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The National Institutes of Child Health and Human Development awarded Phase I and Phase II Small Business Innovative Research Grants to develop The Visible Embryo in 1993 as a first generation internet teaching tool consolidating human embryology teaching for first year medical students.

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Programmed destruction

Weizmann Institute results show the same signaling enzymes can trigger two different processes in the cell sound a warning to biomedical researchers.

Stroke, heart attacks and numerous other common disorders result in a massive destruction of cells and tissues called necrosis. It’s a violent event: As each cell dies, its membrane ruptures, releasing substances that trigger inflammation, which in turn can cause more cellular necrosis. A new Weizmann Institute study may help develop targeted therapies for controlling the tissue destruction resulting from inflammation and necrosis.

The study, conducted in the laboratory of Prof. David
Wallach of the Biological Chemistry Department, focused
on a group of signaling enzymes, including caspase 8,
which was discovered by Wallach nearly two decades ago.
Earlier studies by scientists in the United States, China and
Europe had shown that this group of proteins induces
“programmed,” or deliberate, necrosis intended to
kill off damaged or infected cells.

This revelation had generated the hope that by blocking the induction of necrotic cell death by these proteins, it might be possible to prevent excessive tissue damage in various diseases. But in the new study, reported in Immunity, Wallach’s team sounds a warning.

Research has revealed that under conditions favoring
inflammation—that is, in the presence of certain bacterial
components or other irritants—the same group of signaling
enzymes can trigger an entirely different process in certain
cells. It can activate a previously unknown cascade of
biochemical reactions that causes inflammation more directly,
without inducing necrosis, by stimulating the production
of hormone-like regulatory proteins called cytokines.

The research, mainly based on experiments in transgenic mice lacking caspase 8 in certain immune cells, was spearheaded by postdoctoral fellow Dr. Tae-Bong Kang. Team members Seung-Hoon Yang, Dr. Beata Toth and Dr. Andrew Kovalenko made important contributions to the study.

These findings suggest that prior to developing targeted necrosis-controlling therapies, researchers need to learn more about the signals transmitted by caspase 8 and its molecular partners, as this signaling can lead to several entirely different outcomes.

The scientists need to determine when exactly it results directly in necrosis and when it does not. Clarifying this matter is of enormous importance. Tissue necrosis occurs in a variety of disorders affecting billions of people, from the above-mentioned stroke and heart attack to viral infections and alcoholism-related degeneration of the liver.

Prof. David Wallach’s research is supported by the Leona M. and Harry B. Helmsley Charitable Trust; and Merck Serono. Prof. Wallach is the incumbent of the Joseph and Bessie Feinberg Professorial Chair.

Original article: http://wis-wander.weizmann.ac.il/programmed-destruction#.UUbdbxegJ8E