Welcome to the biweekly electronic newsletter from the Bio-X Program at Stanford University 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 Bio-X or Stanford.

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 113 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 tenfold-plus return on investment, as well as hundreds of publications, dozens of patents filed, and most importantly, the acceleration of scientific discovery and innovation.

In the spring of 2012, we will have a call for proposals for the 6th round of seed grants from our faculty. Competition is intense, and the criteria for the proposals include innovation, high-reward, and interdisciplinary collaboration. To view the different projects that have been funded, please click here.

Every year, two symposia are held at the Clark Center to showcase the seed grant projects. Talks that are presented at the symposia are recorded, and can be viewed here. The next IIP symposium will take place at the Clark Center on February 13, 2012.

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.

News

Study finds iPS cells match embryonic stem cells in modeling human disease
Bio-X affiliated faculty Michael Longaker
Stanford University School of Medicine investigators have shown that iPS cells, viewed as a possible alternative to human embryonic stem cells, can mirror the defining defects of a genetic condition — in this instance, Marfan syndrome — as well as embryonic stem cells can. An immediate implication is that iPS cells could be used to examine the molecular aspects of Marfan on a personalized basis. Embryonic stem cells, on the other hand, can’t do this because their genetic contents are those of the donated embryo, not the patient’s. This proof-of-principle regarding the utility of induced pluripotent stem cells also has more universal significance, as it advances the credibility of an exciting approach that’s been wildly acclaimed by some and viewed through gimlet eyes by others: the prospect of using iPS cells in modeling a broad range of human diseases. These cells, unlike ESCs, are easily obtained from virtually anyone and harbor a genetic background identical to the patient from which they were derived. Moreover, they carry none of the ethical controversy associated with the necessity of destroying embryos. “Our in vitro findings strongly point to the underlying mechanisms that may explain the clinical manifestations of Marfan syndrome,” said Michael Longaker, MD, professor of surgery and senior author of the study, which was published online Dec. 12 in Proceedings of the National Academy of Sciences. Longaker is the Dean P. and Louise Mitchell Professor in the School of Medicine and co-director of the school’s Institute for Stem Cell Biology and Regenerative Medicine. The study’s first author is Natalina Quarto, PhD, a senior research scientist in Longaker’s laboratory.

Study shows how nutrient levels affect enzyme associated with aging process
Bio-X affiliated faculty Anne Brunet
Restricting calorie intake extends life span in many species, and a new study at the School of Medicine helps illuminate how: Low-nutrient conditions activate an enzyme that helps cells complete their normal division process. The researchers discovered that an enzyme called AMPK, found in human cells, plays a role in choreographing the early steps of cell division. The enzyme’s response in restricted-nutrient conditions could be important during normal cell development and in stem or cancer cells, according to the study, which was published online Dec. 1 in Molecular Cell. Cells and organisms must be capable of thriving in a tempest of fluctuating energy levels. AMPK senses when nutrients are scarce, and initiates processes that stabilize the cell’s replication cycle, a function of the enzyme that hadn’t been known before. “We had shown in worms that AMPK is important for the link between dietary restriction and longevity,” said Anne Brunet, PhD, associate professor of genetics and senior author of the study. “This prompted us to investigate its role in mammals.” Studying human cells, the scientists circled in on the enzyme’s role in mitosis, the process cells use to divide their genetic material into two cells. Using a chemical screening method in living cells, the scientists identified 32 proteins directly modified by AMPK, 28 of which were previously unknown. Several of these are involved in cell division. “It’s the first time the screening method has been applied to the AMPK enzyme in living, human cells,” Brunet said.

Scar findings could lead to new therapies, researchers say
Researchers at the Stanford University School of Medicine report that they have identified the molecular pathway through which physical force contributes to scarring in mice. “Our study exposes one of the fundamental mechanisms by which the mechanical environment can directly increase inflammation, which is strongly implicated in scarring,” said Geoffrey Gurtner, MD, professor and associate chair of surgery. Mice genetically engineered to lack an enzyme that is activated by mechanical force demonstrated less inflammation and fibrosis — the formation of excess fibrous connective tissue — in their incisions than mice in a control group, the study found. Inflammation and scar formation also were reduced among mice injected with an organic compound, a small molecule called PF-573228, that blocks this enzyme, which helps cells sense changes in the mechanical environment. While further testing is needed to determine the validity of the findings in humans, the researchers say they hope their work will pave the way for new treatments of fibrotic diseases — disorders caused by scarring, such as pulmonary fibrosis (the buildup of scar tissue in the lungs) — as well as inflammatory diseases, such as rheumatoid arthritis.

Events

Resources

To learn more about Bio-X or Stanford University, please contact Dr. Hanwei Li, the Corporate Forum Liaison of Bio-X, 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.