Enzyme apathetic Alzheimer

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Enzyme apathetic Alzheimer -

ESCAPED an enzyme? These plates characteristics can accumulate in the brains of some people with Alzheimer's disease

because an enzyme can not break b amyloid.

SAN DIEGO - When you hear of insulin, you probably think of diabetes, but perhaps it could soon bring to mind the disease Alzheimer. The connection is an enzyme that breaks insulin and a protein that causes Alzheimer's disease. Now, a preliminary study suggests that dysfunction of this enzyme may be responsible for Alzheimer's disease in some families.

Alzheimer patients suffer from excessive amounts of a protein called b amyloid, which for some reason built into their brain. In some cases, it appears that genetic mutations increase the production of b amyloid. Alternatively enzymes - so far unknown - which break b amyloid simply do not work fast enough. In 1994, researchers found the first candidate: Insulin-degrading enzyme (IDE) breaks down b amyloid in a test tube. FDI but does not seem likely to be clinically important, because it is normally found in the cytoplasm, and b amyloid built between the inner closed cells or vesicles in the cell.

New evidence for the importance of FDI came from Dennis Selkoe, Wesley Farris and colleagues from Harvard Medical School in Boston. Although screening of brain cells to proteins that destroy b amyloid, they discovered that FDI seemed to have more naturally secreted b amyloid. At the annual meeting of the Society for Neuroscience here Farris November 11 reported that blocking FDI activity stopped approximately 70% of b amyloid ventilation in isolated cell membranes from brain tissue. And causing cells to overproduce FDI intensified the rate of b amyloid ventilation.

The team also worked with the geneticist Rudolf Tanzi and his colleagues from Massachusetts General Hospital to see whether mutations in the gene for FDI could contribute to Alzheimer's disease in people with a family history of disease. The Tanzi group provided data on the seven families of Alzheimer's disease appears to be related to the region of chromosome 10 that contains idea. Selkoe's team analyzed the cells of these families and found that members of the same family had significantly fewer b amyloid degradation than normal, suggesting that FDI can contribute to broken disease. The team is looking for more families with Alzheimer's disease that can have such mutations.

The data are "very encouraging," says Alzheimer's researcher Frank Laferla of the University of California, Irvine, but he remains convinced that IDE cleans most of b amyloid . "It will not be a single enzyme that degrades b amyloid," he said.

Related Sites

Summary of the Society for Neuroscience meeting
learn more about Alzheimer's disease from the National Institute on Aging

Hampered Virus Kills Cancer cells

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Hampered Virus Kills Cancer cells -

Scientists have modified a common respiratory viruses to destroy cancer cells while leaving healthy unharmed, said a report in tomorrow's issue of Science . The next step - a clinical trial in human cancer patients - is already underway

The cancer killer pathogen is genetically modified lung and a family member of adenovirus .. Biochemist Frank McCormick and ONYX Pharmaceuticals colleagues in Richmond, California, found that the modified virus is unable to replicate in normal cells, but it develops into cancer cells lacking the gene p53 that suppresses tumor growth. The p53 gene, leaving cells vulnerable to the virus when it is out, is one whose loss or inactivation is linked to the development of 50% of human cancers. Consequently, the virus could be widely applicable in the treatment of cancer, particularly because the loss of p53 also allows to make cancers resistant to conventional chemotherapeutic drugs. The modified virus has killed human tumors implanted in mice while sparing normal cells.

`` What I like is how smart he is, '' said Richard Klausner, director of the National Cancer Institute. `` It has been a longstanding fantasy to find a [anti-cancer] virus. '' However, he warned that `` not all [new cancer treatment] who is intelligent and focused [to tumor cells] will end up being useful. ''

ONYX team tests the safety of the virus in people with cancer of the head or neck that do not respond to conventional therapies. The tests should be completed in 1997. To date, the virus, which is injected directly into the tumors of patients appears to be safe. But it is too early to say whether the virus has the same ability to kill tumors in humans it has in mice.

An American Original: Cancer Deaths Decline

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An American Original: Cancer Deaths Decline -

WASHINGTON, DC - A deadlock that has gripped the longest and most expensive war in modern times - war against cancer - can finally eased. The cancer death rate in the US fell by 2.6% between 1991 and 1995, the National Cancer Institute (NCI) announced today, marking the first sustained decline 6 decades of modern cancer cases.

"This looks like a turning point in the war 25 years on cancer," Donna Shalala, Secretary of Health and Human Services, said in a statement today. "It is not just a blip once, but a trend of real and promising fall." After a 6.4% increase in mortality from cancer between 1971 and 190, the decline suggests that lifestyle changes and improved treatments start paying.

For example, lung cancer mortality among men dropped 6.7%, representing more than half of the overall decline of 4.3% of cancer deaths in men. NCI attributes this decline in part to the 15% decrease between 1955 and 1970, the percentage of men who smoke. For women, however, lung cancer deaths increased, apparently because smoking among women increased in the 1960s increasing numbers of lung cancer offset strong gains against breast cancer because of diagnostic earlier and better treatment, keeping the overall decline in women's cancer mortality to only 1.1%.

African Americans seemed to make the biggest gains. They experienced an overall decline of 5.6% of cancer mortality, compared with an increase of 18.3% between 1971 and 190.

definitive cancer rates for 1995 will not be released before next year, but experts predict the downward trend will remain relatively unchanged. Says the NCI Director Richard Klausner, "The 190s will be remembered as the decade when we turned measurably tide against cancer."

This Little Piggy Going to Market Organ

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This Little Piggy Going to Market Organ -

LONDON - claims in the British media this week that the government is ready to give fire green transplantation of organs from genetically modified pigs in human patients were dismissed as "pure speculation" by a Ministry of Health official. The official said a decision will be announced in 1997.

The London Times and the BBC reported yesterday that the government had accepted the recommendation of an inquiry it was safe to advancing transplants. They reported that the inquiry, chaired by Ian Kennedy, professor of medical law and ethics at the College, London King raised the issue that pig organs could spread to humans potentially dangerous animal viruses. Nevertheless, the Committee has concluded that neither the security nor the ethical issues blocking the way for pig to human transplants. Transgenic pigs are a regulatory protein that helps prevent the immune system from attacking a transplanted organ.

A Ministry of Health official has neither confirmed nor denied that the government planned to approve pigs to humans. "The report will be published in the new year, and we will have to wait until then," he said. A spokesman Imutran, the company based in Cambridge UK, which developed transgenic pigs, says the company n has no information on the content of the report. "speculation is new for us," she said.

Bacchus Knows Best: drugs against cancer in grapes

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Bacchus Knows Best: drugs against cancer in grapes -
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a laboratory of tests indicated that a chemical found in grapes and other fruits and vegetables is a potential antitumor agent. But experts warn that the compound, described in a report in tomorrow's issue of Science , is at least 2 years of testing in humans, and early results do not justify more trips the wine rack.

medicinal chemist John Pezzuto and colleagues at the University of Illinois, Chicago, did not expect it to improve the image of red wine when they began their study. His team was one of many who just a few years began testing some 1,000 plant extracts from around the world for the presence of potential antitumor agents. Their main assay revealed that extracts which inhibit an enzyme called cyclo-oxygenase-1, a cog in the body's inflammatory response. Pezzuto says, "anti-inflammatory agents tend to be good antitumor compounds."

> The team narrowed the 1000 extracts down to three that seemed particularly promising. The most powerful came from Peru roots of Cassia quinquangulata tree, extracts of which are used in traditional medicine to treat fever. Further experiments on a hosted component of the extract called resveratrol, a compound produced in some plants when they are subjected to a stress or pathogen attack. The compound did well in the anti-tumor tests. In addition to inhibition of cyclooxygenase, it impeded the DNA mutations in Salmonella bacteria, increasing the activity of an enzyme in the liver of mice that detoxifies carcinogens, precancerous lesions inhibited in mouse mammary cells, and growth upset of skin tumors in mice exposed to a powerful skin. carcinogenic

Resveratrol is particularly useful as anti-cancer drug candidate because it is easy to obtain: The chemical is abundant in grape skin and has been found in at least 70 other species of plants, including peanuts and mulberries. But experts warn that the compound has a long way to go before the beginning of the pharmacy. "This is a good lead, but it is very early," says Peter Greenwald, director of the division Prevention and fight against cancer from the National Cancer Institute. Greenwald adds that resveratrol is facing at least 2 years' other animal testing and safety testing before it is considered a human cancer prevention trial: "We are certainly far from saying" drink lots of red wine "

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Vaccine protects against cholera in Vietnam

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Vaccine protects against cholera in Vietnam -

A vaccine against cholera cheap performed well in a pilot in Vietnam. The discovery, published in the tomorrow The Lancet , is a breakthrough in the search long and frustrating in developing countries an effective vaccine against cholera, a potentially fatal disease spread by contaminated drinking water.

at the end of 1992, a team led by researchers at the National Institute of Hygiene and Epidemiology in Hanoi, Vietnam, and the National Institute of Child Health and Human Development United States has given the oral vaccine - which is to kill all Vibrio cholerae , the cholera bacteria - to more than 67,000 residents of Hue, Vietnam. A number approximately equal did not receive the vaccine. In 1993, 37 people were vaccinated admitted to a hospital with cholera, against 92 cases in the control group. Thus, the vaccine decreased hospital admissions for cholera by 60%.

Developed and produced at the institute in Hanoi, the vaccine is relatively cheap to produce and easy to distribute as it remains active without refrigeration. He also seems to be equally effective in children and adults. What surprised the researchers, because a similar set, tested vaccine killed in Bangladesh in the 1980s seems to be less strong in children.

"This study is important," said Myron M. Levine, director of the Center for Vaccine Development at the University of Maryland School of Medicine, "because it demonstrates that a developing country can design, produce and evaluate a moderately effective vaccine in a large field trial with little outside help. "

researchers plan to launch a larger trial in Vietnam later this year between the vaccine against placebo. If proven effective, the vaccine could be pressed into service quickly in Vietnam, where more than 3,000 people receive cholera every year. Levine adds that a similar vaccine against other strains of cholera could be produced in developing countries such as Zaire, where an outbreak has killed 12,000 people in the Rwandan refugee camps in July 1994.

Mary Had a Little ... Clone

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Mary Had a Little ... Clone -

Creating a new organism from a single cell was more science fiction than science. Not anymore. Scientists have cloned a sheep using a cell nucleus taken from the udder of an adult sheep, according to a report is expected later this week Nature . The breakthrough has generated a fierce reaction from ethicists and others who fear the prospect of human cloning.

embryologist Ian Wilmut and his colleagues at the Roslin Institute Scotland first increased udder cells in laboratory dishes, then put the nuclei of these cells into egg cells whose DNA had been removed . They found that in the bud, the genome transferred back to embryonic pattern of gene expression, prompting the egg to start dividing. The viable embryo was then placed into the uterus of the ewe that had produced the egg.

Wilmut team first used this technique a year ago, producing lambs with nuclei transplanted from very early embryos. In their latest work, the group reports how cells taken from sheep at any time in their life will do the job. In addition to the lamb of the breast tissue of a sheep 6 years, four children were produced with cores 9 day old embryos and three from the cells of the skin 26 days fetus.

Others have new bodies, mainly amphibians and mice using embryonic nuclei, but failed when they used adult cells. "We now have strong evidence that it is feasible," said researcher Colin Stewart embryo Centre for Research and Development Frederick Cancer National Cancer Institute in Frederick, Maryland.

We thought that in mature somatic cells, certain genes necessary for the development have been transformed permanently, even lost. Thus the success of the group was a "surprise," says Wilmut. "The mechanisms that regulate the expression of genes are more labile than we could have imagined." Finally, Wilmut said he hopes to use nuclear transplantation to create sheep or cattle with genes added to their specific genomes

Theoretically, people could also be cloned. Imagine how much someone would pay for a basketball team fielding five versions of Michael Jordan. Wilmut said Science Now that his group was opposed to human cloning ethically. "We do not know if it will work [in people]," he added. Activists, however, take measures to counteract this possibility. For example, the critic Jeremy Rifkin Biotechnology of the Foundation on Economic Trends announced yesterday his group, as well as some religious leaders and non-governmental organizations, "is determined to mount a global effort opposed human cloning and will seek legislation to ban this technology in every nation. "Several countries - including Germany and the United Kingdom. - Have the laws on the books banning human cloning, but the United States is not among them

A better recipe against Parkinson's disease?

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A better recipe against Parkinson's disease? -

At work. Nurr1, shown in white in the brain of embryonic mice, invites the development of nerve cells of the midbrain dopamine.

People with too little dopamine in their brains develop the debilitating symptoms of Parkinson's disease. Now scientists have identified a molecule that helps the brain get just the right amount of this neurotransmitter. The discovery, published in today's issue of Science * raises the possibility enticing that increasing or restoring the activity of this molecule, called Nurr1, omitting nerve cells could relieve or prevent Parkinson's disease.

researchers already knew that a gene called Nurr1 is most active in brain cells that produce dopamine. To find out what the gene's protein fact, a team led by Thomas Perlmann of the Ludwig Institute for Cancer Research and Lars Olson of the Karolinska Institute, both in Stockholm, Sweden, has created a strain of mice lacking the Nurr1 gene. These mice failed to nurse and died one day after birth. The only physical difference that the group could detect between KO and normal animals of the same age was in the midbrain region, which contains neurons that degenerate in Parkinson's disease. The cells were poorly organized, suggesting that they had never specialized in dopamine-producing neurons.

The team confirmed this suspicion by testing the presence of proteins known to be produced by these particular neurons. Nurr1, tyrosine hydroxylase (an enzyme essential for the production of dopamine) and of other proteins were all absent. Other experiments have suggested that Nurr1 not only causes dopamine cells to form in the first place, but it also helps produce the right amounts of dopamine. "Finding [protein] that affects such a specific [section] brain is very exciting," said neurobiologist Ron McKay of the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. The results raise the tantalizing possibility that the increase or the restoration of Nurr1 activity in failing nerve cells can delay or prevent Parkinson's symptoms.

It may also help researchers track down the cause of the disease. Because Parkinson's disease does not seem to run in families, experts have long sought an external cause, such as a toxic environment. It may now be possible to narrow the search by looking at how the potential toxic substances affect Nurr1. And that could lead to treatment, says molecular biologist Orla Conneely Baylor College of Medicine in Houston, whose team discovered the origin Nurr1: "If we find [toxicants] that inhibit the activity of Nurr1, we can then be able to identify drugs that can counteract that. "

for details, science online subscribers can create a link to the full report.

Moles and melanoma

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Moles and melanoma -

The number and shape of moles on your skin can indicate your risk of malignant melanoma, the most dangerous type of skin cancer. The results, reported in tomorrow's issue of The Journal of the American Medical Association , suggest that doctors should regularly examine moles of patients during physical examinations.

Although researchers have long known that large, irregular shaped moles are most likely to go wrong, Margaret Tucker of the National Cancer Institute and colleagues at Harvard Medical School wanted to identify the relation between the size, number and type of mole and melanoma risk. They asked dermatologists in two research centers on the major skin cancer - the Melanoma Clinic at the University of California, San Francisco, and the pigmented lesion clinic of the Hospital of the University of Pennsylvania - take detailed notes on the characteristics of moles for patients and melanoma moles turned into

having collected data on 738 patients with melanoma and 1,030 melanoma patients, Tucker's team found that subjects with more than 100 small moles -. 2-5 millimeters in diameter - were twice as high a risk of melanoma as did people with fewer moles. In addition, having one mole with an irregular contour or a color marbled also doubled the risk. Patients with 10 or more moles irregular had 12 times the risk of cancer patients without these moles.

The results are not surprising, as other epidemiological studies have implicated the moles as a risk factor for melanoma, said Sewa Legha, a clinical oncologist at MD Anderson Cancer Center in Houston. However, he said, better quantify the risk is important because too few doctors understand the importance of regular skin examinations. "Doctors are not well versed in recognizing abnormal moles," he said. "It should be a part of a routine physical examination." Tucker added that the data his team "allow doctors to determine, based on physical examination, if a person is at moderate risk or very high risk."

Soot and death

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Soot and death -

Scientists have linked two major air pollutants with mortality rates increased in 12 European cities. The findings, published in the issue of tomorrow British Medical Journal , are sure to fuel a contentious debate in Europe and the United States on proposed standards that greatly reduce exposure to air pollutants.

An international team led by Klea Katsouyanni of the University of Athens analyzed the daily fluctuations in the levels of two pollutants - sulfur dioxide and particulates - and mortality rates in cities. They found that the average increase of 50 micrograms per cubic meter either sulfur dioxide or black smoke (small particles) on a given day was associated with an average increase of 3% of deaths in western European cities studied - Athens, Barcelona, ​​Cologne, London, Lyon, Milan and Paris. Such levels of pollutants, however, have been linked to a lower increase in mortality rates in the cities of Eastern Europe and Central Bratislava, Krakow, Lodz, Poznan and Wroclaw sulfur dioxide is linked to increased 0.8% of deaths, and the black smoke she gave up 0.6%.

we do not know why people in Eastern and Central Europe, with higher levels of pollution means, seem to be less exposed to daily increases in air pollution. "It was not an effect we expected," said Katsouyanni. One possibility, she and other experts speculate, is that older people are more vulnerable to the adverse effects of air pollution and because Europeans East have an expected shorter life, their cities are less at risk.

the regional difference is treated in other studies on air pollution and health of the European Union . A European project approach