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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Body temperature depression was noted in rats, mice, and hamsters following intraperitoneal cobaltous chloride administration (25 mg/kg). Intracerebral cobalt injection elicited hypotermia in rats and mice but not in hamsters. Body temperature depression appeared to be centrally mediated in rats and mice and peripherally mediated in hamsters. The effect of intraperitoneal and intracerebral pretreatment with phentolamine, diphenhydramine, propranolol, cimetidine, and naloxone on the mouse rectal temperature response to cobalt (25 mg/kg ip) was noted. Systemic phentolamine injection (intraperitoneal) did not alter the cobalt response, whereas intracerebral administration partially antagonized cobalt-induced hypothermia, indicating that antagonism was mediated centrally. Pretreatment with propranolol and cimetidine failed to modify the temperature response. Intracerebral diphenhydramine did not influence cobalt hypothermia. However, this agent reduced the cobalt response when given intraperitoneally, presumably through a peripheral inhibitory mechanism. The intracerebral injection of naloxone 30 min prior to cobalt slightly enhanced hypothermia, apparently through a central action. Intracerebral 6-hydroxydopamine injection depleted brain norepinephrine and dopamine but exhibited no apparent influence on cobalt-induced hypothermia.
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PMID:Cobaltous chloride-induced hypothermia. II: Pretreatment with sympathoplegics, antihistamines, and narcotic antagonists. 3 17

The mechanisms of the anticonvulsant activity of cannabidiol (CBD) and the central excitation of delta 9-tetrahydrocannabinol (delta 9-THC) were investigated electrophysiologically with conscious, unrestrained cobalt epileptic rats. The well-known antiepileptics, trimethadione (TMO), ethosuximide (ESM), and phenytoin (PHT), were included as reference drugs. Direct measurements were made of spontaneously firing, epileptic potentials from a primary focus on the parietal cortex and convulsions were monitored visually. ESM and TMO decreased the frequency of focal potentials, but PHT and CBD exerted no such effect. Although CBD did not suppress the focal abnormality, it did abolish jaw and limb clonus; in contrast, delta 9-THC markedly increased the frequency of focal potentials, evoked generalized bursts of polyspikes, and produced frank convlusions. 11-OH-delta 9-THC, the major metabolite of delta 9-THC, displayed only one of the excitatory properties of the parent compound: production of bursts of polyspikes. In contrast to delta 9-THC and its 11-OH metabolite, CBD, even in very high doses, did not induce any excitatory effects or convulsions. The present study provides the first evidence that CBD exerts anticonvulsant activity against the motor manifestations of a focal epilepsy, and that the mechanism of the effect may involve a depression of seizure generation or spread in the CNS.
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PMID:The influence of cannabidiol and delta 9-tetrahydrocannabinol on cobalt epilepsy in rats. 11 6

Eighteen patients with nasopharyngeal carcinoma (NPC) were compared to matched controls, before or after cobalt therapy, for the ability of their peripheral blood lymphocytes to: (1) form E and EAC rosettes and (2) mount a proliferative response with PHA, Con A and ALG. A slight decrease in the percentage of E rosettes and a moderate hyporesponsiveness to PHA and Con A were observed before treatment. The statistical significance of these alterations was borderline. Within the group of treated patients a much greater depression, including the response to ALG, was found, although a few long-term survivors responded to mitogens as well as the controls. These findings stress the difficulty of interpreting the results of a longitudinal study of cell-mediated immunity, specific or non-specific, in cancer patients. Finally, by comparing the proliferative response to the three mitogens before and after radiotherapy, it is suggested that their differential effect on these responses might be used in man, as it was in mice, to delineate lymphocyte subpopulations.
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PMID:Lymphocyte subpopulations and mitogenic responses in nasopharyngeal carcinoma, prior to and after radiotherapy. 20 May 72

The trace metals nickel and platinum, which are not substrates for ferrochelatase and thus do not form heme in biological systems, were found to act similaryl to cobalt, and heme itself, in regulating heme metabolism in liver and kidney. These metals induced heme oxygenase activity in both organs with the peak of induced enzyme activity reached approximately 16 hr after single injections in rats. Both metals caused transient depression of cellular glutathione content followed by increases above normal after 12 hr in liver. Nickel and platinum were more potent inducers of heme oxygenase in kidney than in liver (10-13 times normal versus 5-6 times normal). At high concentrations, they inhibited heme oxygenase [heme, hydrogen-donor:oxygen oxidoreductase (alpha-methene-oxidizing, hydroxylating), EC 1.14.99.3] in vitro. Both were active in regulating heme metabolism only when administered in the ionic form. Complexing of the metals with sulfhydryl agents completely blocked their actions on heme metabolism. Administration of cysteine orally prior to or shortly after administration of the metals had a similar blocking effect. Nickel and platinum produced depression of delta-aminolevulinate synthase [succinyl-CoA:glycine c-succinyltransferase (decarboxylating), EC 2.3.1.37] activity in liver, but neigther inhibited this rate-limiting ennzyme for heme synthesis in vitro. Furthermore, despite the substantial decreases in cellular heme and hemoprotein contents mediated by the metal, production of delta-amimolevulinate synthase did not undergo the compensatory increase that would be expected if there were a direct reciprocal feedback relationship between cellular heme level and synthesis of this enzyme. These findings indicate that it is not necessary for metal ions to be chelated in the porphyrin ring in order to regulate the enzymes of heme synthesis and heme oxidation. Accordingly, it is suggested that the iron atom of heme is the proximately active regulator of delta-aminolevulinate synthase and heme oxygenase--actions generally ascribed to the iron-tetrapyrrole complex itself--and that the tetrapyrrole moiety of the complex functions primarily as a means of transport of the metal to regulatory sites in cells.
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PMID:Regulation of heme pathway enzymes and cellular glutathione content by metals that do not chelate with tetrapyrroles: blockade of metal effects by thiols. 26 10

The effects of beryllium addition to a dental cobalt-chromium alloy on biological compatibility as well as physical properties were examined and the following results were obtained. 1. Slight, but significant depression of the rates of cell multiplication was obtained with the experimental groups, i.e., alloy with no beryllium added as well as alloys with beryllium of up to 3.0 per cent by weight, compared to control group, which contained no alloys, but a glass disk. Within the experimental groups no significant difference in the rates of cell multiplication was found between the alloys with beryllium addition ranging from zero up to 2.0% by weight. However, alloy with 3.0% beryllium yielded slight, but significant depression of the rates of cell multiplication. Pure beryllium metal revealed severe cytotoxicity. 2. Cell morphology of the experimental groups confirmed the above results of the rate of cell multiplication. 3. Increase of beryllium within the alloys resulted in increase of tensile strength as well as Rockwell hardness, while elongation and fusion temperature were brought down. 4. Metallographs of alloys and cast specimens confirmed the results of the mechanical properties. The more beryllium was added, the smaller was the alloy crystal observed. 5. Loss of beryllium in the alloy was found during such procedures as melting each metal for making up alloys and casting. It is considered that the present results will be able to lend suggestions to beryllium use in dentistry with regard to biological compatibility as well as physical properties.
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PMID:[A study on the effects of beryllium addition upon biological and physical properties of dental cobalt-chromium alloys (author's transl)]. 28 70

Every week, 8 conscious, chronically instrumented dogs underwent left ventricular (LV) function studies before, during, and after cardiac irradiation with cobalt 60 (myocardial dose of 5,000 rads at 200 rads per day through a 5 X 5 cm port). During the weekly LV function studies, left atrial pressures were raised by rapid infusion of balanced saline solution. Heart rate, aortic pressures, left and right atrial pressures, LV pressure, left ventricular end-diastolic pressure (LVEDP), and maximum rate of rise of LV pressure were recorded. Electrocardiograms were made. Cardiac outputs were obtained by thermodilution. Stroke volume, LV stroke work, and LV minute work were calculated. LV function curves were constructed each week. All dogs lost weight and became irritable after approximately 800 rads. The electrocardiograms showed signs of myocardial injury after 1,200 rads. All variables were slightly depressed during the first 8 weeks following irradiation. At the eleventh week, both left atrial pressure and LVEDP increased significantly and LV function declined. There was also clinical evidence of LV failure at rest and after volume loading. This study documents that external cardiac irradiation, in a therapeutic dose and schedule range, causes depression of LV function. These functional changes were partially reversed when the follow-up study was continued to six months after irradiation.
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PMID:Effect of therapeutic-dose irradiation on left ventricular function in conscious dogs. 47 89

Nickel toxicity was studied in young chicks fed a semi-purified diet. Dietary nickel concentrations of 300 mg/kg and higher resulted in significant reduction in growth rate. Mortality and anemia were observed in chicks receiving 1100 mg/kg nickel. Dietary nickel content of 300 mg/kg resulted in a significant increase in kidney nickel content while higher dietary levels were required to affect the nickel content of other body tissues. Supplementation of nickel toxic diets (500 mg/kg) with 100 mg/kg of cobalt, iron, copper, and zinc did not alleviate the symptoms of nickel toxicity or consistently affect tissue nickel accumulation. The addition of cobalt resulted in a further depression in growth rate when added to the nickel toxic diet. However, subsequent studies showed that this was due to the toxicity of cobalt and no evidence was found for an interaction between these two elements. The lack of interaction of nickel with copper, iron, and zinc is in contrast to the results observed by other investigators at low dietary concentrations of nickel.
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PMID:Studies on nickel metabolism: interaction with other mineral elements. 51 46

Recordings were obtained from single primary auditory neurones in the guinea pig cochlea during perfusion of the scala tympani with solutions containing elevated concentrations of Mg2+, Mn2+ and Co2+, or with lowered concentrations of Ca2+. Such perfusions caused a reversible depression of spontaneous firing rates. This is consistent with the notion that spontaneous firing is the result of background release of excitatory transmitter from cochlear hair cells, in the absence of acoustic stimulation. The above ion modifications also produced varying changes in single neurone response curves to acoustic stimuli. In one half of the 14 neurons studied these changes were also compatible with a classical blockage of synaptic transmission. The other half however, showed little or no change in sensitivity at low frequencies while large threshold elevations occurred at high frequencies.
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PMID:Effect of divalent cations on spontaneous and evoked activity of single mammalian auditory neurones. 57 41

The hypothermic response following intraperitoneal doses (6.25, 12.5, and 25 mg/kg) of cobaltous chloride was investigated in Swiss albino mice. The magnitude and duration of rectal temperature depression were dose related. In each case, maximal hypothermia was evident within 30 min after injection. Body temperature depression was noted 30 min after oral, subcutaneous, intraperitoneal, intravenous, and intracerebral administration of cobaltous chloride. Cobalt was most active when administered intracerebrally, suggesting a central component to the thermolytic response. Rectal temperature depression following cobaltous chloride was dependent on the ambient temperature. The time course of the effect of cobaltous chloride on rectal and cutaneous tail temperature was noted. Cutaneous tail temperature depression occurred throughout the rectal temperature response, suggesting that cobalt may decrease heat production. Pretreatment with atropine sulfate, hexamethonium bromide, or nicotine failed to modify the temperature response to cobalt. Chlorpromazine hydrochloride pretreatment resulted in a partial antagonism of cobalt-induced hypothermia, presumably through a mechanism other than cholinergic blockade.
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PMID:Cobaltous choride-induced hypothermia in mice I: effect of pretreatment with anticholinergic drugs. 66 Apr 60

The study was designed to confirm a previous, unexpected observation of a strong growth depressing effect of 1 microgram cobalt/g in rats fed lactalbumin based diets. The addition of 0.25, 0.5, and 1.0 microgram of cobalt/g to the basal diet containing 0.056 microgram/g depressed growth rates of rats progressively with increasing doses. This depression was overcome by increasing the cobalt supplement to 2 microgram/g, and additional weight gain was observed with 3 microgram/g. Higher concentrations were progressively toxic. Hemoglobin concentrations, hematocrits, and thyroid retention of intravenously injected sodium iodide all were lowest in rats fed the diet containing 1 microgram cobalt/g and increased with lower and higher concentrations of cobalt. The opposite was true for fasting serum glucose levels, which were elevated in rats fed the 1 microgram/g diet and low in rats fed the 3 microgram/g diet or control diet. This biphasic response to cobalt is consistent with the hypothesis that cobalt in low concentrations may have an essential function in the rat. However, an alternative explanation, an interaction of cobalt with a toxic constituent of the diet, has not yet been ruled out.
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PMID:A biphasic response of rats to cobalt. 88 93


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