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)

Patients with active Hodgkin's disease demonstrate a significant depression of cellular immunity. The present study, performed with lymphocytes from 16 untreated patients with active Hodgkin's disease and 13 healthy control volunteers, demonstrate an equivalent IL 2 production in vitro in both groups. Our results, however, demonstrate an abnormal regulation of IL 2 production in patients. A negative control of IL 2 production involving monocytes producing PGE 2 able to induce radiosensitive suppressor T lymphocytes, has been identified previously with cells from healthy donors. In the present study we demonstrate that this negative control is hyper functioning with cells from Hodgkin's disease patients.
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PMID:[Abnormal regulation in the production of IL2 in Hodgkin's disease]. 392 5

An intravenous infusion of (PGE2) prostaglandin E was given for 8 hours on 2-3 consecutive days to 7 normally cycling women during various periods of the luteal phase, and to 1 woman whose luteal phase was prolonged by hCG administration. 3 women were infused with saline solution only. During PGE2 infusion, 2 hourly blood samples showed some variations in progesterone and estradiol levels regardless of the period of the luteal phase; no clear-cut depression was noted. These changes were similar to the spontaneous variations seen in controls. PGE2 did not induce intermenstrual bleeding or premature menstruation, although uterine contractility was markedly increased. In 1 subject, PGE2 was given during the early postovulatory period without interfering with implantation and subsequent normal pregnancy. An increase of cortisol and GH blood levels was also observed during PGE2 infusion. We conclude that PGE in the dosage used is not luteolytic in humans.
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PMID:Prostaglandin E2 and the luteal phase of the menstrual cycle: effects on blood progesterone, estradiol, cortisol, and growth hormone levels. 468 86

PGE2 (prostaglandin E2) had been successfully used in initiating labor in term pregnancies (Karim and Sharma, 1971). This study evaluates the safety and efficacy of prostaglandin for induction of labor in 23 patients (gestational length, 38-41 weeks; mean age, 27; age range, 17 to 40; parity 0 to 6). 20 received an oral PGE2 0.5 mg tablet hourly while 3 received an initial dose of 0.5 mg with 0.5 mg incremental increase hourly. 20 patients delivered vaginally liveborn infants without neonatal depression according to Apgar score and subsequent behavior in the nursery. 2 patients delivered by C-section and 1 was excluded from the study because of inadequate duration of treatment. Mean time to delivery was 5 hours, 47 minutes; mean drug dose, 2.53 mg. Mild transient emesis and diarrhea occurred in 2 patients, and emesis only in 1. Bishop induction score did not correlate with total dose of PGE2 used. Parity correlated negatively with dose necessary to achieve delivery (p0.05). The findings confirm the efficacy and safety of oral PGE, which provides an alternate drug and route for induction of labor. Oxytocin induction is briefly compared with prostaglandin induction.
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PMID:Oral prostaglandin E2 for induction of labor. 482 94

Contrary to published reports, prostaglandin E(1) (PGE(1)) in vitro and in vivo inhibited fasting lipolysis in rats. Adipose tissue lipolysis was inhibited when the tissue was incubated in the presence of PGE(1) and when the compound was administered intravenously. A biphasic plasma free fatty acid (FFA) response was obtained in fasted rats after intravenous injection of 80 micrograms of PGE(1) per kg body weight; plasma FFA concentrations were lowered at 7 min, elevated at 15 min, and at normal concentrations at 30 min. The FFA depression at 7 min was independent of the animal's nutritional state, but the rebound at 15 min did not occur in fed rats. The plasma FFA rebound in fasted rats at 15 min may be a consequence of rapid inactivation of PGE(1), followed by unopposed activity of factors which enhance fasting lipolysis.
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PMID:Effects of prostaglandin E1 on lipolysis and plasma free fatty acids in the fasted rat. 605 87

Several important vasoactive substances are taken up and/or metabolized during a single transpulmonary passage. Such substances include 5-hydroxytryptamine, prostaglandins (PGs) of the E and F series, and peptide substrates (angiotensin I and bradykinin) for angiotensin-converting enzyme (ACE). When these metabolic processes are altered, predictable changes in systemic hemodynamics can follow because of altered arterial concentrations of the vasoactive substances. For example, a single dose of captopril (2 mg/kg, i.v.) given to conscious rabbits caused prolonged depression in pulmonary ACE activity, an effect that coincided with a significant reduction in mean systemic arterial pressure. In another study, total cardiopulmonary bypass in anesthetized dogs was associated with a time-dependent increase in arterial levels of immunoreactive PGE. Coincident with this elevation in PGE was a significant decrease in total systemic vascular resistance. The decrease in resistance was inhibited by pretreatment with indomethacin or by maintaining lung perfusion during extracorporeal circulation (i.e., left heart bypass). Thus, in the intact animal, significant reduction in lung metabolism, induced by either pharmacological or other experimental means, may modify vasoregulation of peripheral circulation. Furthermore, measurement of these metabolic functions may provide biochemical information about the pulmonary microcirculation, which is both the locus of these activities and an early site of acute lung injury.
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PMID:Metabolic functions of the lung and systemic vasoregulation. 608 8

Compared to normal and other neurological disease (OND) controls, multiple sclerosis (MS) pre nylon wool (pre NW) and nylon wool passed (NWP)-peripheral blood cells' natural killer (NK) activity was more sensitive to prostaglandin E (PGE1); it was suppressed to a greater degree and at lower concentrations of PGE1. At the single cell level this was reflected by lower numbers of target-binding cells (TBCs) and fewer killers among the TBCs. ONDs and normal controls were equally sensitive to PGE1. Though PGE-producing cells were depleted in the NWP population of normal and control ONDs, MS patients still had indomethacin-sensitive NK suppressors in the NWP population; these apparently did not suppress at the single cell effector level but at the level of recycling. MS and OND cerebrospinal fluid (CSF) cells' NK activity could not be 'enhanced' by indomethacin. Depression of interferon (IFN)-induced NK by PGE1 was greater in MS than in OND or normal controls perhaps through its effect on IFN-induced recycling. All subjects' cells maintained sensitivity to PGE1 after overnight incubation in the presence of PGE-producing cells (pre NW) or exogenous PGE1. In sharp contrast to normal and OND controls, MS NWP cells were still inhibited by PGE1 even after overnight incubation in the absence of PGE1.
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PMID:Regulation of natural killer cell cytotoxicity by prostaglandin E in the peripheral blood and cerebrospinal fluid of patients with multiple sclerosis and other neurological diseases. Part 2. Effect of exogenous PGE1 on spontaneous and interferon-induced natural killer. 618 56

The immune regulation of phytohemagglutinin (PHA) and concanavalin A (Con A) mitogen responses by prostaglandin (PG)-producing suppressor monocytes was examined in 57 patients with colorectal cancer and 55 normal individuals. The blood lymphocyte responses to either PHA or Con A were significantly depressed in 74% of patients compared to normal controls. The mean PHA response for the patients was significantly lower than that for controls (17,649 versus 25,549 cpm, P = 0.02), while the mean Con A response for the patients was also depressed but not as significantly (13,551 versus 18,623 cpm, P = 0.09). The depression of immune competence was greatest in older patients and those with metastatic disease. The addition of indomethacin (1 microgram/ml) to cell cultures of both patients and normal individuals enhanced the mitogen response, suggesting that PGE-producing suppressor cells were operative in both groups. Among the patient group, however, a differential modulation of the immune response by indomethacin was observed. Thus, the addition of indomethacin restored the PHA response in patients almost to normal levels, while the Con A increase was less pronounced. Even after indomethacin treatment, the Con A proliferative response by lymphocytes was significantly depressed in patients as compared to controls (P = 0.002). To prove that indomethacin was blocking excessive PG production by suppressor monocytes in colon cancer patients, we directly measured PGE2 production by peripheral blood mononuclear cells (PBMCs) using a radioimmunoassay. PBMCs from the patients produced significantly greater amounts of PGE2 compared to controls (10.1 versus 5.1 ng/ml, P = 0.0001). This comparison was still significant after adjustment for age and sex. The increased PGE2 production appeared to be selective, since the levels of two other arachidonic acid metabolites, PGF1 alpha and thromboxane B2, were the same or less than control levels. PG-mediated immune suppression of mitogenesis thus appears to be abnormally increased in colon cancer patients, particularly for the PHA response. This abnormality was partially corrected in vitro by incubation of the PBMCs with indomethacin, a prostaglandin synthetase inhibitor.
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PMID:Prostaglandin E2-mediated suppression of cellular immunity in colon cancer patients. 622 53

Having previously established, that prostaglandins play a role in the regulation of the immune response to polyvinyl pyrollidone, a T-independent antigen, further investigations of the role of prostaglandins and cyclic nucleotides in the control of the immune response to polyvinyl pyrollidone were initiated. Strongly immunogenic (PVP 360,000) and weakly immunogenic (PVP 10,000) molecular sizes of polyvinyl pyrollidone were examined for their effects on splenic PGF2 alpha, PGE and cyclic nucleotide levels. The results show, that PVP 360,000 induces marked changes in PGF2 levels. There is an early marked depression at 2 hours after injection followed by an increase which peaks at 2 hour. At subsequent time intervals (9-10, 13-14 and 16-18 hour) high values were observed, especially in the latter case. cAMP levels undergo significant fluctuations, exhibiting very big rise at 12 and 13 hour post-immunization, cGMP levels are elevated at 2 hour declining thereafter. PGE level in C57Bl mice exhibits very substantial increase at 4-6 hour after immunization, in athymic mice, however, the increase was not significant and was preceded by a profound drop in PGE concentration. PGE level in the splenocytes from athymic mice shows a constant increase till 4 hour after PVP addition, followed by a little decrease at 6-7 hour. cAMP concentration in athymic mice exhibits a drop at 3-4 hour after immunization, followed by an increase at 5-6 hour post-immunization. Indomethacin, an inhibitor of prostaglandin synthetase, blocks the changes in PGF2 and cGMP level but has little effect on cAMP. In contrast, the weakly immunogenic form PVP 10,000 induces a large bimodal increase in cAMP levels peaking at 2 hour and again increasing between 6-8 hour; cGMP levels also rise, but more slowly. The increase in cAMP is blocked by indomethacin even though no comparable increases in PGF2 levels are observed. The changes induced by PVP 10,000 appear to be dependent on T cells since comparable changes are not observed in athymic mice. Although PVP 10,000 is non-immunogenic in normal mice or whole spleen cultures, it is immunogenic in athymic mice and purified B cell cultures. This difference has been traced to an apparent difference in the activation of T cells vs. B cells by PVP 10,000. Lastly, although inhibition of PG synthesis results in an enhancement of the immune response to PVP 360,000, no such enhancement is observed with PVP 10,000. The relevance of prostaglandin and cyclic nucleotide changes to the development of the immune response is discussed.
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PMID:The regulation of the immune response to polyvinylpyrollidone: antigen induced changes in prostaglandin and cyclic nucleotide levels. 625 89

Neuro-effector transmission in the smooth muscle layer of the dog trachea was studied in vitro using the micro-electrode and double sucrose gap methods.1. Electrical field stimulations with short duration (50-100 musec) applied to the whole tissue produced an excitation of the intrinsic nerves, and evoked excitatory junction potentials (e.j.p.s) followed by twitch tension development and subsequent long lasting relaxation of the smooth muscle tissue.2. The effects of field stimulations were abolished by tetrodotoxin (2 x 10(-7)m), and atropine (1.7 x 10(-5)m) selectively blocked both the e.j.p. and twitch tension. On the other hand, propranolol (1.9 x 10(-5)m) suppressed the generation of the prolonged relaxation evoked by the field stimulations.3. E.j.p.s recorded by the double sucrose gap method showed gradual and continuous reduction in amplitude during prolonged exposure in Krebs solution (1-2 hr), and there were no changes in the membrane potential or in the input membrane resistance.4. With application of indomethacin (10(-5)m), a gradual and continuous reduction in the amplitude of e.j.p. was no longer observed, and (after the initial increase in the amplitude) e.j.p.s with a constant amplitude were obtained during 1-1.5 hr. Indomethacin (10(-5)m) modified neither the resting membrane potential nor the input membrane resistance of smooth muscle cells.5. After pre-treatment with indomethacin, low concentrations (10(-11)-10(-8)m) of prostaglandin E(1) or E(2) (PGE series) markedly suppressed the amplitude of e.j.p. with no changes in the resting membrane potential or in the input membrane resistance.6. During the repetitive field stimulation at the stimulus frequency of 0.1-1 Hz, the amplitude of the e.j.p.s was gradually reduced (the depression process). The depression was not affected by applications of prostaglandins, indomethacin or alpha- and beta-adrenoceptor blockers.7. These results indicate that in the dog tracheal smooth muscles, the endogenous PGE series may play an important role in feed-back inhibitory mechanisms, at the nerve terminals related to acetylcholine release.
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PMID:Actions of indomethacin and prostaglandins on neuro-effector transmission in the dog trachea. 627 74

Methoxamine enhanced contractions of mouse vasa deferentia through alpha adrenoceptor stimulation. Additionally, the generation of PGF-like material by the tissue was increased by methoxamine, whereas that of PGE-like material was decreased. The effects of methoxamine on prostaglandin output (stimulation and depression) were antagonized by yohimbine and phenoxybenzamine. Moreover, the stimulating influence of methoxamine on the contractile activity of the preparations was attenuated by the prostaglandin synthesis inhibitors indomethacin and acetylsalicylic acid. The results suggest that methoxamine is able to modify prostaglandin synthesis and output in mouse vasa deferentia, probably through an alpha adrenergic mediated mechanism coupled to the prostaglandin synthesizing system. The fact that indomethacin and acetylsalicylic acid blocked alpha stimulatory responses to methoxamine, suggest a modulatory role for endogenous prostaglandins. Since methoxamine increased PGF levels, this prostaglandin might potentiate the contractile influence of methoxamine.
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PMID:Alpha adrenergic stimulation modified prostaglandins release in vas deferens. 632 37


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