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)

Male weanling rats were made copper deficient with a purified diet containing all known essential dietary nutrients except copper. Copper deficiency was verified by indirect (anemia, growth retardation, hypercholesterolemia, gross pathology, and abnormal electrocardiograms) and direct (tissue copper analysis) criteria. His bundle electrographic and electrocardiographic changes detected in the copper-deficient group consisted most notably of depressed His-Purkinje system conductivity and S-T segment depression. Phosphorus-31 nuclear magnetic resonance spectroscopic analysis of cardiac, renal, and hepatic tissue perchloric acid extracts revealed significant metabolic changes associated with the dietary copper deficiency, including a generalized marked decrease in ATP and phosphocreatine levels and a corresponding increase in inorganic orthophosphate and ADP levels in the various tissues. Tissue-specific changes consisting of elevated ribose 5-phosphate (heart), phosphocholine (heart), and inosine monophosphate (kidney) and decreased glycerol 3-phosphorylethanolamine (liver) and glycerol 3-phosphorylcholine (liver) levels were detected in copper-deficient rats. Microscopic examination of heart tissue from copper-deficient rats revealed extensive disruption of mitochondrial fine structure, including fragmentation of cristae and inner and outer mitochondrial membranes, which resulted in pronounced vacuolization throughout the tissue. Although the physiological and metabolic disturbances manifested in hearts from copper-deficient animals generally mimic myocardial responses to chronic ischemia, the observed changes are interpreted in a broader context to represent the appearance of a copper-dependent cardiomyopathy.
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PMID:Physiological and metabolic characterization of a cardiomyopathy induced by chronic copper deficiency. 663 5

A sensitive (to 5.0 ng/ml) and specific method for analysis of the antidepressant trazodone is described. The method utilizes gas-liquid chromatography with nitrogen-phosphorus detection. Applicability of the method is demonstrated by (1) a pharmacokinetic study in a normal volunteer who received 50 mg trazodone orally and (2) steady-state plasma level determinations of 2 patients receiving trazodone in the treatment of depression.
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PMID:Plasma levels of trazodone: methodology and applications. 670 Nov 85

The relationship of cortisol in blood plasma with plasma calcium and phosphorus was studied from 3 days before to 2.5 days after calving in 12 dairy cows (third or more parity). Cows were in three groups: 1) paretic (displayed hypocalcemic and lateral recumbency), 2) nonparetic (plasma calcium at least 8.0 mg/100 ml), and 3) borderline (plasma calcium less than 8.0 mg/100 ml). Cortisol concentrations from 0 to 1.5 days postpartum reflected the state of calcium stress of the groups, paretic more than borderline and borderline more than nonparetic. Phosphorus was lower from 0 to 1 day postpartum in paretic cows. Calcium and phosphorus were negatively correlated (within cow) with cortisol (-.53, -.37). In experiments with goats, cortisol was released in response to hypocalcemia and displayed no activity in initiating an onset of hypocalcemia when given exogenously. Also, the observation that cortisol-treated goats responded less severely with calcium depression and recovered faster from induced hypocalcemia by ethylene glycol-bis (beta-amino-ethyl ester) N,N'-tetraacetic acid infusions suggests cortisol may aid the animal in recovering from hypocalcemia.
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PMID:Elevated plasma cortisol during induced and spontaneous hypocalcemia in ruminants. 681 10

Acute accidental vitamin D2 (ergocalciferol) toxicosis was diagnosed in a 6-month-old foal with extensive lesions of soft tissue mineralization. In an experimental study, three 18-month-old horses were given ergocalciferol per os at a rate of 9,300, 22,200, or 47,200 IU/kg of body weight/day for 21 days. Clinical signs or lesions were not seen in horses given the low and intermediate doses, whereas the horse receiving the highest dose developed clinical signs and lesions similar to those noted in the foal. Signs included depression, loss of appetite, weakness, limb stiffness with impaired mobility, and cessation of growth or weight loss. Gross and histologic lesions of mineralization of various soft tissues, especially of the endocardium and wall of large blood vessels, were seen in the foal and the horse given the high dose. Marked, persistent, hyperphosphatemia (7.0 to 13.0 mg of P/dl of serum) developed in each horse. The horse given the intermediate dose remained normocalcemic. Horses given the low and high doses became hypercalcemic (13.6 to 14.5 mg of Ca/dl of serum), but serum calcium concentrations varied from day to day and both horses were normocalcemic at necropsy (12.4 to 12.7 mg of Ca/dl of serum). Distal metacarpal bone ash concentrations of calcium, phosphorus, and magnesium of the foal were mg/g of bone ash) 400.5, 180.5, and 5.30, respectively. In the horses, treatment with ergocalciferol also had no significant effect on serum magnesium (1.88 to 2.18 mg/dl of serum) or distal metacarpal bone ash concentrations of calcium (352.5 to 362.5 mg/g of bone ash), phosphorus (182.5 to 184.0 mg/g of bone ash), or magnesium (5.48 to 6.02 mg/g of bone ash).
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PMID:Acute vitamin D2 (ergocalciferol) toxicosis in horses: case report and experimental studies. 697 34

Chronic hypophosphataemia is associated with reversible depression in myocardial performance of the intact heart. To define the basis for this, were studied the mechanical and electrical properties of isolated left ventricular papillary muscles from rats with 6 weeks of phosphorus depletion (P6), 6 weeks of phosphorus repletion and age-matched controls (C). Muscles were perfused with Tyrode's solution (Ca2+ 2.4 mmol.liter-1, 7 = 4.0 mmol . litre-1, dextrose = 5.5 mmol . litre-1) and driven at 0.1 Hz. P6 muscles had slowed isometric relaxation (T1/2R), depressed velocity of shortening and relaxation and prolongation of the transmembrane action potential to 75% of complete repolarisation. These results suggest that the slow relaxation phase may be the result of the prolonged APD75 and that the depressed myocardial performance in the intact heart may be based on impaired relaxation and reduced the velocity of shortening associated with hypophosphataemia. This view is supported by our finding that these alterations are reversible with phosphate repletion.
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PMID:Effects of experimental phosphate deficiency on action potential characteristics and contractile performance of rat myocardium. 707 68

137 patients on maintenance dialysis were studied. All but 2 patients were ambulatory, and all patients demonstrated good to normal strength on manual motor tests. With the exception of systemic lupus erythematosus, no correlation was found between primary diagnosis and patients' fatigue ratings. Laboratory studies of hematocrit, BUN, creatinine, calcium, and phosphorus did not correlate with fatigue ratings for the majority of patients. Fatigue appeared more problematic for patients who had been dialyzing for less than 4 years. Depression was pronounced among patients who reported feeling fatigued upon arising.
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PMID:The problem of fatigue in dialysis patients. 711 Apr 64

Seven patients with advanced cancer underwent whole-body hyperthermia using a nylon and vinyl mesh, water-perfused suit. Treatments were given at 41.8 degrees C for 4 hours. Five patients received concomitant cyclophosphamide with hyperthermia. Compared to baseline (37 degrees C) conditions, there was a significant rise in pulse rate (P less than 0.001), a fall in diastolic pressure (P less than 0.02), and an increase in respiratory rate (P less than 0.001). Toxic effects included fatigue, extremity edema, diarrhea, nausea and vomiting, and respiratory depression in a patient with cerebral metastases. Compared to baseline values, there was a significant increase in serum glucose (P less than 0.02) and decreases in serum calcium (P less than 0.01) and phosphorus (P less than 0.01). Significant elevations in serum LDH and SGOT values occurred 24 hours following hyperthermia, suggesting hepatic sensitivity to heat. The methods used to induce whole-body hyperthermia, as described in this paper, are feasible, permit relatively easy access to the patient, and are potentially applicable in diverse hospital settings such as intensive care units, radiation therapy areas, and conventional rooms. The physiologic alterations that were observed and the toxic effects that were documented indicate that careful monitoring of patients is necessary.
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PMID:Physiologic response and toxicity in patients undergoing whole-body hyperthermia for the treatment of cancer. 723 54

Inoculation of 2 groups of dogs with 1 X 10(9) and 4 X 10(9) Leptospira interrogans serovar icterohaemorrhagiae produced disease varying from transient fever to uremia and death. Clinical signs of disease in the severely affected dogs were fever, dehydration, depression, and icterus. Laboratory changes in serum of infected dogs included increased urea nitrogen, creatinine, phosphorus, alkaline phosphatase, total bilirubin, aspartate aminotransferase, and alanine aminotransferase. Chloride concentration decreased in the serum of dogs with severe disease. The icterus in the infected dogs did not appear to be related to hemolytic anemia.
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PMID:Serum biochemical changes in dogs with experimental Leptospira interrogans serovar icterohaemorrhagiae infection. 727 Oct 27

The inhalation of furfural, 20 mg/m3 by adult rats during 3 months for 5 h daily, 6 times a week, did not change the calcium and phosphorus level in blood serum and in bones, but depressed the activity of alkaline phosphatase in blood serum. The exposure to furfural of immature rats (6-7 weeks old) during 4 weeks caused a depression of blood serum and intestine mucosa alkaline phosphatase activity, elevation of calcium and phosphorus levels in blood serum with concomitant fall in bones, and a decrease in calcium excretion with urine.
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PMID:The influence of furfural inhalation poisoning on calcium and phosphorus metabolism in rats. 731 18

Increasing dietary lead concentrations from 0 to 2000 ppm linearly decreased the weight of two-week-old chicks to approximately 70% of that of the controls. The growth depression caused by the lead was lessened by increasing the dietary calcium and phosphorus levels and was completely counteracted by approximately 2.1% calcium with 1.4% phosphorus. As expected, increasing calcium and phosphorus levels up to 1.2% calcium and .8% phosphorus increased bone ash. Lead had no effect on bone ash.
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PMID:The prevention of chick growth depression due to dietary lead by increased dietary calcium and phosphorus levels. 741 87


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