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  • 1
    ISSN: 1432-0428
    Keywords: Chinese hamster ; spontaneous diabetes ; glucosuria ; ketonuria ; glycogen ; glycogen accumulation ; retina ; Müller cell ; kidney ; distal tubule ; pancreatic islet ; a cell ; Β cell ; D cell ; electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intracellular glycogen deposits were consistently found in the retina, kidney and pancreatic islets of diabetic-ketonuric Chinese hamsters. Accumulation of glycogen in the outer nuclear layer of the retina was mostly associated with severity of the disease, but was not related to age or sex. The type of retinal cell involved in the accumulation of glycogen was not clearly established. However, the position of the affected cell, side by side with retinal neurons, suggests that the glycogen deposits were within Müller cells. These giant glias normally synthesize and store glycogen. All ketonuric Chinese hamsters examined showed some accumulation of glycogen in distal tubules of the kidney. This abnormal glycogen was not found in glucosuric non-ketonuric or in nondiabetic Chinese hamsters. Variable amounts of glycogen were found inΒ cells of pancreatic islets of diabetic hamsters, as reported by others. However, accumulation of glycogen was also found inα and D islet cells from 2 middle aged Chinese hamsters with long term glucosuria and recent ketonuria. Abnormal glucose and glycogen metabolism seem to play an important role in the pathogenesis of diabetes in the Chinese hamster.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-2451
    Keywords: Cytoprotection ; Prostaglandin ; Mucosal blood flow ; Cytoprotektion ; Prostaglandin ; Magendurchblutung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Der Mechanismus der Cytoprotektion von Prostaglandin (PG) auf die Magenmucosa ist unbekannt. Anaesthesierte Kaninchen erhielten in der Gruppe (GR) I (n=8) im. Aspirin (ASA) (100 mg/kg als Bolus, 66 mg/kg/h kontinuierlich) in der GR 11 (n=10) NaCI und in der GR III (n=7) zusätzlich zum ASA, PGE I (0,1 μg/kg/min) als Infusion über 120 min. Der Mucosa-Blutfluß (MBF) wurde mit radioaktiven Mikrosphären gemessen. In der GR I fiel der MBF nach 15 min um 72,3+3,8% (+ SEM) und nach 120 min um 73,1+3,8% (p 0,05 gegen % Änderung in GR II und III). Nach 120 min zeigte sich in der GR I 19,8 + 7,6% der Fundusmucosa hämorrhagisch, in der GR 11 6,1 +5,2% und in der GR 1112,0+ 1,4% (p 0,05 gegen GR II und III). Wir schließen, daß der cytoprotektive Effekt des PGE I auf einer Aufhebung der ASA bedingten Mucosaischämie beruht.
    Notes: Summary The mechanism by which prostaglandins (PG) exert their cytoprotective effect on the gastric mucosa is not known. Anesthetized rabbits received in Group (GR) I (n = 8) i.v. aspirin (ASA) (100 mg/kg as bolus, 66 mg/kg/h continuously), in GR II (n=10) NaCl and in Gr III PGE I (0.1 μg/kg/min) as an infusion for 120 min. Mucosal blood flow (MBF) was measured with radioactive microspheres. After 15 min, fundus MBF had decreased in GR I by 72.3+3.8% (+SEM) and after 120 min by 73.1+3.8% (P 0.05 vs % change in GR II and III). After 120 min, 19.8+7.6% of the mucosa had become hemorrhagic in GR I, 6.1+5.2% in GR II and 2.0+1.4% in GR III (P 0.05 vs GR II and III). We conclude that the cytoprotective effect of PGE I may be mediated through prevention of ASA-induced mucosal ischemia.
    Type of Medium: Electronic Resource
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