Tuesday, November 26, 2013

F.D.A. Orders Genetic Testing Firm to Stop Selling DNA Analysis Service

23andMe, Inc. 11/22/13


Department of Health and Human Services	Public Health Service Food and Drug Administration
	10903 New Hampshire Avenue Silver Spring, MD 20993

Nov 22, 2013

Ann Wojcicki

CEO

23andMe, Inc.

1390 Shoreline Way

Mountain View, CA 94043

Document Number: GEN1300666

Re: Personal Genome Service (PGS)

WARNING LETTER

Dear Ms. Wojcicki,

The Food and Drug Administration (FDA) is sending you this letter because you are marketing the 23andMe Saliva Collection Kit and Personal Genome Service (PGS) without marketing clearance or approval in violation of the Federal Food, Drug and Cosmetic Act (the FD&C Act).

This product is a device within the meaning of section 201(h) of the FD&C Act, 21 U.S.C. 321(h), because it is intended for use in the diagnosis of disease or other conditions or in the cure, mitigation, treatment, or prevention of disease, or is intended to affect the structure or function of the body. For example, your company’s website at www.23andme.com/health (most recently viewed on November 6, 2013) markets the PGS for providing “health reports on 254 diseases and conditions,” including categories such as “carrier status,” “health risks,” and “drug response,” and specifically as a “first step in prevention” that enables users to “take steps toward mitigating serious diseases” such as diabetes, coronary heart disease, and breast cancer. Most of the intended uses for PGS listed on your website, a list that has grown over time, are medical device uses under section 201(h) of the FD&C Act. Most of these uses have not been classified and thus require premarket approval or de novo classification, as FDA has explained to you on numerous occasions.

Some of the uses for which PGS is intended are particularly concerning, such as assessments for BRCA-related genetic risk and drug responses (e.g., warfarin sensitivity, clopidogrel response, and 5-fluorouracil toxicity) because of the potential health consequences that could result from false positive or false negative assessments for high-risk indications such as these. For instance, if the BRCA-related risk assessment for breast or ovarian cancer reports a false positive, it could lead a patient to undergo prophylactic surgery, chemoprevention, intensive screening, or other morbidity-inducing actions, while a false negative could result in a failure to recognize an actual risk that may exist. Assessments for drug responses carry the risks that patients relying on such tests may begin to self-manage their treatments through dose changes or even abandon certain therapies depending on the outcome of the assessment. For example, false genotype results for your warfarin drug response test could have significant unreasonable risk of illness, injury, or death to the patient due to thrombosis or bleeding events that occur from treatment with a drug at a dose that does not provide the appropriately calibrated anticoagulant effect. These risks are typically mitigated by International Normalized Ratio (INR) management under a physician’s care. The risk of serious injury or death is known to be high when patients are either non-compliant or not properly dosed; combined with the risk that a direct-to-consumer test result may be used by a patient to self-manage, serious concerns are raised if test results are not adequately understood by patients or if incorrect test results are reported.

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NYTimes Article

Monday, November 25, 2013

Regional variability of imaging biomarkers in autosomal dominant Alzheimer’s disease

Beta-amyloid plaque accumulation, glucose hypometabolism, and neuronal atrophy are hallmarks of Alzheimer’s disease. However, the regional ordering of these biomarkers prior to dementia remains untested. In a cohort with Alzheimer’s disease mutations, we performed an integrated whole-brain analysis of three major imaging techniques: amyloid PET, [18F]fluro-deoxyglucose PET, and structural MRI. We found that most gray-matter structures with amyloid plaques later have hypometabolism followed by atrophy. Critically, however, not all regions lose metabolic function, and not all regions atrophy, even when there is significant amyloid deposition. These regional disparities have important implications for clinical trials of disease-modifying therapies.

Graphene: The quest for supercarbon

Graphene's dazzling properties promise a technological revolution, but Europe may have to spend a billion euros to overcome some fundamental problems.

Graphene offers a way to make flexible and transparent smartphone screens.

BYUNG HEE HONG

Mr G gazes out from a recruitment poster hanging in an engineering building in Cambridge, UK. His cartoon cape billows out behind him, his sketched-in muscles ripple beneath his costume, his chest is emblazoned with a 'G' inside a hexagon — and his forefinger points straight at the viewer. “I want you for the Graphene Flagship!” declares the cartoon crusader, championing a material as super as he is.

Graphene is the thinnest substance ever made: a single sheet of carbon atoms arranged in a hexagonal honeycomb pattern. It is as stiff as diamond and hundreds of times stronger than steel — yet at the same time is extremely flexible, even stretchable. It conducts electricity faster at room temperature than any other known material, and it can convert light of any wavelength into a current. In the decade since graphene was first isolated, researchers have proposed dozens of potential applications, from faster computer chips and flexible touchscreens to hyper-efficient solar cells and desalination membranes

Hence Mr G's call to arms. The character was created in 2011 to help publicize a multinational push for a Graphene Flagship project: a decade-long, €1-billion (US$1.35-billion), all-European effort to take graphene from the laboratory bench to the factory floor

Most research laboratories still make graphene using the method pioneered in 2004 by Andre Geim and Konstantin Novoselov at the University of Manchester, UK, who went on to win the 2010 Nobel Prize in Physics for their studies. Geim and Novoselov found that they just had to touch a strip of household sticky tape to ordinary graphite — which consists of billions of layers of graphene stacked on top of one another — and they could peel off thin flakes of carbon. By repeatedly splitting those flakes, they were eventually left with graphene². This was a technique that any laboratory could use, and graphene research exploded.

But the method is much too slow and finicky for industrial-scale production. Just one micrometre-sized flake made in this way can cost more than $1,000 — making it, gram for gram, one of the most expensive materials on Earth.

The leading alternative³ relies on chemical vapour deposition (CVD), whereby methane is piped over a catalytic copper foil heated to about 1,000 °C. As the methane breaks down, small islands of pure carbon begin to grow on the foil, linking together to form a patchwork polycrystalline sheet of graphene. Harsh chemicals are then used to etch away the copper to free a sheet of graphene tens of centimetres wide, which can be transferred to a silica or polymer substrate. That process brings costs below $100,000 per square metre, but the product is often riddled with defects, impairing its electrical properties and making it much weaker than flakes produced by the sticky-tape method.

HPV: Sex, cancer and a virus

Human papillomavirus is causing a new form of head and neck cancer— leaving researchers scrambling to understand risk factors, tests and treatments.

Human papillomavirus, seen in a coloured transmission electron micrograph.

PASIEKA/SPL/GETTY

On a sunny day in 1998, Maura Gillison was walking across the campus of Johns Hopkins University in Baltimore, Maryland, thinking about a virus. The young oncologist bumped into the director of the university's cancer centre, who asked politely about her work. Gillison described her discovery of early evidence that human papillomavirus (HPV) — a ubiquitous pathogen that infects nearly every human at some point in their lives — could be causing tens of thousands of cases of throat cancer each year in the United States. The senior doctor stared down at Gillison, not saying a word. “That was the first clue that what I was doing was interesting to others and had potential significance,” recalls Gillison.

Only in 2005 did Gillison finally sit down with a doctoral student to analyse the data. Within an hour, the fruits of those years of labour popped up on the computer screen: people with head and neck cancer were 15 times more likely to be infected with HPV in their mouths or throats than those without¹. The association backed up some of Gillison's earlier work, which showed² how HPV DNA integrates itself into the nuclei of throat cells and produces cancer-causing proteins. Gillison leapt from her chair and began jumping up and down. “The association was so incredibly strong, it made me realize this was absolutely irrefutable evidence,” she says.

Since then, she and a network of other researchers have amassed a mountain of evidence that HPV causes a large proportion of head and neck cancers, and that these HPV-positive cancers are on the rise. The finding has been “a paradigm-shifting realization in the field”, says Robert Ferris, chief of the division of head and neck surgery at the University of Pittsburgh Cancer Institute in Pennsylvania.

Nut Consumption and Mortality

NEJM QUICK TAKE

Nut Consumption and Mortality

New research on nut consumption and mortality is summarized in a short animation.

ORIGINAL ARTICLE

Thursday, November 21, 2013

Vitamin D–Binding Protein and Vitamin D Status of Black Americans and White Americans

NEJM

Large

CONCLUSIONS

Community-dwelling black Americans, as compared with whites, had low levels of total 25-hydroxyvitamin D and vitamin D–binding protein, resulting in similar concentrations of estimated bioavailable 25-hydroxyvitamin D. Racial differences in the prevalence of common genetic polymorphisms provide a likely explanation for this observation. (Funded by the National Institute on Aging and others.)

Risk Calculator for Cholesterol Appears Flawed

By GINA KOLATA

Published: November 17, 2013 721 Comments

Last week, the nation’s leading heart organizations released a sweeping new set of guidelines for lowering cholesterol, along with an online calculator meant to help doctors assess risks and treatment options. But, in a major embarrassment to the health groups, the calculator appears to greatly overestimate risk, so much so that it could mistakenly suggest that millions more people are candidates for statin drugs.

Mark Graham for The New York Times

Dr. Nancy Cook and Dr. Paul M. Ridker of Harvard Medical School found that a new online calculator used to assess heart treatment options overestimated the risks that many people face.

Multimedia

Graphic

Estimating Risk

“It’s stunning,” said the cardiologist, Dr. Steven Nissen, chief of cardiovascular medicine at the Cleveland Clinic. “We need a pause to further evaluate this approach before it is implemented on a widespread basis.”

The controversy set off turmoil at the annual meeting of the American Heart Association, which started this weekend in Dallas. After an emergency session on Saturday night, the two organizations that published the guidelines — the American Heart Association and the American College of Cardiology — said that while the calculator was not perfect, it was a major step forward, and that the guidelines already say patients and doctors should discuss treatment options rather than blindly follow a calculator.

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risk calculator

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November 17, 2013

Friday, November 15, 2013

ANTI HPV-VACCINE VIDEO RAISES FALSE FEARS OF GARDASIL AROUND THE INTERNET

By Nathalie O'Neill @oneillnathalie 15 hours ago

Today in useless fear mongering news, people are apparently afraid of Gardasil now, the vaccine that has the potential to bring the number of people who get newly infected with HPV every year – 14 million – way down. All courtesy of a video from Jenny Thompson of Health Sciences Institute that’s full of claims about women dying after getting the vaccine.

In case you’re seeing something like this on your own Facebook feed, Snopes.com has got you covered:

The message quoted above warns that the Centers for Disease Control (CDC) has already received nearly 12,000 complaints about adverse medical issues related to Gardasil vaccinations, and that 32 young women died after receiving Gardasil vaccinations. Although this information is accurate in a strictly literal sense, it is a misleading presentation of raw data that does not in itself establish a causal connection between Gardasil and the posited medical dangers.

The video can’t hide its political roots: Thompson and the Health Sciences Institute are practically on a slut-hunt. According to Thompson, girls who get the Gardasil vaccine won’t use protection during sex. The implication is that parents should avoid getting their children the Gardasil vaccination, since their pure nine-year-old girls will stay away from sex and STDs anyway — because no one wants their daughter to grow up to be well-informed, sexually active teenager who’s protected from HPV, right? Snopes is on to that too:

Note that this video deals primarily with subjects such as the political and moral issues involved with requiring HPV vaccinations for young girls, the notion that vaccinated girls might mistakenly believe they had been immunized against contracting sexually transmitted diseases (other than HPV), and the claim that cervical cancer deaths can be effectively eliminated through means other than HPV vaccinations. It offers no real evidence that Gardasil vaccinations are dangerous other than to cite the raw VAERS data referenced above (without noting that analysis of those reports failed to establish a causal link between HPV vaccinations and the reported serious adverse events).

Your move, conservative anti-vaccination lobby.

Thursday, November 14, 2013

Food for thought: Eat your way to dementia

Sugar junkies take note: a calorific diet isn't just bad for your body, it may also trigger Alzheimer's disease

Editorial: "Brain diabetes: the ultimate food scare"

SUZANNE DE LA MONTE's rats were disoriented and confused. Navigating their way around a circular water maze - a common memory test for rodents - they quickly forgot where they were, and couldn't figure out how to locate the hidden, submerged safety platform. Instead, they splashed around aimlessly. "They were demented. They couldn't learn or remember," says de la Monte, a neuropathologist at Brown University in Providence, Rhode Island.

A closer look at her rats' brains uncovered devastating damage. Areas associated with memory were studded with bright pink plaques, like rocks in a climbing wall, while many neurons, full to bursting point with a toxic protein, were collapsing and crumbling. As they disintegrated, they lost their shape and their connections with other neurons, teetering on the brink of death.

Such changes are the hallmarks of Alzheimer's disease, and yet they arose in surprising circumstances. De la Monte had interfered with the way the rats' brains respond to insulin. The hormone is most famous for controlling blood sugar levels, but it also plays a key role in brain signalling. When de la Monte disrupted its path to the rats' neurons, the result was dementia.

Poor sensitivity to insulin is typically associated with type 2 diabetes, in which liver, fat and muscle cells fail to respond to the hormone. But results such as de la Monte's have led some researchers to wonder whether Alzheimer's may sometimes be another version of diabetes - one that hits the brain. Some have even renamed it "type 3 diabetes".

115m people globally will get Alzheimer's by 2050

If they are right - and a growing body of evidence suggests they might be - the implications are deeply troubling. Since calorific foods are known to impair our body's response to insulin, we may be unwittingly poisoning our brains every time we chow down on burgers and fries. People with type 2 diabetes, who have already developed insulin resistance, may be particularly at risk. "The epidemic of type 2 diabetes, if it continues on its current trajectory, is likely to be followed by an epidemic of dementia," says Ewan McNay of the University at Albany in New York. "That's going to be a huge challenge to the medical and care systems."

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Tuesday, November 12, 2013

Large NIH projects cut

NATURE | NEWS

Budget woes force institutes to scrutinize expensive, non-competitive programmes.

Sara Reardon

12 November 2013

Rights & Permissions

A sample of the thousands of protein structures solved with the help of a US National Institutes of Health programme that has now been closed down.

And NSF

climate models shows increased tropical cyclone activity over the 21st century

A recently developed technique for simulating large [O(104)] numbers of tropical cyclones in climate states described by global gridded data is applied to simulations of historical and future climate states simulated by six Coupled Model Intercomparison Project 5 (CMIP5) global climate models. Tropical cyclones downscaled from the climate of the period 1950–2005 are compared with those of the 21st century in simulations that stipulate that the radiative forcing from greenhouse gases increases by

over preindustrial values. In contrast to storms that appear explicitly in most global models, the frequency of downscaled tropical cyclones increases during the 21st century in most locations. The intensity of such storms, as measured by their maximum wind speeds, also increases, in agreement with previous results. Increases in tropical cyclone activity are most prominent in the western North Pacific, but are evident in other regions except for the southwestern Pacific. The increased frequency of events is consistent with increases in a genesis potential index based on monthly mean global model output. These results are compared and contrasted with other inferences concerning the effect of global warming on tropical cyclones.
Source

Did climate change cause Typhoon Haiyan?

There is limited evidence that warming oceans could make superstorms more likely.

Quirin Schiermeier

11 November 2013

A large ship that washed ashore in Tacloban, the Philippines, on 10 November during Typhoon Haiyan — the most violent tropical storm on record.

AARON FAVILA/AP PHOTO

As the Philippines assesses the havoc caused by Typhoon Haiyan, which according to some reports has killed as many as 10,000 people, speculation is heating up as to whether the disaster might be a manifestation of climate change. Speaking today on the first day of United Nations climate talks in Warsaw, the head of the Philippines delegation, Yeb Sano, said that he will stop eating until negotiators make "meaningful" progress.

But can the devastating storm be linked to the changing global climate? Nature wades into the evidence.

Was Haiyan the strongest storm ever measured?

Apparently, yes. With sustained wind speeds of more than 310 kilometres per hour, Haiyan was the most powerful tropical cyclone to make landfall in recorded history. The previous record was held by Hurricane Camille, which hit Mississippi in 1969 with wind speeds of just over 300 kilometres per hour.

It is the third time that disaster has struck the Philippines in less than 12 months. In August, Typhoon Trami caused massive flooding on the island of Luzon. And in December 2012, Typhoon Bopha killed up to 2,000 people and caused some US$1.7 billion in damage on the island of Mindanao. Haiyan could easily surpass that figure: its total economic impact could reach US$14 billion, according to a report by a senior insurance analyst at Bloomberg Industries, a data company in New York.

Haiyan's death toll might have been much bigger had so many people in the Philippines not heeded storm warnings and fled at-risk areas.

What’s the difference between a cyclone, a typhoon and a hurricane?

They are just different names for the same type of extreme weather phenomenon occurring in different parts of the world. These storms are called hurricanes in the Atlantic and northeastern Pacific oceans, typhoons in the northwestern Pacific and cyclones in the south Pacific and Indian Ocean.

Are such storms getting worse in a warming world?

This is the million-dollar question, but there is not yet a scientific consensus on how to answer it.

Storms receive their energy from the ocean, so it would seem logical that they would get stronger, and perhaps also more frequent, as the upper layers of tropical oceans get warmer. The potential intensity of tropical storms does increase with warmer sea surface temperatures. However, the effect of warming seas could be counteracted by the apparent increase in the strength of shearing winds — winds blowing in different directions and varying in strength at different altitudes. Shearing winds tend to hinder the formation of storms, or tear them apart before they can reach extreme strength.

On balance, many climate researchers think that it is plausible that tropical-storm activity will rise as the planet warms. There is some evidence¹ that storm intensity has increased over the last three decades, but reliable data are limited to the north Atlantic, where observations are most abundant. In other places, the evidence is not yet conclusive².

The Intergovernmental Panel on Climate Change (IPCC) in its latest report cautiously summarizes the current state of knowledge:

“Time series of cyclone indices such as power dissipation, an aggregate compound of tropical cyclone frequency, duration, and intensity that measures total wind energy by tropical cyclones, show upward trends in the North Atlantic and weaker upward trends in the western North Pacific since the late 1970s, but interpretation of longer-term trends is again constrained by data quality concerns.”

Global climate models are too coarse to resolve relatively small-scale atmospheric disturbances such as tropical storms — despite how prominently these phenomena feature on weather maps. Scientists therefore need to infer the effect of global warming on storm activity from general patterns of atmospheric circulation.What are the models saying?

For example, hurricane researcher Kerry Emanuel of the Massachusetts Institute of Technology in Cambridge has used³ a technique to simulate large numbers of tropical cyclones in climate models. When applied to scenarios of historical and future climate described by six state-of-the-art climate models, his method predicted that both the frequency and intensity of tropical cyclones will increase during the twenty-first century in all tropical ocean regions, except the southwestern Pacific. Emanuel’s study was published too late for inclusion in the latest IPCC report.

The Role of Surface Oxygen in the Growth of Large Single-Crystal Graphene on Copper

Science

The growth of high-quality single crystals of graphene by chemical vapor deposition on copper (Cu) has not always achieved control over domain size and morphology, and the results vary from lab to lab under presumably similar growth conditions. We discovered that oxygen (O) on the Cu surface substantially decreased the graphene nucleation density by passivating Cu surface active sites. Control of surface O enabled repeatable growth of centimeter-scale single-crystal graphene domains. Oxygen also accelerated graphene domain growth and shifted the growth kinetics from edge-attachment–limited to diffusion-limited. Correspondingly, the compact graphene domain shapes became dendritic. The electrical quality of the graphene films was equivalent to that of mechanically exfoliated graphene, in spite of being grown in the presence of O.

F.D.A. Ruling Would All but Eliminate Trans Fats

The Food and Drug Administration proposed measures on Thursday that would all but eliminate artery-clogging, artificial trans fats from the food supply, the culmination of three decades of effort by public health advocates to get the government to take action against them.

Artificial trans fats — a major contributor to heart disease in the United States — have already been substantially reduced in foods. But they still lurk in many popular products, like frostings, microwave popcorn, packaged pies, frozen pizzas, margarines and coffee creamers. Banning them completely could prevent 20,000 heart attacks and 7,000 deaths from heart disease each year, the F.D.A. said.

“This is the final slam dunk on the trans fat issue,” said Barry Popkin, a nutrition epidemiologist at the University of North Carolina, Chapel Hill.

Reward-based hypertension control by a synthetic brain–dopamine interface

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Significance

Essential activities such as feeding and reproduction as well as social, emotional, and mental behavior are reinforced by the brain’s reward system. Pleasure status directly correlates with dopamine levels released in the brain. Because dopamine leaks into the bloodstream via the sympathetic nervous system, brain and blood dopamine levels are interrelated. We designed a synthetic dopamine sensor-effector device that enables engineered human cells, insulated by immunoprotective microcontainers and implanted into the abdomen of mice, to monitor blood-dopamine levels and drive dopamine-dependent secretion of product proteins in pleasure situations associated with palatable food, drugs, or sexual arousal. Hypertensive animals treated with this device, which produces a clinically licensed antihypertensive peptide, had their high blood pressure corrected when exposed to sexual arousal.

Was Arafat Poisoned?

NATURE | BREAKING NEWS

Investigation claims evidence of polonium poisoning in death of Palestinian leader but draws no certain conclusions.

Mark Peplow

07 November 2013

Rights & Permissions

Yasser Arafat died in 2004 in what some now think were suspicious circumstances.

CHRIS HONDROS/GETTY IMAGES

Tests on the exhumed body of the late Palestinian leader Yasser Arafat have found traces of the radioactive isotope polonium-210, prompting renewed claims that he was deliberately poisoned.

"The results could reasonably support the proposition that the death was the consequence of poisoning by polonium 210," says Patrice Mangin, director of the University Centre of Legal Medicine in Lausanne, Switzerland, who led the analysis.

But his lengthy report on the investigations, released yesterday (PDF), is clear that the evidence offers no firm conclusions. “I don’t think it will settle the debate,” says Patrick Regan, a nuclear physicist at the University of Surrey, UK.

Arafat died in a Paris hospital on 11 November 2004 after a month of ill health that included symptoms such as abdominal pain and vomiting. No autopsy was conducted, allowing rampant speculation about the cause of his death. In 2011, news broadcaster Al Jazeera obtained personal belongings that Arafat had used shortly before his death, including a toothbrush and clothing, and commissioned the Lausanne team to investigate.

Former KGB officer Alexander Litvinenko had been killed by polonium-210 poisoning in 2006, and the case inspired the Lausanne team to hunt for the same isotope in Arafat’s effects. Polonium-210 emits alpha particles that rip cells apart like a wrecking ball, destroying a person’s immune system and causing catastrophic organ failure.

To their surprise, the researchers found polonium¹. A piece of Arafat’s underwear stained with urine had a radioactivity of 181 millibecquerels (mBq), almost 100 times higher than normal background levels (see ‘Was Yasser Arafat killed by polonium?’). This prompted a French murder investigation, and his body was exhumed on 27 November 2012. Investigators took samples from his bones, burial shroud and the soil from around the grave.

Mangin's team scoured the samples for the characteristic energy signature of polonium-210’s alpha particles. But they also measured other isotopes that would reveal whether that polonium-210 was from a natural or synthetic source.

Naturally occurring radon-222 decays to give a long chain of daughter products, including lead-210 and subsequently polonium-210, which our bodies contain in trace amounts. Roughly two years after death, those isotopes would normally reach equilibrium so that they emit the same amounts of radiation. But synthetic polonium-210 is made by irradiating bismuth-209 with neutrons, and should contain no lead-210. If Arafat had been poisoned, “a significant enhancement of polonium-210 compared to lead-210 would be a smoking gun,” says Regan.

The results were mixed. Some samples showed unusually high levels of the isotopes – but in many cases their radioactivity was fairly evenly matched. Some even had much more lead-210 than polonium-210, suggesting that the isotopes may have been extracted from bone samples at different rates, further muddying the data. There is certainly no smoking gun in the report, says Regan.

One explanation for the matching isotope ratios could be that Arafat was given a dose of polonium-210 contaminated with lead-210. Although most of the polonium would have decayed by now, lead-210 has a half-life of 22 years, so its radioactivity would barely have declined since Arafat's death. The Lausanne scientists tested a commercial sample, and found that it did contain enough lead-210 to account for this. “It’s a plausible hypothesis,” says Regan.

They also saw elevated levels of a polonium-210 decay product, lead-206, in some samples, providing additional evidence that Arafat died with high levels of polonium-210 in his body. Although the analysis cannot prove foul play, "one doesn't absorb by accident, or voluntarily, a source of polonium", says François Bochud, a colleague of Mangin's and co-author of the report. "From the moment one considers that the polonium was introduced artificially in the organism, that necessarily implies the intervention of a third party.”

Others are less certain. Polonium-210 has a half-life of 138 days, so any radioactivity measured by the team would have been a million times lower than in 2004. “After so many half-lives you can’t reliably say how much polonium was there eight years ago, there’s too much background interference,” says Kai Vetter, head of applied nuclear physics at the Lawrence Berkeley National Laboratory in California. Vetter suggests that the team should survey other commercial polonium samples to back up their lead contamination hypothesis, and re-check the methods they used to extract the isotopes from tissue for systematic errors.

Meanwhile, two other teams, in France and Russia, have received tissue samples, but have yet to report their results. Until then, says Vetter, the Lausanne analysis simply raises more questions about Arafat’s mysterious death.

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