 A Drug to Cure Drug Addiction
SARS may be transmitted through crying
LESS CALORIES, LONGER LIVES
PARIS
Restricting calorie intake could increase the life span of mammals, says a study published by the British journal Science.
The study, performed on mice by scientists from the Massachusetts Institute of Technology and colleagues from universities in Ottawa, Canada and Porto, Portugal, found that mice kept on a low-calorie diet lived 30-percent longer than most other mice.
The scientists showed that a reduction in fat deposits in the body was a likely determining factor in mechanisms connecting increased life expectancy with eating less. MIT biologists Frederic Picard and Leonard Guarente said that this could be the first step in determining a link between the two separate processes of eating and ageing.
Researchers have already singled out a gene called SIR2, which promotes long life in yeast. Now they investigated Sirt1 (short for sirtuin 1), the mouse version of the same gene. When less calories are consumed, Sirt1 represses the activity of the fat controller---known as PPAR-gamma ---which regulates the laying down of fat deposits.
"The first step to long life through dieting, therefore, may involve the body's fat-deposition machinery," Nature said.
The experiments have so far only been carried out on mice. But for humans both anxious to lose weight and live longer, "the establishment of Sirt1 as a central player... is a promising start," the magazine said.
SHED NO TEARS FOR SARS
PARIS
A team of Singaporean researchers found the severe acute respiratory syndrome (SARS) coronavirus in the tears of patients, a discovery that opens up an exciting way for the early detection of SARS, but poses a significant challenge to healthcare workers.
The researchers took tear samples from the tear ducts of 36 patients who'd been suspected with SARS at the Tan Tock Seng Hospital in April last year. Eight of these patients subsequently turned out to have SARS, and in three of those eight cases, the SARS coronavirus was found in the tear samples.
The study, published in the British Journal of Ophthalmology, was headed by Seng Chee Loon of National University Hospital, Singapore. "Many healthcare workers are in close proximity to the eyes of patients and this may be a source of spread among healthcare workers and inoculating patients," the study said.
That means ophthalmologists and other workers should consider beefing up their protective gear when they are treating patients suspected to have the virus.
In May, Chinese scientists announced that the SARS coronavirus had been found in sweat glands and the intestine, raising fears that the disease may spread via contaminated sewage, food, or even a handshake. The typical path of transmission is through the inhalation of airborne droplets that come from an infected person's cough or sneeze.
GENE VARIANTS LOWER STATIN POWER
CHICAGO
The popular cholesterol-lowering class of drugs known as statins appears to be far less effective in people with a certain miscue in genes involved with lipid metabolism, according to a recent study published in the Journal of the American Medical Association.
Researchers from Boston's Brigham and Women's Hospital noticed that patients with a gene variant in the segment of DNA controlling cholesterol synthesis---the object of statins---saw a much less pronounced decline in LDL.
The seven percent of the more than 1,500 volunteers with the genetic miscue reported a 22-percent smaller drop in total cholesterol and a 19-percent drop in LDL than the remaining vo-lunteers. All of the volunteers were given 40mg of the popular drug pravastatin (Pravachol) over a period of 24 weeks.
The researchers said the findings may go some way to explain why statins appear to work better in some patients than others, but that further tests would be needed to confirm their suspicions.
"We suspect [the diminished effect] might persist with other statins, but we're not yet 100-percent sure," said lead author Daniel Chasman, a molecular geneticist. "We also want to know if the [diminished] effect persists with increasing doses."
The findings would appear to bolster the case for "personalized medicine," or the use of genetic screening to guide selection of lipid-lowering therapy. Chasman said he foresees the need to screen patients before prescribing a statin, especially if further analysis suggests similar genetic influences.
A VACCINE AGAINST ADDICTION
LONDON
A British drug company has announced that one of its drugs has helped cure cocaine users of their addiction.
Nearly half of addicts who had participated in the US-based clinical trial of the "vaccine" were able to stay off cocaine for six months, said David Oxlade, chief executive of Xenova.
"The vaccine for cocaine addicts works in very much the same way a regular vaccine works," Oxlade told BBC radio.
According to the company, its anticocaine drug blocks the high experienced by users, instead of fighting the chemical addiction itself. Without the high, the cravings for the stimulant apparently diminish as well.
Oxlade said the vaccine works by attaching cocaine to a larger protein molecule in the body, which then stimulates the immune system to produce antibodies that recognize the cocaine and block its effect. "It stops the cocaine from being able to get across from the blood into the brain, which is where you get the high and, of course, where you get the addiction," he said. The success rate in the clinical trial was "quite remarkable" in its ability to keep addicts off the highly addictive drug for six months, he added.
The Guardian newspaper reported the study had taken place at Yale Medical School using only 22 regular cocaine users and recovering addicts. It said Xenova had embarked on a larger study of 130 patients and would report its findings in 2006.
ANOTHER FOR MULTIPLE SCLEROSIS
SYDNEY
A study published in Nature Neuroscience announced a breakthrough in efforts to develop a vaccine that can help repair damage done to the nervous system by Multiple Sclerosis (MS).
Tana Karnezis, author of the study, found that inhibiting or removing a protein that prevents spinal-nerve regeneration can significantly delay the onset of an MS-like condition in mice.
The research also suggests that the protein, known as Nogo A, may have a hand in initiating MS, said Karnezis, a fellow at Melbourne's La Trobe University. Claude Bernard, director of Latrobe's Neuroimmunology Laboratory oversaw the project.
"This is a very exciting new development in the field of MS," Bernard said. "We have been working on a vaccine which could help stop the deterioration of the disease and may help restore some of the brain function." Bernard added that clinical trials could begin with within the next two years.
The breakthrough was a result of applying knowledge gained from research into spinal cord injuries to MS. The disease has become the most common cause of paralysis in western countries since the eradication of polio and generally strikes people between the ages of 20 and 40.
AND ANOTHER ONE FOR MALARIA
GENEVA
The World Health Organization will help monitor the first clinical trials of a potential malaria vaccine being developed by a team of Japanese scientists, the WHO said.
The phase-one trials scheduled in November or December shall involve initial safety tests of the potential vaccine, known as "SE 36," in a group of adults who have no exposure to malaria, said Zarifah Reed, a vaccine expert at the WHO. The WHO was asked by the researchers at Osaka University to oversee the clinical trials in Japan and their evaluation.
Reed said that the protein on which the potential vaccine is based has been linked to some immunity from the mosquito-borne disease, but it was hard to say how it would react once subjected to human testing.
"We're interested in it because it targets the stage at which the parasite causes the disease, the fever, and the symptoms," Reed said. "We're also very interested in making sure the evaluation, in terms of whether this vaccine keeps going further and further---first into these adults, then African adults, then African children---follows a scientific rationale."
The WHO said, however, that the vaccine may not be ready for another eight or 10 years even if further development, including trials to assess its efficacy, are successful.
GENE FLAW POINTS TO HEART VULNERABILITY
PARIS
Japanese scientists believe a tiny genetic flaw may put some people at far greater risk of heart attack than others. People with a variation in a gene that encodes for a protein called galectin-2 may face a much higher risk of myocardial infarction, their study, published in Nature, says.
Myocardial infarction happens when plaque builds up in the coronary arteries. Plaque can narrow the arteries so much that blood supply to the heart is temporarily interrupted, causing a lack of oxygen that after five or 10 minutes causes cardiac tissue to die and the heart to seize up. The plaque can also rupture the artery wall, causing blood to clot, which may completely block the arterial flow.
One of the key players in this event is a molecule called cytokine lymphotoxin-alpha (LTA), which helps to regulate inflammation.
Scientists led by Toshihiro Tanaka at the Institute of Physical and Chemical Research in Tokyo found that levels of LTA are determined by the lectin protein galectin-2. In turn, levels of galactin-2 depended on variations in a gene, LGALS2, which controlled this protein. In lab-dish tests, they found that one of three variations they studied could reduce galectin-2 by half---a huge fall that they hypothesize is bound to have an effect on secretions of LTA.
Around four percent of Japanese people, they believe, have this specific variant, which is just a single "letter" in the genetic code.
The researchers, however, cautioned that their theory has yet to be tested on the situation in the body, rather than in the far less complicated confines of a laboratory dish. They point out that their search to explore the frequency of the gene variation applies so far only to Japanese, not other populations.
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