Ancient DNA may be misleading scientists

Dating skeletal material with DNA may not be as acurate as thought
Ancient DNA in skeletons has a tendency to show damage in a particular region, resulting in misleading genetic data and mistaken conclusions about the origin of the skeleton, British scientists said.

A group of researchers at the Henry Wellcome Ancient Biomolecules Centre of the University of Oxford, in Britain, made the finding while studying Viking specimens. They found that about half of the specimens had DNA that suggested they were of Middle Eastern origin.

But more detailed analysis revealed that many of the genetic sequences in the double helix molecule, which carries the genetic information of every individual, were damaged at a key base that separates European sequences from Middle Eastern genetic types – damage which made the skeletons appear to have originated in the Levant.

The results are published in the February 2003 issue of the American Journal of Human Genetics.

Damage events appear to be concentrated in specific ‘hotspots’, indicating that a high proportion of DNA molecules can be modified at the same point. These hotspots appear to be in positions that also differ between different human groups. In other words, the DNA damage discovered affects the same genetic positions as evolutionary change.

“Now that this phenomenon has been recognised, it is possible to survey the ancient sequences for damage more accurately, and determine the correct original genetic type – open the way for more reliable future studies,” said Professor Alan Cooper, director of the centre.

Cooper has hopes the finding may have implications for future research. “It also appears that we can use damage cause after death to examine how DNA damage occurs during life – a completely unanticipated, and somewhat ironic result,” he said. “Potentially this allows us to get uniquely separate views of the two major evolutionary processes, mutation and selection.”

Molecule Prompts Blood Stem Cells To Help Repair Heart Damage In Animal Model
ScienceDaily (Apr. 17, 2008) — Researchers at UT Southwestern Medical Center have for the first time used drug-treated blood stem cells to repair heart damage in an animal model, results that might point to methods for healing injuries from heart attacks or disease.
In the study, researchers screened about 147,000 molecules to find one that could transform human blood stem cells into a form resembling immature heart cells. When they implanted blood stem cells activated by this compound into injured rodent hearts, the human cells took root and improved the animals’ heart function.

“The clinical potential is enormous,” said Dr. Jay Schneider, assistant professor of internal medicine and senior author of the study, which recently appeared online and will be published in a future issue of the Proceedings of the National Academy of Sciences.

Despite medical advances in treating and preventing heart attacks, once the heart is damaged it cannot repair itself, said Dr. Schneider, a cardiologist.

“Heart attack is a man-made problem,” he said. “It’s a function of increased longevity and atherosclerosis, which have occurred at no other time in human evolution.”

In the first stage of the current study, which involved mouse stem cells, the researchers screened some 147,000 compounds in UT Southwestern’s Small Molecule Library to see which ones would activate genes known to be at work in the early stages of heart development.

This initial screening sifted out about 1,600 compounds, but the researchers narrowed their focus to a related group of molecules, among the most potent and easy to make, called Shz for sulfonyl-hydrazone.

The researchers then tested the effects of one Shz compound, Shz-3, a molecular variant synthesized by chemists at UT Southwestern, on human blood stem cells. These cells, called PBMCs for peripheral blood mononuclear cells, were cultured with Shz-3 for three days, then for seven days without the drug.

Tests showed that the Shz-treated cells began to create RNAs and proteins found only in heart cells. They were then implanted into the hearts of rats with heart damage. After a week, the function of the rats’ hearts had significantly improved, and after three weeks, the organs contracted as strongly as they did before the damage. Tests showed that the human cells were alive and had incorporated themselves into the heart tissue, although the researchers could not tell whether the human cells had become fully functional, contracting heart cells.

“This functional test is a good first step,” Dr. Schneider said “What this shows is that this drug can act on blood stem cells that are already being used in other clinical trials. This may speed its movement into clinical trials for heart repair.”

Shz compounds do not appear to be toxic in mice, and because the human blood stem cells are washed for seven days after treatment, the compounds are likely not to be harmful to humans, although further tests are needed, Dr. Schneider said.

Further studies will examine precisely what the Shz drugs are doing to the cells, and to identify additional chemical signals that might drive the cells toward a more mature form of heart cell, the researchers said.

Other UT Southwestern researchers in internal medicine involved in the study were lead author Dr. Hesham Sadek, instructor; Britta Hannack, research assistant; Dr. Elizabeth Choe and Dr. Jessica Wang, former residents; Dr. Shuaib Latif, former cardiology fellow; Dr. Mary Garry, former assistant professor; Dr. Daniel Garry, former associate professor; Jamie Longgood, senior research associate in biochemistry; Dr. Douglas Frantz, assistant professor of biochemistry; Dr. Eric Olson, chairman of molecular biology; and Dr. Jenny Hsieh, assistant professor of molecular biology.

The work was supported by the Donald W. Reynolds Foundation, the Esther A. and Joseph Klingenstein Fund, the Ellison Medical Foundation, the Texas Higher Education Coordinating Board, the Welch Foundation and the Haberecht Wild-Hare Idea Program.

Adapted from materials provided by UT Southwestern Medical Center.

Antibiotic Alligator: Promising proteins lurk in reptile blood
Rachel Ehrenberg

Researchers hunting for new antibiotics might get some aid from gator blood. Scientists are zeroing in on snippets of proteins found in American alligator blood that kill a wide range of disease-causing microbes and bacteria, including the formidable MRSA or methicillin-resistant Staphylococcus aureus.

BLOOD BATTALION. Alligator blood harbors proteins that show promise for fighting several disease-causing microbes, including methicillin-resistant bacteria.
U.S. Fish & Wildlife Service

Previous experiments have revealed that gator blood extract cripples many human pathogens, including E. coli, the herpes simplex virus and some strains of the yeast Candida albicans. The serum’s antimicrobial power probably derives from protein bits called peptides. Widespread among reptiles and amphibians, several such germ-fighting peptides have been isolated from the skin of frogs in recent years.

Many of these critters live in “sort of nasty places” that are polluted, and gators probably eat all kinds of sick animals, comments Paul Klein, a reptile infectious disease specialist at the University of Florida College of Medicine in Gainesville. Fierce battles with prey and other gators can leave gaping flesh wounds—but the animals are fairly hardy. These peptides provide a first line of defense—important in the lower vertebrates, who have a slower antibody response than humans, says Klein.

“It seems Mother Nature has built in a circulating system of antimicrobial factories that protect the animals while they are waiting to develop the cell-mediated response that we would develop quickly,” he says.

Fishing around in the reptile’s blood, the scientists identified four or five super-active peptides, reports chemistry doctoral student Lancia Darville of Louisiana State University in Baton Rouge. She collaborated with LSU chemist Kermit Murray and with Mark Merchant of McNeese State University in Lake Charles, La., and presented the work in New Orleans April 6 at a meeting of the American Chemical Society.

While alligators’ immune response is mighty in some regards—they rarely develop tumors, for example—the beasts are by no means immune to all ills, notes Elliott Jacobson of the University of Florida College of Veterinary Medicine in Gainesville. Thirty-three alligators died and 13 more were euthanized when an epidemic caused by mycoplasma, the bacterial group responsible for pneumonia, swept through a gator farm in Florida in 1995. Later dubbed Mycoplasma alligatoris by Jacobson’s colleague Daniel Brown, the previously unidentified bacteria quickly kill their reptilian hosts. “There are unique proteins in amphibians as well,” says Jacobson. “But those animals are in a major decline due to diseases.”

The second one goes along with the one Isha posted. There’s a gene that’s been found in macaque monkeys that actually blocks the AIDs virus, among others. It also suggests that the gene has evolved more than once to provide protection against the viruses.

http://news.yahoo.com/s/hsn/20080301/hl_hsn/monkeygenethatblocksaidsvirusesevolvedmorethanonce;_ylt=Am4GhC5k_U.I5.HwN30MtwTVJRIF

It’s pretty sweet.

Gene That Can Block The Spread Of HIV Discovered

ScienceDaily (Feb. 29, 2008) — A team of researchers at the University of Alberta has discovered a gene that is able to block HIV, and in turn prevent the onset of AIDS.

Stephen Barr, a molecular virologist in the Department of Medical Microbiology and Immunology, says his team has identified a gene called TRIM22 that can block HIV infection in a cell culture by preventing the assembly of the virus.

“When we put this gene in cells, it prevents the assembly of the HIV virus,” said Barr, a postdoctoral fellow. “This means the virus cannot get out of the cells to infect other cells, thereby blocking the spread of the virus.”

Barr and his team also prevented cells from turning on TRIM22 – provoking an interesting phenomenon: the normal response of interferon, a protein that co-ordinates attacks against viral infections, became useless at blocking HIV infection.

“This means that TRIM22 is an essential part of our body’s ability to fight off HIV. The results are very exciting because they show that our bodies have a gene that is capable of stopping the spread of HIV.”

One of the greatest challenges in battling HIV is the virus’ ability to mutate and evade medications. Antiretroviral drugs introduced during the late 1990s interfere with HIV’s ability to produce new copies of itself – and even they are beneficial, the drugs are unable to eradicate the virus. Barr and his team have discovered a gene that could potentially do the job naturally.

“There are always newly emerging drug-resistant strains of HIV so the push has been to develop more natural means of blocking the virus. The discovery of this gene, which is natural in our cells, might provide a different avenue,” said Barr. “The gene prevents the assembly of the virus so in the future the idea would be to develop drugs or vaccines that can mimic the effects of this gene.”

“We are currently trying to figure out why this gene does not work in people infected with HIV and if there is a way to turn this gene on in those individuals,” he added. “We hope that our research will lead to the design of new drugs, or vaccines that can halt the person-to-person transmission of HIV and the spread of the virus in the body, thereby blocking the onset of AIDS.”

The researchers are now investigating the gene’s ability to battle other viruses.

The findings are published in the Public Library of Science Pathogens. http://pathogens.plosjournals.org/perlserv/?request=index-html&issn=1553-7374&ct=1

Barr’s research is funded by the Canadian Institutes of Health Research, the Natural Sciences and Engineering Research Council and the Alberta Heritage Foundation for Medical Research.

Adapted from materials provided by University of Alberta.

Ferg