Thursday, January 14, 2010

“Journal of Biological Chemistry Changes Approach to Manuscript Reviews ... - Earthtimes” plus 3 more

“Journal of Biological Chemistry Changes Approach to Manuscript Reviews ... - Earthtimes” plus 3 more

Journal of Biological Chemistry Changes Approach to Manuscript Reviews ... - Earthtimes

Posted: 14 Jan 2010 08:59 AM PST

Editors say the new mission statement and shift in editorial criteria are in response to changing nature of biological research

BETHESDA, Md., Jan. 14 /PRNewswire-USNewswire/ -- The Journal of Biological Chemistry's editors are unveiling this week a number of changes to the journal's publishing policies. They say the changes are in response to the increasingly interdisciplinary nature of biological research and will help the journal better meet the evolving needs of the scientific community.

(Photo:  http://www.newscom.com/cgi-bin/prnh/20100114/DC37802 )

In an editorial in this week's issue of the JBC, which became available online Friday, the editors announced the journal's new mission statement and laid out changes to how manuscripts are judged by peer review. They also reported that the journal's submission fees have been eliminated to expedite the submission process and hold down costs to authors.

"These developments represent a commitment to publishing the very best science in the JBC," said Dr. Herbert Tabor, the journal's longtime editor-in-chief. "Our new mission statement reflects our understanding that molecular and cellular biology studies are being carried out in a variety of fields, and modifying how our reviewers approach manuscripts will better serve both readers and authors."

When the JBC was established in 1905, its founders set out to publish "anything of a chemical nature in the whole field of biology, whether this touches the plant or animal kingdom." In the decades since, the journal has embraced papers that provide clear "mechanistic insight" into any molecular process, which is to say it accepted papers that not only reported that a molecular process occurred but how or why it occurred.

Now, JBC editors are broadening their definition of "mechanism," in light of path-breaking research being done in new, still-developing fields that, while molecular in the level of analysis, has not yet reached the stage at which it provides the level of detailed mechanistic information expected in more established research areas.

"The fields have evolved so much that you can't always understand mechanistic details fully at the outset," explained JBC Deputy Editor Robert D. Simoni. "We recognize that you cannot in a single paper solve a problem entirely. But, if you develop novel insights into the molecular nature of biological processes that are clear, interesting and important -- and that open the door for answering the next generation of questions -- your paper belongs in the JBC."

In the January issue of ASBMB Today, the member magazine of the American Society for Biochemistry and Molecular Biology, which publishes the JBC and two other journals, Simoni wrote that "a great number of exciting molecular and cellular biology studies are being carried out in neuroscience, developmental biology, cell biology, medical science, biophysics, immunology, microbiology, physiology, etc. We wish to emphasize that ? much of the research in these areas would be very welcome in the JBC."

The "modest course adjustment," he said, also will affect how the journal categorizes manuscripts.

The journal's table of contents will reflect all areas of biology that can be studied at a molecular level. In addition, articles may appear under more than one category, which Simoni said will make finding relevant articles easier for readers and will increase authors' visibility.

To find out more about the Journal of Biological Chemistry, visit www.jbc.org. To read the JBC editorial, visit www.jbc.org/site/home/editorials/toc_changes.xhtml .  To read Simoni's article in ASBMB Today, visit www.asbmb.org/asbmbtoday/asbmbtoday_article.aspx?id=4940.

About the American Society for Biochemistry and Molecular Biology

The ASBMB is a nonprofit scientific and educational organization with more than 12,000 members worldwide. Most members teach and conduct research at colleges and universities. Others conduct research in various government laboratories, at nonprofit research institutions and in industry. The Society's student members attend undergraduate or graduate institutions.  For more information about ASBMB, visit www.asbmb.org.

SOURCE American Society for Biochemistry and Molecular Biology

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Chimp, Human Y Chromosomes Evolving Faster Than Expected - Redorbit.com

Posted: 14 Jan 2010 07:55 AM PST

Posted on: Thursday, 14 January 2010, 11:02 EST

Contrary to a widely held scientific theory that the mammalian Y chromosome is slowly decaying or stagnating, new evidence suggests that in fact the Y is actually evolving quite rapidly through continuous, wholesale renovation.

By conducting the first comprehensive interspecies comparison of Y chromosomes, Whitehead Institute researchers have found considerable differences in the genetic sequences of the human and chimpanzee Ys—an indication that these chromosomes have evolved more quickly than the rest of their respective genomes over the 6 million years since they emerged from a common ancestor. The findings are published online this week in the journal Nature.

"The region of the Y that is evolving the fastest is the part that plays a role in sperm production," say Jennifer Hughes, first author on the Nature paper and a postdoctoral researcher in Whitehead Institute Director David Page's lab. "The rest of the Y is evolving more like the rest of the genome, only a little bit faster."

The chimp Y chromosome is only the second Y chromosome to be comprehensively sequenced. The original chimp genome sequencing completed in 2005 largely excluded the Y chromosome because its hundreds of repetitive sections typically confound standard sequencing techniques. Working closely with the Genome Center at Washington University, the Page lab managed to painstakingly sequence the chimp Y chromosome, allowing for comparison with the human Y, which the Page lab and the Genome Center at Washington University had sequenced successfully back in 2003.

The results overturned the expectation that the chimp and human Y chromosomes would be highly similar. Instead, they differ remarkably in their structure and gene content. The chimp Y, for example, has lost one third to one half of the human Y chromosome genes--a significant change in a relatively short period of time. Page points out that this is not all about gene decay or loss. He likens the Y chromosome changes to a home undergoing continual renovation.

"People are living in the house, but there's always some room that's being demolished and reconstructed," says Page, who is also a Howard Hughes Medical Institute investigator. "And this is not the norm for the genome as a whole."

Wes Warren, Assistant Director of the Washington University Genome Center, agrees. "This work clearly shows that the Y is pretty ingenious at using different tools than the rest of the genome to maintain diversity of genes," he says. "These findings demonstrate that our knowledge of the Y chromosome is still advancing."

Hughes and Page theorize that the divergent evolution of the chimp and human Y chromosomes may be due to several factors, including traits specific to Y chromosomes and differences in mating behaviors.

Because multiple male chimpanzees may mate with a single female in rapid succession, the males' sperm wind up in heated reproductive competition. If a given male produces more sperm, that male would theoretically be more likely to impregnate the female, thereby passing on his superior sperm production genes, some of which may be residing on the Y chromosome, to the next generation.

Because selective pressure to pass on advantageous sperm production genes is so high, those genes may also drag along detrimental genetic traits to the next generation. Such transmission is allowed to occur because, unlike other chromosomes, the Y has no partner with which to swap genes during cell division. Swapping genes between chromosomal partners can eventually associate positive gene versions with each other and eliminate detrimental gene versions. Without this ability, the Y chromosome is treated by evolution as one large entity. Either the entire chromosome is advantageous, or it is not.

In chimps, this potent combination of intense selective pressure on sperm production genes and the inability to swap genes may have fueled the Y chromosome's rapid evolution. Disadvantages from a less-than-ideal gene version or even the deletion of a section of the chromosome may have been outweighed by the advantage of improved sperm production, resulting in a Y chromosome with far fewer genes than its human counterpart.

To determine whether this rapid rate of evolution affects Y chromosomes beyond those of chimps and humans, the Page lab and the Washington University Genome Center are now sequencing and examining the Y chromosomes of several other mammals.

This research was funded by the National Institutes of Health (NIH) and the Howard Hughes Medical Institute (HHMI).

Written by Nicole Giese

David Page's primary affiliation is with Whitehead Institute for Biomedical Research, where his laboratory is located and all his research is conducted. He is also a Howard Hughes Medical Institute Investigator and a Professor of Biology at Massachusetts Institute of Technology.

Full Citation:

"Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content"

Nature, online January 13, 2010.

Jennifer F. Hughes (1), Helen Skaletsky (1), Tatyana Pyntikova (1), Tina A. Graves (2), Saskia K. M. van Daalen (3), Patrick J. Minx (2), Robert S. Fulton (2), Sean D. McGrath (2), Devin P. Locke (2), Cynthia Friedman (4), Barbara J. Trask (4), Elaine R. Mardis (2), Wesley C. Warren (2), Sjoerd Repping (3), Steve Rozen (1), Richard K. Wilson (2), David C. Page (1).

1. Howard Hughes Medical Institute, Whitehead Institute, and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.

2. The Genome Center, Washington University School of Medicine, St. Louis, Missouri, USA.

3. Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Academic Medical Center, Amsterdam, the Netherlands.

4. Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.

---

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Discovery points toward anti-inflammation treatment for blinding ... - EurekAlert

Posted: 14 Jan 2010 08:52 AM PST

[ Back to EurekAlert! ] Public release date: 14-Jan-2010
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Contact: Toni Baker
tbaker@mcg.edu
706-721-4421
Medical College of Georgia

The discovery of an inflammatory mediator key to the blinding effects of diabetic retinopathy is pointing toward a potential new treatment, Medical College of Georgia researchers said.

Interleukin-6, known to contribute to the debilitating joint inflammation of rheumatoid arthritis, also helps ignite inflammation of the retina, a first step in a disease that is the leading cause of blindness is working-age adults, MCG researchers reported online in Investigative Ophthalmology & Visual Science.

The finding has the scientists looking at whether an interleukin-6 antibody, which is showing success in treating rheumatoid arthritis, can halt inflammation in mice with diabetic retinopathy. "We expect that this neutralizing antibody can be used to treat diabetic retinopathy in the future," said Dr. Wenbo Zhang, assistant research scientist in MCG's Vascular Biology Center. Drs. Zhang and Modesto Rojas, senior postdoctoral fellow, are co-first authors on the paper.

Angiotensin II, a powerful constrictor of blood vessels, is typically associated with the kidneys where it plays a vital role in regulating blood pressure. The scientists suspect angiotensin II helps promotes wound healing and regulation of pressure within small blood vessels in the eye.

However in diabetes, angiotensin II levels increase in the eye probably in response to high glucose levels and help promote inflammation, spurring remodeling of blood vessels and tissue destruction, Dr. Rojas said. "Vascular inflammation is one of the first steps to inducing the changes in the retina."

MCG scientists have shown interleukin-6 is a needed accomplice whose previously undetectable levels in the eye also increase, said Dr. Ruth Caldwell, cell biologist a the Vascular Biology Center and the Charlie Norwood Veterans Affairs Medical Center and the study's corresponding author.

With the help of interleukin-6, angiotensin II induces white blood cells to stick to the endothelial cells lining blood vessels of the retina, which slows blood flow. The white blood cells also start producing inflammatory and vascular growth factors that cause blood vessel walls to leak and thicken, further constricting blood flow. Retinal cells start dying from the reduced blood and oxygen supplies that result. In response, the body prompts growth of new blood vessels, presumably to help but instead causing more vision impairment.

If the trigger, high glucose, was temporary, these natural responses might help clear damaged cells and protect the eye. "Inflammation is a compensatory mechanism that gets activated as a survival mechanism," Dr. Rojas said. "If it continues, the effect is bad."

"We have known for along time if patients keep their blood sugar under perfect control, they don't have these problems, but that's hard," Dr. Caldwell adds. "That is why it's such a difficult disease."

To examine interleukin-6's role in the destruction, the researchers injected angiotensin II into the vitreous portion of the eyes of mice missing the gene for the inflammatory factor as well as normal mice. The extra angiotensin did little to the retinal vessels of mice lacking interleukin-6 but vessels in the normal mouse retina mimicked the inflammatory reaction found in diabetic retinopathy. When they reintroduced interleukin-6 to the genetically altered mice, the damage mimicked that of the normal mice. "So when we knock out interleukin-6, we can block the effects of angiotensin II," Dr. Caldwell said.

The scientists want to see whether the interleukin-6 antibody can be used to prevent damage by giving it shortly after the onset of diabetes in rodents and as a treatment by using it later in the disease process.

The research was funded by the National Institutes of Health, the Department of Veterans Affairs and postdoctoral fellowship awards from the Juvenile Diabetes Research Foundation International and the American Heart Association.


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VentiRx Nabs $25M, Gilead Deepens Seattle Roots, Sage Strikes Deal ... - Seattle Post Intelligencer

Posted: 14 Jan 2010 05:25 AM PST

Hope sprang eternal at this year's JP Morgan Healthcare Conference, the annual kickoff event for the biotech industry. A few Seattle biotech companies offered some reasons for people to think a little hope may be justified.

-VentiRx Pharmaceuticals said it raised $25 million to further develop its drugs that stimulate the innate immune system against cancer and allergies. A pair of local investors, Arch Venture Partners and Frazier Healthcare Ventures, chose to re-invest in the Seattle and San Diego-based company, while MedImmune Ventures, a unit of AstraZeneca, led the new round.

-Stephen Friend is at it again. The visionary founder of Sage Bionetworks said he struck a partnership with the world's largest drugmaker, Pfizer, to support Sage's effort to spark an open-source-style movement for biology. Pfizer is paying to support research at Sage to find new cancer drug targets and predict which patients are likely to respond to therapies in development. Terms weren't disclosed.

-Gilead Sciences (NASDAQ: GILD), the world's largest maker of HIV medications, is deepening its roots in the Seattle area with a $50 million respiratory disease research center looking out over Lake Union. The company hasn't yet seen U.S. product sales to justify its $365 million acquisition of Corus Pharma in 2006, although it is hoping to get the green light from the FDA next month to start selling Corus's inhalable antibiotic for cystic fibrosis.

-ZymoGenetics (NASDAQ: ZGEN), the granddaddy of Seattle biotech companies, closed on a financing that netted about $90.9 million. The company plans to use the cash to support R&D, and to boost sales of its lone marketed product, recombinant thrombin (Recothrom) for surgical bleeding.

-Seattle-based Targeted Genetics (NASDAQ: TGEN) said it is allowing itself to be de-listed from the NASDAQ exchange in order to save cash. The longtime gene therapy stalwart is down to the equivalent of six full-time employees.

-The Institute for Systems Biology was found to have the highest scientific impact of any research center in the U.S., and the third highest in a global survey of more than 2,100 research centers, according to an analysis by Spain-based SCImago Research Group. The report looked at total research output, how much each institute collaborates with other centers, the influence of its publications, how often they are cited by other scientists, and other factors.

-SonoSite (NASDAQ: SONO), the Bothell, WA-based developer of portable ultrasound machines, said it plans to spend $100 million to buy back shares of its stock.

-Kineta, the Seattle-based biotech company, raised $942,000 in new capital, according to a regulatory filing. The company is developing anti-viral therapies, as well as drugs for autoimmune diseases.

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