64 research outputs found

    Diagnostic error reduction in the United States and Italy through the intervention of diagnostic management teams

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    A major challenge to most countries is the growing cost of healthcare. The cost of laboratory testing is approximately 3% of the total clinical costs. On the other hand, waste from inappropriate admissions to clinical departments is reported to be as high as 15%. A frequently used approach to save dollars in healthcare is the random reduction in the budget for laboratories, with a focus on reduction of the number of unnecessary laboratory tests. The World Health Assembly has approached the problem by publishing a list of essential in vitro diagnostic tests, in order to achieve a global rationalization of the problem. A much more thoughtful strategy to saving healthcare finance is to improve the efficiency of the diagnostic process. This report presents an opportunity to reduce diagnostic error and increase the efficiency of diagnostic testing. Reduction in time to a correct diagnosis provides a major financial as well as a clinical benefit. In addition, reducing both overutilization and underutilization of laboratory tests while achieving the correct diagnosis is a major benefit to challenged healthcare budgets. One approach taken to achieve major savings in healthcare has been the creation of “Diagnostic Management Teams,” composed of experts in specialty areas of medicine who are primarily based in the clinical laboratory to advise physicians on the selection of only necessary tests and the interpretation of complex test results

    Pathogenesis of Alcoholic Liver Disease–Recent Advances

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65715/1/j.1530-0277.2002.tb02598.x.pd

    Platelet activation in cystic fibrosis

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    Cystic fibrosis (CF) is caused by a mutation of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). We examined platelet function in CF patients because lung inflammation is part of this disease and platelets contribute to inflammation. CF patients had increased circulating leukocyte-platelet aggregates and increased platelet responsiveness to agonists compared with healthy controls. CF plasma caused activation of normal and CF platelets; however, activation was greater in CF platelets. Furthermore, washed CF platelets also showed increased reactivity to agonists. CF platelet hyperreactivity was incompletely inhibited by prostaglandin E(1) (PGE(1)). As demonstrated by Western blotting and reverse-transcriptase-polymerase chain reaction (RT-PCR), there was neither CFTR nor CFTR-specific mRNA in normal platelets. There were abnormalities in the fatty acid composition of membrane fractions of CF platelets. In summary, CF patients have an increase in circulating activated platelets and platelet reactivity, as determined by monocyte-platelet aggregation, neutrophil-platelet aggregation, and platelet surface P-selectin. This increased platelet activation in CF is the result of both a plasma factor(s) and an intrinsic platelet mechanism via cyclic adenosine monophosphate (cAMP)/adenylate cyclase, but not via platelet CFTR. Our findings may account, at least in part, for the beneficial effects of ibuprofen in CF

    Optical measurement of cell membrane tension

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    Using a novel noncontact technique based on optical interferometry, we quantify the nanoscale thermal fluctuations of red blood cells (RBCs) and giant unilamellar vesicles (GUVs). The measurements reveal a nonvanishing tension coefficient for RBCs, which increases as cells transition from a discocytic shape to a spherical shape. The tension coefficient measured for GUVs is, however, a factor of 4-24 smaller. By contrast, the bending moduli for cells and vesicles have similar values. This is consistent with the cytoskeleton confinement model, in which the cytoskeleton inhibits membrane fluctuations [Gov et al., Phys. Rev. Lett. 90, 228101, (2003)

    Laboratory medicine : the diagnosis of disease in the clinical laboratory, 2nd ed./ Edit.: Michael Laposata

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    xxxi, 480 p.: ill, tab.; 28 cm
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