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 s.c. administration of 20 mg/kg of morphine-HCl produced a decrease in the spontaneous locomotor activity (SLMA) of rats. The decrease in SLMA was significantly antagonized by p-chlorophenylalanine (p-CPA). When rats pretreated with p-CPA were given 5-hydroxytryptophan before morphine injection, the marked sedative response to morphine was restored, suggesting that the morphine-induced decrease in SLMA of rats may depend on the release of 5-hydroxytryptamine by morphine. By contrast, the s.c. administration of 5 mg/kg of morphine-HCl produced a significant increase in SLMA of rats. The magnitude of the increase was reduced by atropine, scopolamine or alpha-methyl-p-tyrosine. It appears that both adrenergic and cholinergic mechanisms participate in the increase in SLMA of rats induced by morphine. Both the increase in SLMA produced by 5 mg/kg of morphine and the decrease in SLMA induced by 20 mg/kg of morphine were completely antagonized by the s.c. administration of naloxone-HCl, 0.0625 and 0.25 mg/kg, respectively. Thus, it appears that the receptor with which morphine interacts to produce stimulation is chemically identical with or very similar to the receptor with which morphine combines to induce depression. The former receptors, however, are likely to be located on different neurons from the latter.
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PMID:Effects of humoral modulators and naloxone on morphine-induced changes in the spontaneous locomotor activity of the rat. 0 52

Cyclophosphamide was used to assess the role of suppressor cells in the contact sensitivity reaction. A single painting with 300 microgram and 30 microgram oxazolone produced poor contact sensitivity reactions (ear swelling). Cyclophosphamide (200 mg/kg) 2 days before painting increased the response to the lower doses but had less effect on the response to 3 mg oxazolone. A single feed with 10 mg oxazolone caused strong contact sensitivity while lower doses (10-1000 microgram) caused poor responses. Cyclophosphamide increased the response to the lower doses but not to the highest dose of oxazolone. These results suggested that the poor response to painting and feeding lower doses of oxazolone was due to a suppressor system which was sensitive to cyclophosphamide. A different result was obtained when contact sensitivity was measured by arrival of radioactively labelled cells. Cyclophosphamide had the greatest effect on cell arrival when high doses were fed. This indicates that ear swelling and cell arrival measure separate aspects of the contact sensitivity response. The lower doses of oxazolone, which caused little contact sensitivity, reduced the response to a standard immunizing dose. This low dose unresponsiveness occurred after either painting or feeding (Chase-Sulzberger phenomenon). It did not occur in mice treated with cyclophosphamide before the first exposure to oxazolone. This suggested that the low dose unresponsiveness was due to suppressor cells. The response to oxazolone was also assessed by DNA synthesis in the regional lymph nodes. A small dose of oxazolone (30 microgram) caused a peak of DNA synthesis on day four while a high dose (3 mg) caused a peak on day three. Pretreatment with cyclophosphamide depressed the response to 30 microgram although it increased contact sensitivity. The secondary response was smaller than the primary on days 3, 4 and 5 after immunization but larger on day two. The depression but not the increase was prevented by cyclophosphamide and was probably due to a suppressor system.
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PMID:Contact sensitivity and the DNA response in mice to high and low doses of oxazolone: low dose unresponsiveness following painting and feeding and its prevention by pretreatment with cyclophosphamide. 31 60

The ocular inflammation and antibody production that follow intravitreal injection of rabbit eyes with bovine gamma globulin were suppressed by treatment with Cytoxan by the intramuscular (i.m.) route. The drug suppressed PFC responses of uveal tract and corneal cells when it was administered, beginning as late as 5 days after immunization, if treatment was continued until day 12 or 13. Short-term treatments and treatment with smaller Cytoxan doses were less effective. We noted a good correlation between the presence or absence of ocular inflammation, suppression of ocular PFC responses and depression of serum, aqueous humour and vitreous humour antibody titres. In some treatment groups ocular antibody production seemed to be completely suppressed, while in others antibody production was significantly delayed.
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PMID:The effect of cyclophosphamide on an ocular immune response. I. Primary response. 34 57

BM U2 531, the 2-[2-Cyanaziridinyl-(1)-]-2-[-2-carbamoylaziridinyl-(1)-]-propane, the further development of BM 06 002 is able to compensate the immunosuppressive action of Cyclophosphamide and to increase the carcinostatic action of Cyclophosphamide. These properties are demonstrated 1. by a leucocytosis induced after application of BM 12 531 in rats 2. by a quick restauration of leucocyte depression induced by Cyclophosphamide in rats and dogs 3. by an increase of resistance against an infection (candida albicans) in mice 4. by an increase of antitumour effect of Cyclophosphamide against a DS-carcinosarcoma in rats.
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PMID:Animal experiments on the compensation of the immunosuppressive action of cyclophosphamide by 2-[-2-cyanaziridinyl-(1)-]-2-[-2-carbamoylaziridinyl-(1)]-propane BM 12 531. 34 64

Immunological reactivity was studied in 76 breast cancer patients taking into consideration the extent of disease and mode of treatment. The following tests were used: delayed hypersensitivity skin reaction after application of tissue antigens from mammary cancer and embryonal tissues prepared by Westphal's method (Silber's modification), tuberculin and 2,4-dinitrochlorbenzene (DCNB). Humoral immune reactivity was evaluated with a mikroprecipitation test using antigens from fetal, tumorous and spleen cells. Tests were performed before and after treatment. The results confirm that positive skin reactions are found mostly in stage I and II. In advanced stages depression of all immune reactions was seen. Some changes of immune reactivity depend on the mode of treatment. Immune competence was not depressed by surgical treatment and the most distinct immune depression was provoked by cytostatic chemotherapy. Our observations suggest that the cytostatics Thiophosphamid, Cyclophosphamid and Fluorouracil are immundepressants.
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PMID:[Immune reactions in breast cancer patients (author's transl)]. 41 86

Changes in the immunoglobulin and complement levels in untreated plasmacytoma were compared with those resulting from massive doses of Cyclophosphamide (15--25 mg per kg b. w. at intervals of 10--14 days) applied in combination with double plasmapheresis (involving removal of about 500 ml of plasma). A follow-up of the levels of normal immunoglobulins, paraprotein, total complement and the C3 component revealed a significant decline in the total complement following each single application of this treatment, but the decrease in C3 was nonsignificant. A decline of about 20% in immunoglobulins and of about 15% in paraprotein was observed in relation to the pretreatment values, but only that in the IgM class proved to be of statistical significance. The decrease in proteins was also established with the methods of total protein determination (refractometric or biuret methods) and was found to amount to 1000--3000 mg% after each dose of Cyclophosphamide with plasmapheresis. In the author's view, a combined Cyclophosphamide-plasmapheresis treatment is effective for achieving clinical remission. It should, however, be kept in mind that the effect of protein and paraprotein depression persists for only a few days, hence, to achieve long-term results, this treatment should be repeated in 2--3 week's cycles. The lowered values of humoral immunity indicators do not increase the danger of complications from a clinical aspect, when suitable preventive measures are taken.
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PMID:Follow-up of certain immunologic indicators in the treatment of plasmacytoma with cyclophosphamide in combination with plasmapheresis. 80 59

Female rats were treated with several administration regimens of methylprednisolone, cobra venom anti-complementary factor, and cyclophosphamide in conjunction with polyvinyl sponge implantations. The effect of these drugs on host factors active against bacteria was evaluated with Staphylococcus aureus ATCC 25933, Escherichia coli K-12, and Pseudomonas aeruginosa CDC 7725. One of two implants in each animal was infected with 10(8) of one of the three bacteria, and bacterial and granulocyte content was determined in the infected and control sponges after 48 h. The single large dose of methylprednisolone decreased staphylococcal and E. coli clearance while promoting dissemination of P. aeruginosa. A low chronic dose of the steroid inhibited E. coli chemotaxis only. A higher dose of the steroid administered chronically interfered markedly with S. aureus and E. coli curtailment by the host while leading to enhanced dissemination of P. aeruginosa, accompanied by a precipitous decline in granulocytes. Results with cobra factor resembled the higher chronic dose of steroid enhancing, especially the dissemination of the pseudomonad and its anti-granulocytic propensity. Cyclophosphamide depression of granulocytes revealed the rat's ability to curtail the proliferation of particular S. aureus and E.coli strains even in the absence of leukocytes. This treatment resulted in the rapid spread of P. aeruginosa, leading to the death of some experimental animals. These experiments underline the versatility of this animal model in the study of host and microbial factors influential in infectious disease.
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PMID:Rat polyvinyl sponge model for the study of infections: host factors and microbial proliferation. 82 14

Since maternal-fetal immunogenetic disparity facilitates growth of the fetoplacental unit, nonspecific depression of the maternal immune system by immunosuppressive drugs could result in previously unrecognized adverse effects such as fetal growth retardation. To test this hypothesis, groups of 6 to 8 primigravid Fischer female rats mated with DA or Fischer male rats were treated with saline (controls) or either cyclophosphamide (Cytoxan) or azathioprine (Imuran) in doses similar to those used therapeutically in human subjects. It was found that these drugs caused an increased incidence of fetal death and produced fetal and neonatal growth retardation. Smaller placentas and fetuses reflected a decrease in cell number rather than cell size whereas water, fat, and protein content were only minimally affected. Analyses of mean maternal weight gain, spleen weight assays, and changes in the lymph nodes draining the uterus indicate that effects detrimental to the offspring are primarily the result of immunologic and cytotoxic mechanisms. Moreover, a review of the literature suggests that these immunosuppressive agents are also associated with small-for-gestational age infants in human pregnancies.
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PMID:Fetal growth retardation associated with maternal administration of immunosuppressive drugs. 87 25

The pharmacological effects of repeated administration of 2 mg Kg-1 cytosine arabinoside, 40 mg Kg-1 cyclophosphamide or their combination, all given once weekly for 5 weeks, have been investigated in chicks. Cyclophosphamide did not affect responses to noradrenergic nerve stimulation or phenylephrine, depressed responses of the expansor secundariorum muscle to acetylcholine but sensitised the muscle to direct stimulation. Cytosine arabinoside depressed noradrenergic transmission and enhanced responses of the expansor muscle to phenylephrine and acetylcholine. The combination of both drugs enhanced responses to noradrenergic nerve stimulation due to increased alpha-adrenergic receptor mediated contraction and direct muscle sensitisation. Cyclophosphamide, cytosine arabinoside or their combination produced a non-specific depression of the upper oesophagus and ileum. The exception was the marked increase in response of the ileum from the combination group to agonist drugs, indicating synergism. The non-specific skeletal muscle depressant actions of cyclophosphamide and the combination groups were more pronounced than that of the cytosine arabinoside group.
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PMID:A comparison of the effects of repeated administration of cyclophosphamide, cytosine arabinoside or their combination on smooth and skeletal muscle. 193 22

We have investigated the effects of interleukin 1 (IL-1) administration on the ability of neutropenic mice to resist Pseudomonas aeruginosa challenge in vivo. Cyclophosphamide-treated mice received human rIL-1 beta at 7.0, 0.7, or 00.7 micrograms/kg, according to different regimens, to be challenged with a lethal ip inoculum of pseudomonas cells 5 days after myelosuppression. The repeated exposure of the neutropenic mice to an overall cytokine dosage of 7.0 or 0.7 micrograms/kg during the 4 days after myelosuppression was found to optimally restore the animals' antibacterial resistance. However, when administered as a single injection 24 hr before challenge, the same dosages of IL-1 had lower or no effect in enhancing survival, primarily leading only to a reduction in the amount of antipseudomonal chemotherapy required for cure. The regimen of IL-1 administration conferring optimal protection also resulted in a decrease in the number of pseudomonas cells recovered from the peritoneal cavity of infected mice. This regimen accelerated hematopoietic recovery in cyclophosphamide-treated mice. Assay of serum colony-stimulating activity (CSA) revealed that (a) cyclophosphamide treatment alone significantly increased the level of circulating CSA, (b) administration of a single dose of IL-1 to neutropenic mice induced an early, further increase in serum CSA, followed by depression, (c) a biphasic pattern of CSA response was also evident in mice repeatedly treated with IL-1. These results suggest that regulation of hematopoiesis may have an important role in the induction of antibacterial resistance in myelosuppressed hosts repeatedly treated with low dosages of IL-1.
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PMID:Antibacterial resistance induced by recombinant interleukin 1 in myelosuppressed mice: effect of treatment schedule and correlation with colony-stimulating activity in the bloodstream. 211 38


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