Welcome to the biweekly electronic newsletter from Stanford Bio-X for members of the Bio-X Corporate Forum. Please contact us if you would like to be added or removed from this distribution list, or if you have any questions about Stanford Bio-X or Stanford University.

Seed Grant Program

SEED GRANTS FOR SUCCESS - Stanford Bio-X Interdisciplinary Initiatives Program (IIP)

The Bio-X Interdisciplinary Initiatives Program represents a key Stanford Initiative to address challenges in human health. The IIP awards approximately $3 million every other year in the form of two-year grants averaging about $150,000 each. From its inception in 2000 through the fifth round in 2010, the program has provided critical early-stage funding to 114 different interdisciplinary projects, involving collaborations from over 300 faculty members, and creating over 450 teams from five different Stanford schools. From just the first 4 rounds, the IIP awards have resulted in a 10-fold-plus return on investment, as well as hundreds of publications, dozens of patents filed, and most importantly, the acceleration of scientific discovery and innovation.

The list of 23 awardees for the 6th round of seed grants from 2012 are listed on the Stanford Bio-X website. Please go here to view the list of awardees, along with the titles of their projects and the abstracts of the research. Competition was intense as the awardees were chosen from 118 Letters of Intent (LOIs). Selection criteria included innovation, high-reward, and interdisciplinary collaboration. To view the 114 other IIP projects that have been funded from the first 5 rounds, please click here.

** UPDATE: Sanofi funds 4 new Bio-X IIP Seed Grant projects!

** SAVE THE DATE: ON MONDAY, FEBRUARY 25, 2013, STANFORD BIO-X WILL BE HOLDING ITS NEXT ANNUAL IIP SEED GRANT SYMPOSIUM AT THE CLARK CENTER. The symposium will include 8 podium presentations (or see below under "EVENTS"), followed by a poster session at the end (poster titles coming soon). The IIP symposiums are always well-attended, with the last one in August having over 200 attendants. To view previously recorded talks, please go here.

We are cultivating and are highly successful in building meaningful collaborations with numerous corporate colleagues. New collaborations through our seed grant projects are highly encouraged. To learn about how to get involved, please contact Dr. Hanwei Li or Dr. Heideh Fattaey.

Fellowships

BIO-X FELLOWSHIPS

Every year, graduate students and postdoctoral scholars of Bio-X affiliated faculty are highly encouraged to apply for the Bio-X Fellowships, which are awarded to research projects that are interdisciplinary and utilize the technologies of different fields to solve different biological questions. Students are encouraged to work collaboratively with professors of different departments, thus creating cross-disciplinary relationships among the different Stanford schools. Our fellows have conducted exciting research, resulting in publications in high-impact journals and have been offered excellent positions in industry and academia.

** On Thursday, June 21, 2012, our 18 newest Bio-X Fellowship awardees were announced at the BIO-X FELLOWS SYMPOSIUM. The symposium also consisted of four 15-minute presentations and thirty-five 1-minute research introductions that truly demonstrated the synergy of different yet distinctive disciplines, merged together to address various life bioscience questions. To date, we now have a total of 126 Bio-X Fellows. To view the numerous projects that have been awarded over the years, please click here.

Many fruitful collaborations and relationships have been established with industry through these fellowships. Please contact Dr. Hanwei Li or Dr. Heideh Fattaey if you'd like to learn more about how to get involved with the Bio-X Fellowships.

News

Tuberculosis may lurk in bone marrow stem cells of infected patients, researchers say
Bio-X Affiliated Faculty Dean Felsher

Tuberculosis is a devastating disease that kills nearly 2 million people worldwide each year. Although antibiotics exist that can ameliorate the symptoms, the courses of therapy last for months and don't completely eradicate the disease, which frequently recurs years or decades after the initial treatment. Now, in a classic case of bench-to-bedside research, scientists at the Stanford University School of Medicine have discovered a possible reason for the disease's resistance: The ability of the tuberculosis bacteria to infiltrate and settle down in a particular class of stem cell in the bone marrow. By doing so, the bacteria take advantage of the body's own mechanisms of self-renewal. "Cancer scientists have noted that self-renewing stem cells like these in the bone marrow have properties — such as natural drug resistance, infrequent division and a privileged immune status — that make them resistant to many types of treatment," said Dean Felsher, MD, PhD, professor of oncology and of pathology. "Now it turns out that this ancient organism, Mycobacterium tuberculosis, figured out a long time ago that, for the same reasons, these cells are ideal hosts to invade and in which to hide." Not only did the scientists find genetic material from the bacteria inside the stem cells, they were also able to isolate active bacteria from the cells of human patients with tuberculosis who had undergone extensive treatment for the disease. The findings raise the possibility that other infectious agents may employ similar "wolf-in-stem-cell-clothing" tactics. And, although any new human treatments are likely to still be years away, they suggest a new possible target in the fight against tuberculosis, which infects nearly 2.2 billion people worldwide. ... Felsher is a co-senior author of the study, which was published online Jan. 30 in Science Translational Medicine. [Bikul] Das is the lead author. The research was conducted in collaboration with scientists from the Forsyth Institute in Cambridge, Mass.; the Hospital for Sick Children in Toronto; and several research groups in India.

'Rhythm' of protein folding encoded in RNA, Stanford biologists find
Bio-X Affiliated Faculty Judith Frydman

Your average musical melody doesn't chug along at a single, mechanical speed. It mixes whole notes, quarter notes, sixteenth notes and so on to lay out a specific, complex rhythm. It looks like protein synthesis may work the same way. The sequence of events is elegant: proteins are assembled when ribosomes match mRNA sequences up with specific tRNA molecules. Those tRNAs carry specific amino acids that link together in a chain to form a specific protein. But multiple RNA sequences can encode the same amino acid – some that are translated quickly, and some slowly. Although they all result in proteins with identical composition, the choice of mRNA sequence can dramatically change the rate at which the protein is made. Research from Stanford biology Professor Judith Frydman and researcher Sebastian Pechmann now reveals that this protein synthesis "rhythm" may be evolutionarily adjusted to control the folding of the new protein chain as it emerges from the ribosome. The finding may explain how RNA sequences define the final, folded form of a protein – a fundamental problem in molecular biology, since proteins need to fold in order to function. "For around 50 years, there has been a conceptual gap between the sequence and the final structure," said Pechmann, a postdoctoral scholar in the Frydman Lab. "There's been the sense that there's much more information in the sequence than can be deciphered at the moment." Published online in advance of print last month in the journal Nature Structural and Molecular Biology, the paper analyzes 10 closely related yeast species as a model. Both fast ("optimal") and slow ("non-optimal") codons are evolutionarily conserved, consistently appearing in particular parts of the mRNA transcript, where they appear to strategically slow down or speed up translation. "What they are doing is setting a tune for protein folding," said Frydman.

Beta carotene may protect people with common genetic risk factor for type-2 diabetes, researchers find
Bio-X Affiliated Faculty Atul Butte

Stanford University School of Medicine investigators have found that for people harboring a genetic predisposition that is prevalent among Americans, beta carotene, which the body can convert into vitamin A, may lower the risk for the most common form of diabetes, while gamma tocopherol, the major form of vitamin E in the American diet, may increase risk for the disease. The scientists used a “big data” approach to hunt down interactions between gene variants previously associated with increased risk for type-2 diabetes and blood levels of substances previously implicated in type-2 diabetes risk. In people carrying a double dose of one such predisposing gene variant, the researchers pinpointed a highly statistically significant inverse association of beta carotene blood levels with type-2 diabetes risk, along with a suspiciously high positive association of gamma tocopherol with risk for the disease. “Type-2 diabetes affects about 15 percent of the world’s population, and the numbers are increasing,” said Atul Butte, MD, PhD, associate professor of systems medicine in pediatrics. “Government health authorities estimate that one-third of all children born in the United States since the year 2000 will get this disease at some point in their lives, possibly knocking decades off their life expectancies.”Butte is the senior author of the new study, published online Jan. 22 in Human Genetics. The first author, Chirag Patel, PhD, is a former graduate student in Butte’s lab and now a postdoctoral scholar at the Stanford Prevention Research Center.

Events

Resources

To learn more about Stanford Bio-X or Stanford University, please contact Dr. Hanwei Li, the Bio-X Corporate Forum Liaison, at 650-725-1523 or lhanwei1@stanford.edu, or Dr. Heideh Fattaey, the Executive Director of Bio-X Operations and Programs, at 650-799-1608 or hfattaey@stanford.edu.