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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 41 (1985), S. 1042-1045 
    ISSN: 1420-9071
    Keywords: Liver failure ; hepatitis ; galactosamine ; coenzyme A ; NAD
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Galactosamine, a selective hepatotoxin, produces in rats histologic alterations, which show the characteristics of severe human viral hepatitis. In the present study the efficacy of two different cofactor regimens (coenzyme A, NAD, alpha lipoic-acid, cocarboxylase) in rats with fulminant galactosamine hepatitis were tested. The results showed an improvement of the short-term survival with a short-term treatment and definitely better survival with a long-term regimen with cofactors.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 53 (1975), S. 605-610 
    ISSN: 1432-1440
    Keywords: Vollständiges Fasten ; Stickstoff ; Glukagon ; Blutglucose ; Starvation ; nitrogen ; glucagon ; blood glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Healthy volunteers of ideal weight (12 men and 12 women) were fasted for 6 days, and obese but otherwise healthy subjects (20 men, 28 women) for 6–28 days. In all groups studied a significant increase in urinary nitrogen loss from day 1 to day 3 of fasting was followed by a steady decrease. The early rise in urinary nitrogen excretion coincided with a rise in plasma glucagon levels, suggesting a relation of the latter to increased gluconeogenesis from amino acids. At equal weight greater nitrogen losses were found in men than in women, in both normal and obese subjects. In spite of much higher weight and larger energy expenditure the nitrogen loss in obese subjects however was not higher than in normal ones. Mean daily nitrogen losses varied from 14.5 g (normal and obese men early in starvation) to 3.0 g (obese women after a 4-weeks fast). Calculating the amount of calories derived from body protein (urinary nitrogen ×6.25×4.1) and taking total energy expenditure from tabular metabolic values, the contribution of protein to total calorie output was found to vary from 15% (normal men 6 day fast) to 5% (obese women, 4th week of fasting). The clinical significance of nitrogen loss during therapeutic fasting is discussed.
    Notes: Zusammenfassung Idealgewichtige, gesunde Versuchspersonen (12 Männer und 12 Frauen) wurden während 6tägigen Fastens und adipöse, aber im übrigen gesunde Personen (20 Männer, 28 Frauen) während 6–28tägigen Fastens untersucht. Bei allen Gruppen fand sich während der ersten 3 Fastentage ein signifikanter Anstieg des Stickstoffverlustes im Urin, gefolgt von einem kontinuierlichen Abfall. Der Anstieg der Stickstoffausscheidung erfolgte gleichzeitig mit einem Anstieg des Plasmaglucagons, was für einen Zusammenhang des letzteren mit vermehrter Gluconeogenese aus Aminosäuren spricht. Bei gleichem Körpergewicht waren die Stickstoffverluste der männlichen Probanden größer als bei den weiblichen, sowohl bei normalgewichtigen wie auch bei übergewichtigen Personen. Andererseits war der Stickstoffverlust der adipösen Gruppen trotz viel höherem Körpergewicht und höherer Energieausgabe nicht größer als jener der normalgewichtigen. Der mittlere Stickstoffverlust pro Tag variierte zwischen 14,5 g (normal- und übergewichtige Männer während der ersten Fastentage) und 3,0 g (adipöse Frauen nach 4wöchigem Fasten). Durch Berechnung der aus Protein freigesetzten Kalorienmenge (Urinstickstoff ×6,25×4,1) und Entnahme der Gesamtenergieausgabe aus Stoffwechseltabellen wurde ein Anteil des Proteins an der Gesamtkalorienausgabe von 15% (normalgewichtige Männer bei 6tägigem Fasten) bis 5% (adipöse Frauen nach 4 Fastenwochen) ermittelt. Die klinische Bedeutung des Stickstoffverlustes bei Null-Diät wird diskutiert.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Whipple's disease ; Chronic interstitial nephritis ; Granulomas ; Boeck's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Report is given on a 68-year-old man who suffered primarily from progressive weight loss and repeated episodes of fever and arthralgia. Later, liver dysfunction and renal insufficiency developed. Liver and kidney biopsics disclosed granulomatous hepatitis and nephritis. Because of the morphologic and clinical findings, the diagnosis of Boeck's disease was made. Shortly before death, diarrhea developed. Autopsy revealed a massive systemic involvement in Whipple's disease proven by light and electron microscopy and immunofluorescence. Tuberculoid and epitheloid cell granulomas and isolated giant cells were found in addition to the biopsy findings in skeleton muscles, the small intestine, lymphnodes and bronchi. At autopsy, the kidney showed chronic interstitial nephritis. The literature of kidney involvement in Whipple's disease is reviewed. This is the first case with granulomatous interstitial nephritis and chronic renal insufficiency in an inadequately treated Whipple's disease.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 50 (1972), S. 296-301 
    ISSN: 1432-1440
    Keywords: Coma ; liverfailure ; brain ; edema ; Coenzyme A ; Koma ; Leberinsuffizienz ; Gehirn ; Ödem ; Coenzym A
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung 30 Patienten mit endogenem Leberkoma wurden mit Coenzym A, NAD, α-Liponsäure und Cocarboxylase behandelt. 20 Patienten starben. 16 Patienten wurden autopsiert und zeigten ein Hirnödem. Klinische Zeichen und pathogenetische Mechanismen des Hirnödems werden diskutiert. Unsere Befunde lassen vermuten, daß das Hirnödem und nicht das Leberkoma an sich als unmittelbare Todesursache bei diesen Patienten angesehen werden muß. Aus diesem Grunde sollten Maßnahmen gesucht werden, die die Entstehung des Hirnödems beim endogenen Leberkoma verhindern.
    Notes: Summary 30 patients with endogenous liver coma were treated with coenzyme, A, NAD, α-lipoic acid and cocarboxylase. 20 patients died; 16 were autopsied and showed severe cerebral edema. Clinical signs and pathogenetic mechanisms of cerebral edema are discussed. Our findings suggest that brain edema, not liver coma itself, was the immediate cause of death in these patients. Therefore, measures should be found in the future to prevent and to treat brain edema in endogenous hepatic coma.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1440
    Keywords: Fulminante Lebernekrose ; Hirnödem ; Mannitol ; Kohlehämoperfusion ; Leberzellregeneration ; Fulminant liver necrosis ; Brain edema ; Mannitol ; Charcoal hemoperfusion ; Liver cell regeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The clinical course of a 26 year old female patient with acute liver necrosis and coma due to hepatitis B is reported. The disturbances of conciousness had improved. The patient survived 41 days after the beginning of the coma and developped livercell regeneration and an acute post-hepatitic liver cirrhosis. As a grave complication a septicemia with aspergillus was observed. The patient died because of gastro-intestinal hemorrhage. At autopsy there were no signs of brain edema. The treatment consisted in: daily infusions with coenzyme A, nicotinamid-adenin-dinucleotide, alpha lipoic acid and cocarboxylase to improve the metabolic disorders and the clinical picture; mannitol intravenously to prevent and to treat cerebral edema; 33 charcoal-hemoperfusions to remove toxic substances of acute liver failure. Treatment of the aspergillus infection with 5-fluorocytosine and amphotericine B and infusion of concentrated ascites led to a decompensation of liver functions. From this observation the following conclusions can be drawn: after an acute viral hepatic necrosis, new synthetic functions and improvements of the disturbed intermediary metabolism in regenerated liver-cells can eventually be seen only after twenty-four to thirty days. With systematically applicated mannitol infusions it is possible to treat cerebral edema effectively.
    Notes: Zusammenfassung Es wird der Verlauf einer durch Hepatitis B bedingten, akuten Lebernekrose mit Coma bei einer 26jährigen Patientin beschrieben. Die Bewußtseinsstörung besserte sich. Die Patientin überlebte 41 Tage und entwickelte Leberzellregenerate und eine akute posthepatitische Leberzirrhose. Im Verlauf trat als schwere Komplikation eine Pilzsepsis auf. Die Patientin starb an einer Magendarmblutung. Bei der Autopsie fand sich kein Hirnödem. Die Behandlung beständ in täglichen Infusionen von Coenzym A, Nikotinamid-adenin-dinukleotid, alpha-Liponsäure und Cocarboxylase zur Besserung von metabolischen Störungen und klinischem Bild; Mannitol intravenös, zur Verhinderung und Behandlung des Hirnödems; 33 Kohlehämoperfusionen, zur Entfernung toxischer Substanzen. Behandlung der Aspergillus-Infektion mit 5-Fluorocytosin und Amphotericin B und Infusion des konzentrierten Ascites führten zu einer Dekompensation der Leberfunktionen. Aus dieser Beobachtung können folgende Schlüsse gezogen werden: Nach einer akuten viralen Lebernekrose kann es erst nach 24–30 Tagen zur Wiederaufnahme synthetischer Funktionen und zur Besserung des gestörten Intermediärstoffwechsels in regenerierten Leberzellen kommen. Mit systematischer Mannitol-Therapie ist es möglich, das Hirnödem wirksam zu bekämpfen.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 59 (1981), S. 431-436 
    ISSN: 1432-1440
    Keywords: Renal insufficiency ; Uraemic pericarditis ; 2,3-Butylene glycol ; Acetaldehyde ; 2,3-Diphosphoglycerate ; Niereninsuffizienz ; urämische Perikarditis ; 2,3-Butylenglykol ; Acetaldehyd ; 2,3-Diphosphoglycerat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei 103 Patienten mit Nierenversagen wurden die Blutkonzentration von Pyruvat und einiger seiner Metaboliten sowie die Erythrozytenkonzentration von 2,3-Diphosphoglycerat mit dem Schweregrad der Uraemie verglichen. 2,3-Butylenglykol war beim chronischen Nierenversagen deutlich erhöht und zeigte eine positive lineare Korrelation (2p〈0.001) mit dem Harnstoff; seine Werte lagen noch höher bei entsprechenden Patienten mit urämischer Perikarditis. Bei akuten Nierenversagen lagen sie jedoch unter Berücksichtigung der Abhängigkeit vom Harnstoff nicht über der Norm. Acetaldehyd, Acetoin und Acetat verhielten sich teilweise ähnlich. Die schwere Urämie, klinisch charakterisiert durch die urämische Perikarditis, zeichnete sich unabhängig vom Harnstoff durch besonders hohe Werte von 2,3-Butylenglykol und Acetaldehyd sowie des Pyruvat-Laktat-Quotienten aus. Die nicht hämodialysierten chronischen Uraemiker ließen außerdem den auf Grund der schweren Anämie erwarteten Anstieg des erythrozytären 2,3-Disphosphoglycerats vermissen. Die Störung des oxidativen Glucoseabbaus zwischen Pyruvat und dem Tricarbonsäurezyklus scheint die Urämie biochemisch besser zu charakterisieren als die Harnstoffkonzentration im Blut.
    Notes: Summary The blood concentrations of pyruvate and of some of its metabolites and the red cell 2,3-diphosphoglycerate concentration were compared with the severity of uraemia in 103 patients with renal failure. In chronic renal failure 2,3-butylene glycol was distinctly elevated, and a positive linear correlation (2p〈0.001) with the urea was found. The values were even higher in corresponding patients with uraemic pericarditis, but, — taking into account their relation to the urea —, they were not elevated in acute renal failure. Acetaldehyde, acetoin and acetate behaved in part likewise. Severe uraemia, which clinically was demonstrated by uraemic paricarditis, was characterized biochemically, without regard to the urea, by very elevated values of 2,3-butylene glycol and acetaldehyde and of the pyruvate:lactate ratio. In addition, the chronic patients who were not undergoing regular haemodialysis, did not show the expected rise of 2,3-diphospho-glycerate along with progressive anaemia. The data suggest that the uraemic state is characterized by the impairment of the oxidative glucose metabolism between pyruvate and the tricarbonic acid cycle more precisely than by the blood urea.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 13 (1957), S. 497-499 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary (1) The quotient urea nitrogen: non-protein nitrogen was determined in nephrectomized uremic rats and compared with the quotient in control animals. The quotient in nephrectomized uremic animals was 0.74, in control animals 0.35. The elevation of the quotient is of hepatic origin. (2) The desamination was increased in the liver of nephrectomized uremic animals in comparison to controls; the urea production was unchanged.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 32 (1976), S. 830-832 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Hepatic CoA concentrations and contents were significantly higher in rats having received i.v. CoA injections than in control rats. Maximum hepatic CoA concentrations were found 0.5–1 h after injection. In rat brain, no increase in CoA concentration was detected after i. v. injection of CoA.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 37 (1981), S. 1323-1325 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Severe hepatitis is induced with D-galactosamine hydrochloride in rats. Animals develop brain edema which was treated with mannitol. 1 h after the last mannitol infusion brain water content decreased, but it was not decreased 6 h after treatment. The therapy reduced lethality (p〈0.025). The rigorous brain edema therapy impoved the prognosis of fulminant hepatic failure in the rat.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Acetoin and 2, 3-butylene glycol in blood of renal and hepatic patients are raised, when consciousness is disturbed. There is no correlation between blood levels of acetoin and 2, 3-butylene glycol and the degree of impairment of consciousness. Simultaneous determinations of acetoin and 2, 3-butylene glycol in blood and cerebrospinal fluid show that alterations of the cerebral pyruvic acid metabolism are difficult to detect in circulating blood.
    Type of Medium: Electronic Resource
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