Methicillin-resistant Staphylococcus aureus bacteria, commonly known as MRSA, pose a serious public health threat, causing more than 80,000 skin, lung, and blood infections and killing about 11,000 people annually in the United States . This microbe wreaks its devastation by secreting a toxin, alpha-hemolysin, that punches holes in the membrane of cells, essentially causing them to leak to death. Now, NIH-funded researchers from the University of California, San Diego, have created tiny sponges capable of trapping and binding MRSA’s toxin . When these toxin-laden sponges are injected into mice, they serve as a vaccine—that is, they stimulate the animal’s immune system in a way that protects them from the toxin’s deadly impact.
It would be terrific if we could turn off human genes in the laboratory, one at a time, to figure out their exact functions and learn more about how our health is affected when those functions are disrupted. Today, I’m excited to announce the availability of new data that will empower researchers to do just that on a genome-wide scale. As part of a public-private collaboration between the NIH’s National Center for Advancing Translational Sciences (NCATS) and Life Technologies Corporation, researchers now have access to a wealth of information about small interfering RNAs (siRNAs), which are snippets of ribonucleic acid (RNA) with the power to turn off a gene, or reduce its activity—in much the same way that we use a dimmer switch to modulate a light.
What on earth is this strange-looking critter? Well, among other things, it’s a scientific super model whose photo shoot landed it among the winners of the Federation of American Societies for Experimental Biology’s 2013 BioArt Competition. Researchers use this stingray-like sea creature, called Leucoraja erinacea or Little Skate, as a model organism for studying development.
This image, taken using a stereomicroscope with transmitted light, shows a 10-week-old Little Skate embryo attached to its nutrient-rich yolk sac. Because the skate can develop normally even when removed from its egg case, it provides an accessible system for exploring how genes direct the formation of internal organs.
The diversity found in the natural world can also reveal unexpected insights into human disease. For example, it turns out that the genes controlling development of the Little Skate’s fins are strongly influenced by male sex hormones. And this is the really surprising part: researchers have discovered that the genes activated in the skate fins are the same genes that respond to hormones in human prostate, breast, and skin cancers. So, by studying these genes in this bizarre-looking denizen of the deep, it’s possible to probe the genes that trigger disease in humans.
BioArt, Federation of American Societies for Experimental Biology
BioArt 2013 Exhibit. The public can view an exhibit of the winning art at the NIH Visitor Center. Located in Bethesda, MD, the Center is open from 8:30 a.m.–4:30 p.m. M–F.
NIH support: National Institute of Environmental Health Sciences; National Institute of Diabetes and Digestive and Kidney Diseases
Affecting an estimated 1 in 88 U.S. children, autism spectrum disorder (ASD) is a complicated and diverse group of developmental brain disorders that interfere with language, normal communication, and social interaction. Unlike some other conditions that are caused by mutations in a single gene, as many as 1,000 genes, as well as various environmental factors, are suspected to contribute to the risk of developing ASD. That’s daunting because before we can develop broadly-applicable treatments, we need to figure out which are the key genes, what brain cells they control, and when they are active.
If you’re concerned about your cardiovascular health, you’re probably familiar with “good” and “bad” cholesterol: high-density lipoprotein (HDL) and its evil counterpart, low-density lipoprotein (LDL). Too much LDL floating around in your blood causes problems by sticking to the artery walls, narrowing the passage and raising risk of a stroke or heart attack. Statins work to lower LDL. HDL, on the other hand, cruises through your arteries scavenging excess cholesterol and returning it to the liver, where it’s broken down.