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Abbott And AstraZeneca Extend Relationship To Include Co-promotion Of TRILIPIX(R) (fenofibric Acid)
Abbott and AstraZeneca announced today that they have entered into an agreement for AstraZeneca to co-promote Abbott"s TRILIPIX® (fenofibric acid), a medication for use alone or in combination with a statin to treat certain lipid disorders. Under the terms of the agreement, AstraZeneca will obtain the non-exclusive right to co-promote TRILIPIX alongside Abbott in the United States, excluding Puerto Rico. Specific financial terms were not disclosed.
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What Are Genital Warts? What Causes Genital Warts?
Genital warts are also called venereal warts or condylomata acuminate. Genital warts are one of the most common kinds of STDs (sexually transmitted diseases) or STIs (sexually transmitted infections). According to Medilexicon"s medical dictionary, a genital wart is "a contagious projecting warty growth on the external genitals or at the anus, consisting of fibrous overgrowths covered by thickened epithelium showing koilocytosis, due to sexual contact with infection by human papillomavirus; it is usually benign, although malignant change has been reported, associated with particular types of the virus."
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Medtronic Demonstrates Positive Results On First Pacemaker Designed For Use With MRI
New data announced at Heart Rhythm 2009, the annual congress of the Heart Rhythm Society, demonstrate that patients implanted with the investigational EnRhythm MRI™ SureScan™ pacing system experienced no complications related to the use of magnetic resonance imaging (MRI). Sponsored by Medtronic, Inc. (NYSE: MDT), the study confirms that the pacing system can help cardiac device patients benefit from the use of MRI, a critical imaging technique commonly used in disease diagnosis. Currently, due to safety considerations, there are no implantable pacemakers or defibrillators approved for use with MRI in the United States. Commercially released in Europe last fall, the EnRhythm MRI SureScan system is the world"s first and only pacing system designed and approved for use with MRI.
Mental Health

New Mechanism For Amyloid Beta Protein's Toxic Impact On The Alzheimer's Brain

Scientists have uncovered a novel mechanism linking soluble amyloid í² protein with the synaptic injury and memory loss associated with Alzheimer"s disease (AD). The research, published by Cell Press in the June 25 issue of the journal Neuron, provides critical new insight into disease pathogenesis and reveals signaling molecules that may serve as potential additional therapeutic targets for AD. Amyloid í² protein (Aí²) plays a major pathogenic role in AD, a devastating neurodegenerative disorder characterized by progressive cognitive impairment and memory loss. "Given the mounting evidence that small soluble Aí² assemblies mediate synaptic impairment in AD, elucidating the precise molecular pathways by which this occurs has important implications for treating and preventing the disease," explains senior study author, Dr. Dennis Selkoe from the Center for Neurologic Diseases at Brigham and Women"s Hospital and Harvard Medical School. Dr. Selkoe, Dr. Shaomin Li, and colleagues examined regulation of a cellular communication phenomenon known as long-term synaptic depression (LTD). LTD has been linked with neuronal degeneration, but a role for Aí² in the regulation of LTD has not been clearly described. The researchers found that soluble Aí² facilitated LTD in the hippocampus, a region of the brain intimately associated with memory. The enhanced synaptic depression induced by soluble Aí² was mediated through a decrease in glutamate recycling at hippocampal synapses. Excess glutamate, the major excitatory neurotransmitter in the brain, is thought to contribute to the progressive neuronal loss characteristic of AD. The researchers went on to show that Aí²-enhanced LTD was mediated by glutamate receptor activity and that the LTD could be prevented by an extracellular glutamate scavenger system. A very similar enhancement of LTD could be induced by a pharmacological blocker of glutamate reuptake. Importantly, soluble Aí² directly and significantly decreased glutamate uptake by isolated synapses. "Our findings provide evidence that soluble Aí² from several s enhances synaptic depression through a novel mechanism involving altered glutamate uptake at hippocampal synapses," concludes Dr. Selkoe. "These results have both mechanistic and therapeutic implications for the initiation of hippocampal synaptic failure in AD and in more subtle forms of age-related Aí² accumulation." Future studies are needed to determine precisely how soluble Aí² protein physically interferes with glutamate transporters at the synapse. The researchers include Shaomin Li, Brigham and Women"s Hospital, Harvard Medical School, Boston, MA; Soyon Hong, Brigham and Women"s Hospital, Harvard Medical School, Boston, MA; Nina E. Shepardson, Brigham and Women"s Hospital, Harvard Medical School, Boston, MA; Dominic M. Walsh, University College Dublin, Dublin, Ireland; Ganesh M. Shankar, Brigham and Women"s Hospital, Harvard Medical School, Boston, MA; and Dennis Selkoe, Brigham and Women"s Hospital, Harvard Medical School, Boston, MA. Cathleen Genova Cell Press


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