Scientists at the Gladstone Institute of Cardiovascular Disease (GICD) and Stanford University School of Medicine will collaborate in a new consortium funded by the National Heart, Lung and Blood Institute (NHLBI) to develop stem cell and regenerative medicine therapies. GICD investigators, led by GICD Director Deepak Srivastava, MD, will collaborate with a Stanford team led by Robert Robbins, MD, professor and chair of cardiothoracic surgery, to investigate how to use induced pluripotent stem cells, or iPS cells, to repair damaged heart muscle.
Scientists at the Gladstone Institute of Cardiovascular Disease (GICD) will receive $10 million over the next 6 years to find the genetic causes of congenital heart disease. Congenital heart disease affects 1 percent of all children and often leads to death or long-term illness. The team of investigators, led by Benoit Bruneau, PhD, will focus on the gene networks that underlie the disease and the regulatory factors that turn on and off genes related to congenital heart defects (CHDs). GICD was one of four national centers awarded this highly competitive grant to address CHD at a genome-wide level.
Shinya Yamanaka, MD, PhD, of the the Gladstone Institute of Cardiovascular Disease (GICD) and Kyoto University, has won the 2009 Albert Lasker Basic Medical Research Award for his discovery of a method of reprogramming adult skin cells to become embryonic-like stem cells. Yamanaka, who is the L.K .Whittier Investigator in Stem Cell Biology at Gladstone, and professor of anatomy at UCSF, is one of the youngest recipients of the award, which is seen as a precursor to the Nobel Prize.
Scientists at the Gladstone Institute of Cardiovascular Disease (GICD) have traced the evolution of the four-chambered human heart to a common genetic factor linked to the development of hearts in turtles and other reptiles. The research, published in the September 3 issue of the journal Nature, shows how a specific protein that turns on genes is involved in heart formation in turtles, lizards and humans.
The J. David Gladstone Institutes announced a collaboration with Alitora Systems to develop software technology that facilitates organizational collaboration and enables rapid acceleration of the discovery and evaluation of new drugs. Alitora Systems uses semantic technology to search document and database information in a single collaborative innovation network. The Gladstone collaboration will assist in enhancing Alitora's product offerings for biotechnology and pharmaceutical discovery and development.
Researchers at the Gladstone Institute of Cardiovascular Disease (GICD) have discovered a key switch that makes stem cells turn into the type of muscle cells that reside in the wall of blood vessels. The same switch might be used in the future to limit growth of vascular muscle cells that cause narrowing of arteries leading to heart attacks and strokes, limit formation of blood vessels that feed cancers, or make new blood vessels for organs that are not getting enough blood flow.
Scientists at the Gladstone Institute of Cardiovascular Disease (GICD)have identified for the first time key genetic factors that drive the process of generating new heart cells. The discovery, reported in the current issue of the journalNature, provides important new directions on how stem cells may be used to repair damaged hearts.
Shinya Yamanaka, MD, PhD, of the Gladstone Institutes and Kyoto University is one of seven recipients of Canada's prestigious Gairdner Award. The Gairdner is referred to as the “Baby Nobel,” since many winners then go on to win the Nobel Prize.
Scientists at the Gladstone Institutes of Cardiovascular Disease (GICD) have found that a key enzyme involved in absorbing fat may also be a key to reducing it. The enzyme, acyl CoA: monoacylglycerol acyltransferase 2 or Mgat2 is found in the intestines and plays an important part in the uptake of dietary fat by catalyzing a critical step in making triglyceride, a kind of fat. Triglyceride accounts for nearly one-third of the fat eaten by people in developed countries.
Researchers at the Gladstone Institute of Cardiovascular Disease (GICD) and the University of California, San Francisco have unraveled a complex signaling process that reveals how different types of cells interact to create a heart. It has long been known that heart muscle cells (cardiomyocytes) actively divide and expand in the embryo, but after birth this proliferative capacity is permanently lost. How this transition occurs has not been known. In the current issue of the journal Developmental Cell, the scientists show that the secret to this switch lies in the cells that surround the muscle cells, known as fibroblasts, which send signals that tell cardiomyocytes to divide or get bigger in size. Manipulation of these signals may be able to induce cardiomyocytes to divide again for regenerative purposes after heart attacks.