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  • 1
    Electronic Resource
    Electronic Resource
    Enzymes of Cerebral GABA Metabolism and Synaptosomal GABA Uptake in Acute Liver Failure in the Rabbit: Evidence for Decreased Cerebral GABA-Transaminase Activity (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 42 (1984), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Measurements of the activities of the two key enzymes in cerebral GABA metabolism—glutamate decarboxylase (GAD) and GABA-transaminase (GABA-T)—were performed in normal rabbits and in rabbits with hepatic encephalopathy due to galactosamine-induced liver failure. Furthermore the uptake of GABA by synaptosomes was studied. Hepatic encephalopathy was associated with a marked decrease in the activity of GAB A-T. This decrease in activity was already apparent in galactosamine-treated rabbits before the onset of hepatic encephalopathy. Sera and serum ultrafiltrates of rabbits with hepatic encephalopathy but not of normal rabbits or of rabbits with uremic encephalopathy were shown to inhibit GABA-T activity in vitro. Cerebral GAD activity and synaptosomal GABA uptake in rabbits with hepatic encephalopathy and in untreated animals were not different. These later findings indicate that hepatic encephalopathy is not associated with alterations of presynaptic GABA nerve terminals in the central nervous system. The demonstration of a decrease in cortical GABA-T activity provides indirect evidence for decreased GABA turnover in the brains of rabbits with hepatic encephalopathy and thus is compatible with augmented GABA-ergic inhibitory neurotransmission contributing to the neural inhibition of hepatic encephalopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1984.tb02816.x
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  • 2
    Electronic Resource
    Electronic Resource
    Short- and long-term effects of therapy with interferon-α and pegylated interferon-α/ribavirin on platelet plug formation and von Willebrand factor release in patients with chronic hepatitis C (2005)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 21 (2005), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : A pegylated interferon-alpha-induced decrease in platelet counts may become a limiting factor for continuation of therapy.Aim : To evaluate the effect of pegylated interferon-α administration on platelet plug formation and von Willebrand factor antigen release in patients with chronic hepatitis C.Methods : Thirty patients with chronic hepatitis C (genotype 1; fibrosis 1–3: n = 16, cirrhosis: n = 14) received a single dose of 9 MU interferon-α2a, followed by weekly administration of 180 μg of pegylated interferon-α2a/ribavirin for 48 weeks. Platelet counts, platelet function (collagen–epinephrine-induced closure time) and von Willebrand factor antigen were measured.Results : Platelet counts and collagen–epinephrine-induced closure time decreased by 13% and 16%, respectively, 24 h after the first dose of interferon-α2a, and von Willebrand factor antigen levels increased by 31% (P 〈 0.01) compared with baseline. During a 48-week observation period, platelet counts decreased by a maximum of 33% (P 〈 0.001), von Willebrand factor antigen levels increased by 69% (P 〈 0.001) whereas collagen–epinephrine-induced closure time did not change. In noncirrhotic patients, the increase of von Willebrand factor antigen levels was maintained throughout therapy without a change in collagen–epinephrine-induced closure time. In contrast, in cirrhotics, von Willebrand factor antigen levels did not increase, while collagen–epinephrine-induced closure time was prolonged.Conclusion : Single-dose interferon-α decreases platelet counts but improves platelet function, possibly by the release of von Willebrand factor antigen. Accordingly, long-term antiviral treatment had no effect on collagen–epinephrine-induced closure time, despite the decrease in platelet count in noncirrhotic patients. Such a compensation of decreased platelet counts by increased von Willebrand factor antigen level did not occur in cirrhotics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2004.02305.x
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  • 3
    Electronic Resource
    Electronic Resource
    Diagnosis and current therapy of Wilson's disease (2004)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 19 (2004), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Wilson's disease is an autosomal recessive inherited disorder of hepatic copper metabolism resulting in liver disease and/or neuropsychiatric disease. The diagnosis of neurological disease is straightforward if the following symptoms are present: Kayser–Fleischer rings, typical neurological symptoms and low serum ceruloplasmin levels. The diagnosis is more complex in patients presenting with liver diseases. None of the commonly used parameters alone allows a diagnosis with certainty. A combination of various laboratory parameters is necessary to firmly establish the diagnosis. In the future, limited mutation analysis may play an important diagnostic role. Recently, a group of international experts has proposed a score based on a variety of tests and clinical symptoms. The validity of this score needs to be assessed prospectively. Treatment requires life-long administration of copper chelators (d-penicillamine, trientine). A frequently used alternative is zinc. None of these treatments has been tested by prospective randomized controlled studies. Liver transplantation is reserved for severe or treatment-resistant cases with advanced liver disease, whilst experience with refractory neuropsychiatric disease is limited.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2003.01813.x
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  • 4
    Electronic Resource
    Electronic Resource
    Hemmung der Glukose und Leucin-Resorption durch Somatostatin beim Hund (1981)
    Springer
    Research in experimental medicine 178 (1981), S. 241-246 
    Details
    ISSN: 1433-8580
    Keywords: Somatostatin (growth hormone release inhibitory factor) ; Small bowel absorption ; Glucose ; Leucin ; Somatostatin ; Dünndarmresorption ; Glukose ; Leucin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung In einer Resorptionsstudie an der isolierten Thiry Vella-Schlinge am wachen Hund wurde der Einfluß von Somatostatin (SST) auf die Dünndarmresorption von Glukose und Leucin untersucht. Unter SST wurde eine signifikante, aber nicht totale Hemmung der Glukoseresorption und eine prozentuell geringere signifikante Verminderung der Leucinresorption gefunden.
    Notes: Summary Small bowel absorption of glucose and leucin was investigated under the influence of somatostatin (SST) using an isolated Thiry Vella loop in the unrestrained dog. SST infusion significantly reduced glucose and leucin absorption, inhibiting glucose absorption more than that of leucin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01851013
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  • 5
    Electronic Resource
    Electronic Resource
    Der Aufbau der Placenta-Septen Untersuchungen mit Hilfe der Quinacrinfluorescenzfärbung des Y-Chromatins (1973)
    Springer
    Anatomy and embryology 142 (1973), S. 207-217 
    Details
    ISSN: 1432-0568
    Keywords: Placental septa ; Quinacrine stain ; Y-chromatin ; Decidua cells ; Trophoblast cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Mit Hilfe der Quinacrinfluorescenzdarstellung des Y-Chromatins wurden in Placentarsepten geburtsreifer Placenten mütterliche und kindliche Zellen abgegrenzt. Es ergab sich, daß der Aufbau der Septen nicht einheitlich ist und der Anteil an mütterlichem und kindlichem Gewebe von Septum zu Septum verschieden ist. Den kindlichen großzelligen Elementen entsprechen die X-Zellen und die “clear trophoblastic cells”. Den mütterlichen großzelligen Elementen entsprechen die Deciduazellen.
    Notes: Summary Maternal and fetal cells of placental septa of newborn were determined using the quinacrine fluorescence staining of the Y chromatin. The septa are composed partly of fetal and partly of maternal cells, the proportion of each changing in different septa. Fetal large cells correspond to X-cells and clear trophoblastic cells, maternal large cells correspond to decidua cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00519722
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  • 6
    Electronic Resource
    Electronic Resource
    Colony stimulating activity in acute and chronic endotoxinemia in man (1979)
    Springer
    Cellular and molecular life sciences 35 (1979), S. 1398-1400 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Blood granulocyte-macrophage colony stimulating activity (GM CSF) was measured in 6 normal individuals challenged with low-dose endotoxin and in 63 unselected patients with nonhaematological disorders. 5/63 patients were febrile and 5 other patients showed detectable endotoxin levels, as measured by the Limulus assay. CSA levels showed a rapid increase in normal individuals following endotoxin administration, but were in the normal range in patients with chronic endotoxinemia or in those with febrile disorders. Thus, unlike acute endotoxinemia, chronic endotoxinemia is not associated with elevated activity that promotes growth of myeloid commited stem cells. In addition, fever per se did not coincide with elevated blood CSA levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01964032
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  • 7
    Electronic Resource
    Electronic Resource
    Intestinal neuronal degeneration in a patient with chronic idiopathic intestinal pseudoobstruction (1989)
    Springer
    Digestive diseases and sciences 34 (1989), S. 123-128 
    Details
    ISSN: 1573-2568
    Keywords: chronic idiopathic intestinal pseudoobstruction ; neuronal degeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neuropathological examination of the gut in a patient with chronic idiopathic intestinal pseudoobstruction and temporal lobe epilepsy showed a degeneration of Auerbach's and of Meissner's plexus. The extent of degenerative changes increased in an aboral to oral direction. Neuronal degeneration was characterized by ballooning of the cytoplasm of the ganglial cells, by a hyperargyrophilia, a shortening and dilation of cell processes, and a progressive fragmentation and loss of axoris. In rectal biopsies, a PAS-positive granular material was detected in the cytoplasm of ballooned ganglial cells. A severe peripheral neuropathy with fiber degeneration in the posterior columns and axonal lesions within ventral nerve roots and a more recent fiber degeneration in the lateral columns corresponding to the picture of subacute combined degeneration of the spinal cord and a symmetrical Ammon's horn sclerosis was present. This case of progressive intestinal neuronal degeneration of unknown origin is a newly described condition leading to chronic idiopathic intestinal pseudoobstruction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01536166
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  • 8
    Electronic Resource
    Electronic Resource
    Postsynaptic γ-aminobutyric acid receptors in hepatic coma following portacaval shunt and hepatic artery ligation in the rat (1987)
    Springer
    Metabolic brain disease 2 (1987), S. 195-200 
    Details
    ISSN: 1573-7365
    Keywords: γ-aminobutyric acid (GABA) ; hepatic encephalopathy ; neurotransmission ; receptor binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The specific binding of γ-aminobutyric acid (GABA) to synaptic membranes prepared from the brains of rats with acute liver failure due to portacaval shunt and hepatic artery ligation was measured. No changes in the affinity or the density of the low- and high-affinity binding sites of the GABA receptor were observed, indicating that this model of acute hepatic encephalopathy is apparently not associated with altered GABAergic neurotransmission.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00999610
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  • 9
    Electronic Resource
    Electronic Resource
    A benzodiazepine antagonist does not alter the course of hepatic encephalopathy or neural γ-aminobutyric acid (GABA) binding (1987)
    Springer
    Metabolic brain disease 2 (1987), S. 201-205 
    Details
    ISSN: 1573-7365
    Keywords: antagonist ; benzodiazepine ; hepatic encephalopathy ; coma ; γ-aminobutyric acid (GABA)-ergic ; neural binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The progressive course of hepatic encephalopathy developing in rats after massive hepatic ischemia due to hepatic artery ligation within 48 hr of a portacaval shunt was not altered by the injection of a benzodiazepine antagonist, CGS 8216, in a dose that was sufficient to reverse diazepam-induced coma quickly. The onset of hepatic coma was shortened 20 to 25% by the antagonist, rather than being delayed, as would be expected if hepatic coma were due to a γ-aminobutyric acid (GABA)-ergic effect. The neural binding of GABA by brains from rats in deep hepatic coma was unaffected by the injection of the benzodiazepine antagonist.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00999611
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  • 10
    Electronic Resource
    Electronic Resource
    Role of tryptophan in the elevated serotonin-turnover in hepatic encephalopathy (1998)
    Springer
    Journal of neural transmission 105 (1998), S. 975-986 
    Details
    ISSN: 1435-1463
    Keywords: Keywords: Hepatic encephalopathy ; tryptophan ; serotonin ; branched-chain amino acids ; thioacetamide ; liver failure.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The increase of the brain levels of 5-hydroxyindoleacetic acid (5-HIAA) in hepatic encephalopathy (HE) suggests an increased turnover of serotonin (5-HT). To study the role of tryptophan on the increased brain 5-HT metabolism in HE, we attempted to monitor brain levels of tryptophan in rats with thioacetamide-induced acute liver failure by intravenous infu-sion of branched-chain amino acids (BCAA). The effect of this treatment on 5-HT synthesis and metabolism was investigated in five brain areas. BCAA-infusions (1 and 2 gm/kg/24 h) increased the ratio BCAA/aromatic amino acids in plasma two- and fourfold, respectively, and lowered both plasma and brain levels of tryptophan. At the higher BCAA-dose all parameters suggesting an altered brain 5-HT metabolism (increased brain levels of 5-HT and 5-HIAA, increased 5-HIAA/5-HT ratio) were almost completely normalized. These results provide further evidence for the role of tryptophan in the elevation of brain 5-HT metabolism and for a potential role of BCAA in the treatment of HE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007020050106
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