These stories describe NIGMS-funded medical research projects. Although only the lead scientists are named, they work together in teams to do this research.
Bears hibernate in caves and toads burrow into the ground to protect themselves against harsh conditions. Bacteria take a different tack: They split off a small compartment called a spore. Spores are dormant structures that resist heat, chemicals, radiation and dehydration. When conditions become favorable, the bacterium exits the spore and grows again.
The structure of the spore's protective shell is key to its survival. This shell contains 70 different proteins in concentric layers. Until now, scientists didn't know how the proteins were arranged.
Biologist Patrick Eichenberger and his team at New York University used fluorescent green chemical tags, a microscope and computer analysis to build a map showing the location of spore proteins.
The scientists discovered that spores have four protective layers, including an outer crust never described before.
The soil bacterium the scientists studied doesn't cause any diseases, but its spores are structurally similar to those of the bacteria that cause botulism, tetanus and anthrax.
The research will improve our understanding of these organisms, perhaps leading to new ways to prevent the diseases they cause. —Janelle Weaver
You might use acetaminophen, or Tylenol®, to treat aches and mild fevers. But this inexpensive medicine might also have a role in life-threatening situations like earthquakes, car accidents and war zones to counter a hidden danger—kidney damage.
When people survive major traumatic injuries, it's not uncommon for them to develop kidney failure. That's because when skeletal muscles are seriously injured, their cells burst and dump their contents into the bloodstream. The released contents include proteins, particularly one called myoglobin, that can severely damage the kidneys.
Researchers at Vanderbilt University in Nashville, Tennessee, discovered that if they gave acetaminophen to rats before or after muscle injury, it could alleviate such kidney damage. The doses that worked in rats are comparable to doses that are safe in humans.
If clinical trials prove that the treatment is safe and effective in people, acetaminophen might become a lifesaver in places that lack hospitals and medical equipment—like the sites of natural disasters. The researchers think it might also help prevent similar kidney and tissue damage caused by sickle cell disease, malaria and heart attacks. —Karin Jegalian
If you've ever gotten the flu, you know that we don't have many drugs to treat it. New information from scientists studying one antiflu medicine, amantadine, may pave the way for designing more such drugs.
Biophysicists Mei Hong at Iowa State University and William DeGrado at the University of Pennsylvania discovered how amantadine interacts with a flu protein called M2. This protein launches infection by creating a channel between the flu virus and a healthy cell.
When the researchers determined the detailed, 3-D structure of amantadine bound to M2, they revealed that the drug plugs this channel, preventing infection. They also noticed that amantadine fits loosely inside M2, possibly leaving room for altered versions of the protein to wiggle free and go on to infect a cell. If virus particles containing this version of M2 multiplied, they could lead to a drug-resistant strain.
Already, many strains of the flu resist treatment by amantadine. The biophysicists think that designing drugs that fit into M2 more tightly than amantadine does could provide an effective treatment for the flu that is more difficult for the virus to resist. —Kirstie Saltsman
You've probably heard that scientists have sequenced the entire human genome. But what does this mean for you? If your doctors knew the identity and order of all 3 billion letters in your genome, what could it tell them?
That's what researchers wanted to know. One of them, bioengineer Stephen Quake at Stanford University, volunteered his genome sequence for the study.
He and his colleagues used computer searches to find diseaserelated gene variants. They then analyzed his medical and family history. They even factored in statistical disease risks.
After all the number crunching, they found he had a higher-thanaverage risk for developing a handful of conditions, including heart attacks, thyroid disease, iron overload and certain cancers. Some of these run in his family and some don't. Also, he might respond poorly to certain heart medications—something good to know since he's at increased risk for heart problems.
With this study, the researchers have shown that a person's complete genome sequence can yield clinically useful information. But many challenges remain, including understanding the influence of a person's environment, which can change over time. —Alisa Zapp Machalek