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)

Thirty-one patients suffering from a major depressive illness were entered into a placebo-controlled double-blind study to determine the effectiveness of lithium carbonate in acute depression. Patients were allocated by minimization to receive either lithium or placebo for 6 weeks in 2 parallel groups without crossover. For ethical reasons patients who showed no satisfactory response could be withdrawn at the discretion of the investigator but this was done without breaking the treatment code. More patients were withdrawn from the placebo group than from the lithium group as treatment failures, but in spite of this there was a significant difference in the depression ratings between the 2 groups at weeks 4 and 5 in favour of the active treatment group (p less than 0.04 and p less than 0.03 respectively).
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PMID:Lithium versus placebo in acute depression: a clinical trial. 311 77

We designed experiments to study changes in ventral medullary extracellular fluid (ECF) PCO2 and pH during hypoxemia. Measurements were made in chloralose-urethan-anesthetized spontaneously breathing cats (n = 12) with peripherial chemodenervation. Steady-state measurements were made during normoxemia [arterial PO2 (PaO2) = 106 Torr], hypoxemia (PaO2 = 46 Torr), and recovery (PaO2 = 105 Torr), with relatively constant arterial PCO2 (approximately 44 Torr). Mean values of ventilation were 945, 683, and 1,037 ml/min during normoxemia, hypoxemia, and recovery from hypoxemia, respectively. Ventilatory depression occurred in each cat during hypoxemia. Mean values of medullary ECF PCO2 were 57.7 +/- 7.2 (SD), 59.4 +/- 9.7, and 57.4 +/- 7.2 Torr during normoxemia, hypoxemia, and recovery to normoxemia, respectively; respective values for ECF [H+] were 60.9 +/- 8.0, 64.4 +/- 11.6, and 62.9 +/- 9.2 neq/l. Mean values of calculated ECF [HCO3-] were 22.8 +/- 3.0, 21.7 +/- 3.3, and 21.4 +/- 3.1 meq/l during normoxemia, hypoxemia, and recovery, respectively. Changes in medullary ECF PCO2 and [H+] were not statistically significant. Therefore hypoxemia caused ventilatory depression independent of changes in ECF acid-base variables. Furthermore, on return to normoxemia, ventilation rose considerably, still independent of changes in ECF PCO2, [H+], and [HCO3-].
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PMID:Ventral medullary extracellular fluid pH and PCO2 during hypoxemia. 312 71

This single case study reports on a 74-year-old woman with 48-hour cycles of mood disturbance for 2 years. Every other day she awakened feeling sad with low energy, decreased appetite, fatigue, diminished enjoyment of normal activities, increased irritability, occasional self-deprecatory thoughts, and difficulty concentrating. On alternative days she was active, outgoing, energetic, and cheerful. Her past history was marked by mild postpartum depressions, not requiring treatment, with each of her six pregnancies, and a more severe depression at age 57, which seemed to respond to Premarin. During the recent 2-year period of mood swings, the patient was given trials of several heterocyclic antidepressant medications, but side effects precluded the use of therapeutic doses or durations of treatment. Reluctantly, the patient agreed to a trial of lithium carbonate. After the second week of lithium treatment, at a level of 0.4 mEq/ml, she reported marked improvement, feeling fine every day without mood fluctuations. After almost 1 year at this blood level, she remains asymptomatic. Thus, the patient's cyclic 48-hour unipolar depression responded dramatically and completely to low doses of lithium carbonate.
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PMID:Cyclic 48-hour unipolar depression. 312 83

In our investigations on rats was proofed the qualification of substances 2-Cyanoethyl Urea (CEH), Thymus-Extract and Lithium-carbonate for a potential reducing or shortening of the leucocyte-depression after whole-body irradiation. Intravenous applications of 2-Cyanoethyl Urea in Wistar rats showed no effect not only in the increase of leucocytes but also in variation in portions of leucocytes. In our investigations we could not influence radiogenic phase of leucopenia by application of CEH after 7 Gy whole-body irradiation. Intramuscular injections of thymus extract don't influence the number of leucocytes in peripheral blood in irradiated Wistar rats. The differential blood-count was uninfluenced. Increase in concentration of thymus extract and also higher frequency of the applications effect no changes in blood-count. Leucocyte depression after whole-body irradiation was independent of the application modus of thymus extract. Lithium-carbonate shows a significant increase of leucocytes in peripheral blood in dependence of dosage and frequency of application. After whole-body irradiation with 7 Gy under lithium therapy it was shown that on day 6th after irradiation leucocyte number was significantly higher than in controls. Radiogenic leucopenia phase was reduced significantly by lithium.
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PMID:[Modification of radiogenic leukopenia]. 312 8

The effects of acoustic overstimulation on the endocochlear potential (EP) and on concentrations of ions (K+, Na+, Cl-, H+, HCO3-, and Ca2+) in endolymph were investigated using ion-selective microelectrodes. A slight but significant elevation of the EP and alkalinization of the endolymph were induced by acoustic overstimulation, whereas there was little change in the K+, Na+, Cl-, and HCO3- concentrations. The changes in H+ and HCO3- concentrations implied a depression of PCO2, suggesting an increase in blood flow to the cochlea. On the other hand, the Ca2+ concentration increased abruptly to 48 times the pre-exposure value. In contrast, no significant change in the Ca2+ concentration was observed in cochleae with damaged hair cells. We discuss the mechanism of the tone-induced Ca2+ elevation in endolymph and its effect on hearing acuity.
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PMID:Ionic changes in cochlear endolymph of the guinea pig induced by acoustic injury. 312 86

In response to added catecholamines, isolated trout (Salmo gairdneri) hepatocytes substantially increase the output of glucose into the surrounding medium. This effect is due to activation of glycogen breakdown concomitant with increases in gluconeogenesis and cell respiration. Each metabolic parameter is activated to a similar extent. In hormone-treated and untreated cells, glycogenolysis accounts for more than 97% of glucose production. Activation of glycogen phosphorylase is implicated in the degradation of cell glycogen, while increased flux through the gluconeogenic pathway from lactate is associated with inactivation of pyruvate kinase, possibly through enzyme phosphorylation as indicated by the activity ratio measured at low and saturating concentrations of phosphoenolpyruvate. From studies with specific adrenergic agonists and antagonists, we conclude that stimulation of glycogenolysis and gluconeogenesis in trout hepatocytes is consistent with a beta-adrenergic effect. Results are inconclusive with respect to catecholamine-mediated activation of cell respiration. None of the monitored cell acid-base variables (pH, PCO2, [HCO3-]) are implicated in the catecholamine-dependent changes in metabolic output of hepatocytes. Imposed hypercapnic conditions (increased medium PCO2 and decreased medium pH), which cause changes in cell acid-base parameters, result in a depression of lactate oxidation and gluconeogenesis, while the rate of glycogenolysis is not affected. In addition, the total amounts of glycogen phosphorylase and pyruvate kinase assayable are negatively affected by hypercapnic treatment of hepatocytes. Under hypercapnic conditions, cells are highly responsive to adrenergic agonists. It appears that--especially in the long term--the catecholamine-dependent activation of gluconeogenesis may compensate for the acid-base-dependent shortfall in glucose output by the liver.
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PMID:Interactive effects of catecholamines and hypercapnia on glucose production in isolated trout hepatocytes. 313 Nov 87

The effects of hypercapnia (1% CO2), and the independent effects of changes in extracellular pH (pHe), PCO2 and [HCO3-] on intracellular pH (measured by the DMO method) and lactate metabolism (measured by utilization of 14C-labelled lactate), were examined in rainbow trout hepatocytes in vitro. Simulated uncompensated hypercapnia (high PCO2, low pHe, moderately increased [HCO3-] led to a substantial depression in the production of CO2 (44%) and glucose (51%) from lactate. In simulated compensated hypercapnia (high PCO2, normal pHe, high [HCO3-], metabolism was still significantly inhibited (18-33%). Subsequent multifactorial design experiments determined that variations in PCO2, pH and [HCO3-] independently affected metabolism; increased PCO2 and decreased pH inhibited metabolism, but increased [HCO3-] stimulated metabolism. These results are interpreted in terms of the effects of acid-base variables on enzymatic and transport pathways, and the possible causes of decreased hepatic glycogen stores during in vivo hypercapnia are discussed.
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PMID:Effects of acid-base variables on in vitro hepatic metabolism in rainbow trout. 313 77

The use of ion-sensitive microelectrodes enabled us to follow the dynamic changes in extracellular pH (pHe) together with those in the extracellular concentration of some biologically important ions, particularly K+ and Ca2+. Activity-related changes in pHe were studied in isolated spinal cords of frogs and in spinal cords of rats in vivo. Repetitive electrical stimulation of an afferent input led either to triphasic alkaline-acid-acid changes (90% of frogs) or to triphasic alkaline-acid-alkaline changes (10% of frogs and rats) with the greatest changes in the lower dorsal horns. The transient acid shift by as much as 0.15-0.25 pH units is dominant and builds up during the stimulation. The changes in pHe were also found in response to various adequate stimuli applied to the skin on the hind limb. Using specific inhibitors of Na+/H+ exchange, K+-Cl- co-transport, Cl-/HCO3- exchange, the Na+/K+ pump and carbonic anhydrase, we found pHe homeostasis to be impaired and stimulation-induced changes in pHe decreased. We conclude that the pHe changes evoked by electrical or adequate stimulation of an afferent input are not determined by changes in extracellular strong ion concentration differences due to accumulation of lactate, since we found no effect of NaF, a metabolic blocker of lactate production. However, lactate accumulation has been demonstrated during seizures, spreading depression and anoxia. Recently, it has been recognized that the observed pHe changes can affect permeability of membrane ionic channels, neuronal excitability and glial cell function.
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PMID:Extracellular pH and stimulated neurons. 320 66

Lithium salts, in particular the carbonate and citrate, were formerly in widespread use, forming part of alkaline salt mixtures which were used for treatment of the many disorders belonging to the uric acid diathesis. Among these disorders were mania, depression, acute mania, acute melancholia and periodic depression. Satisfactory prophylactic effects on periodic depression were directly claimed. Daily doses of 3 to 26 mmol of lithium were recommended as standards. Only slight or moderate symptoms of poisoning were reported in a very few cases during the period in question (1860 to 1930), when the popularity of these lithium-containing prophylactic drugs with a favourable therapeutic index was at its peak. Lithium intoxication was not a serious clinical problem until 1949 when Cade introduced his fortuitously effective, but nevertheless high, dosage regimen which was continued until signs of recovery from mania appeared. For the maintenance dose, Cade in principle recommended, but seldom adhered to, 17 mmol/day. Chronic lithium intoxication starts insidiously with silent affliction of the kidneys followed by 'prodromal' symptoms, and when moderate severity has been reached, an accelerating renal vicious circle with decreasing kidney function is imminent. After this point the chronic intoxication resembles acute intoxication. Active detoxification at this, or an earlier stage, leaves the patient with a good chance of recovery. At a later stage, with the occurrence of oliguria, semi-coma or coma, and latent convulsive movement, recovery is less certain. There is no specific antidote for the toxic effects of lithium. Haemodialysis is the most effective treatment for acute lithium poisoning. For patients with impaired, or potentially impaired renal function, peritoneal dialysis may be an alternative, but less effective, treatment. Forced diuresis demands unimpaired renal function, and is little more effective than withdrawal of treatment, supplemented with correction of water and electrolyte balance. Sodium overloading is not recommended. Patients on lithium prophylaxis are treated on an outpatient basis. Prevention of intoxication depends on cooperation between patient and clinician, and possibly on the use of smaller, low risk dosages in most patients.
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PMID:Clinical features and management of lithium poisoning. 328 25

The effects of lithium carbonate on sleep patterns have been investigated both acutely in normal and depressed subjects and chronically in depressed subjects. In normal subjects receiving lithium for two weeks total sleep time did not vary, REM sleep decreased and REM sleep latency increased. In depressed subjects, either on short therm therapy or on long term therapy stages 3 and 4 increased, REM sleep decreased, REM latency increased and REM activity/time spent asleep (an index of REM intensity per minute of sleep) decreased. Plasma lithium levels were negatively correlated with REM sleep percentage and positively correlated with REM sleep latency. Besides, it has been shown in one paper that short term therapy with lithium caused small but significant delays in the sleep-wake circadian rhythm. These effects are of interest in view of polygraphic sleep abnormalities found in affective disorders and possible circadian disturbances accounting for these abnormalities. Indeed lithium might act in correcting spezial sleep abnormalities and/or circadian disturbances. In addition to its predominant use for the prophylaxis of recurrent mania and depression, lithium carbonate has been proposed and tried in the prophylactic treatment of abnormally prolonged sleep episodes featuring the Kleine-Levin syndrome.
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PMID:Lithium carbonate: effects on sleep patterns of normal and depressed subjects and its use in sleep-wake pathology. 331 43


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