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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

Mol Endocrinol. 2002 Nov;16(11):2582-91.
An activated human follicle-stimulating hormone (FSH) receptor stimulates FSH-like activity in gonadotropin-deficient transgenic mice.

Haywood M, Tymchenko N, Spaliviero J, Koch A, Jimenez M, Gromoll J, Simoni M, Nordhoff V, Handelsman DJ, Allan CM.

Andrology Laboratory, ANZAC Research Institute, Sydney, New South Wales 2139, Australia.

FSH mediates its testicular actions via a specific Sertoli cell G protein-coupled receptor. We created a novel transgenic model to investigate a mutant human FSH receptor (FSHR(+)) containing a single amino acid substitution (Asp567Gly) equivalent to activating mutations in related glycoprotein hormone receptors. To examine the ligand-independent gonadal actions of FSHR(+), the rat androgen-binding protein gene promoter was used to direct FSHR(+) transgene expression to Sertoli cells of gonadotropin-deficient hypogonadal (hpg) mice. Both normal and hpg mouse testes expressed FSHR(+) mRNA. Testis weights of transgenic FSHR(+) hpg mice were increased approximately 2-fold relative to hpg controls (P < 0.02) and contained mature Sertoli cells and postmeiotic germ cells absent in controls, revealing FSHR(+)-initiated autonomous FSH-like testicular activity. Isolated transgenic Sertoli cells had significantly higher basal ( approximately 2-fold) and FSH-stimulated ( approximately 50%) cAMP levels compared with controls, demonstrating constitutive signaling and cell-surface expression of FSHR(+), respectively. Transgenic FSHR(+) also elevated testosterone production in hpg testes, in the absence of circulating LH (or FSH), and it was not expressed functionally on steroidogenic cells, suggesting a paracrine effect mediated by Sertoli cells. The FSHR(+) response was additive with a maximal testosterone dose on hpg testicular development, demonstrating FSHR(+) activity independent of androgen-specific actions. The FSHR(+) response was male specific as ovarian expression of FSHR(+) had no effect on hpg ovary size. These findings reveal transgenic FSHR(+) stimulated a constitutive FSH-like Sertoli cell response in gonadotropin-deficient testes, and pathways that induced LH-independent testicular steroidogenesis. This novel transgenic paradigm provides a unique approach to investigate the in vivo actions of mutated activating gonadotropin receptors.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12403847&dopt=Abstract

Mol Endocrinol. 2002 Nov;16(11):2592-602.
Differential regulation of gonadotropin-releasing hormone secretion and gene expression by androgen: membrane versus nuclear receptor activation.

Shakil T, Hoque AN, Husain M, Belsham DD.

Department of Physiology, University of Toronto, Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada M5S 1A8.

Steroid hormones induce rapid membrane receptor-mediated effects that appear to be separate from long-term genomic events. The membrane receptor-mediated effects of androgens on GT1-7 GnRH-secreting neurons were examined. We observed androgen binding activity with a cell-impermeable BSA-conjugated testosterone [testosterone 3-(O-carboxymethyl)oxime (T-3-BSA)] and were able to detect a 110-kDa protein recognized by the androgen receptor (AR) monoclonal MA1-150 antibody in the plasma membrane fraction of the GT1-7 cells by Western analysis. Further, a transfected green fluorescent protein-tagged AR translocates and colocalizes to the plasma membrane of the GT1-7 neuron. Treatment with 10 nM 5alpha-dihydrotestosterone (DHT) inhibits forskolin-stimulated accumulation of cAMP, through a pertussis toxin-sensitive G protein, but has no effect on basal cAMP levels. The inhibition of forskolin-stimulated cAMP accumulation by DHT was blocked by hydroxyflutamide, a specific inhibitor of the nuclear AR. DHT, testosterone (T), and T-3-BSA, all caused significant elevations in intracellular calcium concentrations ([Ca(2+)](i)). T-3-BSA stimulates GnRH secretion 2-fold in the GT1-7 neuron, as did DHT or T. Interestingly GnRH mRNA levels were down-regulated by DHT and T as has been reported, but not by treatment with T-3-BSA or testosterone 17beta-hemisuccinate BSA. These studies indicate that androgen can differentially regulate GnRH secretion and gene expression through specific membrane-mediated or nuclear mechanisms.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12403848&dopt=Abstract

Mol Endocrinol. 2002 Nov;16(11):2628-44.
A new selective peroxisome proliferator-activated receptor gamma antagonist with antiobesity and antidiabetic activity.

Rieusset J, Touri F, Michalik L, Escher P, Desvergne B, Niesor E, Wahli W.

Institut de biologie animale, Universite de Lausanne, CH-1015 Lausanne, Switzerland.

Peroxisome proliferator-activated receptor gamma (PPAR-gamma) plays a key role in adipocyte differentiation and insulin sensitivity. Its synthetic ligands, the thiazolidinediones (TZD), are used as insulin sensitizers in the treatment of type 2 diabetes. These compounds induce both adipocyte differentiation in cell culture models and promote weight gain in rodents and humans. Here, we report on the identification of a new synthetic PPARgamma antagonist, the phosphonophosphate SR-202, which inhibits both TZD-stimulated recruitment of the coactivator steroid receptor coactivator-1 and TZD-induced transcriptional activity of the receptor. In cell culture, SR-202 efficiently antagonizes hormone- and TZD-induced adipocyte differentiation. In vivo, decreasing PPARgamma activity, either by treatment with SR-202 or by invalidation of one allele of the PPARgamma gene, leads to a reduction of both high fat diet-induced adipocyte hypertrophy and insulin resistance. These effects are accompanied by a smaller size of the adipocytes and a reduction of TNFalpha and leptin secretion. Treatment with SR-202 also dramatically improves insulin sensitivity in the diabetic ob/ob mice. Thus, although we cannot exclude that its actions involve additional signaling mechanisms, SR-202 represents a new selective PPARgamma antagonist that is effective both in vitro and in vivo. Because it yields both antiobesity and antidiabetic effects, SR-202 may be a lead for new compounds to be used in the treatment of obesity and type 2 diabetes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12403851&dopt=Abstract

Clin Endocrinol (Oxf). 1998 Nov;49(5):577-81.
A new chemiluminescent assay for the rapid detection of thyroid stimulating antibodies in Graves' disease.

Watson PF, Ajjan RA, Phipps J, Metcalfe R, Weetman AP.

Division of Clinical Sciences Centre, University of Sheffield, Northern General Hospital, UK. p.f.watsoheffield.ac.uk

OBJECTIVE: Thyroid stimulating antibodies (TSAb) are the cause of Graves' disease (GD). At present, these antibodies can only be measured using bioassays, which are generally time consuming and difficult to apply to whole serum. Here we describe a new chemiluminescent assay for the detection of TSAb in serum samples. METHODS: A Chinese hamster ovary (CHO) cell line, stably transformed with a reporter plasmid containing the firefly luciferase gene under the transcriptional control of multiple cAMP responsive elements (CRE), was transfected with the human thyroid stimulating hormone (TSH) receptor. A clonal cell line, (NA-4), was obtained which showed a dose-dependent increase in luciferase activity in response to bovine and human TSH stimulation. NA-4 was subsequently used to study TSAb activity in 42 GD sera. RESULTS: Of the GD sera 25 (60%) produced an increase in luciferase activity of 1.4-9 fold that obtained with control sera. Results were compared with an established bioassay for TSAb, based on the direct measurement of intracellular cAMP, and there was a significant correlation between the two assays (r = 0.8; P < 0.0001). IgG from GD patients, but not controls, also increased luciferase activity in NA-4 cells using concentrations as low as 3 mg/l in selected samples. CONCLUSION: The present report describes a simple, sensitive and rapid assay for the detection of TSAb, with application both in the clinical analysis of GD patient sera and as a potential research tool for use in the isolation of TSAb monoclonal antibodies.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10197071&dopt=Abstract

Anasthesiol Intensivmed Notfallmed Schmerzther. 2002 Nov;37(11):651-8.
[Phylogeny and evolution of hormone systems]

[Article in German]

Feix M, Hoch M.

Institut fur Zoophysiologie der Universitat Bonn, Entwicklungsbiologie, Germany. mfeini-bonn.de

Classically hormones are defined as molecules that are secreted by endocrine glandular or neurosecretory cells into the blood stream and transported to their target tissue where they induce physiological processes at very low concentrations. Studies on the potential origin and the evolution of cell-to-cell communication systems suggest that exocrine pheromones (food signals and toxins) might have been the primitive bioregulatory molecules of unicellular organisms for chemical communication with each other and with the biosphere. The broad distribution and the structural diversity of pheromones suggests that these molecules and their receptors were predecessor modules of cell communication systems in metazoa. Neurosecretory cells, as we find them in Cnidarians, possibly served as basic modules for the evolution of neurohormonal systems of higher animals. Studies on genetic model organisms, such as Drosophila or the mouse, have demonstrated that chemical communication between neighbouring or more distant cells does not just involve endocrine and neurosecretory cells, but also unexpectedly tissues and organs such as the heart or the adipose tissue (e. g. the leptin signalling pathway). Comparative endocrinology could show that molecular components of hormonal systems represent signalling networks that are generally used during cellular communication processes and the differentiation of cell types during ontogenesis. Some of their functions are evolutionarily conserved, others not, as disscussion on steroid hormones and the prolactin signalling pathway will demonstrate.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12404141&dopt=Abstract

Loss of hair changes the appearance of a person, and the identity of the person in social context to a certain extent. Hair growth is a complex biological process, which has not yet been completely understood. A multitude of therapeutic measures, including drugs, surgery, and suppelements have been made available, and used. However, due to the diversity of the problems underlying hair loss, there is no single solution for all hair loss cases. Most of chemical drugs and hair transplantation surgeries are not free from varying degrees of undesirable side effects on health.

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