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September 16, 2009
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A blue laser beam turns on a protein that helps this human cancer cell move. Responding to the stimulus, the protein, called Rac1, first creates ruffles at the edge of the cell. Then it stretches the cell forward, following the light like a horse trotting after a carrot on a stick. This new light-based approach can turn Rac1—and potentially many other proteins—on and off at exact times and places in living cells. By manipulating a protein that controls movement, the technique also offers a new tool to study embryonic development, nerve regeneration and cancer. Courtesy of Yi Wu, the Hahn lab, University of North Carolina.
Up to one-third of people who take the anti-clotting drug Plavix (clopidogrel) to lower their risk of experiencing a heart attack or stroke don't respond to the medicine. Now, University of Maryland School of Medicine geneticist Alan Shuldiner has found a gene variant that's partly to blame. By scanning genetic markers in hundreds of study participants, Shuldiner found that about one in three people share a variation in a gene previously linked to Plavix responsiveness. The variant is less effective at activating Plavix in the body, doubling people's risk of complications from blocked arteries. Next up: searching for additional genes at play.
NIH's National Heart, Lung and Blood Institute also supported this work.
Plasmodium falciparum, the parasite that causes malignant malaria, is responsible for most of the half-billion malaria infections and almost all of the 1.5 million malaria deaths every year. Researchers including University of Massachusetts Amherst entomologist Stephen Rich studied related parasites in chimpanzees to find out when and how malignant malaria originated in humans. Rich, formerly of the University of California, Irvine, traced all human strains of the parasite back to a single chimpanzee strain that may have jumped species through a mosquito as recently as 5,000 years ago. The finding could help researchers develop a malaria vaccine and provide insight into how infectious diseases transmit from animals to humans.
NIH's Fogarty International Center and Director's Pioneer Award also supported this work.
Full story (no longer available)
Article abstract (from the August 3 issue of PNAS)
Some cells are able to push through tough barriers called basement membranes to carry out important tasks—and so can cancer cells, when they spread from one part of the body to another. No one has been able to recreate basement membranes in the lab and they're hard to study in humans, so Duke University researchers led by biologist David Sherwood turned to the simple worm C. elegans. Sherwood identified two molecules that help certain cells orient themselves toward and then punch through the worm's basement membrane. Studying these molecules and the genes that control them could deepen our understanding of cancer spread.
University of Michigan chemical engineer Lola Eniola-Adefeso is trying to create a more efficient heart disease treatment with the help of synthetic white blood cells—hollow plastic beads that look like bubble gum under the microscope. Meanwhile, Connecticut College biochemist Marc Zimmer is investigating why green fluorescent protein (GFP) shines and looking for ways to design brighter proteins to image live organisms, all while he inspires students with glowing animals and exotic field trips. Read more about these envelope-pushing chemists in the September 2009 issue of Findings.