Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new approach to pathogenetic study of hepatic encephalopathy was recently undertaken in order to identify the neurological alterations of the brain which characterize the coma. In this study attention was firstly addressed to a correct and objective evaluation of the comatose state in rats with fulminant hepatic failure induced by galactosamine. For this purpose visual evoked potentials were utilized since this electrophysiological test proved reliable and sensitive on the basis of an extensive pharmacological study. Two different stages of coma were identified in the rat and they were named mild and severe. Receptor binding studies performed on brain membranes of these rats show in the mild stage an increased number of low and high affinity GABA receptors and a decreased affinity of dopamine receptors. The severe stage is characterized by the persistence of only high affinity GABA receptors and a reduced number of dopamine receptors. This imbalance between inhibitory and excitatory receptor systems may explain the generalized central nervous system depression which characterizes the hepatic encephalopathy while the increased number of benzodiazepine receptors found in both stages of coma may account for the brain supersensitivity to sedative administration of patients with liver disease and for the sedative-induced episodes of coma. These receptor alterations may be attributed to a disuse and/or a partial degeneration of nerve terminals due to peripheral neurotoxins (i.e., ammonia, mercaptans, short chain fatty acids) and the decrease of glutamate decarboxylase activity and of zinc levels in brain tissues seems to be respectively a direct and an indirect demonstration of this phenomenon. Bearing in mind the supersensitivity of the GABA-benzodiazepine receptor system and their reciprocal interaction, a benzodiazepine antagonist was administered to rats in mild stage of encephalopathy. Electrophysiological and benzodiazepine binding studies demonstrated that this treatment can temporarily counteract some of the neurological disturbances of the earlier stage of coma and act as antidote of the sedative-induced episodes of coma.
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PMID:Hepatic encephalopathy. Experimental studies in a rat model of fulminant hepatic failure. 299 24

Evidence for increased plasma levels of complexes containing Gc (vitamin D-binding protein) and cellular actin has been previously reported during fulminant hepatic necrosis in man. In order to study this process in more detail, we produced liver injury in hamsters using increasing doses of acetaminophen, with serial collection of sera for up to 168 hr after acetaminophen injection. Hamster Gc was purified using a three-step procedure and was shown to resemble closely human Gc. Polyclonal antihamster Gc was prepared and used in rocket immunoelectrophoresis and radial immunodiffusion studies for quantitation of total serum Gc and the percentage of Gc complexed with actin. Serum Gc levels were depressed in animals having liver damage, and the extent of depression 42 hr after acetaminophen correlated with the extent of elevation of AST. The proportion of the total Gc that was present in the complexed form increased in relation to the severity of the liver disease. In serial studies, diminution in Gc level preceded the rise in AST and increase in the percent complexed. These changes closely resemble observations in man and suggest that the hamster-acetaminophen hepatotoxicity model may be of value in further study of interactions of Gc with intracellular actin components and its role in actin homeostasis in conditions of massive tissue necrosis.
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PMID:Diminished serum Gc (vitamin D-binding protein) levels and increased Gc:G-actin complexes in a hamster model of fulminant hepatic necrosis. 311 82

Intravenous drug abusers (IDA) show an important immunological dysfunction that plays a key role in pathogenesis of infections found in these patients. A defective adherence and chemotaxis has been described at the level of mononuclear phagocytic system (MPS). In this paper, we center on defective chemotaxis. In the face of a chemotactic alteration, the first step is trying to locate the alteration as humoral or cellular; we have used the work sheme proposed by Yousif-Kadaru. Serum of IDA and controls, E. Coli endotoxin-activated and non-activated were used as attractants. Chemotaxis was studied by the morphologic method of Snyderman. Attractant capacity of E. Coli endotoxin activated serum was 55.93 +/- 10.88, similar to that of controls, 59 +/- 10.58. The same was true for non-activated serum, 42.5 +/- 16.8 compared to 44.67 +/- 19.54. That means, according with the scheme proposed, that the alteration is localized in the cell. Some factors that could participate in the pathogenesis of the motor defect are commented in the discussion. The elevation in immunocomplexes titer observed in IDA could depress monocyte chemotaxis, but the defect would be humoral. A deficit in chemotactic factor could be discarded because its production capacity is preserved in IDA. Liver disease, both acute and chronic, is one of the most frequent medical complications in these patients. The cellular localization of depression eliminates any participation in the pathogenesis of chemotactic alteration.
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PMID:Depression of monocyte chemotaxis in intravenous drug abusers (IDA): cell alteration. 324 78

Cardiovascular function, serum ionized calcium (Ca+2), and serum citrate were measured intraoperatively in patients (n = 9) undergoing orthotopic hepatic homotransplantation. Serum citrate increased 20-fold (P less than 0.0006) following transfusion of citrated blood products in the absence of a functional liver. Serum ionized calcium decreased (P less than 0.003) with concomitant decreases in cardiac index (P less than 0.005), stroke index (P less than 0.004), and left ventricular stroke work index (P less than 0.001). Hemodynamic depression and ionic hypocalcemia were reversed following the administration of CaCl2. In contrast to patients with normal hepatic function, who may tolerate large amounts of citrated blood, patients with end-stage liver disease demonstrate acute ionic hypocalcemia with concomitant hemodynamic depression when receiving citrated blood products during the course of hepatic transplantation.
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PMID:Cardiovascular depression secondary to ionic hypocalcemia during hepatic transplantation in humans. 353 71

Aryl hydrocarbon hydroxylase activity was detectable in cultured macrophage monolayers of peripheral blood monocyte origin. Peripheral blood monocytes were isolated from patients with biopsy-confirmed liver disease and healthy volunteers. Macrophage monolayers were prepared and incubated at 37 degrees C. After 24 hr, the aryl hydrocarbon hydroxylase activity and cellular protein concentration were assayed on cell homogenates. The monocyte aryl hydrocarbon hydroxylase activity in cultured macrophages from normal volunteers was 1.23 +/- 0.16 (n = 19). The aryl hydrocarbon hydroxylase activity in macrophage cultures from patients with biopsy-confirmed liver disease was 0.48 +/- 0.05 (n = 20). This represents a significant (61%) decrease in monocyte aryl hydrocarbon hydroxylase compared to controls. The 20 patients have established cirrhosis or early stage liver disease. The established cirrhosis group includes alpha 1-antitrypsin deficiency-associated cirrhosis; primary biliary cirrhosis; alcoholic (Laennec's) cirrhosis; cryptogenic cirrhosis, and hemochromatosis. Early stage liver disease is attributed to methotrexate (Stage III), early stage primary biliary cirrhosis and alpha 1-antitrypsin deficiency. Our results indicate that the depression in monocyte aryl hydrocarbon hydroxylase activity is greater in patients with established cirrhosis than early stage liver disease. Our results further suggest that cultured monocytes from patients with liver disease spontaneously release soluble factors into the culture medium. Incubation of this medium, containing macrophage factors, with isolated hepatocytes significantly depress hepatocyte aryl hydrocarbon hydroxylase activity compared to medium obtained from cultures of monocytes from normal volunteers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Depression of peripheral blood monocyte aryl hydrocarbon hydroxylase activity in patients with liver disease: possible involvement of macrophage factors. 355 13

Case records of horses with equine ehrlichiosis (Ehrlichia equi) at the University of California Veterinary Medical Teaching Hospital and Ackerman Creek Large Animal Clinic were analyzed for evaluation of clinical signs, time of onset, hematologic values, response to treatment, and recovery. Equine ehrlichiosis was found to be seasonal in horses in the foothills of northern California, with higher incidence than reported previously. The horses developed fever, anorexia, depression, limb edema, icterus, and ataxia. Hematologic changes were leukopenia, thrombocytopenia, icterus, anemia, and inclusion bodies in the neutrophils and eosinophils. Diagnosis was made by observing the characteristic inclusion bodies, using a standard Wright's stain. Mortality was low, although complications of opportunistic secondary infection and injury due to ataxia did develop. Treatment with tetracycline resulted in prompt clinical improvement within 24 hours. Chronic cases were not detected. Equine ehrlichiosis should be differentiated from diseases with similar clinical signs including encephalitis, liver disease, purpura hemorrhagica, equine infectious anemia, and equine viral arteritis.
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PMID:Equine ehrlichiosis in northern California: 49 cases (1968-1981). 355 86

The authors administered at least one dexamethasone suppression test (DST) and Hamilton Rating Scale for Depression (HRSD) simultaneously to 30 psychiatric inpatients following detoxification from alcohol. Twenty-five of these were also interviewed using the NIMH Diagnostic Interview Schedule (DIS). Fifteen patients had two or three sequential DSTs at weekly intervals. Seven of the patients were clinically diagnosed as having a major depressive episode based on close observation over 2 to 4 inpatient weeks free of psychotropic medications. Fifty-eight percent of the initial cortisol determinations with the first 2 weeks showed nonsuppression, as did 60% after 2 weeks. While the level of depressive symptoms was initially high (HRSD score greater than 20) for 48% of the 27 patients interviewed within 2 weeks of abstinence, depressive symptoms cleared within 2 weeks in half of these cases. There were no associations between DST results and the presence of DSM-III major depressive disorder (lifetime or current) as assessed by the NIMH DIS, scores on the HRSD, or the presence of liver disease (elevated admission SGOT or SGPT). By the 15th-day of abstinence an examination of the clinical course of depressive symptoms differentiated those patients with a persistent major depressive episode from those with transient, alcohol-related depressive symptoms. An early positive DST had a positive predictive value of 20% for a clinical diagnosis of a major depressive episode, and a negative predictive value of 73%. After 2 weeks the positive and negative predictive values were each 50%.
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PMID:The relationship between depression and the dexamethasone suppression test following alcohol withdrawal in a psychiatric population. 380 27

Human polynuclear neutrophilic function was studied to determine the role of alcohol in the increased susceptibility to infection of chronic alcoholics: in vitro studies investigated the effects of different concentrations of ethanol; in vivo studies included comparison with healthy subjects after alcohol intake, with excessive drinkers without liver disease and with chronic alcoholics with confirmed cirrhosis. In vitro depression of polynuclear neutrophilic function was observed only with significantly higher concentrations of ethanol than encountered clinically. In social and excessive drinkers, phagocytosis was decreased but there was no change in bactericidal activity. On the other hand, in cirrhotic alcoholics chemotaxis, phagocytosis and bactericidal activity were all significantly reduced. A direct action of alcohol alone on polynuclear function would not seem to be the cause of the increased risk of bacterial infection of chronic alcoholics.
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PMID:[Effect of ethanol on human polynuclear neutrophils. In vitro and in vivo study]. 402 7

Two healthy adults with low fumarylacetoacetase activity in fibroblasts and lymphocytes, one a compound heterozygote for the tyrosinaemia and the pseudodeficiency genes and the other a homozygote for the pseudodeficiency gene, produced substantial amounts of succinylacetone when given an intravenous homogentisate load. The level of metabolites correlated with the residual enzyme activity and the genotype, being higher in the compound heterozygote. This subject also showed a small increase of metabolites in urine after an oral tyrosine load. In the pseudodeficiency homozygote a depression of erythrocyte delta-aminolevulinate dehydratase activity was observed after the tyrosine load. In fasting state both individuals have erythrocyte delta-aminolevulinate dehydratase activity below the reference range, indicating a persistently raised concentration of metabolites. Thus, the pseudodeficiency state is not just an in vitro phenomenon, but results in a definite reduction of enzyme activity in vivo. We speculate that the variant gene may predispose to the development of liver disease, possibly not recognized as tyrosinaemia.
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PMID:Concentrations of succinylacetone after homogentisate and tyrosine loading in healthy individuals with low fumarylacetoacetase activity. 406 34

A forty-two year old female with known alcoholic liver disease was given intravenous lorazepam and diazepam for delirium tremens. This resulted in a comatose state with depression of some brainstem reflexes. Her initial EEG showed a pattern of spindle coma with some responsivity of the background. Clinical improvement occurred with cessation of the benzodiazepines and the EEG showed a return to normal patterns. A review of the literature showed no previous description of this pattern in benzodiazepine coma. Two reports of spindle coma are noted with alcohol and imipramine. The prognostic significance of this pattern in drug overdose is therefore not definitive by itself. Outcome is probably more dependent on the clinical condition of the patient and the reversibility of the drug toxicity.
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PMID:Spindle coma in benzodiazepine toxicity: case report. 407 34


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