From: donpat | 3/16/2006 10:05:16 AM | | | | Study says potent cell plays big role in asthma Agents rife in lungs
By Scott Allen, Globe Staff March 16, 2006
A little-known but potent cell in the immune system plays a far bigger role than had been previously thought in asthma, Children's Hospital Boston researchers have found, perhaps explaining why current treatments often fail to control the disease.
The new culprits, called natural killer T cells, were 100 times more abundant in the lungs of people who suffer frequent asthma attacks than in the lungs of healthy people, the researchers found.
They said they believe that these cells, which already have been shown to cause asthma in mice, play a leading role in the inflammation and the buildup of mucus in the airways of asthma patients.
Steroids, which are now the leading treatment for asthma, appear to have little effect on natural killer T cells, the researchers said, and no other treatment is known to work against them, either.
'When I first saw the results . . . I nearly fell off my chair," said Mark Exley, who is an immunologist at Beth Israel Deaconess Medical Center.
Exley, who was not part of the study, said, 'It's certainly a very different approach than anyone else has come up with to date."
The report, published in today's New England Journal of Medicine, points out the shortcomings in the pills and inhalers that most asthma sufferers use to manage the disease. Asthma afflicts 20 million Americans, triple the number in 1980.
Though steroids relieve asthma-related inflammation in the vast majority of patients, the drugs do not fully control symptoms in as many as 20 percent of patients, the researchers said.
People with asthma can develop diminished breathing capacity and routinely suffer attacks of wheezing and shortness of breath, prompting about 2 million emergency room visits each year in the United States. Roughly 5,000 people, including 200 children, die from these attacks.
Moreover, some people with asthma have to take such high doses of steroids to breathe normally that they increase their risk for debilitating side effects such as cataracts, glaucoma, or osteoporosis.
'If we can specifically eliminate natural killer T cells, we should be able to treat asthma much more effectively," said Dr. Dale Umetsu, a Children's Hospital Boston immunologist and coauthor of the study.
The root cause of asthma is unknown, but scientists generally know what happens when dust or strenuous exercise or some other irritant triggers an attack: The patient's immune system goes into overdrive in reaction to the irritant, causing inflammation and mucus buildup as immune-system cells mass in the lungs.
Until now, researchers have believed that a class of immune cells called type 2 helper cells were the leading cause of the inflammation, but the Children's Hospital researchers suspect that this may be a case of mistaken identity. The type 2 helper cells look a lot like natural killer T cells under a microscope, and the technique to clearly detect natural killers has existed only for a few years. As a result, Umetsu said, 'in the past what people thought were type 2 helper cells were really natural killer T cells."
The distinction is bigger than simply a difference in names. Natural killers are far rarer and stronger than type 2 helpers, the researchers said.
The natural killers are able to rapidly summon other cells in the immune system to help expel invaders. Umetsu and a research partner, Omid Akbari, discovered how potent natural killer T cells are in research at Stanford University in 2003: They caused symptoms of asthma in mice using only natural killer T cells.
Their research also found that in humans, natural killers, unlike type 2 helper cells, do not decrease in number when a patient takes steroids.
In the study, Umetsu, Akbari and their colleagues examined specimens from the lungs of 14 people with asthma, six healthy people, and five patients with a lung disease called sarcoidosis.
While the healthy people and the sarcoidosis patients had almost no natural killer T cells in their lungs, the people with asthma had enormous concentrations of natural killers.
In the asthma patients, more than 60 percent of the immune cells were natural killers.
'Conventional type 2 helper cells may not be as important in causing asthma as we thought," Umetsu said. 'We now believe that natural killer T cells may be equally or more important."
Even though the Children's researchers studied a small number of people, outside asthma specialists said their results were persuasive because the difference between the asthma patients' lungs and everyone else's was so large.
'It's a very exciting report," said Dr. George O'Connor, a pulmonologist and asthma researcher at the Boston University School of Medicine. 'These [natural killer T] cells may indeed be important in asthma. We have a lot to learn about what role they play . . . but it does open up a whole new avenue of research."
Umetsu said his lab is looking for a potential treatment that either expels natural killers from the lungs or cuts off the cells' ability to summon other cells. The lab has had limited success so far. However, he believes other asthma researchers will now join in the search for new treatments.
'Clearly, what we are proposing is a very new paradigm for asthma," he said.
Scott Allen can be reached at allen@globe.com.
© Copyright 2006 Globe Newspaper Company.
boston.com |
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From: donpat | 3/16/2006 10:27:17 AM | | | | Re Drug Trials
FYI
Drug trials go haywire for human guinea pigs
By Jennifer Heldt Powell Thursday, March 16, 2006 - Updated: 08:49 AM EST
Ryan Flanagan, 21, was looking to make a little extra money when he volunteered to take an experimental drug developed to treat conditions such as rheumatoid arthritis, leukemia and multiple sclerosis. The healthy college student ended up in a London hospital fighting for his life. He was one of six men to take the drug in a trial run by Waltham-based Parexel International. All ended up in the hospital, two of them in serious condition. Two others in the clinical trial took placebos and were unharmed. Flanagan’s family, according to The Mirror of London, was told he couldn’t breath, his head and neck had swollen to three times their normal size and his legs had turned purple. An otherwise “healthy young man,” Flanagan had seen the drug trial advertised on the Internet. Such devastating side effects are extremely rare, but they highlight the dangers of testing drugs on humans, say researchers. “I think tremendous progress has been made in minimizing the risks, but those risks can never be eliminated,” said Dr. Steven C. Schachter, a Harvard Medical School professor of Neurology and a neurologist at Beth Israel Deaconess Medical School. Parexel was managing the trial on behalf of German-based TeGenero AG, which developed the drug. The volunteers are being cared for at the Northwick Park Hospital while regulators try to figure out what went wrong. One man’s girlfriend said he looked “like the Elephant Man.” “He is like a shell of who he is and this machine is pumping out his lungs,” Myfanwy Marshall told BBC News 24. The test was part of a phase 1 clinical trial, the point at which a drug is given to humans for the first time. It is generally the riskiest. Prior tests are done in laboratories and on animals. TeGenero’s drug showed no signs of safety problems in previous testing, said the company’s chief scientific officer Thomas Hanke. It is supposed to stimulate the body’s own immune system. In the volunteers, it caused an inflammatory response, shutting down their organs.
In the United States, all trials are reviewed by the U.S. Food and Drug Administration and by the institution in which they take place. Still, those considering volunteering should thoroughly review the consent forms and make sure they understand the potential risks, Schachter said. “Patients need to understand that clinical research is an important part of developing therapies, but they’re not proven,” he said.
business.bostonherald.com |
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From: donpat | 3/16/2006 6:57:27 PM | | | | Scientists reveal key protein in H5N1 bird flu virus www.chinaview.cn 2006-03-17 05:09:59
LOS ANGELES, March 16 (Xinhuanet) -- The structure of a key protein of the H5N1 avian influenza virus reveals that certain mutations could ease the deadly virus' spread among people, U.S. scientists reported on Thursday.
In a study published in the March 16 online edition of the journal Science, the researchers led by Ian Wilson at the Scripps Research Institute said they have determined the structure of the hemagglutinin protein.
Hemagglutinin protein, which allows the virus to enter host cells, is the principal antigen on the flu viral surface.
The researchers imaged and analyzed the protein with glycan microarray, after isolating a H5N1 virus sample from a Vietnamese boy who died from the flu in 2004.
The hemagglutinin protein latches on to different cell receptors in avian and human-type flu, which may explain why most bird flu viruses do not spread between humans, according to the researchers.
By now, only three avian influenza viruses have caused pandemics in humans, including the H1N1, the H2N2 and H3N2 strains.
The three viruses aroused flu pandemics in year 1918, 1957 and 1968, respectively, after hemagglutinin of these viruses have become adapted to the human population.
The researchers said both the H2N2 and H3N2 pandemic viruses were avian-human re-assortments, in which some avian gene segments were re-assorted into an already circulating, human-adapted virus.
And the third virus, the H1N1 strain that caused the 1918 Spanish Flu pandemic killing about 50 million worldwide, may have experienced some mutations before jumping from birds to humans.
Although hemagglutinin of the H5N1 virus looked very similar to the H1N1 virus, these mutations do not cause the bird flu virus to prefer human receptor, the researchers found.
"Our conclusion is that the mutations that cause a shift from the avian type to human type specificity on the H1 and H3 frameworks do not cause an equivalent shift in specificity on the H5 framework," the wrote in the Science paper.
However, the researchers noted that some of these mutations may make the H5N1 virus hemagglutinin more likely to bind to human lung epithelial cells, providing a possible "foothold" for the virus in the human population.
"Thus, such mutations provide one possible route by which H5 viruses could gain a foothold into the human population," they said.
With continued outbreaks of the H5N1 virus in poultry and wild birds, further human cases are likely. The potential for the emergence of a human-adapted H5 virus, either by re-assortment or mutation, is a threat to public health worldwide, the researchers said. news.xinhuanet.com |
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From: donpat | 3/17/2006 8:19:06 AM | | | | Biggest physics meeting of the year
Public release date: 17-Mar-2006 Contact: James Riordon riordon@aps.org 301-209-3238 American Physical Society
American Physical Society Annual Meeting, March 13-17 at the Baltimore Convention Center
The American Physical Society (APS) March Meeting, usually the biggest physics meeting of the year anywhere, will occur this year March 13-17 at the Baltimore Convention Center by the harbor in Baltimore, Maryland. The March APS Meeting has traditionally been the showcase for the kind of cutting-edge research results that appear, sometimes not so long afterwards, in the new electronic, communications, computer, and medical diagnosis products that have done so much to shape modern culture.
[SNIP] BUILDING A BETTER VIRUS Viruses are very simple organisms, consisting of little more than a membrane surrounding genetic material. The microorganisms propagate through hijacking other cells by inserting their DNA into their victims, which in turn begin churning out copies of the infecting virus. Rahul Sharma and You-Yeon Won (yywon@ecn.purdue.edu, 765-494-4077) of Purdue are building artificial analogues of viruses designed to deliver therapeutic genetic material, instead of causing disease. The researchers create their artificial viruses with a trio of polymers; one that binds to a DNA molecule and collapses it to a compact size, and two others that encapsulate the DNA in a coating much like a virus' membrane. Although the work is still in early stages, it could lead to an efficient gene therapy method that mimics the ancient and effective infection behavior of natural viruses. (V16.2)
eurekalert.org
That is certainly in the same ballpark as what we are doing! |
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To: donpat who wrote (1034) | 3/17/2006 2:16:12 PM | From: donpat | | | More on fat:
Tests show one in five exposed to 'fat virus'
By Deborah Smith March 18, 2006
OVERWEIGHT people may have a virus to blame.
Blood tests on 2000 Australians, carried out in the US, showed about 20 per cent had been exposed to a virus called Ad-36, which some researchers say can cause weight gain.
The idea that fatness is catching is controversial. However Richard Atkinson, Emeritus Professor of Medicine at the University of Wisconsin in Madison, who did the testing, said a fat virus could help explain the worldwide obesity epidemic.
How Ad-36 causes fatness is not known exactly, but it has been detected in fat cells in people and animals. In the laboratory it stimulates pre-fat cells to become fat cells.
Dr Atkinson said he and colleagues have shown that chickens, mice and marmosets become fatter after infection with Ad-36, one of more than 50 human adenoviruses that usually cause colds, eye infections and diarrhoea.
Tests on more than 500 Americans found about 30 per cent of obese people had been exposed to the virus, compared with 11 per cent of non-obese people. They identified 26 pairs of twins where only one had been infected with Ad-36.
"And just as we predicted, the infected twins were heavier and fatter," said Dr Atkinson, who has established a company that tests for the virus.
But Professor Nick Martin, of the Queensland Institute of Medical Research, who collaborated on the project, said his analysis found no link between Ad-36 infection and body mass index.
theage.com.au |
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To: Kulnor who wrote (1147) | 3/17/2006 2:16:38 PM | From: Kirk © | | | I just sold 40% of my shares here at $2.80 to lock in a gain even if the stock goes to zero.
NNVC chart #1 shows this is a very good level for a double top and a correction back to the blue 50 DMA line where I may consider buying the shares back..
If it busts out... then the 60% of my shares I still have will enjoy the ride. smile
My remaining 60% are all on house money!!! BOOOOYAAA!
investment.suite101.com |
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To: donpat who wrote (1128) | 3/17/2006 2:38:05 PM | From: donpat | | | More on - Nanoparticles make biocompatible capsules
[March 14, 2006]
Yet another use found for nanoparticles
(UPI Science News Via Thomson Dialog NewsEdge)University of Illinois scientists have found yet another use for nanoparticles -- use them to 'armor' lipid molecules.
Steve Granick, a professor of materials science, chemistry and physics, said such nanoparticle-studded capsules would have a variety of uses.
You can treat them as if they were ... very durable objects, he told the Champaign (Ill.) News-Gazette. That would make the capsules useful for such purposes as delivering drugs to specific sites in the body or delivering DNA, proteins and other genetic material in gene therapies.
Granick and graduate student Liangfang Zhang created the tiny nanoparticle-covered capsules of biocompatible lipid molecules that, among other things, could be covered with other reactive molecules to become molecular-scale sensors to detect toxins, tumors, or similar properties, the News-Gazette reported.
The research, which appeared online recently ahead of publication in the journal Nano Letters, was funded by the U.S. Department of Energy.
tmcnet.com |
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