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 antidepressive efficacy of TRH was investigated in 15 endogenous depressive patients in a double-blind cross-over design. The Hamilton depression scale, the AMP (PAS) system, v. Zerssen scale and thermometer scales were used. No therapeutic effect could be demonstrated. The blunted TSH-response to TRH, which has been described by other investigators, was confirmed. There was suggestive evidence of a psychoendocrinological relationship in the sense that the more severe the "somatic depressive" syndrome as calculated from the AMP system, and the more marked the diurnal variation of the endogenous type is, the lower are the basal TSH-values and the smaller the response to TRH. Thus, TRH may become a useful tool to identify subgroups of depressive patient populations.
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PMID:Psychoendocrinological and therapeutic effects of TRH in depression. 40 1

Cholera toxin may depress cell-mediated immunity by stimulation of adenyl cyclase and production of cyclic AMP in cellular systems or when given parenterally to experimental animals. Whether or not similar effects might be found during clinical infection with Vibrio cholerae was the subject of this study. Delayed hypersensitivity reactions to skin test antigens were found to be markedly depressed in Bengali patients with cholera 24 h after fluid repletion. Skin test response rates were lower in children and in adults with the disease than in both normal adults and children or in adults with an equivalent degree of malnutrition. Patients with equal degrees of dehydration due to noncholera diarrhea were significantly less immunosuppressed. Concurrent depression of other manifestations of cell-mediated immunity was not found.
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PMID:Depression of cell-mediated immunity in cholera. 42 32

Adenosine and AMP (5'-adenosine monophosphate) applied by microiontophoresis produced depression of neuronal firing rates in cerebral cortex. A number of antidepressant drugs including examples which are known not to affect noradrenaline uptake systems, potentiated the depressant purine effects. Noradrenaline responses were unaffected or reduced. Purines may therefore be important in the mechanism of action of antidepressant drugs.
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PMID:Antidepressant drugs potentiate suppression by adenosine of neuronal firing in rat cerebral cortex. 43 90

Interactions between some substances (theophylline, noradrenaline, imidazole, ouabain and verapamil) and adenosine or adenosine triphosphate (ATP) were examined by recording the twitch tension of partially magnesium blocked phrenic-rat diaphragm preparations stimulated indirectly. Theophylline (an inhibitor of phosphodieterases) prevented and reversed the neuromuscular depression induced either by adenosine or ATP, and these substances antagonized the neuromuscular facilitation caused by imidazole (an activator of phosphodiesterases); noradrenaline and ouabain did not modify and verapamil increased that depression. These results indicate that the putative purine presynaptic receptor is not the ATPase, that it does not appear to operate by implication of cyclic AMP, but that it could mediate a process involved in the reduction of transmitter release by regulating the entry of calcium that follows the depolorization of the motor nerve endings.
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PMID:Purine effects at the neuromuscular junction and their modification by theophylline, imidazole and verapamil. 47 9

The clinical profile and side-effects of perphenazin-enanthate and fluspirilene were compared in 45 female chronic schizophrenic patients. 100 mg perphenazin-enanthate fortnightly or 8 mg fluspirilene weekly were administered. During the four months' period the psychopathological and somatic symptoms were evaluated by means of the AMP-system and the self-evaluation scale PD-S (v. Zerssen). A covariance analysis was carried out covering 12 AMP syndromes and 6 PD-S factors. The antipsychotic effect of both drugs was similar concerning the paranoid, the hallucinatory-desintegrative and the catatonic syndromes. A significant difference with regard to perphenazin-enanthate was found in the AMP-syndromes of hostility, hypochondria, and autonomic symptoms. Neither drug induced any depression. In the self-rating scale, the factors anxiousness and depressivity were also significantly lower in the perphenazin-enanthate regime. The patients under perphenazin-enanthate required a smaller amount of antiparkinsonian drugs. The more pronounced sedative effect of perphenazin-enanthate can be recommended in hostile and restless schizophrenic patients, whereas fluspirilene should be given to inactive autistic patients.
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PMID:[A comparative study of the longacting neuroleptics perphenazin-enanthate and fluspirilene (author's transl)]. 50 42

80 inpatients were interviewed twice by the same physician with an interval of 24 h. By forming subgroups concerning diagnosis and duration of hospitalization, it was possible to examine the influence of these two criteria on the retest reliability of the following findings: (1) aspects of the interview; (2) AMP symptoms; (3) AMP syndromes; (4) clinical syndrome diagnoses, and (5) nosological diagnoses. The duration of hospitalization (up to 40 days) had no influence on the retest reliability of the described findings. The diagnosis (schizophrenia/depression) had no influence on the well-structured findings (AMP symptoms, AMP syndromes). On the contrary, the diagnosis influenced findings which are not so well structured and defined (aspects of the interview, clinical syndrome diagnoses, nosological diagnoses).
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PMID:[Influence of diagnosis and length of hospitalization on the retest reliability for findings of the first psychopathological test (AMP system)]. 52 Dec 45

We have devised an improved high pressure liquid chromatographic technique whereby serotonin, nucleosides, cyclic nucleotides, namely cAMP and cGMP, and 5'mono-, 5'di-, and 5'tri-nucleotides can be analyzed. The cyclic nucleotides have been measured in picomolar quantities. All nucleotides can be quantitated in a single step separation in 75 min using a 0.0015 M phosphoric acids vs. 1M pH 4.8 ammonium phosphate gradient. 5/10 ml of platelet-rich plasma furnishes an adequate sample for complete analysis. Nucleotide levels in platelets from 16 normal donors expressed in 10(11) platelets are as follows: cAMP, 6.32 (4.15) nanomoles and AMP, 0.32 (0.14); ADP, 2.48 (0.67); ATP 3.78 (0.68); GDP 0.38 (0.07) and GTP, 0.45 (0.07) micromoles. ADP and ATP values are lower than those previously published. However, the total nucleotide level approaches published values. Upon aggregation with thrombin, approximately 50% of ADP and 40% ATP is releaseed. Release is complete by 2 min. Thrombin is the most potent releasing agent with collagen and ADP occupying an intermediate role and epinephrine being the least effective. Upon aggregation cyclic AMP levels diminish along the other nucleotides. Patients with asthma showed depression of ADP, ATP, GDP and GTP levels.
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PMID:Measurement of nucleotide pools in platelets using high pressure liquid chromatography. 57

Glycogen-stimulated rabbit peritoneal exudate cells (polymorphonuclear leukocytes, PMN) produce prostaglandins (PG) and substances which induce alterations (mediators) in experimental animals characteristic of host metabolic responses to infection and other acute inflammatory stresses. The effect of Zn2+ on mediator production and PG synthesis was examined because: Zn homeostasis is perturbed during infection, Zn is known to regulate some cellular functions, and there appears to be an interrelationship between PG synthesis and mediator production. Using exudate cells, 2 mM Zn2+ caused complete inhibition of in vitro PG synthesis as assessed by conversion of [1-14C] arachidonic acid into PG. This concentration of Zn2+ also inhibited production of substances mediating plasma Zn depression, hepatic amino acid "uptake", fever, and neutrophil release from bone marrow. Conversely, Zn2+ did not inhibit in vivo metabolic responses to these mediators. Zn-pretreatment of rabbits or simultaneous injection of Zn2+ and crude PMN-derived pyrogenic activity resulted in prolongation of fever. It is suggested that this action of Zn2+ may be attributed to either stabilization of cyclic AMP through inhibition of phosphodiesterase or a Zn-mediator interaction which stabilizes crude endogenous pyrogen. The potential physiological significance of these results includes: possible potentiation of the host's defense mechanisms by Zn2+ and its utilization for prolongation of fever to determine its effect on potentially temperature-dependent host defense mechanisms.
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PMID:In vitro and in vivo actions of zinc ion affecting cellular substances which influence host metabolic responses to inflammation. 64 Nov 11

Among 83 hospitalized adult psychiatric patients, 22% reported being high caffeine consumers (750 mg or more per day); these patients scored significantly greater on the State-Trait Anxiety Index and the Beck Depression Scale than moderate and low consumers. High consumers described significantly more clinical symptoms, felt that their physical health was not as good, and reported greater use of sedative-hypnotics and minor tranquilizers. Since caffeine modifies catecholamine levels, inhibits phosphodiesterase breakdown of cyclic AMP, and sensitizes receptor sites, association of caffeinism with both anxiety and depressive symptoms is possible.
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PMID:Anxiety and depression associated with caffeinism among psychiatric inpatients. 66 43

Veratridine, ouabain, glutamate and high concentrations of K+, agents which cause depolarization of excitable cells, markedly elevate levels of adenosine 3':5'-monophosphate (cyclic AMP) and guanosine 3':5'-monophosphate (cyclic GMP) in brain tissue, in vitro. Phenytoin inhibits veratridine (5 micron)- and ouabain (100 micron)-induced accumulations of both cyclic nucleotides in slices of mouse cerebral cortex. As little as 10 to 30 micron phenytoin produces a statistically significant depression, and 100 to 400 micron inhibits more than 90%. In contrast, at concentrations up to 400 micron, the drug has little or no effect on elevations of cyclic AMP or cyclic GMP caused by glutamate (10 mM) or K+ (64 mM). The inhibitory action of phenytoin on ouabain-induced elevations of cyclic nucleotides appears to be noncompetitive; inhibition of the veratridine effects probably is also noncompetitive. Tetrodotoxin also inhibits ouabain- and veratridine-induced elevations of cyclic nucleotides in brain slices, but it is 3 orders of magnitude more potent than phenytoin. Like phenytoin, tetrodotoxin does not inhibit the effects of glutamate or K+ on cyclic nucleotide regulation. These data suggest that, similar to tetrodotoxin phenytoin blocks sodium channels in excitable membranes. Possibly this mechanism is responsible for the antiepileptic action of phenytoin.
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PMID:Similar effects of phenytoin and tetrodotoxin on cyclic nucleotid regulation in depolarized brain tissue. 73 31


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