On Admitting Nice, Ethically-Minded People to Med School

By |July 14th, 2011

This week the Times ran a leading story on a new med school admission process, with multiple, mini-interviews, like speed dating. The idea is to assess applicants’ social, communication and ethical thinking (?) skills:

…It is called the multiple mini interview, or M.M.I., and its use is spreading. At least eight medical schools in the United States — including those at Stanford, the University of California, Los Angeles, and the University of Cincinnati — and 13 in Canada are using it.

At Virginia Tech Carilion, 26 candidates showed up on a Saturday in March and stood with their backs to the doors of 26 small rooms. When a bell sounded, the applicants spun around and read a sheet of paper taped to the door that described an ethical conundrum. Two minutes later, the bell sounded again and the applicants charged into the small rooms and found an interviewer waiting. A chorus of cheerful greetings rang out, and the doors shut. The candidates had eight minutes to discuss that room’s situation. Then they moved to the next room, the next surprise conundrum…

This sounds great, at first glance. We all want friendly doctors who get along. It might even be fun, kind of like a game. (Sorry for the cynicism, injected in here, but it’s needed.) I’d even bet that the interviewers and successful interviewees would emerge feeling good about the process and themselves.

But don’t you think most premed students, who get through college, and numerous letters of recommendation, take the MCATS and achieve scores high enough to get an interview, are smart enough to get through this social test without failing? It’s what these young men and women are thinking, internally, that matters. According to the same article, the country’s 134 medical schools have long relied almost entirely on grades and the MCAT to sort through over 42,000 applicants for nearly 19,000 slots.

My math: that means nearly 19 out of 42 (almost half!) of med school applicants get in, here in the U.S.

If we want future doctors who are smart enough to guide patients through tough, data-loaded, evidence-based and ethically-complex decisions, we should make the academic requirements for entry more rigorous, especially in the areas of science, math and analytical thinking.

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Defining a Cluster of Differentiation, or CD

By |May 17th, 2011

One of the goals of this blog is to introduce readers to some of the language of medicine. As much as jargon is sometimes unnecessary, sometimes the specificity and detail in medical terms aids precision.

So what is a cluster of differentiation, or CD?

In medical practice, the two-letter acronym specifies a molecule, or antigen, usually on a cell’s surface. In 1982, an international group of immunologists got together for the First International Workshop on Human Leukocyte Differentiation Antigens. The initial focus was on leukocyte (white blood cell) molecules. The goal was to agree on definitions of receptors and other complex proteins to which monoclonal antibodies bind, so that scientists could communicate more effectively.

A few examples of CDs about which you might be curious:

CD1 – the first-named CD; this complex glycoprotein is expressed in immature T cells, some B cells and other, specialized immune cells in the skin; there are several variants (CD1a, -b, -c…) encoded by genes on human chromosome 1.

CD4 – a molecule on a mature “helper” T cell surface; T lymphocytes with CD4 diminish in people with untreated HIV disease.

CD20 – a molecule at the surface of immature B lymphocytes that binds Rituxan, an antibody used to treat some forms of lymphoma, leukemia and immune disorders.

 

In this schematic, an antibody recognizes a specific molecule, or cluster of differentiation, at a cell surface.

The CDs were named (i.e. numbered) not necessarily by the order of discovery, but by the order of their being deemed as bona fide CDs by HLA Workshop participants. There’s a pretty good, albeit technical, definition in FEBS Letters, from 2009:

Cluster of differentiation (CD) antigens are defined when a surface molecule found on some members of a standard panel of human cells reacts with at least one novel antibody, and there is good accompanying molecular data.

Perhaps the best way to think about CDs is that they’re unique structures, usually at a cell’s surface, to which specific antibodies bind. By knowing the CDs, and by examining which antibodies bind to cells in a patient’s tumor specimen, pathologists can distinguish among cancer types. Another use is in the clinic, when oncologists give an antibody, like Campath – which binds CD52, the responsiveness might depend on whether the malignant cells bear the CD target.

Still, I haven’t come across an official (such as NIH), open-source and complete database for all the CDs. Most can be found at the Human Cell Differentiation Molecules website, and information gleaned through PubMed using the MeSH browser or a straight literature search.

Wikipedia is disappointing on this topic; the list thins out as the CD numbers go higher, and the external references are few. To my astonishment, I found a related page on Facebook. Neither makes the grade.

Where should patients get information about these kinds of things? Or doctors, for that matter?

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TV Meets Real Life Oncology, and Anticipating the MCATs

By |May 13th, 2011

Yesterday I wrote on some tough decisions facing a TV show‘s protagonist. She’s got metastatic melanoma and might participate in a clinical trial when the show resumes.

Now imagine you’re an oncologist, or a real patient with this killing disease – you really need to be on top of new developments, to understand the pros and cons, because someone’s life depends on it.

If you’re the doctor in the relationship, you need keep abreast of current information for all the other tumors types of patients in your care: what are the new findings, if any, what are the limitations of the data. You need to know how the advances apply to an individual person who, most likely, has another condition or two, like high blood pressure or, say, osteoporosis.

Oncologists ought to be familiar with new drugs, and how those compare to old ones, and the side effects, and the distinctions between tumors with and without BRAF mutations. They should know what BRAF stands for.

Melanoma is one form of skin cancer. We understand now there are breast cancer subtypes – with distinct behavior and responsiveness to treatments, with and without inherited and acquired genetic mutations (BRCA-1 and -2 were identified well over 10 years ago; there’s much more known now), dozens of lymphoma forms and innumerable leukemia subtypes. Lung cancer, prostate cancer, brain cancer… Each is a group of diseases.

But the science physicians apply in their work doesn’t just apply in oncology. Even in traditionally “softer” fields of medicine, like pediatrics, doctors need to know how congenital diseases are diagnosed with newer, cheaper methods for testing mutations; in gynecology, doctors need to know about inherited clotting dispositions; in psychiatry, doctors give medicines with complex metabolic effects that involve, or should involve, some grounding in modern neuroscience.

This is why we need to keep the MCAT hard. (I’ll write more on this current issue in medical education, soon.)

Have a great weekend!

ES

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Where Are the Nucleosomes?

By |March 29th, 2011

This clip has had me wondering:

The DNA Dance

The video shows kids dancing on a college campus. They’re wearing tee shirts in any of four colors (representing nucleotides?) and lining up and zip-splitting in a semi-coordinated fashion, and having fun.

That’s fine, but let’s face facts: the exercise has little to do with DNA or understanding genetics at a meaningful level. From the Times Learning Network:

The idea was to connect science with the arts and to facilitate student understanding of the role genetic information plays in our lives. It also works on a metaphorical level, as an allegory for the student-faculty relationship and the college experience.

My initial reaction was puzzlement, then concern about higher education in the U.S. mixed with fear for the next generation of scientists: Where are the nucleosomes? Is the bicyclist like a helicase? What happens if there’s a double-strand break? All these things we should know.

Am I being too harsh?

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Benlysta, A New Treatment for Lupus

By |March 10th, 2011

Lupus, an autoimmune disease, turned up on the front page, right side of today’s Wall Street Journal. It cropped up, also, on the first page of the New York Times business section, and elsewhere. Scientific American published a nice on-line review, just now. The reason is that yesterday the FDA approved a new, monoclonal antibody for treatment of this condition.

The drug, Benlysta (belimumab), targets a molecule called BlyS (B-lymphocyte Stimulator). The newspapers uniformly emphasize that this drug marks some sort of triumph for Human Genome Sciences, a biotech company that first reported on BlyS in the journal Science way back in 1999. BlyS triggers B cells to produce antibodies that, in patients with lupus tend to bind and destroy their own cells’ needed machinery, causing various joint, lung, liver, kidney, brain, blood vessel and other sometimes life-threatening problems. So if and when Benlysta works, it probably does so by blocking aberrant, autoimmune B cell activity.

micrographs of lupus pathology in the kidney, Nephrol Dial Transplant, 25: 153-159 (2010)

The papers don’t give a lot of details on the drug’s effectiveness, except that it appears to help roughly 1 in 11 patients and the main benefit may be that some lupus patients on Benlysta can reduce their use of steroids, which have long-term and toxic effects on many organs. The most recent, major medical publication on a trial on the drug came out in the Lancet, two weeks ago.

Some reported caveats are that the drug has not been adequately tested or approved for patients with severe kidney or neurological manifestations of the disease, and that its activity, marginal as it is, appears to be less in patients of African heritage based on trials completed thus far. Additional trials are in the works.

The drug is expensive, to the updated tune of $35,000 per year. According to the WSJ: “Estimates of how many Americans are affected range from 161,000 to 1.5 million.” (How’s that for a wide ballpark figure? – likely a function of how hard it is to define and establish diagnosis for this disease, which anticipates how hard it will be to measure this drug’s effects, see below.) The same Journal piece says analysts expect the drug to become a blockbuster, with annual sales eventually topping $1 billion.

I’ve been intrigued by lupus ever since I was a second-year medical student, studying pathology before BlyS was discovered and monoclonal antibodies could be bulk-manufactured and tested in clinical trials. The disease’s name – from the Latin term for wolf, refers to the appearance of a facial rash that some patients develop.

Lupus can be scary to treat. One of my clearest late-night memories of my residency was when a 23 year old woman with lupus “rolled in,” as we would say, to the E.R. around 5:30 AM, as I was nearing the end of my then nearly-unrestricted shift. “We’ve got a sickie,” a nurse said as she roused me from my work on a hand-written note about someone else. The patient was dehydrated and gasping for air, and I remember having trouble getting her IV in, but somehow I did and she made it at least to the ICU.

From an immunologist’s perspective, it’s a fascinating condition because it flares and quiets – sometimes on its own – and affects different organs in distinct patterns among patients. The causes of lupus are likely varied. It may be that shutting down BlyS with an antibody is just a fancy and possibly more-targeted, less-toxic way of doing what steroids, like prednisone, do to B lymphocytes.

The problem I’d anticipate with the trials – carried out by my ever-patient, expert rheumatology colleagues – is that it’s sometimes hard to measure disease activity and responsiveness in lupus, apart from the kidney, because so many of the symptoms are subjective. And because the disease can affect so many organs, it’ll be hard to appreciate the drug’s toxicity, as apart from disease in itself.

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Learning About the Cancer Genome Atlas

By |March 2nd, 2011

A tweet from a former research colleague reminded me about the Cancer Genome Atlas, which I’d been meaning to check out. This website covers a project jointly funded by two NIH institutes: the NCI and the National Human Genome Research Institute (NHGRI). The project is about documenting cancer genetics for many, many human tumors.

Cancer Genome Atlas image

Some basics -

We all have genetic sequences we’re born with: our personal genomes. If you were to get your genome sequenced by a company, like 23andMe, they’d get some DNA from any of your cells or body fluid, and sequence your “somatic” or cellular genome. They would identify variants and mutations that you carry in the DNA of all or most of the cells in your body.

Cancer cells often contain genetic mutations that are not present in the patient’s healthy cells. So an individual’s breast cancer genome, for example, might differ from her baseline, inherited genome.

The purpose of the cancer genome project is to sequence DNA present in tumors samples so that researchers can identify specific, genetically distinct cancer forms and, eventually, develop smarter drugs that take aim at those tumor-specific mutations.

The site offers some cool, public-domain pathology and genetics images through a multimedia library. Good to know -

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A New Source of Potential Error in Scientific Research

By |February 17th, 2011

In today’s Times, Nicholas Wade reports on a potentially serious, besides costly, problem for biomedical researchers: Human DNA Contamination Seen in Genome Databases. He writes:

Nearly 20 percent of the nonhuman genomes held in computer databases are contaminated with human DNA, presumably from the researchers who prepared the samples, say scientists who chanced upon the finding while looking for a human virus…

The full report was published yesterday in PLoS One. The investigators, based at the University of Connecticut, screened for a common human sequence in 2,749 non-primate public databases – NCBI, Ensembl, JGI, and UCSC – and found 492 were contaminated with human DNA. Affected sequences included include bacterial, fish, plant and other genomes.

The implications are broad because if the findings in this report are true, scientists throughout the world have drawn inferences and conclusions and published papers based on incorrect DNA sequence information. As the PLoS authors write in their introduction:

The danger in the propagation of errors in scientific discourse has been demonstrated in cases of both scientific fraud as well as incorrectly described or referenced experiments in reviews [1], [2].

abstract double helix (Wikimedia Commons)

Sound familiar? Think of Lies, Damn Lies and Medical Science, as I considered in a December post on the Decline Effect and other problems that cast doubt on research findings we take for granted.

What happened is likely that, over the years and at many separate institutions, researchers handling cells from which DNA would be extracted, or perhaps just handling the DNA and doing sequencing and other experiments with that, contaminated the specimens with their own genetic material. This is a real headache for researchers, or should be.

Yesterday an on-line colleague and patient advocate, Trisha Torrey, (via a Twitter conversation) to the “HeLa bomb” as recounted in Rebecca Skloot’s The Immortal Life of Henrietta Lacks. In that, Skloot describes 1960s researchers who realized that the cells they’d been using for cancer research experiments were contaminated in vitro. HeLa cells tended to grow so rapidly, they’d sometimes overwhelm other cultures growing in nearby petri dishes or flasks. Once scientists realized that the cells they were using weren’t what they thought they were, and that HeLa cells weren’t all the same due to acquired mutations, their results became questionable.

My take is that researchers need to take care, and not make assumptions, such as “the cells I have received for analysis from a colleague’s lab are the cells they are said to be on the label.” Vials get mislabeled, sometimes. Cultures get contaminated by bacteria and fast-growing cell lines. And now it’s evident that at least some published genomes are incorrect.

But also – and more generally, we should constantly be questioning and checking and reviewing our methods and reagents, and whatever forms evidence, especially when results are surprising (think Madoff) and/or have implications for patient care and therapy, because errors do really happen in all realms of medical and scientific research.

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Sad Stats for Science Knowledge in U.S. Schools

By |January 25th, 2011

Today’s Times reports on our nation’s students’ poor science test results. The results are bleak: only 34% of fourth graders scored at a “proficient” level or higher; just 30% of eight graders scored at a proficient level or higher; 21% of twelfth graders scored at a proficient or higher level in science.

The mega-analysis, prepared by the National Center for Education Statistics, derives from 2009 testing of 156,500 fourth-graders and 151,100 eighth-graders, with state-by-state and nationwide metrics of those, and of 11,100 twelfth-graders. Student scores were ranked at one of three science knowledge levels for each peer group: advanced, proficient and basic, as defined by the Department of Education. Only a tiny fraction – as few as 1 or 2% of students – attained “advanced” scores on the science exams.

The complete report card analyzes the data by race, sex, urban vs. rural districts, private vs. public schools and other factors, and includes interactive state maps.

These numbers don’t bode well for our future-docs, or for empowered patients. With 70-80% of high school seniors lacking proficiency in science, informed consent and meaningful participation in health decisions are just theoretical concepts for most U.S. citizens.

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Artificial Red Blood Cells and Platelets from Stem Cells!

By |January 11th, 2011

There’s hematology news today, x 2 (at least):

flexible hydrogel particles resembling RBCs in size and shape (Credit: Timothy Merkel and Joseph DeSimone, University of North Carolina at Chapel Hill)

1. Progress in developing synthetic red blood cells -

A University of North Carolina, Chapel Hill-based research group has created hydrogel particles that mimic the size, shape and flexibility of red blood cells (RBCs). The researchers used PRINT® (Particle Replication in Non-wetting Templates) technology to generate the fake RBCs, which are said to have a relatively long half-life. The findings were reported on-line yesterday in PNAS (abstract available, subscription required for full text). According to a PR-ish but interesting post on Futurity, a website put forth by a consortium of major research universities, tests of the particles’ ability to perform functions such as transporting oxygen or carrying therapeutic drugs have not yet been conducted.

Developing competent, artificial RBCs is a hematologist’s holy grail of sorts, because with that you might alleviate anemia without the risks of transfusion.

2. Progress in using human stem cells to generate lots of platelets -

In an exciting paper published today in Cell Research, investigators stimulated human embryonic stem cells to become platelet-producing cells, called megakaryocytes. According to the article (open-text at Nature PG), the platelets were produced in abundance, appeared typical and clotted appropriately in response to stimuli in vitro. The researchers injected them into mice, used high-speed video microscopy for imaging, and demonstrated that the stem cell-derived human platelets contributed to clot formation in mice, in vivo (i.e., they seem to work).

The research team includes scientists at Harvard Medical School, the University of Illinois and Cha University in Seoul. Several authors are affiliated with either or both of two biotech companies: Stem Cell and Regenerative Medicine International (address in Marlborough, MA) and Advanced Cell Technology (headquarters in Santa Monica, CA; lab in Marlborough, MA).

Platelets are tiny blood cells essential in wound repair and clotting upon injury. For some patients with bone marrow disorders, such as leukemia, or chemotherapy-induced thrombocytopenia (low platelets) with bleeding, there’s a significant transfusion demand for this blood component. If safe, functional human platelets could be manufactured from self-replicating stem cells in a lab, that would significantly reduce the need for platelets in the blood supply.

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Lessons from the Wakefield Case

By |January 6th, 2011

I was almost at a loss for words today, besides having read the morning paper on the upcoming ESP study in a major psychology journal with questionable stats, and my having seen last night the first story on the British Medical Journal‘s report that completely, and maybe finally, discredits Dr. Andrew Wakefield’s anti-vaccine crusade which has caused needless morbidity and deaths in children from preventable illnesses in the U.S. and elsewhere.

So many others have written on Wakefield’s fraud, and considered the role of the press in perpetuating the notion that vaccines cause autism, I wasn’t going to cover it here on ML. But I do think there are a few instructive points from this “lesson” about medical communication and news:

1. People aren’t always rational in their decisions about health care. (This is an understatement.)

2. When most of the population (including journalists and, sadly, some doctors) are ignorant in basic science and statistics, misinformation spreads easily. In effect, our limited educations render us vulnerable to speculation and hype. A result “sounds good” or plausible, so we believe it, never mind the details -

3. Sometimes even educated people are so desperate for an explanation, or for a solution to a medical problem, that they’ll believe a smooth-talking scientist or doctor because they want to believe what he’s saying is true. If vaccines were to cause autism, that would give people a sense of control, i.e. a way to avoid autism.

The truth is that, for the most part, we still don’t know why diseases occur in some people and not in others. Not understanding can be a frustrating, unsatisfying circumstance, because it makes us feel powerless.

That’s it for today.

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On the Value of Open-Mindedness

By |January 3rd, 2011

Three recent stories lead me to my opening topic for the year: the value of open-mindedness. This characteristic – a state of receptiveness to new ideas – affects how we perceive and process information. It’s a quality I look for in my doctors, and which I admire especially in older people.

Story #1 – on the questionable effects of echinacea

Echinacea Purpurea flower (Wikimedia Commons)

The first article, published in the Dec 21 Annals of Internal Medicine, considers the potential of echinacea in treating the common cold. The results of a 4-armed, randomized study involving 719 patients with symptoms of an acute respiratory infection (“a cold”) were inconclusive, at best. A skeptic might say of the trial, sponsored by the National Center for Complimentary and Alternative Medicine (NCCAM), that it proves once and for all that echinacea is therapeutically useless. Another reader, perhaps versed in the flower-derived substance’s purported effects in other and earlier cultures, might charge that the investigators chose the wrong preparation, derived from roots of the E. angustifolia and E. Purpurea species, or that the researchers picked the wrong dose to observe an effect of the drug on the duration and intensity and biological effects of a common cold.

I’ve never tried echinacea and have no financial or other particular interest in this compound. But having read the article a few times, I’m disappointed, even unsettled by the results. After so many studies, many of which are referenced in the Annals paper, and now this costly, NIH-sponsored finding of what’s essentially no effect, it’s hard to say that echinacea is helpful to anyone. At the same time, I don’t think there’s sufficient information to say that it doesn’t work in preventing or reducing the intensity of an upper respiratory tract infection, or that it doesn’t work in some individuals who have symptoms like a runny nose and sore throat.

According to the ACP Internist (where I am a contributor):

…The study’s lead author, Bruce Barrett, MD, PhD, told USA Today that echinacea’s supporters would probably consider the findings positive but that those who oppose it for the common cold would consider the study “the nail in the coffin.” The director of the study’s primary funding source, the National Center for Complementary and Alternative Medicine, told USA Today that the center doesn’t plan to support future similar research, since existing data make clear that Echinacea’s benefit for the common cold, if any, is “very modest.”

Still, we don’t know if echinacea might work better as a tea prepared from dried roots or somehow otherwise ingested by people who are sick, as opposed to the pill compound that was given to participants in the Annals study, or if an extract compounded from a different combination of Echinacea flower species might do the trick.

So if a doctor’s open-minded and her patient wants to try taking echinacea tea for a blossoming cold, she might tell the patient that there’s not much evidence based on published trials of the herb, and that in fact so far the echinacea data aren’t supportive of a meaningful effect in any patient group. At the same time, there’s probably little risk of trying echinacea, in that it seems to have few untoward effects. And the patient and physician might then observe what happens, and draw limited if any conclusions based on that person’s individual, n=1 experience with echinacea.

A closed-minded doctor might tell her patient that echinacea isn’t worth trying, in any form. In her mind, she considers the substance is a sort of natural or home-remedy that has no role in modern medicine. She might even feel it’s a waste of her time to discuss the alternative treatment with her patient, and perceive the patient as being uncooperative if he or she tries taking it against her advice.

Echinacea - "white swan" variety, Wikimedia Commons

Patients’ attitudes vary, as do their doctors, and given a choice of physicians patients probably choose doctors whose personal philosophies roughly align with their own.

For now what I’ll say is this: I respect it when a doctor admits uncertainty, and is willing to try something of low cost and low toxicity, for which the evidence is thus-far unclear. (Of course, if we extend this argument to a discussion of more costly and potentially toxic drugs – like new cancer treatments, we’d need to weigh more carefully the potential harms of a treatment against the unproved benefit.) In principle, though, I like the approach of an open-minded doctor, who recognizes the limitations of published data, and is willing to explore an unproved approach to a problem in a way that’s transparent: as long as the doctor doesn’t sell the echinacea, and is honest with the patient about the lack of evidence to support its use, it seems OK.

Paper #2 – on an incredible effect of known placebos

Another, curious December story, Placebos without Deception: A Randomized Controlled Trial in Irritable Bowel Syndrome, appeared in the strictly on-line journal PLosONE. The article is perhaps more definitive, as it is more puzzling: the investigators observed that when people with irritable bowel syndrome (IBS) took placebo drugs in a clinical trial, even though they knew they were receiving a placebo and not real medication, they felt significantly better than those patients who didn’t receive the open-label, placebo treatment.

As a reader and scientist, I cannot understand this observation except to say most likely it’s an experimental fluke. But the study’s statistics were strong, and the trends internally consistent, rendering it likely that what the investigators reported could be reproduced. The patients’ symptoms are highly subjective in IBS, although they can be debilitating and costly. My conclusion, trying to be open-minded about a result that seems improbable if not impossible, is that maybe there are things we don’t really understand about how “medicine” affects humans.

The ethical implications of this finding – that “placebos work” – are interesting, if it’s true (which I wouldn’t conclude based on this one study reported in PLoS, or anywhere). For now what I’d say is the results are intriguing. I’m curious to see if these results are reproduced, and how the ethical implications will be ironed out in our modern medical community.

Piece #3 – on the brain’s maturity, flexibility and “cognitive fitness”

Finally, I’ll note a Dec 31 op-ed piece that appeared in the Times: This Year, Change Your Mind, by Dr. Oliver Sacks, the neurologist and author. In this thoughtful essay, he considers the adult brain’s “mysterious and extraordinary” power to adapt and grow: “I have seen hundreds of patients with various deficits — strokes, Parkinson’s and even dementia — learn to do things in new ways, whether consciously or unconsciously, to work around those deficits.”

With appropriate and very-real respect, I question Sacks’ objectivity on this subject – he’s referred some of the most outstanding (i.e. exceptional) neurological cases in the world. And so it may be that his careful reports are perfectly valid but not representative; for most of us, the adult brain’s capacity to establish new circuitry for language learning or music appreciation may be limited. What his stories do show is that unimaginably strange things happen in our brains, at least occasionally. And maybe we should just accept that and take notes (as he does so carefully), and keep an open mind –

Finally, he writes:

…all of us can find ways to stimulate our brains to grow, in the coming year and those to follow. Just as physical activity is essential to maintaining a healthy body, challenging one’s brain, keeping it active, engaged, flexible and playful, is not only fun. It is essential to cognitive fitness.

I’m inspired by the notion of keeping a fluid, active mind. It’s not easy to keep abreast of new data, and to read the literature critically. While some people become more withdrawn in adulthood, resting on comfortable routines and reliable sources, I choose the opposite: reading blogs, scanning Twitter, checking out lectures on YouTube, watching new TV shows, listening to my kids and students. How much better it is to approach information with an open mind, to take it in and contemplate its ramifications, than to simply say “no, that’s impossible.” As far as my doctors are concerned, I hope that’s their attitude, too.

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A Play About the Life and Work of Dr. Rosalind Franklin

By |November 11th, 2010

Last weekend I snagged a last-minute ticket to see Photograph 51, a new play about the work and life of Rosalind Franklin. Her data, possibly stolen, enabled Francis Crick and James Watson to decipher and model the double-helix structure of DNA.

The intimate production, enacted by the small Ensemble Studio Theatre on the second floor of a nondescript building on West 52nd Street, affords a fresh look, albeit partly fictionalized, into important moments in the history of science. Most of the scenes take place in a research lab in post-War London, at King’s College, where Franklin took on a faculty appointment.

Franklin’s story starts like this: She was born in 1920 to a Jewish family in London. She excelled in math and science. She studied physical chemistry at Cambridge, where she received her undergraduate degree in 1941. After performing research in photochemistry in the following year on scholarship, she joined the British Coal Utilisation Research Association (BCURA) and carried out basic investigations on the micro-structure of coal and carbon compounds, and so earned a Ph.D. from Cambridge University. She was a polyglot, and next found herself in Paris at the Laboratoire Central des Services Chimique de l’Etat, where she picked up some fine skills in x-ray crystallography.

You get the picture: she was smart, well-educated and totally immersed in physical chemistry before, during and after WWII. Single-minded and focused, you might say –

Franklin in Photograph 51 wears a simple brown dress with large black buttons straight down the middle of her lithe frame. Her lipstick and haircut seem right, but her three inch heels, even after a few years of experiencing the joie de vivre in Paris, or just being holed up in a research institute there, seem a tad too high for such a pragmatic soul. The lab set is perfect with its double-distilling glassware, wooden pegs on racks, tall metal stools with small, flat circular seats, light microscopes, heavy metal desks with file drawers and a contentious cast of characters.

As this narrative goes, Franklin spurns socializing with most of her colleagues. They find her difficult. She spends nearly all of her time and late hours using x-rays to generate crystallographic images of DNA and making detailed notes and related calculations. Eventually a lab assistant gives her key data, Photograph 51, to her colleague, Maurice Wilkins, who is inexpert in crystallography and cannot independently interpret the structure. While Franklin continues working at a measured pace, refusing to rush into publishing a model until she’s sure of her findings and the implications, Wilkins shares the image with Watson and Crick. They move quickly, publish first in Nature and, later, win the Nobel Prize for the discovery. Meanwhile Franklin leaves Wilkins’ lab and starts a new project on the structure of tobacco mosaic virus. She dies at the age of 37 of ovarian cancer, likely caused or effectuated by the radiation to which she exposed herself at work.

It’s a sad story, but instructive, engaging and very well-done, so much that it’s haunted me for days. Hard to know what’s real –

According to a program note from Anna Ziegler, the playwright: “this play is a work of fiction, though it is based on the story of the race to the double helix in England in the years between 1951 and 1953.” Ziegler refers to several books from which she drew material: The Dark Lady of DNA (by Brenda Maddox), The Double Helix (by James Watson) and The Third Man of the Double Helix (by Maurice Wilkins).

My favorite part is Franklin’s statement at the beginning: “We made the visible, visible.”


For a (depressing) counterpoint to this play’s version of events, you can take a look at Nobel Laureate James Watson’s 2007 TED lecture on YouTube. “She was a crystallographer,” he says of Franklin, and other things, before delving into his late-life happiness and current ventures in cancer genetics and autism studies.


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Stem Cells, Breast Reconstruction and a Magazine Cover

By |October 26th, 2010

The cover of the November print edition of Wired features large, unnatural-appearing cleavage. Inside and toward the back of the issue, a curious article ties together stem cells and the future of breast reconstruction. It got my attention.

Wired, November 2010 issue

The detailed and admittedly interesting piece, by Sharon Begley, describes what’s science or science fiction: first humans, such as some plastic surgeons, remove adipose tissue, a.k.a. fat, by a well-established cosmetic surgery procedure called liposuction, from a body part where there’s a fat surplus – such as the belly or backside; next, laboratory workers purify and grow what are said to be stem cells from that that fat; finally, they use a nifty, calibrated and expensive device to inject those fatty stem cells where women want, such as in a hole or dimpled breast where a tumor’s been removed.

The story starts, unfortunately and distractingly, with a portrait of a male, enterprising and PowerPoint presentation-giving CEO of a biotech company, Cytori Therapeutics. Toward the end of the article, the author provides stats to support the potential business. Ultimately, improved breast cancer survival means that greater numbers of women will live more years after a lumpectomy or mastectomy, she explains. The reconstruction market may expand further, still, because some women opt for prophylactic mastectomies upon positive genetic testing for a BRCA mutation. Others, without cancer or high risk, might simply want to use these adipose-derived stem cells for cosmetic breast augmentation. What’s clear, if nothing else, is that women’s breasts are perceived as a commodity.

In between the money elements of the discussion, there’s some cool science about adipose-derived stem cells, which according to the cited scientists are quite prevalent in fatty tissue and relatively easy to grow if you give them some blood to feed on in the lab. A putative advantage of the cells is that they draw blood vessels to the area of engraftment, which is a concern to this oncologist (me) and, evidently, to an FDA panel that has not yet approved of this innovative method of breast reconstruction in women who’ve had breast tumors.

I’m not convinced, at least from what’s reported in this Wired article, that the cells used in this process are true stem cells, based on the high numbers the scientists describe finding so readily, and in rich proportions, in human fat tissues. It could be, for example, that what they’re isolating are really primitive adipose cells that can, indeed blend into the breast tissue and even recruit blood vessels as described, but aren’t true, pluripotent stem cells – the kind that can form any kind of blood cell or heart cell or neuron. Perhaps stem cells just sound sexy, at least to investors.

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Everybody’s Talking About Stem Cells

By |October 12th, 2010

Last week, doctors injected embryonic stem cells into a human patient with an acute spinal cord injury. The procedure took place at Shepherd Center, a hospital and research center for spinal cord and brain injury in Atlanta, GA. The patient was the first to receive human stem cells derived from an embryo in an FDA-approved research protocol in the U.S.

The phase I trial, sponsored by Geron Corporation of Menlo Park, CA, is primarily intended to evaluate the treatment’s safety. The company has developed a way to culture and purify oligodendrocyte progenitor cells (OPCs – primitive neuronal cells) from human embryonic stem cells (h-ESCs). These precursor cells, obtained from human embryonic tissue, can be coaxed, at least in vitro, to develop into one of various mature cell types, including neurons).

So what defines stem cells?

Stem cells are considered pluripotent, meaning that they have the capacity to differentiate, or mature, into specialized, distinct cell forms depending on nearby cells and stimulatory molecules in their environment. Mature cells, by contrast, have already “decided” what kind of tissue they’ll grow into – whether that’s part of the eye, or the heart, liver tissue, nervous system or any other body component.

The idea behind stem cell therapy for spinal cord injury is to provide the wounded spine with fresh, primitive cells that might grow into neurons and replace those that have been damaged. The protocol is highly-experimental.

There are three major sources of human stem cells:

1. Adult stem cells are relatively abundant in the bone marrow.

2. Cord blood cells; as are found in the placenta and umbilical cord after delivery of a newborn;

3. Embryonic stem cells, as were used in this protocol, are typically removed from surplus material after IVF.

You can learn more about human stem cells on the NIH website here.

(and belated happy birthday, JL!)

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The Music of H.I.V.

By |October 6th, 2010

Yesterday I came upon something I’d never heard before: Alexandra Pajak, a graduate student at the University of Georgia, merges art and science in a novel way. She composed a new work, the Sounds of HIV, based on the virus’s genetic sequence.

A CD, produced by Azica records, will be available later this month. A ScienceRoll post, by Bertalan Meskó, clued me into this fascinating project. He shared the artist’s explanation of her work:

Sounds of HIV is a musical translation of the genetic code of HIV, the Human Immunodeficiency Virus.  Every segment of the virus is assigned music pitches that correspond to the segment’s scientific properties.  In this way, the sounds reflect the true nature of the virus.  When listening from beginning to end, the listener hears the entire genome of HIV.

In English, the nucleotides Adenine, Cytosine, Uracil/Thymine, and Guanine are abbreviated with the letters A, C, T, and G.  Since A, C, and G are also musical pitches in the Western melodic scale, these pitches were assigned to the matching nucleotides.  To form two perfect fifths (C-G and D-A), “D” was arbitrarily assigned to musically represent Uracil.  I assigned the pitches of the A minor scale to the amino acids based on their level of attraction to water…

According to a May, 2010 post in the Daily Scan, the artist has assigned pitches to each viral segment’s properties:

…The composition’s Prelude and Postlude correspond to the first and last 100 nucleotides, and the sections named after the proteins (Proteins 1-9) represent translations of the amino acid sequences…

Upon searching further, I tracked down some partial HIV music clips, available now, at ClassicsOnline. The start of the prelude sounds calm and lovely to my rock-trained ears; other portions are distinct and lively.

I look forward to more listening!

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Back to Basics – But Which Ones?

By |August 6th, 2010

A front-page story on the Humanities and Medicine Program at the Mount Sinai School of Medicine, here in Manhattan, recently added to the discussion on what it takes to become a doctor in 2010. The school runs a special track for non-science majors who apply relatively early in their undergraduate years. Mount Sinai doesn’t require that they take MCATs or the usual set of premedical science courses – some college math, physics, biology, chemistry and organic chemistry – before admission.

The idea of the program is two-fold: first, that the traditional med school requirements are a turn-off, or barrier, to some young people who might, otherwise, go on to become fine doctors; second, that a liberal arts education makes for better, communicative physicians and, based on the numbers published in a new article, a greater proportion who choose primary care.

Today Orac, a popular but anonymous physician-scientist blogger, considers the issue in a very long post. His view, as I understand it, is that if doctors don’t know enough science they’ll be vulnerable to misinformation and even quackery.

On the side of the spectrum, perhaps, Dr. Pauline Chen, a surgeon who puts her name on her blog and essays. In a January column, “Do You Have the Right Stuff to Be a Doctor?” she challenged the relevance of most medical schools’ entry requirements.

I see merit on both sides:

It seems fine, even good, for some students to enter medical school with backgrounds in the humanities. Knowledge of history, literature, philosophy, art history, anthropology and pretty much any other field can enhance a doctor’s capability to relate to people coming from other backgrounds, to recognize and describe nonparametric patterns and, perhaps, deliver care. Strong writing and verbal skills can help a doctor be effective in teaching, get grants and publish papers and, first and foremost, communicate well with patients and colleagues.

Still, there’s value in a doctor’s having a demonstrated aptitude in math and science. Without the capacity to think critically in math and science, physicians may not really understand the potential benefits and limitations of new medical findings. What’s more, doctors should grasp numbers and speak statistics well enough so they can explain what often seems like jumbled jargon to a patient who’s about to make an important decision.

Thinking back on my years in medical school, residency, fellowship, research years and practice in hematology and oncology, I can’t honestly say that the general biology course I took – which included a semester’s worth of arcane plant and animal taxonomy – had much value in terms of my academic success or in being a good doctor. Chemistry and organic chemistry were probably necessary to some degree. Multivariable calculus and linear algebra turned out to be far less important than what I learned, later on my own, about statistics. As for physics and those unmappable s, p, d and f orbitals whereabout electrons zoom, I have no idea how those fit in.

What I do think is relevant was an advanced cell biology course I took during my senior year.  That, along with a tough, accompanying lab requirement, gave me what was a cutting-edge, 1981 view of gene transcription and the cell’s molecular machinery. Back then I took philosophy courses on ethical issues including autonomy – those, too, proved relevant in my med school years and later, as a practicing physician. If I could do it again, now, I’d prepare myself with courses (and labs) in molecular biology, modern genetics, and college-level statistics.

My (always-tentative) conclusions:

1. We need doctors who are well-educated, and gifted, in the humanities and sciences. But for more of the best and brightest college students to choose medicine, we (our society) should make the career path more attractive – in terms of lifestyle, and finances.

(To achieve this, we should have salaried physicians who do not incur debt while in school, ~European-style, and who work in a system with reasonable provisions for maternity leave, medical absences, vacation, etc. – but this is a large subject beyond the scope of this post.)

2. There may not be one cookie-cutter “best” when it comes to premedical education. Rather, the requirements for med school should be flexible and, perhaps, should depend on the student’s ultimate goals. It may be, for instance, that the ideal pre-med fund of knowledge of a would-be psychiatrist differs from that of a future orthopedist or oncologist.

3. We shouldn’t cut corners or standards in medical education to save money. As scientific knowledge has exploded so dramatically in the past 30 years or so, there’s more for students to learn, not less. Three years of med school isn’t sufficient, even and especially for training primary care physicians who need be familiar with many aspects of health care. If admission requirements are flexible, that’s fine, but they shouldn’t be lax.

Critical thinking is an essential skill for a good doctor in any field. But that kind of learning starts early and, ideally, long before a young person applies to college. To get that right, we need to go back to basics in elementary and high school education. If students enter college with “the right stuff,” they’ll have a better understanding of health-related topics whether they choose a career in medicine, or just go to visit the doctor with some reasonable questions in hand.

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On Sergey’s Search (for a Cure for Parkinson’s Disease)

By |July 8th, 2010

This week I brushed up on Parkinson’s disease. What drew me into this mini-review is an informative article, “Sergey’s Search,” that appeared in the July (print) issue of Wired and is now available on-line. The feature, by Thomas Goetz, offers insight on what it’s like to know that you’ve got a genetic disposition to Parkinson’s, details on some enzymes implicated in the illness and, further, considers what might be done to help future patients.

I recommend this article to any of my readers who are interested in genetics, Parkinson’s and/or what some even consider as a new era for health-related research.

There’s a lot to take in –

The Wired story starts with Google co-founder Sergey Brin. A Moscow native and, more recently, a California swimmer, Brin’s got his reasons for concern. He’s got a strong family history, for one thing: the illness has affected both his mother and aunt. It turns out Brin has a genetic disposition to develop the condition because he shares the disease-associated G2019S mutation with his mom. As Goetz explains, this alteration in the DNA segment of the gene encoding LRRK2, a leucine-rich repeat kinase, involves a single-nucleotide switch of an adenine for a guanine.

(I’ll add this, just in case you’re interested: the gene encoding LRRK2, or dardarin, resides at human 12q12 – that’s the long arm of chromosome 12. The G2019S nomenclature indicates that the mutation results in a change at the 2019th amino acid position along the protein’s encoded structure, so that a glycine, normally present, is replaced by a serine molecule at that spot. A fascinating tidbit, news to me today, is that when the gene was first cloned in 2004 the researchers, who’d studied several affected families of Basque origin, called it dardarin, derived from the Basque word dardara, meaning tremor.)

The G2019S mutation is relatively common among Ashkenazi Jews. Still, not all of those who carry the mutation develop the disease, and not all who have the disease have this particular mutation. Other genetic variants have been identified, and it’s not clear exactly how these wreak havoc with LRRK2′s function. Enzymes like LRRK2, a kinase, usually transfer ATP molecules from one protein to another. The presumption is that in Parkinson’s, abnormalities in this enzyme’s function – whether they’re caused by this particular mutation or another – somehow lead to loss of dopamine-producing cells in the brain.

Back to Sergey’s story -

“Brin didn’t panic,” Goetz reports (a point I’d emphasize too). Rather, he was reassured by his mother’s experience and high level of functioning with the disease. She still goes skiing (among other things one’s mother might do), he reasons.

What Brin is doing, along the lines of Goetz’s Decision Tree approach, is cutting his risk as best he can. He exercises regularly, doesn’t smoke, and funds research.

Like other rock star informaticists before him (think of Netscape founder James H. Clarke, who launched Healtheon and Steve Case, who started Revolution Health – these are my examples), Brin is struck by the slow pace of medical investigation:

“Generally the pace of medical research is glacial compared to what I’m used to in the Internet,” Brin says. “We could be looking lots of places and collecting lots of information. And if we see a pattern, that could lead somewhere.”

If only medical research could be more like Google…

Some clinical background:

Parkinson’s, a progressive and often debilitating neurological condition, affects a half million or so people in the U.S. As a practicing as a physician, I cared for many patients who had this illness. Although I would see them for other reasons, it was hard not to notice, and know, the characteristic tremor, rigidity and shuffling walk of those affected. The onset of symptoms is usually insidious, slow and unnerving.

As Goetz indicates, most of what doctors understand about Parkinson’s comes from observing patients in the clinic. Illness emerges, it’s thought, as the number of dopamine-producing cells in the brain diminishes. Dopamine is a neurotransmitter, a molecule that transmits messages between cells or groups of cells within the nervous system. Since around 1967, when the drug Levodopa was first marketed, doctors have prescribed this and other pills for people who have Parkinson’s. While these meds can ameliorate symptoms, these don’t reverse the unstoppable deterioration of body and, ultimately, the mind.

One problem with Parkinson’s research and treatment is that once the disease becomes evident, it’s hard – probably too late – to reverse the loss of dopamine-producing cells. Most people don’t develop symptoms until dopamine production is around 20 percent of normal levels. Now, with the advent of genetic markers and potential to “catch” this disease early on, there’s an opportunity for early intervention.

One promising area for Parkinson’s research:

LRRK2 is a kinase, a kind of enzyme that’s over-active in some cancers. Already, pharmaceutical companies have developed specific kinase inhibitors; a dozen or so are already FDA-approved for treatment of particular cancers, and many more are in the pipeline.

What excites me, in all of this, is the possibility that these drugs might be effective in patients with Parkinson’s disease. And because the same enzyme – LRRK2, or dardarin – is implicated in cases without the particular G2019S mutation, it may be that these drugs would work even in cases that lack this particular genetic feature. (There are examples in oncology, in terms of tumor genetics and responsiveness to targeted drugs, that would support this contention, but that’s just theory for now.) The bottom line, as I see it, is that these new drugs should be carefully tested in clinical trials.

Sergey’s view:

One of the key ideas in Goetz’s piece has to do what he considers and may well be a revolutionary approach to medical research.

…Brin is after a different kind of science altogether. Most Parkinson’s research, like much of medical research, relies on the classic scientific method: hypothesis, analysis, peer review, publication. Brin proposes a different approach, one driven by computational muscle and staggeringly large data sets. It’s a method that draws on his algorithmic sensibility—and Google’s storied faith in computing power…

In what may indeed be a “fourth paradigm” of science, as attributed to the late computer scientist Jim Gray, there’s an inevitable evolution away from hypothesis and toward patterns.

As I understand it, Brin seeks to invert the traditional scientific method by applying Google-size data-mining power to massive and very imperfect data sets in health. Already, he and his colleagues have accomplished this by Google’s Flu Trends, which several years ago beat the CDC to an epidemic’s discovery by two weeks.

You should read this article for yourself, as I’m afraid I can’t adequately describe the potential powers of computational health and science analyses that might be applied to well, pretty much everything in medicine. This goes well beyond a new approach to finding a cure for Parkinson’s disease.

This story, largely based in genomics and computational advances, reflects the power of the human mind, how the gifted son of two mathematicians who fell into a particular medical situation, can use his brains, intellectual and financial resources, and creativity, to at least try to make a difference.

I hope he’s successful!

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DNA Comes Home, or Maybe Not

By |May 25th, 2010

Earlier this month employees at most of 7500 Walgreens pharmacies geared up to stock a new item on their shelves: a saliva sampler for personal genetic testing. On May 11, officials at Pathway Genomics, a San Diego-based biotech firm, announced they’d sell over-the-counter spit kits for around $25 through an arrangement with the retailer. A curious consumer could follow the simple package instructions and send their stuff in a plastic tube, provided in a handy box with pre-paid postage, for DNA analysis.

DNA helix structure (Wikimedia Commons)

Once the sample’s in the lab, the cost of genomics testing depends on what, and how much, you want to know. Pathway offers a variety of options. A pre-pregnancy planning report would check to see if you carry mutations for each of 37 inherited diseases – conditions as varied as beta thalassemia, cystic fibrosis and familial Mediterranean fever – for $179. A profile of tests for genes involved in metabolizing specific drugs, such as Plavix and Coumadin, goes for $79. A vaguer, health conditions panel suggests a propensity to develop particular diseases including Type II diabetes and melanoma. This series runs $179 if purchased separately, but might be had for less through a discounted package rate. A genetics ancestry evaluation lists for $249.

Within two days, after some controversy and a receipt of a letter from the FDA Office of In Vitro Diagnostic Device Evaluation and Safety addressed to James Plante, Founder and CEO of Pathway (dated May 10), Walgreens nixed the plan. Now, Congress wants to know more about direct-to-consumer personal genomics testing. On May 19, the House Committee on Energy and Commerce sent letters to Plante and the CEOs of two major competitors – Navigenics and 23andMe. House Committee Chairman Henry Waxman and colleagues have some questions about how samples are processed and the accuracy of the results:

“The Committee is requesting information from the companies on several aspects of the tests:  How the companies analyze test results to determine consumers’ risk for any conditions, diseases, drug responses, and adverse reactions; the ability of the companies’ genetic testing products to accurately identify any genetic risks; and the companies’ policies for the collection, storage, and processing of individual genetic samples collected from consumers.

The Federal Trade Commission has cautioned consumers about genetic testing kits since 2006.  Still, personal genomics tests are readily through available on-line sales. You can get the 23andMe “DNA Test for Health and Ancestry Information” from the manufacturer or at Amazon.com for $499. Navigenics takes a distinct approach by marketing its genetic tests strictly as a laboratory service for medical practitioners and so, thus far, avoids some rules regarding in vitro diagnostic tools.

New York State, my home, is one region where Walgreens wouldn’t have sold the kits in stores. That’s because of stricter state laws regarding genetic testing.

Dan Vorhaus, writing for the Genomics Law Blog, provides a considered analysis:

At present, whether a genetic test is subject to FDA regulation largely depends on how it is developed and marketed. The literature, as well as current FDA regulatory policy, divides genetic tests into two primary categories:

(i) in vitro diagnostic test kits (also sometimes referred to as IVD kits or, simply, as genetic test kits), which may be sold by their manufacturers directly to consumers, testing laboratories, clinicians or other approved recipients, depending on the device; and

(ii) laboratory developed tests (or LDTs, also sometimes referred to as “home brew” assays), which are not sold directly to the general public or to physicians; rather, a testing service (as opposed to the actual test itself) is marketed, and samples (e.g., of saliva) are collected and submitted to the laboratory for evaluation.

The FDA regulates IVD kits as medical devices…

Up until now personal genomics testing companies have had few constraints, and little profit. What’s clear from the recent news is that we’ll be hearing more about these kits – their manufacture, distribution, accuracy and interpreting results. And that doctors, for our part, have some serious studying to do. Whether the test results go directly to patients, or not, they’re sure to raise many legitimate questions. We’ll need some solid answers about the testing process in itself, besides meaningful responses about what’s found in our DNA.

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Uncertainty Rules (on Eyjafjallajokull, volatility and a patient’s prognosis)

By |April 20th, 2010

(on Eyjafjallajokull, volatility and a patient’s prognosis)

Eyjafjallajökull, April 2010 (Wikimedia Commons, attr: David Karnå)

As pretty much anyone traveling in Europe this week can tell you, it’s sometimes hard to know what happens after an unusual, disruptive event. Volcanologists – the people most expert in this sort of matter – can’t say for sure what the spitfire at Eyjafjallajokull will do next.

It comes down to this: the volcano’s eruption could get better or it could get worse. Or it might fluctuate for a while. If the situation persists, there’s no telling if its course will stutter, like seizures of varying intensity in a person with untreated epilepsy, or if it will flare sporadically like disease exacerbations in patients with MS and then, with some luck, peter out.

Some wonder if the ash might spread westward over the ocean, affecting distant cities like New York and Chicago. Unlikely, it seems to me, but this is far afield from my area of expertise.

What I do know is oncology, and so how I’m thinking about Eyjafjallajokull in medical terms – I want to know the prognosis: how bad and extensive will be the damage, how much will it cost, and in a few weeks or (please, volcanologist, don’t say it could be months) from now, how we can know for sure when the situation has cleared.

Aside from a few pulmonologists who rushed in to say there’s not much to worry about the silica-laden aerosolized dust particles, most scientists who’ve been interviewed have been cautious. I admire their candidness about what they don’t know.

For example, yesterday NPR’s All Things Considered offered this assessment:

“The volcanic eruption that has grounded planes and closed airports throughout Europe appears to be slowing down. But before travelers start rejoicing, Icelandic scientists have a warning: The eruption could start up again any time.

The website of the American Geophysical Union offers some explanations provided by Dr. John Eichelberger, Volcano Hazards Program Coordinator at the U.S. Geological Survey who, it happens, was grounded in Europe after attending a scientific conference:

“Although we’re pretty good at saying when an eruption will start, we’re not so good at saying when it’s going to end. You go mainly on the basis of history, what the volcano has done before. In the case of this volcano, the last time it erupted it was active for over a year. The other factor is how the wind is blowing…

Today, the BBC published several scientists’ opinions including these differing views:

Dr John Murray, an Earth scientist from the Open University in Milton Keynes, said that the ash had “significantly diminished” and the ice over the crater itself had melted…”This is the stage we have been waiting for: the steam explosions due to water being trapped within the erupting lava will have virtually ceased, and the activity has changed to lava outpouring,” he said. …Ash may resume at any time, but it is likely to be less pronounced and prolonged than before.”

But Dr Sue Loughlin from the British Geological Survey pointed out that a decrease in the volcano’s activity might not mean the end of the eruption all together. “There’s seismic activity ongoing, which means the eruption is ongoing…

You get the idea, a volcano in Iceland exploded for the second time in two months, putting much of Europe at a stand-still. Business travelers, vacationers, and companies had to stop and make new arrangements and even compromises. Disappointment and frustration ensued, besides some anger toward those whose job it is to decide if it’s safe to fly.

Going back to medicine – I’m thinking of a patient I once cared for with a non-Hodgkin’s lymphoma. When her disease struck, she was a young mother like me who led a complicated life with lots of responsibilities.

The type of lymphoma she had was uncommon; she sought multiple expert opinions regarding her exact diagnosis and treatment. My colleagues and I didn’t all agree about chemotherapy and radiation, and she was uncertain of how to proceed. Ultimately she opted for surgery and six months of chemotherapy. At the end of all that, she wanted to know if the lymphoma would come back.

“We can never be sure,” I told her. There’s really no choice but to watch and wait.

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Nice Nerds Needed

By |April 12th, 2010

In last weekend’s edition of NPR’s Wait Wait…Don’t Tell Me!, host Peter Sagal asked a panelist about a serious problem facing the Pentagon: There’s a shortage of nerds, a.k.a. geeks.

Space Shuttle Atlantis (NASA image, Wikimedia Commons)

Happily, Houston Chronicle deputy editor and blogger Kyrie O’Connor came to the right answer.

On the quiz show, Sagal reported that Regina Dugan, head of DARPA (the Pentagon’s research arm and developer of the early Internet), recently testified before the House Armed Services Committee about her concern for our country’s most famous five-sided structure’s looming intellectual deficit.

“The decline in science education in this country means fewer nerds are being produced, a fact which has serious national security implications,” Sagal said in summary.

“Nerds molt into tech geeks. Tech geeks grow into scientists and scientists maintain the United States technical superiority,” he explained. No worries, though –

Sagal suggests the current nerd shortage will self-correct based on the predictable laws of high-school ecosystems. (To listen to his short description of this evolutionary process, check the track for Panel Round 2, after minute 4:48.)

Wired covered, earlier, the same story on DARPA’s looming technogeek shortage and Dugan’s forward-thinking statement on the matter:

…outlined her vision for the future of the Pentagon’s blue-sky research arm, with everything from plant-based vaccines to biomimetics making the short list. But none of it’s possible, she told the panel, without more investment in American universities and industry to cultivate the techies of the future…

So we lack sufficient math and science education to support the Pentagon’s needs for cutting-edge technology. And we all know that American businesses are losing out for the same reasons.

My concern is health, that some turned-on science and math-oriented kids should grow up and become physician-scientists or even plain-old, well-trained doctors who are good at interpreting graphs and applying detailed, technical information to patients with complex medical conditions. Last week I wrote that better education would improve health and medical care delivery in the U.S. This seems like an obvious point, but the more common discussion strikes on the need for math and science education to support hard technology in industry.

We’re facing a shortage of primary care physicians, oncologists and other doctor-types. Lots of clever and curious young people are turning away from medicine. The hours are too long, the pay’s too low, and the pressure is too great. If we want doctors who know what they’re doing, we should invest in their education and training, starting early on and pushing well past their graduation from med school.

Sure, we like physicians who are kind and honest people and can talk to them in ways they understand. This is crucial, but only to a point – we still depend on doctors to know their stuff.

I like doctors who are nice nerds. We need more of those, too.

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