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)

The effect of daily therapeutic doses of 100 mg benzbromarone (Normurat) and 2.0 g probenecid on the purine metabolism of 40 test subjects was investigated. Fasting-hyperuricemia was used as the model and particular attention paid to the mechanisms of renal elimination. Urate concentration remains under the solubility threshold when benzbromarone is administered, in contrast to medication with probenecid. The significantly greater hypouricemic effect of benzbromarone correlates with a significant rise in the excretion and clearance of uric acid in comparison to probenecid, accompanied by a stronger depression of tubular reabsorption. Serum levels, clearances and reabsorption rates demonstrate the prolonged effect of the benzofurane derivative Normurat even during strict fasting. Supplementary allantoin and urea determinations gave no indication of increased enterobacterial uricolysis. Normurat was well tolerated, side effects were not noted.
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PMID:[The effect of benzbromarone on fasting-hyperuricemia as a model (author's transl)]. 66 30

Studied were the acute, subchronic, and chronic toxicity of the Pharmachim tylosin tartrate as well as the tolerance of chicken broilers and turkeys. The mean lethal dose of the antibiotic at subcutaneous application to 28-32 day-old broilers was 620 mg/kg; the oral dose was 1500 mg/kg. In the case of 42-45-day-old broilers these values were 740 and 5400 mg/kg. The LD50 at i/v infusion for 75-77-day-old ones was 48 mg/kg. Beside the age and route of introduction toxicity was found to depend on the initial biologic activity of tylosin tartrate. The subcutaneous injection of tylosin tartrate at the rate of 30 mg/kg for 20 days did not lead to changes in the appetite, behaviour, growth, and structure of viscera. A 42-day treatment at the same rate, however, resulted in slightly manifested and fully reversible dystrophic changes in the liver and kidneys. Higher doses (90 and 150 mg/kg) led to transient depression, stunting of growth, and a rise of the urea level and the activity of blood transaminases as well as to moderate destructive changes in the liver and kidneys. The stimulation of growth and the improvement of feed conversion (without deviations in the clinical and biochemical indices of the blood and the structure and development of the viscera in broilers) were recorded after the application of a water-soluble formula of tylosin tartrate for a period of 98 days offered via the drinking water in amounts equal to or exceeding 2 to 4 times the ED50. Turkeys' tolerance for the preparation was evaluated as very good so far as single i/m injective applications were concerned in doses exceeding 3, 5, and 10 times the average effective rates, no differences in this respect being noted with the comparative use of tylosin tartrate produced by the Elanco firm.
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PMID:[Toxicity studies of Pharmachem's tylosin tartrate for broilers and turkeys]. 74 15

Young male rats (100-130 g) were fed diets of equal energy content containing o.5, 1,2,3,5, and 18% lactalbumin consumed either freely or in restricted amounts. The rats receiving low protein diets failed to grow and mature. Those consuming the 0.5 and1% protein diets given freely developed the characteristic features of kwashiorkor including edema, while those receiving the diets in restricted amounts developed the characteristic features of marasmus. The rats fed low protein diets had low plasma levels of essential amino acids; however, the lysine level was well maintained. The plasma levels of nonessential amino acids, especially glycine, alanine, and aspartic and glutamic acids were raised in marasmic rats but were reduced in rats fed low protein diets ad libitum. Young and severly malnourished rats appeared to have limited ability to synthesize urea. Therefore, they excreted more ammonia and other nitrogenous substances such as ethanolamine, and when given an amino acid load, intermediary metabolites of the ingested amino acids. Rats fed low protein diets showed diminution of total liver DNA, RNA, and protein. In addition to the reduction of protein synthesis resulting from decreased cellular RNA, ribosomes from the livers of protein-deficient rats had reduced ability to synthesize proteins. This defect was associated with the detatchment of the ribosomes from endoplasmic reticulum membrane and the elevation of the proportion of monosomes to polyribosomes. Malnutrition did not produce any change in the turnover rate of liver RNA. Protein deficiency caused significant depression of serum insulin, thyroxine, and corticosterone levels. Theoverall conclusion is that mammalian metabolism is well adapted to dietary intake and that this adaptation is achieved through dietary control of synthesis and release of key metabolic hormones.
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PMID:Experimental protein and energy in the rat. 80 70

The present study was designed to develop an animal model applicable to the clinical patient in the investigation of the pathogenesis of septic shock. The model currently described is a lightly anesthetized, unrestrained monkey, carefully monitored during a 24 hour observation period. Varying doses of live Excherichia coli organisms were infused intravenously during a 30 minute period, and a variety of hemodynamic, respiratory and metabolic parameters were monitored. Doses of organisms varied between 7.6X10(9) and 3.0X10(11) organisms per kilogram of body weight, and there was no obvious correlation between size of dose and survival time. Two of nine experimental monkeys survived the Excherichia coli, while times of death of the remaining monkeys varied between three and 27 hours. Two control monkeys, not administered organisms, survived the 24 hour period with minimal changes in all measured parameters. Results reveal two patterns in response to organism administration. These were early acute death, after three to four hours, and prolonged life, death after 20 to 27 hours. The acute response was characterized by marked systemic hypotension, hypoglycemia, hypoinsulinemia, increased lactate level, decreased pH or respiratory depression. The other type of response involved profound sustained hypotension with hypoglycemia and hypoinsulinemia in most monkeys and elevations in lactate, blood urea nitrogen potassium creatinine, serum glutamicoxalacetic, lactic dehydrogenase and fractionatedlactic dehydrogenase levels. Depressions in respiration were not evident in the group which survived a longer period of time. Renal fibrin thrombi, prominent in baboons administered Escherichia coli, were absent in the rhesus monkey regardless of the size of the dose of organisms. The results of this study suggest the operation of a multifactiorial mechanism in septic shock with interactions between hemodynamic and metabolic factors varying within the species.
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PMID:Physiopathologic responses of the rhesus monkey to live Escherichia coli. 82 5

The renal clearance of furosemide and tetraethylammonium (TEA) were compared in 10 patients with hypertensive nephropathy. BUN and creatinine ranges were 10 to 88 mg/dl and 0.9 to 3.8 mg/dl, respectively. Diuretics were discontinued 48 hr prior to the study, and 2 consecutive clearances (ml/min/1.73 m2BSA) of creatinine were performed. The patient then received a bolus followed by a constant infusion of furosemide-14C and tetraethylammonium-14C (analyzed by specific methodology for plasma and urine), both in subpharmacologic doses. After 40-min equilibration sequential 20-min clearance periods were obtained. Both the clearance of furosemide (range 17 to 133) and TEA (range 99 to 443) correlated negatively with BUN and serum creatinine and positively with creatinine and urea clearances. Thus, by using a constant-infusion technique we demonstrated that the renal clearance of furosemide is depressed by azotemia in man and that there was greater depression with furosemide than with TEA.
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PMID:Depression of renal clearance of furosemide in man by azotemia. 83 33

Trans-1,2-dichloroethylene (t-DCE), an industrial solvent, proved to be moderately toxic when studied in small laboratory animals. In adult female rats brief (8 h) and prolonged (8 h daily, on 5 consecutive days a week, for more than 16 weeks) inhalation of 200 ppm--the current TLV/MAC in various countries--produced histological evidence of slight to severe fatty degeneration of the liver lobules and Kupffer cells. In addition marked pulmonary hyperaemia and alveolar septal distention were noted. Fibrous swelling of the cardiac muscle (with striation) just barely maintained) and hyperaemia remained detectable for as long as 14 h post-exposure, but only occurred at 3000 ppm/8 h. A concentration of 1000 ppm/8 h was required to produce a fall in blood albumin, urea nitrogen, alkaline phosphatase activities and erythrocyte count. The cited concentrations failed to produce prenarcotic symptoms of narcosis (central nervous system (CNS) depression). The LD50 was found to be 6.0 ml/kg i.p. and 1.0 ml/kg p.o. for female rats, and 3.2 ml/kg i;p. for female mice. In some of the rats killed in these experiments the organ changes were found to be identical to those observed after inhalation.
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PMID:Toxicity studies on trans-1,2-dichloroethylene. 85 30

Based on the results of an open trial with Ro 8-1998 (chemic name: N,N-dimethyl-3-(1-methyl-5H-dibenzo(a,d)cycloheptene-5-ylidene)-propylamine N-oxide hydrochloride) in 11 endogenous depressed outpatients a double-blind trial with imipramine was proposed. Therapeutic efficacy and side effects of Ro 8-1998 and imipramine were compared in a double-blind trial with 30 patients who were newly hospitalized. Most of them suffered from endogenous depression. On days 0, 5, 10, 15 and 20 the patients were examined and the symptoms were documented with the AMP system, the Hamilton scale for depression, a behaviour rating and the "global depression rating Zurich". Ro 8-1998 caused a decrease of systolic blood pressure, an increase of heart frequency and urea. Twelve out of 15 patients showed a decrease of white blood cells. In four patients the number of white blood cells dropped below 4,000. Statistical analyses proved both substances to be potent antidepressants. The therapeutic efficacy of Ro 8-1998 was at least equal to that of imipramine. Further trials with bigger groups of patients are necessary to show whether the trend towards a better antidepressant efficacy of Ro 8-1998 can be reproduced.
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PMID:Open trial and double-blind clinical trial of the antidepressant Ro 8-1998 in comparison with imipramine. 87 18

Fatal myopathy similar to "capture myopathy" described for African game was diagnosed in a wild white-tailed deer. Clinical signs included depression, inability to rise or stand, and myoglobinuria. Values for serum creatine phosphokinase, glutamic oxaloacetic transaminase, and blood urea nitrogen were high. The deer died 42 hours after capture. At necropsy the muscles of the limbs had a waxy, "cooked" appearance and the kidneys were brown. Microscopic findings included severe degeneration and fragmentation of skeletal muscle fibers, nephrosis, centrilobular hepatic necrosis, myocardial degeneration, and anoxic neuronal degeneration.
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PMID:Myopathy and myoglobinuria in a wild white-tailed deer. 97 70

The effects of hypophysectomy and short-term GH replacement on insulin release and on some aspects of glucose metabolism in isolated rat islets of Langerhans were investigated. The effects on body, pancreas and adrenal gland weights, and on the levels of blood plasma constituents were also measured. Three to four weeks after hypophysectomy the early and late phases of insulin release from islets incubated with high concentrations of glucose, but not with low concentrations of glucose or with xylitol, leucine, arginine, tolbutamide, citrate or butyrate, were significantly lowered. Short-term GH replacement partially reversed the depression in glucose-stimulated insulin release. This reversal effect was not dependent on the increase in body weight of rats after GH replacement when the fall in adrenal gland but not in pancreas weight was also reversed. Nine out of the 12 plasma constituents measured, including glucose, were maintained in the control range of levels, but albumin, inorganic phosphate and urea nitrogen levels were altered after hypophysectomy or GH replacement. Three to four weeks after hypophysectomy, total glucose oxidation and glucose utilization by the islets were slightly depressed. Hypophysectomy appeared to slow down glucose 6-phosphate utilization in the islets. However, the functional capacity of the glucose phosphorylating, glucose-6-phosphate and 6-phosphogluconate dehydrogenase activities were not changed. Short-term GH replacement caused improvements in these islet functions.
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PMID:Effects of hypophysectomy and short-term growth hormone replacement on insulin release from and glucose metabolism in isolated rat islets of Langerhans. 110 38

In the unicellular green alga Chlamydomonas reinhardi (strain y-1), synthesis of the enzymes required for urea hydrolysis is under substrate induction control by urea and under end product repression control by ammonia. Hydrolysis of urea if effected by the sequential action of the discrete enzymes urea carboxylase and allophanate lyase, collectively called urea amidolyase. The carboxylase converts urea to allophanate in a reaction requiring biotin, adenosine 5'-triphosphate, and Mg2+. The lyase hydrolzyes allophanate to ammonium ions and bicarbonate. Neither activity is present in more than trace amounts when cultures are grown with ammonia or urea plus ammonia, or when they are starved for nitrogen for 8 h. Urea in the absence of ammonia induces both activities 10 to 100 times the basal levels. Addition of ammonia to an induced culture causes complete cessation of carboxylase accumulation and an 80% depression of lyase accumulation. Ammonia does not reduce urea uptake by repressed cells, so it does not prevent induction by the mechanism of inducer exclusion. The unicellular green alga Chlorella pyrenoidosa (strain 3 Emerson) also has discrete carboxylase and lyase enzymes, but only the carboxylase exhibits metabolic control.
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PMID:Metabolic control of urea catabolism in Chlamydomonas reinhardi and Chlorella pyrenoidosa. 111 94


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