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  • 1990-1994  (4)
  • protein kinase C  (2)
  • Atrial fibrillation  (1)
  • Pancreatic exocrine cell antibodies  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Translocation of protein kinase C α and ζ in rat glomerular mesangial cells cultured under high glucose conditions (1994)
    Springer
    Diabetologia 37 (1994), S. 838-841 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic nephropathy ; glomerular mesangial cells ; protein kinase C ; isoenzymes ; high glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The activities and expression of protein kinase C isoenzymes were examined in glomerular mesangial cells cultured under high glucose conditions. Exposure of cells to high glucose concentrations (27.8 mmol/l) for more than 3 days resulted in a significant elevation of protein kinase C activities in the membrane fraction. Of the protein kinase C isoenzymes, the levels of protein kinase C α significantly increased in the membrane fraction after 3 days of exposure to glucose, and protein kinase C ζ increased after 5 days of exposure. Levels of protein kinase C δ and ε remained unchanged and protein kinase C Β and γ were not detected. These results indicate that protein kinase C α and ζ are translocated under high glucose conditions possibly through different mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404342
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Pancreatic cytokeratin: an antigen of pancreatic exocrine cell autoantibodies in Type 1 (insulin-dependent) diabetes mellitus (1990)
    Springer
    Diabetologia 33 (1990), S. 363-370 
    Details
    ISSN: 1432-0428
    Keywords: Pancreatic exocrine cell antibodies ; cytokeratin ; Type 1 (insulin-dependent) diabetes mellitus ; islet cell antibodies ; pancreatic exocrine cells ; pancreatic islet
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Autoantibodies reacting with human pancreatic exocrine cells were investigated by immunofluorescent techniques in 107 patients with Type 1 (insulin-dependent) diabetes mellitus, 20 first-degree relatives of the Type 1 diabetic patients, 347 patients with Type 2 (non-insulin-dependent) diabetes, 34 with alcoholic pancreatitis, 26 with rheumatoid arthritis and 107 normal control subjects. Both immunoblotting analysis and double-immunostaining methods were used to characterize the antigens targeted by the pancreatic exocrine cell autoantibodies. Sera positive for human pancreatic exocrine cell cytoplasm, producing a “fine fibrillar” pattern, were found in 21% (23/107) of the Type 1 diabetic patients. The autoantibodies were present in 39% (15/38) of Type 1 diabetic patients diagnosed within 3 months, and the prevalence decreased with duration of diabetes. The antibodies were of the IgM class in 87% (13/15) of recent-onset Type 1 diabetes cases, but IgG-autoantibodies became more prevalent with increasing duration of diabetes. Three out of 347 (0.9%) Type 2 diabetic patients and 4 of 20 (20%) first-degree relatives of Type 1 diabetic patients had autoantibodies targeted against pancreatic exocrine cells. None of the patients with alcoholic pancreatitis or rheumatoid arthritis and none of the control subjects had these antibodies. Immunoblotting analysis and double-immunostaining demonstrated that the autoantibodies reacted with 40 kilodalton cytokeratin in pancreatic exocrine cell cytoplasm. The antibody was absorbed by the Triton X-100-insoluble fraction of pancreatic extract. These results indicate the presence of distinct autoantibodies to pancreatic exocrine cells in Type 1 diabetes. This suggests the provocative concept that the cytoskeletal system of pancreatic exocrine cells is involved in the pathogenetic process of Type 1 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404641
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Efficacy of disopyramide in conversion and prophylaxis of post-thyrotoxic atrial fibrillation (1991)
    Springer
    European journal of clinical pharmacology 40 (1991), S. 215-219 
    Details
    ISSN: 1432-1041
    Keywords: Atrial fibrillation ; disopyramide ; thyrotoxicosis ; cardioversion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Rhythm conversion in patients with post-thyrotoxic atrial fibrillation (AF) has been performed with disopyramide in order to evaluate the conversion rate and to test its effect on the maintenance of sinus rhythm after cardioversion. The duration of AF ranged from 9 to 122 months (mean 31.8 months). Of 81 patients, 12 (15%) with relatively short duration AF were converted to sinus rhythm with disopyramide. The remaining 69 patients required DC cardioversion, which restored sinus rhythm in 58 patients. The 58 DC-converted patients were divided into two groups: a disopyramide group (D group) and a non-disopyramide group (non-D group). The D group received disopyramide 300 mg per day for 3 months after DC cardioversion and the non-D group did not receive anti-arrhythmic drugs. During the early observation period, only one patient relapsed in the D group into AF, but 5 successive patients in the non-D group reverted to AF, forcing discontinuation of the non-D protocol. A second DC cardioversion performed on 3 of those 5 patients was followed by maintenance therapy with disopyramide 300 mg per day, and they remained in sinus rhythm. With the inclusion of those three subjects, sinus rhythm was still present in 44 of the total of 58 patients converted by DC (76%) at the time of follow-up (64 months). Thus, disopyramide was effective in rhythm conversion and it was essential for the maintenance of sinus rhythm after cardioversion in patients with post-thyrotoxic AF.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00315198
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Roles of Ca2+ and protein kinase C in regulation of prostaglandin E2 release by cultured rabbit gastric epithelial cells (1993)
    Springer
    Digestive diseases and sciences 38 (1993), S. 1426-1434 
    Details
    ISSN: 1573-2568
    Keywords: cultured rabbit gastric cells ; prostaglandin E2 release ; protein kinase C ; Ca2+ ; cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prostaglandin (PG) has been reported to be one of the important protective factors in the gastric mucosa. However the mechanism of the regulation of endogenous PG production has not been well studied. We investigated the possible roles of Ca2+, cAMP, and protein kinase C (PKC) in the regulation of PGE2 release from cultured rabbit gastric mucosal cells. PGE2 was measured by radioimmunoassay. A23187 (Ca2+ ionophore) at 2×10−6 M significantly increased PGE2 release. Deprivation of Ca2+ from the medium blocked the A23187-induced increase of PGE2. TMB-8 (a putative inhibitor of Ca2+ release from intracellular stores) did not have any significant effects on the increase of PGE2-induced by A23187. Thus, A23187 increased PGE2 through the influx of extracellular Ca2+. W7 or compound 48/80 (calmodulin inhibitors) did not alter the response of PGE2 caused by A23187. Exogenous administration of cAMP, forskolin (an activator of adenylate cyclase), or 2-chloroadenosine (a possible activator of adenylate cyclase through adenosine A2 receptor) had neither significant effects on PGE2 release nor an effect on A23187-induced increase of PGE2 release. 12-O-tetradecanoylphorbol 13-acetate (TPA, an activator of PKC) significantly stimulated PGE2 release in a dose-dependent fashion, whereas another phorbol ester with no biological activity did not. A23187 at 0.8×10−6 M, but not cAMP, potentiated the TPA-induced increase of PGE2. Mepacrine (a phospholipase A2 inhibitor) reduced the A23187-and TPA-induced increase of PGE2. These results suggest that Ca2+ and protein kinase C may play important roles in the regulation of PGE2 release by cultured rabbit gastric cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01308599
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    Paper (German National Licenses)
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