Health Meaning

A hospital's imaging magnetic resonance imaging (MRI) room has no space for credit cards. MRI magnets used to paint accurate pictures of your insides are strong enough to pull a screwdriver out of your hands from a meter away. , Portable devices can be cheaper more in store, however. The researchers report in the next week Physical Review Letters that high-quality images of at least some parts of the body like the lungs, can be made using a magnet to 10 times lower than that native art pin refrigerators.

With traditional MRI, someone slipped into the hole of a giant superconducting magnet that generates a field some 20,000 times stronger than the Earth. The field aligns the nuclei of hydrogen atoms within the body, leaving the spinning atoms as tiny synch bar magnets. Then a brief advice electromagnetic pulse nuclei so they flicker like quirky tops. The whirling atoms emit an electromagnetic wave of its own which can be detected. By adding a second weak magnetic field to change the frequency of the atoms in different places, researchers can map the density of water molecules and build a clear picture of the tissues and internal organs.

Ron Walsworth of Harvard-Smithsonian Center for Astrophysics in Cambridge, Massachusetts, and his colleagues took a slightly different approach. They used a pioneering technology several years ago by physicist from Princeton University William Happer: First align atomic nuclei in gas rubidium with a laser, and then allow them to mix with a helium gas -3 (helium least one neutron). When the atoms collide, a portion of the alignment is gradually transferred to the helium atoms. toxic rubidium atoms can then be removed. Because the helium atoms are an inert gas, they can stay lined up for a few minutes at a time, even without a magnetic field.

In one test, researchers have inflated the lungs of a rat with polarized helium gas and makes high quality photos cavities with a resolution of one millimeter. The magnetic field used to adjust the rotation rate them was only 40 times stronger than the Earth. "It is embarrassing simple," Walsworth said. "You and your brother can liquidate your own magnet and get an MRI as well as what you get in a hospital," he said, although Science NOW is not recommended.

Researchers had known that such a low field imaging with tissue could be done, but no one had bothered to put all the pieces together, says Walsworth. Still, others are impressed: "It's a beautiful piece of work," says Alex Pines, a Lawrence Berkeley National Laboratory physicist in California. "They are very sharp images."

traditional MRI magnets can cost a million dollars, says Pines. The technique could lead to MRI at low price Laptop for imaging the lungs, they say it. Happer added that the lungs are only the beginning. Replacing helium with xenon gas, which is absorbed like oxygen in the blood, also allow researchers to take small budget MRI arteries and brain he predicted.

clinical researchers received a bioethics kit for Christmas, and some may be afraid to open it. He arrived this month in the form of a draft report of the National Bioethics Advisory Commission (NBAC) President calls for tighter controls on research on stored samples of blood and tissue. NBAC says its goal is to protect donor privacy.

The "matter tissue", as bioethicist Robert Yale Levine called, has become a hot topic. Stored tissue may contain a goldmine of information for researchers tracking the spread of the disease, hunting, disease genes and the study of human genetic variation. And it is a huge resource: NBAC calculates that American institutions hold more than 282 million samples of archived human tissue. People who have donated the equipment probably gave general consent for its use, but ethicists argue that the more specific consent may be needed now

CCNB -. A group of 17 members, lawyers, ethicists and health professionals chaired by Princeton President Harold Shapiro of the University - suggests that, in many cases, the identity of the samples secretly encoded by a third party to make them truly anonymous . If a researcher does not want to do, NBAC said, research should go to a local ethics panel, or the Institutional Review Board for approval. NBAC also said that researchers may need to get a new donor consent, particularly for certain genetic studies that provide more than minimal risk to economic or psychological harm.

These are among the 16 recommendations in the draft report of CCNB, which is drawing mixed reactions from the research community. Pathologist John Trojanowski, a specialist in Alzheimer's disease at the University of Pennsylvania, objected that the proposed new notice and consent requirements are so onerous that they "bring research to the judgment." But others were more accepting. Judith Greenberg, who oversees the operations of a large collection of human tissue for the National Institute of General Medical Sciences, said the new report "appears to have reached a fairly reasonable balance." NBAC has set a deadline of 17 January for public comment and may vote on a final report early next year.

biomedical and scientific groups began an intense lobbying effort to convince Congress to resist conservative campaign to block federal support for research human stem cells. Both parties should encounter Capitol Hill in the coming weeks. The first skirmishes could take place as early as 23 and 24 February, when Donna Shalala, Secretary of Health and Human Services (HHS), and Harold Varmus, director of the National Institutes of Health (NIH), before committees of appropriations Congress to defend their 00 budget proposals.

row erupted this week as conservative members of the House and Senate, demanding a change in policy, sent angry letters to the Clinton administration. The Conservatives have attacked an HHS-NIH decision to fund research on human stem cells. These cells, which scientists hope to develop in a variety of transplantable tissues are derived from aborted fetuses and human "spare" embryos in fertility clinics. In a letter of 16 February to Shalala, eight Republican senators, including Sam Brownback of Texas and Jesse Helms of North Carolina, have expressed concern that this research could "give incentives for the killing of human embryos."

Five days earlier, 70 House members led by abortion opponent Jay Dickey (R-AR) had written a letter to Shalala as severe, complaining that HHS misinterpreted a recent law that bans US funding for research that involves the destruction of human embryos. In January, HHS found that the law does not apply to embryonic stem cells because they can not grow naturally in embryos. Indeed, Varmus announced January 19 that researchers may soon be funded to study these cells ( Science , 22 January, p. 465). But members of Dickey group - which includes prominent conservative Republicans such as Henry Hyde (IL), Richard Armey (TX) and Tom DeLay (TX) - disagree vehemently. HHS has read the law too restrictive, they claim; Congress intended to block not only the destruction of the embryo, but also "looking after dependent or destruction or injury of a human embryo."

Neither Shalala nor Varmus yet responded to Conservative calls. But today, 70 scientific groups, academic, and patients sent a petition to Congress, prepared by the Association of American Medical Colleges (AAMC), which calls for research on stem cells. This field, communication AAMC said, holds "enormous potential for the treatment of many diseases" and should be allowed to go ahead.

H Ebden B RIDGE , UK - A recent sharp increase the number of deaths from variant Creutzfeldt-Jakob disease (vCJD) in Britain has caused concern that an epidemic long dreaded the fatal brain disease is imminent. But the numbers may be a statistical fluke, scientists write in tomorrow's issue of The Lancet .

Researchers agree that vCJD, to which some 39 Britons have died since 1995, can be caused by eating meat from cows with bovine spongiform encephalopathy (BSE), better known as disease mad cow. Millions of British people may have been exposed to meat from cows infected during a BSE epidemic that peaked in the late 1980s; but nobody knows how many are likely to be victims of vCJD, or how long the disease develop in the average patient

So far the figures have been reassuring. In each of the first three quarters of 1998, only two deaths were reported. But in the last quarter of '98, the number suddenly jumped to nine. This may be a coincidence, a team of scientists led by Robert Wills of the CJD Surveillance Unit in Edinburgh write in their analysis. But it could also signal the beginning of a larger increase, says one of the authors, Simon Cousens of the London School of Hygiene & Tropical Medicine. "I do not want to prejudge the issue," said Cousens, "but I would not be surprised if it was the beginning of an upward curve." It is unlikely that the apparent increase is due to increased vigilance among doctors, writing team, because vCJD is a high profile disease for years.

The scientists and the public are now eagerly awaiting the latest data. So far, there has only been one confirmed death vCJD in the first quarter of 1999, but that means little, because it usually takes months for cases confirmed to arrive. It will be 6 to 9 months before there is more certainty, Cousens said. "Certainly I'm concerned about the numbers," said John Collinge, head of the Neurogenetics department at Imperial College School of Medicine in London.

Microsoft CEO Bill Gates and his wife Melinda will announce a contribution of $ 25 million to the International AIDS Vaccine Initiative (IAVI), the largest single philanthropic gift ever made to the research against AIDS, science has learned. "Bill and Melinda Gates are very excited and pleased to work with organizations making such a difference in global health," says Trevor Neilson, a spokesman for the William H. Gates Foundation.

IAVI will receive 5 $ million per year for the next 5 years of the foundation, which last June gave the new York-based non-profit of $ 1.5 million. According to Neilson, $ 13.5 million will fund up to three new international teams of vaccine development against AIDS. another $ 3.5 million will support these two teams met last year to develop vaccines against HIV specifically for Kenya and South Africa. Between 2.5 million and $ 3.5 million will go to the program of applied research, advocacy and trial preparation IAVI in developing countries, and operational support. "This historic act of generosity will allow us to dramatically accelerate scientific endeavor, "said Seth Berkley, president of IAVI.

The new grant will be two chests of IAVI to nearly $ 50 million and is expected to significantly increase the capacity of the Institute to carry out development and human trials of these vaccines. The National Institutes of Health is by far the biggest player in the field, now spend $ 0 million annually in R & D vaccine against HIV. The iconoclastic IAVI, however, hopes to address the problem of a novel angle, marrying academics from both rich and poor countries with cash-strapped businesses.

Today

is Sir James Black's birthday, a British pharmacologist who revolutionized the treatment of heart disease and ulcers of his discovery of two important drugs.

In an attempt to find a drug that would relieve the pain of angina, discovered black propranolol, which target beta receptors in the heart, preventing hormones like adrenaline to stimulate and increase the heart rate and oxygen demand. Others followed the discovery of a multitude of new beta-blockers for the treatment of heart attacks, hypertension and migraine. Black also discovered cimetidine b, a compound that calms stomach ulcers by blocking the receptors that stimulate gastric acid secretion.

Black was knighted in 1981 and received a share of the Nobel Prize in Physiology or Medicine in 1988 for its drug discovery.

[Source: Britannica Online ]

Today is the 74th anniversary of Baruch Blumberg, an American research physician whose work has led to a blood test and a vaccine against hepatitis B. as head of geographic medicine and genetics section of the national Institutes of health, Blumberg has traveled the world and collected blood samples from remote ethnic groups to study the hereditary variations in blood proteins.

in 1963 while testing the blood of Australian aborigines, Blumberg detected a foreign molecule which was rare in North America. It was also discovered that this molecule, which he named the antigen, reacted with antibodies in the blood of hemophiliacs who were monitored for the strains of hepatitis. Three years later, he identified the antigen in the context of hepatitis B. Blood banks soon began testing the virus, and in 1971, the incidence of post-transfusion hepatitis had fallen 25% in the United States. A vaccine of his work became commercially available in 1982. Blumberg, who is now affiliated with Fox Chase Cancer Center in Philadelphia, received a share of the Nobel Prize in Physiology or Medicine in 1976.

[Source:EmilyMcMurrayEd notable scientific Twentieth Century (Gale Research Inc., ITP, 1995)]

The idea of ​​replacing faulty genes with functional ones is appealing, but it has come under severe criticism from a voluntary patient with a deficit hereditary enzyme died last fall ( science , 17 December 1999, p. 2244). Now a first report from a different research team suggests that, at least for hemophilia, there are reasons for cautious optimism about a new gene therapy.

People with hemophilia have inherited a genetic defect that limits the production of blood clotting factors. This puts them at risk of dying from trauma or internal bleeding. regular and costly transfusions currently allow most hemophiliacs to keep their disease in check. The purpose of this treatment is to maintain a level of coagulation factor which is 1% or more of the level in normal blood.

Hoping to find better treatment of hemophilia, hematologist Katherine High of the Children's Hospital of Philadelphia and colleagues started working on a gene therapy strategy there 6 years. After the success with mice and dogs, they started a preliminary clinical trial with three patients. The team injected the volunteers in the thigh with a virus that has been modified to carry a gene encoding a clotting factor. Muscle tissue near infected, where cells have intensified their production of clotting factor, the team reports in the March Nature Genetics

Although this test preliminary -. To test safety, not efficacy - used very low doses of the virus, patients responded well. Someone required 50% less of clotting factor during the first 100 days after injection, and one needed 80% less. The third patient showed no clear answer. The researchers found no side effects.

High is "cautiously optimistic" that the therapy could provide a new way to treat hemophilia, perhaps by converting severe forms of the disease in a milder condition more manageable. Although early results are "far from being a clear case of successful gene therapy," says molecular biologist Kotoku Kurachi of the University of Michigan, Ann Arbor, he said that the treatment could be very useful - if higher doses are safe and treated tissue continues to produce clotting factor over the long term.

The fountain of youth that keeps the immortal cancer cells can be disabled by a mutated enzyme, the researchers say.

The key cancer cell immortality are the telomeres of the cell, repetitive stretches of DNA at the ends of chromosomes that can protect the chromosomes when they divide. Researchers have learned that telomeres get shorter and shorter each time a cell divides; Once they are gone, the cell dies. Cells in semen, bone marrow and other tissues that divide are frequently an enzyme called telomerase that prevents telomeres shrink. Because cancer cells are also telomerase, scientists have suspected that the enzyme allows cancer cells to continue to divide without dying. Many laboratories test whether compounds which block the enzyme can slow tumor growth.

oncologists William Hahn, Robert Weinberg and colleagues at the Whitehead Institute in Cambridge, Massachusetts, mutated gene for part of the enzyme and inserted into human cells cultured from tumors of the colon, ovary and breast. The mutant unit linked with other building blocks to create a telomerase enzyme that dud supplanted the native enzyme. In seven weeks, all cells have stopped dividing, scientists report in October Nature Medicine . In another indication that cancer cells persist because they maintain their telomeres, the cells that began with longer telomeres in the experience lived longer than those with shorter telomeres.

The results are "an exciting step forward in validating telomerase" as a drug target against cancer, said Louis Zumstein, a molecular biologist at Introgen Therapeutics in Houston, Texas. But a drug antitelomerase would be no miracle solution, as it would allow cancer cells to continue dividing until their telomeres were gone. such latency, Hahn said, could allow cancer cells to develop resistance to a drug finding another way to maintain their telomeres. the wisest approach, Zumstein said, would be to combine a telomerase inhibitor with additional drugs.

A new analysis of older studies sparked a debate about whether the use of mammograms to screen women for breast cancer saves lives. After reviewing eight published studies on the effectiveness of screening, a team of scientists found that both showed no benefit while six others were potentially biased and therefore of little use. But other researchers strongly dispute the conclusions

Much of the debate about mammograms sought to determine if they are useful for women in their 40s. most scientists accepted the benefits for women over 50 and proven ( Science , 21 February 1997, p. 1056 and April 4, 1997, p. 27). But new issues of meta-analysis that conclusion.

internist Peter Gøtzsche from the Nordic Cochrane Centre in Copenhagen and his colleague Ole Olsen watched eight screening effectiveness studies conducted since 1963. In each study, women were randomly assigned to either a group that mammograms regular checks, or to a control group that did not get the chest x-ray procedure. In six studies, the Danish duo claims, the two groups differed significantly in age or socioeconomic status, can skew the results in either direction, or the authors describe their randomization procedure thoroughly enough to convince Gøtzsche Olsen and that the subjects had an equal chance of being in the two groups. Of the two studies, the authors consider well randomized and therefore impartial - one from Canada and one in Malmö, Sweden - nor found that mammograms increased life expectancy. Therefore, "breast cancer screening by mammography is unjustified," the team writes in Lancet tomorrow .

"Nonsense," says Daniel Kopans radiologist at Massachusetts General Hospital in Boston . the bias and Gøtzsche Olsen report are trivial, he says, for example, they dismiss a study in Gothenburg, in Sweden, because the control group was older, on average, than the mammography group - but a months. And the Canadian trial was so much prejudice that one of the licensees studies, he said. Significantly more women in the group of mammography than in the control group began in the Canadian experience with cancer advanced breast, Kopans said, a difference that he and others suspect perhaps arisen because nurses assigned to women in the other group also conducted an initial manual breast examination and may have affected women with pieces within the group of mammography in the hope they would be diagnosed more quickly, said Kopans. A survey of a subset of Canadian data found no evidence of bias, but Kopans and others are suspects.

Gøtzsche stands by its results. Scrutinizing the effectiveness of mammography is particularly important, he said, because this process disadvantages, too: Mammograms often produce false positives, which cause anxiety and may lead women to undergo unnecessary biopsies or surgery . Each mammography study was dissected and supported for years, and Gøtzsche also provides that people will come gunning for his study. "We look forward to the scientific debate that will come now," he said.

cancer research and send humans to Mars may seem light years away, but advances in technology have put them on the same flight path. Last week, NASA and the National Cancer Institute (NCI) announced that each intends to spend annually $ 10 million for the next 5 years in a coordinated effort to develop devices that could both detect speed cancer on the Earth and keep astronauts healthy during long stays from home.

to beat the enthusiasm for the idea, NASA Administrator Dan Goldin and NCI Director Richard Klausner brought together two dozen molecular biologists, geneticists, pharmacologists and chemists to discuss how nanotechnology and bioengineering can revolutionize health care on Earth and in space. "We bring the hospital medicine," said David Baltimore, president of the California Institute of Technology in Pasadena and chairman of the working group NASA / NCI on biomolecular systems and technologies. "It's a tremendous opportunity."

Goldin and Klausner hatched the idea of ​​collaboration 3 years ago at a dinner hosted by Bruce Alberts, president of the National Academy of Sciences, and flew through their agencies. Under the new agreement, the NCI and NASA disburse grants separately, but be free to complete each other projects. Klausner gains access to the expertise of the space agency in the small and light construction equipment, while Goldin enhances the scientific credibility of the human spaceflight program of NASA and strengthens links with the biological community in full boom.

The astronauts to Mars may be in space for more than 4 years, bombarded by hazardous radiation and situations where face even minor accidents - such as a tear in a spacesuit - could prove disastrous. The fight against these threats may call for machines that can detect genetic damage at a very early stage, robotic sensors injected into astronauts continuously monitor their health and spatial self-healing combination. These innovations have revolutionary implications for improving health care on Earth, says Klausner.

Of course, the issue of health could be questionable if humans do not take long trips in space. "Why not learn to build robots to do business on Mars?" asked Stanford geneticist David Botstein a population panel on April 13 to discuss the new collaboration. Even Baltimore noted that "radiation problem is very serious" and predicted that it will be difficult to overcome. But Goldin says both robots and humans in the end account will be needed for the exploration of Mars.

The strain of the virus responsible for almost all cases of AIDS appeared in the 1930s, say scientists who have used a "clock molecular "to date the origin of HIV. The discovery, published in the June 9 issue of Science , casts doubt on the idea that the controversial vaccine against the AIDS pandemic contaminated polio sown in the late 1950s

the origin of AIDS is much clearer today than it was in the early 1980s, when the new disease blindsided the scientific establishment. Virologists have identified the chimpanzee virus that likely led to HIV, while epidemiologists searched in old and forgotten samples of medical records to identify early cases. Yet traces of direct evidence stops with HIV positive blood sample drawn in 1959 in what is now the Democratic Republic of Congo. How and when the chimpanzee virus entered the human remains uncertain.

To look further into the murky past of HIV, theoretical biologist Bette Korber of Los Alamos National Laboratory in New Mexico and his colleagues used a statistical model to the clock of the evolution of the gene of HIV of the envelope, which encodes a protein spines protrude from the surface of the virus. With the help of a supercomputer, the Korber group compared 159 gene sequences from the virus in the so-called Group M, which causes most cases of AIDS worldwide. Assuming that the differences between genes accumulate at a constant rate, the researchers calculated that the common ancestor of all virus group M occurred between 1915 and 1941 - most likely in 1931. They believe that the virus had already jumped to humans at present; invasion later, he would have several viral strains entrants before spreading from person to person. - A highly unlikely scenario called Korber

The study impresses other scientists in the field. "It is the best by a long way analysis has been done in this area," says molecular evolutionist Paul Sharp of Nottingham University in the UK If confirmed, early date would crush the hypothesis. - recently described in a book called river (Science, November 12, 1999, p 1305.) - That the AIDS pandemic was triggered by an oral vaccine against polio contaminated inadvertently by the chimpanzee virus.

Millions of people suffer from inflammatory bowel disease, which causes a painful set of symptoms and is difficult to treat. Now researchers have developed a technique that works well in mice -. Using bacteria to deliver soothing compounds directly to the site of inflammation

Two common forms of inflammatory bowel disease, ulcerative colitis and Crohn's disease, impose episodes rectal bleeding, abdominal pain, weight loss and diarrhea. There is no cure. Instead, patients face a life of a drug. They also risk the side effects of long-term treatment.

One approach is to imitate his way of reducing inflammation in the body. In humans and other mammals, this signal is given by proteins called cytokines. Molecular biologist Lothar Steidler and colleagues at the Interuniversity Institute for Biotechnology in Flanders, Belgium, designed harmless bacteria called Lactococcus lactis to produce the anti-inflammatory cytokine IL-10. The researchers then injected the The amended. lactis in two strains of mice, one designed to develop colitis and another that was given a gastrointestinal irritant to mimic colitis. In both groups, the inflammation has decreased by about half, the researchers report in the August 25 issue of Science .

The technique is "an inexpensive way to provide large amounts of an immunomodulatory factor directly the site of inflammation," says gastroenterologist Brian Dieckgraefe Washington University Medical School in St. Louis, Missouri. But he warns that the technique has some problems. Among other things, the bacteria do not remain in the colon and should be replenished daily.

Related Sites
For more information on this project
Crohn's disease and inflammatory Foundation of America

ATLANTA - Some of the biggest dangers to human health lurk in the animal kingdom. About three out of four "emerging" diseases affect human populations from animals, according to an inventory of all human pathogens presented here Sunday at the International Conference on Emerging Infectious Diseases. The study highlights the risk of ecological disturbances, such as the construction of new suburbs in the forests, which bring more people into contact with animals

Emerging diseases -. Those who are new to the human population, expanding their geographical range, or suddenly explode - often transmissible from vertebrate animals to humans or vice versa, researchers have noted for years. Hantavirus is widespread in rodents, for instance. The West Nile virus spends most of its life cycle in birds. And the most devastating disease emerge in recent history - AIDS - is thought to have originated in chimpanzees. epidemiological theory also predicts that diseases with an animal reservoir may cause more frequent relapses than those limited to human hosts, says biologist Mark Woolhouse of the University of Edinburgh in the UK. Yet no one has ever investigated whether zoonoses, diseases transmitted by animals are called, are actually more common in emerging diseases that among infectious diseases in general.

"It took several months of trawling through three books," to know, said Woolhouse. In the end, he and his colleagues concluded there are currently 1709 known pathogens - viruses and bacteria to fungi, protozoa and worms - that afflict humanity. 832 of these, 49% are zoonotic, the team concluded; but among the 156 diseases that are considered emerging, there were 114 zoonoses - which is 73%. To put it differently, said Woolhouse, zoonoses are three times more likely to emerge as nonzoonotic diseases and epidemiologists vigilant should keep an especially careful eye on pathogens of animal origin.

Yale medical entomologist Durland Fish appropriate. "The focus on emerging diseases should be in the field and should be geared much more environmentally friendly," said Fish. "As it is now, we wait until we have an epidemic of some new zoonotic pathogen and then try to understand what it is and why it took place."

Related Sites
Global Aspects of emerging and potential zoonoses: a WHO perspective
The International Conference on Emerging Infectious Diseases

London - The record was huge - tens of British dead, tens of thousands of destroyed livelihoods or are afflicted, 170,000 cattle slaughtered, and a bill of $ 7.5 billion. Yesterday, an independent panel reported that the BSE epidemic in Britain was caused by a series of errors and misunderstandings on many levels. But in the end, the committee found "no heroes or villains" and no government cover-up. "If action had been taken earlier, the infection could have been reduced," said the chairman of the committee Lord Philips reporters after the results were published on October 26th. "But the situation was bad before someone knew what was going on. "

the report in 16 volumes concludes the official on the epidemic of bovine spongiform encephalopathy investigation, or bovine spongiform encephalopathy, a brain disease that affects cattle, and his mortal human counterpart, variant Creutzfeldt-Jakob disease (vCJD). beef consumption infected with BSE is now considered the main cause of the current epidemic of vCJD in Britain. So far, nearly 80 people have died of the disease since the first case was reported in 1995, and future loss estimates vary widely ( Science , September 1, p. 1452).

despite criticism of previous British government officials have sought to minimize the risk of BSE, the new report avoids an outright condemnation of the government or senior officials. But while refusing to point the blame on someone, the three-member committee reviews all. Politicians have failed to provide a balanced picture of the risks of BSE, scientists still incredibly expected to come with clear answers to a mysterious threat to health. Communication broke down between departments and between staff and senior ministers. Farmers, producers of animal feed and slaughterhouses ignored safety regulations. Legislative obstacles - such as regulations of the European Union - have prevented swift action

Scientists do not escape unscathed .. One of the key scientific advisory committees, headed by zoologist Richard Southwood of University of Oxford in 1988 promoted precautions to reduce the risk of transmission of BSE to humans - thought to be a risk away at the time. But he failed to make this clear vision in a final report, Philips said. Administrators of science are equally guilty, the report said. In one case, Chief Medical Officer Sir Donald Acheson proposed a "search supremo" to coordinate research and identify gaps in knowledge, but it was opposed by the research councils - main group of the UK organizations funding - and the Ministry of Agriculture, Food and fisheries, who feared losing their autonomy.

the British government and the House applauded the findings. "The report contains many lessons for the public administration", said Agriculture Minister Nick Brown. A lawyer for the families of the victims, David Body, called the findings "a more comprehensive employment and appropriate "and warns journalists to read the full report before reaching a conclusion.

Related site
The entire Philips report

London - The record was huge - tens of British dead, tens of thousands of destroyed livelihoods or are afflicted, 170,000 cattle slaughtered, and a bill of $ 7.5 billion. Yesterday, an independent panel reported that the BSE epidemic in Britain was caused by a series of errors and misunderstandings on many levels. But in the end, the committee found "no heroes or villains" and no government cover-up. "If action had been taken earlier, the infection could have been reduced," said the chairman of the committee Lord Philips reporters after the results were published on October 26. "But the situation was bad before someone knew what was going on. "

the report in 16 volumes concludes the official on the epidemic of bovine spongiform encephalopathy investigation, or bovine spongiform encephalopathy, a brain disease that affects cattle, and his mortal human counterpart, variant Creutzfeldt-Jakob disease (vCJD). beef consumption infected with BSE is now considered the main cause of the current epidemic of vCJD in Britain. So far, nearly 80 people have died of the disease since the first case was reported in 1995, and future loss estimates vary widely ( Science , September 1, p. 1452).

despite criticism of previous British government officials have sought to minimize the risk of BSE, the new report avoids an outright condemnation of the government or senior officials. But while refusing to point the blame on someone, the three-member committee reviews all. Politicians have failed to provide a balanced picture of the risks of BSE, scientists still incredibly expected to come with clear answers to a mysterious threat to health. Communication broke down between departments and between staff and senior ministers. Farmers, producers of animal feed and slaughterhouses ignored safety regulations. Legislative obstacles - such as regulations of the European Union - have prevented swift action

Scientists do not escape unscathed .. One of the key scientific advisory committees, headed by zoologist Richard Southwood of University of Oxford in 1988 promoted precautions to reduce the risk of transmission of BSE to humans - thought to be a risk away at the time. But he failed to make this clear vision in a final report, Philips said. Administrators of science are equally guilty, the report said. In one case, Chief Medical Officer Sir Donald Acheson proposed a "search supremo" to coordinate research and identify gaps in knowledge, but it was opposed by the research councils - main group of the UK organizations funding - and the Ministry of Agriculture, Food and fisheries, who feared losing their autonomy.

the British government and the House applauded the findings. "The report contains many lessons for the public administration", said Agriculture Minister Nick Brown. A lawyer for the families of the victims, David Body, called the findings "a more comprehensive employment and appropriate "and warns journalists to read the full report before reaching a conclusion.

Related site
The entire Philips report

The virus that causes hepatitis C (HCV) has frustrated researchers because of his stubborn refusal to grow in the laboratory. Without an abundant supply of the virus, researchers have had a difficult time determining how the virus causes infection and how to fight it with drugs. Now, a team partly solve this problem. They created a better "replicon" viruslike which produces HCV proteins efficiently without relying on virus itself

Twelve years, researchers have identified HCV as the elusive pathogen that was the cause of liver disease in some people who had received blood transfusions. Donated blood is now screened for the virus, reducing the number of new HCV infections. But it is estimated that 1% of the population of the United States has been infected with the virus, which can persist in the body for many years. Over time, it can damage the liver and increase the risk of cancer.

Last year, Ralf Bartenschlager the Gutenberg University in Mainz, Germany, and colleagues reported that they had made an HCV replicon. In other words, they took the HCV genome apart and reassembled it, editing rooms and adding new parts ( Science , July 2, 1999, p. 110). They removed the genes that enable the virus to infect human cells, for example, and nestled in other genes that allow researchers to identify which cells hosts took the replicon.

The replicon system was ineffective, however, the production of the HCV proteins around 1 million host cells. To boost production, a team led by Charles Rice at Washington University in St. Louis rebuilt the system. They studied Bartenschlager data, looking for genetic mutations that might allow the replicon to be more productive. They identified 10 mutations, one of which, called S1179I, was exceptional. Replicon with this mutation produces abundant viral protein in one of the 10 host cells, the researchers report in the December 8 issue of Science .

The innovation has attracted the interest of industrial and academic scientists who are racing to develop treatments for hepatitis C should make it possible "for investigators to study the effects of drugs antivirals and host controls that regulate HCV replication, "says Frank Chisari of the Scripps research Institute in la Jolla, California.

Cancer turns deadly when it spreads from a tumor and attack organs throughout the body. two research groups have now demonstrated a trick tumors use to travel: they induce the growth of lymphatic vessels, which serve as highways. By identifying this strategy, the teams hope they have opened up new possibilities to stop the spread of cancer.

malignant cancer cells have no difficulty swimming in blood and lymphatic system, a network of conduits which is part of the immune system response. Previous work has shown that tumors can open a door to the rest of the body by activating the growth of blood vessels, but it is unclear if they could grow their own lymphatic vessels also. A response was possible there about 2 years, when the researchers developed the first marker that specifically mark the lymphatic vessels, which makes them easy to spot under a microscope. In the February issue of Nature Medicine , two teams reported using the new marker to watch tumors grow new lymphatic vessels to grow.

For a better look at the process, both the teams tumor cells an unfair advantage: they boosted levels of natural proteins that stimulate the growth of lymphatic vessels. Cancer researcher Mihaela Skobe Massachusetts General Hospital (MGH) in Boston and colleagues added a gene for a growth factor called VEGF-C for cancer cells of the human breast. When these cells were injected into mouse mammary pads, they formed tumors that had four and a half times the concentration of the lymphatic vessels in the form of tumors from cells with normal levels of VEGF-C gene. In addition, the more cancer cells spread to the lymph nodes and lungs of mice injected with VEGF-C cells, suggesting that the rebels tumor cells were able to use the additional lymphatics to infiltrate other body parts. Meanwhile, a team led by Steven Stacker cancer researcher at the Ludwig Institute for Cancer Research in Melbourne, Australia, reported a growth factor linked, VEGF-D, also encourages the growth of blood vessels lymph and spread of cancer.

both groups say the lymphatic system deserves more attention of cancer researchers. "This may be one of the most important steps in the spread of cancer," says Stacker. In the future, he said, it could be possible to use levels of VEGF-C and VEGF-D to predict the risk of cancer spreading from a particular tumor, information that could help doctors choose the best treatment for a patient. in addition, Stacker said, VEGF-C and VEGF-D these could be promising targets for cancer drugs.

Related Sites
MGH / Harvard Cutaneous Biology Research Center
angiogenesis Lab, Ludwig Institute for Cancer Research in Melbourne, Australia

SAN FRANCISCO -. Scientists dream of one day using a single chip studded with DNA to help determine the health risks of drugs, food additives and industrial chemicals. Now, this technique has passed a preliminary test with flying colors, the researchers reported here on March 26 at a meeting of the Society of Toxicology.

The principle is simple. The researchers exposed laboratory animals to a chemical, then extract the genetic material called mRNA (which is produced only by active genes) of their cells. A microarray chips or so-called DNA tests for the activity of thousands of genes at once. The profile of active genes should reveal exactly what the toxin is an animal -. If the signal can be distinguished from normal changes in gene activity

few months, Cynthia Afshari the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina, put the new technology to the test. Using microarrays 1,700 genes that may be important in the response of rats to toxins, the team Ashfari first product of genomic fingerprint for two types of liver toxins well studied: phenobarbital and three members of a diversified chemical class of compounds called peroxisome proliferators. Then they did a blind test of rat mRNA from another laboratory.

By comparing gene activity in these 26 extracts the two references, postdoc Hisham Hamadeh of Ashfari correctly identified all the rats that had been exposed to a peroxisome proliferator or phenobarbital derivative. He also acknowledged that several rats were exposed to a wild-card consists not in the database. Hamadeh made only one mistake, misidentification of a wild-card sample as a weak analog of phenobarbital; it was actually an unrelated compound.

The accuracy of DNA matrix surprised scientists who filled the room for the presentation of Afshari. "This work is important," said J. Christopher Corton, the CIIT Centers for Health Research in Research Triangle Park, North Carolina. Toxicologists have a long way to go before they can use genomic tests to predict a wide range of toxicities, he added. But the work of Afshari shows that the objective can be achieved much more quickly than expected, Corton said.

Related Sites

Summary of presentation
home of Cynthia Afshari Page

AIDS not only causes immense human suffering, it is also a significant financial burden. The cost of prevention and care in the developing world will more than quadrupled to $ 9.2 billion annually by 05, according to an international group of experts. The report, published online June 22 by Science , was designed to guide discussions at a special session on HIV / AIDS of the General Assembly of the United Nations this week. "We wanted to give people [numbers] to work with," says economist Lori Bollinger Futures Group International in Glastonbury, Connecticut.

Omit the developed world, where the cost of AIDS is not a major issue, the Panel reviewed 135 nations, including low-income countries in sub-Saharan Africa and in middle-income countries like Brazil and Thailand. They estimated that about $ 4.8 billion will be needed to reduce the rate of infection While prevention programs such as the reduction of mother to child transmission and distribution of condoms. Adequate care and support for those infected, including supervision of orphans, will add $ 4.4 billion more. The study does not include funds to develop new drugs and vaccines.

So where should the money come from? The authors note that as of now, the countries studied are spending $ 1.8 billion annually on HIV / AIDS. To offset the shortfall, they suggest that a third to half of the money could come from local sources such as government, private sector and individual donations, with foreign funds, which make up the rest. But the ability of countries to pay will be different, the panel said sub-Saharan Africa and parts of Asia, up to 80% may come from abroad, while countries like Brazil could pay 0% bill themselves [

"it was the first analysis that really got us pretty close to what the actual expenditure," says tropical medicine expert Paul de Lay the uS Agency for International development in Washington, DC from the main weakness of the study, he notes, is that it ignores the additional costs for basic infrastructure, such as building hospitals and training people. Although difficult to assess, these factors could add billions more to the bottom line, Lay said.

Related site

The Joint United Nations Programme on HIV / AIDS

Like all animal tissues, cancerous tumors need blood to survive, and one of the hottest areas of research cancer is to find ways to block the blood supply. Now scientists have created a new treatment that destroys blood vessels supplying tumors in mice while leaving others unscathed blood vessels. Scientists say the findings could eventually lead to new therapies against cancer in humans.

Cancer researchers have high hopes when scientists reported in 1997 that two new drugs, angiostatin and endostatin, prevented the growth of blood vessels and dramatically reduced in tumors mouse. Many of these so-called anti-angiogenesis drugs are in clinical trials, and early results look promising. But these drugs all have one major drawback: Although they stop or slow tumor growth, they do not destroy existing blood vessels of the tumor. This should be possible because the inner walls of tumor vessels are covered with a protein called tissue factor (TF) not present in normal blood vessels.

biochemists from the University Yale Zhiwei Hu and Alan Garen exploited this difference to create a new drug that seeks blood vessels of the tumor and destroys them. The drug, known as Icon is a unique compound consisting of two parts, which recognizes the blood vessels coated with TF and another that causes the immune system to attack them. The researchers speculated that these two components together should attack the tumor vessels without harming normal ones. To test icon, they injected a virus genetically designed to produce seven mice with cancer of the human prostate.

In the early edition of the October 2 Proceedings of the National Academy of Sciences , they report that tumors in mice decreased steadily for about 0 days with only a small sliver remaining at the end of the experiment. In contrast, tumors in the seven control mice grew rapidly and they died within 63 days. The treatment was effective against human melanoma tumors in mice as well, and scientists believe it may struggle against a range of cancers.

Harvard biologist Cancer Judah Folkman, who studies the anti-angiogenesis drugs, said "the novel researchers and elegant approach" may lead to new therapies that can be tested for human cancers. "This is a very important document," says Folkman.

Related Sites

homepage Alan Garen
Angiogenesis Foundation

Researchers have discovered how HIV can penetrate the tight nucleus of an infected cell, a necessary step for the virus to replicate. Somehow, the virus sabotages the nuclear membrane with numerous punctures. The discovery could provide a new target for future drugs against AIDS.

The HIV (HIV) breeds entering the nucleus of a cell and supported. Once inside, copies of HIV DNA in its genome RNA, which slips into the cell's DNA. Then, when the cell prepares to divide, it copies inadvertently viral genome into RNA, the model for the manufacture of proteins. These proteins then assembled into new HIV particles which can infect other cells. To make more than one copy, the virus uses a protein called Vpr which stops the cell from normal cell division cycle. As a record skipping, the cell can not progress in the division, but the viral genome transcribed into RNA, again and again.

virologist Warner Greene and colleagues at the University of California, San Francisco, and Northwestern University Medical School, wanted to know how the virus stops the cell cycle. The team used video fluorescence microscopy to track the movement of proteins related to cell cycle-in and out of the cell nuclei, watch how traffic varies with the presence of Vpr. "I am astonished," said Greene. Vpr was present when the buttons appeared on the membrane surrounding the nucleus. Some curved until they burst, breaking the seal between the cytoplasm and the nucleus by an unknown mechanism. Reporting in the Nov. 2 issue of Science , the team suggests that these offenses can give HIV easy access to the nucleus. Normally, it is too large to pass through the membrane.

The conclusion only increases the respect of researchers for HIV. "It's blowing holes in the nuclear envelope, and it is just as radical as you can get," says cell biologist Katherine Wilson of the Johns Hopkins University School of Medicine. Wilson said the finding may encourage drug designers to consider Vpr as a potential antiviral target. "It is an important document," she said, "because it's making us look in a new direction."

Related Sites

Videos of Science article
Greene laboratory homepage
Wilson Homepage laboratory

CHICAGO - While thousands enter the new year sneezing and coughing winter colds, a company pharmaceutical said it might have something to offer. A new antiviral drug shortens the course of colds by one day, according to results of a clinical trial large Phase III published here on December 17 at the Interscience Conference on Antimicrobial Agents and Chemotherapy.

Americans spend $ 3.5 billion annually remedies against colds, which target only the symptoms. The new drug, pleconaril, attack instead of a group of viruses called rhinoviruses, which cause about half of all colds. Jointly developed by ViroPharma Inc. of Exton, Pennsylvania, and Aventis Pharmaceuticals, based in Strasbourg, France, PLECONARIL acts like a molecular glue, preventing rhinoviruses that erupted in the cells to release their genes to copy.

To test how cold the drug controls in adults, Frederick Hayden of the University of Virginia School of Medicine have coordinated a clinical trial of 2,096 adults across the United States and Canada who had moderate to severe runny nose and at least one other symptom, such as a sore throat, nasal congestion, cough, muscle aches, or general malaise. Patients were randomized to receive either the drug or a placebo and took the pills until their runny had relaxed for 2 days.

self rating patient revealed that it took 2.9 days until their symptoms were half as severe as on the first day, compared to 3.9 days for the placebo group . The second day of the cold, the rhinovirus can be cultured from nasal mucus samples in 85% of placebo patients, but only 60% of patients taking the drug. ViroPharma, which funded the study, is also the pleconaril trial on children with colds and try to determine whether the drug can completely prevent the common cold, said Mark McKinlay, vice president of research and society development.

Although drug shortens the disease in just a day or two, "you can not expect much more with a disease that is measured in days," says virologist Scott Hammer of Columbia University. If the Food and drug Administration approves peconaril, the drug could be on the market in autumn 02. - in time for the fight winter colds of next year

Related Sites

ongoing trials of ViroPharma pleconaril
Facts about colds

CAMBRIDGE, UK - For survivors of the atomic bombs on Japan fell at the end of the Second World War, burns and disfiguring diseases radiation-induced were too real and scary. Now researchers have a strong new evidence of a more insidious effect in others blighted by nuclear weapons :. Unexplained DNA mutations atomic tests in Kazakhstan in the early days of the Cold War

As indicated in Science , Yuri Dubrova and colleagues at the University of Leicester, UK the blood collected from three generations of 40 families in the district Beskaragai Kazakhstan, a desert region particularly affected by four surface atomic tests between 1949 and 1956. the researchers examined DNA minisatellite subjects - short repetitive sequences pepper genome. In each subject they examined eight minisatellite DNA regions that are prone to mutations. The mutation rate naturally rich in this DNA enables researchers to detect statistically significant increases in mutation rates in small populations.

When the data returned, "I could not believe my eyes," says Dubrova. As compared to control families in a non-irradiated part of Kazakhstan, people exposed to radioactive fallout had a rate of transfer about 80% higher, and their children showed an average increase of 50% over Sonder, Dubrova's group found an effect related to the apparent dose in children. - proof that the radiation, not a another environmental factor, induced mutations

These findings challenge the conventional view that the radiation inflicts his punishment. DNA only by direct corruption of nucleic acids, said Dudley Goodhead, director of Genome stability Unit . radiation Medical Research Council UK and Harwell Goodhead indicates that the mutation rate found in Kazakhstan is "too large magnitudes" to be counted by direct damage to the DNA of the germ line - DNA that is passed from parent to child. But exactly how long-term exposure to low-dose radiation leads to a high rate of mutation is unknown.

What these changes mean for germline health is a mystery, said Bryn Bridges of Cell Mutation Unit Medical Research Council in Brighton, UK. But evidence is mounting that Minisatellites affect gene transcription and hiking the risk of contracting certain diseases. Screening for these mutations may offer a new tool for radiation exposure monitoring, says William Morgan, director of the Research Laboratory of Radiation Oncology at the University of Maryland School of Medicine in Baltimore.

Related Sites
homepage of Dubrova
Information on nuclear testing in Kazakhstan Development Gateway Kazakhstan

Scientists use own red blood cells of a patient to deliver needed drugs directly to cells in the body. A new test of the art suggests that effectively delivers steroids in the lungs of patients with cystic fibrosis; In addition, a single dose lasts for at least a month. In the long term, scientists hope the technique could also be applied for uses as diverse as gene therapy and HIV treatments.

Many treatments, such as modified genes and new drugs are too heavy to cross cell membranes and do their job. Mauro Magnani and colleagues at the University of Urbino, Italy, wanted to overcome this problem. To do this, immersed blood cells in saline. Differences in osmotic pressure between the solution inside of the elongated cells in the pores in the cell membranes, allowing large molecules to be pressed. When the cells were removed from the solution, they chewed their usual size with the medicament sealed within. A pilot study found that cells released the steroid dexamethasone in the blood of patients with chronic obstructive pulmonary disease, and remained in the circulating blood for 7 days.

Now, a second study found similar success with cystic fibrosis. In the June issue of Gene Therapy , Magnani's team reports that this method of delivery offers dexamethasone, which is also used to treat this disease, for the blood of patients for 1 month. In both studies the drug was sealed in RBCs of patients in an inactive form, before being decomposed by enzymes in the cell to a size that may leak into the blood. Magnani believes that the technique has far-reaching applications. Red blood cells can carry new compounds such as modified genes and cells can also be modified to attract specific immune cells that may harbor germs such as HIV and tuberculosis.

"There is a great strategy," says biochemist Philip Low, Purdue University in West Lafayette, Indiana. "He should certainly be able to achieve the [cache] virus that is not accessible to conventional therapy. "

Related Sites
The homepage of Philip Low
NIH brochure cystic fibrosis

A small molecule blowing power plants tumor cells but leaves normal cells unharmed may provide a model for new drugs against cancer. The molecule is drawn to the unique electrical properties of mitochondria energy production in tumor cells, and once ensconced, kick off a series of events leading to cell suicide.

Best known for his role as power generators cells, mitochondria also influence whether a cell lives or dies. When stressed, mitochondria rupture or leak, factors that activate enzymes that release dismantle the entire cell. This process is called apoptosis. A molecule that jumps-starts apoptosis in tumor cells - and only the cells - could be a useful drug against cancer

The researchers led by geneticist Valeria Fantin from Harvard Medical School in Boston screened more 16,000 small molecules. see if were taken selectively by the tumor cells. A molecule called F16 has passed the test. The reason, says Fantin is that F16 has a positive charge and is drawn into the mitochondria of cancer cells, the inner compartments are charged more negatively than in normal cells. More importantly, once in the mitochondria, F16 triggers apoptosis, the team of Fantin reports in the July 15 issue of Cancer Cell .

One potential drawback, noted molecular geneticist Andreas Strasser Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, is that F16 can damage normal cells with high metabolic activity. In the absence of in vivo data critical to the safety of this compound, it can not be considered a promising cancer drug, he said. Even so, the study may renew interest in the therapeutic potential of this class of molecules (delocalized lipophilic cations), say Yardin Yosef, a molecular biologist at the Weizmann Institute of Science, and Chausovsky Alexander, vice president of research Zetiq Technologies in Rehovot, Israel.

related sites
Councillor site of Fantin
Background on apoptosis and cancer chemotherapy
More on apoptosis

DENVER -. There are over 2 decades, the United States began to eliminate lead additives in gasoline and paint. But new research suggests that many children living in large cities are still at risk of lingering lead in soil. Study finds contaminated soil in Indianapolis is correlated with elevated blood lead levels in children, and other cities are likely to have similar problems.

In the 1970s lead poisoning has been identified as a serious threat to children, causing disorder behaviors, permanent drop in IQ, paralysis and even death. Children are more vulnerable because, before the age of six, they absorb about 80% of all the lead they ingest, while adults absorb about 15%. These revelations have spurred legislation to reduce lead exposure, but an important source of lead may have been overlooked, said geochemist Gabriel Filippelli at Indiana University-Purdue Indianapolis (IUPUI).

Filippelli and graduate student Mark Laidlaw tested some 100 samples of surface soil of the world Indianapolis and found that high levels of lead were omnipresent. Lead in the soil is left on auto emissions before unleaded gasoline was said Filippelli. Not surprisingly, the levels are higher near busy roads, but water and wind have spread more slowly. He then compared the levels of soil with lead levels in the blood recordings in children of public health. "There is a halo of high levels of lead around the city, and is linked particularly to the lead levels in the blood of children," he said. Filippelli reported the results of his study this week at the meeting of the Geological Society of America.

lead risks in the soil have been neglected, said Filippelli. The children come into contact with lead in playgrounds and even their own backyards, and follow in their homes, he said. This could explain why high levels of lead in the blood have been found in children living in brick houses, which tend to have some paint, and do not play near roads.

"We thought we had solved the problem when we took the lead in gasoline," said environmental toxicologist Howard Mielke of Xavier University in New Orleans, which found lead levels Similar to other cities. "The good news is the problem is solvable," he said. The new study found that 95% of the lead was in the top 13 centimeters of soil to remove the top layer of soil in areas where children play would go a long way toward reducing exposure.

Related Sites
IUPUI lab biogeochemistry
information on lead poisoning, the National Library of Medicine

The devastating Ebola virus might be able to steal a victim to another, speculate scientists have confirmed a link between Ebola and bird viruses. The results suggest that the Ebola virus has evolved from the same ancestor as bird retroviruses, raising the possibility that the birds could still be carriers. However, the same research also has a good side :. A mutant version of an Ebola protein could lead to a promising new vector for gene therapy

biochemist David Sanders of Purdue University in West Lafayette, Indiana, and co workers made the discovery while studying a glycoprotein molecule on the surface of the virus that allows it to break into the host cells. The team used a variety of biochemical techniques to determine the structure of the glycoprotein and study the complex sequence of changes that the virus makes to the glycoprotein entering cells.

The Ebola glycoprotein appears to be very similar to the structure and function of glycoproteins found in some bird retroviruses, the team reports in the December 15 issue of Journal of Virology . The possibility of a common evolutionary past is very strong, says Sanders. But he is quick to warn that the natural host of the Ebola virus is unknown, and epidemiological studies are needed to determine if birds are involved.

The team also found a way to put the Ebola potentially beneficial use. A mutated version of the virus that has failed a particular region of the glycoprotein was much more effective to penetrate into the cells, making it a promising candidate for use in gene therapy. Ebola is one of the few viruses that attack the lungs directly from respiratory tract rather than in the bloodstream; thus, the shell could be used to create an inhalation treatment. Sanders is considering the combination of the shell of an Ebola virus with the mutated virus glycoprotein with a second, less deadly that would provide the genetic information needed to address diseases such as lung cancer or cystic fibrosis.

Previous genetic evidence pointed to a similarity between Ebola and bird retroviruses, says molecular geneticist Paul McCray from the University of Iowa in Iowa City, but "it is a fascinating link to say that they are related in terms of evolution. "the mutant protein is another exciting product research, he added.

Related Sites
David Sanders website
information Ebola Centers for Disease Control and Prevention
information filoviruses, the category that includes Ebola