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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

Int J Biol Markers. 2002 Jul-Sep;17(3):196-200.
Natural history of estrogen receptor-negative, progesterone receptor-positive breast cancer.

Nikolic-Vukosavljevic D, Kanjer K, Neskovic-Konstantinovic Z, Vukotic D.

Department of Experimental Oncology, Institute for Oncology and Radiology of Serbia, Belgrade, Yugoslavia. tunfosky.net

The biological significance of estrogen receptor-negative but progesterone receptor-positive breast carcinomas is not clear. In the present study the aggressiveness of breast carcinomas in relation to ER and PgR status has been investigated. The probability of disease-free survival in 297 node-negative breast carcinoma patients was monitored during a follow-up ranging from six to 96 months (median 45 months). Steroid hormone receptor content was assayed with the biochemical method recommended by the EORTC. The probability of disease-free survival was significantly worse for patients with ER-negative, PgR-positive carcinomas compared to the other three steroid hormone receptor phenotypes. Our results suggest that ER-negative, PgR-positive breast carcinomas are biologically different in terms of aggressiveness from the other steroid hormone receptor phenotypes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12408471&dopt=Abstract

Scand J Gastroenterol. 2002 Oct;37(10):1149-55.
Gastrectomy has no effect on bone regeneration in rats despite a decrease in bone mass.

Zellin G, Hakanson R, Linde A.

Dept. of Oral Biochemistry, Goteborg University, Sweden.

BACKGROUND: Gastrectomy, specifically the removal of the acid-producing part of the stomach (fundectomy), is known to cause osteopenia. This effect has been ascribed to the elimination of a hypothetical osteotropic peptide hormone, presumably produced in the oxyntic mucosa. Since osteopenia is due to a disturbed balance between bone formation and resorption, we assessed the effect of gastrectomy on osteogenesis, more specifically mandibular orthotopic bone regeneration. METHODS: Adult rats were either gastrectomized or sham-operated. Two weeks later, unilateral 5-mm transosseous defects were made in the mandibles and covered with microporous barrier membranes (GORE-TEX Membrane). After 6 weeks of healing. bone-bridging of the defects was analyzed by computerized light microscopic image analysis. Furthermore, bone mass was analyzed in the contralateral untreated mandibular side, in calvarial bone, and in femora by morphometry and dry/ash weights. RESULTS: While gastrectomy resulted in a clearly decreased bone mass, manifested as increased marrow spaces in all bones and as decreased dry and ash weights in femora, no difference in mandibular bone healing rate was found between the groups. CONCLUSIONS: Since secluding of the defect space by membrane barriers implies that osteogenic cells have to be recruited primarily from intra-osseous stem cells by their proliferation and differentiation into actively bone-forming osteoblasts, the results indicate that gastrectomy has no effect on these processes. The findings thus imply that the disturbed balance in bone remodeling caused by gastrectomy, resulting in osteopenia, may be due to stimulated bone resorption rather than to reduced bone formation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12408519&dopt=Abstract

Mar Environ Res. 2002 Sep-Dec;54(3-5):275-8.
Effect of cortisol and urea on flavin monooxygenase activity and expression in rainbow trout, Oncorhynchus mykiss.

El-Alfy A, Larsen B, Schlenk D.

Department of Environmental Sciences, University of California, Riverside 92521, USA.

Expression of flavin-containing monooxygenase(s) (FMO) correlates with salinity exposure in certain species of euryhaline fish, such as the rainbow trout, Oncorhynchus mykiss. The mechanism(s) by which salinity regulates FMO is unclear. Adult rainbow trout were infused through the dorsal aorta with either cortisol or urea. At 500 ng/ml, cortisol caused a significant increase in FMO-catalyzed thiourea oxidase activity in gill and liver microsomes. FMOI expression, however, was significantly increased by the high cortisol dose only in gill microsomes. The levels of TMAO and urea were not altered by cortisol. In the liver, urea infusion caused an increase in hepatic FMO activity. FMO expression and activity correlated with elevated tissue urea levels, but TMAO concentrations were not related. These results indicate that FMO expression and activity may be partially controlled by the osmoregulatory/stress hormone. cortisol, and concentrations of the organic osmolyte, urea, in the rainbow trout.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12408576&dopt=Abstract

Mol Endocrinol. 1999 Apr;13(4):566-77.
Homologous regulation of the gonadotropin-releasing hormone receptor gene is partially mediated by protein kinase C activation of an activator protein-1 element.

White BR, Duval DL, Mulvaney JM, Roberson MS, Clay CM.

Department of Physiology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins 80523, USA.

Homologous regulation of GnRH receptor (GnRHR) gene expression is an established mechanism for controlling the sensitivity of gonadotropes to GnRH. We have found that expression of the GnRHR gene in the gonadotrope-derived alpha T3-1 cell line is mediated by a tripartite enhancer that includes a consensus activator protein-1 (AP-1) element, a binding site for SF-1 (steroidogenic factor-1), and an element we have termed GRAS (GnRHR-activating sequence). Further, in transgenic mice, approximately 1900 b.p. of the murine GnRHR gene promoter are sufficient for tissue-specific expression and GnRH responsiveness. The present studies were designed to further delineate the molecular mechanisms underlying GnRH regulation of GnRHR gene expression. Vectors containing 600 bp of the murine GnRHR gene promoter linked to luciferase (LUC) were transiently transfected into alpha T3-1 cells and exposed to treatments for 4 or 6 h. A GnRH-induced, dose-dependent increase in LUC expression of the -600 promoter was observed with maximal induction of LUC noted at 100 nM GnRH. We next tested the ability of GnRH to stimulate expression of vectors containing mutations in each of the components of the tripartite enhancer. GnRH responsiveness was lost in vectors containing mutations in AP-1. Gel mobility shift data revealed binding of fos/jun family members to the AP-1 element of the murine GnRHR promoter. Treatment with GnRH or phorbol-12-myristate-13-acetate (PMA) (100 nM), but not forskolin (10 microM), increased LUC expression, which was blocked by the protein kinase C (PKC) inhibitor, GF109203X (100 nM), and PKC down-regulation (10 nM PMA for 20 h). In addition, a specific MEK1/MEK2 inhibitor, PD98059 (60 microM), reduced the GnRH and PMA responses whereas the L-type voltage-gated calcium channel agonist, +/- BayK 8644 (5 microM), and antagonist, nimodipine (250 nM), had no effect on GnRH responsiveness. Furthermore, treatment of alpha T3-1 cells with 100 nM GnRH stimulated phosphorylation of both p42 and p44 forms of extracellular signal-regulated kinase (ERK), which was completely blocked with 60 microM PD98059. We suggest that GnRH regulation of the GnRHR gene is partially mediated by an ERK-dependent activation of a canonical AP-1 site located in the proximal promoter of the GnRHR gene.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10194763&dopt=Abstract

Mar Environ Res. 2002 Sep-Dec;54(3-5):685-9.
Residues of 14C-4n-nonylphenol in mosquitofish (Gambusia holbrooki) oocytes and embryos during dietary exposure of mature females to this xenohormone.

Thibaut R, Monod G, Cravedi JP.

UMR 1089 Xenobiotiques, INRA/ENSAT/ENVT, Toulouse, France.

In order to assess in fish the maternal transfer of alkylphenolic compounds to the progeny, the identification and quantification of the labelled compounds present in oocytes and embryos was conducted after dietary exposure of mature female mosquitofish to 14C-4n-nonylphenol during vitellogenesis and embryogenesis respectively. Radioactivity found in bile and liver extracts accounted for 0.9-0.6 and 0.2-0.1% of ingested radioactivity for females exposed during vitellogenesis and embryogenesis respectively. The amount of extractable radioactivity present in oocytes and embryos was 0.19 and 0.07% of the ingested dose respectively. The radio-HPLC profiles obtained from bile, liver, oocyte and embryo extracts were similar. They showed the presence of 4n-NP-glucuronide as the major metabolite and traces of unchanged 4n-NP. The other metabolites corresponded to 8-hydroxynonylphenol, 9-(4-hydroxyphenyl)-nonanoic acid and para-hydroxybenzoic acid which is the final product of the alkyl chain oxidation. Our results indicate that exposure of ovoviviparous female fish to 4-NP during vitellogenesis and embryogenesis leads to the contamination of the progeny by 4-NP and its metabolites.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12408636&dopt=Abstract

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