Publications by authors named "Ragland B"

The significance of cyclooxygenase-2 (COX-2) expression in mesenchymal tumors has not been completely described. We analyzed clinicopathologic variables and COX-2 protein expression in all mesenchymal tumors of the GI tract that were treated at our institution between 1990 and 2002. Paraffin-embedded specimens were immunohistochemically stained for KIT and COX-2 protein.

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A "mitochondrial hypothesis" of late onset Alzheimer's disease (AD) has been proposed. Biochemical studies indicate that there is a significant decrease in cytochrome oxidase (CO) activity as well as perturbed CO I and CO III mRNA levels in platelets and brain tissue from Alzheimer's patients. Using the electrophoretic mutation detection technique SSCP and DNA sequencing, we have identified 20 point mutations in the mitochondrial-encoded CO subunits (CO I, II, and III) in AD and age-matched control brain samples.

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The activated protein C resistance (APCR) assay is the test of choice to screen for factor V Leiden. We evaluated the effect of lupus anticoagulant on the baseline clotting time of the second-generation APCR assay with plasma samples from 54 patients to determine whether a falsely low APCR ratio could be predicted. We also assessed whether a modification of the assay could make it more reliable in the presence of strong lupus anticoagulants.

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A 32-year-old male presented with fever, mental status changes, renal dysfunction, cytopenias and hemolysis. His platelet count was 14,000/microL, hemoglobin 5.7 g/dL and LDH 2,636 U/L.

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Adherence of the enteric protozoan parasite Entamoeba histolytica is mediated by an N-acetyl D-galactosamine (GalNAc)-specific lectin, a heterodimer of heavy (170 kDa) and light (35/31 kDa) subunits. The gene families encoding the lectin subunits were characterized using clamped homogeneous electric field (CHEF) gel electrophoresis in the strain HM1:IMSS. The heavy subunit was shown to be encoded by a family of five hgl genes, which were physically mapped to five distinct HindIII restriction fragments.

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Amebic destruction of neutrophils and macrophages is contact-dependent. Adherence is mediated by a galactose-specific surface lectin on the amebic membrane. The pathway by which contact-dependent cytolysis of the target cell occurs is unknown.

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