BioSpace to Power 2009 BIO Career Fair

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Help an Air Crash Victim Find a Job

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Russo Partners Launches Blog, Twitter Feed

The blog, where the agency intends to talk about PR insights as well asexcerpts from recent conversations from the healthcare community, islocated at http://www.rxforpr.com, as well as linked to our new Web site, which was created by bfw Advertising.

Russo Partner's new Twitter feed for client and agency news is accessible here: http://www.twitter.com/russopartners.

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Grubb Releases New Sales Data

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Arlene Lieberman Appointed to Barney & Barney LLC Board

Paul Hering, managing principal and CEO of San Diego-headquartered insurance brokerage Barney & Barney, announced that Arlene Lieberman, a principal of the firm, has been appointed to serve on the firm’s board of directors.  This governing board is made up of senior leadership and has responsibility for overall governance matters and setting strategic direction for the 100 year old firm.

Arlene is a principal of Barney & Barney and serves as a practice group leader in the employee benefits department.  In this position she manages a team of 17 insurance sales and service professionals.  She has dedicated over 27 years to the insurance industry and is responsible for the development and design of employee benefit packages for large national and international employer groups. As an expert on insurance legislation and regulations, she is an aggressive advocate for her clients. 

Barney & Barney LLC is a California based privately held risk management and insurance brokerage firm providing solutions, services and products in commercial property and casualty insurance, employee benefits, workers’ compensation, executive personal lines, and surety for the past 100 years. The firm also offers value added services in alternative risk financing, business continuity and loss control.

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Asterand Partners with BioWisdom on Data Deal

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Moores Center Launches Drug Effectiveness Center

Researchers at the Moores Cancer Center at the University of California, San Diego are taking advantage of a five-year, $7.5 million grant from the National Institutes of Health (NIH) and sophisticated imaging technologies at the newly established In Vivo Cellular and Molecular Imaging Center (ICMIC) – one of only eight in the country – to develop new ways to detect early cancers that require treatment and monitor the effectiveness of new molecular-based cancer therapies.

The new center, which is led by Robert Mattrey, MD, professor of radiology at the UC San Diego School of Medicine and co-principal investigator David Vera, PhD, professor of radiology, is one of only three such centers in the nation to receive funding recently from the NIH’s National Cancer Institute.

Researchers will focus initially on three main basic research projects – all of which are aimed at translating laboratory findings in animals to the clinic. Mattrey and recent Nobel Prize winner Roger Tsien, PhD, professor of pharmacology, chemistry and biochemistry at UC San Diego, are leading a project to improve the ability to characterize the aggressiveness of certain tumors. According to Mattrey, cancers that express an enzyme called a matrix metalloproteinase tend to be aggressive and are likely to spread. Such enzymes are instrumental in breaking down tissues, enabling cancers to escape and enter the bloodstream and/or lymphatic system and metastasize, or spread, to distant sites.

Mattrey and Tsien are developing imaging contrast agents to use with ultrasound that will help them detect such enzymes in prostate and breast cancers. Determining the likelihood that a cancer could be aggressive has implications for treatment decisions, especially for diseases where the treatment adds risk, Mattrey said. For example, a 60-year-old man who is diagnosed with aggressive prostate cancer might elect to undergo surgery, whereas a man with a slow-growing malignancy might decide to wait and let physicians monitor his tumor.

In another project, Vera and co-investigator Stephen Howell, MD, professor of medicine at the UC San Diego School of Medicine, will use nuclear imaging and ultrasound to virtually crawl inside of cancer cells and monitor the presence and activity of an experimental platinum-based chemotherapy drug – in essence to find out if the therapy is hitting its targets and working or not. 

Because drugs are expensive, drug companies want to know if agents are hitting targets before they invest hundreds of millions of dollars in testing and development, rather than waiting the months that it can sometimes take for some drugs to have any kind of visible effect. Doctors and patients would like to know a therapy’s efficacy much sooner than that in order to pursue a different treatment option.

The Moores UCSD Cancer Center is one of the nation’s 41 National Cancer Institute-designated Comprehensive Cancer Centers, combining research, clinical care and community outreach to advance the prevention, treatment and cure of cancer.

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UCSD Study Shows Growth Factor Protects Brain Cells in Alzheimer's

Memory loss, cognitive impairment, brain cell degeneration and cell death were prevented or reversed in several animal models after treatment with a naturally occurring protein called brain-derived neurotrophic factor (BDNF).  The study by a University of California, San Diego-led team - published in the February 8, 2009 issue of Nature Medicine - shows that BDNF treatment can potentially provide long-lasting protection by slowing, or even stopping the progression of Alzheimer's disease in animal models.

BDNF is normally produced throughout life in the entorhinal cortex, a portion of the brain that supports memory. Its production decreases in the presence of Alzheimer's disease. For these experiments, the researchers injected the BDNF gene or protein in a series of cell culture and animal models, including transgenic mouse models of Alzheimer's disease; aged rats; rats with induced damage to the entorhinal cortex; aged rhesus monkeys, and monkeys with entorhinal cortex damage. 

In each case, when compared with control groups not treated with BDNF, the treated animals demonstrated significant improvement in the performance of a variety of learning and memory tests.  Notably, the brains of the treated animals also exhibited restored BDNF gene expression, enhanced cell size, improved cell signaling, and activation of function in neurons that would otherwise have degenerated, compared to untreated animals. These benefits extended to the degenerating hippocampus where short-term memory is processed, one of the first regions of the brain to suffer damage in Alzheimer's disease.

The study was supported by the National Institutes of Health, the California Regional Primate Research Center, the Veterans Administration, the Alzheimer's Association, the State of California, the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation and the Shiley Family Foundation.  Tuszynski is scientific founder of Trophin Therapeutics, a company that may potentially benefit from the research results.

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Stem Cell Research Uncovers Mechanism for Type 2 Diabetes

Taking clues from their stem cell research, investigators at the University of California San Diego (UC San Diego) and the Burnham Institute for Medical Research (Burnham) have discovered that a signaling pathway involved in normal pancreatic development is also associated with type 2 diabetes. Their findings, recently published in Experimental Diabetes Research, could provide a potential new target for therapy.

Pamela Itkin-Ansari, PhD, assistant adjunct professor at the UC San Diego School of Medicine and Burnham; Fred Levine, MD, PhD, professor and director of the Sanford Children’s Health Research Center at Burnham, and colleagues showed that the Wnt signaling pathway is up-regulated in insulin-producing cells of pancreases from adults with type 2 diabetes.

“It is now clear that progenitor cells, cells with the capacity to become insulin producing cells, reside in the adult pancreas,” said Itkin-Ansari. “The key to harnessing those cells to treat diabetes is to understand the signaling pathways that are active in the pancreas under both normal and disease conditions. In the course of that research, we found that Wnt signaling activity, which plays a critical role in the development of the pancreas, re-emerges in type 2 diabetes.”

In many tissues, the Wnt signaling pathway – a series of protein interactions that control several genes –plays a role in normal development as well as in cancer.  In this study, the scientists compared the expression of different proteins in the Wnt pathway in the pancreas from adults with type 2 diabetes and those from healthy individuals. The researchers discovered that cells from those without the disease had low levels of beta-catenin, a protein that enters cell nuclei and activates certain genes. Insulin-producing beta cells from people with type 2 diabetes had increased levels of the protein.

This study was funded by grants from the California Institute for Regenerative Medicine, the National Institute of Diabetes and Digestive and Kidney Diseases, the Juvenile Diabetes Research Foundation and the JW Kieckhefer Foundation.

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Scripps Research Scientists Create First Crystal Structure of an Intermediate Particle in Virus Assembly

Gertsman et al determined the crystal structure of the assembly intermediate at the far right and found that the subunits (representative structure is in purple) forming the particle had a different structure from that in the mature particle at far left (representative subunit structure is in gray). The arrow shows the change in particle with maturation, correlated with the change in subunit structure.

LA JOLLA, CA, February, 6, 2009-

A research team at the Scripps Research Institute has been able to produce the first crystal structure of a virus particle caught in the midst of assembling its impenetrable outer protein coat.  The structure, described February 8 in an advance online publication of the journal Nature, provides fresh insights into the elegant dance that viral proteins perform to create the infectious structure that causes all manner of misery and disease, say researchers. While the virus they studied, HK97, only infects bacteria, well-known viruses such as herpes and HIV are also known to assemble an"

"The principles of this multi-stage protein coat assembly will likely be similar across all complex viruses," says the study's senior author, Scripps Research Professor John E. Johnson. "But this process has never been seen before at this resolution, and now we known that what we thought happens, doesn't."

That's important, Johnson says, because if scientists understand how a virus builds its protective coat, they may be able to medically target vulnerabilities in the first stage of that assembly. "We believe that without its final shell to protect it, an immature virus will be much more defenseless to antiviral agents," he says.
Knowing how viruses build these vessels to protect the naked viral DNA inside is also useful in the field of medical nanotechnology, he adds. 

The work was supported by grants from the National Institutes of Health.

The Scripps Research Institute is one of the world's largest independent, non-profit biomedical research organizations, at the forefront of basic biomedical science that seeks to comprehend the most fundamental processes of life.

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Scripps Group Studies Blindness

A collaborative team of scientists from the Scripps Research Institute and other institutions has shed light on the causes of and potential treatment for two blinding conditions known as macular telangiectasia (MacTel) and retinal angiomatous proliferation (RAP), types of macular degeneration. Though based on mouse studies, the research bolsters the idea that humans suffering from these and other eye conditions may be able to help preserve function by adding antioxidants to their diet, and explains why this would work. The team also devised a new cell-based gene therapy technique that could eventually offer another option for arresting vision loss from these diseases. 

The work, led by Scripps Research Professor Martin Friedlander, M.D., Ph.D., was reported in an advance, online edition of the Journal of Clinical Investigation on February 2, 2009. The research is also likely to apply to a range of other neurodegenerative conditions, including vision loss from Huntington's and Alzheimer's diseases and inherited retinal degenerations, such as retinitis pigmentosa.

Many forms of blinding degenerative eye conditions are tied to the abnormal proliferation of new blood vessels in the eyes, or neovascularization. Treatment of these conditions has generally focused on blocking continued neovascularization, but this typically only slows disease progression because new growth eventually wins out, leading to continued damage and vision loss.

The MacTel Foundation and the National Institutes of Health supported this work.

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Scientists at Scripps Research Identify Inflammatory Bowel Disease Mutation

A team of scientists at The Scripps Research Institute has linked a mouse mutation to an increased susceptibility for developing inflammatory bowel disease (IBD)—represented in humans as Crohn's disease and ulcerative colitis, which together are estimated to affect more than a million people in the United States. The findings may one day lead to new and better treatments for the disease.
The work was published in the February 6, 2009 Early Edition of the Proceedings of the National Academy of Sciences (PNAS).

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Moores Scientists Uncover Leukemia Indicator

Scientists at the Moores Cancer Center at the University of California, San Diego, Stanford University School of Medicine and other centers have identified a mechanism by which a chronic form of leukemia can progress into a deadlier stage of the disease. The findings may provide physicians with an indicator of when this type of cancer – chronic myeloid leukemia (CML) – is progressing, enabling them to make more accurate prognoses for the disease and improved treatment choices.

The findings, reported online during the week of February 16, 2009 in the Proceedings of the National Academy of Sciences, also shed light on the development of potentially treatment-resistant leukemia stem cells and provide insights for new strategies against CML and other cancers.

Led by Jamieson and Irving Weissman, MD, director of the Stem Cell Biology and Regenerative Medicine Institute at the Stanford University School of Medicine, the researchers discovered that when a molecular off-switch called glycogen synthase kinase (GSK) 3 beta becomes faulty in chronic stage CML cells, it fails to turn off another protein, beta-catenin. This in turn enables pre-leukemia stem cells to develop into leukemia stem cells and expand their numbers, leading to progression to the more dangerous “blast crisis” stage of CML. This errant off-switch is a potential therapeutic target, Jamieson explained.

Much of the work received funding from the National Institutes of Health, the California Institute of Regenerative Medicine and the Moores UCSD Cancer Center.

The Moores UCSD Cancer Center is one of the nation’s 41 National Cancer Institute-designated Comprehensive Cancer Centers, combining research, clinical care and community outreach to advance the prevention, treatment and cure of cancer.

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New Scripps Research Technique Clears Research Path for Hemorrhagic Fever Diseases

A team from the Scripps Research Institute has developed a novel method for studying arenaviruses, rodent-borne viruses that can cause hemorrhagic fever  diseases. Currently, no licensed vaccines are available against arenaviruses and drug therapies are extremely limited. This development opens new avenues for vaccine development and identification of anti-viral drugs to combat human pathogenic arenaviruses.

Some arenaviruses can cause severe disease in humans. For example, Lassa virus causes Lassa fever, a hemorrhagic fever disease endemic to sub-Saharan Africa, whereas other arenaviruses are responsible for a variety of South American hemorrhagic fever diseases. Infections with hemorrhagic fever arenaviruses are characterized by damage to the vascular system, and may be associated with disease symptoms that can be relatively mild, severe or deadly. Victims who recover from their illnesses may suffer post-infection health problems, especially hearing loss in the case of infection with Lassa virus. 

The work was published in the February 10, 2009 Early Edition of the Proceedings of the National Academy of Sciences (PNAS). See http://www.pnas.org/content/early/2009/02/10/0900088106.abstract.

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Salk Identifies Fruit flies as cancer lab model

Fruit flies and humans share most of their genes, including 70 percent of all known human disease genes. Taking advantage of this remarkable evolutionary conservation, researchers at the Salk Institute for Biological Studies transformed the fruit fly into a laboratory model for an innovative study of gliomas, the most common malignant brain tumors.

Better models for research into human gliomas are urgently needed. Last year alone, about 21,000 people in this country were diagnosed with brain and nervous system cancers, Senator Edward M. Kennedy the most famous among them. About 77 percent of malignant brain tumors are gliomas and their prognosis is usually bleak. While they rarely spread to elsewhere in the body, cancerous glial cells quickly infiltrate the brain and grow rapidly, which renders them largely incurable even with current therapies.

The researchers are hoping that through their combined efforts new discoveries from the fly model can be rapidly translated into mouse and human brain tumor studies and lead to development of new therapies for this deadly cancer.

The work was supported by the National Institutes for Neurological Disorders and Stroke and the American Brain Tumor Association.

For information on the commercialization of this technology, please contact Dave Odelson at 858-453-4100, x 1223 (dodelson@salk.edu) in the Salk Office of Technology Management and Development.

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