Research Report: New class of antimalarial compounds uncovered

By Lynne Friedmann

An international team led by the Genomics Institute of the Novartis Research Foundation and The Scripps Research Institute has discovered a family of chemical compounds that could lead to new antimalarial drugs.

When a malaria-infected mosquito bites a person, the Plasmodium parasite enters the human body where it begins a complicated life cycle: first infecting liver cells, then entering red blood cells where it grows and multiplies eventually releasing toxins that cause illness and in severe cases death. Most antimalarial drugs are only effective during the parasite’s blood stage, and those that work in the liver have notable side effects.

In the new study, researchers screened thousands of candidate compounds known to act against malaria parasites in the blood. Of these, 15 percent looked like they might also work in the liver. Researchers then identified the strongest drug-development candidates by mining the data for groups of related compounds that showed liver activity. This led to a cluster shown to be activity in both the blood and liver stages of the parasite. These compounds have the additional advantage of being chemically unrelated to current antimalarial drugs, and therefore less likely to face existing drug resistance.

Findings appear in Science Express. News release at http://bit.ly/udJy7Q.

Disease linked to wind currents

Kawasaki Disease (KD) is a serious childhood disease often mistaken for an inconsequential viral infection. Tragically, if not diagnosed or treated in time, KD can lead to irreversible heart damage. In surprising findings, an international team of scientists suggest that KD cases are linked to large-scale wind currents that track from Asia to Japan and also traverse the North Pacific.

Because of seasonality of the disease in many regions (including San Diego), an international team including researchers from the UCSD School of Medicine, Rady Children’s Hospital, and the Scripps Institution of Oceanography, investigated a set of atmospheric and oceanographic measures, which revealed a link to pressure patterns and associated wind flow during the months prior to major KD epidemics in Japan in 1979, 1982, and 1986.

Wind currents, which can cross the Pacific in less than one week, may explain why KD cases recorded in Japan, San Diego, and Hawaii show a nearly synchronized seasonal peak from November through March. The findings could aid efforts to isolate the cause of KD, which so far has eluded health officials.

The paper appears in Scientific Reports.  More information at http://bit.ly/sLwEd5.

Heart defects in Down Syndrome

A study involving fruit flies and mice has pinpointed two genes responsible for congenital heart defects; a major cause of infant mortality and death in people born with Down syndrome.

Researchers from UCSD, the Sanford-Burnham Medical Research Institute, and the University of Utah report that the genes, when produced at elevated levels, work together to disrupt cardiac development and function.

Down syndrome occurs when individuals have three, instead of the usual two, copies of human chromosome 21. Studies have identified a region of chromosome 21 (called DS-CHD) that plays a critical role in causing congenital heart defects in those with Down syndrome. But identifying the culprit genes is challenging using traditional experimental models. Instead, scientists devised an approach to successfully untangle the problem by first testing fruit flies for all possible pair-wise genetic interactions that might disrupt the function of the simple, fluid-pumping fly heart. After candidates pairs were found, researchers tested the effects of increasing the levels of corresponding genes in the hearts of experimental mice.

The findings appear in the online journal PLoS Genetics. News release at http://bit.ly/sd6sZ5.

Lynne Friedmann is a science writer based in Solana Beach.

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Posted by Staff on Nov 27, 2011. Filed under Research Report. You can follow any responses to this entry through the RSS 2.0. You can leave a response or trackback to this entry

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