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)

Synaptic transmission between mechanosensory and motor neurons of the gill withdrawal reflex in Aplysia can undergo both short-term and long-term modulation. One form of short-term synaptic depression lasting minutes can be evoked by the peptide Phe-Met-Arg-Phe-amide (FMRFamide), and is mediated by the lipoxygenase pathway of arachidonic acid. We report here using cell culture, that the same monosynaptic sensory-to-motor component of the gill withdrawal reflex can also undergo long-term synaptic depression lasting 24 h after five applications of FMRFamide over a 2-h period. The long-term depression evoked by FMRFamide is transmitter-specific. Dopamine or low-frequency stimulation of sensory neurons, which also produce short-lasting synaptic depression in vivo, failed to evoke a long-term change. As is the case for long-term presynaptic facilitation of this connection with serotonin, the long-term depression, but not the short-term, can be blocked when applications of FMRFamide are given in the presence of anisomycin, a reversible inhibitor of protein synthesis. Thus, heterosynaptic depression parallels heterosynaptic facilitation in having a long-term as well as a short-term form, and in both cases the long-term modulation requires the synthesis of gene products not essential for the short-term changes.
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PMID:Long-term heterosynaptic inhibition in Aplysia. 336 86

The effect of S-adenosyl-L-methionine sulfate tosylate (FO-1561) on survival time in various brain damage models (cerebral anoxia or ischemia) was studied. 1) In KCN-induced or normobaric anoxia of ddY mice, FO-1561 (30-100 mg/kg as amount of S-adenosyl-L-methionine) administered intravenously 15-30 min prior to the treatment showed significant increase of survival time dose-dependently. 2) In asphyxic anoxia of Wistar rats, FO-1561 (100 mg/kg) administered intravenously 15 min prior to the treatment (cessation of artificial respiration) delayed the time until the disappearance of electrocorticogram. 3) In cerebral ischemia of Mongolian gerbils, FO-1561 (50 mg/kg) injected five times at 1 hr interval intraperitoneally 3 hr after the unilateral ligation of common carotid arteries showed significant increase of survival time. These results suggested that FO-1561 may be effective in ameliorating cerebral anoxic or ischemic damage, without observing any side effects like sedation and motor depression which pentobarbital showed with the effective doses in these damage models.
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PMID:[The effect of S-adenosyl-L-methionine sulfate tosylate (FO-1561) on survival time in various brain damage models]. 340 5

We report a case of methionine synthase deficiency associated with cellular immune deficiency discovered in a 14-year-old boy. Principal findings were: developmental delay, recurrent upper and lower respiratory tract infections, megaloblastic anemia, discovered at 3 months of age, unresponsive to cyanocobalamin and poorly responsive to folinic acid. Biochemical studies showed: an abnormal deoxyuridine suppression test despite normal serum folate, cobalamin and transcobalamin levels; a normal intracellular uptake of these two coenzymes; and an absolute requirement of methionine for fibroblast growth, suggestive of defective methionine synthesis. An absence of methionine synthase activity in the patient's bone marrow and a profound depression of this activity in lymphocytes and liver were found. Hypergammaglobulinemia with variable lymphopenia, depressed lymphocyte transformation after lectin or recall-antigen stimulation, defective delayed-type hypersensitivity and decreased natural killer activity were noted as well. The patient died at the age of 14.
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PMID:Megaloblastic anemia and immune abnormalities in a patient with methionine synthase deficiency. 342 20

Two 12-day experiments were conducted with Large White turkeys to determine which amino acids are deficient in a diet containing dehulled soybean meal as the sole source of protein. A 22% protein basal diet composed of 43.3% glucose monohydrate, 45.4% dehulled soybean meal, .5% DL-methionine, 6% stabilized fat, and added minerals and vitamins served as the negative control. Two positive control diets were formed by substituting either 16.5% dehulled soybean meal or a mixture containing amounts of essential amino acids equivalent to those in the added dehulled soybean meal in place of an equal amount of glucose monohydrate in the basal diet. Nine additional diets were formed by removing one or more amino acids from the mixture. Each of the 12 diets in a block design was fed to two pens of males and two pens of females with 8 birds per pen from 7 to 19 days of age in each experiment. Average body weight gain of poults fed the 22% protein diet with added amino acids approached that of poults fed the 30% protein diet (288 vs. 300 g, respectively). Removal of the amino acid mixture from the 22% protein diet depressed body weight gain by 19.0%. Depressions of 19, 16, 11, 7, and 6% in body weight gains resulted from the removal of valine, threonine, lysine, phenylalanine (or tyrosine or glycine), and isoleucine, respectively. A decrease of 5% was required for significance (P less than or equal to .05). When evaluated by this deletion technique, effects of valine and threonine deficiency were more pronounced than effects of lysine deficiency in dehulled soybean meal for young turkeys.
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PMID:Deficient amino acids in protein of dehulled soybean meal for young turkeys. 344 40

The first cases of fulminant hepatic failure due to paracetamol poisoning were reported in 1966, and in the United Kingdom this condition is now responsible for more cases of acute hepatic failure than any other cause. Adults account for the majority of serious and fatal cases of paracetamol poisoning and it is extremely rare for young children to ingest sufficient paracetamol to cause more than minimal liver damage. A single measurement of the plasma paracetamol concentration is an accurate predictor of liver damage provided that it is taken not earlier than 4 hours after ingestion of the overdose. Peak disturbance of liver function occurs 2 to 4 days after the overdose, often accompanied by mild jaundice, after which recovery is usually rapid and complete. In a few patients, fulminant hepatic failure, manifested by increasing jaundice and encephalopathy, may develop by the third to fifth day. Acute renal failure may complicate paracetamol poisoning, often in the context of severe liver damage. Renal failure, which is often non-oliguric, typically becomes apparent 24 to 72 hours after overdosage. The treatment of paracetamol intoxication should include gastric lavage, which has been shown to be of value for up to 6 hours after ingestion of a paracetamol overdose. Further general treatment may include parenteral fluid replacement and a prophylactic infusion of dextrose (5-10%) in patients at risk of hepatic failure. Specific protective agents in those patients at risk of paracetamol-induced liver damage include N-acetylcysteine and methionine which are most effective if given within 8 to 10 hours of ingestion of the overdose. Hepatic and renal failure should be managed conventionally. In recent years in the United Kingdom there has been a gradual decline in the number of hospital admissions and the number of deaths from aspirin poisoning. Salicylates in overdose directly stimulate the respiratory centre and so cause a respiratory alkalosis. Metabolic acidosis occurs in severe poisoning because of impairment of the oxidative metabolism of energy substrates. At very high salicylate concentrations respiratory depression may occur, possibly associated with neuroglycopenia, adding respiratory acidosis to the worsening metabolic acidosis. In addition to a mixed acid-base disturbance, hypokalaemia and hypoglycaemia may be present. Nausea and vomiting increase the fluid deficit. If dehydration is sufficiently severe, decreasing cardiac output may hasten development of lactic acidosis and acute renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Non-narcotic analgesics. Problems of overdosage. 355 83

Two trials were conducted to compare the performance of Nicholas Large White turkey poults fed diets with three levels of copper in diets with two sources of methionine. A corn-soybean meal diet, containing 26.5% protein, was used. The two methionine sources were fed at 0 and .06% in diets containing 0, 500, and 750 ppm of copper supplied by CuSO4 X 5H2O. The basal diet contained no supplemental choline and sulfate-free trace minerals were used. The addition of 500 ppm of copper from copper sulfate to the diet improved body weight, feed efficiency, and feed consumption. However, the addition of 750 ppm of copper resulted in a depression of all of the parameters. The addition of both methionine sources significantly improved body weight, feed consumption, and feed efficiency at all levels of copper supplementation. No significant difference was attributed to the two sources of methionine as the response to the two sources was the same at all levels of copper supplementation.
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PMID:Influence of three levels of copper on the performance of turkey poults with diets containing two sources of methionine. 361 32

Several chick bioassays were conducted to evaluate means of ameliorating ethionine toxicity. Supplementing a corn-soy diet marginally deficient in sulfur amino acids (methionine + cystine) with .075% D,L-ethionine reduced weight gain in 8-day-old chicks by 70% compared to gains of unsupplemented controls. Dietary addition of .50% DL-methionine prevented reduction in weight gain and feed intake resulting from ethionine supplementation whereas feeding supplemental L-cystine was without effect. Supplementation of the ethionine-containing diet with either choline or betaine ameliorated the growth depression, although neither compound was able to completely overcome the toxic effects of ethionine. Dietary ethionine did not affect plasma levels of free methionine or cystine but did increase plasma free glycine 6-fold. Dietary addition of .50% DL-methionine caused normalization of plasma glycine levels whereas it elevated plasma methionine concentration. Although results suggested the possibility of ethionine-induced serine or threonine deficiency, dietary additions of .75% L-serine or .75% L-threonine failed to improve chick weight gain. These studies suggest that ethionine, in addition to affecting transsulfuration and transmethylation activity may exert specific effects on certain amino acids in tissue pools.
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PMID:Amelioration of ethionine toxicity in the chick. 365 79

Two trials were conducted to compare the effects of supplements of methionine and cysteine on the growth and immune responses of broiler chicks fed corn-soy diets. The basal diet contained 21% crude protein, 3,255 kcal metabolizable energy/kg diet, .35% methionine, .37% cysteine, and .13% choline. Additions to the basal diet were methionine (.063, .25, .85, and 1.45%), or cysteine (.203%), or a combination of methionine (.063%) and cysteine (.153%). Total antibody and 2-mercaptoethanol-resistant antibodies, immunoglobulin G (IgG), were determined in chicks inoculated intraperitoneally at 14 days of age and serially bled at 4, 7, and 10 days postinoculation. Thymus-derived (T)-cell-dependent in vivo mitogen response to phytohemagglutinin-P (PHA-P) was assessed via wing web swelling. The methionine requirement for growth (0 to 3 wk of age) was found to be no more than .413% of the diet (.35% in the basal diet plus .063% added). Addition of 1.45% methionine to the basal diet resulted in significant depression (P less than .05) in growth. The antibody responses generally peaked at 7 days postprimary inoculation. Both methionine and cystine supplementation at low levels resulted in improvement in the cell mediated PHA-P responses as well as in the IgG (T-cell-dependent) responses. High supplemental methionine (1.45%), however, caused significant (P less than .05) depressions in both responses. Equimolar additions of methionine and cysteine (16.8 mmol/kg diet) showed that cysteine was about 84 and 70% as efficacious as methionine in the IgG and the PHA-P stimulation (PHA-I), respectively, in healthy chicks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy of cysteine in replacing methionine in the immune responses of broiler chicks. 367 Dec 89

Propidium iodide, an antitumor compound, was diffused into crystals of a complex between RNase A and deoxytetraadenylate (dpA)4). This complex has four deoxyoligomers bound per protein molecule. A difference Fourier analysis at 2.9 A showed that the principal binding site for the propidium in the crystals was a hydrophobic depression on the side of RNase away from the active site and apparently involves methionine 13 and phenylalanine 8. Binding of propidium at this site produces small conformational changes that effect binding of nucleotides at the active site of the enzyme. Fluorescence titrations in the presence and absence of nucleotide inhibitors suggested that propidium iodide is a competitive inhibitor of the enzyme with a Kl of approximately 1 mM. No significant binding of propidium to the 16 nucleotides of single-stranded DNA associated with each protein molecule was observed.
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PMID:Propidium binding to a ribonuclease-DNA complex: X-ray and fluorescence studies. 368 65

An experiment was conducted with 576 female Cobb feather-sexed chicks to study the influence of methionine (MET) and selected nutrient (SN) supplementation on the performance of chicks fed high Cu levels. Day-old chicks were allotted randomly to pens for the 22-day experiment. A 3 X 2 X 2 factorial arrangement of treatments was used which included Cu at 0, 400, and 800 mg/kg, MET at 0 and .4%, and SN at 0 and 20%. A significant (P less than .001) Cu X MET X SN interaction was found for gain. Supplemental MET reversed the growth depression observed in birds fed 400 but not 800 mg/kg Cu. Additions of 400 and 800 mg/kg Cu to the basal diet depressed (P less than .001) feed consumption by 8.6 and 19.4%, respectively. Hepatic Cu concentrations increased linearly (P less than .001) with increasing dietary Cu and were not influenced (P greater than .10) by supplemental MET or SN. Liver weights increased linearly (P less than .001) with increasing dietary Cu and were higher (P less than .05) for chicks on diets supplemented with SN, but lower (P less than .05) for those with diets supplemented with MET. The interaction of MET X SN was significant (P less than .001) for serum Cu; chicks supplemented with SN in conjunction with MET had the lowest (P less than .05) serum Cu concentrations. Serum glutamic-oxaloacetic transaminase (SGOT) activity was not influenced (P greater than .10) by dietary Cu, but SN supplementation resulted in a 10% elevation (P less than .001) in SGOT activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interaction of dietary nutrient concentration and supplemental copper on chick performance and tissue copper concentrations. 368 58


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