Peter Kasson has been working hard on a new approach to improve the Windows SMP core stability.

»folding.typepad.com/news/2008/03···cli.html

At first glance, it bears an uncanny resemblance to a piece of modern art. A grid of red, yellow, and green spots glows against a glassy black backdrop in an abstract composition no larger than a microscope slide.

There comes a time in many a cell's life when it feels the need to reproduce. But before it can split into two, it must fashion a second set of genetic instructions to pass on to the new cell.

When Berkeley professor of biochemistry and molecular biology Mike Botchan first began studying chromosome copying, basic questions about the process remained unknown. He wanted to understand how and where DNA replication began. Over the past three decades, Botchan has been instrumental in piecing together the story of what he calls "the elaborate dance of replication."

»sciencematters.berkeley.edu/arch···ory3.php

Howard Hughes Medical Institute researchers have identified small pieces of ribonucleic acid (RNA) that suppress the spread of breast cancer to the lungs and bone. The new research shows that the most invasive and aggressive human breast cancer tumors are missing three critical microRNA molecules. When the researchers put those molecules back into human breast cancer tumors in mice, the tumors lost their ability to spread.

"The tiny RNAs prevent the spread of cancer by interfering with the expression of genes that give cancer cells the ability to proliferate and migrate," said senior author Joan Massagué, a Howard Hughes Medical Institute researcher at Memorial Sloan-Kettering Cancer Center.

»www.medicalnewstoday.com/articles/93593.php

It is a whole new science with important implications for the treatment of disease - most notably cancer.

Epigenetics is the study of molecular modifications which sit on top of the DNA in our cells, in effect switching our genes on and off; telling our cells how they should behave.

Scientists are now realising that if those epigenetic markings are disrupted, causing a gene to become incorrectly active or silent, a healthy cell could become diseased.

»news.bbc.co.uk/2/hi/health/7155854.stm

Another mention in The Economist of "Folding@home, run by Vijay Pande and his team at Stanford University" in this article ---> »www.economist.com/printedition/d···0202635

UNTIL recently there were only two ways to speed up a volunteer-computing project: persuade more people to take part, or wait for users to upgrade their PCs to faster models. But in October 2006 the creators of Folding@home, a popular volunteer-computing project run by Stanford University that analyses protein folding, gave its users another option

»www.economist.com/printedition/d···0202613

Mario R. Capecchi's earliest memories are of his mother being arrested by the Nazis.

Enzymes are a picky lot. Of the many thousands of molecules drifting through their environment, most enzymes will react with only one-its preferred substrate, or target.

BOSTON - Two genetic mutations raise the risk of rheumatoid arthritis, one by as much as 87 percent, researchers reported on Wednesday in a discovery that sheds more light on a complex and baffling disease.

They said their findings also show a link between rheumatoid arthritis and other diseases caused when the immune system mistakenly attack healthy tissue, such as lupus.

People who had two copies of one gene, found in a region known as STAT4, had a 60 percent higher risk of rheumatoid arthritis, the international team of researchers reported in New England Journal of Medicine.

»www.msnbc.msn.com/id/20611541

The first new genes for three decades linked to multiple sclerosis have been identified by UK and US researchers.

Approximately 60,000 people in the UK suffer from the incurable disease of the nervous system.

The finding, published in two journals, will not lead directly to new tests or treatments, as experts say as many as 100 more genes may play a role in MS.

However, a Cambridge University researcher said he now expected swifter progress to reveal them all.

»news.bbc.co.uk/2/hi/health/6919613.stm

Genes don't act alone to cause disease and there may be no 'junk' DNA, landmark study finds

By E.J. Mundell
HealthDay Reporter

WEDNESDAY, June 13 (HealthDay News) -- In what's being hailed as a milestone in human genetics research, an international consortium of scientists announced Wednesday new data that could revolutionize how scientists study health and disease.

An exhaustive look at only 1 percent of the human genome produced two major findings: a vast amount of seemingly useless genes formerly called "junk DNA" may, in fact, be crucial to regulatory processes governing cells; and "epigenetic" factors outside of genes are probably big players behind many diseases.

Story Continues

"Two professors at the University of Oklahoma say they've developed a protein that can stop the spread of certain cancer cells without damaging normal cells.

Thomas Pento and Roger Harrison helped develop a fusion protein that keeps some types of cancer cells from ingesting a vital protein called methionine. The fusion protein doesn't affect normal cells because, unlike cancer cells, they can be healthy without that protein.

Chemotherapy and radiation therapies kill normal cells along with cancer cells, and they also often cause sickness and hair loss."

»www.newsday.com/news/health/ny-h···th-print

The devil is in the details, or so the old adage goes. Jhih-Wei Chu understands that better than anyone. A UC Berkeley professor of chemical engineering, Chu models the behavior of proteins atom by painstaking atom. By understanding how proteins interact with other molecules, as well as larger structures in the cell, he is developing a new way to target medicines, design novel materials, and ultimately improve our understanding of cell behavior.

»sciencematters.berkeley.edu/arch···ory3.php

Article Date: 27 Apr 2007 - 5:00 PDT

Several teams of scientists this week report discovering more genes linked to Type 2 Diabetes and describe the achievement as bringing science closer to understanding the genetics of the origins and progress of this modern disease.

The various papers are published in Science and Nature Genetics this week.

The unravelling of the human genome five years ago opened the door to a cascade of research projects looking for genes that might be involved in many common diseases. These studies have acquired the name genome-wide association (GWA) projects.


»www.medicalnewstoday.com/healthn···id=69176

Stanford University's Folding@home distributed computing project has seen its capacity more than double in the last month thanks to the addition of idle processor cycles from hundreds of thousands of PlayStation 3 consoles.


Total computing power of the system is now at around 700T Flops (floating point operations per second), with nearly 400T Flops of that coming from roughly 250,000 PlayStation 3 consoles, Sony Computer Entertainment Inc. (SCEI) said Wednesday.

»news.yahoo.com/s/pcworld/2007042···S_MWM0F

"The ribosome is in some respects the prototypical nanomachine," says Jamie Cate, a UC Berkeley professor of biochemistry, molecular biology, and chemistry.

Cate is among the leaders in the current effort to map the ribosome's structure.

The Register: Folding@Home comes to the PS3
"Sony is to let Playstation 3 users run Folding@home on their consoles, helping the study of Parkinson's, Alzheimer's, cystic fibrosis and many cancers."

A blue fluorescent protein has an added extra that makes it a useful tool for biophysical studies, says a team of US researchers.


"Fluorescent proteins can be used in protein biophysics to track the folding status of proteins."

Andreas Bommarius, from the Georgia Institute of Technology in Atlanta, and colleagues, investigated the natural function of a fluorescent protein from the marine bacterium Vibrio vulnificus.

»www.rsc.org/Publishing/Journals/···blue.asp

Researchers find that a protein activated to repair DNA damage also activates tanning, which can protect against melanoma

Scientists have determined that while it fixes damage to DNA caused by UV rays, the protein p53 also controls the mechanism for tanning. A powerful protein known as p53 has long been considered the master regulator of the genome because of its amazing ability to repair damaged DNA. Now scientists at Harvard's Dana-Farber Cancer Institute have discovered that p53 not only mends genetic material but also kicks off the chemical cascade that results in tanning.

Scientific American