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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

Biochem J. 1999 Mar 1;338 ( Pt 2):427-32.
Thyroid hormone promotes the phosphorylation of STAT3 and potentiates the action of epidermal growth factor in cultured cells.

Lin HY, Shih A, Davis FB, Davis PJ.

Molecular and Cellular Medicine Program, Department of Medicine, Albany Medical College, Albany, NY 12208, USA.

We have examined the effects of l-thyroxine (T4) on the activation of signal transducer and activator of transcription 3 (STAT3) and on the STAT3-dependent induction of c-Fos expression by epidermal growth factor (EGF). T4, at a physiological concentration of 100 nM, caused tyrosine phosphorylation and nuclear translocation (i.e. activation) of STAT3 in HeLa cells in as little as 10-20 min. Activation by T4 of STAT3 was maximal at 30 min (15+/-4-fold enhancement; mean+/-S.E.M.) in 18 experiments. This effect was reproduced by T4-agarose (100 nM) and blocked by CGP 41251, genistein, PD 98059 and geldanamycin, inhibitors of protein kinase C (PKC), protein tyrosine kinase (PTK), mitogen-activated protein kinase (MAPK) kinase and Raf-1 respectively. Tyrosine-phosphorylated MAPK also appeared in nuclear fractions within 10 min of treatment with T4. In the nuclear fraction of T4-treated cells, MAPK immunoprecipitate also contained STAT3. The actions of T4 were similar in HeLa and CV-1 cells, which lack thyroid hormone receptor (TR), and in TR-replete skin fibroblasts (BG-9). T4 also potentiated the EGF-induced nuclear translocation of activated STAT1alpha and STAT3 and enhanced the EGF-stimulated expression of c-Fos. Hormone potentiation of EGF-induced signal transduction and c-Fos expression was inhibited by CGP 41251, geldanamycin and PD 98059. Therefore the non-genomically induced activation by T4 of STAT3, and the potentiation of EGF by T4, require activities of PKC, PTK and an intact MAPK pathway.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10024519&dopt=Abstract

J Clin Endocrinol Metab. 1999 Feb;84(2):751-5.
Mutational analysis of the follicle-stimulating hormone (FSH) receptor in normal and infertile men: identification and characterization of two discrete FSH receptor isoforms.

Simoni M, Gromoll J, Hoppner W, Kamischke A, Krafft T, Stahle D, Nieschlag E.

Institute of Reproductive Medicine of the University, Munster, Germany.

In a search for pathophysiological causes of idiopathic male infertility we investigated the occurrence of mutations of the FSH receptor in 48 men with this disorder. The entire FSH receptor gene was analyzed by single stranded conformation polymorphism analysis (SSCP). A heterozygous point mutation without functional consequences, exchanging Val to Ala in codon 341, was found in one patient. SSCP analysis led to the identification of 2 polymorphisms in exon 10 associated in 2 discrete FSH receptor allelic variants, i.e. Thr307-Asn680 and Ala307-Ser680. The frequency and distribution of the two allelic variants was further analyzed in 86 proven fathers and 75 infertile men by SSCP (codon 307) and restriction fragment length polymorphism (codon 680). The 2 receptor isoforms showed similar Mendelian distribution in proven fathers and in infertile men. Serum FSH, inhibin B, and combined testicular volume did not differ between subjects with different receptor isoforms. Binding studies in transiently transfected COS-7 cells showed similar binding affinity for the two receptor variants. Moreover, the Ala307-Ser680 and the Thr307-Asn680 FSH receptors responded in vitro to FSH with comparable cAMP production. These data suggest that different isoforms of the FSH receptor with similar functional properties exist in normal and infertile men. We conclude that mutations of the FSH receptor or the FSH receptor genotype do not play a pathogenic role in male idiopathic infertility. The possibility that different FSH isoforms might interact differently with the 2 receptor variants remains to be investigated.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10022448&dopt=Abstract

Arch Pharm Res. 2003 Jan;26(1):58-63.
Ginsenoside-Rb1 acts as a weak phytoestrogen in MCF-7 human breast cancer cells.

Lee YJ, Jin YR, Lim WC, Park WK, Cho JY, Jang S, Lee SK.

College of Engineering, Institute of Biotechnology, Department of Bioscience and Biotechnology, Sejong University, Seoul, Korea. yjleejong.ac.kr

Ginseng has been recommended to alleviate the menopausal symptoms, which indicates that components of ginseng very likely contain estrogenic activity. We have examined the possibility that a component of Panax ginseng, ginsenoside-Rb1, acts by binding to estrogen receptor. We have investigated the estrogenic activity of ginsenoside-Rb1 in a transient transfection system using estrogen-responsive luciferase plasmids in MCF-7 cells. Ginsenoside-Rb1 activated the transcription of the estrogen-responsive luciferase reporter gene in MCF-7 breast cancer cells at a concentration of 50 microM. Activation was inhibited by the specific estrogen receptor antagonist ICI 182,780, indicating that the estrogenic effect of ginsenoside-Rb1 is estrogen receptor dependent. Next, we evaluated the ability of ginsenoside-Rb1 to induce the estrogen-responsive gene c-fos by semi-quantitative RT-PCR assays and Western analyses. Ginsenoside-Rb1 increased c-fos both at mRNA and protein levels. However, ginsenoside-Rb1 failed to activate the glucocorticoid receptor, the retinoic acid receptor, or the androgen receptor in CV-1 cells transiently transfected with the corresponding steroid hormone receptors and hormone responsive reporter plasmids. These data support our hypothesis that ginsenoside-Rb1 acts a weak phytoestrogen, presumably by binding and activating the estrogen receptor.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12568360&dopt=Abstract

Can J Anaesth. 1998 Nov;45(11):1116-22.
Haemodynamic and catecholamine responses to calcitonin gene-related peptide during volatile anaesthesia.

Takeda S, Tomaru T, Inada Y.

Department of Anesthesiology, Showa University Fujigaoka Hospital, Yokohama, Japan.

PURPOSE: Calcitonin gene-related peptide (CGRP) produces vasodilatation, hypotension, and tachycardia. Tachycardia induced by CGRP may be due to sympathetic activation. Volatile anaesthetics attenuate activation of arterial baroreflexes. We examined the haemodynamic and endocrine effects of CGRP infusion (4 micrograms.kg-1) during anaesthesia with either enflurane or isoflurane in dogs. METHODS: Measurements of haemodynamic variables and hormone assays for plasma catecholamines were made before, during, and after CGRP infusion. Anaesthesia consisted of induction with 25 mg.kg-1 pentobarbital, followed by either enflurane (n = 7) or isoflurane (n = 7) to achieve a 1.0 end-tidal minimum alveolar concentration in oxygen 100%. RESULTS: Mean arterial pressure and systemic vascular resistance decreased (P < 0.01) and the reductions in both variables were similar during CGRP infusion in both groups. Cardiac index (CI) was increased (P < 0.01) in the enflurane group throughout the study while CI increased (P < 0.01) only during infusion in the isoflurane group. Heart rate (HR) remained unchanged (from 135 +/- 6 bpm to 134 +/- 7 bpm) in the enflurane group but tended to increase (from 162 +/- 9 bpm to 171 +/- 9 bpm) in the isoflurane group during infusion. Intergroup differences in HR were found (P < 0.05). Plasma epinephrine concentrations increased (from 42.4 +/- 12.7 pg.ml-1 to 115.3 +/- 41.8 pg.ml-1, P < 0.01) during infusion in the isoflurane group. However, these increases were suppressed (from 46.6 +/- 23.2 pg.ml-1 to 64.7 +/- 32.4 pg.ml-1) to a greater extent in the enflurane group. CONCLUSION: The haemodynamic responses, except for HR, of CGRP infusion are similar during enflurane and isoflurane anaesthesia. Suppression of tachycardia induced by CGRP is greater with enflurane than with isoflurane. The differences in HR may be due to the roles of catecholamine responses resulting from the anaesthetic-induced sympathetic suppression.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10021964&dopt=Abstract

No Shinkei Geka. 1999 Jan;27(1):85-7.
[Carbamazepine induced hyponatremia]

[Article in Japanese]

Inamura T, Kuba H, Morioka T, Muratani H, Muraishi M, Hisada K, Fukui M.

Department of Neurosurgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

Carbamazepine (CBZ) is a drug which can induce the syndrome of inappropriate antidiuretic hormone (SIADH). Until 1980's, there were reports regarding CBZ-induced SIADH, but it is rarely reported these days. We here report two cases of CBZ-induced SIADH. Hyponatremia in these cases was rapidly improved by withdrawal of administration of CBZ. According to the previous reports, the rate of hyponatremia in patients receiving CBZ is not small. It ranges from 48% to 31%. As CBZ is frequently used for patients with epilepsy and neuralgia, not only their blood CBZ concentration but also their serum Na level should be monitored.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10024990&dopt=Abstract

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