Health Meaning

It warms the heart of a mother to see her child has inherited his nose, hair, or smile. But could it also have transmitted a trigger for diabetes? Researchers working with mice now suggest that insulin antibodies transferred from mother to child during pregnancy and breastfeeding may trigger type 1 diabetes in some children.

Type 1 diabetes develops when the body's immune system mistakenly kills insulin-producing beta cells of the pancreas. Insulin is a hormone that allows cells to absorb blood sugar. Without enough insulin, sugar levels in the blood increases unchecked and eventually damage every system in the body - resulting in kidney failure, heart disease, poor circulation, and blindness. symptoms of diabetes are brought out after 60% to 80% of beta cells have been destroyed. full blown diabetes is marked by quantities of antibodies specific for insulin in the blood increases. Such antibodies are proteins created by the immune system in response to the destruction of beta cells, but until now, they were considered as secondary effects of the disease.

Surgeon Ali Naji and his team at the University of Pennsylvania School of Medicine in Philadelphia asked whether specific insulin antibodies passed from mother to child could revive the autoimmune response causes diabetes. The team implanted two days old embryos of diabetes mouse strain prone in either normal home moms or prone diabetes. Only 15% of pups birthed and nursed by normal adoptive mothers eventually developed diabetes compared with 73% of pups birthed and nursed by adoptive mothers prone diabetes, the researchers report in the April issue of Nature Medicine .

to study the potential role of antibodies passed from mother to offspring, the team then developed diabetes-prone mice that did not make antibodies against insulin. When females mated with males prone diabetes, their young were much less likely to develop diabetes than are puppies prone diabetic mothers who pass on antibodies.

This research brings a new controversy in the study of diabetes, says diabetologist Mark Atkinson of the University of Florida College of Medicine in Gainesville. previous human studies have shown that fathers genes can predispose their children to diabetes, while this study clearly demonstrates a maternal influence as well. In addition, these results suggest that, in some cases, but not all, antibodies play a pathogenic role in the development of diabetes. "It is simply a fantastic study," said Atkinson.

Related Sites
American Diabetes Association
Diabetes Dictionary

The first signs of the disease Huntington's disease occurs in middle age: Jerks and muscle spasms are followed over the years by the worsening of memory and loss muscle control. Although a mutated gene is to blame, it is not clear how it causes symptoms. Now scientists studying mice and human cells affected by Huntington's disease have shown that chronic damage to mitochondria, cells of the plants plays an important role.

Huntington's disease is inherited by a person over 10 000 in the United States. The mutated gene adds unusually long chains of glutamine, an amino acid in a protein huntingtin (htt), and in general, the more glutamine chains corresponding to an earlier onset and more severe neurological symptoms. But scientists still do not know for sure what normal htt made or how the abnormal version of throws a wrench in the works.

neurologist and biochemist Timothy Greenamyre Alexander Panov from Emory University School of Medicine in Atlanta and his colleagues believe that mitochondria are an important factor in Huntington's disease. Mitochondria of the team examined are from mouse and human cells affected by Huntington's disease. They found that the long chains of glutamine in the stick abnormally htt protein in the outer membrane of mitochondria and allow ions to flow freely in and out. Accordingly, mitochondria "run" like a battery exploited, reports the team in the July 1st issue of Nature Neuroscience . In addition, Greenamyre and Panov found that pepper mitochondria with too much glutamine can not properly regulate calcium, which can reach toxic levels and kill the cell

But all body tissues htt -. So why the abnormal protein hit the cells of the nervous system so hard? Probably because neurons live so long, said Panov. As cells age, their mitochondria become less efficient. This problem is particularly acute for neurons because they are not often replaced as cells elsewhere. The subtle mitochondrial damage caused by mutant htt can exacerbate the wear and tear of natural aging, said Panov. This could explain why the disease remains at rest until the Middle Ages.

The debate on the role of mitochondrial damage in Huntington's disease fluctuated for years between scientists, says neurologist Kenneth Fischbeck of the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. "But this research should help resolve the issue and to focus the research."

Related Sites
The site of Timothy Greenamyre
The site Kenneth Fischbeck
Information about Huntington's Disease from the National Institute of Neurological Disorders and Stroke
Disease Huntington Society of America

People with the disease Parkinson's struggle with progressive worsening tremors, stiffness, poor balance, and abnormally slow movement. The drugs relieve these symptoms, but there is still no cure for the disease. Now researchers say it might be possible to slow its progression with a compound called coenzyme Q ₁₀ .

called coenzyme because it improves the performance of other enzymes, Q ₁₀ is also a powerful antioxidant. Antioxidants help protect cells against the harmful oxidation - the biological equivalent of rust. Q ₁₀ is also known to play a critical role in the normal functioning of the energy generators of cells, the mitochondria. Previous studies have found that people with Parkinson's disease have mitochondrial dysfunction and low levels of Q ₁₀ . And over the last decade, neurologists Clifford Shults of the University of California, San Diego, and Flint Beal of Cornell University in Ithaca, New York, showed that rodents with symptoms like sickness Parkinson were able to control their movements much longer when given Q ₁₀ .

To determine if Q ₁₀ could help people with Parkinson's disease, Shults and Beal have teamed up with researchers from 10 research centers across the country. They recruited 80 people in the early stages of Parkinson's disease to be one of three doses of Q ₁₀ or placebo. The researchers then followed the progress of each patient for 16 months, monitoring symptoms each with a battery of standardized tests. The progression of Parkinson's disease was slowed by 44% in the group taking the higher dose of Q ₁₀ , reports the team in the October 15 issue of the Archive of Neurology . Blood tests taken before and after the Q ₁₀ The treatment showed an increase of mitochondrial activity, indicating an improvement in mitochondrial function. Encouragingly, none of the patients experienced serious side effects.

The results clearly show that mitochondrial dysfunction plays a role in the progression of Parkinson's disease, said neurobiologist Virginia Lee of the University of Pennsylvania in Philadelphia. Although it needed more research before the drug can be approved as a treatment for Parkinson's disease, the study provides "clear and convincing support" for the hope that Q ₁₀ can slow the disease, she said.

related sites
site Clifford Shults
site Flint Beal
the site of Virginia Lee
basic information on Parkinson's disease NINDS

Checking clogged arteries could someday be as simple as a blood test. Researchers report that a relatively quick and inexpensive analysis of chemicals in the blood can reliably detect the disease and indicate its seriousness.

coronary artery disease, the leading cause of death in the United States, results when fats clog the arteries that supply blood to the heart. Currently, patients doctors screen for the disease by checking a laundry list of risk factors, including high cholesterol, smoking and obesity. But they can not be sure until they donned a catheter into the coronary arteries and to take X-ray films that reveal their status. This procedure, called angiography is invasive time-consuming, and expensive. Biochemist David Grainger of Addenbrooke's Hospital in Cambridge, UK, and his team say they have found an effective alternative to a powerful technique borrowed from analytical chemistry.

The technique, called proton nuclear magnetic resonance (1H NMR), the reflected light from a sample records placed in a magnetic field and zapped with radio waves. Any chemical has such a unique spectrum that digital emission footprint. The Grainger team sampled serum (blood with clotting cells) removed 36 people with coronary artery disease diagnosed by angiography and 30 healthy people. After analyzing the spectra with a statistics program, the team was able to diagnose the samples with an accuracy of 92%. Differences in the amount of lipoproteins - a type of fat - were the most significant indicators of the disease, they found

The team also demonstrated that 1 H NMR can indicate the severity of the disease: They attributed precisely 76 other patients. to one of three categories - benign (an affected artery), moderate (two arteries in difficulty), and large (all three coronary arteries blocked). These results, as well as the ease with which the technique can be done, make NMR suitable for clinical use, the team argues in the November 25 issue Nature Medicine .

"This study is a beautiful integration of analytical chemistry, clinical medicine and biostatistics" said chemist and toxicologist Mark Viant the University of California, Davis. The technique capture huge amounts of data that can be exploited for new ideas on how the diseases progress, says toxicologist Marion Miller, also at UC Davis.

Related Sites
Bio David Grainger
Marion Miller website

the benefits of exercise for the heart have long been touted, but we do not know how, for example, jogging protects the blood vessels against cardiovascular disease. Now scientists suggest that simply will get your blood is what helps. In experiments with cow arteries, they find that the fast-flowing blood has anti-inflammatory effect as powerful as that of certain steroid medications that protect the arteries.

Scientists have known for years that the hardened plates that are a big factor in heart disease tend to form in areas where the blood slows and inflammation in these areas contribute to the disease . Curiously, when the walls of the vessels experienced increased drag faster blood flow, the cells lining the walls of blood vessels are more certain molecules that protect the arteries. Link the evidence together, Scott Diamond, a biomedical engineer at the University of Pennsylvania in Philadelphia, has suggested that the trail itself could activate anti-inflammatory pathways as do many steroid medicines like dexamethasone.

Diamond and his colleagues have endothelial cells cow arteries in a special chamber that mimics the conditions of flow of arterial blood. They reported a steroid receptor in the cytoplasm of cells with green fluorescent protein. When they pumped fluid on the cells to create a shear stress, the receiver has looked into the cell nucleus - as if the cell was exposed to dexamethasone. Once inside the nucleus, the activated receptor a steroid-sensitive gene, reports the online team in January 24 Traffic . Finally, the team repeated the experiments in the segments of human arteries and found a similar effect.

The work is important because it really connects changes in blood flow with protection against heart disease, says Peter Davies, a vascular biologist at the University of Pennsylvania, which is not associated with the project. "This system can be the manifestation of [exercise's] protective effect." The next step, Diamond and Davies agree, is to see if the increased blood flow that triggers anti-inflammatory pathway in living animals.

Related Sites
Background information on atherosclerosis
Scott L. diamond site
Peter F. Davies site

A mysterious disease that causes flu-like symptoms and pneumonia rapidly around the world last week after sickening dozens Asia. More than 0 people in seven countries have fallen ill in recent weeks, according to the World Health Organization (WHO), and at least four died. These figures raise concerns about a new and uncontrollable pandemic.

Researchers are desperately trying to determine the cause of severe acute respiratory syndrome (SARS), WHO has called the disease. Hospital staff seem to be more at risk, suggesting that close contact with a patient is necessary for infection. But until now, scientists are not even sure that the infection is viral or bacterial - much less how it spreads, or the best way to treat and prevent. The researchers tried to "a wide range phenomenal" diagnostic tests on samples available, says Klaus Stöhr, an expert from the flu to WHO in Geneva, but they were all negative. "We really have to start from zero and put aside all our hypotheses "in the search for a culprit, he said.

Initial symptoms include high fever, muscle aches, sore throat and headache, sometimes followed by pneumonia and acute respiratory distress. "This kind of flu screams," said Brian Hjelle, a virologist at the University of New Mexico, Albuquerque. Indeed, some initially thought that the epidemic could be linked to a small outbreak of a virulent strain of bird flu, called H5N1, which has killed a man in Hong Kong last month and sickened her 9 year old son ( Science , 7 March, p. 1504). But such a link has been found, and most scientists say that if the disease was the flu, doctors have recognized now.

Other potential candidates include human parvovirus, or something that looks like Nipah, a paramyxovirus that triggered a deadly epidemic among pig farmers in Malaysia in 1999, said CJ Peters, director of the Center for biodefense at the University of Texas Medical Branch in Galveston. Having studied deadly epidemics in many parts of the world, Peters said. "I do not know who gave me such a feeling of danger"

At the same time, the new home puts public fears bioterrorism and biodefense bloated budgets perspective reaffirming the impact of naturally occurring diseases, said Marjorie Pollack, which monitors the epidemic ProMED, an electronic reporting system in the world. says Pollack :. ". Mother Nature is by far the worst bioterrorist there "

With Gretchen Vogel reportage in Berlin

Related Sites
World Health Organization
health updates on SARS of the US Centers for Disease Control and Prevention

The mice were created "completely by accident," says Suzie Chen biologist at Rutgers University in Piscataway, New Jersey. Chen and colleagues studied obesity at the time. For their experiments, they created mutant mouse lines by inserting bits of foreign DNA. They noted that one of their germinated mutant mice, the dark cancerous tumors, which were found to be melanoma lesions. The research team put the fat study for melanoma -. A disease for which there were few good animal models

They determined that the inserted DNA, designed to create fat mice had inadvertently landed in the middle of a region of the gene that encodes a neurotransmitter glutamate receptor, causing an abnormal production of the receptor. glutamate receptors were once thought to be limited to the brain, but have recently turned into the bone and skin. Partnering with researchers from other institutions, laboratory Chen has created a new line of mice that expressed too much of a glutamate receptor. These mice also had a melanoma disease as a human, which propagate through the body. Cells taken from their tumors showed a disorder of glutamate receptor gene. The researchers also found expression even glutamate receptor in about a third of human melanoma specimens have been tested. This finding, Chen said, shows that a mutation affecting the glutamate receptor gene "may be relevant, but can not show that it is the cause in one way or the other humans." The work was published online April 21 in Nature Genetics .

This mouse model was long overdue "because its highly metastatic mimics the behavior of deadly aspect of human disease," says David Fisher, a melanoma researcher at Harvard Medical School in Boston . However, he said, the involvement of the glutamate receptor gene is still not yet fully understood. Lynda Chin, Harvard University, says that "this particular receptor may or may not be a great player, but this data tells you is that this pathway could be important. "

Related Sites
CDC fact sheet skin cancer
homepage Suzie Chen

BALTIMORE, Maryland- - Biology does not get much more basic - or much more work - histology, examination of the finer details of tissue samples. Now, researchers say they have developed a laser-based approach that can produce 3D high resolution images in a fraction of the time required for traditional techniques.

histology usually involves freezing a tissue sample, cut into thin slices and staining with dyes that label different components. Researchers take images and digitally colored sections recombine to reconstruct a three-dimensional view. But such reconstructions are often hampered because the blades can move components around.

So, a group led by Jeff Squier, a physicist laser at Colorado School of Mines Golden, turned to a laser capable of shooting light pulses lasting only 20 quadrillionths of a second. Such short pulse lasers are useful for imaging of fluorescent molecules within the upper fabric layer and for the removal of thin layers of tissue. Squier's team decided to put the two jobs at once.

In one experiment, the team used the laser to scan the brain tissue of rats engineered to express a fluorescent protein in cells that line the blood vessels in the cerebral cortex. They shot a series of low-intensity infrared pulses, which triggered the protein designed to emit photons of light yellow. The light is captured by a camera and stored on a computer. Then the researchers bent the laser enough to take off the first 10 microns of tissue. They repeated imaging and ablation steps several times and then used a computer to integrate the image file in a 3D view of the vasculature of the brain of a rat. Squier presented the findings here on June 2 at the meeting of the Conference on Lasers and Electro-Optics.

"It is a very promising technique," said Virginijus Barzda a biophysicst at the University of Toronto in Canada. Barzda noted that this technique enables researchers to produce images with a resolution of about 1 micron much better than conventional techniques such as magnetic resonance imaging that peers through tissue. But because the laser destroyed the sample Barzda and others say it is unlikely to be useful for traditional clinical pathology tests on human tissue, because doctors generally prefer to save the samples so they can be reviewed later.

The idea was simple, cooling, and controversial: the Chamorro people of Guam who feasted on a traditional delicacy, bats giant fruit may have ingested enough a toxin develop a rare and fatal neurodegenerative disease. Now this hypothesis, released last year, has been given a boost. In the August 12 issue of Neurology , the researchers report that the bats museum specimens frugivorous Guam, also known as flying foxes, are chock full of the neurotoxin BMAA.

For decades, scientists have struggled to explain a significant impact on Guam of a motor neuron disease that combines features of amyotrophic lateral sclerosis and Parkinson's dementia, with symptoms ranging from uncontrolled trembling at paralysis. One hypothesis leading disease related to the consumption of seeds of the cycad plant. These are used to make the tortilla flour and contain BMAA and another neurotoxin, cycasin. Residents can remove most toxins, however, by thoroughly washing the seeds.

Last year ethnobotanist Paul Cox, director of the National Tropical Botanical Garden in Kalaheo, Hawaii, noted that another local specialty, bats giant fruit Guam, like to eat seeds and cycads suggested that cycad neurotoxins have accumulated to dangerous levels in the bat meat ( science now, March 29, 02). But the evidence was only circumstantial. More bats have been killed and eaten on Guam immediately after the Second World War, when weapons became readily available, coinciding with a peak incidence of neurodegenerative disease

Now Cox and ethnobotaniste Sandra Banack of California State University, Fullerton, have the first tangible evidence for their theory. Examine the skin tissue from three 50 bats Guam museum at the University of California, Berkeley, they found concentrations of BMAA hundreds of times higher than in the cycad flour. Cox said he was "stunned". The pair is now planning further research on how changes in power levels influence BMAA bats to better understand biomagnification cycads.

"Research seems to answer many questions that we all had about Guam's disease," said John Stein, a neurophysiologist engine at the University of Oxford, UK, hopes the study will encourage scientists hunting for the cause of various neurodegenerative disorders to "seek more common [environmental] toxins that could be similar to BMAA."

related sites
Recipe for dogfish soup
Cox site
the site Banack

although smoking has long been linked to lung cancer, only 10% of heavy smokers develop the disease. Why them? One factor may be the activity of DNA repair enzymes that can undo some of the damage caused by smoking. A new study finds that smokers with a powerful repair enzyme are much more likely to get lung cancer.

About 150,000 people die from lung cancer each year in the United States. Many cases dates back to smoking, which causes the DNA in lung cells mutate at a high rate. Because the enzymes can solve this type of damage, repair the DNA scientist Zvi Livneh of the Weizmann Institute of Science in Rehovot, Israel, and colleagues wondered if the enzymes could be defective in smokers who develop cancer lung.

To find out, Livneh team looked for a common DNA repair enzyme called OGG1, in the blood of 68 patients with non-small cell lung cancer and 68 healthy individuals ; both groups included smokers and nonsmokers. The researchers extracted OGG1 from blood samples and DNA was added that they synthesized in the laboratory. The DNA samples carried the kind of damage that smoking causes.

OGG1 was less active than normal in 41% of cancer patients and 4% of healthy participants, they report September 3 Journal of the National Cancer Institute . Smoking with slow OGG1 were 10 times more likely to have lung cancer than those whose enzyme normally works and 0 times more likely than nonsmokers with normal enzyme activity. Nonsmokers with bad OGG1 were 10 times more likely to have cancer. This suggests that the reduced OGG1 activity could be lung cancer risk factor in the general population -. Not only in smokers

The results are "novel" and "significant", said Samuel Wilson, a biochemist at the National Institute of Sciences of Environmental Health. He added that if the findings hold, they could lead to earlier detection and prevention of lung cancer.

Related Sites
Zvi Livneh
Lung cancer information

for the first time, a study of pregnant women infected with HIV found that co-infection with malaria has significantly increased the risk of transmission of the AIDS virus her child before or during birth of a mother. According to a report in the November issue of AIDS , some of these pregnant women in Uganda had nearly three times the risk of transmitting the AIDS virus to their babies.

Little is know about how other diseases affect the chances of a mother passing HIV to her fetus. To assess the risk for malaria, epidemiologist at Johns Hopkins University Heena Brahmbhatt turned to a set of data from a large study by his adviser, Ronald Gray, in collaboration with several Ugandan research groups. These researchers assessed 746 pregnant women with HIV and their babies in the Rakai district of Uganda from 1994 to 1999. Brahmbhatt found 93 cases in which the researchers recorded the HIV status of the child and had also retained placenta. Of the 15 babies whose mothers had placental malaria, she found that six (40%) were infected. However, the spread of HIV in only 12 of the 78 infants (15%) whose infected mother has not had malaria in their placentas.

The results were statistically significant, leading the authors to conclude that the tests are "urgently needed" to assess whether drugs against malaria can reduce HIV transmission to the fetus. "If our findings pan out, there may be a case for the removal of malaria much more aggressive in women infected with HIV during pregnancy," says Gray.

The story is complicated, however. Another study, in press at Emerging Infectious Diseases , found that the number of parasites in the placenta is crucial: Low levels actually offer some protection against HIV, while higher levels are increasing risk, said lead investigator of the study, Richard Steketee of the US Centers for Disease Control and Prevention in Atlanta. Gray Hopkins said he and his colleagues plan to check the levels of parasites in the placenta of Uganda.

Steketee suspects that the intensity of malaria infection alters the immunity of the mother in various ways, affecting the ability of HIV to be transmitted in utero. "It would be important for someone to look at this time," said Steketee. "These are not easy studies and they are not cheap, but the impact could be considerable."

Related Sites
The mother-child transmission of overflight of HIV from the World of the Organization Health
Roll Back Malaria, malaria during pregnancy

Although nature seems to strive for the perfect balance between form and function, it does not always realize it. Sometimes there is a good reason :. A new study suggests that if human lungs were designed to function optimally their most important task - the exchange of oxygen and carbon dioxide between the blood and air - They'd be prone to disasters

gas exchange is the purpose of the lung. It requires several square kilometers worth of boots membranes in tiny bags and packaged in the human torso. To reach the small sacs called alveoli, where gas exchange takes place, the air must flow through a series of tubes of smaller and smaller called bronchioles.

Although necessary to provide air, bronchioles take place in the lungs that might otherwise used for gas exchange. The best design lung would seemingly find a perfect balance between the need to have fairly wide bronchioles to minimize the friction of air flow while keeping the maximum volume available for recess.

Unexpectedly, this is not what happens in our lungs, Bernard Sapoval of the Ecole Polytechnique in Palaiseau, France, and colleagues report in the February 12 issue of Nature . Our bronchioles are wider than they need to be to minimize the resistance, and the team Sapoval think they know why: security. The researchers' calculations show that if the lungs have been optimized for the exchange of gases, even a minor narrowing of a bronchiole would considerably increase the resistance to air flow - which could mean the difference between inhalation effortlessly and panting like an asthmatic. Asthma, in fact, is an excellent example of why a small excess volume does not hurt; during an asthma attack, the bronchioles constrict, making the effortful breathing. If our bronchioles started narrower, the same amount of constriction would make breathing almost impossible.

If the optimal design for gas exchange has a dangerous side effect, said Hiroko Kitaoka the University of Osaka in Osaka, Japan, perhaps Savopal and quantitative approach to his colleague can find the best compromise. It may be that nature has already found. As Sapoval said, "our lungs are built on the safe side."

Related site
website Hiroko Kitaoka

As spreads malaria resistant to drugs, researchers have intensified their search for new ways to fight against the scourge of mosquitoes. Now they have identified three genes that control how the mosquitoes themselves fight the malaria parasite. The results indicate that drugs or genetic changes that Beef immune response of mosquitoes could one day help stop malaria spreading.

When a mosquito bites a person infected with malaria, it ingests unicellular Plasmodium parasites that cause disease. Within 10 minutes the matt parasites; in a day it is fixed in the wall of the gut of the mosquito; and after 3 weeks he made his way to the salivary glands of the insect, ready to jump into the next human, mosquito bites. But even within a given species that some mosquitoes carry malaria. The researchers suspected that differences in immune mosquito proteins might be responsible.

mosquitoes To identify these proteins, molecular biologists Mike Osta, George Christophides and Fotis Kafatos of the European Molecular Biology Laboratory in Heidelberg, Germany, engineering to miss certain immune genes. One at a time, they inactivated 100 of these genes using RNA strands that block a specific gene to its corresponding protein. A week later, they let the modified mosquitoes feed on infected mice with a parasite malaria line that has been genetically modified to glow green when alive, but turn black after death. Then they killed the mosquitoes, dissected their guts, and counted the living and dead parasites under a microscope.

Silencing a gene called LRIM1 more than tripled the number of live parasites, the researchers report in March 26 number science . This suggests that the gene normally helps kill insects Plasmodium . In contrast, silencing one of two other genes, CTL4 and CTLMA2 has caused mosquitoes to kill many more parasites than usual, suggesting that proteins they are somehow protecting Plasmodium . If the results are valid for the parasite of human malaria, chemicals that block or stimulate two protective genes the parasite killing gene could slow the spread of malaria, said Osta.

"It's impressive work," parasitologist said Kim Williamson of Loyola University of Chicago, but there is a long way to go before that wild mosquitoes can be controlled in this way;. For example, researchers must show that the three genes controlling resistance to Plasmodium species that infects humans. However, the approach is promising, she said, because when it is to infect mosquitoes, "the parasite is relatively vulnerable."

Related Sites
Kafatos lab
Background of the malaria life cycle
background on the WHO malaria

This is the nightmare of every owner :. Mold hidden inside a house. It is also the cause of many insurance claims and lawsuits against the manufacturers, in which people attribute a variety of ailments in the mold. Now a report from the Institute of Medicine (IOM) found that the wet conditions can aggravate asthma and cause coughing and wheezing in healthy people. But it found no evidence of a convincing link with other symptoms, including acute pulmonary hemorrhage in infants, as has been proposed.

In response to growing concerns about mold, called Centers for Disease Control and Prevention IOM to examine the scientific evidence of health effects in 01. The Panel found that moisture aggravates symptoms asthma for those sensitive to mold. But he failed to support arguments about his role in other health problems. The evidence is only suggestive that dampness or visible mold causes a disease of the lower respiratory tract, such as bronchitis and asthma in healthy children, the report said. And because of a lack of studies done well, the panel could not say if there was a link to oblivion, chronic fatigue, cancer, or other conditions.

Part of the challenge of linking adverse health effects wet conditions is that, in addition to mold, bacteria and they host mites; moisture also causes chemicals to be released from the decomposition of furniture and building materials. Most studies have not teased apart these variables, the panel found. The committee calls for better ways to measure what people are exposed to agents and called for national guidelines to prevent excess moisture or eliminate existing buildings.

Perhaps as much as 10% of homes in North America is moist enough to lead to infections of asthma or minor, said David Miller of Carleton University in Ottawa. This adds a significant burden on public health, he said, one that is focused by people who can not afford to repair leaky roofs or other problems. But it is difficult to quantify exactly how big the problem is compared to other types of indoor air pollution, or where it should stand on the agenda of public health, said epidemiologist Jonathon Samet Johns Hopkins School of Public Health University in Baltimore.

Related Sites
the IOM report
pan on information from the Environmental Protection Agency

A small study of children with influenza in Japan estimated that the influenza virus can thwart a drug that was thought to be relatively foolproof. The paper, published in the August 28 issue of The Lancet , just as some countries stockpiled the same antiviral drug against pandemic influenza. researchers flu say there is no need to stop storage, though - the drugs must always be useful

The last major global flu pandemic, the Spanish flu of 1918, killed 50 million people .. another great pandemic could be in the works if the avian flu H5N1 highly virulent, which killed at least 24 people in Asia last winter takes a form that can be transmitted from person to person. Because the preparation of a vaccine against such a virus might take six months, antiviral drugs are the first line of defense against pandemic flu. Although the flu virus may develop resistance to some older drugs, new drugs called neuraminidase inhibitors that target an enzyme that makes an envelope of the influenza virus protein, appeared more waterproof. Thus, some countries have started to store any of these drugs, oseltamivir (sold as Tamiflu).

The United States is among them, according to a federal pandemic flu plan released today. The United States has stockpiled enough oseltamivir to treat 1 million people, officials said. The plan also describes measures to increase vaccine manufacturing capacity and how national and local health care providers should respond.

The Lancet report, however, suggests that the influenza virus develops resistance to oseltamivir easier than was thought. Virologist Yoshihiro Kawaoka of the University of Tokyo and his colleagues in Japan and the United States has collected virus samples from 50 children after a 5-day course of oseltamivir for an episode of the flu. In nine samples, 18% of children, the virus had developed mutations that made it resistant to the drug.

But this does not mean antivirals will not work against a pandemic, says Kawaoka, who is also at the University of Wisconsin, Madison. On the one hand, the changes that make an oseltamivir-resistant virus may make it less pathogenic, he said. In an accompanying editorial, Anne Moscona of Mount Sinai School of Medicine in New York noted that another drug in this class, zanamivir, may be less likely to become resistant.

Moreover, adds expert Arnold Monto flu the University of Michigan, Ann Arbor, strains of avian influenza will not necessarily become resistant to oseltamivir as easily. Monto, who sits on an international committee that recently recommended the storage of neuraminidase inhibitors in August 13 Weekly Epidemiological Record , concludes: "The message for most of us, governments. should stockpile "

Related Sites
neuraminidase Inhibitor susceptibility Network statement supporting the antiviral storage
US response Ministry pandemic Health and Human Services and preparedness Plan

The National Institutes of Health (NIH) today announced that it has suspended a large clinical trial testing whether the COX-2 Celebrex can prevent colon polyps. Those taking the drug had an increased risk of heart attacks compared to volunteers taking placebo, results which echo similar results with another COX-2 inhibitor -. Vioxx, which forced him to be uprooted from the market on September 30

Elias Zerhouni, director of the NIH, which funded the suspended trials, and dozens of others to prevent cancer or Alzheimer's disease with Celebrex, said in a press conference that he has ordered a review of all studies funded by NIH COX -2 inhibitors.

Celebrex, manufactured by pharmaceutical giant Pfizer, has been under a microscope since the pharmaceutical company Merck announced it was withdrawing Vioxx from the market. A study testing the Vioxx capacity to stem polyps in 2,0 volunteers found that after 18 months, participants on Vioxx were twice as likely to suffer a heart attack or stroke than those taking placebo. The withdrawal of Vioxx has raised questions about whether the problems with Vioxx could infest other COX-2 inhibitors as well. Earlier this month, the FDA added a warning to the COX-2 inhibitor Bextra, which against its use in patients undergoing bypass surgery.

Pfizer has defended Celebrex as safe, but is now evaluating new data. The study of the National Cancer Institute funded, involving 2,000 people, was to test whether Celebrex could prevent colon polyps, a precursor of colon cancer in patients at risk. After further examination after the withdrawal of Vioxx, and the addition of cardiovascular experts to the security of the test supervisory board data, the DSMB concluded that patients taking a high dose of Celebrex had an increase of 3.4 times the risk of heart attacks or stroke versus placebo; those on a moderate dose had a 2.5-fold increase risk

Since the announcement this morning of the suspension of the trial, at least two related trials were temporarily halted. a colon prevention study polyp began recruiting this year and aimed for 1,0 participants, and breast cancer treatment trial who also started this year with the aim to recruit 2,700 women, said Charles Geyer, director of medical Affairs for the National Surgical adjuvant Breast Bowel project (NSABP), a group that performs cancer trials and is itself funded by the NIH. So far, the NIH is apparently not suspend other trials of Celebrex, including two that have more than 1,000 participants - at least not immediately, in part, Zerhouni said, because another Celebrex trial that closely resembles suspended the trial did not find the same problems. But investigators are holding their breath. "There are big questions to be answered about whether we continue," said Peter Lance University of Arizona in Tucson, who heads a large colon polyp prevention trials, expected to enroll 1,0 people.

SAN FRANCISCO, CALIFORNIA - Some cancers keep them- same as compact tumors while others aren 't content until they have spread throughout the body. What makes more aggressive than the other? One explanation, according to a new study, is the presence of a protein normally present in neurons. Experts say the work may offer a new target in the fight against colon and other cancers.

As cells become cancerous, they produce more of a protein called b-catenin. The protein acts as a molecular switch, turning specific genes and off. Reasoning that b-catenin could turn on other genes that help cancer along, such as those that make the spread, biologists cancer Avri Ben-Ze'ev and Nancy Gavert of the Weizmann Institute of Science in Israel and his colleagues are looking for these genes.

Ben-Ze'ev colleagues examined the effect of extinguishing b-catenin on other, other functions within cells. In the current study, they scanned some of the genes involved in these processes and found a gene called L1CAM, the protein is well known for nerve cells son together. To determine whether L1CAM has a role in cancer, the researchers studied for its protein in normal cells of the skin, non-cancerous cells in culture, and aggressive melanomas from 11 patients. While normal cells contained no protein L1CAM, many cancers harbored. When the team blocked the activity of L1CAM in cultured cells of human colon cancer cell growth has slowed dramatically.

The role of L1CAM in cancer seems to make more aggressive disease. When the team has transformed the gene into a set of colon cancer cells and injecting them into the mouse spleen, the cells distributed in the livers of animals; cells that do not make protein L1CAM stayed put. The protein appears to help cancer spread in people too: 50% of patients with colon cancer with high amounts of L1CAM protein in their tumors had cancer spread to 5 years of treatment, compared with only 14% of people with low levels, researchers reported here since December 13 at a meeting of the American Society for Cell Biology.

L1CAM could prove to be a prognostic factor for cancer development and a potential target for treatment, says cancer biologist Michael Shtutman of Ordway Research Institute in Albany, New York. Furthermore, it could be a useful tool to help researchers understand how cancers invade tissues and metastasize, he said.

Related site

• information on colon cancer from the National Cancer Institute

In the turmoil and confusion of an emergency operating room, it is not surprising for occasional surgical sponge to go missing. But when the sponge is left inside a patient, there is no harmless error. Now there may be a way to detect stray sponges before the patient leaves the OR. radio frequency ID (RFID), as those used to prevent shoplifting, can be sewn in surgical sponges, according to a new study. If the idea catches on, the technology could prevent hundreds of infections and deaths caused by forgotten sponges every year.

surgical sponges are small plots gauze used to absorb fluid, wipe instruments, and able to support the body's tissues during surgery. The average abdominal surgery uses about 50 sponges. the operating room nurses count the sponges before and after surgery to ensure that none have gone, but in an emergency or complex surgery, it can be difficult to keep track of exactly how sponges were used and where they all went. Very occasionally - only about 1 in every 16,000 surgeries -. A sponge is accidentally left inside the patient's body, which leads to a potentially serious infection

In that month's number Archives of Surgery , Alex Macario surgeon to Stanford University School of Medicine in Palo Alto, California, and colleagues describe a monitoring system that they hope to eliminate that risk. An RFID tag sewn into each surgical sponge acts as a tracking device. To test the technology, a surgeon placed a sponge marked somewhere in the body cavity of an abdominal surgery patient who had consented to the study. A second surgeon, who did not see where the sponge was hidden, waving an RFID detection wand over the patient's abdomen. When the rod was marked directly on the RFID sponge, the RFID chip picked up radio waves the wand and sent a signal, making the wand beep. In four trials with a total of 8 patients, the surgeon can locate the sponge hidden in less than three seconds each time.

"This is a proof of concept very nice," said Atul Gawande, a surgeon at Brigham Women's Hospital in Boston and Harvard School of Public Health. The RFID technology is very fast, adds, but unless the RFID tags are very cheap, it could be costly. - the US uses about 2 billion surgical sponges annually RFID sponges developed by ClearCount Medical Solutions, which hopes to make the technology available fall.

related site

• case study of a surgical sponge restraint

Weight gain can be a serious problem for patients taking antipsychotic drugs for schizophrenia - not only drugs have a sedative effect that slows people down, but they also stimulate the appetite, a combination that can mean a significant weight gain. It turns out that this is also what some antihistamines, which counteract allergic reactions are. Now, scientists say they have identified a common mechanism: the two types of drugs act on the same histamine receptor in the brain. Knowledge should help drug manufacturers to avoid this side effect in the next generation of antipsychotic drugs and other drugs.

Previous research had already suggested that the actions of a particular enzyme, AMP kinase (AMPK), are directly related to appetite control, apparently by an action on the H1 histamine receptor. To see if antipsychotic drugs cause excessive production of the enzyme, researchers led by neuroscientist Solomon Snyder of Johns Hopkins University in Baltimore, Maryland, injected mice with clozapine, an antipsychotic medication commonly prescribed. The injection resulted in quadrupled AMPK activity in the brains of mice. The researchers then gave the mice leptin, an appetite suppressant hormone, and saw the AMPK levels down.

The scientists then established the link of histamine giving elevated clozapine to mice lacking H1 receptor. In this case, the mouse does not react with high levels of AMPK, showing that stimulation of the enzyme by the drug depends on the stimulation of the H1 histamine receptor, researchers report online this week in the Proceedings of the National Academy of sciences . "We have now connected a whole class of antipsychotics to natural brain chemicals that trigger appetite," said Snyder.

The first antipsychotic, chlorpromazine, was originally designed as an antihistamine when was invented in the early 1950s, neuropsychopharmacologist Bryan Roth notes the University of North Carolina, Chapel Hill. Roth previous research has shown that many antipsychotics, besides targeting neurotransmitters linked to schizophrenia appears to activate signaling pathway mediated by H1 receptors But now, he said, the mechanism has been permanently nailed he said.. "I think this will go a long way toward convincing pharmaceutical companies and regulators that medication taken by humans we need to avoid hitting the receiver to avoid weight gain. "

Related Sites

• Information on atypical antipsychotics
• About histamine

In the days following the death of Ludwig van Beethoven, friends and admirers came to see her body and cut her hair for the memories. Recent chemical analysis of one of these stolen locks has now led scientists to conclude that medical treatment may have accelerated Beethoven's death by his deteriorating lead poisoning.

Four months before his death in March 1827, Beethoven began to suffer from excessive abdominal swelling, perhaps due to cirrhosis. To drain fluid, his doctor, Andreas Wawruch, pierced her abdomen with a needle. Researchers have known since 05 that Beethoven had suffered from a severe lead poisoning. The most recent study of his hair, led by forensic pathologist Christian Reiter of the Medical University of Vienna in Austria, links the two problems.

As the hair grows, it absorbs substances, including lead, from the bloodstream. For his research, Reiter analyzed two hairs with a spectrograph and created a daily log of the internal chemistry of Beethoven in his last 4 months. The composer received abdominal punctures four times on his deathbed, draining between 7.7 and 14 liters of fluid from his body each time. The amount of lead in the hair spiked after each composer abdominal puncture. The correlation suggests that palliative measure worsened the lead poisoning, and Reiter accuses lead salts used to clean the wound as a likely culprit. Reiter speculates that lead has worsened cirrhosis of the composer and hastened his death. The English translation of his study appears in the latest issue of The Beethoven Journal .

"The fact doctor may have killed [Beethoven] with lead poisoning," says William Walsh, director of research at the Health Research Institute and Pfeiffer Treatment Center in Warrenville, Illinois . Walsh, who orchestrated an earlier chemical analysis of hair from Beethoven, spent 30 years conducting a forensic analysis of hair.

Reiter reported lower levels of lead to the end of Beethoven's life that made the Walsh studies. as a result, Walsh said, the two scientists will work together to reach consensus on possible levels of lead. "There are limits to what you can do with hair," he said . "There is a lot of data showing that chemical analysis is completely reliable when you get a few inches of the scalp."

Related Sites

• The Ira F. Brilliant Center for Beethoven studies
• The film "Hair Beethoven"
• health research Institute and Pfeiffer Treatment Center

Mention resistant staph bacteria, and most people think about the almost invincible strains - formally called methicillin-resistant Staphylococcus aureus (MRSA) --What infect immunocompromised individuals and patients in hospitals. But in recent years, MRSA strains that are more virulent began to spread outside hospitals and attack people in perfect health ( Science , 14 March 03, p. 1639) . Now, researchers say they have discovered how these bugs, which some see as a major threat to public health, do their damage.

Typically transmitted in prisons, schools and locker rooms, "community associated" MRSA (CA -MRSA) can cause serious infections of the skin and soft tissue, pneumonia and an infection of the blood known the bacteremia name, sometimes with fatal consequences. Why bacteria are so virulent is uncertain. Many believe it is because all CA-MRSA strains carry the gene for a toxin called (PVL) Panton-Valentine; A recent Science document suggests that this molecule plays an important role in CA-MRSA caused by pneumonia ( Science , 23 February, p. 1130).

But some scientists disagree. "We fight about PVL much," said Michael Otto, a researcher at the Rocky Mountain Laboratories, part of the National Institute of Allergy and Infectious Diseases in Hamilton, Montana. He was not convinced by the Science paper, and points out that pneumonia occurs in about 2% of CA-MRSA. PVL does not appear to play a role in skin infections and soft tissue or bacteremia, said Otto.

Now his team found another group of biochemical guilty. They found that CA-MRSA strains produce called phenol-soluble modulins peptides (PSM) in much larger quantities than do strains . hospital When the researchers knocked the genes for four of these peptides, the so-called PSMs of α-type, CA-MRSA bacteria have become much softer in mice: skin infections were less severe, and bacteremia was less often fatal. Apparently, the peptides are the most virulent microbe, the authors concluded

Learn why PSM-aS are destructive, the researchers added the peptides in human neutrophils -. A class of white blood cell that engulfs the bacteria --In the test tube. Neutrophils have started to collapse within 5 minutes, and less than an hour, many have been completely destroyed. So PSMs seem to strike a defense system, said Otto, giving vent MRSA.

"I have no doubt that these peptides contribute to the virulence of Staphylococcus aureus ," said Francois Vandenesch the University of Lyon in France, which has long defended the hypothesis and PVL co-author of science paper.. But he still believes PVL plays a major role as well

Henry Chambers, who is studying MRSA at the University of California, San Francisco, said PSMs that form "an attractive alternative explanation" for PVL - but both can be important. If the results of Otto maintain, Chambers said, they offer researchers a series of new drug targets.

Related site

• More CA-MRSA, the Centers for Disease Control and Prevention

BOSTON -. Two prominent researchers evaluated the downright depressing state of vaccine research against AIDS and urged the National Institutes of Health (NIH) to correct its course.

in the plenary discussions back-to-back at the 15th Conference on retroviruses and opportunistic infections today, Ronald Desrosiers, director of the New England Primate Research Center in around Southborough, said he thought the NIH - the largest funder of the research of vaccine against AIDS - had "lost its way," spending too much money on development and testing products and not enough on basic research. Virologist Neal Nathanson, professor emeritus at the University of Pennsylvania who formerly headed the Office of the NIH AIDS Research, echoed the plea Desrosiers that more money go to, innovative studies at risk.

The trigger for unusually harsh public criticism of the field came last fall when a vaccine against AIDS that many considered the best prospect in developing bombed in large clinical trials ( science , 16 November 07, p. 1048). Recapping this failure, Desrosiers, who is testing vaccines against AIDS in monkeys, went to claim that an effective vaccine is not even on the horizon. "None of the products in the pipeline any chance of being effective," said Desrosiers, because the field is hampered by many unknowns, such as understanding of the immune responses that a vaccine must elicit. "We must make a better job of making the clinical trial only products that show very promising. "

clinical studies receive about a third of the nearly $ 0 million that the NIH dedicated to the research of vaccine against AIDS year, the majority from the National Institute of allergy and infectious diseases (NIAID). in January, Desrosiers and 13 other private researchers wrote NIAID Director Anthony Fauci about their concerns that the field was the drift. "the letter was a good outside tweak something I was already thinking," said Fauci Science at the meeting here. Fauci said NIAID plans to organize a vaccine against AIDS day "summit" on March 25 to explore how to move forward. It will be open to the public and webcast. "The real question is the balance we want between research and development of discovery," Fauci said. "We need to take a time out."

Related Sites

• conference home page
• More information on vaccines against AIDS

can fat - even lots of it - to be healthy? A provocative study of fat grafts in mice suggests for the first time that the answer may be yes. Although some types of fat are known to be worse than others, no one had directly investigated whether certain types of fat can be a good thing. Researchers say the work is preliminary, but intriguing

For most overweight people, excess fat is in one of two areas :. Deep inside the abdomen (visceral fat) or around the hips and legs (subcutaneous fat). Researchers have recognized for some time that visceral fat is the greatest evil. People with lots of it are much more prone to diabetes, heart disease and other problems that people with excess subcutaneous fat. But he does not know exactly why. The fat itself different, or because of its location in the question of the body?

To probe this question, C. Ronald Kahn, director of obesity research at the Joslin Diabetes Center in Boston, and colleagues designed a relatively simple experiment. They transplanted fat in 42 mice naturally plump, healthy. The mice were divided into four groups that have undergone different types of operations. In some cases, the researchers added visceral fat and subcutaneous abdominal. In others, they nestled visceral fat or subcutaneous fat in the flanks of the animal, the approximate equivalent hips. Thirteen other animals formed a control group; they were made, but received no additional fat.

Kahn team found some surprising benefits to the subcutaneous fat. The mice with fat transplanted subcutaneously into the abdomen won only about 60% of the weight packed with the control group, who, like most mice, continued to grow. These transplant recipients also had higher levels of glucose and insulin. Mice that got subcutaneous fat in additional subcutaneous areas also performed better than controls, but not as good as the first group. Those who had visceral fat added to their visceral cavity were the worst off, the group said today in Cell Metabolism . Autopsies on the mice confirmed that the transplanted fat was still in place.

The conclusion suggests that subcutaneous fat may be beneficial to health, says Kahn. "That's the surprise twist in the story."

The implications are that "the subcutaneous fat produces something that is good for you, and that visceral fat produces something that is bad for you," says Richard Bergman, diabetes and obesity researcher at the University of Southern California in Los Angeles. Although some studies have correlated excess subcutaneous fat in people with improved insulin levels, the new work is "the most comprehensive study to date" consideration of this, says Philipp Scherer, diabetes and obesity researcher at the University of Texas Southwestern Medical Center in Dallas.

But for Bergman, the conclusion was so unexpected that it is keen to see more evidence, including an index on "magic factor" that could explain the interest of health. "Putting the subcutaneous fat in the visceral compartment is something that happens naturally, so it is difficult to interpret," he said.

Peer pressure can lead adolescents to start smoking, but their DNA keeps hooked on the buzz of nicotine in their adult lives. So says a new study that found that people with variations in specific genes are more likely to become addicted if they start smoking in adolescence. The work may explain why some people find it harder to quit smoking and also stresses the importance of preventing children from smoking in the first place.

Previous research has shown that people who start smoking in adolescence are more likely to be heavy smokers as adults; They also find it more difficult to quit than those who start first turn later in life. Some genes may influence whether people are hooked on cigarettes during their teenage years, but no one had shown that. Three recent studies have shown that people with only one change of base nucleotides in genes encoding cell receptors that bind to nicotine - the chemical addictive in cigarettes - were more likely to develop lung cancer ( Science NOW, April 2). Because genes help produce the buzz of nicotine, a team led by Robert Weiss, a geneticist at the University of Utah in Salt Lake City, wanted to determine whether the variations in their sequences determine if people develop stronger addiction to cigarettes.

The research team compared the genes of receptors 2827 adults currently smoke more than a pack a day and have been enlightening on average for more than 30 years. 1051 smokers who started smoking at 16 or younger were 1.5 times more likely to have an addiction to nicotine worse if they had a particular pattern of six changes from a single base in the genes than those with other genetic models. However, subjects who had the same gene pattern, but started smoking after 16 years had no increased risk of a more severe habit, suggesting that addiction risk window of this particular genetic variation opens only during the teen years, the researchers report today in PLoS Genetics .

It is unclear how the genetic variant increases the chances of being caught young smokers. One possible explanation is that the adolescent brain responds differently to nicotine. "It could be that your brain matures, you become less susceptible to the addictive effects of nicotine because the genetic component that affects how nicotine interacts with these receptors may have less effect," said Chris Amos, genetic epidemiologist at University of Texas MD Anderson Cancer Center in Houston, who was not involved in the study.

Norman Edelman, a pulmonologist at the medical Center of Stony Brook University in New York, said the results show highlight the need to focus more on preventing adolescents from smoking. "most smokers, perhaps 0%, are hooked on cigarettes as adolescents or young people," he notes. "We spend a lot of 'efforts on smoking cessation in adults, but we do not spend enough on the prevention of smoking among children, which is really important because this place where the damage is done, according to this study. "

Fifteen years of genetic sleuthing finally paid .: researchers have nailed the gene that seems to cause an inherited form of neuroblastoma, a cancer of the nervous system that primarily affects children. Scientists are optimistic that the results will help them develop disease screening for some families, and lead to potential new therapies.

about 15 years, a family riddled with neuroblastoma arrived at the Philadelphia Children's Hospital (CHOP); even a grandmother had developed the disease. Pediatric oncologist John Maris realized that he had a rare clue to his hands. Only 700 children in North America are diagnosed with neuroblastoma, and only 1% of those with familial, transmitted through other family members. Maris asked permission to draw blood for DNA tests and was invited to a barbecue with the family; he came armed with needles and collected blood samples at the kitchen table. Over time, Maris and his colleague Yael Mosse reached to hospitals in Belgium, Italy and elsewhere to look for other families like this. Finally, they found 20 to 1 total of 49 people with neuroblastoma and 127 without

In search of the shared DNA, the researchers quickly hosted on a region of chromosome 2. This led them to mutations in a gene called. ALK , which, when activated, can promote cancer. The defective form of ALK , a dominant allele, appeared in all concerned, as well as in healthy parents, who had passed down, reports Team online this week in Nature . They also found ALK some brothers and sisters who were healthy, making them wonder if these young people were high-risk neuroblastoma. ALK has also been implicated in lung cancer and lymphoma, although there are different molecular defects.

The families studied here who wear ALK mutation, make up a small minority of those affected by neuroblastoma, however. Most children are the only ones in their family with the disease, develop spontaneously for no apparent reason. Could the discovery of ALK family in neuroblastoma help children who inherit the gene?

To find out, researchers studied tumor samples from children with neuroblastoma who did not inherit the disease. They found that 12% had ALK mutations in their tumors. In addition, a handful of children with no family history of the mutation carried ALK mutations in all cells of the body, which means they have developed a spontaneous mutation in utero before continuing to develop neuroblastoma. Together, these pieces suggested ALK had a role in neuroblastoma spontaneous and familial, although oncologists are still trying to unravel exactly what it might be.

Meanwhile, CHOP is preparing to offer ALK tests for all patients newly diagnosed neuroblastoma. This will help doctors determine how common ALK mutations in neuroblastoma tumors and help to identify children who may have developed mutations before birth. For those who are ALK carriers - harboring the gene in their normal cells as well as cancerous - CHOP offer tests for the brothers and healthy sisters, in the sense that if these children are also testing positive, they can be given regular, non-invasive screening to catch the disease in its early stages. Mosse considers it essential, because by his estimation, the risk of developing neuroblastoma when wearing a ALK mutation is at least 50%. Most children with neuroblastoma are diagnosed when the disease has already spread and has a rate of approximately 30% survival.

"We have the chance not only to have found this gene, but to be able to do something about it," said Mosse. She is particularly grateful that the culprit is a gene that is activated to cause cancer - as opposed to one that is silenced, then triggers the disease - because the drugs can suppress. One ALK inhibitor is in a Phase I trial for lung cancer, and the company, Pfizer, is ready to test it in neuroblastoma. Mosse awaiting trial to open in 6 months.

"It is clear that these changes are real," said pediatric oncologist Susan Cohn of the University of Chicago Comer Children's Hospital. "It is incredibly exciting." One thing that is unknown, she said, is whether ALK inhibiting drugs work on all types of neuroblastoma tumors, because all tumors carry them. This is something that only clinical trials will tell, she said.

As if black rats have a bad reputation already. A study published today in PLoS One suggests that a century ago, these rodents, already blamed for the spread of bubonic plague in medieval Europe and considered one of the worst invasive species on planet, wore a disease that killed off two species of native rats of Christmas island in the Indian ocean.

Ocean islands are notorious extinction hotspots, because endemic species evolved with few predators or competition. When invasive species (or people) arrive, the native animals are often as helpless as the flightless dodo, which was hunted to extinction in the 17th century.

The same fate awaited Maclear of rats and Bulldog, who lived on Christmas Island. Both species were abundant at the time of the first scientific expedition to the island in 1887, but their populations began to decline in 1899, when black rats arrived with the SS Hindustan . In 108, the two species have been declared extinct. Shortly before their final disappearance of Maclear rats were reported sick and seen crawling along the trails. Visit naturalists of the time attributed the symptoms to a type of sickness (trypanosomiasis) transmitted by invasive black rats to sleep, but many modern researchers instead suggested the crossing with black rats as the main cause of extinctions.

Alex Greenwood of Old Dominion University in Norfolk, Virginia, and colleagues set out to solve the mystery of extinctions. They collected samples of 21 historic rat skins of Christmas Island, stored in natural history museums in the United Kingdom. 100 years specimens were then examined for genetic signs of interbreeding and the presence of pathogens sleeping sickness.

The researchers analyzed the skins of black rats, both extinct and alleged cross. The results showed "no consistent genetic difference" between the black rats and supposed hybrids, say the authors, that the specimens labeled as hybrids are actually black rats. Greenwood, results eliminate hybridization as the main cause of extinction.

Some also tested positive for skin Trypanosoma lewisi , a parasite from the group of organizations responsible for the fatal bedroom sickness and Chagas disease in humans. The trypanosome is transmitted by fleas carried by black rats, which are immune to its effects. But for endemic rats that had no resistance, the parasite would probably have been fatal. Greenwood says this study implies that invasive species and environmental destruction are not the only causes of extinction. "The disease can play a role as well," he added.

Amy Pedersen, parasitology at the University of Sheffield in the UK said that despite the small number of samples, " excellent arguments for authors extinction mediated disease ". It is likely that infectious diseases could contribute to future extinctions, especially species that are also facing other challenges, she added.

Rod cells in our eyes help us see in dim light. They also ensure that the cones, other light-sensitive cells on which we depend for vision, enough food, a new study reveals. The findings may shed light on a common cause of blindness.

Approximately 100,000 people in the United States have retinitis pigmentosa, a hereditary retinal incurable disease that leads to blindness. Over 40 genes may contribute to disease, often damaging important proteins in the cells of the retina. initial symptom loss, night vision disease, occurs when stems begin to die off. This attrition usually begins in childhood, and even if it is inconvenient, most people get by with their cones - the photoreceptor cells that operate in bright light. But when those affected reach adulthood, the cones begin to die, too, ultimately resulting in total blindness. This has confused the scientists, because defective genes are not active in the cones, as in the stems.

To crack this mystery, Constance Cepko biologist from Harvard University and his colleague Claudio Punzo, a postdoctoral researcher, first evaluated earlier theories. Some researchers believe that when the stems are dead, they produced a toxin that killed cones. Others have speculated that, because the stems use a lot of oxygen in the retina, their death could leave a large amount of oxygen that overloads and damages the remaining cones. But none of them seemed to match the trend, Cepko said, so he and Punzo decided to look for a new explanation.

The researchers measured the activity of genes in four different strains of mice with defective stem cells. They found more than 0 genes that are activated at about the same time, the cones began to die, many of them related to cell metabolism.

"That was our first clue that maybe the cells do not receive enough nutrients," says Cepko. Several of these genes were linked to a protein known as the mammalian target of rapamycin, or mTOR, which leaves the cell whether it has enough nutrients. - especially glucose But if the harsh famine long enough, mTOR directs the cell to digest is exactly what the cones were

in determining whether a drop-off glucose was killing cones, the researchers injected abdominally some of the mice with insulin to increase their glucose levels. the shots do not cause the cones to hang on a little longer long, but they still died a few weeks later.

Cepko and Punzo think the cones could starve because of crumbling architecture of the retina. a thin layer of cells, known as name of the retinal pigment epithelium (RPE), covers the rods and cones like a circus tent and provides their nutrients. Rods outnumber cones in the retina significantly, so that when they die, most of the "tent poles" of RpEs die with them. Collapses tents, cones lose their nutrient connection, and they starve slowly. The study is published online this week in Nature Neuroscience .

"I think it's very exciting," said Rafael Caruso, an ophthalmologist with the US National Eye Institute in Bethesda, Md. "It's a new approach to the problem." Caruso said researchers "do a pretty convincing case for their conclusions," especially because the same mutations in mice tested are also found in humans.

Unfortunately, both Cepko Caruso and agree that the finding does little to researchers seeking treatments. But it suggests a new framework for thinking about the problem. Exploring different ways to get nutrients into the cones, Cepko said, researchers may one day be able to help people with retinitis pigmentosa retain their daytime vision for a longer period of time.

Stem cells fans are in a frenzy about the upcoming change in presidential politics and held press conferences Abrim enthusiastically, if not the content. But at a meeting today at the Center for American Progress (CAP) in Washington, DC, to publish a report A Life Sciences Crucible , some differences emerged on how the new administration should proceed to normalize stem cell research and from political winds that buffeted during the Bush administration.

CAP wants President-elect Barack Obama to quickly issue a decree clearing the restrictions Bush and Congress to pass a bill that explicitly allows researchers funded by the federal access to cell lines derived human embryonic stem after August 01.

But Amy Comstock Rick, chief patient-centered Coalition for the advancement of medical research, warned that it was important to see how the decree reads . Orders may come and go, she noted, so it should not be used to specify search criteria. Instead, she said the order is to simply put the whole subject "where it belongs" - in the capable hands of the NIH. Similarly, she said, his group opposes a new law which she said would not be "conducive to making flexible decision."

CAP also calls for a special working group for clinical research using embryonic stem cells to create within recombinant DNA Advisory committee of the NIH. the Coalition for the advancement of medical research disagrees with that, too. It's just another layer of national oversight on matters that should be left to committees existing institutional oversight, said Rick. "separate Special Structures" to oversee the research on stem cells still smack of political motivations.

looks like the cries may have disappeared from the world of politics on stem cells, but it is far from over.

National Institutes of Health will devote most of its $ 8.2 billion to research the economic stimulus bill for requests of grant funding it has already received and to complement existing grants. A smaller amount of approximately $ 100 million to $ 0 will go to new grant applications it receives in the coming months.

Speaking Wednesday afternoon in Washington, DC, to a packed auditorium of representatives of universities and associations, Acting Director Raynard Kington said NIH would soon issue a request for applications for new grants "challenge" of up 'to $ 500,000 per year for 2 years. These grants will challenge for research on certain areas of science or public health think that NIH can make significant progress within 2 years. NIH will create an abbreviated application process for these grants, peer-reviewed, but did not say which areas will be targeted.

Because the NIH must spend stimulus money in these 2 years, he is under pressure to start sending money to the beneficiaries as soon as possible. Therefore, Kington said, it will not issue a massive call for new applications. Instead, it will mainly seek to add money to existing grants and fund grant requests it has received and reviewed by peers.

All grants 2 years resulting from the stimulus package will come with the unusually rigorous reporting requirements, Kington said, including reporting the number of jobs created or maintained. He has repeatedly said that the NIH would be "embarrassed" if the institutions do not spend money or increase their local economies. He expects the beneficiaries to "hire people and make purchases and advance science," he said.

Because the goal of the stimulus bill is to improve the economy of the nation, Kington said NIH would also be sensitive to the geographic distribution of subsidies it gives.

Kington gave few details about NIH plans, but said more details would be available soon.