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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Breast Cancer Res Treat. 1998;52(1-3):227-37. ["Cited in Books","window.top.location='/entrez/query.fcgi?tool=pmcited&cmd=search&db=books&term=10066085[pmid]'","",""],
Time-dependence of hazard ratios for prognostic factors in primary breast cancer.

Hilsenbeck SG, Ravdin PM, de Moor CA, Chamness GC, Osborne CK, Clark GM.

Department of Medicine, University of Texas Health Science Center at San Antonio, 78284-7884, USA. suncology.uthscsa.edu

Some prognostic factors, such as steroid receptors, appear strongly related to outcome in early studies with short follow-up, but as follow-up matures the relationships appear to weaken. We investigated this phenomenon for several factors (tumor size, axillary lymph nodes, S-phase fraction, estrogen receptor (ER) status, and adjuvant therapy) in a large sample of breast cancer cases (N=2,873) with up to 17 years of follow-up for disease-free survival (DFS). Subjects in the study were identified from patients who had hormone receptor assays performed in our laboratory. Analysis of DFS included fitting a multivariate Cox proportional hazards model, testing for nonproportionality, and examining diagnostic plots. The assumption of proportional hazards was violated for several factors including ER, tumor size, and S-phase fraction. For ER, the hazard ratio was initially less than 1.0, indicating a good effect on prognosis, but increased at later times to values greater than 1.0, indicating a bad effect on prognosis. In contrast, the hazard ratios for tumor size and S-phase were initially high and decreased asymptotically toward 1.0 over time. Analysis of p53 expression in a subset of cases yielded qualitatively similar results. We conclude that several standard prognostic factors (ER, tumor size, S-phase fraction) and possibly other investigational factors have important but nonproportional effects on hazard. It is likely that violation of proportional hazards is common and not limited to breast cancer. Failure to recognize violations of proportional hazards can lead to both over- and under-estimation of the effects of important prognostic factors.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10066085&dopt=Abstract

Twin Res. 1998 Sep;1(3):154-5.
Genetic risk factors in tumours of the testis: lessons from twin studies.

Lambalk CB, Boomsma DI.

Research Institute for Endocrinology, Reproduction and Metabolism, Department of Obstetrics/Gynaecology, Academic Hospital, Free University, Amsterdam, The Netherlands. cb.lambalzvu.nl

A threefold increase for testicular carcinoma has been reported in male dizygotic twins. In this comment we suggest the hypothesis that over-exposure to endogenously hypersecreted Follicle Stimulating Hormone (FSH) may underlie the pathogenesis. This is supported by several findings. 1) FSH hypersecretion in mothers of dizygotic twins is most likely an autosomal trait implicating the possibility of male offspring with the same hormone characteristic. 2) In testicular carcinoma higher levels of cyclin D2 are found. This is an FSH dependent stimulatory regulator of mitosis. 3) There is a marked similarity between geographical distribution in occurence of dizygotic twinning and testicular carcinoma. 4) Men undergoing surgery for testicular carcinoma have higher FSH concentrations and males with Down syndrome have higher FSH levels and are more at risk to develop testicular carcinoma. We suggest to study FSH secretion in males of familial dizygotic twins and furthermore the risk of developing testicular carcinoma in males with elevated FSH. These men with one testicle and/or with dysfunctioning Sertoli/Leydig cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10051341&dopt=Abstract

Endocrinology. 1999 Mar;140(3):1111-7.
Thyroid hormones act primarily within the brain to promote the seasonal inhibition of luteinizing hormone secretion in the ewe.

Viguie C, Battaglia DF, Krasa HB, Thrun LA, Karsch FJ.

Reproductive Sciences Program, University of Michigan, Ann Arbor 48109-0404, USA.

In the ewe, thyroid hormones are required for the seasonal suppression of GnRH and LH secretion, thereby maintaining an annual rhythm in reproductive activity. The primary site of action of thyroid hormones is unknown; in particular, there is no evidence to distinguish a central from a peripheral action. In this study, we test the hypothesis that thyroid hormones can act directly within the brain to promote GnRH/LH seasonal inhibition. Ovariectomized estradiol-treated ewes were thyroidectomized late in the breeding season to prevent seasonal LH inhibition. T4 was then infused for 3 months, either peripherally or centrally. Neuroendocrine reproductive state was monitored by assaying the LH concentration in biweekly blood samples. Central infusion of low dose T4, which restored a physiological concentration of the hormone in cerebrospinal fluid of these thyroidectomized ewes, promoted the neuroendocrine changes that lead to anestrus. The serum LH concentration in these animals fell at the same time as the seasonal LH decline in euthyroid controls. Neither this same T4 dose infused peripherally nor vehicle infused centrally was effective; LH remained elevated, signifying blockade of the mechanism for anestrus. Our results provide strong evidence that thyroid hormones can act directly within the brain to promote seasonal inhibition of neuroendocrine reproductive function in the ewe.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10067833&dopt=Abstract

J Am Coll Nutr. 2003 Feb;22(1):43-51.
Plasma selenium and plasma and erythrocyte glutathione peroxidase activity increase with estrogen during the menstrual cycle.

Ha EJ, Smith AM.

Department of Human Nutrition, The Ohio State University, Columbus, Ohio 43210, USA.

OBJECTIVE: This study was designed to determine the timing and magnitude of changes in selenium status in relation to the fluctuation of 17-beta-estradiol during the menstrual cycle and the effect of different phases of the menstrual cycle on dietary selenium intake. METHODS: Plasma 17-beta-estradiol and plasma and erythrocyte selenium and glutathione peroxidase (GPx) activity were measured in fasting blood samples collected in the morning at four times over three phases of the menstrual cycle: early follicular (EF: days 1-3 menstruation), periovulatory (PO; E-1: 1 day before estrogen peak and E: during estrogen peak) and mid-luteal (ML: 7-9 days after ovulation) in healthy women (n = 14) aged 21 to 39 years and with regular menstrual cycles (26 to 30 days). The estrogen peak was confirmed by measurement of the luteinizing hormone surge. Dietary records (three-day) coincided with blood collection for each phase. RESULTS: Plasma selenium and plasma and erythrocyte GPx activity were greatest during the periovulatory phase, coinciding with the estrogen peak. No differences were observed for erythrocyte selenium or dietary selenium throughout the cycle. A linear relationship existed between estradiol and plasma selenium (p < 0.0027), plasma GPx activity (p < 0.0001), and erythrocyte GPx activity (p < 0.0001). CONCLUSIONS: These results indicate that blood selenium parameters fluctuate during the menstrual cycle such that the phase of the cycle should be considered when assessing selenium status.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12569113&dopt=Abstract

J Soc Gynecol Investig. 1999 Jan-Feb;6(1):27-31.
The effects of sex steroids on human umbilical artery and vein.

Fausett MB, Belfort MA, Nanda R, Saade GR, Vedernikov Y.

Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, USA.

OBJECTIVE: To define the vascular actions of selected sex steroids on human umbilical artery and vein and to determine whether there are any gender-specific differences in vasorelaxation between umbilical cord vessels of male and female fetuses. METHODS: Segments of umbilical artery (n = 12) and umbilical vein (n = 8) from male and female fetuses were suspended in organ baths of Krebs solution for isometric tension recording. The vessels were contracted using 60 mM potassium chloride followed by exposure to increasing concentrations (10(-7) to 10(-4) M) of sex steroid hormones (estradiol-17 beta, estriol, estrone, testosterone, and progesterone). A specific estrogen receptor antagonist (ICI 164, 384) was used to attempt to block the estradiol effect. Changes in tension were recorded. RESULTS: Of the agents tested, estradiol-17 beta had the greatest effect (25-29% relaxation at 10(-4) M concentration), which was uninhibited by a specific receptor antagonist. The other steroids tested had no significant effect, even at 10(-4) M concentration. The umbilical artery is slightly more sensitive to the effects of estradiol than the umbilical vein. There were no gender-specific differences noted in either artery or vein harvested from male or female fetuses. CONCLUSION: Estradiol-17 beta in supraphysiologic concentrations has a non-receptor-mediated vasorelaxation effect on human umbilical blood vessels.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10065423&dopt=Abstract

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