These stories describe NIGMS-funded medical research projects. Although only the lead scientists are named, they work together in teams to do this research.
Poor sanitation and disasters like earthquakes and tsunamis can promote the spread of cholera, a water-borne, diarrheal disease that annually kills tens of thousands of people. Scientists devised a quick, inexpensive way to detect cholera toxin that might help limit the spread of the disease.
The new technique uses a special sugar and microscopic beads called nanoparticles. About 100 million nanoparticles lined up would measure just a millimeter.
A team led by chemist J. Manuel Perez at the University of Central Florida in Orlando created nano-particles coated with the sugar dextran, which resembles the receptor the cholera toxin uses to invade intestinal cells. If cholera toxin is present in a water sample, it will bind to the sugar-coated nanoparticle and is then easily detected by a handheld machine.
The test would allow relief workers to identify contaminated water on the spot, instead of having to send samples to a lab. Workers could then restrict access to such water more quickly, possibly preventing a cholera epidemic.
The technique might also be adapted as an inexpensive cholera treatment that would be particularly valuable in the developing world. —Erin Fults
You may never have heard of ARDS (acute respiratory distress syndrome), but it is a leading cause of death in intensive care units. Doctors don't know exactly what triggers it, and there are no specific drugs to treat it.
ARDS often follows a serious injury or infection. It begins when an overzealous inflammatory response floods the lungs with fluid, preventing oxygen uptake and causing major organ failure.
Immunologist Laurie Kilpatrick at Temple University School of Medicine in Philadelphia may have discovered how to rein it in. By studying ARDS in rats, she was able to prevent many of its symptoms by blocking the action of a specific enzyme.
This enzyme, known as deltaprotein kinase C, activates white blood cells called neutrophils. Part of our first-line defenses, neutrophils spew out toxins to kill bacteria and other invaders. These chemicals also inflame nearby tissues. Blocking delta-protein kinase C shuts down neutrophils and seems to halt the cascade of inflammation.
The finding points to a possible drug target for ARDS and could also help explain what causes this out-of-control inflammatory reaction. —Hadley Leggett
For the first time, researchers have coaxed human cells to form 3-D tissues that look and work like organs.
The "organoids" function like intestines. They contain all the major intestinal cell types and display characteristic intestinal structures, including fingerlike projections. They are able to absorb nutrients and secrete proteins, just like our own intestines.
Developmental biologist James Wells and his team at Cincinnati Children's Hospital Medical Center created one batch of organoids from human embryonic stem cells and one from induced pluripotent stem (iPS) cells. Like embryonic stem cells, iPS cells, which came from human skin biopsies, can turn into virtually any cell type in the body.
The two cell types were put in separate laboratory containers and exposed to growth-promoting proteins. Within a month, the cells in each container morphed into four different cell types and formed a tissue that resembled a fetal intestine.
The study will shed light on how human intestines develop and function. The work might also be useful in treating certain bowel diseases or designing drugs that are more easily absorbed through the intestines. —Erin Fults
Whether you are well nourished—even before you become a parent—might affect the health of your descendants.
Researchers observed decades ago that if food was scarce during a man's lifetime, his grandchildren had higher-than-average rates of diabetes, obesity and cardiovascular disease.
Clearly, the descendants were inheriting something that increased their risk of these diseases, but what was it? Normally, gene sequences are passed unchanged from parent to child.
A new study by biochemist Oliver Rando of the University of Massachusetts Medical School suggests that changes in the activity of genes—seemingly without changes in their DNA sequence—might be responsible.
Rando found that when male mice were fed a low-protein diet, the activity of hundreds of genes in the animals' offspring changed. In particular, genes that manufacture fats were more active. Making too many fats can lead to obesity and related diseases. These same genes also displayed an altered pattern of chemical tags that regulate gene activity through a process called epigenetics.
Scientists are still trying to understand how epigenetic changes occur and how such changes might affect the metabolism and disease risks of future generations. —Kirstie Saltsman