Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to isolate and characterize genes whose expression may be altered in breast malignancy, we screened a cDNA library with a polyclonal anti-serum against breast-cancer-metastasis membranes and isolated several immunopositive clones. One of these, AJ1, was analyzed in detail and found to be expressed at varying levels as a 3.3-kb mRNA in all of 143 breast cancers. High expression was associated with lymph-node involvement (p = 0.03). Comparison between high- and low-expressing groups showed a significant difference at 4 and 6 years for both overall (p = 0.004 and p = 0.002 respectively) and disease-free (p = 0.0001 and p = 0.04 respectively) survival, but not at 11 years. AJ1 was expressed at much lower levels in non-malignant biopsies as compared with malignant tissue (p = 0.001). Expression was observed in breast-cancer cell lines MCF-7, ZR-75-1, T47D, MDA-MB-231 and HBL 100. Partial sequence analysis of the 620 bp clone showed complete homology with human heat-shock protein 89 alpha. In addition to being heat-inducible in all the breast cell lines examined, AJ1 levels were increased by estradiol (blocked by cyclohexamide and tamoxifen), EGF, oxytocin and vasopressin in a time-dependent manner in MCF-7 cells and by estradiol, EGF, prolactin and hydrocortisone in T47D cells. In MDA-MB-231 cells, EGF caused down-regulation of AJ1 mRNA levels. The increasing evidence for the association of heat-shock proteins with steroid receptors suggests that AJ1 may play an important role in the control of estrogen-receptor transcriptional activity in breast cancers.
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PMID:Clinical and biological significance of HSP89 alpha in human breast cancer. 173 10

The hormonal changes in maternal serum during parturition induced by amniotomy and oxytocin (OXY) infusion or oral prostaglandin E2 (PGE2) medication have been compared in 68 patients (33 women in the PGE2 group, 35 in the oxytocin group). The effect of PGE2 differed from that of oxytocin. Thus the prostaglandin elicited increases in total estriol (p < 0.001) and decreases in prolactin (p < 0.01), TSH (p < 0.05) and HPL (p < 0.05) from the basal level to that immediately before parturition. Maternal serum cortisol levels rose to the same extent in both treatment groups (p < 0.001). The significant (p < 0.05) increase occurred earlier among women receiving PGE2 (two hours into therapy), even though labor pain was experienced later in this group. The serum estriol elevation in these patients was significant three hours after start of therapy (p < 0.05). A similar time course was noted for the decrease of serum prolactin in PGE2 treated patients. The drop in maternal serum levels of HPL and TSH in the PGE2 group was significant only immediately prior to partus. Neither PGE2 nor oxytocin induced changes in maternal serum levels of HCG or alpha-fetoprotein or estradiol. Oxytocin but not PGE2 lead to a decrease in maternal serum progesterone concentrations; this was significant (p < 0.05--p < 0.01) only late in labor. Mixed umbilical serum levels of the hormones mentioned above were the same regardless of method of induction. Hence the increased maternal estriol concentrations during PGE2 treatment were not reflected in fetal blood. It is suggested that increases in maternal estriol levels during PGE2 medication are due to effects on the maternal enterohepatic circulation rather than on the fetoplacental unit. Irrespective of maternal treatment umbilical serum from female newborns contained statistically higher (p < 0.05) levels of estradiol and HCG than serum from male children.
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PMID:Changes in serum hormone levels during labor induced by oral PGE2 or oxytocin infusion. 616 Jul 19

A case of pre-eclampsia is described where suspicion of placental insufficiency arose due to low estriol levels and a positive oxytocin challenge test (OCT). The cause, however, of these findings was later proven to be strictly fetal. It is concluded that low estriol levels and a positive OCT may be caused by a decreased placental capacity but specific tests of placental function, as for instance estimations of HPL in plasma and/or a DHAS-test, should be used to verify or rule out a suspicion of placental insufficiency.
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PMID:Incorrect diagnosis of placental insufficiency in a patient with pre-eclampsia. 644 32

The purpose of this study was to evaluate, in vivo and in vitro, the influence of ritodrine and oxytocin on the placental release of human chorionic gonadotrophin (HCG) and placental lactogen (HPL). The in-vivo study was performed on maternal sera collected before and 1 h after the onset of either ritodrine treatment (50 micrograms i.v./min; administered to 15 women at risk of premature labour) or oxytocin infusion (2 mU i.v./min; administered to 21 women for acceleration of slow labour). The in-vitro study was performed on human term placental explants incubated in the presence of 4-400 ng ritodrine/ml or 15-1500 microU oxytocin/ml. HCG and HPL were measured by radioimmunoassay on maternal sera and incubation media. Maternal circulating concentrations of HCG and HPL remained unaffected after 1 h of ritodrine or oxytocin treatment. The in-vitro release of HCG and HPL by placental explants was not modified when ritodrine or oxytocin was added to the incubation media. The lack of influence of ritodrine and oxytocin on the placental secretion of HCG and HPL suggests that beta 2-adrenergic and oxytocin receptors are not involved in the releasing process.
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PMID:In-vivo and in-vitro assessment of the influence of ritodrine and oxytocin on the placental secretion of human chorionic gonadotrophin and placental lactogen. 867 Dec 88