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)

Two breeds of commercial broiler chicks were used to investigate possible breed differences and to determine the effect of methionine and lysine on arginine requirements. Graded levels of arginine were added to a glucose-casein diet with or without added methionine and to a corn-soybean meal diet with and without added lysine and/or methionine. The arginine requirement of chicks receiving the glucose-casein diet with and without supplemental methionine was found to be 1.46 per cent and 1.55 per cent of the diet, respectively. No breed differences were found. When arginine was added to a corn-soy diet containing 1.53 per cent arginine, with or without supplemental methionine, no response was obtained indicating that this level of arginine was adequate. When this diet was supplemented with lysine to bring it up to the lysine level of the casein diet, a growth depression occurred which was overcome by the addition of 0.20 and 0.25 per cent arginine, respectively, in the absence and presence of supplemental methione. These levels of arginine exceeded the requirements determined for chicks fed the glucose-casein diet. In chicks fed the glucose-casein diet, muscle creatine increased with each level of added arginine with or without supplemental methionine. Creatinine excretion also increased with each level of added arginine in the absence of supplementary methionine but when methionine was added creatine excretion reached a plateau at the level of arginine which satisfied the chick's growth requirement.
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PMID:The effect of methionine and lysine levels on the arginine requirement of the chick. 116 68

The changes of immunoglobulin-G and creatinine levels in mid-altitude were investigated in rabbits. The animals living at sea level were exposed to 2240 m altitude for 22 days period. When compared with sea level values; immunoglobulin-G levels were significantly low. Serum creatinine level decreased significantly in the 2nd day, then reached the sea level amount on the 12th day. On the 22nd day a significant increase was observed. It was concluded that the decrease in immunoglobulin-G values may be due to the depression of protein synthesis. The increase in plasma creatinine level would be explained by the decrease in urine.
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PMID:Immunoglobulin-G and creatinine levels in rabbits in altitude adaptation. 128 59

The urinary excretion rates of diethyl phosphate and diethyl phosphorothioate and changes in blood cholinesterase activities were studied in fifteen persons self-poisoned either by the organophosphorus pesticide quinalphos (twelve persons) or by chlorpyrifos (three persons). The organophosphate poisoning was always indicated by a significant depression of serum and/or red blood cell cholinesterase activities. The return of serum cholinesterase activity in the range of referent values took more than 30 days and had a different course in different persons. The most rapid increase in red blood cell acetylcholinesterase activity was noted within 24 h after the first treatment with oximes Pralidoxime and/or HI-6. None of the spot urine samples, collected daily after admission of persons to hospital, contained measurable quantities of the parent pesticide. There was no correlation between the maximum concentration of total urinary diethylphosphorus metabolites normalized to creatinine and the initial inhibition of blood cholinesterase activities measured in samples collected on the day of admission to hospital. The excretion of metabolites followed the kinetics of a biphasic reaction. The half-time of urinary metabolites concentration decrease in the fast excretion phase in quinalphos poisoned persons was 5.5-14.2 h (eight persons) and 26.8-53.6 h (four persons) and in chlorpyrifos poisoned persons 3.5-5.5 h. The half-time for the slow excretion phase ranged from 66.5 to 127.9 h in all persons and for both compounds. For a given person, the rates of excretion of diethyl phosphate and diethyl phosphorothioate were about the same. However, in quinalphos poisoned persons the proportions of single metabolites in total diethylphosphorus metabolites varied with the initial maximum concentration of total metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary excretion of diethylphosphorus metabolites in persons poisoned by quinalphos or chlorpyrifos. 137 16

The effect of the proteinase-inhibitor aprotinin on blood loss and homologous blood requirement in cardiac surgery was investigated. In a prospective study, 902 adult patients were treated with high-dose aprotinin (total greater than 5 x 10(6) kallikrein inactivator units [KIU]; group A), while 882 patients without aprotinin administration served as the controls (group C). Both groups were operated on between January 1987 and October 1989, and included patients with primary coronary artery bypass grafting (n = 525 group C, n = 560 group A), valve replacement (n = 292 group C, n = 264 group A), or combined procedures (n = 65 group C, n = 78 group A), as well as cardiac reoperations (n = 91 group C, n = 110 group A). The average blood loss 36 hours postoperatively in the aprotinin group was 679 +/- 419 mL, compared with 1,038 +/- 671 mL in the control group (P less than 0.05). Total homologous blood requirement was also significantly less in group A (942 +/- 1,630 mL) compared with group C (1,999 +/- 2,283 mL) (P less than 0.05), a reduction of 53%. Serum creatinine concentrations did not show intergroup differences on the first postoperative day (group A, 1.2 +/- 0.7; group C, 1.3 +/- 0.5 mg/dL) or on discharge from the intensive care unit (ICU). Thus, impairment of renal function as a consequence of aprotinin treatment was not observed. Three patients developed signs of mild circulatory depression after injection of aprotinin, which responded promptly to vasopressor therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High-dose aprotinin in cardiac surgery: three years' experience in 1,784 patients. 137 36

Gram-negative bacterial infections were documented in 6 neonatal New World camelids (5 Ilamas and 1 alpaca). The organisms isolated from blood before death or from multiple organs after death were Escherichia coli (n = 3), Actinobacillus sp (n = 1), and Klebsiella pneumoniae (n = 1). Only 2 crias survived, and 1 became blind secondary to retinal detachment and ocular inflammation, which developed after treatment for bacterial infection. Abnormal events during the perinatal period (prematurity, dystocia, cesarean section, weak at birth) were reported in all 6 crias. Signs of depression, convulsions, and/or coma were observed in all animals. Diarrhea and respiratory distress were also noticed in the 3 crias that died shortly after admission. Serum immunoglobulins were assessed, but without the benefit of a stall-side test specific for Ilama immunoglobulins. All crias were suspected to have poor transfer of maternal immunoglobulins. Hemograms and serum biochemical values prior to the initiation of treatment were obtained on 5 of the 6 crias. Total nucleated cells ranged from 1,400 to 23,100 cells/microliter. Four of the 5 crias has a left shift, and 2 crias had toxic neutrophils. Serum glucose concentrations, measured in 5 of 6 crias, ranged from 83 to 293 mg/dl. Serum creatinine values were high in 2 of 5 crias, 1 of which had acute tubular necrosis. Three crias with high serum electrolyte (sodium, chloride, or potassium) values subsequently died. Arterial blood gas values were assessed in 3 crias, 1 of which had respiratory alkalosis and mild hypoxemia.
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PMID:Gram-negative bacterial infection in neonatal New World camelids: six cases (1985-1991). 142 94

Thirty-three cases of infective endocarditis presenting during a 6.5 year period to a district general hospital were analysed retrospectively. The annual incidence was 22 cases per million population. Twenty-two cases had pre-existing cardiac disease, mainly valvular disease-usually rheumatic (nine cases) and prosthetic valves (10 cases). Recognizable precipitants such as recent surgery were uncommon. Two cases presented after deliberate drug overdose possibly due to depression exacerbated by systemic disease. Symptoms were usually non-specific. All but two cases had murmurs and most were pyrexial. Splinter haemorrhages and clubbing were seen in about 20% of cases. Viridans-type streptococci were the commonest infecting organisms (14 cases). Staphylococcal infection (six cases) was confined to intravenous drug abusers and patients with prosthetic valves. Five cases were culture negative. Cardiac failure was present in 13 cases at presentation and developed in seven others during treatment. Acute valve replacement was necessary in eight cases, and late replacement in three. Renal impairment (plasma urea > 8 mmol/l and/or plasma creatinine > 120 mumol/l) occurred in 19 cases during the course of their illness. Embolic phenomena occurred in 12 patients and mostly involved the central nervous system. In the 8 fatal cases, the cause of death was cardiac failure in six, cerebrovascular accident in one, and myocardial infarction in one. Four of the six patients who subsequently died of cardiac failure had been referred for surgery. Both those who were not referred had coexisting medical problems. Factors associated with increased mortality were age, male sex, cardiac failure (P < 0.01), renal impairment (P < 0.05), and embolic phenomena (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infective endocarditis in a district general hospital. 143 86

A quantitative analysis of the molecular weight (MW) profile of urinary protein by SDS-PAGE was performed in streptozotocin (STZ)-injected, non-ketotic diabetic rats (DM group), diabetic rats receiving dipyridamole (DM-DIP group), normal rats (C group) and STZ-injected rats with near-normal glycemia due to insulin treatment (DM-INSULIN group). In the DM group, decrease of a small MW protein (SMWP) (MW 19.5 k) was found at 2.5 weeks, and an increase of larger MW proteins (LMWP) (MW 68 [albumin], 55 and 29 k) together with a decrease of SMWPs (MW 19.5 and 15 k) was found at 15 weeks, as compared to the C group: the MW profile of urinary protein in the DM-INSULIN and C groups was indistinguishable. At 15 weeks, creatinine clearance (Ccr) was significantly depressed and an increase in the mesangial matrix with electron dense deposits was evident in the DM group. The urinary protein abnormalities were partially corrected and the reduction of Ccr was absent in the DM-DIP group with no effect on glomerular morphology. STZ-induced diabetes in rats is accompanied by a reduction of urinary SMWP, and a subsequent increase of LMWP and depression of Ccr: dipyridamole ameliorates urinary protein abnormalities and prevents the reduction of Ccr.
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PMID:Abnormal molecular weight profile of urinary protein in rats with streptozotocin-induced diabetes. 144 72

Neopterin is a validated marker of the activation of cell-mediated immunity in a variety of disease states. We measured neopterin and creatinine concentrations in the plasma and urine of 22 schizophrenic and 26 depressed patients admitted acutely to hospital, and compared results with those in a large group of normal controls. Neopterin/creatinine ratios were normal in the schizophrenic patients, but significantly elevated in the plasma of depressed patients. In each diagnostic group, the use of psychotropic drugs before admission had no effect on the neopterin ratios observed. Our findings indicate altered cell-mediated immunity in depression.
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PMID:Neopterin measurement provides evidence of altered cell-mediated immunity in patients with depression, but not with schizophrenia. 148 78

This study was designed to determine the incidence, etiology and consequences of severe hypermagnesemia. We retrospectively reviewed all hospital admissions over a 5-year period from 1984 to 1989 and identified 8 cases of severe hypermagnesemia (serum Mg > or = 6.0 mg/dl) due to magnesium ingestion. All but 1 patient were elderly (mean age 70 +/- 6 years). The etiology when identified was due to magnesium-containing cathartics (n = 3) or antacids (n = 3). The total amount of magnesium ingested was not excessive, but bowel disorders that may have enhanced absorption (such as active ulcer disease, gastritis, colitis, perforated viscus, massive gastric dilatation) were present in 7 of the 8 patients. Unexpectedly, only 1 had preexisting renal failure. Renal function was found to be normal in 1, only mildly to moderately impaired in 5 (creatinine < 3.6 mg/dl) and severely impaired in 2 (creatinine 7.6, 15.7 mg/dl). Clinical sequelae of hypermagnesemia were hypotension (n = 7), bradycardia (n = 2), respiratory depression (n = 3), EKG abnormalities (n = 6), depressed mental status (n = 5). Hypocalcemia (range 5.7-7.4 mg/dl) more severe than could be attributed to either hypoalbuminemia or acute renal failure was present in 7. A low anion gap (range-2 to 9) was present in 5. Most striking was the fact that despite clinical sequelae, the hypermagnesemia was unsuspected in 6 of the 8 cases. Hypermagnesemia can occur without severe renal insufficiency in association with bowel disease, particularly in elderly individuals, and may be a clinically unrecognized cause of cardiovascular dysfunction, hypocalcemia and neurologic or respiratory depression.
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PMID:Unsuspected morbid hypermagnesemia in elderly patients. 148 3

The depression of renal function caused by cyclosporin does not generally reflect permanent kidney damage but is caused by a reversible vasoconstriction, with no relevant changes in tubular function. Serum creatinine may remain within the normal range during therapy, but any decline in renal function can be detected by a rise in serum creatinine above the baseline value. Measurements of glomerular filtration rate before and during therapy have shown the degree of renal dysfunction in individual patients to correspond to their rise in serum creatinine. The cause of renal vasoconstriction is uncertain but animal experiments have highlighted several possibilities. These include: (1) albumin leakage with circulatory volume contraction; (2) enhanced Ca mobilization in contractile cells; (3) activation of a renin-like enzyme in vessel walls; and (4) renin accumulation in the renin-producing cells of the afferent arteriole. Such mechanisms, although seeming to operate at different doses, may act in unison at high doses, when renal function is most severely depressed.
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PMID:The effect of cyclosporin on renal function. 150 31


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