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The National Institute of General Medical Sciences (NIGMS), one of the National Institutes of Health, supports all research featured in this digest. Although only the lead scientists are named, coworkers and other collaborators also contributed to the findings.

In This Issue... August 16, 2012

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Screenshot from the Re-creating Kidneys video

Cool Video: Re-creating Kidneys

Alejandro Sánchez Alvarado • Stowers Institute for Medical Research

About the size of toenail clippings, planarians are freshwater flatworms that can re-form from tiny slivers. This feature not only lets them repair themselves, but it lets them reproduce by breaking apart and then creating new worms. Many planarian bodily systems operate like ours. By studying how these features are reconstituted as the worms regenerate, scientists might move one step closer to replacing human tissue and cells lost to disease or injury. This image shows a cross-section of a flatworm. The magenta clusters and green specks throughout the planarian are structures that push waste toward bile ducts. The structures, which comprise the animal's excretory system, are like our kidneys in that they are lined with specialized cells. The ducts employ filtration methods similar to our kidneys, too. One key difference, though, is that flatworms can regenerate their excretory systems from next to nothing. To better understand how this regeneration happens, researchers removed the heads from planarians and watched as new excretory systems grew within a week. They uncovered a gene, EGFR5, that is necessary for the excretory structures to re-form during regeneration and for maintaining them in the intact animal. Studying similar genes in mammals could shed light on how we maintain our kidneys—and might repair damaged ones. Read more... Link to external Website

Zinc-finger nucleases (pink, orange, red and blue) crossing cell membranes. Credit: Carlos Barbas, Scripps Research Institute.

Scientists Put a Finger on How to Cut DNA Safely

Carlos Barbas • Scripps Research Institute

Zinc-finger nucleases (ZFNs) are genetically engineered proteins that bind and cut DNA within cells to disrupt specific genes. Since the development of ZFNs as research tools, scientists have used viruses to deliver them into cells, but the use of viruses has been linked to unintended damage to the cells' genetic material and other potentially serious complications. But research now shows that ZFNs can enter cells unassisted. Using this approach, scientists effectively disrupted a gene HIV needs to enter cells, without causing collateral damage to the host genome. This technique paves the way for the development of a new strategy for treating HIV infection and other diseases. Read more... Link to external Website

This work also was supported by the NIH Common Fund.

Caption: Zinc-finger nucleases (pink, orange, red and blue) can cross the inner and outer membranes of cells to make changes to the DNA inside the nucleus. Credit: Carlos Barbas, Scripps Research Institute. High res. image (JPG, 179KB)
Eternal clock

Researchers Find Molecule that Helps Control Biological Clock

Steve A. Kay • University of California, San Diego

The biological clock controls daily behaviors like sleeping and waking, as well as physical processes like cyclical patterns of metabolic activity. To keep our blood sugar levels in the normal range, the clock helps stimulate the liver's glucose production during times of the day when we're not eating, for instance, during sleep. A chemical, KL001, appears to slow the clock and inhibit sugar production in liver cells. Scientists learned that KL001 works by binding and preventing the breakdown of a known clock protein, cryptochrome. Their finding could suggest a new approach for treating diabetes, a metabolic disease linked to aberrant blood glucose levels. Read more... Link to external Website

This work also was supported by NIH's National Institute of Mental Health.

Caption: Some proteins affect the body's biological clock, which governs processes like glucose production.
X-ray of human hands with rheumatoid arthritis

Researchers Identify Enzyme's Role in Inflammation

Kevin Tracey • The Feinstein Institute for Medical Research

When cells detect signs of infection, they activate a protein complex called the inflammasome, which triggers inflammation. This defense response is necessary, but, if persistent, it can be harmful and cause arthritis, colitis and other diseases. Offering a potential new drug target for inflammation-related illnesses, researchers have identified another player in the inflammasome activation pathway: an enzyme dubbed PKR. When the scientists turned PKR off by deleting the gene or inhibiting the enzyme with chemicals, the inflammasome was unresponsive to its usual inducers and failed to set off inflammation.

This work was also supported by NIH's National Institute of Diabetes and Digestive and Kidney Diseases.

Caption: Rheumatoid arthritis is a disease associated with chronic inflammation.High res. image (JPG, 97KB)
Copper deposits

Copper Finds Another Way Out of the Body

Svetlana Lutsenko • Johns Hopkins University School of Medicine

Like many other metals, copper is necessary for maintaining human health, but too much can impair organ function. The body usually rids itself of excess copper by excreting it through the liver's bile. But in people with Wilson's disease, a condition in which a defective copper exporter leads to excess copper and liver damage, the metal also leaves the body through urine. By studying a mouse model of Wilson's disease, a group of collaborative researchers discovered a small molecule that transports copper to the kidneys. This small molecule might eventually form the basis for a diagnostic test as well as a possible treatment for Wilson's disease. Read more... Link to external Website

This work was also supported by NIH's National Institute of Diabetes and Digestive and Kidney Diseases.

Caption: In nature, copper is found in rocks and deposits. In the body, copper is essential for processes like respiration, cardiovascular function and neurological signaling.

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This page last reviewed on August 16, 2012