Philippine Herbal Medicine

BCM researchers awarded national funding

HOUSTON -- (September 30, 2008) -- Twelve Baylor College of Medicine researchers have been awarded funding through the U.S. Department of Health and Human Services along with researchers from six additional Texas institutions, Senator Kay Bailey Hutchison (R-TX) announced.

"This funding will help Texas health institutions expand their knowledge and understanding of science and medicine," said Hutchison.

"The research represented by these grants covers many important fields of study at Baylor College of Medicine," said Dr. Peter G. Traber, president and CEO at BCM. "We appreciate Senator Hutchison's leadership in support of biomedical science."

Researchers at BCM receiving funding include:

• Dr. Jue (Jade) D. Wang, assistant professor of molecular and human genetics, received $2,302,500 for her project, The Molecular Interface of Replication Elongation and the Cellular Environment from the Office of the Director at the National Institutes of Health. Wang also received the 2008 National Institutes of Health Director's New Innovator Awards, a program to support young scientists early in their careers, earlier this year.
• Dr. Aleksandar Milosavljevic, associate professor of molecular and human genetics, received $1,364,573 for his project, Epigenomics Data Analysis and Coordination Center at BCM from the National Institute on Drug Abuse.
• Dr. Olivier Lichtarge, professor of molecular and human genetics, received $423,459 for his project, Functional Determinants in G Protein-Coupled Receptors from the National Institute of General Medical Sciences.
• Dr. H. Daniel Lacorazza, assistant professor of pathology and immunology, received $383,750 for his project, Transcriptional Regulation of Development and Maintenance of Memory T Lymphocytes from the National Institute of Allergy and Infectious Diseases.
• Dr. Jenny Chang, associate professor of medicine and medical director of the Lester and Sue Smith Breast Center at BCM, received $475,325 for her project, Targeting Notch, PI3K-AKT and other novel pathways in breast cancer stem cells from the National Cancer Institute.
• Dr. David Corry, associate professor of medicine-immunology, received $697,014 for his project, Molecular Phenotypes for Lung Diseases from the National Heart, Lung, and Blood Institute.
• Dr. Karen Cullen, associate professor of pediatrics-nutrition, received $360,449 for her project, Family Eats: Cancer Prevention for Families from the National Cancer Institute.
• Dr. Graeme Mardon, professor of pathology, received $274,764 for his project, Molecular Genetics Emphasizing Vision Research from the National Eye Institute.
• Dr. Mary Mariscalco, associate professor of pediatrics-critical care, received $183,632 for her project, Research Training in Pediatric Critical Care Medicine from the National Heart, Lung, and Blood Institute.
• Dr. Hardeep Singh, assistant professor of medicine-health services research, received $421,506 for his project, Using Electronic Data to Improve Care of Patients with Known or Suspected Cancer from the Agency for Healthcare Research and Quality.
• Dr. Susan Marriott, professor of molecular virology and microbiology, received $223,295 for her project, Transforming Potential of Emerging Human Retroviruses from the National Institute of Allergy and Infectious Diseases.
• Dr. Virginia Moyer, professor of pediatrics, received $299,764 for her project, Safe Passages: A Toolkit to Ensure Quality Transitions from NICU to Ambulatory Care from the Agency for Healthcare Research and Quality.

Fewer doses of anthrax vaccine comparable to current dosing regimen

HOUSTON -- (September 30, 2008) -- Three injections of anthrax vaccine given into the muscle stimulate comparable antibody responses and cause fewer adverse reactions than four doses given under the skin, said a consortium of researchers that included those from Baylor College of Medicine in a report in the current Journal of the American Medical Association.

"We expect that reducing the number of adverse reactions will lead to a higher level of acceptability of the vaccine," said Dr. Wendy Keitel, professor of molecular virology and microbiology at BCM and director of the Vaccine Treatment and Evaluation Unit at BCM. "And reducing the number of times the vaccine is given will reduce the cost and complexity of delivering the entire program."

Eliminating second dose

Anthrax vaccine is primarily given to people who are at risk for repeated exposure to anthrax spores, such as military personnel deployed to areas where they face an increased risk of infection with the bacteria and people who work with the organism in the laboratory. Eliminating the second dose of the currently recommended schedule would make it easier to fully vaccinate someone, said Keitel.

Researchers studied the ability of a reduced dose schedule to stimulate immune responses and reactions at the vaccine injection site in 1,005 healthy adults between the ages of 18 and 61 years who had not previously received the anthrax vaccine. Study participants were placed at random into one of six groups. Some groups received four scheduled doses at weeks 0, two and four weeks and six months; some groups received placebo as the second dose at two weeks; and some received only placebo injections.

Muscle vs. under the skin

Researchers evaluated antibody responses to the vaccine in the study participants seven months after they received the first dose and found that giving fewer injections into the muscle was comparable to the usual schedule of four given under the skin. They also noted fewer and milder side effects in those who received injections into the muscle rather than under the skin.

Other BCM researchers contributing to the study are Dr. Hanaa El Sahly, assistant professor of molecular virology and microbiology, Nanette Bond, P.A.C., study coordinator, and staff from the Vaccine Research Center. Contributing institutions include University of Alabama at Birmingham, Walter Reed Army Institute for Research, Mayo Clinic, and Emory University School of Medicine.

The study was funded and sponsored by the Centers for Disease Control and Prevention. The CDC was responsible for the development, study protocol and for statistical analyses.

The study can be found at www.jama.ama-assn.org/.

My Project 10100 Submission: Mitochondrial Repair

Here is an example of what I think is a passable submission to Google's Project 10100, with a focus on mitochondrial science. I could probably run one up for LysoSENS-like work as well, but one thing at a time.

Bring Mitochondrial Repair to Phase 1 Trials

What one sentence best describes your idea? (maximum 150 characters):

Our mitochondria degrade over the years, contributing greatly to age-related disease and frailty - but medical technology can fix this problem.

Describe your idea in more depth. (maximum 300 words):

I propose that the most promising of nascent mitochondrial repair technologies be funded from their present early-stage standing to readiness for Phase I clinical trials in humans. As a condition of funding, methodologies will be published free of restriction for any group to further develop and bring to market. This will be accomplished with the aid of a non-profit research organization like the Methuselah Foundation, with a history of raising matching funds for large donations, so as to maximize the impact of the funding program.

Mitochondria are tiny power plants inside our cells, churning away to turn food into energy. They were once free-roaming bacteria and have retained their own mitochondrial DNA, distinct from our own nuclear DNA. As our mitochondria fail, however, so do we. The Mitochondrial Free Radical Theory of Aging points to progressive damage to our mitochondrial DNA as an important - and arguably the most important - root cause of age-related degeneration, disease, and frailty.

At present, a range of plausible technologies exist to repair mitochondrial DNA, replace mitochondrial DNA, or make damage to this DNA irrelevant. These technologies stand at varying points between ideation and animal trials: whole-body replacement of mitochondrial DNA was demonstrated in mice as early as 2005, for example, as has the process of allotopic expression: moving a single important mitochondrial gene into the cellular nucleus, such that the necessary proteins are still made, and a damaged mitochondrion continues to function.

These technologies are progressing very slowly and with a paucity of funding, partly because this is the nature of early research, partly because of perverse regulatory incentives. This is unacceptable when considered against a) the comparatively low cost of basic research in this age of biotechnology, and b) the vast potential benefits to humanity. Philanthropic funding can overcome these hurdles.

What problem or issue does your idea address? (maximum 150 words):

Consequences of damaged mitochondrial DNA include failing organs, clogged arteries, neurodegeneration, and much more. This is the Mitochondrial Free Radical Theory of Aging, well supported by decades of evidence. A working repair technology pushed into the clinical system has the potential to entirely remove this large contribution to disease and frailty. But first it must be finalized from the promising beginnings presently in the laboratory.

Regulatory bodies like the FDA restrict all application of medical science to specific, named diseases; this makes early stage research to produce a general repair technology for mitochondria unprofitable. It would be hard to license, as a developer would struggle to make money on that license. Yet it costs little to move established research to Phase I trial readiness - $1 million is a fortune for a single laboratory - and developers leap at license-free medical technology. This is where careful philanthropy can unjam the gridlocked system.

If your idea were to become a reality, who would benefit the most and how? (maximum 150 words):

A mitochondrial repair technology demonstrated to be ready for human trials, free of licensing cost, free from intellectual property restrictions, and unjammed from the system of perverse incentives in early-stage research stands to benefit everyone. It will be as universally beneficial a medicine as aspirin; the elderly will benefit immediately upon availability, we will benefit from it in decades to come, and our children will benefit when their bodies too start to run down.

Everyone has mitochondria, and mitochondrial degeneration is a universal condition, bringing myriad forms of suffering and pain. We got rid of tuberculosis and smallpox as soon as we could, so why not this? Repair of mitochondrial DNA damage is a very plausible near-future win for everyone, given where the science is today. We can make it happen.

What are the initial steps required to get this idea off the ground? (maximum 150 words):

I envisage the opening labor as follows: 1) Identify the existing non-profit research group and volunteer cadre to run this project - my vote is for the Methuselah Foundation, given their record and contacts within the research community, and the way their mission aligns with that of this project; 2) Identify the best groups and laboratories presently engaged in mitochondrial repair and related research; 3) Develop prospective work, milestone, and funding plans with researchers; 4) Start raising matching funds through existing channels; 5) Select the initial funding opportunities from the best of those produced, and get the researchers to work.

From there, I would like to see established a low-overhead but effective volunteer group of researchers and advocates to manage the cycle of grants, matching fundraising, and evaluation of progress and new research opportunities going forward.

Describe the optimal outcome should your idea be selected and successfully implemented. How would you measure it? (maximum 150 words):

The optimal outcome, after the completion of the project, is: a) for one or more different repair technologies to be successfully readied for Phase 1 human trials; b) protocols and methods to be fully detailed and published, free of restriction; c) multiple medical development concerns to be working on bringing applications to market in diverse regulatory regions; d) independently funded follow-on research taking place with the aim of improving upon the initial technology; e) matching fundraising to effectively continue even after the Google grant is complete.

Sample metrics for success include: a) the breadth and effectiveness of the technologies developed; b) the quality of the published material; c) range of developers working on applications; d) the range of independently funded lines of work spawned by this philanthropic funding; and, most crucially, e) the amount of matching funding and independent research and development funding drawn by this philanthropic project.

If you'd like to recommend a specific organization, or the ideal type of organization, to execute your plan, please do so here. (maximum 50 words):

The ideal organization is a research non-profit with existing connections to scientists already involved in mitochondrial repair research, a very low cost of operation for delivered funding, and a history of raising matching funds for large donations. The ideal example is the Methuselah Foundation, as you might have gathered.

Deactivating a cancer growth promoter

HOUSTON -- (September 26, 2008) -- Three enzymes called phosphatases that shut down a molecule called SRC-3 (steroid receptor coactivator 3) could provide a new pathway for fighting cancer, particularly tumors of the breast and prostate, said researchers at Baylor College of Medicine in a report that appears in the current issue of the journal Molecular Cell.

"This kind of information provides a target for the production of drugs against cancer," said Dr. Bert O'Malley, chair of molecular and cellular biology at BCM. "One can already find drugs that stimulate or inhibit phosphatases in other disease processes."

O'Malley and his colleagues had already determined that SRC-3 is an oncogene or cancer-promoting gene as well as a master switch in the cell. Phosphorylation or adding a phosphate molecule activates its cancer-promoting activities. In this study, the researchers identified three phosphatases that promote removal of the phosphate and thus halt the activity of SRC-3.

Of the three identified, PDXP, PP1, and PP2A, PP1 not only stops SRC-3 activity, it also stops the degradation of the co-activator. SRC-3 then builds up in cells, but without the phosphate, it is a dead molecule that does not function and may even further inhibit tumor growth.

Providing new avenues for fighting cancer is an important outcome of basic science, said O'Malley, who is also associate director for basic research in The Dan L. Duncan Cancer Center at BCM. "In cancer right now, many drugs work the same way. They are toxic to all cells. Because the cancer cell grows faster, the drug is more toxic, but there is nothing selective about the process. In the past decade, we have realized that there has to be a better, more intellectual approach to cancer. In fact, some already exist."

For example, the drug Herceptin targets breast cancer cells that carry the protein Her2/neu. Finding drugs that stop the activation of SRC-3, found at high levels in some breast tumors, could provide another avenue of treatment that could target just the cancer cells.

One study, published by Dr. C. Kent Osborne, director of the Lester and Sue Smith Breast Center at BCM, showed that women whose tumors have both the Her2/neu protein and high levels of SRC-3 are less likely to be helped by drugs such as tamoxifen and more likely to die quickly of their disease. Finding a way to stop Her2/neu and shut down SRC-3 could make the tumor cell's growth controllable, O'Malley said.

Others who took part in this work include Chao Li, Yao-Yun Liang, Xin-Hua Feng, Sophia Y. Tsia and Ming-Jer Tsai, all of BCM.

Funding for this study came from the National Institutes of Health and the Welch Foundation.

This report can be found at www.molecule.org.

For more information on basic research at Baylor College of Medicine, please go to www.bcm.edu/fromthelab.

Laura Arnold named to BCM Board of Trustees

HOUSTON -- (September 26, 2008) -- Baylor College of Medicine has named Laura Elena Muñoz Arnold, president of the Arnold Family Foundation, to its board of trustees.

The board announced the appointment Wednesday.

"Laura Arnold's business, legal and community service experience, along with her dedication to education initiatives, will be of great benefit to the college's leadership in planning our strategic missions," said Dr. Peter G. Traber, BCM president and CEO. "We are thrilled to have her as a trustee of the college."

A magna cum laude graduate of Harvard College and a graduate of Yale Law School, Arnold also has a master's of philosophy in European Studies from the University of Cambridge.

The Arnold Family Foundation, founded in 2004, supports education initiatives and social and human services programs.

Arnold also serves on the Houston regional board of Teach for America. She was a co-founder, executive vice president and general counsel at Houston-based Cobalt Energy International, a private equity exploration and production company. She joined Cobalt after working in the New York law firm of Wachtell, Lipton, Rosen & Katz, where she was a corporate attorney specializing in mergers and acquisitions.

Following graduation from the University of Cambridge, she was a professor of international relations in Mexico at the Centro de Estudios Profesionales de Chiapas "Fray Bartolomé de las Casas" and at the Instituto Tecnológico y de Estudios Superiores de Monterrey in Tuxtla Gutiérrez, Chiapas. During the 2000-2001 term, she clerked for the Honorable Judith W. Rogers of the U.S. Court of Appeals for the District of Columbia Circuit.