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)

(1) Subcutaneous or intra-abdominal injections of 8 mg of HgCl2/100 g body weight markedly depressed hepatic fatty acid synthetase activity of chicks at 1 h post-injection. The depression occurred despite the fact that the chicks continued to eat up until the time they were killed. Under these same conditions, the hepatic activity of acetyl-CoA carboxylase (EC 6.4.1.2) was not affected by HgCl2, while the activity of the mitochondrial system of fatty acid elongation was stimulated. (2) When 2-mercaptoethanol was included in the incubation medium for a highly purified preparation of fatty acid synthetase, 500 muM HgCl2 was required to show definite inhibition of the enzyme. When 2-mercaptoethanol was omitted, 50 muM HgCl2 was inhibitory and 100 muM HgCl2 abolished enzyme activity. (3) 2 mM dithiothreitol completely protected the purified fatty acid synthetase preparation from inhibition by 100 muM HgCl2. When dithiothreitol was added after the addition of enzyme to the mercury-containing medium, protection of the enzyme was not complete. (4) Dialysis of cytosol fractions from chicks injected with HgCl2 against 500 vol. of 0.2 M potassium phosphate buffer (pH 7.0) containing 1 mM EDTA and 10 mM dithiothreitol for 4 h at 4 degrees stimulated the fatty acid synthetase activity of the fractions. Dialysis of cytosol fractions from noninjected chicks under the same conditions was without effect on fatty acid synthetase activity. (5) These data support the hypothesis that the inhibitory effect of HgCl2 administered in vivo on hepatic fatty acid synthetase activity in chicks is mediated through the interaction of mercury with the sulfhydryl groups of the enzyme.
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PMID:Mercury inhibition of avian fatty acid synthetase complex. 0 Jan 50

Neuron cell bodies of Helix pomatia were voltage-clamped with a 300-millisecond depolarizing test pulse (pulse II) delivered I second after a depolarizing conditioning pulse (pulse I). The outward current, measured 200 milliseconds after the onset of pulse. II, exhibited a strong depression that was dependent on the presence of pulse. I. The maximum depression of the pulse II outward current occurred when pulse I voltages lay in the range over which calcium influx is inferred to be greatest; depression of the pulse II current subsided as pulse I potentials approached the putative calcium equilibrium potential. In the presence of extracellular [ethylenebis(oxyethylenenitrilo)]tetraacetic acid (EGTA) or D600, the intensity of the pulse II current became largely independent of pulse I, approaching the values of maximal depression seen in normal Ringer solution. On the other hand, lowering the intracellular pH with extracellular carbon dioxide-carbonate buffer had no measurable effect on the outward currents. Other experiments showed that it is primarily the calcium-dependent, outward-current hump of the N-shaped late current-voltage curve that is depressed by presentation of the conditioning pulse. It was concluded that distinct from an early potassium-activating role, calcium entering during a depolarization leads, during a subsequent depolarization, to a depression of the calcium-activated potassium system that persists for many seconds.
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PMID:Calcium-dependent depression of a late outward current in snail neurons. 1 21

Patients attending their family practitioner with emotional disturbance manifesting predominantly as anxiety were treated once daily for 4 weeks with either a pure anxiolytic, potassium clorazepate, or a formulation of a specific antidepressant together with an anxiolytic, fluphenazine/nortriptyline, in accordance with a double-blind, completely randomized design. After the first week the patients receiving fluphenazine/nortriptyline were showing a better response in terms of total symptomatology as well as anxiety, tension and depression taken separately, and after 4 weeks treatment this trend reached statistically significant levels on both the physicans' ratings and the patients' self-ratings for overall symptomatology (p less than 0-05) as well as anxiety and tension on the physicians' scale (p less than 0-01). Side-effects were infrequent, with the exception of drowsiness which was complained of by 42% of the patients receiving clorazepate. Although simple and convenient to take, a once daily benzodiazepine formulation of fixed dose is likely to be too inflexible to achieve optimal therapeutic effect in many patients. These results are in accord with accumulating evidence for the importance of a depressive aetiology underlying the majority of so-called anxiety states in family practice. Anxiolytic, in the absence of specific antidepressant, therapy is unlikely to be adequate for these patients, and may lead to long-term palliative use of benzodiazepines incurring a risk of dependence.
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PMID:Anxiety states in family practice: an evaluation of the need for antidepressant as well as anxiolytic therapy. 2 Nov 16

Treatment of chronic uremia by hemodiafiltration requires replacement of the filtrate. Using Ringer's solution alone, there is a depression of pH because of bicarbonate loss. To bring the acid base status back to normal, sodium lactate in increasing concentrations (283 mg% = 32 mM/1, 361 mg% = 40 mM/1; 462 mg% = 51 mM/1; 508 mg% = 57 mM/1) was added to the replacement fluid. The optimal concentration is 450 mg% (=50 mM/1) sodium lactate, provided the following conditions are fulfilled: (a) substitution after the filter; (b) mixing ratio of blood and substitution fluid 1:2. Using 12-15 liters of substitution fluid during a 5 hr treatment, the added lactate amounts to 60 g (=0.54 M). With continuous addition of lactate, the serum concentration of lactate is 3.5 times normal and the concentration of serum pyruvate 4 times normal. An excess lactate concentration, according to Huckabee [1,2], was thus not observed. The sieving coefficients were the following: sodium, potassium, urea, lactate, pyruvate, and phosphate 1; chloride greater then 1; calcium and protein less than 1. Serum osmolality fell, on the average, 9 mOsmol/1 during diafiltration.
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PMID:Acid base status during treatment of chronic uremia with diafiltration. 2 47

After incubation at pH 10 or higher, Bacillus thuringiensis spores and endotoxin, at concentrations above 0.1 IU/ml, affected transport parameters in the isolated midgut of Manduca sexta larvae. (Toxic activity was lost during roughly 1 week at pH 11.) About 60% of the short-circuit current was inhibited, and the remainder was reversibly inhibited by anoxia. Electrical resistance was reduced by about 55% and oxygen uptake stimulated by about 30%. Influx of potassium from blood-side to lumen-side ('active' flux) was unaffected but flux in the reverse direction was nearly tripled. These results suggest that hydrolysis of the toxin yields an inhibitor of potassium transport, presumably a polypeptide. It is argued that inhibition is not primarily by uncoupling of oxidative phosphorylation, but instead by interference with an active depression of the efflux of potassium from lumen-side to blood-side.
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PMID:Mechanism of inhibition of active potassium transport in isolated midgut of Manduca sexta by Bacillus thuringiensis endotoxin. 4 81

The effects of a 0.5 g/kg body weight arginine infusion on plasma inorganic phosphates and potassium were examined in nineteen normal subjects. Plasma phosphorus displayed a highly significant (p less than 0.001) fall with a maximum depression below baseline of 1.11 +/- 0.15 mg/100 ml or 33 +/- 3% (mean +/- SEM); there was a significant correlation (p less than 0.01) between this fall and the insulin peaks induced by arginine. Plasma potassium levels displayed a distinct and significant increase in eleven of the twelve subjects studied; the maximum increase above baseline was 1.02 +/- 0.14 mEq/1 or 27 +/- 4.5% (p less than 0.001). No change occurred in blood pH values determined in four subjects. In six normal subjects, the test was repeated with the addition of somatostatin (250 micrograms bolus, followed by 500 micrograms/hr), which abolished the insulin and growth hormone response to arginine. It also abolished the fall in plasma phosphorus but appeared (if anything) to augment the increase in potassium. These findings show that arginine is responsible for a fall in plasma phosphorus related to the insulin response, and for an increase in plasma potassium of clinical significance, the mechanism(s) of which, however, are still obscure.
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PMID:Arginine-induced hypophosphatemia and hyperkaliemia in man. 4 74

70 chronic alcoholics in the withdrawal state, 45 with convulsions and 25 controls without convulsive seizures, were tested with respect to electrolyte changes and acid base balance in serum or blood and cerebrospinal fluid (CSF). It was of special interest to note that there was a partial independence between magnesium levels in serum and CSF. Thus the serum level has only a limited liability as to magnesium depletion suggested to be responsible for seizure precipitation. In the seizure group a slightly but significantly lower magnesium, potassium and calcium in CSF and a significant decrease of potassium and calcium in serum were revealed. In the nonzeizure controls a similar decrease of magnesium in serum and potassium in CSF was observed while serum potassium and calcium in CSF and serum remained in low normal range. In both groups there was a prominent respiratory alkalosis. The role of magnesium depression for seizure precipitation is discussed with respect to the concomitant changes of other electrolytes and acid base disturbances.
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PMID:Electrolyte changes and acid base balance after alcohol withdrawal, with special reference to rum fits and magnesium depletion. 6 5

Interaction between epileptic foci and spreading depression (SD) was studied in the cerebral cortex of rats anesthetized with Nembutal. At comparable discharge rates, picrotoxin and penicillin caused complete and partial SD blockade respectively, strychnine and Metrazol were ineffective and Aldactone facilitated SD. Conversely, the duration of SD-induced blockade of epileptic activity was maximal for Aldactone and minimal for picrotoxin. Treatment of the picrotoxin focus with tetrodotoxin (10(-4)M) reduced the discharge rate and reinstated SD propagation into the focus. [K+]e measured with ion-selective K+ electrodes 1 mm below the cortical surface increased to 8 mM in penicillin foci blocking SD and remained below 5 mM in Aldactone foci. It is concluded that the differential effect of various convulsants on SD propagation depends on the potassium concentration in the depth of the focus rather than on the discharge rate or on the mechanism of the the epileptogenic effect.
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PMID:Differential effects of cortical speading depression on epileptic foci induced by various convulsants. 7 46

We have investigated the effects of quinidine on the force of contraction and the intracellularly recorded action potential in papillary muscles isolated from human hearts. All preparations were obtained from patients undergoing corrective open heart surgery. The following results were obtained: (1) quinidine had a depressant effect on myocardial contractile force; (2) quinidine reduced the maximal upstroke velocity of the action potential; (3) quinidine shortened the plateau phase and prolonged the terminal repolarization of the action potential; (4) at higher concentrations quinidine reduced the resting potential; and (5) the depression by quinidine of both the plateau and the force of contraction was antagonized by isoprenaline. It is concluded that quinidine reduces the membrane conductances for sodium, calcium, and potassium ions. All of these actions of quinidine may contribute to the antiarrhythmic effects of the drug. The negative inotropic effect of quinidine can be explained by a depression of the calcium conductance at the myocardial cell membrane. The results show that earlier findings in laboratory animals regarding the effects of quinidine on the upstroke velocity and repolarization phase of the action potential are applicable to the human heart.
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PMID:Electrophysiological study of human ventricular heart muscle treated with quinidine: interaction with isoprenaline. 9 19

Spreading depression (SD) of EEG activity was elicited by microinjection (5 microliter) of 5% potassium chloride into the caudate nucleus (n = 7) or hippocampus (n = 3) during stereotactic brain surgery in patients with focal epilepsy. An electrode-cannula assembly for eliciting and recording the slow potential waves of SD is described. The parameters of SD in human brain are similar to those in lower mammals. Functional ablation by SD can be used as a diagnostic tool in neurosurgery.
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PMID:Functional ablation by spreading depression: possible use in human stereotactic neurosurgery. 9 40


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