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BACKGROUND: Glutamine synthetase is involved in the recycling of synaptically released glutamate and GABA and in the detoxification of ammonia. It is present in the Müller cells of the neural retina but not in the retinal pigment epithelial (RPE) cells of adult mammals. In human retinal pathological conditions glutamine synthetase has also been detected in RPE cells. In this case glutamine synthetase may provide the cells with glutamine needed for proliferation. Proliferation is also intense during retinal development. METHODS: We studied the distribution of glutamine synthetase immunoreactivity in fetal bovine retinae, especially in the RPE. The maturity of the RPE was demonstrated by histochemical detection of gamma-glutamyltranspeptidase, alkaline phosphatase and Na/K-ATPase as marker enzymes for the blood-retina barrier and by electron microscopy. RESULTS: We found that in the first 3 months of gestation glutamine synthetase immunoreactivity is located exclusively in the RPE. During the 3rd month the marker enzymes of the blood-retina barrier begin to appear. From the 4th month on, RPE cells are glutamine synthetase immunonegative. CONCLUSION: Glutamine in RPE cells in early development may supply glutamine for the intensely proliferating cells in the retina. Glutamine synthetase immunoreactivity in human retinal pathological conditions may indicate reinduction of an enzyme used in earlier development.  相似文献   
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The use of endophenotypes (intermediate quantitative traits) is one strategy that may provide valuable information about the neural mechanisms underlying disease etiology and facilitate discovery of susceptibility genes. For a trait to be an appropriate endophenotype, several key features should exist. In this article we discuss validating potential electrophysiological endophenotypes for schizophrenia based on conventionally accepted criteria. We focus on applying a twin study design and model fitting techniques to evaluate whether three event-related potential paradigms (P300, P50, and MMN) meet criteria as valid endophenotypes of schizophrenia.  相似文献   
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Three cultivars of broccoli seeds (Brassica oleracea var. italica), cv. Tiburon, cv. Belstar and cv. Lucky, and two cultivars of radish seeds (Raphanus sativus), cv. Rebel and cv. Bolide, were germinated for three and five days and safety aspects such as microbiological counts and biogenic amines were investigated. Cytotoxicity evaluation was also carried out. Broccoli and radish sprouts contained numbers of mesophilic, psychrotrophic, total and faecal coliform bacteria which are the usual counts for minimally processed germinated seeds. Putrescine, cadaverine, histamine, tyramine, spermidine and spermine increased during sprout production although these levels were below those permitted by legislation (5 mg/100 g of edible food). Broccoli and radish sprouts demonstrated no toxic effects on proliferation and viability of HL-60 cells and should be included in our diets as healthy and safe fresh foods.  相似文献   
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Background/Aims: Meckel syndrome is an autosomal‐recessive disease characterized by a combination of renal cysts, anomalies of the central nervous system, polydactyly and ductal plate malformations (DPM), which are hepatic anomalies consisting of excessive and abnormal foetal biliary structures. Among the genomic loci associated with Meckel syndrome, mutations in four genes were recently identified. These genes code for proteins associated with primary cilia and are possibly involved in cell differentiation. The aim of the present work was to investigate the formation of the primary cilia and the differentiation of the hepatic cells in foetuses with Meckel syndrome. Methods: Sections of livers from human foetuses with Meckel syndrome were analysed by immunofluorescence, immunohistochemistry and electron microscopy. Results: The primary cilia of the biliary cells were absent in some Meckel foetuses, but were present in others. In addition, defects in hepatic differentiation were observed in Meckel livers, as evidenced by the presence of hybrid cells co‐expressing hepatocytic and biliary markers. Conclusions: Defects in cilia formation occur in some Meckel livers, and most cases show DPM associated with abnormal hepatic cell differentiation. Because differentiation precedes the formation of the cilia during liver development, we propose that defective differentiation may constitute the initial defect in the liver of Meckel syndrome foetuses.  相似文献   
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