Tramadol, buy tramadol, antibiotics, Weight Loss drugs, weight loss herbs, weight loss herbal formula, weight loss, hair loss, hair growth, baldness, Rx Online, pharmaceuticals, DHEA, Lutein, Prescription, Prescription drug, prescription medications, hormone.

DreamPharm Products:

Lutein-20||Herbs for headache, fever, and migraine || Milk thistle||Saw palmetto|| Triple B Super Vision||Garlic, Ginger, and Grapeseed Extract|| Ginseng and Ginkgo||Hair Million|| DHEA||Coenzyme Q10|| Sleep Aid herbal formula - natural sleep aid||Herbal Breath - herbs for bad breath problems.|| Weight loss herbal formula for menopause and pms||Ginkgo biloba|| Colon cleansing, Laxative||ViaVita, Lecithin for healthy liver

Fatty acids resources:

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

J Endocrinol. 2002 Sep;174(3):499-507.
Insulin and IGF-I are necessary for FSH-induced cytochrome P450 aromatase but not cytochrome P450 side-chain cleavage gene expression in oestrogenic bovine granulosa cells in vitro.

Silva JM, Price CA.

Centre de Recherche en Reproduction Animale, Faculte de Medecine Veterinaire, Universite de Montreal, 3200 Sicotte, St-Hyacinthe, Quebec J2S 7C6, Canada.

The earliest biochemical indicators of ovarian follicle deviation in cattle include lower oestradiol and free IGF concentrations in subordinate compared with dominant follicles. We determined if decreases in FSH, IGF-I or insulin cause decreased P450 aromatase (P450arom) or P450 cholesterol side-chain cleavage (P450scc) mRNA expression in oestrogenic bovine granulosa cells in vitro. In the first experiment, cells obtained from small follicles (2-5 mm diameter) were cultured in serum-free medium supplemented with physiological concentrations of FSH, IGF-I and insulin for 4 days. A decrease in specific hormone concentration was produced by replacing 70% of spent medium with medium devoid of FSH, insulin, or insulin and IGF-I on day 4 and again on day 5 of culture. Cultures were terminated on day 7. A reduction in FSH concentrations during the last 3 days of culture decreased P450arom and P450scc mRNA levels. A reduction in insulin reduced P450arom but not P450scc mRNA levels, and a reduction of both insulin and IGF-I concentrations further decreased P450arom mRNA levels and decreased P450scc mRNA levels. In a second experiment, cells obtained from small follicles (2-5 mm diameter) were cultured with insulin (100 ng/ml) without FSH for 4 days, and then insulin was withdrawn from the culture and FSH added for a further 3 days. The withdrawal of insulin decreased (P<0.02) oestradiol accumulation and reduced P450arom mRNA to below detectable levels, but did not affect P450scc mRNA levels. The addition of FSH transiently increased oestradiol secretion and P450arom mRNA levels, but P450arom mRNA levels were undetectable at the end of the culture period. The addition of FSH significantly enhanced P450scc mRNA levels and progesterone accumulation. These data demonstrated that a reduction of insulin-like activity reduced aromatase gene expression in bovine follicles without necessarily affecting progesterone synthetic capability, and thus may initiate follicle regression in cattle at the time of follicle divergence.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12208671&dopt=Abstract

J Endocrinol. 2002 Sep;174(3):509-16.
Clodronate inhibits adrenocortical cell proliferation and P450c21 activity.

Fassnacht M, Franke A, Dettling A, Hahner S, Zink M, Wudy S, Allolio B.

Department of Medicine, Endocrine and Diabetes Unit, University of Wuerzburg, 9700 Wuerzburg, Germany. M.Fassnachedizin.uni-wuerzburg.de

Bisphosphonates (BPs), specific inhibitors of osteoclasts, are well established in the management of skeletal metastases in breast cancer. Recent studies have suggested that these compounds may also directly influence tumor cell proliferation. As adrenocortical cancer frequently leads to bone metastases, we investigated the effects of clodronate (CLO) in the human adrenocortical cancer cell line NCI-H295 and in primary cultures of bovine adrenocortical cells. Both the non-amino BP CLO and the amino BP pamidronate (PAM) exhibited a dose-dependent antiproliferative effect in both cell types (cell viability in NCI-H295 cells: 100 microM CLO: 98+/-8%; 500 microM CLO 76+/-6%; 1000 microM CLO 53+/-2; 10 microM PAM 96+/-3%; 50 microM PAM 46+/-6%; 100 microM PAM 11+/-1% vs untreated control cells: 100+/-10%; P<0.01). FACS analysis in NCI-H295 cells treated with either CLO or PAM demonstrated both apoptotic and necrotic cell death. However, while during PAM treatment cell number and hormone secretion decreased in parallel, we observed specific impairment of steroidogenesis in the presence of CLO with a dose-dependent increase in the 17-OH-progesterone/cortisol ratio (100 microM CLO 134+/-30%; 500 microM CLO 284+/-10%; 1000 microM CLO 545+/-130% vs 100+/-20% in control cells; P<0.01). Further analysis in ACTH-stimulated bovine adrenal cells using stable isotope dilution/gas chromatography-mass spectrometry demonstrated CLO-induced inhibition of adrenal 21-hydroxylase (P450c21) activity leading to a dose-dependent increase in the 17-OH-progesterone/11-deoxycortisol ratio. In conclusion, we demonstrate a dose-dependent antiproliferative effect of CLO and PAM in adrenocortical cells. In addition, for the first time, we describe a suppressive effect of CLO on steroidogenesis via inhibition of adrenal 21-hydroxylase (P450c21) activity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12208672&dopt=Abstract

J Endocrinol. 2002 Sep;174(3):R13-7.
Liver receptor homologue-1 is expressed in human steroidogenic tissues and activates transcription of genes encoding steroidogenic enzymes.

Sirianni R, Seely JB, Attia G, Stocco DM, Carr BR, Pezzi V, Rainey WE.

Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, University of Texas Southwestern Medical Center, Dallas, Texas, USA.

In the current study we test the hypothesis that liver receptor homologue-1 (LRH; designated NR5A2) is involved in the regulation of steroid hormone production. The potential role of LRH was assessed by first examining expression in human steroidogenic tissues and second by examining effects on transcription of genes encoding enzymes involved in steroidogenesis. LRH is closely related to steroidogenic factor 1 (SF1; designated NR5A1), which is expressed in most steroidogenic tissues and regulates expression of several steroid-metabolizing enzymes. LRH transcripts were expressed at high levels in the human ovary and testis. Adrenal and placenta expressed much lower levels of LRH than either ovary or liver. To examine the effects of LRH on steroidogenic capacity we used reporter constructs prepared with the 5'-flanking region of steroidogenic acute regulatory protein (StAR), cholesterol side-chain cleavage (CYP11A1), 3beta hydroxysteroid dehydrogenase type II (HSD3B2), 17alpha hydroxylase, 17,20 lyase (CYP17), 11beta hydroxylase (CYP11B1) and aldosterone synthase (CYP11B2). Co-transfection of these reporter constructs with LRH expression vector demonstrated that like SF1, LRH enhanced reporter activity driven by flanking DNA from StAR, CYP11A1, CYP17, HSD3B2, and CYP11B1. Reporter constructs driven by CYP11A1 and CYP17 were increased the most by co-transfection with LRH and SF1. Of the promoters examined only HSD3B2 was more sensitive to LRH than SF1. The high level of ovarian and testicular LRH expression make it likely that LRH plays an important role in the regulation of gonadal function.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12208674&dopt=Abstract

Br J Pharmacol. 2002 Sep;137(2):153-61.
Beta 3-adrenoceptor in rat aorta: molecular and biochemical characterization and signalling pathway.

Rautureau Y, Toumaniantz G, Serpillon S, Jourdon P, Trochu JN, Gauthier C.

Laboratoire de Physiopathologie et de Pharmacologie Cellulaires et Moleculaires, INSERM U533, Hotel-Dieu, Nantes, France.

1. We have previously demonstrated that beta(3)-adrenoceptor (beta(3)-AR) stimulation induces endothelium-dependent vasorelaxation in rat aorta through the activation of an endothelial NO synthase associated with an increase in intracellular cGMP. The aim of the present study was to localise beta(3)-AR to confirm our functional study and to complete the signalling pathway of beta(3)-AR in rat aorta. 2. By RT-PCR, we have detected beta(3)-AR transcripts both in aorta and in freshly isolated endothelial cells. The absence of markers for adipsin or hormone-sensitive lipase in endothelial cells excluded the presence of beta(3)-AR from adipocytes. The localization of beta(3)-AR in aortic endothelial cells was confirmed by immunohistochemistry using a rat beta(3)-AR antibody. 3. To identify the G protein linked to beta(3)-AR, experiments were performed in rat pre-treated with PTX (10 microg kg(-1)), a G(i/0) protein inhibitor. The blockage of G(i/0) protein by PTX was confirmed by the reduction of vasorelaxation induced by UK 14304, a selective alpha(2)-AR agonist. The cumulative concentration-response curve for SR 58611A, a beta(3)-AR agonist, was not significantly modified on aorta rings from PTX pre-treated rats. 4. At the same level of contraction, the relaxations induced by 10 microM SR 58611A were significantly reduced in 30 mM-KCl pre-constricted rings (E(max)=16.7+/-8.4%, n=5), in comparison to phenylephrine (0.3 microM) pre-constricted rings (E(max)=49.11+/-11.0%, n=5, P<0.05). In addition, iberotoxin (0.1 microM), glibenclamide (1 microM) and 4-aminopyridine (1 mM), selective potassium channels blockers of K(Ca), K(ATP), and K(v) respectively, decreased the SR 58611A-mediated relaxation. 5. We conclude that beta(3)-AR is preferentially expressed in rat aortic endothelial cells. Beta(3)-AR-mediated aortic relaxation is independent of G(i/0) proteins stimulation, but results from the activation of several potassium channels, K(Ca), K(ATP), and K(v).

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12208771&dopt=Abstract

J Biol Chem. 2002 Oct 25;277(43):40181-4. Epub 2002 Sep 02.
Biological evidence that SOCS-2 can act either as an enhancer or suppressor of growth hormone signaling.

Greenhalgh CJ, Metcalf D, Thaus AL, Corbin JE, Uren R, Morgan PO, Fabri LJ, Zhang JG, Martin HM, Willson TA, Billestrup N, Nicola NA, Baca M, Alexander WS, Hilton DJ.

Walter and Eliza Hall Institute of Medical Research and the Cooperative Research for Cellular Growth Factors, PO Royal Melbourne Hospital, VIC 3050, Australia. greenhalgehi.edu.au

Suppressor of cytokine signaling (SOCS)-2 is a member of a family of intracellular proteins implicated in the negative regulation of cytokine signaling. The generation of SOCS-2-deficient mice, which grow to one and a half times the size of their wild-type littermates, suggests that SOCS-2 may attenuate growth hormone (GH) signaling. In vitro studies indicate that, while SOCS-2 can inhibit GH action at low concentrations, at higher concentrations it may potentiate signaling. To determine whether a similar enhancement of signaling is observed in vivo or alternatively whether increased SOCS-2 levels repress growth in vivo, we generated and analyzed transgenic mice that overexpress SOCS-2 from a human ubiquitin C promoter. These mice are not growth-deficient and are, in fact, significantly larger than wild-type mice. The overexpressed SOCS-2 was found to bind to endogenous GH receptors in a number of mouse organs, while phosphopeptide binding studies with recombinant SOCS-2 defined phosphorylated tyrosine 595 on the GH receptor as the site of interaction. Together, the data implicate SOCS-2 as having dual effects on GH signaling in vivo.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12208853&dopt=Abstract

Hair growth is a sophisticated biological process, which is still not thoroughly 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.

Hair Million is an alternative solution to cope with hair loss problems. Anecdotally, it shows prositive results and improvement especially for age-related hair thinning and hair loss for a fraction of people who take it. We do not know the mechanisms of action as to how Hair Million works to help stop hair loss, and promote hair growth. We only know by anecdotal observations. There has been no clinical trials nor placebo controlled statistical analysis on the efficacy of Hair Million on hair loss and hair growth.

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.

DreamPharm Online Healthy Supplements || Lutein || Progesterone Cream || Natural herbal formula for hair loss problems ||