91 research outputs found

    Multiple sclerosis genomic map implicates peripheral immune cells and microglia in susceptibility

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    Ergosterol biosynthesis in Yeast

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    Verrucous Carcinoma of the Nasal Septum and Columella

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    Tumours of the nasal septum are rare. They mostly concern squamous cell carcinomas. Verrucous carcinomas are exceptional, with only three well-documented cases in the literature. We operated such a tumour, localized both on the columella and nasal septum.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

    Human type 2 diabetes: morphological evidence for abnormal beta-cell function.

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    The exact nature of the beta-cell defect in type 2 diabetic patients is still unclear. beta-Cell mass reduction has been reported but remains controversial. A preliminary study of a large series of patients has demonstrated that in most, the beta-cell defect is not related to a decreased beta-cell mass. Amyloid deposits are observed in the islets of some type 2 diabetic patients but also in normoglycemic subjects. Because it has been claimed that these deposits interfere with beta-cell function, we evaluated in situ the effect of insular amyloid deposits on beta-cell transcription and translation. Pancreases were obtained at autopsy from 28 normoglycemic patients and 41 type 2 diabetic patients. Staining with hemaluneosin and Congo red was used to analyze the general features of the islets and the presence of amyloid deposits, respectively. Immunohistochemistry for proinsulin was performed with an antibody recognizing the junction between B-chain and C-peptide, thus specifically labeling the Golgi area where proinsulin is produced. In seven patients, we evaluated insulin gene transcription by in situ hybridization of proinsulin mRNA combined with Congo red staining, and we evaluated insulin storage by double immunostaining for insulin and amylin. In many type 2 diabetic patients, the islets appeared entirely normal. Amyloid deposits were found in 57% of diabetic subjects and 33% of normoglycemic age-matched control subjects. The percentage of amyloid-infiltrated islets varied from 0.4 to 74%. beta-Cells from amyloid-containing islets still had specific Golgi proinsulin labeling. In obese type 2 diabetic patients, the number of beta-cells with abnormal expression of proinsulin in the whole cytoplasm was significantly higher than in normoglycemic control subjects. Proinsulin mRNA was significantly reduced in islets with amyloid deposits when compared with amyloid-free islets, but the mean reduction did not exceed 16%. Insulin was still present in the beta-cells of amyloid-containing islets, and its amount, estimated by measurement of the insulin-labeling optical density, was not statistically different from that in amyloid-free islets. In conclusion, even in amyloid-containing islets, beta-cells maintain active insulin transcription and translation and normal insulin storage. Taking into account that in most cases only a small proportion of islets are infiltrated by amyloid, the limited reduction in proinsulin mRNA is unlikely to play a major role in the pathogenesis of diabetes

    Pilomatrix carcinoma.

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    A 43-year-old man presented with a tumour of the medial part of the right eyebrow. A biopsy was performed and histological examination revealed a malignant transformation of a 'calcifying epithelioma of Malherbe'. A secondary wide excision was performed. Clinical and pathological findings of this extremely rare tumour are reviewed. Factors influencing the prognosis are proposed, based on a compilation of the literature.Case ReportsJournal ArticleSCOPUS: ar.jinfo:eu-repo/semantics/publishe

    Localization and serum concentration of secretory component during massive necrosis of human liver.

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    The serum concentration of secretory component was monitored in 9 patients with massive liver necrosis. During acute cytolysis, no increase in serum secretory component levels was observed. Later on, patients with fulminant evolution displayed minor elevations. Values as high as those usually found in acute hepatitis were only observed in cases with delayed liver failure. In these patients, levels were elevated before failure, dropped as liver failure developed, and rose again during recovery. This evolution of serum secretory component level cannot be accounted for by a defective liver clearance of circulating secretory component. It rather suggests a release into the blood of secretory component produced in the liver by cells other than damaged hepatocytes, possibly during liver regeneration. In 3 cases, secretory component localization in the liver was demonstrated by immunocytochemistry and was compared with that in normal liver and in obstructive jaundice. In normal liver, it was restricted to portal bile duct cells and lumens. In obstructive jaundice, additional secretory component staining was found in bile canaliculi. After fatal liver necrosis, secretory component was localized to portal ducts and to a variable proportion of the cholangiocytelike cells belonging to the numerous extraportal proliferating ducts. In these structures, 0.1%, 21%, and 4% of the cells were stained 3, 8, and 30 days after maximal cytolysis, respectively. Remaining hepatocytes and bile canaliculi or bile plugs were unstained. Therefore, portal cholangiocytes and extraportal cholangiocytelike cells are probably essential sources of secretory component in human liver. We propose that proliferation of extraportal cholangiocytelike cells, expression of secretory component synthesis by these cells, and their inability to secrete secretory component in a disorganized biliary tree result in the elevated serum concentration of secretory component observed after acute liver necrosis

    Hypertrophic osteoarthropathy and thyroid cancer

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    SCOPUS: ar.jinfo:eu-repo/semantics/publishe
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