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)

In our clinical trial we have compared the effect of high doses of prednisone, ACTH alone or ACTH and cyclophosphamide on plasma and CSF albumin and IgG levels. We have found that the treatment with high doses of prednisone is more effective in the suppression of CNS IgG synthesis than ACTH, or cyclophosphamide. However the significance of this immunological phenomenon in the pathogenesis of MS is a very complex problem, since we have not observed any correlation between the depression of the intrathecal IgG synthesis and clinical results of MS treatment.
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PMID:Therapeutic trials of multiple sclerosis and intrathecal IgG production. 301

The role of anticonvulsants, particularly carbamazepine, in the treatment of manic-depressive illness has been the subject of multiple recent studies. Overall, carbamazepine has achieved a 55% to 65% clinical response in mania. The drug has a time course and efficacy rate similar to those of neuroleptics and lithium. Studies have not uncovered a relationship between clinical response and carbamazepine levels in plasma or the CSF, but a relationship was found in one study between the drug's principal metabolite and clinical response. Patients who are severely depressed, manic, anxious, or dysphoric before treatment appear to be good responders to carbamazepine. In one trial, 40% of the manic patients taking carbamazepine experienced a marked response. In depression a moderate or better response to carbamazepine was attained by 50% of patients in one study. Some evidence indicates that carbamazepine can potentiate the efficacy of other medications, including lithium.
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PMID:The use of anticonvulsants in manic-depressive illness. 305 72

Pretreatment plasma ratios of tryptophan (Trp) and tyrosine (Tyr) to other large neutral amino acids were determined in 27 depressed patients who completed a double-blind trial of citalopram, a selective serotonin uptake inhibitor, against maprotiline, a selective noradrenaline uptake inhibitor. The Trp ratio and the Tyr ratio were decreased in the total patient sample as compared with healthy controls. Plasma Tyr ratio was normal in the endogenous, but significantly decreased in the non-endogenous depressives. There was no significant relationship between the plasma Trp ratio and the probenecid-induced accumulation of 5-HIAA in the CSF, or between the plasma Tyr ratio and HVA level in CSF, whereas the CSF level of MHPG correlated significantly with the plasma Tyr ratio. There was a significantly positive correlation between the Trp ratio, the Tyr ratio, their sum and the final Hamilton depression score in 14 patients treated with citalopram; on the whole, this association was evident also in the endogenous and non-endogenous subgroups. In 13 patients on maprotiline there was a significantly positive correlation between the plasma Tyr ratio and the percent reduction of Hamilton depression score; this association was poor in the endogenous, whereas a trend towards a correlation remained in the non-endogenous subgroup. The results suggest that the plasma Trp and Tyr ratios may be determinants of clinical improvement in depressed patients to treatment with citalopram and maprotiline. However, further studies are needed on larger patient samples to allow a firm conclusion.
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PMID:Plasma tryptophan and tyrosine ratios to competing amino acids in relation to antidepressant response to citalopram and maprotiline. A preliminary study. 308 Jul 81

A new experimental model was employed to investigate alterations of cerebral metabolic activity in rats subjected to extensive subarachnoid hemorrhage (SAH). The hemorrhages were produced in anesthetized animals by inserting 0.37 ml fresh autologous arterial blood into the subarachnoid space. Rats that underwent sham operations received subarachnoid injections of mock CSF to study the effects of sudden raised intracranial pressure (ICP). Forty-eight hours after subarachnoid injection, the unanesthetized rats were given intravenous injections of [14C]2-deoxyglucose. Experiments were terminated 45 min later by decapitation, and the brains were removed and frozen. Regional brain metabolic activity was studied employing quantitative autoradiography. In comparison with control animals, cerebral metabolic activity was diffusely decreased following SAH. Statistically significant decreases in metabolic activity of less than 34% were observed in 17 of 30 brain regions studied. The largest percentage reductions were in regions displaying the highest basal metabolic rates. Subarachnoid injections of mock CSF also produced depression of cerebral metabolic activity, but quantitatively these changes were not as pronounced as in the hemorrhage group. These studies demonstrate regional changes in brain function following SAH. The data relate these changes to both the presence of blood in the subarachnoid space and sudden raised ICP.
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PMID:Regional cerebral metabolic activity in the rat following experimental subarachnoid hemorrhage. 310 55

The concentration of thyrotropin-releasing hormone (TRH), a tripeptide (pyroglutamylhistidylprolin-amide), in the CSF of drug-free patients with DSM-III major depression, somatization disorder, and peripheral neurological disorders was measured with a sensitive and specific radioimmunoassay. The depressed patients had markedly higher CSF TRH concentrations than the other patient groups, and this finding could not be attributed to any demographic variables. The elevation of TRH in CSF provides further evidence of hypothalamic-pituitary-thyroid dysfunction in depression.
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PMID:Elevation of immunoreactive CSF TRH in depressed patients. 314 69

The onset of therapeutic effectiveness of carbamazepine is generally very rapid in the treatment of seizure and paroxysmal pain disorders, shows some lag in the treatment of mania, and exhibits the longest lag in depression. These time course variations may indicate that different mechanisms underlie the efficacy of carbamazepine in the differential neuropsychiatric syndromes. Biochemical and pharmacological data suggest that the anticonvulsant effects of carbamazepine are related to "peripheral-type" benzodiazepine and alpha 2-noradrenergic receptor systems and to its ability to stabilize sodium channels. GABAB (baclofen-like) actions appear to be involved in antinociceptive, but not anticonvulsant, effects. The relatively acute time course of antimanic efficacy may be related to the above-mentioned mechanisms or to other effects related to systems postulated to be altered in the manic syndrome. These effects might include carbamazepine's ability to increase acetylcholine in the striatum, decrease probenecid-induced levels of CSF homovanillic acid (HVA) in man and dopamine turnover in animals, decrease CSF norepinephrine in manic patients, inhibit adenylate cyclase activity (in response to norepinephrine, dopamine, adenosine, or ouabain), decrease GABA turnover, or act as a vasopressin agonist. Efficacy in depression may be related to actions in man that take time or chronic drug administration to develop, such as increases in plasma tryptophan, decreases in CSF somatostatin, decreases in thyroid indices, and increases in urinary free cortisol excretion and, in animals, increases in substance P sensitivity and increases in brain adenosine receptors. The ability of carbamazepine to block the development of lidocaine- and cocaine-induced seizures also requires chronic administration, suggesting that these seizure models may provide a unique perspective for understanding mechanisms of time-dependent effects.
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PMID:Time course of clinical effects of carbamazepine: implications for mechanisms of action. 328 May 60

In order to investigate the role of serotonergic mechanisms in depressive disorders, the fenfluramine challenge test was performed in 31 patients suffering from different types of depression. The strategy was to select a simple method (i.e., easier to perform than CSF studies for instance) to be applied to a wide range of patients, as close as possible to everyday cases in a clinical setting (i.e., not only to such severe or highly selected groups as is normally the case in biological research in psychiatry). The neuroendocrine test (which consisted of the measurement of variations in the secretion of prolactin, growth hormone and Cortisol after the administration of 60 mg dl-fenfluramine p. o.) did not correlate with symptoms of behavior patterns previously identified with a "serotonin deficit" (i. e., suicidal behavior or attempts, lowering of the control of impulses, sleep disturbances) but only with the severity of the diagnosis (in the DSM-III hierarchical scale) or with indexes of endogeneity (Newcastle scale). This fact could be explained by methodological artifacts (i. e., dlfenfluramine is not a clean probe, showing influence in the dopamine and noradrenaline metabolism; the absorption of fenfluramine was not controlled) or by the fact that the involvement of serotonin in affective disorders is not a selective, isolated dysfunction, but is integrated in more complex interrelationships. Nevertheless, our preliminary findings (even without the results of the comparison with a control group and the evaluation of a few more data and cases) do coincide with the absence of predictors or the lack of specific patterns of response of symptoms with new selective re-uptake blockers of serotonin antidepressants.
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PMID:The fenfluramine challenge test in the affective spectrum: a possible marker of endogeneity and severity. 328 85

In anesthetized spinal cats, perfusion of lumbosacral spinal cord with artificial CSF containing manganese (1.5-3.0 Mm/l) or cobalt (6.0 mM/l) ions, led to reversible suppression of negative dorsal root potentials (DRP), induced by stimulation of ipsilateral hindlimbs' afferent nerves. The depression of the DRP proceeded in connection with the depression of presynaptic inhibition of extensor monosynaptic reflexes induced with impulse volleys in the group I flexor muscle afferents. The depression of inhibition was not associated with changes in amplitudes of testing monosynaptic reflexes. The DRP is concluded to have a synaptic origin.
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PMID:[Suppression of the dorsal root potentials of the cat spinal cord by manganese and cobalt ions]. 341 29

Eleven baboons, anaesthetised with ketamine, had catheters introduced into the cisterna magna. Morphine was injected at lumbar level intrathecally in six and epidurally in five. Cisternal CSF was sampled hourly and the morphine concentration measured using a high pressure liquid chromatograph. In two cases following intrathecal injection peaks of 180 ng/ml at 4 hours, and 2,200 ng/ml at 3 hours were detected. In the latter case there was associated error in sampling therefore this baboon had a repeat injection four weeks later. The maximum level of morphine obtained then was 139 ng/ml at 4 hours. In the epidural group peaks of 113 ng/ml and 53 ng/ml at 1 hour were measured in 2 baboons and 27 ng/ml at 6 hours in a third. In all six other baboons following either procedure no morphine was detected in the cisterna. We conclude that morphine injected either intrathecally or epidurally in primates does migrate centrally in varying quantities. This finding would seem to have some bearing on the unpredictability of reported episodes of respiratory depression following intraspinal morphine.
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PMID:Cisternal cerebrospinal fluid concentrations of morphine following intrathecal and epidural administration in the baboon. 342 84

Pharmacokinetic studies of five biological response modifiers (BRMs) show diverse regulator functions on effector cell responses and a capacity to cause the secretion of specific soluble factors. Of the five BRMs tested, MVE-2, Poly ICLC, OK-432, and alpha beta IFN were capable of stimulating both natural killer (NK) cell and macrophage (M phi) tumoricidal activity, whereas BM 41-332 augmented only NK cells. Following one treatment with the aforementioned BRMs, M phi activity remained elevated for a longer period (10-14 days) than did NK cell activity (6-9 days). Of particular interest, multiple treatment with BRMs led to a downregulation of NK cell activity (hyporesponsiveness). Three soluble secretory products were induced by these BRMs (colony stimulating factor, CSF; prostaglandin E, PGE; and interferon, IFN). Treatment with MVE-2 and Poly ICLC led to a significant increase in bone marrow cellularity and GM-CFV-C. Results of studies with the cyclo-oxygense-inhibited indomethacin indicate that CSF and PGE are produced and/or secreted by different cellular mechanisms. The depression of effector cells (NK, bone marrow, and GM-CFU-C), as the result of cyto-reductive treatment with cyclophosphamide, could be reversed by treatment with MVE-2. A significantly earlier time to recovery of these effector cells was achieved following MVE-treatment. When MVE-2 was used as an adjuvant to initial tumor cyto-reductive chemotherapy, more successful antitumor response was achieved, indicating that MVE-2 functioned to elevate a substantial effector cell response as well as reconstituting bone marrow cellularity.
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PMID:Biological response modifiers: regulators of the cellular immune system and adjuvants in antitumor therapy. 348 34


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