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No Sex For 40 Million Years? No Problem

Posted by tumicrobiology on March 20, 2007

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A group of organisms that has never had sex in over 40 million years of existence has nevertheless managed to evolve into distinct species, says new research published today. The study challenges the assumption that sex is necessary for organisms to diversify and provides scientists with new insight into why species evolve in the first place 

The research, published in PLoS Biology, focuses on the study of bdelloid rotifers, microscopic aquatic animals that live in watery or occasionally wet habitats including ponds, rivers, soils, and on mosses and lichens. These tiny asexual creatures multiply by producing eggs that are genetic clones of the mother — there are no males. Fossil records and molecular data show that bdelloid rotifers have been around for over 40 million years without sexually reproducing, and yet this new study has shown that they have evolved into distinct species.

Using a combination of DNA sequencing and jaw measurements taken using a scanning electron microscope, the research team examined bdelloid rotifers living in different aquatic environments across the UK, Italy and other parts of the world. They found genetic and jaw-shape evidence that the rotifers had evolved into distinct species by adapting to differences in their environment.

Dr Tim Barraclough from Imperial College London’s Division of Biology explained: “We found evidence that different populations of these creatures have diverged into distinct species, not just because they become isolated in different places, but because of the differing selection pressures in different environments.

“One remarkable example is of two species living in close proximity on the body of another animal, a water louse. One lives around its legs, the other on its chest, yet they have diverged in body size and jaw shape to occupy these distinct ecological niches. Our results show that, over millions of years, natural selection has caused divergence into distinct entities equivalent to the species found in sexual organisms.”

Previously, many scientists had thought that sexual reproduction was necessary for speciation because of the importance of interbreeding in explaining speciation in sexual organisms. Asexual creatures like the bdelloid rotifers were known not to be all identical, but it had been argued that the differences might arise solely through the chance build-up of random mutations that occur in the ‘cloning’ process when a new rotifer is born. The new study proves that these differences are not random and are the result of so-called ‘divergent selection’, a process well known to cause the origin of species in sexual organisms.

Dr Barraclough adds: “These really are amazing creatures, whose very existence calls into question scientific understanding, because it is generally thought that asexual creatures die out quickly, but these have been around for millions of years.

“Our proof that natural selection has driven their divergence into distinct species is another example of these miniscule creatures surprising scientists — and their ability to survive and adapt to change certainly raises interesting questions about our understanding of evolutionary processes.”

Note: This story has been adapted from a news release issued by Imperial College London.

Science Daily

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Study: Antiviral protein may fight Ebola

Posted by tumicrobiology on March 20, 2007

German scientists have found an antiviral protein shown to inhibit other viruses might protect against Ebola and Marburg virus infections.

The Ebola and Marburg viruses belong to the Filoviridae family and cause severe hemorrhagic fever in humans and non-human primates. Filovirus infections are characterized by high fever, hemorrhages and shock and are responsible for mortality rates up to 90 percent. Currently, there is no vaccine or therapy available for treating infected patients.

In a previous study researchers found the zinc finger antiviral protein, or ZAP, capable of inhibiting Moloney murine leukemia virus and Sindbis virus replication.

In the new study, ZAP was tested for its antiviral activity in cells infected with Ebola and Marburg. Results showed up to 95 percent inhibition of Ebola, while Marburg was less significantly inhibited suggesting the antiviral effectiveness of ZAP may depend on the filovirus species.

The study conducted at the Bernhard-Nocht Institute for Tropical Medicine in Hamburg is reported in the Journal of Virology.

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Bacterial Virus Gene Confers Disease Resistance In Tall Fescue Grass

Posted by tumicrobiology on March 20, 2007

Researchers at North Carolina State University have discovered that inserting a specific gene from a bacterial virus into tall fescue grass makes the grass resistant to two of its biggest enemies
The NC State researchers showed that the inserted gene – the T4 lysozyme gene, a gene found in bacteriophages, or bacterial viruses – conferred high resistance to gray leaf spot disease in six of 13 experimental grasses. Three of the six resistant grasses also showed high resistance to brown patch disease. These two diseases are arguably the most important – and severe – fungal diseases affecting tall fescue grass.

The finding has the potential to have wide applications in engineering resistance to a variety of fungal diseases in not only tall fescue grass – the most widely planted turfgrass in North Carolina and a commonly utilized grass in the southeastern United States – but various other crops.

The collaborative research involves four faculty members: Dr. Ron Qu in the Department of Crop Science, Drs. H. David Shew and Lane Tredway from the Department of Plant Pathology, and Dr. Eric Miller, in the Department of Microbiology. The research was mainly performed by Dr. Shujie Dong, a post-doctoral researcher who was a graduate student of Qu’s, with assistance from two other scientists in Qu’s lab – Drs. Jianli Lu and Elumalai Sivamani.

About half of the turfgrass planted in North Carolina – one million acres – is tall fescue grass, a cool-season grass that has a high tolerance for the heat and drought of North Carolina summers, Tredway says. It is ubiquitous in the Southeast, found on lawns, golf courses and commercial acreages.

Gray leaf spot disease is caused by the Magnaporthe grisea fungus, the pathogen that also causes rice blast – the major disease of rice plants. Gray leaf spot causes round or oval tan spots that turn gray when there’s high humidity. It infects blades to make the grasses die rapidly.

Brown patch disease, caused by the soil-dwelling fungus Rhizoctonia solani, a major pest to various plant species, brings about circular, brown lesions on grass. Lawns with brown patch disease appear wilted, even if watered sufficiently, the researchers say.

Miller, the microbiologist, says that the bacterial viruses exist widely in different environments, and produce an array of products that are harmful to bacteria; as viruses attempt to spread, which they need to do in order to survive and thrive, the T4 lysozyme gene produces the enzymes that chew through the bacterial cell walls.

Miller says that the lysozyme now made by the grass does essentially the same thing to a fungus when it tries to infect, thereby providing anti-fungal properties in tall fescue and allowing the grass to withstand fungal disease.

Tredway says the benefits of potential applications may be felt economically and environmentally.

“A lot of money is spent on fungicides, which also have an impact on the environment,” he said. “Disease-resistant plants have the potential to reduce those economic and environmental impacts for many years.”

Qu says that future research will replicate this experiment in the field, rather than just in the lab, and that other disease resistance genes show anti-fungal properties in tall fescue. He also hopes to study how the group’s genetically altered plants interact with other important fungal diseases to further test their anti-fungal mettle.

Much of the work was funded by NC State’s Center for Turfgrass Environmental Research and Education and the Turfgrass Council of North Carolina.

Reference: “Expression of the Bacteriophage T4 Lysozyme Gene in Tall Fescue Confers Resistance to Gray Leaf Spot and Brown Patch Diseases”

Authors: Shujie Dong, H. David Shew, Lane P. Tredway, Jianli Lu, Elumalai Sivamani, Eric S. Miller and Rongda Qu, North Carolina State University

Published: February 2007 in Transgenic Research

Note: This story has been adapted from a news release issued by North Carolina State University.

Source: North Carolina State University
(Sciencedaily)

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Too Much Or Too Little Sleep Increases Diabetes Risk

Posted by tumicrobiology on March 27, 2006

Men who sleep too much or too little are at an increased risk of developing Type 2 diabetes, according to a study by the New England Research Institutes in collaboration with Yale School of Medicine researchers.

The data published in the March issue of Diabetes Care were obtained from 1,709 men, 40 to 70 years old. The men were enrolled in the Massachusetts Male Aging Study and were followed for 15 years with home visits, a health questionnaire and blood samples.

Six to eight hours of sleep was found to be most healthy. In contrast, men who reported they slept between five and six hours per night were twice as likely to develop diabetes and men who slept more than eight hours per night were three times as likely to develop diabetes, according to the lead author, H. Klar Yaggi, M.D., professor in Yale's Department of Internal Medicine, pulmonary section. Previous data from the Nurses Health Study have shown similar results in women.

"These elevated risks remained after adjustment for age, hypertension, smoking status, self-rated health status and education," Yaggi said.

He said researchers are just beginning to recognize the hormonal and metabolic implications of too little sleep. Among the documented effects, Yaggi said, are striking alterations in metabolic and endocrine function including decreased carbohydrate tolerance, insulin resistance, and lower levels of the hormone leptin leading to obesity. The mechanisms by which long sleep duration increase diabetes risk requires further investigation.

"There is a lot of interest in determining whether sleep disturbances such as a reduced amount of sleep or disorders like sleep apnea may actually worsen the metabolic syndrome," said Yaggi. Metabolic syndrome is a cluster of risk factors including high blood pressure, obesity, high cholesterol and insulin resistance which increase the risk for heart disease and stroke.

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Co-authors include Andre Araujo and John McKinlay. The research was supported in part by the National Institute on Aging, the National Institute of Diabetes and Digestive and Kidney Disorders, the Yale Mentored Clinical Research Scholars Program from the National Center for Research Resources, and a career development award from the Veterans Affairs Health Services and Research and Development Service.

Diabetes Care 29: 657-661 (March 2006)

(TUMDF posted this information here for you TU Microbiologists)

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Diagnostic blood test inventor dies

Posted by tumicrobiology on March 27, 2006

LONDON, March 27 (UPI) — British immunologist Robin Coombs, inventor of a widely used blood test named for him, has died at the age of 85.

Coombs invented the test that's used to diagnose anemia and to test for the presence of antigens in Rh disease, which affects about 4,000 babies a year because the mother's blood is incompatible with that of her fetus.

The British Society for Immunology, a group he helped found, reported Coombs died Jan. 25, but his death was not widely reported in the British press until this month, The New York Times said Monday.

Robert Royston Amos Coombs was born in London and grew up in South Africa and spent most of his academic career at Cambridge University, retiring during the late 1980's.

He is survived by his wife, Anne; a son, Robert; a daughter, Rosalind; and four grandchildren.

Copyright 2006 by United Press International. All Rights Reserved.

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