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FDA Recommends Gardasil Recipients Sit, Lie Down After Receiving Vaccination
In a posting aimed at health care professionals, FDA on its Web site on Wednesday said that recipients of Merck"s human papillomavirus vaccine, Gardasil, should be closely observed afterward for 15 minutes while they remain seated or lying down to avoid the possibility of fainting, the Wall Street Journal reports. FDA said that since October 2007, Gardasil"s labeling for both health care providers and patients has included a discussion about fainting. The agency said the strengthened recommendation comes in response to reports of "traumatic injuries" among some recipients who experienced fainting (Corbett Dooren, Wall Street Journal, 6/10). Gardasil protects against the strains of HPV that cause most cases of cervical cancer and genital warts. The Centers for Disease Control and Prevention recommends that girls ages 11 and 12 receive the three-dose vaccine before they are sexually active. Girls and women ages 13 to 26 who have not been vaccinated or completed the vaccine series also should receive the vaccine (CDC fact sheet, June 2008). On Wednesday, FDA also approved changes to Gardasil materials that place warnings about fainting in a more prominent place on drug labels and handouts. The agency said that the new recommendations are intended to "prevent falls and injuries" (Wall Street Journal, 6/10).
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New Path For Cocaine Addiction Research
Cocaine is one of the oldest drugs known to humans, and its abuse has become widespread since the end of the 19th century. At the same time, we know rather little about its effects on the human brain or the mechanisms that lead to cocaine addiction. The latest article by Dr. Marco Leyton, of the Montreal Neurological Institute (MNI), McGill University and the McGill University Health Centre, which was published in the journal Biological Psychiatry on May 15, 2009, not only demonstrates a link between cocaine and the reward circuits in the brain but also associates the susceptibility to addiction with these mechanisms.
Cardiovascular

Viral Mimic Induces Melanoma Cells To Digest Themselves

Recent research has uncovered an unexpected vulnerability in deadly melanoma cells that, when exploited, can cause the cancer cells to turn against themselves. The study, published by Cell Press in the August issue of the journal Cancer Cell, identifies a new target for development of future therapeutics aimed at selectively eliminating this aggressive skin cancer which is characterized by a notoriously high rate of metastasis and treatment-resistance. "Although considerable effort has been devoted to the search for molecular mechanisms that contribute to the chemo- and immunoresistance of melanoma, the average survival of patients with inoperable metastases remains less than 10 months," explains senior study author Dr. Maria S. Soengas from the Melanoma Laboratory at the Spanish National Cancer Research Centre in Madrid, Spain. Melanoma has multiple complex genetic aberrations that make the cells difficult to destroy with current treatments. One process that has not been studied in great detail with regards to melanoma is a type of autophagy (literally, self-eating) that involves sequestration of components within the cell for eventual degradation. Previous work has linked autophagy with both cancer cell death and survival and it is not clear whether this process might be a viable target for future drug development. Dr. Soengas and colleagues designed a series of studies to examine the interplay between autophagy and cell death in the context of tumor cell-selective elimination of melanoma cells. The researchers discovered that melanoma cells retain the ability to recognize and respond to double-stranded RNA (dsRNA) located inside the cell cytoplasm. Most animal cells contain single-stranded RNA and see dsRNA, which is associated with viruses, as a threat. The melanoma cells responded to administration of the dsRNA mimic polyinosine-polycytidylic acid (pIC) by inducing an immune response that led to autophagy. However, the method of delivering the pIC to the melanoma cells was critical and required a carrier called polyethyleneimine (PEI) to ensure delivery of pIC to the cell cytoplasm. The researchers went on to show that pIC links autophagy to apoptosis, a well studied cell death pathway. Significantly, the cell autonomous anti-tumor activity of pIC was observed even in animals with a suppressed immune system, a condition common to melanoma patients. "Altogether, our results provide the proof of principle for dsRNA sensors as therapeutic targets to overcome the inherent resistance of melanoma cells to current anticancer treatments," says Dr. Soengas. Importantly, the pIC-PEI complex has two exciting advantages over other anticancer agents. "First, pIC-PEI can induce both autophagy and apoptosis in an efficient manner while other compounds are just partial inducers of one of the two processes. Second, pIC-PEI has a significant anti-melanoma activity in experimental mouse models without noticeable side effects." The researchers caution that further research is required before these results can be translated to the clinic. The researchers include Damia` Tormo, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Agnieszka Checinska, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Direna Alonso-Curbelo, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Eva Perez-Guijarro, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Estela Canon, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Erica Riveiro-Falkenbach, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Tonantzin G. Calvo, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Lionel Larribere, Spanish National Cancer Research Centre (CNIO), Madrid, Spain" Diego Megias, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Francisca Mulero, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Miguel A. Piris, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Rupesh Dash, Virginia Commonwealth University, School of Medicine, Richmond, VA; Paola M. Barral, Virginia Commonwealth University, School of Medicine, Richmond, VA; Jose÷´ L. Rodriguez-Peralto, Hospital Universitario, Madrid, Spain; Pablo Ortiz-Romero, Hospital Universitario, Madrid, Spain; Thomas Tuting, University of Bonn, Bonn, Germany; Paul B. Fisher, Virginia Commonwealth University, School of Medicine, Richmond, VA; and Maria S. Soengas, Spanish National Cancer Research Centre (CNIO), Madrid, Spain. Cathleen Genova Cell Press


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