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Some Black Women With Advanced Breast Cancer Opt Against Treatment, Study Finds
A new study has found that some black women with advanced breast cancer declined treatment with chemotherapy or radiation, though researchers did not know the reason why so many of the women opted against treatment, HealthDay/Las Vegas NOW reports. For the study, researchers examined records for 107 women with cases of advanced breast cancer that were reported at one inner-city hospital between 2000 and 2006. Eighty-seven percent of the women were black, and 29% of them had breast cancer tumors that did not respond well to new, targeted treatments. Of all women, 20.5% declined chemotherapy and 26.3% opted against radiation.Lead researcher Monica Rizzo, an assistant professor of surgery at the Division of Surgical Oncology at the Emory University School of Medicine, said the reason why the women declined treatment is not clear, adding, "We looked at marital status, as well as religious background, of those women, and unfortunately, we were not able to find any clear identifier." Researchers speculated that fear of the medical system, poverty and cultural differences might play a role. Rizzo"s group has started a community outreach program through which a nurse practitioner and social worker follow up with breast cancer patients (Reinberg, HealthDay/Las Vegas NOW, 5/22). An abstract of the study is available online.
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Lawmakers, Officials Distort The Facts To Support Or Oppose Health Overhaul
"Confusing claims and outright distortions have animated the national debate over changes in the health care system," the Associated Press reports. The AP lists examples:
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Quality Of Care Delivery In Colorectal Cancer Improved By Educational Initiatives
A study of targeted educational initiatives between the clinical staff at Fox Chase Cancer Center and the hospitals within their Partners program suggest that educational interventions by academic cancer centers can improve quality of care for cancer patients at community hospitals. The study, to be presented at the 2009 Annual Meeting of the American Society of Clinical Oncology, looked specifically at the number of lymph nodes that were surgically removed in colorectal cancer patients at Fox Chase"s partner hospitals and the impact that educational initiatives by clinical staff had on improving the number of nodes removed.
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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