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 purpose of this study was to determine whether the energy metabolism of an experimental rodent sarcoma was selectively depressed by the combination of inhibition of glycolysis and respiration. In vivo phosphorus-31 nuclear magnetic resonance spectroscopy was used to monitor the response of tumor or brain high-energy phosphate compounds to insulin hypoglycemia, rhodamine 123, or both agents in fasting rats with subcutaneous methylcholanthrene-induced sarcomas. Insulin or rhodamine 123 alone produced a similar 50% to 60% reduction in tumor adenosine triphosphate (ATP) concentration compared with controls injected with saline solution (p less than 0.05, one-way analysis of variance [ANOVA]). The combination of insulin plus rhodamine 123 resulted in a 90% reduction of tumor ATP concentration, which was significantly different from the effect of either agent alone (p less than 0.05, one-way ANOVA). Brain phosphocreatine and ATP concentrations were unchanged by these agents. Administration of dimethyl sulfoxide (DMSO)/glycerol, the vehicle for rhodamine, produced a 35% reduction of tumor ATP, which was similar to the effect of insulin alone but significantly different from rhodamine. The combination of DMSO/glycerol plus insulin hypoglycemia resulted in a 70% reduction in tumor ATP, which was significantly elevated compared with the combination of rhodamine plus insulin. Glucose deprivation induced by insulin, and combined with the inhibition of oxidative phosphorylation, produces an additive depression of tumor energetics. The drug vehicle DMSO/glycerol significantly depresses tumor energy metabolism, presumably because of its DMSO component, which may explain the previously reported antineoplastic efficacy of this solvent. Combinations of inhibitors directed at different points of tumor metabolism produced an enhanced depression of tumor energetics, whereas host tissue was protected.
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PMID:Inhibition of tumor high-energy phosphate metabolism by insulin combined with rhodamine 123. 304 41

The nonlactating period should be regarded as a preparatory phase for the next lactation, rather than a rest phase from the preceding one. During the early dry period, a diet should be provided that meets nutrient requirements for energy, protein, calcium, phosphorus, selenium, vitamins, and other minerals. This can usually be accomplished by feeding a blend of roughages with little or no grain and providing a vitamin and mineral supplement. The diet during the late dry period, or transitional stage, should provide increased energy (an additional 3 to 4 Mcal), and a PP preventive regimen can be instituted at this time. Five to six pounds of concentrate containing 200 gm of an ammonium sulfate and chloride mixture and 6 gm of niacin can be added to the diet to aid in the transition to lactation. Feeding of high-calcium, lactating-cow grain mix should be avoided until after parturition. Stress should be minimized at and after parturition, and a quiet maternity area should be available. The normal depression in dry matter intake at parturition should be minimized; feeding high-quality roughages at this time is beneficial. Concentrate consumption should be increased gradually following parturition, and careful attention to the soluble and undegradable protein fractions of the diet is warranted. In group feeding situations, introduction to the energy-dense, high-lactation ration should probably be avoided for the first 10 to 14 days postpartum, until the cow is acclimated to the forage mix. Body overconditioning should be avoided. However, attempts to manipulate body condition during the dry period tend to be unrewarding and counterproductive. Following these guidelines should reduce the incidence of metabolic diseases in high-producing dairy cattle.
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PMID:Feeding the dry cow to avoid metabolic disease. 306 14

To evaluate the hypothesis that depressed neuromuscular transmission causes dithiobiuret (DTB)-induced muscle weakness in rats, the temporal development of impaired treadmill performance and deficits in the nerve-elicited muscle contractions were compared during daily treatment with the toxicant (DTB, 1 mg/kg/day X 6 days). Diminished treadmill test performance after 4 days of treatment marked the initial detection of impaired motor function. At this time fading (loss of tension during tetanus) of gastrocnemius contractions elicited in response to 100-Hz sciatic nerve stimulation occurred in DTB-treated rats but not in controls. After 5 and 6 days of treatment, treadmill failure became complete, tetanic fade worsened dramatically, and peak contractile tension measured during trains of nerve stimulation (10-250 Hz) decreased progressively. Appearing by Day 6 were marked body weight loss, dehydration, hypothermia, and a depression in serum concentrations of thyroid hormones. Total oxygen content of the blood was not reduced at any time during treatment, and serum concentrations of glucose, sodium, potassium, calcium, chloride, and phosphorus in DTB-treated rats on Day 6 were similar to those of control animals. Therefore, hypoxia, hypoglycemia, or a serum electrolyte imbalance do not initiate or modulate the neuromuscular toxicity. Light microscopic evaluation of liver, kidney, lung, thyroid, and other organs in intoxicated rats was unremarkable and in skeletal muscles and selected sites of brain, spinal cord, and sciatic nerve no morphologically significant lesions were observed. Even when DTB-intoxicated rats were maintained in a state of flaccid muscle weakness for 5 continuous days, peripheral nerve lesions proximal to the intramuscular nerves were not detected. Thus, depressed neuromuscular transmission appears to be the primary cause of the flaccid muscle weakness and no evidence was obtained that nonneural effects of DTB initiate or modulate this effect.
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PMID:Temporal analysis of dithiobiuret neurotoxicity in rats and assessment of potential nonneural causes. 311 11

Studies of myocardial function in patients with hypophosphatemia have yielded conflicting results. Systolic time intervals were performed in 19 patients during and after the correction of hypophosphatemia; 11 had severe (0.9 +/- 0.15 mg/dL) and eight had moderate (1.4 +/- 0.11 mg/dL) hypophosphatemia. Controls were 14 patients with normal serum phosphorus levels. No patient with hypophosphatemia had clinical congestive heart failure. When hypophosphatemia was corrected, improvement in left ventricular performance was seen only in patients with severe hypophosphatemia (p less than 0.001); in eight patients left ventricular performance was normal during hypophosphatemia but showed significant improvement with its correction (p less than 0.01). Patients with moderate hypophosphatemia showed no significant change. Our results confirm the findings of O'Conner et al, whose study is the only previous one to demonstrate hypophosphatemia-induced myocardial depression in humans. Contradictory results from other studies may be explained by the inclusion of patients with moderate hypophosphatemia and failure to repeat measurements after the correction of hypophosphatemia. We conclude that reversible depression of myocardial performance is seen in hypophosphatemia only when it is severe. In some cases, normal left ventricular performance improves when hypophosphatemia is corrected.
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PMID:Reversible depression of myocardial performance in hypophosphatemia. 335 91

In a historical cohort study, acute renal failure developed in 16.5% of 157 patients with rhabdomyolysis over a two-year study period. Underlying clinical, laboratory, and causative factors associated with the development of acute renal failure were examined. Factors predictive of renal failure in this setting, determined by multiple logistic regression analysis, included the degree of serum creatine kinase, serum potassium, and serum phosphorus level elevation; the degree of depression of serum albumin level; and the presence of dehydration at presentation or sepsis as the underlying cause. The predictive model that was developed correctly classified 93% of subjects and was statistically validated.
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PMID:Factors predictive of acute renal failure in rhabdomyolysis. 338 1

Alcoholic depression of left ventricular function was produced in normal hamsters by the administration of increasing concentrations of alcohol in drinking water (up to 50%) for 6 months. The result was assessed by phosphorus-31 nuclear magnetic resonance of isolated perfused hearts and high-pressure liquid chromatography of freeze-clamped tissues. Hemodynamic data and myocardial oxygen consumption were also monitored. Alcoholic hamsters had significantly higher inorganic phosphate and lower ATP levels, while maintaining normal intracellular pH, phosphocreatine, and creatine. Although coronary flow and oxygen consumption were maintained at normal levels, hamsters ingesting 50% ethanol had significantly lower left ventricular developed pressure and dP/dt. Treatment with verapamil during long-term ethanol consumption prevented the development of these metabolic and functional abnormalities. It is hypothesized that alcohol produces membrane abnormalities leading to adverse ion flux, and that these are largely prevented by concurrent administration of verapamil.
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PMID:The preventive effect of verapamil on ethanol-induced cardiac depression: phosphorus-31 nuclear magnetic resonance and high-pressure liquid chromatographic studies of hamsters. 356 6

The case is described of a 43 year old woman with spasmophilic syndrome. For 12 years she had suffered from fainting fits, marked morning asthenia, anxiety, depression, widespread arthromyalgia, blood pressure fluctuations, precordial pains, paresthesia and painful nocturnal cramp. This clinical picture appeared in a subject with a double left kidney and stones in the supernumerary ureter, enlargement of the pancreatic head and tail revealed by a CAT scan and an earlier cholecystectomy. Given the multiplicity of symptoms diagnosis was necessarily by a process of elimination. The data providing grounds for optimism were a positive Chvostek's sign, stable calcium phosphorus profiles, a reduction in ionised calcium and favourable eletromyographic readings.
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PMID:[A case of spasmophilic syndrome]. 360 Nov 38

A study was done to examine the effects of aluminum, magnesium, and boron on major mineral metabolism in postmenopausal women. This communication describes some of the effects of dietary boron on 12 women between the ages of 48 and 82 housed in a metabolic unit. A boron supplement of 3 mg/day markedly affected several indices of mineral metabolism of seven women consuming a low-magnesium diet and five women consuming a diet adequate in magnesium; the women had consumed a conventional diet supplying about 0.25 mg boron/day for 119 days. Boron supplementation markedly reduced the urinary excretion of calcium and magnesium; the depression seemed more marked when dietary magnesium was low. Boron supplementation depressed the urinary excretion of phosphorus by the low-magnesium, but not by the adequate-magnesium, women. Boron supplementation markedly elevated the serum concentrations of 17 beta-estradiol and testosterone; the elevation seemed more marked when dietary magnesium was low. Neither high dietary aluminum (1000 mg/day) nor an interaction between boron and aluminum affected the variables presented. The findings suggest that supplementation of a low-boron diet with an amount of boron commonly found in diets high in fruits and vegetables induces changes in postmenopausal women consistent with the prevention of calcium loss and bone demineralization.
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PMID:Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women. 367 98

Phosphorus-31 magnetic resonance (31P MR) spectroscopy was used to obtain serial in vivo measurements of cerebral adenosine triphosphate (ATP), phosphocreatine (PCr), inorganic phosphate (Pi), and intracellular pH levels in rats during temporary global cerebral ischemia and reperfusion. Three groups of 4 rats each that recovered from permanent bilateral vertebral artery occlusion were placed in a MR spectrometer and subjected to remotely controlled bilateral carotid artery occlusion lasting 6, 15, or 30 minutes followed by 1 hour of reperfusion. Four additional rats that developed systemic hypotension (2 during a 6-minute occlusion and 2 during a 15-minute occlusion) were also studied. 31P MR spectra were obtained in each rat before, during, and after ischemia. Rats in which MR spectra showed metabolic recovery underwent a second occlusion followed by reperfusion and sacrifice. In the 12 normotensive rats, metabolic alterations began within 3 minutes after the onset of global ischemia. By the end of the occlusion period, cerebral ATP had decreased by 20 to 100% in 10 rats and PCr had decreased by 15 to 75% in all 12; Pi increased by 25 to 240%. The mean intracellular pH decreased from 7.33 to 6.9 +/- 0.6. The degree of metabolic deterioration during ischemia was not related to the duration of occlusion. During reperfusion, ATP, PCr, Pi, and intracellular pH returned to normal in 4 rats; 5 rats had partial metabolic recovery, and 3 had minimal or transient metabolic recovery followed by progressive deterioration. All rats that developed systemic hypotension had a decrease in ATP, PCr, and intracellular pH and an increase in Pi during the initial occlusion. Each had transient partial recovery in ATP during reperfusion, and 2 had slight recovery of PCr. The onset of hypotension was followed by depletion of these metabolites, progressive increase in Pi, and progressive intracellular acidosis. All rats that deteriorated metabolically after reversal of carotid occlusion died by the end of the reperfusion period or soon after. The 8 rats that recovered from the first occlusion were subjected to a second period of ischemia, during which each rat showed severe depletion of metabolites. During the second reperfusion, only 1 rat showed significant metabolic recovery, which lasted only 30 minutes and was followed by progressive deterioration. Severe global cerebral ischemia was associated with a progressive decline in both ATP and PCr, whereas less complete ischemia seemed to be characterized by stabilization or recovery of ATP and continued depression of PCr.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sequential in vivo measurement of cerebral intracellular metabolites with phosphorus-31 magnetic resonance spectroscopy during global cerebral ischemia and reperfusion in rats. 369 5

The biochemical mechanism of acute contractile failure in the hypoxic rat heart was investigated using phosphorus nuclear magnetic resonance to measure intracellular acidosis and the concentrations of phosphocreatine, adenosine triphosphate (ATP), and inorganic phosphate while cardiac mechanical function was simultaneously monitored. The cytosolic free [ADP] was calculated from the creatine kinase equilibrium expression. Mechanical activity, phosphocreatine and ATP concentrations, and intracellular pH all decreased after the onset of hypoxic perfusion. Neither a reduction in ATP concentration nor limitation in its rate of production contributed to the early contractile failure. Calculations suggest only a modest (approximately 10%) difference in cytosolic free energies of ATP hydrolysis. Neither the time course nor the extent of depression of mechanical function correlated well with intracellular acidosis. In conjunction with other observations, these results were consistent with the view that the myocardial inotropic state may be directly responsive to the ambient PO2. The overall rate of ATP turnover was assessed from measurements of oxygen utilisation and lactate production in both normoxic and hypoxic hearts. Surprisingly, despite more than an 80% reduction in mechanical activity during hypoxia, no significant decrease in the rate of ATP utilisation was noted during hypoxia. This suggests that unidentified non-contractile processes may hydrolyse ATP at relatively higher rates during hypoxia.
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PMID:Biochemical mechanisms of acute contractile failure in the hypoxic rat heart. 370 37


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