Health Meaning

The humble stool sample can be much more valuable than most people think. By carefully sifting through the genetic content of stool samples, researchers have developed a test that can detect colon and rectum in their early, most curable stages.

Although colorectal cancer is highly curable when caught early, it remains the second leading cause of cancer death in the United States. This is because many people do not seek preventive screening. The most effective tool detection is colonoscopy, which requires doctors to snake 2 meters long endoscope into the large intestine (slowly around curves, please) to look for abnormalities and tumors. In addition to being significantly uncomfortable, colonoscopies are also expensive. A simpler method of screening, analysis of blood samples for traces of stools (a symptom of colorectal cancer) is rarely conclusive.

The new technique involves testing samples of stool of a gene called CPA . Movements CPA can trigger the growth of tumors and mutated CPA is found in almost all malignant colorectal tumors. Now oncologists Bert Vogelstein and Kenneth Kinzler and their team at the Kimmel Cancer Center at Johns Hopkins University in Baltimore have shown that mutant CPA DNA can be detected in necrotic cells of the intestinal mucosa in faeces . The team used PCR - the standard method for DNA replication - to amplify the CPA DNA in stool samples from 74 patients. Samples containing mutated CPA dysfunctional protein gene products, allowing them to be easily identified.

The precise detected mutated ART CPA DNA in 61% of patients already diagnosed with cancer of precancerous colon at an early stage and identified mutations in 50% of patients known to have tumor benign, the team reports in the January 31 the New England Journal of Medicine . The test produced no false positives for a group without cancer.

"This work must absolutely be prosecuted," said Barbara Conley, an oncologist at the National Cancer Institute in Bethesda, Maryland. Although Conley stressed that more work needs to be done to improve test sensitivity she said it could one day provide a welcome alternative to colonoscopy.

Related Sites
Vogelstein / Kinzler Laboratory
information on colon cancer NCI

Stress can make people nervous, have ulcers, and even dying young. If that were not enough, new research suggests it may contribute to bad skin and play a role in hair loss. Scientists have found that the main body stress hormone triggers skin cells to multiply the oily lipid and to testosterone -. A key culprit in both baldness and excessive hair growth, depending on where it occurs

During a stressful event- -Say a final exam - the brain releases corticotropin (CRH), a master stress hormone that directs the body to pump adrenaline, tense muscles, or shiver. But researchers do not believe that CRH had an effect on the skin. Researchers have long thought the stress responses of the skin - such as tanning to prevent sunburn -. Was triggered by the immune system, which releases chemicals in the first signs of damage

Dermatologist Christos Zouboulis of the Free University of Berlin, Germany, and colleagues examined the effect of CRH on cells cultured from human sebaceous glands. These glands are located at the base of hair all over the body except the palms and soles. They house sebocyte called cells that are lipids, oily compounds that coat and protect the skin at low levels, but cause oily skin and acne in high concentrations.

The team found that Zouboulis sebocytes to CRH and have receptors for the hormone on their surfaces. Sebocyte meet CRH seepage up to 60% fat, the team reports in the May 14 issue of Proceedings of the National Academy of Sciences . HRC also caused the crank 50% cells of more than one enzyme which makes testosterone, which has been linked to both the male pattern baldness and hirsutism.

Call of labor "a big step forward" in understanding the skin stress response, biologist Andrzej Slominski skin of the University of Tennessee Health Science Center, Memphis, said that the production of the hormone stress of testosterone and oil in sebocytes could lead to new topical treatments for a variety of skin and hair disorders. Until then, the stress management courses are highly recommended.

Related Sites
Free University dermatology department page

Bacterial infections may trigger high levels of brain steroid which can make infants too sleepy to wake up when they encounter difficulties in breathing, suggests new research on lambs . Although a link between infections and sudden infant death syndrome (SIDS) has been suspected, this is the first time a clear mechanism was found that could explain such a link.

SIDS usually occurs during an infant sleeps at night. An emerging theory holds that the condition is caused by bacterial toxins encountered by virtually all infants in the first year of life. Researchers have proposed several theories to explain how these toxins could kill infants, but so far there has been little experimental evidence to back them up.

Now physiologist Saraid pool Monash University in Melbourne, Australia, found that even slight bacterial infection can cause brain levels of steroids to increase dramatically, leading lambs to become extremely drowsy and difficult to wake. In a trial involving 12 lambs a mild infection with Escherichia coli caused levels of allopregnanolone steroids in the blood to increase by 50%. The results were even more dramatic in the brain, where levels of allopregnanolone, which is known to have sedative and anesthetic properties, increased by two to three times. If the same thing happens in humans, even a mild infection could blunt the ability of infants to awaken, says billiards. "If they develop breathing problems during sleep that cause their blood oxygen in the fall, they are not the appropriate response exciting that allows them to wake up."

John Newnham, Director of Women and Infants Research Foundation in Perth, Australia, said the finding is an important step towards the understanding of SIDS. "This helps us with the idea that infection is involved." The research has been accepted for publication in the journal Pediatric Research later in the year.

Related Sites
Monash University Department of Physiology
General information on SIDS from the National Institute of Child Health and Human Development of the United States

Lupus, an incurable disease that strikes more than 16,000 Americans a year, causes the body's immune system to turn against itself, creating antibodies that will fight and kill their own cells. In a significant move, geneticists are now saying that a small change in a single gene contributes to the development of the disease in some people.

Lupus Symptoms can vary from joint pain, fever, arthritis, rash, and sensitivity to light for kidney and blood-clotting problems of life in danger. Although the disease seems to run in families, researchers have yet to identify the gene or genes that cause. However, mouse studies showing symptoms of lupuslike suggested that a gene called PDCD1 - which is known to help the body recognize foreign cells -. May play a role

Geneticist Marta Alarcon-Riquelme of Uppsala University in Sweden led an international team of researchers whether PDCD1 is also associated with lupus in humans . The team recruited 2510 people of European-American, Mexican, and African-American descent families with single or multiple cases of lupus, and families with no known history of the disease. The team decoded PDCD1 DNA of each person and found a single mutation - a change in a nucleotide letter of the genetic code -. Associated with lupus in 12% percent of European Americans and 7% of Mexicans

based on the location of the mutation in the DNA code, researchers believe that the mutation prevents a protein called RUNX1 of binding to the PDCD1 gene [ParcequeRUNX1estpensépouraiderlescellulescopientl'ADNcettedéconnexionpourraitperturberlacapacitédescellulesimmunitairesàdistinguerlesproprescellulesducorpscontrelesmicrobesenvahisseursenempêchantlescellulesd'exprimerlabonnequantitéde PDCD1 , the team argued in October 28 Nature Genetics . This mutation is not the only cause of lupus, though; it has also been found in 5% of European Americans and 2% of Mexicans who do not have lupus. And mutation was almost nonexistent in the African American population.

"This is a great advance for researchers to work with and we now have a testable hypothesis to continue," said rheumatologist Paul Utz of Stanford University in California. The next step, Utz said, is whether RUNX1 really play a role in the regulation of PDCD1 gene.

Related Sites
homepage Utz
Lupus Foundation of America

, the tiny disc-shaped platelets floating in the veins of the help blood clot, protect against excessive blood loss after injury. But new evidence shows that these cells have a darker side too. Researchers studying mice have shown that some are sticky platelets than normal can contribute to clogged arteries, which can lead to serious health problems.

atherosclerosis, or clogging of the arteries, is a major contributor to heart disease. The disease develops as white blood cells called monocytes cells attach to the walls of blood vessels, then the inventory to create fat deposits resembling hardened cottage cheese. Enough of this "plate" may reduce or block blood flow. Platelets are known to bind to monocytes, the doctors suspected a role in arterial disease. And in fact, inhibiting platelet drugs such as aspirin may help prevent blood clots in narrowed arteries. But he does not know if platelets contribute to arterial disease in the first place or just exacerbate the disease once it develops.

molecular physiologist Klaus Ley University of Virginia, Charlottesville, and his team studied activated platelets, hoping to find an answer. Activated platelets are revved beyond the resting state, but not yet committed to the formation of blood clots. For 12 weeks, the team injected platelet both resting and activated in mouse designed to be susceptible to atherosclerosis. They found that activated platelets express a molecular adhesive called P-selectin which attaches briefly arterial walls. This contact with the walls buffered with a chemokine residue, chemicals which attract monocytes. The mice injected with activated platelets developed plaque deposits that were 39% larger than those of mice injected with platelets rest online reporting team on December 16 in Nature Medicine . Mice can not produce P-selectin was not affected by injection of activated platelets.

Calling the study "stylish and exceptionally deep," cardiologist Anthony Rosenzweig of the Harvard Medical School and Massachusetts General Hospital in Charlestown said the next step will be to confirm that the platelet induce atherosclerosis in humans. Hematologist Zaverio Ruggeri from the Scripps Research Institute in La Jolla, California, said the findings could point to useful treatments that could prevent or slow the progression of atherosclerosis.

Related Sites
Klaus Ley website
Zaverio the site Ruggeri
Anthony Rosenzweig's website
basic information on atherosclerosis of American Heart Association

In war zones around the world, bandits steal food intended for starving civilians. One of the most feared pathogens medicine performs the same kind of piracy, new research suggests. To obtain the iron it needs to keep the bacteria Staphylococcus aureus steals the essential mineral from human blood cells. The chemicals that stop the crime could offer a new type large need antibiotics to kill dangerous infections resistant to drugs.

S. aureus causes diseases ranging from ear infections to meningitis. Antibiotics that kill it quickly lose their punch. Half of all hospital-acquired staph infections now resist all but one antibiotic, vancomycin. Some strains learn to avoid even one, so that new ways to kill the bug are urgently needed.

Nutrition is a possible weak point. S. aureus , like other bacterial pathogens and like us, needs iron to keep its engines running. There are a few years, a team led by Olaf Schneewind, now of the University of Chicago, hungry S. aureus for iron and took one of its proteins in the act. The protein had caught a chemical containing iron called heme in hemoglobin, the protein that makes red blood cells red

Now the postdoc Schneewind Eric Skaar has unraveled a conspiracy between this protein and six other that allows the microbe pilfer iron human red blood cells. Collectively, these proteins are known as surface determinants iron-regulated, or ISD proteins. After S. aureus hole punches protein in the red blood cell, Isd proteins form a bucket brigade flying heme in hemoglobin and pries out of his iron to feed the bacteria, Skaar, Schneewind and colleagues report in the 7 February science . They also identified two other proteins called sortases Isd proteins that bind to the cell wall so they can do their job. This means that drugs that block the way, perhaps by blocking sortases could prevent even the most wicked S. aureus strains to get the iron they need to grow, says Skaar.

"I liked [the study] much," said Klaus Hantke microbiologist at the University of Tübingen in Germany, adding that it offers the best description yet of how a bug extract iron from heme. But S. aureus and other microbes have backup plans for iron, he warns, to block flying heme iron may not kill them.

Related Sites
Backgrounder on antibiotic resistance
Centers for prevention pages S Disease Control. aureus , which are resistant to two common antibiotics, methicillin and vancomycin

pharmaceutical giants Merck and Aventis Pasteur decided to combine their experimental vaccines against HIV in a double blow. In tests on monkeys, the combination vaccine may work better than one of the two companies separately in human trials strategies. "We were driven by the data," says Emilio Emini, who heads the vaccine program against Merck HIV in West Point, Pennsylvania.

Merck and Aventis Pasteur, based in Lyon, France, the developed two vaccines against AIDS that the point of HIV genes into harmless virus. as explained Emini, Merck found in monkey studies between various combinations of vaccines against the other that the adenovirus-based HIV vaccine company continued with a booster dose of canarypox Aventis / vaccine against HIV has led to some of the strongest immune responses they observed. human trials of the Merck vaccine followed by Aventis preparation are awaiting US regulatory approval and could start in the coming months.

the proposed clinical trial is "an experience that needs to be done," said the vaccine against AIDS researcher Norman Letvin of Beth Israel Deaconess medical Center in Boston, Massachusetts. Letvin, who has directed several of these comparative studies in monkeys himself, said there are "very good data" that the smallpox virus such as canarypox can powerfully stimulate the so-called killer cells, warriors Immunity that selectively target and destroy cells infected with HIV and other invaders.

Merck also new data from a study of the human being. the company announced ago 2 years on monkey studies that led the company to launch human trials of vaccines against AIDS this year with a different strategy ( science , April 6, 01, p. 24). first they were vaccinated with an HIV gene sewn into a circular piece of bacterial DNA. they were then stimulated with the adenovirus / vaccines against HIV. But Emini said the first results of DNA studies in humans have disappointing. "Unfortunately, the DNA does not work as well in humans as it does in monkeys," he said.

Emini and colleagues plan to present their new monkey studies and human data from their trials, at a meeting of AIDS in Banff, Canada, which begins March 29.

a huge boost in funding for HIV prevention efforts could prevent up to 29 million new infections by 2010, according to a new analysis. Access to HIV Prevention: Closing the Gap , released today by a panel of AIDS experts known as the Global Working Group on HIV Prevention, provides that the group called the first book of the gap between the efforts to stop transmission of the virus and the continuing needs.

According to the report, in 02 the world spent $ 1.9 billion in low- and middle-income on prevention efforts such as condom distribution, education campaigns, counseling and voluntary testing programs, antiretroviral therapy for infected pregnant women and their newborns, and drug users and offers needles own treatment. This amount should be tripled by 05, estimates of the working group, if the world wants to avert 29 million new infections by 2010. "Without immediate intensification of HIV prevention interventions, we may see an explosion of HIV, "said Helene Gayle of the Bill & Melinda Gates Foundation, which co-convened the working group with the family Foundation Henry J. Kaiser.

The report, based on data from the Joint United Nations Programme on HIV / AIDS (UNAIDS), records how many effective prevention strategies still do not reach the majority of people most at risk of infection by HIV. Only 5% of pregnant women infected with HIV, for example, have access to drugs that can prevent transmission to their babies. More than 80% of injecting drug users have no access to so-called programs of "harm reduction" and only 42% of those at risk have condoms available.

Not only the rich governments must invest more in "combination prevention" efforts, the report concludes, but as if companies and foundations. "The realistic investment now will reap huge benefits in the future "says member of the working group Catherine Hankins of UNAIDS." This is not a dream. We really believe that this can happen if we are committed, and scale. "

Related Sites
Kaiser
Gates Foundation The Foundation

A steroid inhibitor which shrinks the prostate gland - and low-dose treated baldness - also helps to prevent the cancer prostate, the researchers found. The findings come from a massive test, 7 year nearly 19,000 men. But although the drug called finasteride, caused a 25% reduction in prostate cancer, it also increased the risk of aggressive prostate cancer in people diagnosed with the disease. Doctors now hope to find out who is most likely to benefit from the drug.

When finasteride was approved in 1992, it was designed to treat men with an enlarged prostate. (His hair-restoring properties were noted later.) The doctors also asked whether its ability to block the natural conversion of testosterone into a more potent male hormone called dihydrotestosterone, in the prostate may prevent cancer. Previous research had linked male hormones at the onset of prostate cancer. Some scientists worry that many men might start taking finasteride as a preventive measure before it has been proven to do the job. So they quickly - many at the time said too quickly - launched Prostate Cancer Prevention Trial, 18.882 recruiting older healthy men aged 55 and dividing them into two groups at random. A received finasteride, and the other received a placebo.

After 7 years, the researchers, led by Ian Thompson of the University of Texas Health Science Center at San Antonio, met with 060 men. In the finasteride group, 18%, or 804 men had developed prostate cancer. In the placebo group, the number was 24% or 1147 men. (The typical incidence is about 6%, the team believes it has found more because the biopsies were performed systematically at the end of the study.) The difference was so striking that Thompson and his colleagues arrested study a year ahead of

The drug has side effects, however, including problems with sexual arousal. Of greater concern were the highest rates of prostate cancer classified as aggressive. He developed in 6.4% of men in the finasteride group, compared to 5.1% in the placebo group

The difference in cancer rates of the most serious prostate, although small, "looks like a phenomenon, "said Peter Scardino, chief of urology at the cancer Center Memorial Sloan-Kettering in New York City notes that the increase could be misleading;. it is possible, for example, that the drug alters architecture of cancer cells in the prostate, making them only look worse. anyway, Scardino said, the study should be followed by others that evaluate the effect of the drug, for example, men high risk of prostate cancer.

Related Sites
Background on cancer prevention Trial prostate
National prostate cancer Coalition
information finasteride NIH

Radiation is one of the most effective means of killing germs, but it has been used clinically to treat only the cancer. This may be about to change. For the first time, researchers have turned radiotherapy against infection.

With antibiotic resistance on the rise in bacteria, medical researchers are looking beyond traditional drug therapies. One possible source of new weapons is radioimmunotherapy (RIT), a technique used to treat cancer patients. RIT works as a radiation treatment, but tumors blasting zone with radiation from outside, individual radioactive atoms are injected into the blood and circulate through the body. The trick is to fix the atoms emitting radiation to antibodies to proteins for locking onto the surface of the tumor cell. This ensures that the tumor cells overlap with RIT molecules while normal cells are spared the radiation DNA-blasting.

To see if RIT could be useful against an invading pathogen, Kate Dadachova, biologist at the Albert Einstein College of Medicine antibody in New York, and colleagues designed to bind to the surface of Cryptococcus neoformans , a tenacious fungus that plagues AIDS patients. In a paper published online this week in the Proceedings of the National Academy of Sciences , the team shows the courage to RIT as a fungus fighter. When infected mice were injected with the antibody alone, they died just as quickly as untreated mice. But when radioactive bismuth-213 or rhenium-188 atoms have been hung on the antibody, infections began to clarify and the survival of the mice increased up to 60% at the end of the tests. And the best news is that RIT does not seem to kill the bone marrow, a side effect that has limited the use of RIT in the treatment of cancer. Given this initial success in mice Dadachova believes that any kind of infection can potentially be treated with RIT.

"The data clearly indicate that RIT can be effectively used to treat fungal infections," said Gregory Adams, an oncologist at the Fox Chase Cancer Center in Philadelphia. Adams warns, however, that there could have difficulty scaling technique from mouse to man, and there could be damage to long-term tissue radiation.

Related Sites
research RIT Adams
About radiotherapy