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 5 conscious piglets with implanted electrodes in the antrum pylori, duodenum, jejunum and ileum, electromyographic activity was recorded daily on a multichannel recorder with a time constant of 0.03 s for intestinal and of 1 s for gastric recordings, and simultaneously integrated at 20 s intervals. PGE2 was infused for 2 h in relatively low doses of 0.1 and 1 microgram/kg/min, to avoid excessive hypersecretion, which would disguise direct effects. Each dose was tested once in each animal with a 1 week interval. Infusion of 0.1 microgram/kg/min revealed no significant changes in antral and small intestinal electrical activity. One microgram/kg/min however induced a strong depression of fast oscillations until the end of the infusion and prolongation of the inhibitory phase in the antrum following a duodenal phase of regular spiking activity. Intestinal segments displayed a prolongation of the quiescent phase and a decrease in the integrated area curve of the phase of irregular spiking activity. Recurrence of the phase of regular spiking activity was unaltered in either segment. These data suggest that the direct effect of PGE2 on gastrointestinal motility in the piglet is a partial inhibition of intestinal contractions.
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PMID:Influence of prostaglandin E2 infusion on gastrointestinal electrical activity in the conscious piglet. 188 9

The haemolytic activity of the total Complement (CH50) and the fractions C3 and C4 were assayed in rats transplanted with Yoshida's tumor and then treated with hCG, LH-FSH and PGE2. A relevant increase, only concerning the values of the CH50 and C3 fraction, was observed in all animals in the early days after the transplantation, probably due to a sort of stress "by transplantation". Afterwards, hCG and PGE2 induced an increase in CH50 and C3 values, but not in the C4 fraction. Treatment with LH and FSH led to a very slight increase in the CH50 and C3. In the following days, as a consequence of the cachexia, a progressive reduction of the values of the Complement was observed in all animals. Those treated with hCG also showed a little increase of survival. The authors suggest that the increase in CH50 and C3 fraction induced by the treatment with hCG and PGE2 could be an expression of increase of the aspecific humoral immunity, as a compensatory mechanism of the cell-mediated immunological depression which occurs during neoplasias.
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PMID:[Complement behavior in rats bearing Yoshida tumors subjected to treatment with gonadotropin and PGE2]. 193 Sep 5

Preliminary studies suggest that administration of fish oil fatty acids may be beneficial in several immunological diseases; therefore, we studied the effect of fish oil dietary supplementation on the expression of Ia in stimulated murine peritoneal macrophages. Rats (n = 19) and mice (n = 27) on standard rodent feeding were separated in experimental (E) and control (C) groups that received fish oil or saline solution, respectively, daily for 4 weeks by esophageal gavage. Cholesterol serum levels were significantly lowered by fish oil (E vs C, P less than 0.01). E and C groups were injected intraperitoneally with Listeria monocytogenes (LM) and peritoneal cells were harvested 4 and 7 days after infection. Decreased expression of Ia induced by LM was found in rats (C = 49.68 +/- 5.09%, E = 16.95 +/- 4.3%, P less than 0.01) and mice (C = 47.38 +/- 7.63%, E = 26.66 +/- 1.92%, P less than 0.01). Animals with a more pronounced depression of serum cholesterol (reduction of 44.04 +/- 1.52% of baseline levels) had more depression of Ia expression (6.47 +/- 1.22%, P less than 0.001 vs control). Reduction of Ia expression was not related to PGE2 production by peritoneal cells. Reduction of Ia expression by fish oil could induce down-regulation of antigen presentation and alloreactivity.
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PMID:Fish oil dietary supplementation reduces Ia expression in rat and mouse peritoneal macrophages. 211 44

The Complement is one of the major effectors of the humoral aspecific immune system building up a defence mechanism of the organism. As it is known that some hormonal substances like gonadotropin (hCG) and some hormone-like substances (PGE2) influence the entire immunitary system, we wanted to see if they had specific action on the Complement. The measurement of CH50 was carried out using Mayer's method, derived by Ferrazzi and modified by us. Fractions C3 and C4 were measured by means of immunochemistry using Beckman nephelometer. The treatment with hCG (1,000 U + 10 Lf tetanus toxoid) caused an increase in the CH50 and in the fraction C3, while the fraction C4 was not modified. The treatment with PGE2 (0.25 microgram/rat/die) caused a higher increase of CH50 and C3 fraction. It seems possible to acknowledge C3 involvement in the variation of the Complement's haemolytic activity and this could confirm the intervention of the "alternative pathway". The notable increase in the activity of the Complement induced by hCG and PGE2 could indicate an alternative mechanism of activation of the aspecific humoral immunity in the defence of the organism in all those physio-pathological situations where these substances cause a state of depression of cellular mediated activity.
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PMID:Modification of the complement induced by PGE2 and gonadotropins. 212 14

Heart fragments obtained from human right atrium contain 1.5 +/- 0.2 micrograms of histamine per gram of wet tissue. Human heart spontaneously synthesizes significant amounts of PGI2, PGF2 alpha, PGE2 and TxA2. The Ca2+ ionophore A 23187 (0.5-3 micrograms/ml) dose-dependently induces histamine release and prostanoid production. Histamine (0.5-1 micrograms/kg/min) infusion in 10 normal donors produced an increase in heart rate and a significant depression of the ST segment. Selective H1 receptor stimulation in patients undergoing cardiac catheterization resulted in a decrease of the mean aortic pressure and of coronary vascular resistance.
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PMID:Histamine and human heart. 240 15

Current theories of affective disorders do not account for many of the biological markers replicated in patient studies. We link many biological findings in a reasonable physiological relationship, compatible with mechanisms of action of pharmacological and electroshock therapies for depression. We propose that excessive phospholipase-A2 (PLA2) activity disrupts membrane fluidity, composition, and therefore, the activity, of membrane-dependent proteins. Similar disruptions in these proteins are documented in depressed patients and can be accounted for by excessive PLA2 activity. This paradigm accounts for disturbances in the activity of Na-K-ATPase, beta2- and alpha2-adrenergic receptors, MAO, norepinephrine and serotonin uptake, and imipramine binding. Disturbances in other membrane-dependent proteins, tyrosine and tryptophan hydroxylase, can explain the biogenic amine hypothesis. Inhibition of glucocorticoid receptor and TRH receptor binding to their respective ligands by PLA2 may explain patient nonsuppression in the Dexamethasone Suppression Test and poor response in the TRH stimulation test. Physiological regulators of PLA2 activity; calcium, cortisol, estrogen, progesterone, and PGE2 are documented abnormalities in some patients with affective disorders and consistent with excessive PLA2 activity. Thus, postpartum depression and premenstrual tension syndrome may be described in the paradigm. The mechanisms of action of tricyclic antidepressants, lithium, electroconvulsive shock, and some novel antimanic agents can be described in terms of alterations of PLA2 activity. Interestingly, ethanol perturbs membrane fluidity and membrane-bound enzymes in a manner similar to excessive PLA2 activity. A hereditary factor predisposing patients to affective disorders may be a gene defect at either PLA2 or in its regulation.
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PMID:Are disturbances in lipid-protein interactions by phospholipase-A2 a predisposing factor in affective illness? 256 35

The effect of the bone resorptive cytokines IL-1 alpha, IL-1 beta, and TNF on bone formation was studied in an in vitro system. All three cytokines were profoundly inhibitory, with the rank order of potency IL-1 beta greater than IL-1 alpha greater than TNF. Inhibition was mediated by a depression of differentiated osteoblast functions, including alkaline phosphatase expression and matrix synthesis. Osteoblast proliferation was not affected. Bone formation inhibition was independent of PGE2 production, indicating a direct effect of cytokines on osteoblasts. High concentrations of IL-1 beta (10 U/ml) abrogated IGF-1-stimulated bone formation, providing evidence for the hypothesis that cytokines act as 'uncoupling factors'. Conversely, high concentrations of IGF-1 circumvented inhibition by IL-1 beta (0.1-1.0 U/ml). The interaction of cytokines and bone growth factors with osteoblasts are likely to be of critical importance in the regulation of bone mass at local inflammatory sites.
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PMID:Effect of immune cytokines on bone. 265 11

The rat uterus generates and releases prostaglandins (PGs) of the series 2 as well as PGs of the series 1. The main purposes of the present study are to compare the effects of norepinephrine (NE) on the production and outputs of PGE1, PGE2 and PGF2 alpha by the uterus isolated from ovariectomized rats, treated or not with 17-beta-estradiol and to explore also, whether the effects of NE on PG synthesis are mediated through alpha, beta or both types of adrenoreceptors. Segments of control uterine horns obtained from ovariectomized rats generated and released into the incubating solution, equal amounts of PGE1, PGE2 and PGF2 alpha and propranolol (10(-6) M) or phentolamine (10(-6) M) failed to alter this basal production of PGs. Norepinephrine (3 X 10(-6) M) significantly depressed the outputs of PGE1 and PGF2 alpha but enhanced, also significantly, the release of PGE2. In the presence of the beta-adrenoreceptor blocker, propranolol, the reduction induced by NE on the output of PGE1 was not altered, but the stimulatory influence of NE on the release of PGE2 as well as the depression on the output of PGF2 alpha, were abolished. On the other hand the diminution evoked by NE on the release of PGF1 and PGF2 alpha as well as the increment induced on PGE2 output, were inhibited by the presence of phentolamine in the incubating solution. Uterine horns from ovariectomized rats treated with 17-beta-estradiol released into the incubating solution significantly more PGF2 alpha than PGE1 or PGE2. NE, either alone of in the presence of alpha 0 or beta-adrenoceptor blockers, did not modify this pattern of PG production. A possible mechanism(s) of action for NE on PG synthesis is discussed.
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PMID:Norepinephrine alters PGE2/PGE1 output ratio in isolated uterus from ovariectomized rats. 287 85

Plasma prostaglandin E1 and E2, and quantitative and qualitative measures of immune function, were determined in depressed patients and healthy controls. Prostaglandin E2 was significantly elevated in the depressed group, and prostaglandin E1 showed a trend in the same direction. Lymphocyte stimulation responses, as measured by phytohemagglutinin, concanavalin A, and pokeweed mitogen, were significantly lower in the depressed group. Helper and suppressor T cell percentages did not significantly differ in the two populations. In the depressed group, prostaglandin E1 showed a significant inverse correlation with concanavalin A, and prostaglandin E2 showed a similar trend. These preliminary data suggest prostaglandins of the E series may be related to abnormalities of cellular immunity previously documented in depression.
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PMID:Depression, immunocompetence, and prostaglandins of the E series. 293 97

The depression of interleukin-2 synthesis represents a major dysfunction within the cascade of immunologic defects induced by mechanical and thermal trauma. This study was undertaken to elucidate the negative control mechanisms that were responsible for the deficiency of IL-2 production in polytraumatized patients. Peripheral blood mononuclear cells (PBMC's) from 29 patients (average age, 35.8 years; average ISS, 35) were separated on post-trauma days 1, 3, 5, 7, 10, 14, and 21 and cultured as untreated cells (C), cells treated with indomethacin (C + INDO), and cells depleted of adherent cells (C-AC). Cell cultures were assayed for proliferative responses to PHA, IL-2 synthesis, PGE2 production, gamma-interferon levels, and phenotyping studies. On all days post-trauma there was found a marked reduction of IL-2 production compared to controls with a highly significant nadir from day 5 to day 10 with an almost 80% inhibition of IL-2 (p less than 0.005). C + INDO cells showed increases of IL-2 synthesis over untreated cells ranging from 48% (Day 1) to 220% (Day 7). Removal of adherent cells (C-AC) did not reverse the suppression of IL-2 production. gamma-interferon levels were depressed in parallel with IL-2 levels but did not increase with C + INDO. The phenotyping of the PBMC's showed highly significant suppression of OKT3+, OKT4+, and IL-2R+ lymphocytes as well as a highly significant elevation of the monocyte (p less than 0.005) count. There was a highly significant increase of PGE2 synthesis from monocytes, due to the monocytosis and to a higher capacity of synthesis of the individual cells following trauma. PGE2 levels peaked on Day 5 and 7 post-trauma at 400% of control (p less than 0.005). These data suggest that the suppression of IL-2 synthesis post trauma is caused mainly by two factors: the excessive PGE2 output of inhibitory monocytes and inadequate function in immature and/or blocked lymphocytes. The partial restoration of IL-2 synthesis by indomethacin suggests that blockade of the cyclo-oxygenase pathway as an immunomodulating therapy may reverse some of the immunologic abnormalities in multiple trauma patients.
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PMID:Prostaglandin E2 (PGE2)-dependent suppression of interleukin alpha (IL-2) production in patients with major trauma. 295 32


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