As part of the commitment to efficient and effective paperless clinical trials, Target Health will be releasing Target e*CTMS in early October. Target e*CTMS will be residing in our new portal and will take a clinical trial from “cradle to grave.” There will be project management, financial management and even the ability to draw data from other EDC applications. We are building the software collaboratively with another CRO, confirming that we are the only eCRO to CROs.

For more information about Target Health or any of our software tools for clinical research, please contact Dr. Jules T. Mitchel or Ms. Joyce Hays. Our software tools are designed to partner with both CROs and Sponsors.

Target Health is pleased to announce that Dr. Mitchel will be speaking at The Second Annual Skin Workshop, entitled “New Developments in Dermaceuticals and Wound Care.” The meeting will take place on Tuesday September 30, 2008 (10:00 AM – 4:00 PM) at The New Jersey Center for Biomaterials (145 Bevier Road, Piscataway, NJ 08854. The meeting is being co-sponsored by Dr. Bozena Michniak-Kohn, Director of the Laboratory for Drug Delivery, The New Jersey Center for Biomaterials, and The New Jersey Chapter of the Controlled Release Society and Hill Top Research. Good meeting for those interested in Dermatology.

Marauding 1) ___ cause the tissue damage that underlies heart attacks, sunburn, Alzheimer’s and hangovers. But scientists at the Stanford University School of Medicine say they may have found ways to combat the carnage after discovering an important cog in the body’s molecular detoxification machinery. The culprit molecules are 2) ___ by-products called free radicals. These highly unstable molecules start chain reactions of cellular damage – an escalating storm that ravages healthy tissue. A totally new pathway for reducing the damage caused by free 3) ___, such as the damage that happens during a heart attack, has been found. Before the study, scientists knew that heart muscle could be preconditioned by alcohol to resist heart attack damage; for instance, it is known that moderate drinkers tend to have smaller, less severe heart attacks than teetotalers. But scientists didn’t understand how pre-conditioning worked. To figure out how alcohol protects heart 4) ___ from free-radical damage, the Stanford team tested alcohol pretreatment in a rat heart-attack model. They compared the enzymes activated during the attacks to those switched on with no alcohol. Surprisingly, the treatment activated aldehyde dehydrogenase 2 (ALDH2), an obscure alcohol-processing 5) ___. Alcohol pretreatment increased the enzyme’s activity during heart attack by 20%, leading to a 27% drop in the associated damage. Although this enzyme was discovered a long time ago, this research group knew nothing about the enzyme except that it helps remove 6) ___ when people drink. The enzyme 7) ___ an aldehyde molecule, a toxic byproduct of the ethanol in alcoholic beverages. But aldehydes are also formed in the body when free radicals react with fat molecules. It’s very easy for free radicals to find 8) ___ and oxidize it to aldehydes. Inside cells, the accumulating aldehydes permanently bind and damage cellular machinery and DNA. Such damage occurs in many diseases, from heart attack and Parkinson’s to sun-induced aging of the skin. After learning of ALDH2’s novel role in reducing the damage, the team searched for a molecule that could make the enzyme function even better. They enlisted the Stanford High Throughput Bioscience Center, to find a molecule that heightened the enzyme’s activity. The winner of this contest was a tiny molecule that reduced heart attack 9) ___ by 60% in the rat model. The molecule, Alda-1, has a surprising mode of action: it protects ALDH2 itself from aldehyde attack. The enzyme, it turns out, was being hobbled by the very 10) ___ it removes. Because Alda-1 is small, it should be easy to adapt for pharmacological use. So far, Alda-1 has been tested only in the rat model, but the Stanford lab is investigating other possible applications, such as fighting neurodegenerative disease and sun damage on the skin. In addition to its lofty medical applications, Alda-1 could also have a much lowlier use: fighting hangovers. Many nasty hangover symptoms are due to aldehyde buildup. The tiny molecule may also improve alcohol tolerance and reduce susceptibility to free-radical diseases in people with a common ALDH2 mutation. The mutation affects 40% of people of Asian descent and causes an 11) ___ for alcohol.

ANSWERS: 1) molecules; 2) oxygen; 3) radicals; 4) muscle; 5) enzyme; 6) alcohol; 7) neutralizes; 8) fat; 9) damage; 10) chemical; 11) intolerance