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  • Articles: DFG German National Licenses  (6)
  • Electronic Resource  (6)
  • 1990-1994  (3)
  • 1985-1989  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Role of alcohol in clinical nephrology (1985)
    Springer
    Journal of molecular medicine 63 (1985), S. 948-958 
    Details
    ISSN: 1432-1440
    Keywords: Alcoholism ; Fetal alcohol syndrome ; Genitourinary tract malformations ; Phosphate and magnesium depletion ; Rhabdomyolysis ; Acute renal failure ; Hypertension ; Alkohol ; Alkoholische Embryopathie ; Urogenitaltraktschädigung ; Phosphatund Magnesiumdepletion ; Rhabdomyolyse ; Akutes Nierenversagen ; Hypertonie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Nephrologisch wichtige Störungen des schwereren Alkoholismus manifestieren sich auf verschiedenen Ebenen. Eine direkte Schädigung der Nieren und abführenden Harnwege ist bislang ausschließlich bei alkoholischer Embryopathie nachgewiesen. Beim Erwachsenen dominieren unspezifische und komplexe Elektrolytstörungen mit Akzentuierung im Alkohol-Entzugssyndrom. Die Niere ist nicht selten primäre Ursache verschiedener Störungen, sie trägt ferner zur — oft inadäquaten — Kompensation extrarenal entstandener Stoffwechselstörungen (z.B. Phosphatmangel, Hypoglykämie) bei. Der alkoholassoziierten Uratretention, hervorgerufen durch Hyperlaktatämie oder Erhöhung derβ-Hydroxybuttersäure, kommt — wegen meist mäßiger Ausprägung — für die Entwicklung einer hyperurikämischen Nephropathie nur geringe Bedeutung zu. Alkoholexzeß (akut oder chronisch) prädisponiert zur Rhabdomyolyse mit konsekutivem Nierenversagen. Möglicherweise ist bei schwerem Alkoholismus und Myopathie die Vulnerabilität der Nieren für andere Noxen gesteigert. Bei der Ratte wird das Glyzerin-induzierte akute Nierenversagen durch Alkoholvorbehandlung verstärkt. Alkohol begünstigt ferner bei Normotonikern und Hypertonikern einen Blutdruckanstieg, der seinerseits das Risiko einer Nierenschädigung erhöht.
    Notes: Summary Different nephrological derangements are observed in severe alcoholics. Until now the direct toxicity of ethanol is only shown in the fetal alcohol syndrome with various malformations of the genitourinary tract. In the adult the kidney is often involved in the development, maintenance and counterregulation of complex electrolyte disturbances like phosphate and potassium hypoglycemia etc. The alcohol associated retention of urate, induced by hyperlactatemia and/or increasedβ-hydroxybutyrate concentration is only rarely complicated by urate nephropathy. Alcohol intoxication (acute and chronic) predisposes to rhabdomyolysis with the risk of acute renal failure. There are some hints that chronic alcoholism with myopathy increases the vulnerability of the kidney for further toxic agents. In rats glycerol induced renal failure is enhanced by alcohol pretreatment. Finally, regular alcohol consumption raises the blood pressure, which per se is a risk factor for renal damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01738150
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Independence of enhanced protein catabolism from glucocorticoids in chronically uremic rats (1989)
    Springer
    Research in experimental medicine 189 (1989), S. 339-345 
    Details
    ISSN: 1433-8580
    Keywords: Chronic renal failure ; Catabolism ; Corticosterone ; RU 38 486 ; Nt-methylhistidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Patients with chronic renal failure are prone to develop negative nitrogen balance resulting clinically in wasting and malnutrition. To study the role of glucocorticoids in the pathogenesis of uremic catabolism, we determined urinary excretion rates of urea and Nt-methylhistidine in chronically uremic rats with and without RU 38 486, a potent antiglucocorticoid. In comparison to pair-fed non-uremic animals, chronically uremic rats displayed significantly enhanced ureagenesis, as demonstrated by increased urinary urea excretion, and myofibrillar protein breakdown, as indicated by increased excretion rates of urinary Nt-methylhistidine. The administration of RU 38486 to chronically uremic rats, however, did not result in a normalization of urinary excretion of Nt-methylhistidine. Similarily, the antiglucocorticoid did not influence the extent of ureagenesis in our uremic animals, as it was demonstrated by comparable levels of urinary urea excretion. This suggests that glucocorticoids are not involved in the pathogenesis of enhanced catabolism in chronic renal insufficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01855039
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Renal proteinases and kidney hypertrophy in experimental diabetes (1994)
    Springer
    Diabetologia 37 (1994), S. 567-571 
    Details
    ISSN: 1432-0428
    Keywords: Key words IDDM, streptozotocin, tubules, glomeruli, collagenase, gelatinase, cathepsins, hypertrophy.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary IDDM is associated with an increase in kidney size, which is due to cellular hypertrophy and progressive matrix accumulation within the glomerulus and throughout the tubulointerstitium. The present study addressed the potential role of cysteine and metalloproteinases in renal hypertrophy of short-term diabetes. Three weeks after induction of streptozotocin diabetes in rats, intraglomerular gelatinase activity (streptozotocin: 23±4 vs control: 44±3 mU/µg DNA) and cathepsin L+B activity (streptozotocin: 6.7±0.8 vs control: 9.3±0.7 U/µg DNA) were significantly decreased. Insulin treatment completely prevented the decline in glomerular proteinase activity (gelatinase: 37±6 mU/µg DNA; cathepsin L+B: 9.6±0.9 U/µg DNA). In isolated proximal tubules a similar pattern of enzyme activity could be observed. Three weeks of diabetes caused a significant decline in cathepsin L+B activity (streptozotocin: 28±2 vs control: 37±3 U/µg DNA). Insulin treatment again prevented the decline in these tubular proteinase activities. In parallel, kidney weight increased by 22 % and glomerular protein/DNA ratio rose by 17 % in untreated diabetic rats. Diabetic rats receiving insulin displayed a normal glomerular protein/DNA ratio and the kidney weight was increased by only 5 %. These results show that renal hypertrophy of early diabetes is closely associated with a decline in both glomerular and tubular proteinase activity. Adequate insulin substitution prevented renal hypertrophy and the reduction in proteinase activity. [Diabetologia (1994) 37: 567–571]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403374
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Renal proteinases and kidney hypertrophy in experimental diabetes (1994)
    Springer
    Diabetologia 37 (1994), S. 567-571 
    Details
    ISSN: 1432-0428
    Keywords: IDDM ; streptozotocin ; tubules ; glomeruli ; collagenase ; gelatinase ; cathepsins ; hypertrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary IDDM is associated with an increase in kidney size, which is due to cellular hypertrophy and progressive matrix accumulation within the glomerulus and throughout the tubulointerstitium. The present study addressed the potential role of cysteine and metalloproteinases in renal hypertrophy of short-term diabetes. Three weeks after induction of streptozotocin diabetes in rats, intraglomerular gelatinase activity (streptozotocin: 23±4 vs control: 44±3 mU/μg DNA) and cathepsin L + B activity (streptozotocin: 6.7±0.8 vs control: 9.3±0.7 U/μg DNA) were significantly decreased. Insulin treatment completely prevented the decline in glomerular proteinase activity (gelatinase: 37±6 mU/μg DNA; cathepsin L + B: 9.6±0.9 U/μg DNA). In isolated proximal tubules a similar pattern of enzyme activity could be observed. Three weeks of diabetes caused a significant decline in cathepsin L + B activity (streptozotocin: 28±2 vs control: 37±3 U/μg DNA). Insulin treatment again prevented the decline in these tubular proteinase activities. In parallel, kidney weight increased by 22% and glomerular protein/DNA ratio rose by 17% in untreated diabetic rats. Diabetic rats receiving insulin displayed a normal glomerular protein/DNA ratio and the kidney weight was increased by only 5%. These results show that renal hypertrophy of early diabetes is closely associated with a decline in both glomerular and tubular proteinase activity. Adequate insulin substitution prevented renal hypertrophy and the reduction in proteinase activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403374
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Intraglomerular fibronectin accumulation and degradation in obese Zucker rats (1991)
    Springer
    Diabetologia 34 (1991), S. 786-789 
    Details
    ISSN: 1432-0428
    Keywords: Fibronectin ; diabetes mellitus ; isolated glomeruli
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The obese Zucker rat is a classic model of non-immune mediated spontaneous focal glomerulosclerosis. An important initiating hallmark of glomerulosclerosis in this model is mesangial matrix expansion. Fibronectin, a highly biologically active glycoprotein, is a normal constituent of mesangial extracellular matrix. Using a quantitative method based on enzyme immunoassay we assessed the intraglomerular fibronectin content and its degradation in obese Zucker rats and their lean littermates. In the obese Zucker rats the glomerular fibronectin content was significantly higher in comparison to the controls (88±6 vs 48±4 ng/103 glomeruli). Furthermore, proteinase activity against fibronectin was significantly reduced in the glomeruli of obese Zucker rats when compared to control animals (at pH 5.4: 186±6 U/mg protein vs 286±14 U/mg protein, at pH 7.4: 152±12 U/mg protein vs 193±12 U/mg protein). These data demonstrate that in obese Zucker rats there is a glomerular accumulation of fibronectin which we propose is at least partly due to diminished proteolytic digestion. Whether accumulation of intraglomerular fibronectin contributes to progressive glomerulosclerosis remains a matter of debate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00408351
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Chromatographic investigations on biodegraded crude oils (1985)
    Springer
    Chromatographia 20 (1985), S. 407-416 
    Details
    ISSN: 1612-1112
    Keywords: Gas chromatography-mass spectrometry ; Size exclusion chromatography ; Crude oil analysis ; Biodegradation ; Biological markers ; C- and H-isotopes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Summary Microorganisms have been isolated from a biodegraded crude oil from the Gifhorn trough, Lower Saxony. A non-degraded crude oil, related to the same source rock as the biodegraded one, was inoculated with the microorganisms found and the course of biodegradation thus initiated was followed by gas and liquid chromatographic techniques. The influence of biodegradation on commonly used oil-to-oil correlation parameters was investigated in detail.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02265482
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    Paper (German National Licenses)
    Fulltext
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