Cisternas and Atwater observed that while both the 1575 and 1960 earthquakes were clear in the stratigraphic record, having covered marsh and meadow with up to 2 feet of sand, stratigraphic analysis pointed to no such significant sand deposition in layers associated with the quakes of 1737 and 1837.

Cisternas and Atwater concluded that, though tsunamis were indeed associated with these last two earthquakes, they were not nearly as sizeable as the earthquake-generated waves of 1575 and 1960, nor did their associated quakes expend much of the accumulated stress at the fault. The scientists propose that the earthquakes of 1737 and 1837 shook the earth on a much smaller scale than their sixteenth century predecessor, making 1575 the quake from which we should base history of 1960’s giant. In other words, massive fault dislocation from that earthquake was produced by energy that had remained “locked in” since 1575.

This 385 year gap fits the timeline for large earthquake recurrence. Additionally, Cisternas and Atwater’s study provides a wake-up call to seismologists content to consult history for earthquake understanding. No longer can it be assumed that the shaking of one quake stifles the same region from shaking again soon. Rather, giant earthquakes can still occur, even if mediocre ones have not-so-long-ago set the Earth ringing in the very same spot.

.MGW.

--Gender Mentor Makes us Wonder--

The Y chromosome is reporting to work early. With the release of last month’s Baby Gender Mentor Home DNA Gender Testing Kit, the presence of Y chromosome DNA has been employed to reveal fetal sex in record time: just 5 weeks after conception.

This test outpaces present methods of sex determination by a long shot; chorionic villus sampling and amniocentecis do not reveal male or female status until weeks 10 and 15, respectively. Both tests are used predominantly to screen for chromosomal abnormalities like Down syndrome, or for genetic defects, such as cystic fibrosis and Tay-Sachs disease. These tests also reveal fetal sex in this process. The Gender Mentor test, on the other hand, was specifically designed to reveal a baby’s sex.

This kit is for ''the type of woman who can't wait to open Christmas presents," says Sherry Bonelli, president of Mommy's Thinkin', the company that designed Gender Mentor. Indeed, as Bonelli intended, eager parents-to-be can now quench their curiousity and paint the nursery pink (or blue) with plenty of time to spare. And they don’t need to consult a physician to gain this knowledge of sex; Bonelli’s genetic test is directly marketed to consumers. Offered outside the usual context of medical consulation, it can be purchased online for $25. Acu-Gen Labs in Lowell, Massachusetts, charges $250 more for processing, for a grand total of 275$.

How does this test actually work? Lab tests analyze the fetal DNA floating in a finger-prick sample of a pregnant woman’s blood. (A finger-prick blood sampling kit is included in the Gender Mentor package.) Because human DNA is so similar from person to person, the best way to distinguish fetal DNA from maternal DNA is if there is Y chromosome in the sample- that is, if the fetus is a boy. Thus, Acu-Gen tests for the presence of Y chromosome DNA. A woman whose blood sample shows it can expect a boy. Likewise, absence of Y chromosome DNA in a pregnant woman means that a girl is on the way.

C.N. Wang, scientific director of Mommy’s Thinkin’, reports that Gender Mentor is designed to showcase the power of a new DNA analysis technique that holds promise for serious clinical uses, from early cancer testing to prenatal diagnosis of Down syndrome. These are the applications to which most scienctists are directing their attention. Free-cell DNA associated with tumors, for example, could make blood tests standard for detection in cancer patients, who would otherwise require chemotherapy. At this stage, however, the test is not used as a diagnostic tool.

Bioethicists are concerned about implications of Gender Mentor. They worry that this product will be used as a means for selecting sex, inciting couples unhappy with the determined sex to abort. Arthur Caplan, chairman of the department of medical ethics at the University of Pennsylvania, warns that being only five weeks into a pregnancy changes the moral view for people. “Ending a pregnancy early is easier to do [at 5 weeks] than at 20 weeks,“ Caplan said.

Previously, procedures like CVS and amniocentesis have escaped this concern; they are powerless to determine fetal sex until later stages when a) most mothers-to-be have already chosen to continue their pregnancies and b) the State becomes legally interested in the viability of the fetus.

But Bonelli claims that sex-selection via abortion is a non-issue in the United States. Here, she says, there are no dowries or other other culturally specific influences which fuel the boy preference prevalent in places like China and India.

However, despite Bonelli’s claims, sex selection is not absent from reproductive clinics in America. At the Genetics and IVF Institute in Fairfax, Virginia, a technology called MicroSort, which separates sperm into X and Y specimen based on weight, is part of the current commercial effort to standardize sex selection. The Virginia-based clinic has received 1,300 requests for MircroSort procedures since it opened in 1995. The Micrsort technique costs 5000 dollars per sitting compared to Gender Mentor’s 275 (kit + lab test). Incidentally, it appears that sex-selection in the United States is becoming a profitable industry. And why are Americans taking part?

One reason reported: to achieve “balanced” families – families with equal (or close to equal) numbers of boys and girls. In 2000, the Scottish couple Lousie and Alan Masterton made international headlines in their fight with the Human Fertilzation and Embryology Authority. They saught to “balance their family" by selecting for a girl to replace a lost daugter, Nicole. "We are missing the female element," said Louise Masterton, mother of 4 boys. The HFEA denied the Masterton’s requests, however, holding fast to the creed that sex-selction should be reserved for medical purposes, such as avoiding sex-linked diseases.

Beyond family balancing, Microsort reports that Americans are also seeking to sex-select to control gender order. Couples may want to raise a boy first, and then bring the girl home. A nation of little sisters in the making?

Though sex selection may or may not become widespread in the U.S., the idea of a direct-to-consumer genetic test like Gender Mentor does raise questions. In a report from the Human Genetics Commission, chairman Philip Webb addresses the role of this technology in America: “Genetic testing will become much more prevalent in future and has the potential to deliver significant health benefits,” he claims, “but it is important that direct testing is now somewhat regulated in such a way that we can gain the benefits of our new knowledge.” Webb’s statement serves as a reminder that genetic technology is progressing on a fast track, along which Americans may or may not be regulated. The option provided by Gender Mentor- to determine fetal sex as early as 5 weeks- poses to parents the question of whether knowledge of a child’s sex so soon after conception would be beneficial. Gender Mentor could make such knowledge readily available. But who will mentor minds struggling to answer this question?

.MGW.

AutumnWords

2005-09-24T05:17:00.000-07:00

~She doesn't wear a Jacket~

Drugs lace their lingo.
Sex swims on their lips.
Smoke coats their convo;
She laughs at darted quips.

Crack bridges barriers
And booze opens doors.
Powder pushes pulses;
Inhibition hits the floor.

Inhibition is the jacket
That she rarely ever wears.
It doesn’t let her move enough.
Its color doesn’t dare.

And it’s autumn in the city,
Her steps are rushing-free.
She doesn’t don that jacket.
She’s asked: how can this be?

"My drug is in the sun’s shot.
My sex is in the grass.
That fog that coats my memory
Too shimmers on lake-glass."

You ask her if she’s crazy.
You query of her joy.
You seek to sweet-corrupt her.
You’re carved of natural boy.

She answers you with wind-words
Racing on the breeze...
She answers you with eyes-wide:
“I love life. This is me.”

~September 11th: Birthday~

September eleven years ago,
And I had just turned twelve.
September 11th: birthday morn.
Cake waiting on the shelf.

Friends & cards & bows abound;
Kodak moments many,
Laughter licks the candle wicks.
I live a day of plenty…

September 11th: wake me now.
Gifts hold less allure.
It takes the cake 2 not take
4 granted,
as be4.

2 remember and 2 relish
In knowing that I can
Stride free, work hard, laugh lovingly
& live my master plan.

2 remember we inhabit
Land unaccustomed 2
Terror tumbling towers.
It’s not something we knew…

We may not have nightly worried
If our fathers came home late…
I may not have been too grateful
For all richness, on my plate.

September 11th: birthday.
Celebratory. True.
September: sweet America.
I'm glad 2 salute you.

~Sapphire 30~

Hello, September,
And I remember-
Your natural highs, my butterflies,
Summer-end starts, two beautiful eyes…

Once more September!
2 our surprise.
How swiftly summer 4 autumn vies,
As wet-gold sun leaves leafs gold-dry.

& Some of the boldest gold still lies

in memory,
Within.

Embrace us, sapphire-thirty.

~A Poem, Sans Title~
2WK

Inject your dreams with energy
Clasp them in your mind;
Don’t let the daily ground state
Absorb them, in its grind.

Not everything can stand out.
In fact, much must stand in.
The moves that make us human
Are often dull and dim.

But fire fuels the interim;
It blazes under flesh…
Though some days it may smolder,
And these are days that mesh.

Yet meshing days march steadily
To meet the days that glow,
Yes, these -The days that burn us-
These are days we know.

We know them by the risk-rush
They scatter on our skin.
We feel them in the fame we claim,
When we craft, stand out, or win.

And b4 we’ve known them long enough
To pace their bold-fast race,
The highest times, they flee us,
Leaving slow ones, in their place.

Perhaps slow days are vital tho,
Like catching breath and air.
Maybe time’s a state of mind;
State excited’s always there.

Inject your dreams with energy;
And on the slow-burn days,
Process them incessantly.
Your interim will blaze.

Yes, set your “I will’s” higher still,
No matter interim’s base.
Intent arms your ability.
Just right flows your life’s pace.

SummerWords

2005-08-21T22:09:00.002-07:00

~Science Writers We, Virginia & Me~

There's a pulse and it's live and it's different,
And I sense that it beats in us both.
We know what intrigues us: cold science-
And warmly we write of its growth...
Its growth and its place in this vast world!
This earth of a spin science-spun,
Where daily technology marches
Under watch of the moon and the sun.
This moon and that sun, they are beauteous.
Their rays bring new light to dark times
Just as our vibrant words will embrace this-
This science that unites mankind.

~Make Yourself~

In your element, you can be
as fierce and as fast as your will can see.

You
can

push your heart to burst,
endure keen pain, ignore plain thirst,

surge through trials,
and sweat through hills,

embracing heat,
imbibing chills

To make yourself
As diamond-hard
As any king
On any card.

This is your hand--
Why would you play
Like other winners of today?
If they are special,
So are you-
If special all,
Is any true?

The only way that you should sleep
Is knowing that your talent’s deep,
And deeply-worked
And longly-saught
And carved in ways
Others are not.

The greatest thing that you can do
is carve a unique, fiercesome you.
So carve, my friend, and I’ll stand by,
encourage with a loving eye…
And you can know, behind the scenes,
I’m loving carving unique-me.

~Love2LiveLearn~

2 i's in a "vision";
They belong to the word.
2 eyes on a vision...
They belong 2 me!
and to this
Infinite energy,
This zealous intent,
That's riding the crests of our youths,
Splendid-spent!

Mmm, let us learn, and
Oh! let us grow.
4 there's so much 2 love,
And wavelengths 2 know.

~Primitive Elegant~

Primitive-elegant.
Exists such a glow?
One wild as wolf tracks,
One gentle as snow…

Can the same swift steps that race ‘neath the moon
Waltz, graceful-light, to the violin’s tune?
Does snow-pearl skin, unaccustomed to earth
Blaze like skin bronzed after riverside mirth?

And how do they join,
Fair-mannered & fierce?
Can such distinct spirits
Share one gorgeous sphere?...

So that when coalesced,
They’d sing songs of merge,
With lines painting Venice,
but still praising birds.

On pine-lined paths I forge crystal dreams;
My pulse pushes fast at silk-sand-woven seams.
I’ll race you, bear-lightning.
I’ll pace you, harp-song.
Primitve elegant?
It’s here lived,
all along

~Innocence 4 Wisdom~

Hawks in her arteries,
Eagles in her eyes…
All her life
They’ve stretched their wings
And lead to swift surprise.

And though they’ve done this boldy,
Catching others’ sight,
They’ve not yet
Done it wildly,
Nor flown aggressive flight.

But now their pulse is quickened.
Their blood beats colder, too.
They’ve learned to soar
With shielded hearts;
Winds changed in knowing you.

~SummerWords~
(adapted from John Mosefield's "Sea-Fever")

I must go down to the seas again
For the call of the running tide
Is a wild call and clear call
That may not be denied.

I’ll sail down to the seas again
To that wild-hearted life
To the whale’s way and the gull’s way
Where the wind’s a whetted knife.

And I’ll wear summer stars in evening eyes
Drink sea breezes with lime
And cherish every sun-kissed step
Of a wave-licked summertime.

~Dare2Speak~

Dare 2 speak
And I ensure
That others content
2 endure
The dim of dismal timid more
Will secret-silently implore
For yet a sparkling waves-worth more
Of the vibrant starlit shore
That is your radiant spirit,
That does 4ever soar!

~Goodnight~
(2MIL)

Suddenly in summer steps when I was wild-walking,
Free as foam on wave crests,
Not looking and not knowing,
A new sun… !
It crested hills of forethought, warming sweet-cooled notions
Speckling me with light that I’d thought set,
In calmer oceans.

This sun, it burned a liking burn!
With playful rays of blink,
And extensions of such mention
Behind bright bronzing wink…

Though I was slow to notice, Yes.
Wrapped in beams of winter-spring.

And this sun,
it seeks to roll in grass!
To tumble, sing, and play.
It’s warmed me on the tennis court;
It’s kissed me, end of day.
Alive its light makes other steps!
Giving color, taking chill…
Where-how-why did it arrive right here?
I’ll ask it, yes I will.
For
No, I did not just now know,
In this wild-walking June
How simple-fast a face of sun
Could shoot me to the moon.

Goodnight!That moon amazes me
But for the sun I sleep.
4 this aura-sphere of lively-hot
That’s summer-sprung on me

~Sangria Night~

on cobble streets
in spanish heat
two sets of feet went walking

and stopped
in shade of Giralda
so lips could halt their talking

to sip the red and deep and dark
the night flavor, sangria!
a nectar of the old-world Spain…

Long live summer-Sevilla!

~Gettysburg College Commencement 2005~
(2 my classmates)

Gettysburg, you're looking good.
Your caps, your gowns, your smiles,
This sparkle you give off today...
It's going to take you miles.

It's exponential, your potential.
Could not graph it on Excel.
The input range would shoot the moon;
The output- hard to tell.

You've lived 4 years of orange and blue
They've tempted your mind's palette.
Now you're striding off to paint the world.
And shape it with your mallet.

Shall we take a moment here in May
To envision what you'll do?
A ragin' sea of possibility!
Hold on, I beg of you-

You may start slowly... you might race!
Take the time you need.
Not many days will grace the clock
Before you find your speed.

Your skills are many, Gettysburg.
Take a speedy stock.
The liberal arts have laced you well,
From economist to jock.

Yes, CEO is quite your color.
Film director fits you, too.
You could operate in every state.
Design condos in Peru.

Stitched with versatility
You think critically and long.
But you're also quite adept at
Javascript and improv song.

So when you start, wherever you are,
In an office, on a track.
You'll be armed with all the talents
That a Gburg degree packs.

And other souls may get caught up
In that nine to five-ish thing.
But you will "do great work" each day;
You'll make those moments sing!

And when the boss does fret and shout,
"This company needs vision!
Our motto hasn't changed in years-
Our ideas lack precision."

You'll be on top of this endeavor
And stroll up to his door-
"Ideas you've got?" the boss will say.
Why, I've got twenty-four.

Meanwhile the names of co-workers
Will all be ones you know.
You'll greet your fellow office mates
Like Esther at servo.

One day one May you might say, Hey!
I think I'll go explore.
You'll hop a plane to Ireland;
Bike 'round an Irish moor.

And on the trail you'll pass some kids
Fighting with their tent;
You'll fix that thing up with finesse;
Your GRAB days were well-spent.

On British Air, as you jet home,
You'll make a new connection.
The Frenchman in the next seat down
Is off to a convention...

He's in the business your in.
He asks you for your card.
That French you studied in McKnight
Made that far from hard.

And suddenly the pilot
Announces from the front
"This plane has turned around about!
We've hit a violent front."

Several hours after hearing this,
Your plane lands in Dubai.
Your non-western had you dreaming this
While others start to cry.

And if you've not already,
One noon you might be strolling
And catch a glimpse of him! (or her!)
Your heart will set to rolling.

Love will prove a wild spark~
For it is equal art and game.
Marriage may be in your cards;
Solo flight may light your flame.

And when your son plays Shakespeare
And needs medieval garments
Costume-design skills are at hand.
Thank you, liberal arts requirements!

From Natural Light to Crystal Light,
Your beverage tastes may alter.
But memories of spring fest days
Will never ever falter.

So sweet years will dance from one to next
And one day you'll be eighty,
Sitting on your favorite swing
With your favorite man or lady...

You've just returned from swing dance class.
It's time to feed the yak.
Your 9 iron needs polishing.
But you stop... and ponder back...

Through four scores of life lived so full
You could not have fit more in.
A cool peace overwhelms you now,
From your toes up to your chin.

It was 2005 when you set sail, alive
Liberated by liberal arts.
You persisted in creativity
Through a million ends & starts...
* * *
Yes, today's start is a special one.
Let's step up to the line...
The gun's been fired, Gettysburg.
It is our time to shine.

~Warm Fusion~

Metal cold-
Behold.
Precision in this place,
Of acid and fire,
Where you lift higher
Every element’s possibility-
Where you synthesize
Products from particles
That otherwise rest alone.
What’s the greatest thing you’ll ever learn?

Chemistry-
Chance it.
You pour solutions into cylinders
And your eyes light up.
Your passion is fashioned in proteins.
Pleasure is knowing their properties.
Promise is in their potential.
You will not break the promise to yourself
To conquer knowledge new.
Dedicated you,
Seeking delta for the world.
Beautiful.

And in the midst,
Would you nanosecond-venture
A new experiment?
Would you risk?
And pour your solution
Out of you, into flesh?
Would you chance the burn
That could accompany
What some might call the sweetest periodic fire?

You ask "how to measure
one’s
love against finding the cure for cancer, which would permit
millions
to experience
this love."
There is no balance to weigh my answer, but

Could love not be a
catalyst
in the reaction that is your noble pursuit of novel chemistry?

Could not embracing its emotion awaken you further and
activate
pathways of thought, otherways blocked & dead?

Or do u see love as simple distraction, preventing great reactions
From dancing in your head?

Warning:
Love’s equation is variable-ridden.
There is no control.
The solution’s hidden.
It is physical, it is organic-
Dare to chance a chem romantic?

No, it’s not perfect.
And there is no proof.
Though it is proven
That one must
Improvise, compromise, fling safety glass from cautious eyes…
Stakes are high. This is true;
Love might combust, unless you trust
The bluest flames, embrace their pulse,
Let them hurl you high & inspire
You.
Perspire in Kelvin you never knew…

And Oh! To feel what the Hydrogen knows
When it dances and basks in the Oxygen’s glow;
Unquenchable sigma.
Perhaps that which is greater than this
Is less than life’s discovered.
Would you risk to bond?

But wait, scientist -
you risk everyday…Yes.

So, perhaps the truth spun down is resolute solute:
My elements do not have the
Perfection you’d require
To kindle such life fire.
And perhaps you theorize
A chemistry of little size
To be yielded in mixing of “Me” + “U”.
May be true.

And I could accept this notion of null, I could.
For chemistry is not to be forced. It is natural-beautiful in its spontaneity.
I’d agree,
For I feel its radiance within me! Its entropy…
And existing in an excited state,
I seek simply to wholly radiate
This electric-shine-mine before considering to combine
In a thunderbolt compound.

And, thus, I could comprehend your precipitations
Of desires
for thunder of another color,
for electricity not found in “Me”,
But easily innate in an isotope of “Her”.
Sure.
Reactions flow this way.

And again, the monatomic state
Might be the wavelength
you appreciate.
This, too, can glow an oh-so-great!
Okay.

But sometimes I think deeper, too, and conjecture otherwise, I do.
It is the method scientific;
Let me be a bit specific-
My hypothesis ensuing?
You might be closed,
unsure, or just afraid
to expose
your beta sheets to my alpha particles…

So that I can’t help but speculate
What reaction could precipitate,
If two orbitals of beating heart
Were prevented from pulsing apart.

I wonder if you then would find
The warmest fusion of all time.

& I wonder if
this
could help you change the world…

.MGW.