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)

In a group of depressed patients who had either been treated with or considered suitable for monoamine oxidase (M.A.O.) inhibitor therapy, a highly significant decrease in conjugated tyramine output was observed after an oral tyramine load compared with normal controls. However, there was no difference in conjugated isoprenaline output between the two groups after isoprenaline ingestion, even though this amine is almost solely metabolised by what is likely to be the same conjugation mechanism. Whilst some explanation in terms of altered gut motility is conceivable, it seems more likely that the apparent deficit in tyramine conjugation in depression represents an increase in functional M.A.O. activity. Consequently, this enzyme would metabolise a greater proportion of available amine, causing a proportionately large decrease in the smaller conjugate pool.
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PMID:Is there an increase in monoamine-oxidase activity in depressive illness? 4 26

This review set out to answer several questions related to tumour immunology and the gut. It is evident that in patients with gastrointestinal cancer there is a general depression of the immune response and this seems to be correlated with the stage of the disease. Paradoxically a specific immune response against definable tumour antigens can be demonstrated, both cellular and humoral mechanisms being involved although the complexities of this paradox require further analysis. Immunotherapy has been employed in gastrointestinal tumours in a sporadic way. The results suggest that gastrointestinal neoplasms may respond at least as well as other tumours. A firm conclusion awaits the results of controlled trials in which the bulk of the tumour has been effectively dealt with by other means or where combined immunochemotherapy is being used.
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PMID:Tumour immunology and the gut. 5 Feb 55

General evidence of malnutrition such as loss in body weight associated with intestinal parasitism has been attributed to decreased food intake, to intestinal malabsorption, and to change in host basal metabolism. To establish the relative importance of these factors in this regard, rats with trichinosis were studied. The weights of infected and uninfected animals were followed after being placed on one of three feeding regimens for 1 week--stock diet ad libitum, intraduodenal nutrition, and intravenous nutrition. Infected rats on a stock diet lost weight whereas those on the other two regimens maintained the same weight pattern as uninfected counterparts. The maintainance of body weight occurred despite alterations at the level of the intestinal brush border as indicated by a depression of intestinal disaccharidase activities (sucrase and lactase) and by reduction of monosaccharide absorption (measured as accumulation of beta-methyl glucoside) in the proximal, heavily infected region of the small intestine. There was no compensatory increase in enzyme activity nor in the absorptive capacity in the distal gut. Results support the conclusion that inadequate oral food intake rather than changes in basal metabolism or intestinal pathophysiology accounts for weight loss during the intestinal phase of infection.
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PMID:Enteral and parenteral feeding to evaluate malabsorption in intestinal parasitism. 11 Jan 62

45 children were admitted to hospital after ingesting varying quantities of diphenoxylate (Lomotil). One died and 44 recovered without any sequelae. Four patients were comatose, 32 were drowsy, and 9 suffered respiratory depression. No correlation was found between ingested dose and the severity of symptoms. Because of its action in rendering the gut atonic, removal of diphenoxylate by gastric lavage is mandatory, even in patients admitted at least 24 hours after drug ingestion. Naloxone is the narcotic antagonist of choice, and should be used in all cases where suspected diphenoxylate poisoning leads to respiratory depression or coma. The use of Lomotil as an antidiarrhoeal agent in children is difficult to justify.
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PMID:Lomotil poisoning in children. 43 9

Species IgG antibody given intravenously 3-4 hours prior to oral immunisation with Vibrio cholerae led to a specific depression of both the systemic and loca limmune response. One vibriocidal unit of IgG antibody, which itself would given undetectable levels of circulating specific antibody, was significantly immunosuppressive. The suppression is considered to be due to central repression of the antigen-reactive lymphocyte, rather than to antigen exclusion at the gut mucosal surface. The repression appeared less pronounced in some immunoglobulin classes than in others.
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PMID:The suppressive effect of circulating specific antibody on the response to oral immunisation with Vibrio cholerae. 53 81

In a prospective study to determine the frequency of thrombocytopenia in patients treated with intravenous heparin sodium of porcine gut origin, only four of 120 patients with suspected venous thromboembolism showed a depression of the platelet count to below 150 x 10(9)/L. In two of these patients, heparin was not considered to be the cause of thrombocytopenia because the platelet count, which fell transiently, rose again while heparin therapy was continued. These results indicate that thrombocytopenia is an uncommon complication of anticoagulant therapy with heparin derived from porcine gut mucosa.
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PMID:Thrombocytopenia found uncommonly during heparin therapy. 57 85

Feeding trials with guarbeans or its protein- or carbohdrat-rich fractions with cattle, poultry and rats are briefly summarized. The protein fraction of the bean contains toxic substances of unknown structure. The toxic effect is diminished by heating. In case of addition of the carbohydrate-rich fractions of the bean in the feeding experiments depression of growth is observed probably in connection with the bad utilization of the galactomannan or the decrease of fodder consumption due to the expanding volume of the fodder in the gut.
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PMID:[Guar II. Feeding Trials with Animals]. 96 Oct 62

Taurocholate transport by everted ileal gut sacs was studied in physiological media containing graded amounts of sodium ions. Significant uphill transport of taurocholate was observed when the bulk of NaCl was replaced by osmotic equivalents of mannitol or choline chloride. Seventy-seven percent of control transport activity was observed when 36 milliequivalents per liter of Na+ were present in the incubation medium with mannitol acting as the isosmotic replacement, and 74% of the control transport was retained when 31 milliequivalents per liter of Na+ were present in the incubation medium with choline chloride acting as the osmotic replacement. Lowering the Na+ concentration to 19 milliequivalents per liter (i.e., 84% replacement of Na+) still allowed for 69% of the uphill transport observed in the control incubations. Taurodehydrocholate transport by ileal everted sacs was more sensitive to decreased Na+ concentrations; 29% of control transport was observed at 31 milliequivalents per liter of Na+. A kinetic analysis comparing the transport of taurocholate with taurodehydrocholate, the triketo analogue, at different concentrations of Na+ indicated that the apparent affinity of the transport system for Na+ is greater in the presence of taurocholate than in the presence of taurodehydrocholate. The ability of taurodehydrocholate to depress taurocholate transport is less in media of low Na+ concentration. Finally, in vivo intestinal perfusion studies demonstrated that the depression of taurocholate absorption, following Na+ removal, is reversible. These results are in agreement with the idea that Na+ has a physiological role in intestinal bile salt transport, and that the affinities of the anionic bile salt and the sodium cation for the transport system appear to be cooperative in that one enhances the binding of the other.
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PMID:Ionic requirements for the active ileal bile salt transport system. 99 69

The objective of this study was to investigate the mechanism by which ethanol inhibits intestinal absorption of sugars. In vitro experiments on hamster jejunum have shown that the presence of ethanol in the mucosal solution caused an inhibition of the net transport of water and glucose. There was also a decrease in the intracellular water content and an increase in the intracellular sodium and potassium concentration of the gut tissue. In contrast, the intracellular glucose concentration decreased in the presence of ethanol. These ethanol-induced changes were directly related to the ethanol concentration of the mucosal solution. In the presence of 450 mM (2%) ethanol in the mucosal solution, there was also a significant inhibition of transmural potential difference, estimated glucose metabolism, and both unidirectional fluxes of sodium. The net flux of sodium to the serosal side however did not decrease significantly. These effects of ethanol cannot be fully explained by its osmotic action, and it is suggested that the ethanol-induced reduction in glucose transport could be mainly the result of an interference with the carrier-mediated coupled entrance of glucose and sodium across the brush border. A depression of cellular metabolism could also have played a role in this process.
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PMID:Effect of ethanol on sodium-dependent glucose transport in the small intestine of the hamster. 113 33

The systematic chemical control of cancer requires a quantitative knowledge of the pharmacologic disposition of antitumor drugs in both healthy and malignant tissues in the body. Pharmacokinetic models can predict the drug concentration in both tumor sites and healthy organs and hence may provide a predictive capability regarding both antitumor action and concomitant toxicity. Adriamycin is an anthracycline antibiotic that has been demonstrated to possess a broad spectrum of antitticularly solid tumors. Its major toxicity is manifested by the depression of normal cell proliferation in the bone marrow and a delayed dose-dependent cardiac toxicity eventually resulting in congestive heart failure. This study is concerned with the development of a predictve analytic model for the pharmacokinetics of adriamycin. The analytic approach embodies a physiologic multicompartmental model as a framework. This model postulates that specific organs or tissue masses may be simulated by a compartment whose elements consist of physiologic properties such as tissue volume and blood flow and pharmacologic behavior such as tissue binding and metabolic activity. A mass balance is set up across each compartment and all compartments are linked by an independent blood compartment. The mass balance includes terms representing inflow and outflow of the drug as well as its metabolism, protein-binding, and other pharmacologic behavior. A model has been developed that has ten compartments which represent the plasma, heart, liver, kidney, lung, lean tissue, adipose tissue, gut, bone marrow, and spleen. Solutions of the system of equations yield the time course of the drug in each organ. Predictions of adriamycin concentration-time curves in the ten tissues after intravenous (iv) administration were generated using this model. With few exceptions, agreement between predicted and actual tissue data in rabbits was excellent. Human plasma levels of adriamycin were predicted and comparison with patient data demonstrated a reasonable first approximation.
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PMID:Preliminary pharmacokinetic model for adriamycin (NSC-123127). 117 72


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