22 research outputs found

    Gesichtsschädel und Parapharyngealraum

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    Iopromide

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    Characterization of glycoconjugates of human gastrointestinal mucosa by lectins. I. Histochemical distribution of lectin binding sites in normal alimentary tract as well as in benign and malignant gastric neoplasms.

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    Labeled lectins with binding specificity to the hexose components of mucus glycoproteins (HPA, RCA I, PNA, Con A, WGA, and UEA I) were used to demonstrate structural differences in the glycoprotein composition of various cell types of the normal, benign and malignant gastrointestinal mucosa. While in the RCA I, UEA I, and WGA binding of normal mucus secreting cell types only quantitative differences were observed, the mucus in the surface epithelial cells of gastric mucosa and in the colonic goblet cells was characterized by the absence of PNA, Con A, and PNA, HPA binding sites, respectively. These lectins, however, showed a strong binding to the supranuclear, Golgi-region in the undifferentiated or activated forms of these cells. Even the staining intensity of the luminal membrane surfaces of the non mucinous parietal and chief cells was often stronger by PNA, HPA, and RCA I lectins than that of the mucus secretions in the highly differentiated mucus cells. These results indicate the existence of either heterogeneous glycoprotein components or mucus molecules with variations in the degree of glycosylation of their oligosaccharide chains in the different cells. The latter seems more likely since in benign and malignant alterations lectin binding sites appear in great density, which were found to be characteristic of the undifferentiated mucus cells or for the non mucinous cells of the normal gastric mucosa. Similarly in some gastric cancers which do not stain with the periodic acid-Schiff reaction at all, large amount of free or neuraminic acid substituted PNA binding sites can be detected. </jats:p

    Treatment and imaging of intracranial atherosclerotic stenosis: current perspectives and future directions

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    BACKGROUND AND PURPOSE: Intracranial atherosclerosis is a common cause of stroke worldwide. It results in ischemic stroke due to different mechanisms including artery-to-artery embolism, in situ thrombo-occlusion, occlusion of perforating arteries, and hemodynamic failure. In this review, we present an overview of current treatment and imaging modalities in intracranial atherosclerotic stenosis. METHODS: PubMed was searched for relevant articles in English that evaluated the treatment and imaging of intracranial atherosclerotic stenosis (ICAS). RESULTS: Aggressive medical management, consisting of dual antiplatelet therapy and intensive risk factor management, is important in patients with ICAS because of a substantial risk of recurrent stroke, approximately 20% in the first year, in patients on aspirin or warfarin alone. Recent trials have suggested that, aggressive medical therapy results in better outcome as compared with intracranial stenting. However, the question remains what the optimal treatment strategy would be in patients with recurrent strokes in the setting of failed aggressive medical therapy. Moreover, controversy exists whether a subgroup of patients with symptomatic ICAS could benefit from intracranial stenting if selection is based on radiological evidence of hemodynamic failure. With regard to imaging, transcranial Doppler ultrasound and magnetic resonance angiography are useful screening tests for exclusion of ICAS, but need confirmation by other imaging modalities when stenosis is suggested. Computed tomography angiography has a high positive and negative predictive value for detection of intracranial luminal stenosis of 50% or higher, but performs worse than digital subtraction angiography with regard to establishing the exact degree of luminal stenosis. Novel imaging techniques including high-resolution CT and MRI better identify plaque characteristics than conventional imaging methods. CONCLUSIONS: Currently, aggressive medical management remains the standard of care for patients with ICAS. Further research is needed to identify high-risk subgroups and to develop more effective treatments for ICAS patients
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