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A Radiologist Reflects on the Boston Marathon Bombings: NEMC – 22 Radiologists, 22 Residents with 16 Staff Members Onsite

Posted in Interviews with Scientific Leaders, tagged , , , , , , on May 16, 2013| Leave a Comment »

Reporter: Aviva Lev-Ari, PhD, RN

Article ID #50: A Radiologist Reflects on the Boston Marathon Bombings: NEMC – 22 Radiologists, 22 Residents with 16 Staff Members Onsite. Published on 5/16/2013

WordCloud Image Produced by Adam Tubman

A radiologist reflects on the Boston Marathon bombings

 

By Wayne Forrest, AuntMinnie.com staff writer

May 16, 2013 — Monday, April 15 — Patriots’ Day in Boston — started much like any other day for radiologist Dr. Robert Ward of Tufts Medical Center. But it turned out to be anything but normal after two bombs exploded at the end of the Boston Marathon, sending dozens of injured people to Tufts with battlefield-like injuries.

Ward is chief of musculoskeletal imaging and has been on the job at Tufts for more than five years. He’d finished his administrative duties for the day and was reading routine imaging studies when he received a text from his wife shortly before 3 p.m. A friend, who is a gastroenterology fellow at Boston University and was running in the marathon, told Mrs. Ward there had been explosions heard near the race’s finish line.

Dr. Robert Ward

Dr. Robert Ward from Tufts Medical Center.

“My first inclination was that there was some sort of minor mischief; maybe someone dropped some firecrackers or something like that into a garbage can,” Ward said. “Then a colleague poked his head into the reading room and said there were explosions, limbs were lost, and there were several people dead. At that point, it became an entirely different matter.”

Marathon bombings

Soon thereafter, Ward, the city, the nation, and the rest of world would come to learn that two homemade bombs had been detonated within seconds of each other about 200 yards apart along the path to the finish line. In the end, three people died and more than 260 bystanders and runners were injured, some hurt so severely that they lost limbs.

On a normal Boston Marathon day, most patients at Tufts present with dehydration, or a couple of days after the race, people arrive with extremity abnormalities. There are 22 radiologists and 22 residents at the medical center, with 16 or 17 staff members onsite at any given time.

Word spread quickly that bombing victims were on their way to the level I trauma center.

“I elected to go down to the ER,” Ward recalled. “Patients were starting to come in, probably five times the normal number of people who are in the emergency department [at that time of day]. That place was really in a chaotic manner.”

He estimated there were 13 marathon patients in the emergency room, most of whom were young and probably runners. Most injuries were isolated to the lower extremities; a fair number of patients had skin ripped away from their bodies. What’s more, the limbs of many patients were embedded with the “strangest foreign bodies [and] shrapnel like we have never seen before.”

Some patients had BBs lodged in their extremities, as well as what Ward described as twisted, metallic items that must have been 2 to 4 inches in size. “Generally, those [objects] don’t make it deep into tissue unless there is a substantial explosion, which was obviously the case,” he said.

Onsite care

For the marathon, medical personnel and physicians often take the day off and donate their time to treat race-related injuries and other ailments at a makeshift facility near the finish line. On this day, having that kind of medical expertise so close to the bombings “made for an extraordinary rapid response,” Ward said. “It was almost like battlefield medicine in a sense.”

Under normal circumstances, Tufts’ protocol is to acquire two right-angle x-rays of leg and ankle injuries to determine their extent and location.

“Because of the emergent nature of the injuries, we would get one x-ray and [patients] would go straight to the operating room,” Ward explained. “It is purely a time issue. With some of the bizarre shrapnel fragments that we were seeing, it was hard to believe they were actually inside people.”

Patients with injuries above the waist received a CT scan of the chest, abdomen, and pelvis.

Ward stayed in the emergency department for about 30 minutes, collaborating with a fellow radiologist in the reading room. He later joined the rest of his colleagues, all of whom stayed late into the evening to process all the image interpretations that needed to be done.

Radiology was one of several departments at Tufts that rallied additional personnel to respond to the emergency conditions. The orthopedic department, for example, called in its entire staff to assist in the operating room.

Ward described the coordination between the radiologists and the surgeons as “seamless,” adding that communication between caregivers functioned the same as during any other day at the medical center.

“We have a very well-patterned response, and we were doing our job the same way we do every day, except with a little bit more intensity, given the experience,” he added. “When consultations were necessary, the lines of communication were open.”

Lessons learned

In the wake of the Boston Marathon bombings, Tufts will likely review its emergency response to the event and modify its disaster protocol, if needed, just as it regularly assesses its preparedness through periodic drills.

Within the past 18 months, Tufts was upgraded from a level II to a level I trauma center, which included the implementation of protocols for trauma and potential disaster scenarios.

“In the global sense, we are in the business of helping people, and every day you wake up and have to be aware that you never know what’s going to come your way,” Ward reflected. “You have to be ready, and vigilance is key in every aspect, whether it’s homeland security or taking care of patients who are victims of dramatic, unforeseen events. It brings an urgency to the importance of quality care and making sure that everyone in the department is ready to go at any moment.”

A few days after the tragedy, Ward and a colleague dined at a Boston restaurant while still wearing scrubs, as they had come straight from work. At the end of their dinner, the server insisted that they allow the restaurant to pay for their meal in gratitude for their service. The server told them his friend was treated in the neuro intensive care unit at Tufts during that week and had recently been discharged.

“We were both speechless,” Ward recalled. “That’s just us doing our jobs. The real tragedy is the people who wanted to go see a race, were running in the marathon, and were victims of this tragic incident. We are in the business of helping people. Whatever we can do to help is why we went into this endeavor to begin with.”

Related Reading

Haiti after the earthquake: A radiologist’s story, January 22, 2010

Is your department prepared for disaster? You might be surprised, September 5, 2007
Copyright © 2013 AuntMinnie.com

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Country’s Genetic Diversity can predict the success of its Economy: On Economics and Genetics

Posted in Computational Biology/Systems and Bioinformatics, Genome Biology, Genomic Testing: Methodology for Diagnosis, Health Economics and Outcomes Research, Personalized and Precision Medicine & Genomic Research, Population Health Management, Genetics & Pharmaceutical, tagged , , , , on October 16, 2012| Leave a Comment »

Reporter: Aviva Lev-Ari, PhD, RN

 

Economics and genetics meet in uneasy union

Use of population-genetic data to predict economic success sparks war of words.

10 October 2012 Corrected: 

  1. 12 October 2012
The United States has the right amount of genetic diversity to buoy its economy, claim economists.

picture: D. ACKER/BLOOMBERG VIA GETTY

“The invalid assumption that correlation implies cause is probably among the two or three most serious and common errors of human reasoning.” Evolutionary biologist Stephen Jay Gould was referring to purported links between genetics and an individual’s intelligence when he made this familiar complaint in his 1981 book The Mismeasure of Man. 

Fast-forward three decades, and leading geneticists and anthropologists are levelling a similar charge at economics researchers who claim that a country’s genetic diversity can predict the success of its economy. To critics, the economists’ paper seems to suggest that a country’s poverty could be the result of its citizens’ genetic make-up, and the paper is attracting charges of genetic determinism, and even racism. But the economists say that they have been misunderstood, and are merely using genetics as a proxy for other factors that can drive an economy, such as history and culture. The debate holds cautionary lessons for a nascent field that blends genetics with economics, sometimes called genoeconomics. The work could have real-world pay-offs, such as helping policy-makers to “reduce barriers to the flows of ideas and innovations across populations”, says Enrico Spolaore, an economist at Tufts University near Boston, Massachusetts, who has also used global genetic-diversity data in his research.

But the economists at the forefront of this field clearly need to be prepared for harsh scrutiny of their techniques and conclusions. At the centre of the storm is a 107-page paper by Oded Galor of Brown University in Providence, Rhode Island, and Quamrul Ashraf of Williams College in Williamstown, Massachusetts1. It has been peer-reviewed by economists and biologists, and will soon appear in American Economic Review, one of the most prestigious economics journals.

The paper argues that there are strong links between estimates of genetic diversity for 145 countries and per-capita incomes, even after accounting for myriad factors such as economic-based migration. High genetic diversity in a country’s population is linked with greater innovation, the paper says, because diverse populations have a greater range of cognitive abilities and styles. By contrast, low genetic diversity tends to produce societies with greater interpersonal trust, because there are fewer differences between populations. Countries with intermediate levels of diversity, such as the United States, balance these factors and have the most productive economies as a result, the economists conclude.

The manuscript had been circulating on the Internet for more than two years, garnering little attention outside economics — until last month, when Science published a summary of the paper in its section on new research in other journals. This sparked a sharp response from a long list of prominent scientists, including geneticist David Reich of Harvard Medical School in Boston, Massachusetts, and Harvard University palaeoanthropologist Daniel Lieberman in Cambridge.

In an open letter, the group said that it is worried about the political implications of the economists’ work: “the suggestion that an ideal level of genetic variation could foster economic growth and could even be engineered has the potential to be misused with frightening consequences to justify indefensible practices such as ethnic cleansing or genocide,” it said.

“Our study is not about a nature or nurture debate.”

The critics add that the economists made blunders such as treating the genetic diversity of different countries as independent data, when they are intrinsically linked by human migration and shared history. “It’s a misuse of data,” says Reich, which undermines the paper’s main conclusions. The populations of East Asian countries share a common genetic history, and cultural practices — but the former is not necessarily responsible for the latter. “Such haphazard methods and erroneous assumptions of statistical independence could equally find a genetic cause for the use of chopsticks,” the critics wrote.

They have missed the point, responds Galor, a prominent economist whose work examines the ancient origins of contemporary economic factors. “The entire criticism is based on a gross misinterpretation of our work and, in some respects, a superficial understanding of the empirical techniques employed,” he says. Galor and Ashraf told Nature that, far from claiming that genetic diversity directly influences economic development, they are using it as a proxy for immeasurable cultural, historical and biological factors that influence economies. “Our study is not about a nature or nurture debate,” says Ashraf. 

“It seems like the devil is in the interpretation more than the actual application of the statistics,” says Sohini Ramachandran, a population geneticist at Brown University who provided the genetic data for the study. She adds that Galor and Ashraf used estimates of genetic diversity that she and her colleagues specifically developed to overcome many of the confounding factors caused by the overlapping genetic and cultural histories of neighbouring countries.

Galor and Ashraf are not the first economists to use genetic-diversity data. Spolaore has also found that the differences in genetic diversity between countries can predict discrepancies in their level of economic development2. But he is clear that this is not necessarily a causal relationship:  “In my view it’s not genetic diversity itself that is responsible for this correlation,” he says. “A lot of this could be culture.”

Some say that the field needs a dose of rigour. Many studies linking genetic variation to economic traits make basic methodological errors, says Daniel Benjamin, a behavioural economist at Cornell University in Ithaca, New York. He is part of the Social Science Genetics Association Consortium, a group that brings together social scientists, epidemiologists and geneticists to improve such studies. Problems that medical geneticists have known about for years — such as those stemming from small sample sizes — crop up all too often when economists start to work with the data, he says.

For instance, while searching for genetic associations with factors such as happiness and income in a study of 2,349 Icelanders, Benjamin and his colleagues found a statistically significant association between educational attainment and a variant in a gene involved in breaking down a neurotransmitter molecule3. But the researchers could not replicate this association in three other population samples — a test for false positives that is standard practice in medical genetics — and the team now has reservations about the association. If the field is to develop fruitfully, “I think it’s essential for us to have geneticists involved”, says Benjamin. “We couldn’t do it without their help and insight.”

Nature 490, 154–155 (11 October 2012) doi:10.1038/490154a

Corrected:

In the original text, we wrongly attributed to Enrico Spolaore the opinion that using genetic data in economics could help policy-makers to set immigration levels. He actually suggested that the work could reduce barriers to the flows of ideas and innovations across populations. The text has been amended to reflect that.

References

  1. Ashraf, Q. & Galor, O. Am. Econ. Rev. (in the press).

    Show context

  2. Spolaore, E. & Wacziarg, W. Q. J. Econ. 124, 469–529 (2009).

    Show context

  3. Benjamin, D. J. et al. Annu. Rev. Econ. 4, 627–662 (2012).

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Opposite effects of neurosteroids on the HPA axis: Resolving a paradox

Posted in Innovations in Neurophysiology & Neuropsychology, tagged , , , , , , , on September 30, 2012| 7 Comments »

 

Reporter: Howard Donohue, PhD (EAW)

The hypothalamic-pituitary-adrenal (HPA) axis – which can be thought of as a series of closely linked endocrine structures in the brain – has a key role in triggering the body’s stress response through the secretion of cortisol. In explaining how the HPA axis is itself regulated, for example how its activity is increased in response to a perceived environmental threat, we can infer that the diverse brain areas with which it shares neural interconnections have a crucial role (for a review, see [1]). An equally important question relates to how the activity of the HPA axis is returned to normal when the stress response is no longer needed. To answer this, it is well known that the same “neurosteroid” hormones released by the HPA axis that trigger stress-related biological adaptations also serve to dampen its activity through a “negative feedback” mechanism. In re-defining the biological model of how neurosteroids control the HPA axis, a study led by Jamie Maguire, PhD at Tufts University (Boston, MA) provides some fascinating insights [2]. Moreover, this study has some extremely interesting and counter-intuitive implications for understanding the functions of the “inhibitory” brain chemical gamma-aminobutyric acid (GABA), which is best known for opposing the effects of “excitatory” brain chemicals in order to balance the flow of electrical activity in the brain.

To study how the HPA axis is regulated by neurosteroids, Maguire’s team performed investigations in mice using the neurosteroid tetrahydrodeoxycorticosterone (THDOC). The investigators found that THDOC, when applied to a discrete population of cells in the thalamus called the paraventricular nucleus (PVN), resulted in a decrease in blood levels of corticosterone (the mouse equivalent of the human stress hormone, cortisol). This finding highlights the importance of the PVN as a key anatomical locus in the brain where neurosteroids act, and is consistent with the traditional view of neurosteroids as “negative regulators” of the HPA axis. However, in mice that underwent a stressful “restraint” procedure, it was found that a prior treatment with THDOC (thirty minutes before the stressful experience) resulted in augmentation of corticosterone levels (i.e. relative to mice that underwent the stressful experience but did not receive prior THDOC treatment). In parallel, it was shown that while application of THDOC normally decreased the electrical activity of PVN cells, it actually led to increases in mice that had undergone restraint. Taken together, these findings provide evidence that neurosteroids can have opposite effects on the HPA axis depending on the “stressed” state of the organism.

Thinking about how a neurosteroid hormone can exert opposite effects on PVN cells in the thalamus may be confusing, but what may be more confusing is that these different actions depend on the same “inhibitory” brain chemical, GABA (a neurotransmitter), as well as the same molecular “machinery” (or receptors) with which GABA interacts. This was demonstrated by using mice in which a particular sub-component (or subunit) of the GABA receptor, the gamma subunit, had been genetically deleted; neurosteroids had absolutely no effect on the activity of the HPA axis (neither positive nor negative) in these gamma subunit-deficient mice.

How is it possible to explain the seemingly paradoxical finding that neurosteroids can exert opposite effects on the HPA axis through the same neurotransmitter system? In addressing this question, it is important to remember that although neurotransmitters may be thought of as excitatory or inhibitory, their ability to trigger these effects depends solely on the molecular and cellular apparatus with which they interact. Normally, the inhibitory actions of GABA upon the electrical activity of nerve cells depend on the maintenance of an “electrochemical” gradient by a “transporter” molecule called KCC2 (which transports chloride ions out of cells). Maguire’s team showed that “dephosphorylation” (i.e. the removal of a small chemical moiety – the phosphate group – which is covalently bound at a specific site on the molecule) of KCC2 resulted in lower detectable levels of this transporter in the PVN. Similarly to innumerable other examples in biology where dephosphorylation (or the reverse, phosphorylation) serves as an exquisite regulatory mechanism for controlling the activity of molecular networks, removal of the phosphate group from KCC2 acts as a molecular “switch” that causes the breakdown of the electrochemical gradient. The outcome is that GABA has an excitatory influence on neural activity instead of the inhibitory influence with which it is usually associated.

In common with many important contributions to scientific understanding, these findings should serve as a reminder that it is often necessary to challenge and question what is already “accepted” in our theoretical models, in the light of unexpected and sometimes counter-intuitive experimental results. Whatever the line of scientific inquiry may be, the reward for doing so will be a deeper and more comprehensive understanding of the natural phenomena being studied. The findings of Maguire and colleagues, published in the Journal of Neuroscience, have possible therapeutic implications for disorders associated with disrupted function of the HPA axis, including epilepsy and depression.

References

1. http://www.nature.com/nrn/journal/v10/n6/full/nrn2647.html

2. http://www.jneurosci.org/content/31/50/18198.long

 

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Sequenom Center for Molecular Medicine diagnostic services: MaterniT21 Plus test detects for T18 and T13.

Posted in Bio Instrumentation in Experimental Life Sciences Research, Biological Networks, Gene Regulation and Evolution, Biomarkers & Medical Diagnostics, Chemical Genetics, Computational Biology/Systems and Bioinformatics, Genome Biology, Genomic Testing: Methodology for Diagnosis, Health Economics and Outcomes Research, Molecular Genetics & Pharmaceutical, Personalized and Precision Medicine & Genomic Research, Pharmaceutical R&D Investment, Population Health Management, Genetics & Pharmaceutical, tagged , , , , , , , , on August 15, 2012| Leave a Comment »

 

Tufts Health Plan to Cover Sequenom’s MaterniT21, Pathwork’s Tissue of Origin Tests

Reporter: Aviva Lev-Ari, PhD, RN

http://www.genomeweb.com/mdx/tufts-health-plan-cover-sequenoms-maternit21-pathworks-tissue-origin-tests

NEW YORK (GenomeWeb News) – Tufts Health Plan will begin covering Sequenom’s MaterniT21 Plus trisomy 21 test and Pathwork Diagnostics‘ Tissue of Origin test starting Oct. 1.

In an update to providers posted on its website, the health plan said that it may authorize coverage of the MaterniT21 test for patients who are plan members if they are at least 35 years old when they give birth; have a fetal aneuploidy screening test result including maternal serum screening and/or ultrasound evaluation that indicates the possibility of trisomy 21; or the plan member has a family history or prior pregnancy involving aneuploidy.

In a research note Oppenheimer analyst David Ferreiro said that Tufts Health Plan has approximately 1 million lives under coverage and a network of 90 hospitals and 25,000 healthcare providers.

“We view this decision as an incremental positive for [Sequenom] and as validation of the value proposition MaterniT21 presents to payors,” he said. “The adoption rate is encouraging and could positively impact payor decisions, further entrenching,” the company.

Two weeks ago, Sequenom said that in the second quarter revenues from its Sequenom Center for Molecular Medicine diagnostic services rose five-fold to $8.1 million driven by the MaterniT21 Plus test, which was launched in the fall. The test also detects for T18 and T13.

As adoption of the test continues to ramp at an increasing rate, the San Diego-based company increased its internal goal of billed MaterniT21 Plus tests for 2012 to 50,000 from an earlier goal of 40,000.

The company has stopped announcing coverage decisions by individual plans following an incident in the spring in which Coventry Health Care National Networkterminated a coverage decision for MaterniT21 Plus one week after Sequenom said that Coventy would cover the test. Sequenom said at the time that Coventry’s decision was without cause and was not a judgment on the company, Sequenom CMM, or its products.

In a statement today to GenomeWeb Daily News, a Sequenom spokesperson declined to disclose the terms of the contract with Tufts Health Plan. She said that Sequenom CMM has more than 26 million live under contract, and “we operate as an out-of-network laboratory where we are not yet contracted and bill payors accordingly.”

Tufts Health Plan also said that it will begin coverage of Pathwork Diagnostics’ Pathwork Tissue of Origin test, beginning on Oct. 1. The test is for the identification of challenging tumors, including poorly differentiated, undifferentiated, and metastatic cancers.

The plan said it may authorize coverage of the test if it is ordered by an oncologist and the plan member is diagnosed with metastatic cancer; the clinical evaluation has not identified the primary site of the cancer; the pathology report is submitted to Tufts Health Plan for review; and the pathology examination is unable to conclusively identify the primary site, or has identified two or more possible primary sites.

Use of the test to confirm a diagnosis will not be covered by the health plan.

 

 

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