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  • 1
    ISSN: 1432-0649
    Keywords: 04.80.Nn ; 07.60.Ly ; 95.55.Ym
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract We describe preliminary experimental results concerning the operation of a 3 m arm-length Michelson interferometer with two Fabry-Perot cavities whose mirrors and beam splitter are suspended independently by wires. The reflected light beams from the two Fabry-Perot cavities are recombined to obtain interference at a photo-detector; this scheme is necessary for future power-recycled laser interferometers used to detect gravitational waves. The fundamental properties of the interferometer are presented, including the power spectral density of the displacement noise.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Hypoglycaemia ; rat embryo culture ; congenital malformation ; growth retardation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary As congenital malformations may be caused by perturbations of glycolytic flux on early embryogenesis [16], effects of hypoglycaemia were investigated by using rat embryo organ culture. Nine and one-half day old rat embryos were grown in vitro for 48 h (day 9 1/2 to 11 1/2) in the presence of hypoglycaemic serum for different hours during the culture period. Hypoglycaemic serum was obtained from rats given insulin intraperitoneally. On exposure to hypoglycaemic serum during the first 24 h of culture (day 9 1/2 to 10 1/2), embryos showed marked growth retardation and had increased frequencies of neural lesions (42.7% versus 0%, p〈0.01), in contrast to hypoglycaemic exposure during the second 24 h of culture (day 10 1/2 to 11 1/2), where only minor growth retardation and low frequencies of neural lesions (2.4% versus 0%, NS) were seen. Even exposure to hypoglycaemic serum for a relatively short period (8 h) during the first 24 h of culture resulted in neural lesions at the frequency of 9.3–13.3%. The embryos exposed to hypoglycaemia demonstrated decreased glucose uptake and lactic acid formation, indicating decreased energy production via glycolysis that constitutes the principal energy pathway at this stage of embryonic development. These results suggest that hypoglycaemia during critical periods of embryogenesis has adverse effects on the development of the embryo and these effects might be mediated through metabolic interruption of embryogenesis.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Islet cell antibodies ; Type 1 (insulin-dependent) diabetes ; Epstein-Barr virus ; peripheral blood lymphocytes ; transformation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet cell antibodies are usually detected in the sera of almost all Type 1 (insulin-dependent) diabetic patients within several months after onset of the disease. The antibodies then disappear quite early during the course of the disease. The present study was undertaken to detect islet cell antibody-producing clones in peripheral blood lymphocytes of Type 1 diabetic patients whose islet cell antibodies could not be detected in sera. Epstein-Barr virus-transformed lymphocytes were employed to enhance the production of antibodies and to detect the clones from peripheral blood lymphocytes. Peripheral blood lymphocytes were obtained from 40 islet cell antibody-negative Type 1 diabetic patients, 10 antibody-positive Type 1 diabetic patients, 30 Type 2 (non-insulin-dependent) diabetic patients and 40 normal control subjects. Epstein-Barr virus-transformed lymphocytes were cultured for 4 weeks and the culture supernatants were used for assay of islet cell antibodies. Islet cell antibody assays were performed by immunohistochemical methods using peroxidase-labelled protein A for IgG antibodies, peroxidase-labelled anti-human IgM antibodies for IgM antibodies and fresh frozen human pancreatic tissue. IgG-islet cell antibodies were detected in 26 islet cell antibody-negative patients (65%), eight antibody-positive patients (80%) and one Type 2 diabetic patient (3%) in the culture supernatants. Islet cell antibodies in the supernatants could not be detected in any of the control subjects. IgM-islet cell antibodies could not be detected in any of the patients or control subjects. These findings indicate that islet cell antibody-producing clones exist in peripheral blood lymphocytes from Type 1 diabetic patients whose islet cell antibodies cannot be detected in their sera and IgG-islet cell antibodies might be a specific characteristic of Type 1 diabetes. The detection of islet cell antibodies from Epstein-Barr virus-transformed lymphocytes may be useful in examining the role of autoimmune mechanisms in the development of disease.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Islet cell antibody (ICA) ; Type 1 (insulin-dependent) diabetes ; peroxidase-labeled protein A ; incidence of ICA ; ICA titres
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have developed a new method of detecting islet cell antibodies using peroxidase-labeled protein A, and have determined the incidence of ICA in Type 1 (insulin-dependent) diabetes in Japan. In our method, fresh frozen sections of human pancreas and serum samples were incubated and then treated with peroxidase-labeled protein A at room temperature. Conjugates of peroxidase and protein A were subjected to Sephadex G-200 column chromatography, and only the 80,000 dalton peak was employed. The treated sections were allowed to react with haematoxylin and eosin (HE) to confirm the localization of islet cells. With this method, human pancreatic tissues can be used regardless of age and blood type, and the stained sections can be stored for more than 5 years. Serum samples obtained from 52 patients with Type 1 diabetes, 54 with Type 2 (non-insulin-dependent) diabetes and 100 control subjects were examined. In patients with Type 1 diabetes, islet cell antibodies were detected in 14 of 14 (0.5 years after onset), 3 of 6 (0.5–1 years after onset), 7 of 16 (1–5 years after onset) and 2 of 16 (more than 5 years after onset). In contrast, only 4 of 54 patients with Type 2 diabetes and none of the controls were ICA positive. It is concluded that, with our newly developed method using peroxidase-labeled protein A, ICA is present in all Japanese Type 1 diabetic patients whose diabetic manifestations are less than 0.5 years duration from onset.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Hyperglycaemia ; embryogenesis ; rat embryo culture ; malformation ; sorbitol ; myo-inositol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To demonstrate the myo-inositol depletion hypothesis in hyperglycaemia-induced embryopathy, rat conceptuses of 9.5 days of gestation in the early head-fold stage were grown in vitro during neural tube formation for 48 h with increasing amounts of glucose. The effects of an aldose reductase inhibitor and the myo-inositol supplementation were also investigated. Sorbitol and myo-inositol contents were measured in separated embryos and extra-embryonic membranes including yolk sac and amnion at the end of culture. After addition of 33.3 mmol/l and 66.7 mmol/l glucose to the culture media, the myo-inositol content of the embryos was significantly decreased by 43.1% (p〈0.05) and 64.6% (p 〈 0.01) of the control group, while a marked accumulation of sorbitol was observed (25 and 41 times that of the control). Although the addition of an aldose reductase inhibitor (0.7 mmol/l) to the hyperglycaemic culture media containing an additional 66.7 mmol/l glucose significantly reduced the sorbitol content of embryos to approximately one-eighth, the myo-inositol content of embryos remained decreased and the frequency of neural lesions was unchanged (23.1% vs 23.9%, NS). Supplementation of the myo-inositol (0.28 mmol/l) completely restored the myo-inositol content of the embryos and resulted in a significant decrease in the frequency of neural lesions (7.1% vs 23.9%, p 〈 0.01) and a significant increase in crown-rump length and somite numbers. Much less significantly, sorbitol accumulation was also observed in the extra-embryonic membrane in response to hyperglycaemia, neither hyperglycaemia nor the myo-inositol supplementation modified the myo-inositol contents of the extra-embryonic membrane. We conclude that the mechanism of hyperglycaemia-induced teratogenicity was mediated by the myo-inositol depletion of the embryo at a critical stage of organogenesis.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Glucose transporter ; embryogenesis ; hyperglycaemia ; rat embryo culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the expression of glucose transporter genes and protein in embryo and yolk sac during organogenesis and the regulation of glucose transporters during culture in hyperglycaemic media. Erythrocyte-type glucose transporter (GLUT 1) and brain-type glucose transporter (GLUT 3) mRNA were expressed in embryo and yolk sac. The expression of GLUT-1 and GLUT-3 mRNA was abundant on day 9–11 and day 9–10 in the embryo, respectively, and day 9–14 and day 10–11 in the yolk sac, respectively. The levels of GLUT-1 protein in the embryo increased in parallel with the expression of GLUT-1 mRNA during the corresponding period. Immunohistochemical staining of GLUT-1 protein was found principally in the neuroepithelial cells surrounding the neural tube in the embryo on day 10 and appeared in the microvessels surrounding the neural tube after day 12. To test whether the expression of glucose transporter genes and protein was suppressed during hyperglycaemia, conceptuses were cultured in high glucose medium. The abundant expression of GLUT-1 protein was not decreased during culture in high glucose media for 24 h (day 9–10) and was only down-regulated by prolonged exposure to this media for 48 h (day 9–11). We have demonstrated the predominant expression of the high affinity glucose transporter (GLUT 1 and GLUT 3) genes and (GLUT 1) protein in embryo during the early period of organogenesis. The persistently abundant expression of glucose transporter during the critical period of neural tube formation (day 9–10) even in the presence of hyperglycaemia may explain one of the mechanisms of increased glucose flux into the neuroepithelium, which may lead to neural tube defects.
    Type of Medium: Electronic Resource
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