Science Weekly: Uranium wars

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Alok Jha looks at the power of uranium, a new climate change map and synthetic vocal chords

Science Weekly Extra: Climate change map unveiled

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Listen to the entire launch event of the government’s 4C climate change map

Growth at Target Health

Without the terrific support of our clients and great staff, some of whom have been working with/ at Target Health for over 10 years, nothing would be possible. 

As the recession hits home, it is key for small business such as Target Health Inc. to take the lead in America’s recovery. Therefore, Target Health is pleased to announce three new hires as part of our natural growth: 1) Statistician, 2) SAS programmer and 3) Web programmer. This 8% increase in staff represents what America needs to get out of the doldrums. By hiring additional staff, there is also the need to provide office space, computers, supplies, etc. which make a lot of other companies happy. We encourage all small businesses to follow our lead. 

For more information about Target Health and our software tools for paperless clinical trials, please contact Dr. Jules T. Mitchel (212-681-2100 ext 0) or Ms. Joyce Hays. Target Health’s software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website at

Color Plays Musical Chairs In The Brain

Color is normally thought of as a fundamental attribute of an object: a red Corvette, a blue lake, a pink flamingo. Yet despite this popular notion, new research suggests that our perception of color is malleable and relies heavily on biological processes of the eye and 1) ___. The brain’s neural mechanisms keep straight which color belongs to what object, so one doesn’t mistakenly see a blue flamingo in a pink lake. But what happens when a color loses the object to which it is linked? Research at the University of Chicago has demonstrated, for the first time, that instead of disappearing along with the lost object, the color latches onto a region of some other object in view – a finding that reveals a new basic property of 2) ___. The research shows that the brain processes the shape of an object and its color in two separate 3) ___ and, though the object’s shape and color normally are linked, the neural representation of the color can survive alone. When that happens, the brain establishes a new link that binds the color to another visible 4) ___. “Color is in the brain. It is constructed, just as the meanings of words are constructed. Without the 5) ___ processes of the brain, we wouldn’t be able to understand colors of objects any more than we could understand words of a language we hear but don’t know,” said Steven Shevell, a University of Chicago psychologist who specializes on color and vision. Shevell’s findings are reported in a paper, “Color-Binding Errors During Rivalrous Suppression of Form,” in the current issue of Psychological Science. The work expands the understanding of how the brain is able to integrate the multiple features of an object, such as shape, color, location and velocity, into a unified whole. “An aspect of human vision that we normally don’t appreciate is that different features of an object, including color and shape, can be represented in different parts of the brain,” said Shevell. If a person sees a basketball coming, it is perceived as having a particular color, shape and velocity. “The knitting together, or what can be called ‘neural gluing,’ of all those different features so we see a unified object is a complex 6) ___ done by the brain and our research focused on how the brain does that.” To study how the brain represents the color of 7) ___, the researchers used a technique called binocular rivalry. The technique presents a different image to each eye and thus pits signals from the right eye against signals from the left. The brain has difficulty integrating the two eyes’ incompatible 8) ___. When the signals from the two eyes are different enough, the brain resolves the conflicting information by suppressing the information from one of the 9) ___. This feature of the brain, was exploited with a method that caused the shape from one eye to be suppressed but not its color. The researchers first showed subjects vertically oriented green stripes in the left eye and a horizontally oriented set of red stripes in the right eye. The brain cannot fuse them in a way that makes sense. So the brain sees only horizontal or vertical. For their study, the researchers developed a new form of the technique that allowed the horizontal pattern to be suppressed without eliminating its red color, which continued on to the brain. At this point, the brain has a musical chairs problem. Both the red and green colors reach consciousness but with only the one vertical pattern one object but two colors. The surprising result was that the “disembodied red, which originated from the unseen horizontal pattern in one eye, glued itself to parts of the 10) ___ seen vertical pattern from the other eye. According to Shevell, that proves the idea of neural binding or neural gluing, where the color is connected to the object in an active neural process. “To us it seems automatic,” Shevell added. “Every basketball has a color. Every shirt has a color, but the brain must link each object’s color to its shape.” The research is funded by the National Institutes of Health.


  • 1) brain; 2) sight; 3) pathways; 4) shape; 5) neural; 6) function; 7) objects; 8) signals; 9) eyes; 10) consciously

Joseph Priestley – 1767

In 1767, the chemist Joseph Priestley stood in his laboratory one day with an idea to help English mariners stay healthy on long ocean voyages. He infused water with carbon dioxide to create an effervescent liquid that mimicked the finest mineral waters consumed at European health spas. Priestley’s man-made tonic, which he urged his benefactors to test aboard His Majesty’s ships, never prevented a scurvy outbreak. But, as the decades passed, his carbonated water became popular in cities and towns for its enjoyable taste and later as the main ingredient of sodas, sparkling wines, and all variety of carbonated drinks. Missing from this nearly 250-year-old story is a scientific explanation of how people taste the carbonation bubbling in their glass. A somatosensory system transmits sensory information within the body from protein receptors to nerve fibers and onward to the brain, where a sensation is perceived. Common sensory information includes taste, touch, pain, and temperature. According to an article published in Science (2009 16 October: 443-445), a research team has reported that they have discovered the answer in mice, whose sense of taste closely resembles that of humans. It appears that the taste of carbonation is initiated by an enzyme tethered like a small flag from the surface of sour-sensing cells in taste buds. The enzyme, called carbonic anhydrase 4, interacts with the carbon dioxide in the soda, activating the sour cells in the taste bud and prompting it to send a sensory message to the brain, where carbonation is perceived as a familiar sensation. Of course, this raises the question of why carbonation doesn’t just taste sour. Since it is known that carbon dioxide also stimulates the mouth’s somatosensory system. Therefore, according to the authors, what we perceive as carbonation must reflect the combination of this somatosensory information with that from taste. The taste of carbonation is quite deceptive. When people drink soft drinks, they think that they are detecting the bubbles bursting on their tongue. But if one drinks a carbonated drink in a pressure chamber, which prevents the bubbles from bursting, it turns out the sensation is actually the same. What people taste when they detect the fizz and tingle on their tongue is a combination of the activation of the taste receptor and the somatosensory cells, which is what gives carbonation its characteristic sensation. It is hypothesized that our sense of taste generates only a limited palate of distinct qualities: the familiar sweet, sour, salty, bitter and savory tastes. Much of the flavor of food (the “tickling of taste buds”) comes from a combination of this taste information with input from other senses like touch and smell. Over the past decade, there has been tremendous progress in identifying the basis for detection of the five major taste qualities. Indeed, previous studies have identified the receptor proteins and cells responsible for sweet, bitter, and savory taste and the receptor cells for sour detection. Recent work from a number of groups has suggested taste buds might detect other qualities, such as fat and metallic tastes. It also indicated that the gas carbon dioxide induces strong responses in taste nerves. The body senses carbon dioxide on many levels – in the somatosensory system (including touch and pain), smell, and in the brain and blood to control respiration, but how it is detected in taste was quite unclear.

Risk of Parkinson’s Disease is 5X for Gaucher Disease Carriers

Target Health is pleased to announce that it has been deeply involved in a drug development program in Gaucher Disease. 

Parkinson’s disease (PD), a neurological condition that typically causes tremors and stiffness in movement, affects about 1 to 2% of people over the age of 60. The chance of developing PD increases with age and involves a combination of environmental risk factors and genetic susceptibility. Gaucher disease (GD) occurs when an individual inherits two defective copies of the GBA gene, which codes for an enzyme called glucocerebrosidase. This enzyme breaks down a fatty substance called glucocerebroside, which, when not properly disposed of, can harm the spleen, liver, lungs, bone marrow and, in some cases, the brain. The enzyme functions in a part of the cell called the lysosome, where cellular components are broken down, or metabolized, for recycling. In the past, it was thought that people who carry just one altered GBA gene were unaffected. However, in recent years, research groups completed small studies suggesting that carriers of GBA alterations may have an increased risk of developing PD. According to an article published in the New England Journal of Medicine (2009;361:1651-1661), it has been confirmed that carriers of GD face a risk of developing (PD) more than five times greater than the general public. In previous studies, several genes have been linked to PD. However, the current work conclusively shows that mutations in the gene responsible for GD are among the most significant risk factors found to date for PD. The discovery was made by investigators from the National Human Genome Research Institute (NHGRI) and the National Institute on Aging (NIA), in collaboration with scientists from 16 research centers across four continents. The research team examined the frequency of GBA alterations in 5,691 patients with PD, including 780 Ashkenazi Jews, a population in which a particular type of GD is more prevalent. Those data were matched against 4,898 unaffected controls, which included 387 Ashkenazi Jews. Results showed that at least one of the two common GBA alterations was found in 3.2% of PD patients and 0.6% of controls. Among the Ashkenazi subjects, 15.3% of those with PD carried a GBA alteration compared to 3.4% of the controls. In addition to screening for the two common alterations, five of the research centers sequenced the entire GBA gene in 1,642 non-Ashkenazi patients with PD and 609 non-Ashkenazi controls. Using this more thorough method, it was found many additional alterations associated with PD, and showed that 7% of patients carried an alteration, indicating that it is important to look beyond the two common alterations to gain a true picture of risk in the general population. Besides significantly increasing the risk of PD, GBA alterations also appear to increase the likelihood of early disease onset. According to that study, PD patients with GBA alterations developed symptoms an average of four years earlier than other Parkinson’s patients. Overall, it was found that the association between GBA and PD is not confined to any single ethnicity or to specific GBA mutations, though it was found that some gene alterations are seen more frequently in certain populations. Compared with the general population, in which GBA alterations occur in fewer than one out of 100 people, GBA alterations occur in at least one out of 16 people of Ashkenazi descent. However, many GBA mutation carriers as well as patients with GD never develop Parkinson’s disease, so this appears to be only one of several risk factors involved.


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Viral Link to Chronic Fatigue Syndrome

Chronic fatigue syndrome (CFS) is a condition of prolonged and severe tiredness or weariness (fatigue) that is not relieved by rest and is not directly caused by other conditions. To be diagnosed with this condition, tiredness must be severe enough to decrease the ability to participate in ordinary activities by 50%. Symptoms of CFS are similar to those of most common viral infections (muscle aches, headache, and fatigue). They come on within a few hours or days and last for 6 months or more. Main symptoms are 1) Fatigue or tiredness, never experienced to this extent before (new onset), lasting at least 6 months and not relieved by bed rest; 2) Fatigue that is severe enough to restrict activity (serious fatigue develops with less than one-half of the exertion compared with before the illness). According to an article published online in Science (8 October 2009), a potential retroviral link to CFS has been discovered. The virus, XMRV, was first identified by Robert H. Silverman, Ph.D., professor in the Department of Cancer Biology at the Cleveland Clinic Lerner Research Institute, in men who had a specific immune system defect that reduced their ability to fight viral infections. “The discovery of XMRV in two major diseases, prostate cancer and now chronic fatigue syndrome, is very exciting. If cause-and-effect is established, there would be a new opportunity for prevention and treatment of these diseases,” said Silverman, a co-author on the CFS paper. Commonality of an immune system defect in patients with CFS and prostate cancer led the researchers to look for the virus in the patient’s blood samples. The study identified XMRV DNA in the blood of 68 of 101 (67%) CFS patients. In contrast, it was found in only eight of 218 healthy subjects (3.7%). The study not only found that blood cells contained XMRV but also expressed XMRV proteins at high levels and produced infectious viral particles. The study results were also supported by the observation of retrovirus particles in patient samples when examined using transmission electron microscopy. The data demonstrate the first direct isolation of infectious XMRV from humans. These compelling data allow the development of a hypothesis concerning a cause of this complex and misunderstood disease, since retroviruses are a known cause of neurodegenerative diseases and cancer in man. Retroviruses like XMRV have also been shown to activate a number of other latent viruses. This could explain why so many different viruses, such as Epstein-Barr virus, which was causally linked to Burkitt’s and other lymphomas in the 1970s, have been associated with CFS. It is important to note that retroviruses, like XMRV, are not airborne.

Newly Reported Hypertension After Military Combat Deployment

High-stress situations, such as combat deployments, are a potential risk factor for hypertension. Although stress is postulated to increase blood pressure, the underlying role of stress on hypertension is not well established. As a result, a study published in Hypertension (2009;54:966-973), was performed to determine the relations between combat deployment-induced stress and hypertension. The Millennium Cohort baseline questionnaire (2001-2003) was completed by 77,047 US active-duty and Reserve/National Guard members. Follow-up was completed by 55,021 responders 3 years later. Multivariable logistic regression was used to estimate the 3-year risk of newly reported hypertension, adjusting for general and mental health, demographics, and occupational and behavioral characteristics. After applying exclusion criteria, the analyses included 36,061 service members. Subanalyses of deployers included 8,829 participants. Newly reported hypertension was identified in 6.9% of the cohort between baseline and follow-up, many of whom had deployed on military operations in support of the conflicts in Iraq and Afghanistan. After adjusting, deployers who experienced no combat exposures were less likely to report hypertension than nondeployers (odds ratio: 0.77). Among deployers, those reporting multiple combat exposures were 1.33 times more likely to report hypertension compared with noncombat deployers. Although military deployers, in general, had a lower incidence of hypertension than nondeployers, deployment with multiple stressful combat exposures appeared to be a unique risk factor for newly reported hypertension.

TARGET HEALTH excels in Regulatory Affairs and works closely with many of its clients performing all FDA submissions. TARGET HEALTH receives daily updates of new developments at FDA. Each week, highlights of what is going on at FDA are shared to assure that new information is expeditiously made available.

FDA Authorizes Emergency Use of IV Antiviral Peramivir for H1N1

The FDA has announced that, in response to a request from the CDC, it has issued an emergency use authorization (EUA) for the investigational antiviral drug peramivir intravenous (IV) in certain adult and pediatric patients with confirmed or suspected 2009 H1N1 influenza infection who are admitted to a hospital. Specifically, IV peramivir is authorized only for hospitalized adult and pediatric patients for whom therapy with an IV drug is clinically appropriate, based on one or more of the following reasons:

  1. the patient is not responding to either oral or inhaled antiviral therapy, or
  2. when drug delivery by a route other than an intravenous route — e.g., enteral (absorbed by the intestines) or inhaled — is not expected to be dependable or feasible;
  3. for adults only, when the clinician judges IV therapy is appropriate due to other circumstances.

The FDA has reviewed the available scientific data and has concluded that the criteria for authorizing the emergency use of IV peramivir have been met. There are no FDA-approved intravenously administered antivirals for the treatment of influenza. Peramivir is the only intravenously administered influenza treatment currently authorized for use under EUA for 2009 H1N1 infections. The EUA authority allows the FDA, based on the evaluation of available data, to authorize the use of unapproved or uncleared medical products or unapproved or uncleared uses of approved or cleared medical products following a determination and declaration of emergency, provided certain criteria are met. The authorization will end when the declaration of emergency is terminated or the authorization is revoked by the agency. For more information, see or call 1-800-CDC-INFO (1-800-232-4636).

For more information about our expertise in Regulatory Affairs, please contact Dr. Jules T. Mitchel or Dr. Glen Park.