Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Effect of Portacaval Anastomosis on Electrically Stimulated Release of Glutamate from Rat Hippocampal Slices (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 56 (1991), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: To evaluate the effects of chronic liver failure on release of the excitatory transmitter glutamate, electrically stimulated Ca2+-dependent and Ca2+-independent release of glutamate in the absence or presence of NH4+ was studied in superfused slices of hippocampus from portacaval-shunted or sham-operated rats 4 weeks after surgery. Spontaneous and stimulation-evoked release of glutamate was higher in shunted rats in the presence of normal or low Ca2+ concentrations, and this release was depressed by 5 mM ammonium chloride. These findings suggest that portacaval shunting results in increased levels of extracellular glutamate in brain, probably due to a decreased reuptake of glutamate into perineuronal astrocytes, shown in previous studies to undergo neurqpathological changes following portacaval shunting. Changes in the inactivation of transmitter glutamate could be responsible, at least in part, for the neurological dysfunction resulting from sustained hyperammonemia and portal-systemic shunting resulting from chronic liver failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1991.tb02041.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Amino Acid Changes in Autopsied Brain Tissue from Cirrhotic Patients with Hepatic Encephalopathy (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 49 (1987), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Brain tissue was obtained at autopsy from nine cirrhotic patients dying in hepatic coma and from an equal number of controls, free from neurological, psychiatric, or hepatic diseases, matched for age and time interval from death to freezing of dissected brain samples. Glutamine, glutamate, aspartame, and γ-aminobutyric acid (GABA) levels were measured in homogenates of cerebral cortex (prefrontal and frontal), caudate nuclei, hypothalamus, cerebellum (cortex and vermis), and medulla oblongata as their O-phthalaldehyde derivatives by HPLC using fluorescence detection. Glutamine concentrations were found to be elevated two- to fourfold in all brain structures, the largest increases being observed in prefrontal cortex and medulla oblongata. Glutamate levels were selectively decreased in prefrontal cortex (by 20%), caudate nuclei (by 27%), and cerebellar vermis (by 17%) from cirrhotic patients. On the other hand, GABA content of autopsied brain tissue from these patients was found to be within normal limits in all brain structures. It is suggested that such region-selective reductions of glutamate may reflect loss of the amino acid from the releasable (neurotransmitter) pool. These findings may be of significance in the pathogenesis of hepatic encephalopathy resulting from chronic liver disease. Key Words: Hepatic encephalopathy—Hyperammonemia— Cerebral amino acids—Glutamine—Glutamate—γ-Aminobutyric acid. Lavoie J. et al. Amino acid changes in autopsied brain tissue from cirrhotic patients with hepatic encephalopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1987.tb00949.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Reduced sensory and motor nerve conduction velocities in moderate drinkers (2000)
    Oxford, UK : Blackwell Publishing Ltd
    Addiction biology 5 (2000), S. 0 
    Details
    ISSN: 1369-1600
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The mechanism responsible for peripheral nerve dysfunction in chronic alcoholism has not been fully elucidated either in terms of its relationship to the quantity of alcohol consumed or to nutritional status. As part of a series of studies to address these issues, the effects of moderate drinking (60–90 g ethanol per day) or heavy drinking (〉 100 g ethanol per day) on peripheral nervous function and thiamine status was measured in 73 patients admitted to a detoxification unit. Electromyographic evaluation revealed significant reductions in median and ulnar sensory and motor nerve conduction velocities in both moderate drinkers (n = 30) and heavy drinkers (n = 43) compared to age-matched controls. Twelve moderate drinkers and 25 heavy drinkers manifested clinical neurological signs of peripheral neuropathy. Thiamine deficiency, as revealed by erythrocyte transketolase activation assay, was detected in two moderate drinkers and seven heavy drinkers but was not significantly correlated with electromyographic alterations with the exception of ulnar nerves. These findings provide evidence for significant early peripheral nerve dysfunction in moderate drinkers and a possible contributory role of thiamine deficiency to the ulnar nerve conduction deficits. Whether deficits in other water-soluble vitamins or a direct neurotoxic effect of ethanol are implicated in alcoholic peripheral neuropathy awaits further studies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1080/13556210071298
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Alterations of thiamine phosphorylation and of thiamine-dependent enzymes in Alzheimer's disease (1996)
    Springer
    Metabolic brain disease 11 (1996), S. 81-88 
    Details
    ISSN: 1573-7365
    Keywords: Alzheimer's Disease ; thiamine ; thiamine phosphorylation ; thiamine monophosphate ; thiamine diphosphate ; thiamine-dependent enzymes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is a growing body of evidence to suggest that thiamine neurochemistry is disrupted in Alzheimer's Disease (AD). Studies in autopsied brain tissue from neuropathologically proven AD patients reveal significantly reduced activities of the thiamine phosphate dephosphorylating enzymes thiamine diphosphatase (TDPase) and thiamine monophosphatase (TMPase) as well as the thiamine diphosphate-dependent enzymes, pyruvate dehydrogenase complex, α-ketoglutarate dehydrogenase (αKGDH) and transketolase. Reductions in enzyme activities are present both in affected areas of AD brain as well as in relatively well conserved tissue. Decreased TDP concentrations and concomitantly increased TMP in autopsied brain tissue from AD patients and in CSF from patients with Dementia of the Alzheimer Type suggests that CNS thiamine phosphorylation-dephosphorylation mechanisms are disrupted in AD. αKGDH is a rate-limiting enzyme for cerebral glucose utilization and decreases in its activity are associated with lactic acidosis, cerebral energy failure and neuronal cell loss. Deficiencies of TDP-related metabolic processes could therefore participate in neuronal cell death mechanisms in AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02080933
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Plasma and CSF Benzodiazepine Receptor Ligand Concentrations in Cirrhotic Patients with Hepatic Encephalopathy: Relationship to Severity of Encephalopathy and to Pharmaceutical Benzodiazepine Intake (1998)
    Springer
    Metabolic brain disease 13 (1998), S. 201-210 
    Details
    ISSN: 1573-7365
    Keywords: Hepatic Encephalopathy ; “endogenous benzodiazepines” ; benzodiazepine receptors ; flumazenil ; cirrhosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Increased plasma and CSF concentrations of substances which bind to brain benzodiazepine receptors have previously been reported in cirrhotic patients with hepatic encephalopathy (HE). However, their relationship to previous intake of pharmaceutical benzodiazepines has not been clearly established. In the present study, plasma levels of benzodiazepine receptor ligands (BZRLs) were measured using a sensitive radioreceptor assay in 12 control subjects with no evidence of hepatic, neurological or psychiatric illness, 11 cirrhotic patients without HE, 24 cirrhotic patients with moderate (grade I-II) HE and in 45 cirrhotic patients with severe (grade II-IV) HE. In addition, CSF concentrations of BZRLs were measured in 8 cirrhotic patients with HE and an equal number of age-matched controls. Recent intake (within 10 days) of pharmaceutical benzodiazepines was assessed by detailed review of medical files, and interviews with the patient, at least one family member as well as the pharmacist. Significantly increased plasma concentrations of BZRLs were observed in cirrhotic patients with severe encephalopathy (p〈0.02) compared to controls and to cirrhotic patients without (or with mild) neurological impairment. Increased plasma BZRLs could be accounted for by prior exposure to benzodiazepine medication in all cases. CSF concentrations of BZRLs in cirrhotic patients were not significantly different from control values. These findings do not support a role for “endogenous” benzodiazepines in the pathogenesis of HE in chronic liver disease but suggest that pharmaceutic benzodiazepines administered to cirrhotic patients as sedatives or as part of endoscopic work-up could have contributed to the neurological impairment in some patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1023271908568
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Activities of neuronal and astrocytic marker enzymes in autopsied brain tissue from patients with hepatic encephalopathy (1987)
    Springer
    Metabolic brain disease 2 (1987), S. 283-290 
    Details
    ISSN: 1573-7365
    Keywords: hepatic encephalopathy ; glutamic acid decarboxylase ; glutamine synthetase ; choline acetyltransferase ; autopsied brain tissue ; γ-aminobutyric acid (GABA) ; glutamate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Activities of the γ-aminobutyric acid (GABA) and cholinergic nerve-terminal marker enzymes glutamic acid decarboxylase (GAD) and choline acetyltransferase (CAT) as well as the astrocytic enzyme glutamine synthetase (GS) were measured in homogenates of dissected brain tissue obtained at autopsy from nine cirrhotic patients dying in hepatic encephalopathy and an equal number of control subjects matched for age, agonal status, and time interval from death to freezing of autopsied material. GAD activities varied as a function of agonal status in control samples, confirming a previous report, but were unchanged in brain tissue from cirrhotic patients, suggesting no loss of integrity of presynaptic GABA nerve terminals in this disease. On the other hand, GS activities were selectively decreased by 25% (P 〈 0.01) in caudate nuclei of cirrhotic patients, reflecting, no doubt, the severe astrocytosis consistently observed in this brain structure. CAT activities, expressed per milligram of protein, were found to be increased by 30% (P 〈 0.01) in the prefrontal cortex of cirrhotic patients. Whether such changes result from a relative increase in CAT as a consequence of losses of astrocytic protein or reflect altered cholinergic function in hepatic encephalopathy associated with chronic liver disease awaits further study.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00999698
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Loss of [3H]kainate and of NMDA-displaceable [3H]glutamate binding sites in brain in thiamine deficiency: Results of a quantitative autoradiographic study (1995)
    Springer
    Neurochemical research 20 (1995), S. 1155-1160 
    Details
    ISSN: 1573-6903
    Keywords: Thiamine deficiency ; glutamate ; NMDA receptors ; AMPA receptors ; kainate receptors ; autoradiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies suggest that alterations of brain glutamate synthesis and release occur in experimental thiamine deficiency. In order to assess the integrity of post-synaptic glutamatergic receptors in thiamine deficiency, binding sites for [3H]glutamate (displaced by NMDA), [3H]-kainate, and [3H]quisqualate (AMPA sites) were evaluated using Quantitative Receptor Autoradiography in rat brain following 14 days of treatment with the central thiamine antagonist pyrithiamine. Compared to pair-fed controls, brains of symptomatic thiamine-deficient animals contained significantly fewer NMDA-displaceable binding sites in cerebral cortex, medial septum and hippocampus. It has been suggested that NMDA-receptor mediated glutamate excitotoxicity plays a role in the pathogenesis of neuronal loss in thiamine deficiency. If such is the case, the selective loss of NMDA binding sites in cerebral cortex and hippocampus offers a possible explanation for the relative nonvulnerability of these brain regions to pyrithiamine-induced thiamine deficiency. [3H]quisqualate (AMPA) binding sites were unchanged in all brain regions of pyrithiamine-treated rats whereas [3H]kainate sites were significantly reduced in density in medial and lateral thalamus. The decline in these binding sites may be due to neuronal loss in pyrithiamine-induced thiamine deficiency. Alterations of glutamatergic synaptic function involving both NMDA and kainate receptor subclasses could contribute to the pathogenesis of neurological dysfunction in Wernicke's Encephalopathy in humans.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00995378
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...