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 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

Previous studies demonstrated alterations of thyroidal economy in untreated diabetes mellitus both in man and experimental animals. To test the role of beta-hydroxybutyric acid (BHB) and acidosis in generating such changes, we studied the pituitary-thyroid axis of streptozotocin-diabetic rats, BHB or ammonium chloride (NH4Cl)-treated normal rats. Serum TSH, pituitary content and pituitary concentration of TSH, serum T4, T3 and free T4 (FT4), were all measured by RIA. In short term (2 days) diabetic rats the pituitary content of TSH was normal whereas the concentration (per mg of protein) was elevated (p less than 0.05 versus control group). Serum TSH (p less than 0.05), serum T4 (p less than 0.05), serum T3 (p less than 0.01) and serum FT4 (p less than 0.05) were all significantly decreased. In long term (30 days) untreated diabetic rats serum changes were similar to the short term diabetic group, though the pituitary content of TSH was significantly decreased (p less than 0.05). Animals treated with NH4Cl had no variations from controls. However, rats treated with BHB displayed a significant decrease in pituitary content of TSH (p less than 0.05), pituitary concentration of TSH (p less than 0.05) and in plasma TSH (p less than 0.01), and normal thyroid hormones in serum. No significant changes were seen in the TSH response to TRH in 2 or 30 days untreated diabetic and in BHB - treated animals. The data suggest that BHB, although not NH4Cl acidosis, may be capable of inducing a moderate depression of pituitary and plasma TSH of a lesser magnitude of that accompanying the full, long term diabetic state in the rat.
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PMID:Effects of diabetes, beta-hydroxybutyric acid and metabolic acidosis on the pituitary-thyroid axis in the rat. 316 31

Tumours produce substances that inhibit the expression of cell-mediated immunity, in the form of delayed-type hypersensitivity in mice. Phenol-saline extracts of bovine ocular squamous cell carcinoma (BOSCC) which have immunotherapeutic activity in cattle were able to immunize mice against this depressive effect. Such immunization was effective against products of BOSCC, a spontaneous rat tumour, three of four human tumour cell lines and (in other experiments) mouse tumours. Phenol-saline extracts of mouse tumour cell lines were immunogenic (protective against depression of delayed-type hypersensitivity) in mice. Fractions of BOSCC phenol-saline extracts which were immunotherapeutically active in cattle were generally also protective in mice. The protective activity was lost after treatment with proteinase K, and was present in the supernatant after precipitation with 55% ammonium sulphate. It was not affected by treatment with RNase or DNase or by heating to 50 degrees C for 2 h. It was present in gel filtration fractions with an apparent molecular weight of 10,000-37,000 daltons. The immunogenic factor in mice and the immunotherapeutic factor in cattle may be related to each other.
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PMID:Depression of cell-mediated immunity by tumour cell products: induction of resistance by immunotherapeutically active extracts of bovine ocular squamous cell carcinoma. 359 86

An alkaline, followed by an acid-going transient, characterizes acid-base changes in the interstitial space during spreading depression in a variety of brain structures. In rat, such changes are associated with a significant rise in brain lactate content. How brain proton buffers behave during spreading depression is unknown. Techniques to significantly improve the response time of gas permeable membrane semimicroelectrodes for carbon dioxide and ammonia are reported. Measurements with such electrodes, when coupled to measurements of hydrogen ion concentration (from microelectrodes), permit rapid changes to be determined in bicarbonate concentration or ammonia and ammonium ion concentration, respectively. Bicarbonate concentration fell from 30 +/- 1 (n = 16) to 14 +/- 1 mM (n = 16) during spreading depression. On the other hand, ammonia concentration rose from 2.3 +/- 0.1 to 4.4 +/- 0.3 microM (n = 17) while ammonium ion concentration rose from 116 +/- 11 (n = 17) to 382 +/- 30 microM (n = 17) during spreading depression. Bicarbonate changes probably reflect titration of brain bicarbonate stores by accumulated lactic acid. Similar physicochemical changes do not explain the rise in ammonia and ammonium ion concentrations. Instead, elevation of the latter can only result from an increase in ammonia content of the interstitial space.
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PMID:Bicarbonate and ammonia changes in brain during spreading depression. 362 Oct 35

Portasystemic encephalopathy has been a major deterent to the utilization of total or non-selective shunts. A procedure to determine the maximum rate of urea synthesis (MRUS) has been developed and a depression in the ability to synthesize urea has been shown to correlate closely with the development of encephalopathy. Utilizing this procedure and a modified ammonium tolerance curve, a controlled comparison was instituted between selective and non-selective shunts. Following a non-selective or total shunt, there was a definite deterioration in both the MRUS and the ammonium chloride tolerance curve which was accompanied by a high rate of clinical encephalopathy. In marked contrast, the selective shunt, which maintains portal venous perfusion of the liver, showed little or no change in the MRUS and the ammonium chloride tolerance curve following the selective shunt and there was a very low incidence of encephalopathy. The difference between the non-selective and selective shunt in maintenance of urea synthesis, metabolism of ammonium chloride, and the development of clinical encephalopathy show the selective shunt procedure to be definitively superior in this regard.
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PMID:The metabolic basis of portasystemic encephalopathy and the effect of selective vs nonselective shunts. 441 59

Laboratory tests were conducted with four organophosphorus insecticides, Bay 37289 (O-ethyl O-2,4,5-trichlorophenyl ethylphosphonothioate), diazinon [O,O-diethyl O-(2-isopropyl-4-methyl-6-pyrimidinyl) phosphorothioate], Dursban (O,O-diethyl O-3,5,6-trichloro-2-pyridyl phosphorothioate), and Zinophos (O,O-diethyl O-2-pyrazinyl phosphorothioate), applied to a sandy loam at rates of 10 and 100 mug/g to determine whether these materials caused any serious effects on microbial activities related to soil fertility. All insecticides showed an effect on fungi and bacteria for the first and second week of incubation, but, subsequently, the populations returned to levels similar to those obtained in the controls. All insecticide applications increased ammonium production, but, in some instances, there appeared to be a slight depression of nitrification. Sulfur oxidation was equal to or better than that obtained with untreated soil in most cases. There was no significant effect on phosphorus mineralization. Oxygen consumption indicated that microbial respiration increased in proportion to the concentration of insecticides, suggesting the possibilities of microbial degradation of the insecticides or their degradation products and of uncoupling oxidative phosphorylation.
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PMID:Effect of four organophosphorus insecticides on microbial activities in soil. 546 62

Decreased ammonium (NH4+) excretion is associated with hyperkalemia. To determine if potassium could directly influence renal ammonia production, we investigated ammoniagenesis by rat and canine renal cortical tissues in vitro at different potassium concentrations. Renal tissue from normal and acidotic rats and normal dogs incubated in glutamine, lactate, and 7 to 10 mEq/liters of potassium or 25 mEq/liters of potassium produced significantly less ammonia than slices incubating in glutamine, lactate, and 4 to 5 mEq of potassium. Glutamate accumulation, which follows glutamine deamidation, did not decrease and even increased at 25 mEq/liters of potassium. With glutamine as the sole substrate, decreased ammoniagenesis was seen only at higher potassium concentrations (greater than 16 mEq/liters) than when lactate was also present. The depression to glutamine ammoniagenesis by high concentrations of potassium was partially obliterated in an anaerobic environment. When glutamate replaced glutamine as the precursor, renal ammonia produced by slices in 7 and 25 mEq/liters was again significantly lower than by slices incubating in 4 mEq/liters. We blocked glutamine synthesis by rat kidney slices with dl-methionine dl-sulfoximine when glutamate was the renal ammonia precursor. This essentially allows glutamate deamination to produce ammonia. Potassium depressed glutamate deamination significantly at 7 mEq/liters (decreases 13%) and at 25 mEq/liters of potassium (decreases 35%) as compared to 4 mEq/liters. The above findings are consistent with a major depressive effect of in vitro potassium on glutamate deamination in rat and canine kidneys. Other evidence, especially from rat tissue studies, suggests that potassium also may affect glutamine deamination directly. Rat kidney slices incubating in the high potassium medium of 7 mEq/liter or greater also consumed less oxygen in the presence of glutamine (P less than 0.01), oxidatively decarboxylated less glutamine (P less than 0.02) and produced less glucose from glutamine (P less than 0.01).
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PMID:Effects of in vitro potassium on ammoniagenesis in rat and canine kidney tissue. 612 28

Adenosine monophosphate (AMP) deaminase and 5'-nucleotidase, the two enzymes involved in the disposal of AMP, have been detected in different regions of normal rat brain and in animals subjected to heightened neuronal activity (leptazol-induced convulsions) and to depression of the central nervous system (CNS) by the administration of barbiturates. They have also been estimated in the CNS of animals subjected to anoxia or treated with lithium and ammonium salts. The AMP deaminase activity was found to be highest in cerebellum and lowest in cerebral cortex, while the 5'-nucleotidase activity was found to be highest in brain stem and lowest in cerebellum. The AMP deaminase activity was elevated in all the regions of brain during the preconvulsive and convulsive periods. The activity returned to normal during recovery. The activity of 5'-nucleotidase was found to be depressed in the preconvulsive and post-convulsive periods. The enzyme was also found to be depressed in all the three regions after the administration of barbiturates. Administration of lithium or ammonium salts of induction of anoxic states resulted in an increase in the activity of AMP deaminase in all the three regions of brain. These results are discussed in relation to the probable production of cyclic AMP and cyclic guanosine monophosphate (GMP) which may have depressive and excitatory roles, respectively, in brain. It appears that increased AMP deaminase activity is associated with increased neuronal activity while depression of 5'-nucleotidase activity is associated with conditions of decreased CNS excitability.
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PMID:Studies on AMP deaminase and 5'-nucleotidase in rat brain under different experimental conditions. 625 52

GABA applied by iontophoresis produced GABA-induced currents (GCs) and GABA-induced depolarizations (GDs) which were recorded intracellularly from cat dorsal root ganglia (DRG). Lowering the temperature (37 to 27 degrees C) of the preparation depressed the amplitude of GCs while prolonging their rise-time and decay time. This depressant action was mainly due to a hyperpolarizing shift in the GABA equilibrium potential (EGABA). GABA responses could also be depressed by alkalinization of the superfusion solution or addition of putative chloride pump inhibitors, e.g. SITS, furosemide or bumetanide. However, the mechanism by which these latter procedures depressed GABA responses was not due to a shift in EGABA as occurred with lowered temperature. Instead we suggest that alkalinization or the putative chloride pump inhibitors affect the chloride channel or some other site associated with the GABA receptor complex and cause the depression we observed. GABA responses could be facilitated by lowering the pH of the superfusion solution or by injecting ammonium ion into a DRG. These results suggest that a temperature-sensitive, inwardly directed chloride pump that is resistant to SITS, furosemide or bumetanide, operates in cat DRG.
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PMID:The effects of temperature, pH and Cl-pump inhibitors on GABA responses recorded from cat dorsal root ganglia. 630 67

Pretreatment with ammonium acetate (NH4Ac) (6 mmol/kg s.c.) approximately doubled the time morphine-treated mice remained on a hot surface and similarly increased muscular incoordination by diazepam, but NH4Ac treatment alone had no effect. Thus, hyperammonemia is capable of altering drug action and must be considered along with impaired drug metabolism in enhanced drug responses associated with liver disease. Experiments in vitro showed that acetylcholine-induced catecholamine release from bovine adrenal medulla is depressed as much as 50% by 0.3 mM NH4Ac and KCl-induced contractions of guinea-pig ileum were inhibited 20% by 5 mM NH4Ac. Addition of excess calcium reversed the depression in both tissues, but calcium-independent catecholamine release by acetaldehyde was not blocked by NH4Ac. These results suggested that ammonia blocks calcium channels. Parallels in the actions of NH4Ac and the calcium channel blocker verapamil support this concept. Both verapamil (10 mg/kg i.p.) and NH4Ac pretreatment enhanced morphine analgesia- and diazepam-induced muscular incoordination and antagonized amphetamine-induced motor activity, and neither verapamil nor NH4Ac affected the convulsant action of metrazol. The data suggest that hyperammonemia exerts a calcium channel blocking action which enhances the effects of central nervous system depressants and certain opioid analgesics.
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PMID:Modification of drug action by hyperammonemia. 632 92


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