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)

Experiments on pyrolaxon-immobilized cats evidence that diazepam produces depression of evoked potentials in the specific, nonspecific and associative brain structures upon an electric stimulation of the visceral and somatic nerves, and also with accoustic and photostimulation; Meprotan (meprobamate) in doses of 40-100 mg/kg neither changes nor increases, and in doses of 100-150 mg/kg, reduces the amplitude of evoked potentials and at the sme time forces down the arterial pressure. Amizyl (benactyzine) inhibits the potentials evoked by stimulation of the vagus. The amplitude of responses arising on stimulation of the inferior cardiac, celiac and sciatic nerves, and also with acoustic and photostimulation neither changes nor increases.
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PMID:[Effect of tranquilizers on impulse conduction in the afferent pathways of visceral nerves]. 3 65

Detailed complement system studies were performed in 22 patients with adult coeliac disease. Activation products of C3 were observed in the fresh sera of all untreated patients, while only 4 had activation products of factor B of the alternate pathway. Levels of C4 and C3 were lower than normal mean, but only the depression of C4 reached a level of statistical significance. The amounts of circulating C3 activation products were significantly reduced when the patients were on a gluten-free diet. There is thus evidence that activation of the classical pathway of the complement system takes place in adult coeliac disease, and there is an association between gluten ingestion and the complement activity. We suggest that a possible mechanism of tissue injury in this disease is activation of complement factors by a humoral immune reaction to dietary gluten in the intestinal wall.
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PMID:Complement system studies in adult coeliac disease. 59 55

Fourteen coeliac patients on a gluten free diet (GFD) and 10 on a normal diet were studied by lymphocyte transformation in response to PHA to assess the integrity of cell-mediated immunity (CMI). Transformation was depressed in the majority taking a normal diet, with improvement after a GFD. In some patients the depression may have been due to a serum factor, as transformation was more nearly normal when the lymphocytes were cultured in pooled AB serum than in their own serum. There was no correlation between transformation and nutritional deficiencies. Mantoux tests were performed in some of these and other coeliac patients and there was a very significant reduction in the incidence of positive tests compared with controls. These findings provide evidence of depressed CMI in coeliac patients taking a normal diet with improvement on a GFD and may be of relevance to the high risk of malignancy in coeliac disease, further strengthening the case for a strict GFD.
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PMID:Depressed cell-mediated immunity in coeliac disease. 108 62

An experimental model of acute aortic dissection has been designed in an effort to examine myocardial contractility and systolic arterial pressure as factors influencing the progression of dissection. Thirty mongrel dogs divided into three experimental groups underwent left thoracotomy and construction of a standard intimal tear in the proximal descending aorta. Nine of ten animals in the control group showed progression of the aortic dissection a mean of 81.5 percent of the distance from the aortotomy to the celiac axis. Group II consisted of ten dogs pretreated with propranolol. The myocardial contractility (dp/dt) was significantly depressed in this group without change in systolic pressure. However, progression of dissection occurred in nine of ten animals as in the control group. In Group III, ten dogs were pretreated with trimethaphan lowering the systolic blood pressure to 90 mm. Hg and depressing the dp/dt to levels equal to those of Group II. There was no progression of aortic dissection in any of the animals in this group. The results indicate that, under these experimental conditions, depression of myocardial contractility alone has no inhibitory effect on the progression of dissection. When controlled hypotension is added to myocardial depression, aortic dissection is inhibited completely.
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PMID:Control of acute aortic dissection. 113 95

Zinc nutritional status was examined in 10 adult patients with biopsy-proven celiac disease; five of these patients were clinically well on gluten-free diets at the time of study. Plasma zinc and taste acuity were used as indices of zinc nutrition. Depression of plasma zinc and lowered taste discrimination were observed among the untreated patients, and some patients who were otherwise in clinical remission also had impaired zinc nutrition. With confirmation of plasma copper depression in patients with celiac sprue, these observations indicate that trace metal deficiency is another common nutritional complication of adult celiac disease.
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PMID:Zinc nutrition in celiac sprue. 126 87

Intestinal disaccharidase activities were determined in 294 jejunal biopsies obtained from 254 children with various disorders of the small bowel, and alkaline phosphatase activity was measured in 251 biopsies. In normal mucosa a broad range of enzyme activity was found corresponding with the data in the literature. A primary disaccharidase deficiency was observed in 5 children with congenital sucrase-isomaltase deficiency and in a 12-year-old Egyptian boy with acquired lactase deficiency. A secondary generalized depression of disaccharidase activity and a diminution of alkaline phosphatase activity existed chiefly in patients who had severe or moderate mucosal damage, also in active coeliac disease and during gluten loading, in protracted diarrhoea of infancy, chronic malabsorption of unknown origin and agammaglobulinemia. During remissions enzyme activities recovered together with mucosal improvement. Low levels of enzyme activities were also seen in some cases of protracted diarrhoea of infancy and chronic malabsorption of unknown origin although only mild mucosal lesions were demonstrated.
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PMID:[Intestinal disaccharidase and alkaline phosphatase activities of jejunal biopsies in small bowel diseases of children (author's transl)]. 127 85

Some children with coeliac disease show behavioural disorders such as depression and other signs which have been correlated with reduced central monoamine metabolism. We have therefore investigated the brain availability of the monoamine precursors tryptophan and tyrosine in 15 untreated children with coeliac disease and 12 treated children with coeliac disease as well as in 12 control children. Significantly decreased plasma concentrations of tryptophan were found in untreated children (mean (SD) 13 (4) mumols/l, p less than 0.001) compared with treated children (31 (13) mumols/l), and in both groups of coeliac children when compared with control children (81 (22) mumols/l). A significantly lower ratio of plasma tryptophan to large neutral amino acids (tyrosine, valine, isoleucine, leucine, and phenylalanine) was also observed, which could indicate impaired brain availability of tryptophan in coeliac children and was more pronounced in untreated children. The impaired availability of tryptophan could produce decreased central serotonin synthesis and in turn behaviour disorders in children with coeliac disease.
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PMID:Plasma precursor amino acids of central nervous system monoamines in children with coeliac disease. 177 52

The intermediary pathways in the bombesin-induced somatostatin release were examined in isolated perfused rat stomach obtained from male rats that were fasted overnight. The stomachs were perfused by way of the celiac artery. On coinfusion of 1.0 mumol/L tetrodotoxin and 1 nmol/L bombesin, a significant depression in release of somatostatin was observed compared with that observed with bombesin alone. The 5-minute integrated somatostatin response after treatment with tetrodotoxin and bombesin was 173% +/- 14% of basal, which was significantly lower than that observed with bombesin alone (394% +/- 59% of basal, P less than 0.05) but significantly higher than that observed with medium-199 alone (95% +/- 7% of basal, P less than 0.05); this indicated that approximately 70% of the bombesin-stimulated somatostatin release was indirectly mediated through neural pathways, while a significant (approximately 30%) segment of it was mediated by nonneural mechanisms. To test if the 30% somatostatin release was secondary to gastrin release in response to bombesin, gastrin antiserum and bombesin (1 nmol/L) were coadministrated in the presence or absence of tetrodotoxin (1 mumol/L). Gastrin antiserum alone did not significantly affect basal release of somatostatin but caused a significant inhibition (approximately 23%) of bombesin-provoked somatostatin release. Coadministration of gastrin antiserum and tetrodotoxin attenuated bombesin-stimulated somatostatin release. Gastrin (1 mumol/L) alone significantly stimulated somatostatin release (150% +/- 10% of basal), which was completely attenuated in the presence of gastrin antiserum. Tetrodotoxin did not affect bombesin-elicited gastrin release, confirming that bombesin-stimulated gastrin release was directly mediated. To determine the nature of the neural pathways mediating the bombesin-induced somatostatin release, atropine (100 nmol/L) was used. Atropine inhibited bombesin-induced somatostatin release to the same extent as tetrodotoxin, indicating that cholinergic pathways mediated bombesin-induced somatostatin release. These results show that almost all the somatostatin response to bombesin is indirectly mediated, and is composed of a major neural (cholinergic) and a minor nonneural pathway. The nonneural mechanism appears to be contributed primarily by gastrin released in response to bombesin, which apparently has a short paracrine positive feedback effect on somatostatin release.
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PMID:Role of gastrin in bombesin-stimulated somatostatin release. 197 61

Effects of celiac plexus block (CPB) on systemic and splanchnic circulation, especially of liver and kidney, were investigated in twenty nine mongrel dogs. CPB was performed by an anterior approach through a catheter placed in a paraaortic compartment using 7 mg.kg-1 of 2% mepivacaine. Tissue blood flow measurement was performed by a hydrogen clearance method in eleven dogs, and vascular blood flow was measured in eighteen dogs by an electromagnetic flow meter. Swan-Ganz catheter was inserted to measure mean arterial pressure (ABP), heart rate (HR), central venous pressure (CVP), mean pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP) and cardiac output (CO). Then stroke volume (SV), systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were calculated. Following CPB, ABP, HR, CVP and C.O. were significantly decreased at 7 to 9%. PAP decreased at 5%. PCWP, SV, SVR and PVR were unchanged. The hepatic arterial blood flow increased significantly, and portal venous blood flow decreased after CPB transiently, and then recovered to control value or to a higher level at 60min after CPB. The tissue blood flow of the liver tended to increase, but the change was not significant. In the kidney, both arterial and tissue blood flows increased significantly after CPB. The results suggest that following CPB, hepatic and renal tissue blood flows increased because of the increments of their arterial blood flows, unless a profound systemic hemodynamic depression occurred.
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PMID:[Effects of celiac plexus block on splanchnic circulation--II: Changes in the systemic hemodynamics and the blood flow of the liver and kidney in dogs]. 281 Jun 98

Fast nicotinic transmission was studied in vitro in neurons of isolated cat celiac ganglia. In the absence of nerve stimulation, neurons could be classified into three types: silent neurons, synaptically activated neurons, and spontaneously discharging neurons. In all three types, fast synaptic activation could be obtained in single neurons by stimulating with a single pulse both the splanchnic nerves or one of the peripheral nerves connected to the ganglia. During repetitive nerve stimulation, a gradual depression of the central and peripheral fast nicotinic activation occurred, which was not affected by phentolamine plus propranolol, domperidone, atropine, or naloxone. Repetitive nerve stimulation was followed by a long lasting discharge of excitatory postsynaptic potentials and action potentials that decreased gradually with time. This discharge, which was probably due to presynaptic or prejunctional facilitation of acetylcholine release from cholinergic terminals, was reduced by the application of phentolamine plus propranolol, domperidone, or atropine and increased with naloxone. The existence of the mechanisms described in this study reflects the complexity of the integrative processes at work in neurons of the cat celiac ganglia that involve fast synaptic cholinergic activation.
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PMID:Patterns of fast synaptic cholinergic activation of neurons in the celiac ganglia of cats. 290 69


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