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Schumer Preparing Strong Public Plan Option
Sen. Charles Schumer, D-N.Y., a member of the key Senate Finance Committee and advocate for a government-run health insurance plan, said yesterday he would abandon all other possible compromises in favor of immediately creating a public plan that "would operate on "a level playing field" with private insurers," CongressDaily reports. Other proposals have included a plan that would establish health insurance co-ops with government seed money or "trigger" the creation of a public plan only if private insurers fail to meet certain targets for containing costs and improving access.
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Large Abdominal Wall Lipoma Causes Bowel Obstruction
Proteus syndrome is a complex disorder associated with varied, disproportionate, asymmetric overgrowth of many body parts and unregulated adipose tissue. The overgrowth seen in Proteus syndrome is progressive and difficult to manage. Patients with Proteus syndrome require repeated treatment for the progressive overgrowth of tissue over a long period. Aggressive treatment may cause severe functional and cosmetic consequences, so surgical intervention is often delayed until it is absolutely necessary.
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The Government Of Canada Reaches Another Important Milestone With The Chemicals Management Plan
The Honourable Leona Aglukkaq, Minister of Health, and the Honourable Jim Prentice, Canada"s Environment Minister, today announced the release of the draft screening assessments and risk management scope documents for 18 substances assessed in Batch 6 of the Chemicals Management Plan. The Government has reached the halfway point in its commitment to assess approximately 200 high-priority substances as part of the Chemicals Management Plan.
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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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