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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





BMC Genomics. 2002 Aug 21;3(1):25.
In silico and in situ characterization of the zebrafish (Danio rerio) gnrh3 (sGnRH) gene.

Torgersen J, Nourizadeh-Lillabadi R, Husebye H, Alestrom P.

Department of Biochemistry, Physiology and Nutrition, Norwegian School of Veterinary Science, PO Box 8146 Dep, N-0033 Oslo, Norway. jacob.torgerseeths.no

BACKGROUND: Gonadotropin releasing hormone (GnRH) is responsible for stimulation of gonadotropic hormone (GtH) in the hypothalamus-pituitary-gonadal axis (HPG). The regulatory mechanisms responsible for brain specificity make the promoter attractive for in silico analysis and reporter gene studies in zebrafish (Danio rerio). RESULTS: We have characterized a zebrafish [Trp7, Leu8] or salmon (s) GnRH variant, gnrh3. The gene includes a 1.6 Kb upstream regulatory region and displays the conserved structure of 4 exons and 3 introns, as seen in other species. An in silico defined enhancer at -976 in the zebrafish promoter, containing adjacent binding sites for Oct-1, CREB and Sp1, was predicted in 2 mammalian and 5 teleost GnRH promoters. Reporter gene studies confirmed the importance of this enhancer for cell specific expression in zebrafish. Interestingly the promoter of human GnRH-I, known as mammalian GnRH (mGnRH), was shown capable of driving cell specific reporter gene expression in transgenic zebrafish. CONCLUSIONS: The characterized zebrafish Gnrh3 decapeptide exhibits complete homology to the Atlantic salmon (Salmo salar) GnRH-III variant. In silico analysis of mammalian and teleost GnRH promoters revealed a conserved enhancer possessing binding sites for Oct-1, CREB and Sp1. Transgenic and transient reporter gene expression in zebrafish larvae, confirmed the importance of the in silico defined zebrafish enhancer at -976. The capability of the human GnRH-I promoter of directing cell specific reporter gene expression in zebrafish supports orthology between GnRH-I and GnRH-III.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12188930&dopt=Abstract [PubMed]



Redox Rep. 2002;7(3):145-51.
Catecholamine effects on cardiac remodelling, oxidative stress and fibrosis in experimental heart failure.

Bonnefont-Rousselot D, Mahmoudi A, Mougenot N, Varoquaux O, Le Nahour G, Fouret P, Lechat P.

Laboratoire de Biochimie B, Coeur et Vaisseaux, Groupe Hospitalier Pitie-Salpetriere (AP-HP), 47 boulevard de l'Hopital, 75651 Paris Cedex 13, France. dominique.rousselosl.ap-hop-paris.fr

The aim of the study was to assess the relationships between oxidative stress, cardiac remodelling and fibrosis on an experimental model of heart failure with adrenergic stimulation. Large myocardial infarction (approximately 50% of the left ventricle myocardium) was obtained by ligation of the left coronary artery of normotensive male Wistar rats. Sham animals were submitted to left thoracotomy without coronary ligation. In order to perform cardiac stimulation by catecholamines, mini-osmotic pumps were implanted in animals 10 weeks after surgery to deliver noradrenalin for a 2-week period. At the end of this period, the following investigations were performed: haemodynamics, morphometry, fibrosis quantification, plasma and tissue catecholamine assay and oxidative stress status. Coronary ligation induced dilatation of left ventricle with compensatory hypertrophy of the right ventricle and of the remaining left ventricle myocardium. This remodelling process was associated in non-infarcted myocardium with increased collagen infiltration and increased oxidative stress. Ten weeks after surgery, the chronic administration of noradrenalin for 2 weeks did not increase oxidative stress. Noradrenalin, however, induced inotropic stimulation and myocardial hypertrophy, but to a lesser extent in infarcted rats compared to sham rats. Our results suggest that noradrenalin infusion to levels in excess of those seen post-infarction is associated with fibrosis and oxidative stress. Moreover, noradrenalin in infarcted animals caused additional fibrosis without further increasing oxidative stress. The mechanism of catecholamine-induced fibrosis may thus involve different processes such as ischaemia, increased mechanical stress, cytokines and neurohormones.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12189044&dopt=Abstract



J Natl Cancer Inst. 2002 Aug 21;94(16):1226-37.
The effects of adrenomedullin overexpression in breast tumor cells.

Martinez A, Vos M, Guedez L, Kaur G, Chen Z, Garayoa M, Pio R, Moody T, Stetler-Stevenson WG, Kleinman HK, Cuttitta F.

Cell and Cancer Biology Branch and Vascular Biology Faculty, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA. martineail.nih.gov

BACKGROUND: Adrenomedullin is a secreted peptide hormone with multiple activities. Several reports have indicated that adrenomedullin may be involved in tumor survival, but this has not been directly shown. Here we evaluate the in vitro and in vivo effects of adrenomedullin overexpression in human breast cancer cells. METHODS: The human breast cancer cell lines T47D and MCF7, both of which express low basal levels of adrenomedullin, were stably transfected with an expression construct that contained the coding region of the human adrenomedullin gene or with empty expression vector. Properties of the transfected cells were assessed by proliferation and apoptosis assays, in vitro and in vivo angiogenesis assays, cell migration experiments, and xenograft implants. The effect of synthetic adrenomedullin on human ovarian (ECV) cancer cell motility was also tested. Western blot analysis was used to compare expression levels of several genes whose products are associated with cell growth and regulation of apoptosis. RESULTS: T47D and MCF7 cells transfected with the adrenomedullin construct both expressed high levels of adrenomedullin mRNA and protein. Compared with cells transfected with empty vector, cells that overexpressed adrenomedullin displayed a more pleiotropic morphology, an increased angiogenic potential both in vitro and in vivo, and less apoptosis after serum deprivation. T47D and MCF7 cells did not display measurable motility, but ECV ovarian cancer cells treated with synthetic adrenomedullin were more motile than saline-treated ECV cells. Adrenomedullin-overexpressing T47D cells had higher levels of proteins involved in oncogenic signal transduction pathways (such as Ras, Raf, PKC, and MAPKp49) and lower levels of pro-apoptotic proteins (such as Bax, Bid, and caspase 8) than T47D cells transfected with empty vector. In a preliminary in vivo experiment, three of 10 nude mice injected with adrenomedullin-overexpressing T47D cells developed xenograft tumors, whereas none of the 10 nude mice injected with cells carrying the empty plasmid developed tumors. CONCLUSIONS: These results further support the role of adrenomedullin as a survival factor for tumors. Development of physiologically efficient inhibitors of adrenomedullin may prove useful in the clinical management of cancer.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12189226&dopt=Abstract



Congest Heart Fail. 1999 Nov-Dec;5(6):275-282.
Diagnosis and assessment in heart failure.

Dargie H.

Clinical Research Initiative in Heart Failure, West Medical Building, University of Glasgow, G12 8QQ Glasgow, United Kingdom.

Heart failure is a common and growing problem. Its optimal and effective management and the evaluation of new therapies require assessment of underlying etiology, type of cardiac dysfunction, severity, prognosis, and response to therapy. Unfortunately, the lack of a universally agreed definition of heart failure and uniform criteria make an accurate and complete diagnosis of heart failure difficult. Currently, a wide range of investigations and assessments is available, including assessment of symptoms, exercise performance, and cardiac function. In particular, left ventricular (LV) ejection fraction (EF) is widely used and a good marker of the severity of LV dysfunction and prognosis. It is now being recognized that the early identification and treatment of patients with asymptomatic LV dysfunction may prevent subsequent progression to symptomatic heart failure. Recently, attention has focused on the neurohormonal activation that occurs early in heart failure, and especially increasing evidence suggests that plasma levels of neurohormones and brain natriuretic peptides, may be useful biochemical markers in the diagnosis and assessment of heart failure at an early stage. Further evaluation of this neurohormonal activation and treatments directed towards it may provide considerable benefits in improving patient morbidity and mortality. (c)1999 by CHF, Inc.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12189297&dopt=Abstract [PubMed - as supplied by publisher]



Congest Heart Fail. 1999 Jul-Aug;5(4):171-179.
Atrial natriuretic peptides in the diagnosis and treatment of congestive heart failure.

Vesely DL.

Departments of Medicine, Physiology, and Biophysics, University of South Florida Health Sciences Center and James A. Haley Veterans Hospital, Tampa, FL 33612.

Atrial natriuretic peptides (ANPs) consist of a family of peptides (atrial natriuretic factor [ANF], long acting natriuretic peptide, vessel dilator, kaliuretic peptide, urodilatin, brain natriuretic peptide [BNP], and C type natriuretic peptide [CNP]) which are synthesized within the heart, except for urodilatin. Of these natriuretic peptides, the vessel dilator radioimmunoassay (RIA) of a single plasma sample is the most sensitive and specific in the diagnosis of early (i.e., NYHA class I) congestive heart failure (CHF). Vessel dilator is beneficial in the treatment of CHF, enhancing of urine flow two- to 13-fold and sodium excretion three- to four-fold for 3 hours after stopping its infusion. This 37 amino acid peptide hormone simultaneously decreases systemic vascular resistance 24%, pulmonary vascular resistance 25%, pulmonary capillary wedge pressure 33%, and central venous pressure 27% while increasing cardiac output 34%, cardiac index 35%, and stroke volume index 24% in individuals with CHF. (c)1999 by CHF, Inc.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12189309&dopt=Abstract [PubMed - as supplied by publisher]







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DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells. Our bodies produce decreasing amount of DHEA as we get older. various health benefits: To deter aging, improve sexual function/erectile dysfunction, treat cognitive decline, enhance athletic performance, facilitate weight loss, improve strength, prevent osteoporosis, enhance immunomodulation for rheumatic conditions, and treat depression.





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