Monday 18 December 2006

Anti-aging ingredient ready for market

Source: UPI
A new anti-aging ingredient developed by university researchers in Australia may be available in skin products as soon as next year.
Known as GGC, the ingredient is a forerunner for the anti-oxidant glutathione and has a number of possible health benefits, the University of New South Wales researchers said. Glutathione is a defense for detoxifying harmful compounds implicated in cancer, diabetes, aging and other diseases and degenerative conditions in the body.
University researchers said after nine years they developed a new, cost-effective way to manufacture GGC, which has been licensed to Biospecialties Australia.
Researchers said they expected the ingredient would be used in foods, health and beauty products, dietary supplements and anti-aging creams.
Natural dietary sources of GGC are available, including milk whey protein and garlic in diluted concentrations, researchers said. The new GGC product could allow for more effective doses.

Copyright 2006 by United Press International. All Rights Reserved.

'Clumping' Protein Linked To Return Of Ovarian Cancer

Johns Hopkins scientists have discovered that women treated for ovarian cancer are at increased risk of a rapid and potentially fatal recurrence if their tumor cells have high levels of a binding protein that triggers abnormal growth and slows down cell death, both hallmarks of malignancy.Now there's the possibility that testing for NAC-1 protein in cancer tissue removed during surgery might identify women most at risk for recurrence and guide doctors and patients to greater vigilance and extended therapy," said Ie-Ming Shih, M.D., Ph.D., associate professor of pathology at Johns Hopkins Kimmel Cancer Center. The research also suggests that drugs capable of blocking NAC-1 activity may be a useful strategy in preventing and treating recurrences as well.
A report on the research, the first to link NAC-1 to cancer, appears in the December 5 issue of the Proceedings of the National Academy of Sciences.
"Because recurrent cancers are often what really kill patients, and most ovarian cancer is diagnosed when it's already advanced, our findings offer women a better chance of catching or preventing recurrent disease early and increasing survival," says Shih.
An estimated at least 60 percent of advanced-stage ovarian cancer patients who appear to be disease-free after initial treatment develop recurrent disease, according to the researchers.
When the investigators compared levels of NAC-1 among primary and recurrent tumor samples taken from 338 ovarian cancer patients from two hospitals, they found that levels of NAC-1 were significantly higher in recurrent tumors compared with primary tumors taken from the same patient. Women whose primary cancers had high levels of NAC-1 were more likely to suffer a recurrence within one year.
Studying the functions of NAC-1, the researchers genetically modified cells so they made both NAC-1 and a component of the protein found at the ends of natural NAC-1 that is a binding site. In the modified cells, N130 capped off NAC-1 proteins disrupting their ability to bind with each other. This action can prevent tumor formation and kill cancer cells in experimental mice. Shih says that in the future, drugs that mimic N130 can be used to treat cancer.
This research was supported by the Department of Defense and the National Institutes of Health.
Co-authors of the published research include Kentaro Nakayama, Naomi Nakayama, Jim J.-C. Sheu, Antonio Santillan, Ritu Salani, Natini Jinawath, Robert E. Bristow, Robert J. Kurman, and Tian-Li Wang from Johns Hopkins; Ben Davidson from the Norwegian Radium Hospital, Oslo, Norway; and Patrice J. Morin from the National Institute on Aging, NIH.
Nakayama, K. "A BTB/POZ protein, NAC-1, is related to tumor recurrence and is essential for tumor growth and survival." Proceeding of the National Academy of Science, Vol 103:49: pp18739-18744.
Source:
Johns Hopkins Medical Institutions and Sciencedaily

Boost For New Cancer Therapies

Scientists have revealed the critical role a key enzyme plays in helping cells divide in what could prove an important breakthrough for new cancer therapies.
Cells divide to form two identical cells as part of the body's natural development and replenishment processes but when cells divide in an abnormal manner, tumours can develop.
Research has shown that an enzyme called 'Polo kinase' is involved in normal cell division but that it also goes into overdrive in cancer helping cells to multiply in an uncontrolled way.
Clinical trials on drugs that block the actions of Polo kinase started in the United States last year but the complete picture of how the enzyme assisted the cell-division process has not been clear until now.
Writing in the highly respected science journal, Nature, a team of researchers from the Universities of Manchester and Newcastle-upon-Tyne have described a new way in which the enzyme works.
"Enzymes are proteins that speed up or 'catalyse' the body's chemical reactions such as those required for normal cell division," explained Professor Andrew Sharrocks, lead researcher in Manchester's Faculty of Life Sciences.
"As its name suggests, the enzyme we have studied is from a group known as kinase enzymes which use a particular chemical -- a phosphate -- to catalyse the reactions that lead to cell division.
"Our study has identified a new target protein that uses these phosphate groups to switch on genes and alter the properties of cells.
"When the actions of enzymes like Polo kinase go unchecked, cells divide in an uncontrolled manner to form tumours. However, if we block their activity using chemical inhibitors the cells can no longer divide and the cancer cannot grow and spread."
The identification of a new key step in which Polo kinase functions confirms the choice of this enzyme as a target for anti-cancer drug development and will spur on efforts in this direction.
Indeed, as scientists now have a much greater understanding of the mechanisms involved, it might enable them to either develop more effective drugs or suggest different situations in which the drug can be used.
"Kinase inhibitors are proving to be very effective at killing off rogue cells and trials on patients elsewhere have been promising with fewer toxic effects than current cancer treatments," said Professor Sharrocks.
"Our research on Polo kinase will help with this line of drug development and hopefully produce more effective kinase-blocking chemicals that will one day treat patients with different types of cancer."

Source:
University of Manchester and Sciencedaily

Just How Useful Are Animal Studies To Human Health?

Just How Useful Are Animal Studies To Human Health?
Animal studies are of limited usefulness to human health because they are of poor quality and their results often conflict with human trials, argue researchers in a study online in the British Medical Journal.

Before clinical trials are carried out, the safety and effectiveness of new drugs are usually tested in animal models. Some believe, however, that the results from animal trials are not applicable to humans because of biological differences between the species.
So researchers compared treatment effects in animal models with human clinical trials.
They used systematic reviews (impartial summaries of evidence from many different studies) of human and animal trials to analyse the effects of six drugs for conditions such as head injury, stroke and osteoporosis.
Agreement between human and animal studies varied. For example, corticosteroids did not show any benefit for treating head injury in clinical trials but did show a benefit in animal models. Results also differed for the drug tirilazad to treat stroke - data from animal studies suggested a benefit but the clinical trials showed no benefit and possible harm.
Some results did agree. For instance, bisphosphonates increased bone mineral density in both clinical trials and animal studies, while corticosteroids reduced neonatal respiratory distress syndrome in animal studies and in clinical trials, although the data were sparse.
Animal studies are generally of poor quality and lack agreement with clinical trials, which limits their usefulness to human health, say the authors. This discordance may be due to bias, random error, or the failure of animal models to adequately represent clinical disease.
Systematic reviews could help translate research findings from animals to humans. They could also promote closer collaboration between the research communities and encourage an interative approach to improving the relevance of animal models to clinical trial design, they conclude.

Source:
BMJ-British Medical Journal
and Sciencedaily
'Clumping' Protein Linked To Return Of Ovarian Cancer
Johns Hopkins scientists have discovered that women treated for ovarian cancer are at increased risk of a rapid and potentially fatal recurrence if their tumor cells have high levels of a binding protein that triggers abnormal growth and slows down cell death, both hallmarks of malignancy.
"Now there's the possibility that testing for NAC-1 protein in cancer tissue removed during surgery might identify women most at risk for recurrence and guide doctors and patients to greater vigilance and extended therapy," said Ie-Ming Shih, M.D., Ph.D., associate professor of pathology at Johns Hopkins Kimmel Cancer Center. The research also suggests that drugs capable of blocking NAC-1 activity may be a useful strategy in preventing and treating recurrences as well.
A report on the research, the first to link NAC-1 to cancer, appears in the December 5 issue of the Proceedings of the National Academy of Sciences.
"Because recurrent cancers are often what really kill patients, and most ovarian cancer is diagnosed when it's already advanced, our findings offer women a better chance of catching or preventing recurrent disease early and increasing survival," says Shih.
An estimated at least 60 percent of advanced-stage ovarian cancer patients who appear to be disease-free after initial treatment develop recurrent disease, according to the researchers.
When the investigators compared levels of NAC-1 among primary and recurrent tumor samples taken from 338 ovarian cancer patients from two hospitals, they found that levels of NAC-1 were significantly higher in recurrent tumors compared with primary tumors taken from the same patient. Women whose primary cancers had high levels of NAC-1 were more likely to suffer a recurrence within one year.
Studying the functions of NAC-1, the researchers genetically modified cells so they made both NAC-1 and a component of the protein found at the ends of natural NAC-1 that is a binding site. In the modified cells, N130 capped off NAC-1 proteins disrupting their ability to bind with each other. This action can prevent tumor formation and kill cancer cells in experimental mice. Shih says that in the future, drugs that mimic N130 can be used to treat cancer.
This research was supported by the Department of Defense and the National Institutes of Health.
Co-authors of the published research include Kentaro Nakayama, Naomi Nakayama, Jim J.-C. Sheu, Antonio Santillan, Ritu Salani, Natini Jinawath, Robert E. Bristow, Robert J. Kurman, and Tian-Li Wang from Johns Hopkins; Ben Davidson from the Norwegian Radium Hospital, Oslo, Norway; and Patrice J. Morin from the National Institute on Aging, NIH.
Nakayama, K. "A BTB/POZ protein, NAC-1, is related to tumor recurrence and is essential for tumor growth and survival." Proceeding of the National Academy of Science, Vol 103:49: pp18739-18744.
Source:
Johns Hopkins Medical Institutions
In 2003, breast cancer incidence in the United States dropped sharply, and this decline may largely be due to the fact that millions of older women stopped using hormone replacement therapy (HRT) in 2002, according to a new analysis led by researchers at The University of Texas M. D. Anderson Cancer Center.At the 29th annual San Antonio Breast Cancer Symposium, the investigators report that there was an overall 7 percent relative decline in breast cancer incidence between 2002 and 2003, and that the steepest decline - 12 percent - occurred in women between ages 50-69 diagnosed with estrogen receptor positive (ER-positive) breast cancer. This is the kind of breast cancer that is dependent on hormones for tumor growth.
From this, the researchers conclude that as many as 14,000 fewer women were diagnosed with breast cancer in 2003 than in 2002, a year in which the American Cancer Society estimates 203,500 new cases of breast cancer were diagnosed.
"It is the largest single drop in breast cancer incidence within a single year I am aware of," says Peter Ravdin, M.D., Ph.D., a research professor in the Department of Biostatistics at M. D. Anderson.
"Something went right in 2003, and it seems that it was the decrease in the use of hormone therapy, but from the data we used we can only indirectly infer that is the case," he says.
"But if it is true, the tumor growth effect of stopping use of HRT is very dramatic over a short period of time, making the difference between whether a tumor is detected on a mammogram in 2003 or not," says Ravdin.
The study's senior investigator, Donald Berry, Ph.D., professor and head of the Division of Quantitative Sciences at M. D. Anderson, says he was, at first, very surprised by both the magnitude and the rapidity of the decline in incidence, but adds "it makes perfect sense" if you consider that use of HRT may be an important contributing factor to breast cancer development.
"Incidence of breast cancer had been increasing in the 20 or so years prior to July 2002, and this increase was over and above the known role of screening mammography," he says. "HRT had been proposed as a possible factor, although the magnitude of any HRT effect was not known. Now the possibility that the effect is much greater than originally thought all along is plausible, and that is a remarkable finding."
HRT provides both estrogen and sometimes also progestin hormones to women who are postmenopausal. The ongoing Women's Health Initiative study of 16,608 women 50-79 years old using HRT was prematurely stopped in July, 2002 when the combination of estrogen and progestin was found to significantly increase the risk of developing invasive breast cancer.
Ravdin said about 30% of women older than 50 had been taking HRT in the early years of this decade, that about half of these women stopped using HRT in late 2002 after the results of the large study were announced. "Research has shown that ER-positive tumors will stop growing if they are deprived of the hormones, so it is possible that a significant decrease in breast cancer can be seen if so many women stopped using HRT," he says.
"It takes breast cancer a long time to develop, but here we are primarily talking about existing cancers that are fueled by hormones and that slow or stop their growing when a source of fuel is cut," Berry adds. "These existing cancers are then more likely to make it under mammography's radar."
But the researchers stress that because the analysis is based solely on population statistics, they cannot know for certain the reasons why incidence declined. "We have to sound a cautionary note because epidemiology can never prove causation," he says. They considered whether other effects may be involved (such as decreased use of screening mammography and changes in the use of anti-inflammatory agents, SERMs or statins) but only the potential impact of HRT was strong enough to explain the effect."
To conduct the study, Ravdin, Berry, and researchers at the National Cancer Institute (NCI) and Harbor UCLA Medical Center analyzed data from nine regions across the country that contribute data to the NCI's Surveillance Epidemiology and End Results (SEER) database, from which national cancer incidence statistics are derived.
They examined rates of breast cancer in the United States from 1990 to the end of 2003 and found that while incidence increased at 1.7 percent per year from 1990 to 1998, it began to decrease, relative to other years, 1 percent each year from 1998 to 2002. When that 1 percent increase was adjusted for age in each of those years, incidence from 1998 to 2002 stayed about the same, Ravdin says. "There were more cases of breast cancer being diagnosed, but that was because women were getting older and entering the higher risk pool."
But by the end of 2003, there was a 7 percent, age-adjusted decrease in the number of breast cancer cases diagnosed. With further analysis, the researchers discovered that decline in incidence was far greater in ER-positive breast cancer (8 percent) compared to ER-negative breast cancer (4 percent). And when they looked at women 50-69 years old, the decline in ER-positive cancer was 12 percent, compared to 4 percent in ER-negative breast cancers. After adjusting for age, the researchers concluded that there was an absolute decline of about 14,000 fewer women diagnosed with breast cancer in 2003 than in 2002.
The study was funded by grants from the National Cancer Institute and from M. D. Anderson.
Coauthors also include Kathy Cronin, Ph.D., and Nadia Howlader from the National Cancer Institute, and Rowan Chlebowski, M.D., Ph.D., from Harbor UCLA Medical Center.
Source:
University of Texas M. D. Anderson Cancer Center

Protozoan encounters with Toll-like receptor signalling pathways: implications for host parasitism

Ricardo T. Gazzinelli and Eric Y. Denkers

Abstract
Toll-like receptors (TLRs) have emerged as a major receptor family involved in non-self recognition. They have a vital role in triggering innate immunity and orchestrate the acquired immune response during bacterial and viral infection. However, the role of TLRs during infection with protozoan pathogens is less clear. Nevertheless, our understanding of how these parasitic microorganisms engage the host TLR signalling system has now entered a phase of rapid expansion. This Review describes recent insights into how parasitic protozoans are sensed by TLR molecules, and how the TLR system itself can be targeted by these microbial pathogens for their own survival.

Source: Nature

Microbe Fixes Nitrogen At A Blistering 92 deg C, May Offer Clues To Evolution Of Nitrogen Fixation

A heat-loving archaeon capable of fixing nitrogen at a surprisingly hot 92 degrees Celsius, or 198 Fahrenheit, may represent Earth's earliest lineages of organisms capable of nitrogen fixation, perhaps even preceding the kinds of bacteria today's plants and animals rely on to fix nitrogen. The genetic analysis reported in the Dec. 15 issue of Science supports the notion that the gene needed to produce nitrogenase -- an enzyme capable of converting nitrogen gas, that's unusable by life, to a form like ammonia that is useable -- arose before the three main branches of life -- bacteria, archaea and eukaryotes -- diverged some 3.5 billion years ago, according to oceanographer Mausmi Mehta, who recently received her doctorate from the UW, and John Baross, UW professor of oceanography. This is opposed to the theory that the nitrogenase system arose within archaea and was later transferred laterally to bacteria.
"There's been lots of evidence that point to high-temperature archaea as the first life on Earth but the question has been, 'So why can't we find archaea that fix nitrogen at high temperatures"'" says Baross, who's been on a 20-year quest to find just such a microbe. Archaea are single-celled organisms that live under extreme environmental conditions, such as the high temperatures and crushing pressures below the seafloor. If heat-loving archaea were the first life on the planet, they would have needed a usable source of nitrogen, Baross says.
Known as FS406-22 because of the fluid and culture samples it came from, the archaeon discovered by the UW researchers is the first from a deep-sea hydrothermal vent that can fix nitrogen, says Mehta, first author on the Science paper.
It was collected at Axial Volcano on the Juan de Fuca Ridge off the coast of Washington and Oregon. Fixing nitrogen at 92 C smashes the previous record by 28 C, a record held by Methanothermococcus thermolithotrophicus, an archaeon that was isolated from geothermally heated sand near an Italian beach and fixes nitrogen at temperatures up to 64 C.
Nitrogen is necessary for all life because it is an essential part of amino acids and proteins. To be used by organisms, gaseous nitrogen must be converted to other compounds, or "fixed," which can only be done by certain bacteria and specific archaea. Nitrogen can be fixed into ammonia, nitrate and other products that can be used by land and sea plants, which in turn are eaten by higher animals.
Today's oceans contain nitrogen both as a dissolved gas and as nitrate. Ocean water that percolates down into the seafloor can pick up enough heat from volcanism deep in the earth to cause the fixed nitrogen to revert to its gaseous form. Venting water hotter than 30 C contains very little nitrate so organisms in areas where the subseafloor temperatures are higher would lack nitrogen in a form they can use.
The discovery of FS406-22's nitrogen fixing capabilities at 92 C, therefore, widens the realm of where life can grow in the subseafloor biosphere and other nitrogen-limited ecosystems, perhaps even on other planets, Mehta says.
Scientists have speculated since 1981 that nitrogen fixation was occurring at hydrothermal vents because vent animals had completely different nitrogen isotope ratios than non-vent deep sea animals.
The work that led to FS406-22 was supported by Washington Sea Grant, based at the UW, and the NASA Astrobiology Institute. Mehta worked five years doing some 600 enrichments, with FS406-22 being the only one she was could wean off fixed nitrogen completely. An unimpressive looking sphere of a microbe, FS406-22 is able to grow with gaseous nitrogen as its sole source of nitrogen at temperatures ranging from 58 to 92 C, with the fastest growth at 90 C.
The genetic analysis shows FS406-22 as having one of the deepest-rooted genes and the most primordial characteristics in terms of gene sequence, Baross says.
"We propose that among diazotrophic archaea, the nitrogenase from FS406-22 might have retained the most ancient characteristics, possibly derived from a nitrogenase present in the last common ancestor of modern life," the co-authors conclude in their report.

Source:
University of Washington and Sciencedaily

Young Women Unfamiliar With Safety, Effectiveness Of IUD

The IUD might be one of the best-kept birth control secrets for young women, according to researchers at the University of Rochester Medical Center.
Their study, published in this month's journal Obstetrics & Gynecology, revealed that most young women who sought birth control after a first pregnancy were unaware of the safety and effectiveness of modern intrauterine devices (IUD). An IUD is a small T-shaped device that is inserted into the uterus by a health care provider. It provides long-term birth control by preventing sperm from fertilizing eggs.
"Modern IUDs are safe, effective, and reversible, but only about 2 percent of U.S. women use them," said Nancy L. Stanwood, M.D., M.P.H., assistant professor of Obstetrics and Gynecology at the University of Rochester Medical Center. Suspecting the low use of IUDs was related to awareness, Stanwood's study aimed to estimate knowledge of IUDs among young pregnant women.
In the study, nearly 200 pregnant women, ages 14 to 25, were asked about their contraceptive history, plans, and knowledge. They were also asked if they had heard of IUDs, and if they knew anything about them. Half of the women in the study said they had heard of IUDs, but 71 percent were unaware of their safety and 58 percent did not know about their effectiveness in preventing pregnancy.
"Those results have significant implications, especially when you consider that only 9 percent of the women surveyed had planned their current pregnancy," Stanwood said. "More than half said they wanted to wait at least four years before becoming pregnant again, and more than a quarter said they never wanted to be pregnant again."
Though not widely used in the U.S., today's IUDs have been proven to be highly effective in preventing pregnancy and are also quite safe, Stanwood said. Modern IUDs have failure rates similar to tubal ligation, but are not permanent and do not require surgery.
Pregnancy rates for women using IUDs are 0.1% in the first year and are 2 percent over a total of 10 years. Compared to other more popular methods, pregnancy rates for condom users are 14 percent in the first year with typical use and 3 percent with perfect use. For birth control pills, the rate is 3 to 8 percent in the first year with typical use and 0.1 percent with perfect use.
"Young women choosing contraception after a pregnancy would benefit from counseling about the relative safety and effectiveness of IUDs, allowing them to make fully informed contraceptive decisions," Stanwood said.

Source: University of Rochester Medical Center and Sciencedaily

Researchers Barcode DNA Of Venice Museum's Vast Fungi Collection

In the storerooms of a Venice, Italy, museum, a University of California, Berkeley, scholar and Italian experts are at work on a rare collection, but the objects aren't Renaissance paintings or the art of ancient glassblowers. Instead, the team is collecting samples from the largest and best preserved collection of fungi in Italy to create an unprecedented DNA database
These 28,000 samples of fungi that represent 6,000 species - many of which are quite rare - are housed at the Venice Museum of Natural History, a partner with UC Berkeley for this ambitious project. The collection also is one of the largest in Europe.
The project was publicly announced in Italy today (Wednesday, Dec. 13) at the prestigious Venetian Institute of Sciences, Letters and Arts.
"We are building up a huge molecular database that will be available to the entire scientific community," said Matteo Garbelotto, UC Berkeley adjunct associate professor of ecosystem sciences and principal investigator of the project. "In addition to aiding research on the productivity of forests and agricultural ecosystems, this database will greatly aid the diagnosis of plant diseases."
Fungi are a kingdom of organisms that include yeasts, mushrooms and mold. They are essential to most terrestrial ecosystems, channeling nutrients in the soil and making them available for the growth of plants, including trees and agricultural crops. "Without fungi, there would be no forests," Garbelotto pointed out.
A large number of fungi are also plant pathogens and cause serious diseases of crops and trees, especially when transported to new areas of the world through the global trade of goods and movement of people. In addition, some species of fungi can lead to human illness, including pneumonia, skin infections, allergies and asthma.
Garbelotto is perhaps best known for his work in the identification of Phytophthora ramorum, the fungus-like plant pathogen that made its way from Europe to the United States. The pathogen is responsible for sudden oak death, the disease that has caused widespread dieback of tanoaks and coast live oaks in California and southwest Oregon.
"In the case of exotic plant diseases, DNA information may be used, as it is in criminal forensics, to identify possible culprits and to understand how they were introduced," said Garbelotto. "This provides governments with pivotal information needed to avoid repeated introductions of pathogens."
Garbelotto is working with Italian mycologist Giovanni Robich and Luca Mizzan, curator of Marine Biology at the Venice Museum of Natural History, to sort through the samples in the museum, which are being sent to Garbelotto's lab at UC Berkeley for DNA sequencing and analysis.
The Venice Natural History Museum is part of the Musei Civici Veneziani, a network of 11 museums in Venice. It is housed in the Fontego dei Turchi, a Byzantine-style palace on the Grand Canal that dates back to the 12th century. Before it was established as a museum in 1923, it had served as a trading depot for Turkish merchants.
"Often museums are seen as places where people just go and see things," said Garbelotto, who is doing this work during a sabbatical leave from UC Berkeley. "This shows that museums are actually involved in cutting-edge research. Providing a database of this scope is pretty novel."
Museum curator Mizzan said the museum's vast collection of fungi got a kick start when the Venice Society of Mycology formed in the late 1980s to monitor the mycological flora in the Lagoon of Venice and surrounding areas. The collected samples represented over 1,200 species of fungi and formed the foundation of the museum's present collection.
Garbelotto noted that the relatively young age of the samples has been critical to obtaining good quality tissue for DNA analysis. The samples come from throughout Europe, with a significant number representing species found elsewhere in the world.
Rather than sequencing the entire genome of each species, the researchers are focusing on a non-coding region of the ribosomal DNA that is known to be unique in each species. The length of the region varies from around 450 base pairs to 900 base pairs, depending upon the taxa from which it is sampled.
"If you're going to cross-compare species, you've got to amplify the same region," said Sarah Bergemann, the post-doctoral researcher in ecosystem science who is heading the lab analysis work at UC Berkeley. Bergemann is working with Amy Smith, staff research associate at Garbelotto's lab, to process the samples Garbelotto sends from Italy.
"This will be important for people who study the evolutionary characteristics of fungi," said Bergemann. "They'll be able to use our database for cross comparisons. It's also useful for people who study species distribution. For example, if you want to figure out how some species are related to one another, and you know something about their taxonomy, you can go back to their DNA to see if the morphological characteristics match their molecular code."
Without the DNA fingerprint, researchers traditionally need to wait for fungi to fruit or mushroom to identify them. "This can be very limiting because mushrooms are only produced seasonally, with some species only fruiting once every several years," said Garbelotto. "The database we are creating will allow people to identify the fungi present in plants, in the soil and in the air at any time."
The project, which began in April, is expected to be completed by the end of 2007. "We do not know of any similar project in Europe, at least of this dimension," said Enrico Ratti, the museum's scientific director.
"The importance of this project is in the cooperation between different subjects, namely private collectors, a private association, a public municipal museum and a foreign university," said Giandomenico Romanelli, director of the Musei Civici Veneziani. "We think that this is an exemplar model, to be followed in subsequent projects. Furthermore, in our philosophy, natural science collections are public goods that everybody belonging to the scientific community should be able to take advantage of."

Source: University of California - Berkeley and Sciencedaily

Linchpin Discovered In Insulin Metabolism; Gene Might Contribute To Type II Diabetes

Scientists from the new interdisciplinary LIMES (Life & Medical Sciences) Centre at the University of Bonn have identified a new gene which could play an important role in the development of diabetes. Flies in which this hereditary factor is defective are also significantly smaller than other members of their species and live appreciably longer. The gene seems to have such a crucial function that it has hardly changed in just under a billion years: it is found in flies, but in a similar form it is also found in mice and humans. In the current issue of the prestigious journal Nature the Bonn researchers have published two articles on this topic.
Sometimes science resembles a relay race: in 1996 the biochemist Professor Waldemar Kolanus discovered a group of cellular proteins, the cytohesins, and described their function in the immune system. Two of his colleagues at the LIMES Centre in Bonn have now found a totally new and completely unexpected function of these proteins which is very relevant to medicine. "We wanted to know whether there were also cytohesins in the fruit fly drosophila and what functions they have there," the evolutionary biologist Professor Michael Hoch reminisces. He and his team were in fact successful. They discovered a protein which is very similar to the cytohesins in mammals. Even more interestingly, fruit flies in which the genetic blueprint for this gene is defective are smaller in size. So the researchers nicknamed cytohesin 'Titch'. "The effect on the insect's growth showed us that 'Titch' could play a key role in the metabolism of insulin -- a completely new role for cytohesins," Professor Hoch says.
New drugs for diabetes
The maximum size of plants or animals is written into their genes. Yet whether they exploit this potential is influenced by a number of other factors. One of them is insulin. Mammals produce increased amounts of this hormone after eating as a reaction to the increasing blood sugar level. Via a complicated sequence of reactions it ensures that muscles and other organs absorb blood sugar. What is more, however, the cascade of insulin signals also determines size and number of the body cells during growth. Apparently, 'Titch' plays a key role in this shower of signals. "The fruit fly larvae increase their weight 200-fold in the first three days after hatching," Michael Hoch explains. "If their 'Titch gene' has mutated, they grow visibly more slowly." A series of additional observations support the thesis that 'Titch' is extremely important for the metabolism of insulin in drosophila. If there were a cytohesin with a similar function in mammals, this would, for instance, be of great interest for research into diabetes.
In parallel to Michael Hoch's research, Professor Michael Famulok produced an active substance that inhibits cytohesins, known as SecinH3. 'We fed this inhibitor to mice,' he explains. Unlike fruit flies, the rodents do not have just one cytohesin at their disposal, they have four. Professor Famulok wanted to find out whether they play a similar crucial role in the insulin metabolism of mice as 'Titch' does in the fly and discovered the following: "Liver cells of the animals treated with SecinH3 reacted to insulin not nearly as strongly as they should." Medical people know this effect: this insulin resistance is regarded as a warning signal for the onset of Type II diabetes.
Six million people suffer from this type of diabetes in Germany alone. It is triggered by an unhealthy diet and lack of exercise, and the tendency is rising. Michael Famulok now thinks new drugs are on the cards. "There is a class of switch molecules which are activated by cytohesins. This activation is apparently necessary to pass on the signals. If we manage to stimulate the switch molecules with a suitable active substance, we might possibly be able to thereby reverse the resistance to insulin." A new method described by Michael Famulok in the Nature paper could help in the search for this kind of drug. With its help his team has already found the inhibitor SecinH3.
A long life thanks to a genetic defect
The joint ancestor of the fruit fly and the mouse lived at least 900 million years ago. Nevertheless, 'Titch' and the corresponding cytohesin in mice are so similar that SecinH3 is effective with both. "We have fed the inhibitor to our fly larvae," Michael Hoch explains. "They then developed as if their 'Titch gene' were defective." This hereditary factor also has a completely different effect, which really sets the researchers' imagination going. Flies which have a 'Titch' defect live a lot longer than others of their species. "An exciting effect,' Michael Hoch thinks. 'We certainly must investigate this further."
Source: University of Bonn and Sciencedaily.

Microbe Fixes Nitrogen At A Blistering 92 C, May Offer Clues To Evolution Of Nitrogen Fixation

A heat-loving archaeon capable of fixing nitrogen at a surprisingly hot 92 degrees Celsius, or 198 Fahrenheit, may represent Earth's earliest lineages of organisms capable of nitrogen fixation, perhaps even preceding the kinds of bacteria today's plants and animals rely on to fix nitrogenThe genetic analysis reported in the Dec. 15 issue of Science supports the notion that the gene needed to produce nitrogenase -- an enzyme capable of converting nitrogen gas, that's unusable by life, to a form like ammonia that is useable -- arose before the three main branches of life -- bacteria, archaea and eukaryotes -- diverged some 3.5 billion years ago, according to oceanographer Mausmi Mehta, who recently received her doctorate from the UW, and John Baross, UW professor of oceanography. This is opposed to the theory that the nitrogenase system arose within archaea and was later transferred laterally to bacteria.
"There's been lots of evidence that point to high-temperature archaea as the first life on Earth but the question has been, 'So why can't we find archaea that fix nitrogen at high temperatures"'" says Baross, who's been on a 20-year quest to find just such a microbe. Archaea are single-celled organisms that live under extreme environmental conditions, such as the high temperatures and crushing pressures below the seafloor. If heat-loving archaea were the first life on the planet, they would have needed a usable source of nitrogen, Baross says.
Known as FS406-22 because of the fluid and culture samples it came from, the archaeon discovered by the UW researchers is the first from a deep-sea hydrothermal vent that can fix nitrogen, says Mehta, first author on the Science paper.
It was collected at Axial Volcano on the Juan de Fuca Ridge off the coast of Washington and Oregon. Fixing nitrogen at 92 C smashes the previous record by 28 C, a record held by Methanothermococcus thermolithotrophicus, an archaeon that was isolated from geothermally heated sand near an Italian beach and fixes nitrogen at temperatures up to 64 C.
Nitrogen is necessary for all life because it is an essential part of amino acids and proteins. To be used by organisms, gaseous nitrogen must be converted to other compounds, or "fixed," which can only be done by certain bacteria and specific archaea. Nitrogen can be fixed into ammonia, nitrate and other products that can be used by land and sea plants, which in turn are eaten by higher animals.
Today's oceans contain nitrogen both as a dissolved gas and as nitrate. Ocean water that percolates down into the seafloor can pick up enough heat from volcanism deep in the earth to cause the fixed nitrogen to revert to its gaseous form. Venting water hotter than 30 C contains very little nitrate so organisms in areas where the subseafloor temperatures are higher would lack nitrogen in a form they can use.
The discovery of FS406-22's nitrogen fixing capabilities at 92 C, therefore, widens the realm of where life can grow in the subseafloor biosphere and other nitrogen-limited ecosystems, perhaps even on other planets, Mehta says.
Scientists have speculated since 1981 that nitrogen fixation was occurring at hydrothermal vents because vent animals had completely different nitrogen isotope ratios than non-vent deep sea animals.
The work that led to FS406-22 was supported by Washington Sea Grant, based at the UW, and the NASA Astrobiology Institute. Mehta worked five years doing some 600 enrichments, with FS406-22 being the only one she was could wean off fixed nitrogen completely. An unimpressive looking sphere of a microbe, FS406-22 is able to grow with gaseous nitrogen as its sole source of nitrogen at temperatures ranging from 58 to 92 C, with the fastest growth at 90 C.
The genetic analysis shows FS406-22 as having one of the deepest-rooted genes and the most primordial characteristics in terms of gene sequence, Baross says.
"We propose that among diazotrophic archaea, the nitrogenase from FS406-22 might have retained the most ancient characteristics, possibly derived from a nitrogenase present in the last common ancestor of modern life," the co-authors conclude in their report.

(Source: Sciencedaily)

Scientists Find Potential Weapon Against Tuberculosis Infection

The discovery of a unique copper-repressing protein in the bacterium that causes tuberculosis in humans may pave the way toward new strategies for halting tuberculosis infection.
Scientists have known that when macrophages - the host’s immune cells - swallow an invading bacterium, they dump excessive amounts of copper onto the invader in an effort to kill it. While all cells need copper to function, too much of the metal ion causes cell death.
“But the invaders fight back with their own defense,” says Adel Talaat, a microbiologist at the University of Wisconsin-Madison School of Veterinary Medicine. “They block the excess copper.”
In a paper published in the January 2007 issue of Nature Chemical Biology, Talaat and colleagues from Texas A&M University and University of Saskatchewan in Saskatoon, Canada describe a unique protein repressor that they have identified as the mechanism used by invading bacterium cells to fight off the host’s copper attack.
Prior to the discovery of this repressor protein, scientists did not know exactly how invading bacterium protected themselves from copper ions used by the body as a defense against infection.
“With this discovery, we can now pursue ways to deactivate the repressor protein,” says Talaat. “Our goal is to disable the tuberculosis bacterium from fighting back against the host body’s defense mechanisms, so that we can stop tuberculosis.”


Source: University Of Wisconsin-Madison

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