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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







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Glucocorticoids are involved in the modulation of the release of parturition hormones from the fetal membranes and placenta, where their actions are determined by the prereceptor glucocorticoid metabolizing enzyme 11beta-hydroxysteroid dehydrogenase (11beta-HSD). Two distinct isozymes of 11beta-HSD have been characterized. In the fetal membranes, 11beta-HSD1 is the predominate isozyme; it converts biologically inert 11-ketone glucocorticoid metabolites into active glucocorticoids. Sequence analysis of the cloned 11beta-HSD1 gene revealed a putative glucocorticoid response element in the promoter region. However, whether glucocorticoids modulate 11beta-HSD1 expression in the fetal membranes is unknown. In this study, 11beta-HSD1 and glucocorticoid receptor (GR) were coexpressed in the chorionic trophoblast. Radiometric conversion assay and Northern blot analysis revealed that both 11beta-HSD1 reductase activity and mRNA levels were increased by dexamethasone (1 microM, 0.1 microM) in the cultured chorionic trophoblast, and the effects were blocked by GR antagonist RU486 (1 microM). Prior induction of 11beta-HSD1 by dexamethasone potentiated the subsequent stimulation of prostaglandin H synthetase 2 expression and secretion of prostaglandin E(2) by cortisone in the chorionic trophoblast. There is colocalization of 11beta-HSD1 and GR in the chorionic trophoblast. By binding to GR, glucocorticoids induce the expression of 11beta-HSD1 by a possible intracrine mechanism, thereby amplifying the actions of glucocorticoids on prostaglandin production in the fetal membranes. This cascade of events initiated by glucocorticoids may play an important role in the positive feed-forward mechanisms of labor.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12390875&dopt=Abstract



Biol Reprod. 2002 Nov;67(5):1509-21.
Expression of steroidogenic factor 1 in the testis requires an interactive array of elements within its proximal promoter.

Scherrer SP, Rice DA, Heckert LL.

Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas 66160, USA.

Steroidogenic factor 1 (SF-1) is an orphan nuclear receptor that is important for expression of genes involved in sexual differentiation, testicular and adrenal development, and hormone synthesis and regulation. To better understand the mechanisms required for SF-1 production, we employed transient transfection analysis and electrophoretic mobility shift assays to characterize the elements and proteins required for transcriptional activity of the SF-1 proximal promoter in testicular Sertoli and Leydig cells and adrenocortical cells. Direct comparison of SF-1-promoter activity in testis and adrenal cell types established that a similar set of regulatory elements (an E box, CCAAT box, and Sp1-binding sites) is required for proximal promoter activity in these cells. Further evaluation of the E box and CCAAT box revealed a novel synergism between the two elements and identified functionally important bases within the elements. Importantly, DNA/protein-binding studies uncovered new proteins interacting with the E box and CCAAT box. Thus, in addition to the previously identified USF and NF-Y proteins, newly described complexes, having migration properties that differed between Sertoli and Leydig cells, were observed bound to the E box and CCAAT box. Transient transfection analysis also identified several Sp1/Sp3-binding elements important for expression of SF-1 in the testis, one of which was previously described for expression in the adrenal gland whereas the other two were newly disclosed elements.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12390883&dopt=Abstract



Biol Reprod. 2002 Nov;67(5):1593-604.
Spatiotemporal expression of epidermal growth factor receptor messenger RNA and protein in the hamster ovary: follicle stage-specific differential modulation by follicle-stimulating hormone, luteinizing hormone, estradiol, and progesterone.

Garnett K, Wang J, Roy SK.

Department of Obstetrics and Gynecology, University of Nebraska Medical Center, 984515 Nebraska Medical Center, Omaha, Nebraska 68198-4515, USA.

Spatiotemporal expression, endocrine regulation, and activation of epidermal growth factor receptor (EGFR) in the hamster ovary were evaluated by immunofluorescence and in situ hybridization localization. Whereas granulosa cells (GC) of primordial through large preantral (stage 6, 7-8 layers GC) follicles had low immunoreactivity, granulosa cells of antral follicles, theca, and interstitial cells had intense EGFR immunoreactivity. EGFR expression in GC of primordial and small preantral follicles increased progressively from estrous through proestrous, but a significant increase occurred in mural GC of antral follicles following the gonadotropin surge. Interstitial cells around small preantral follicles had strong immunofluorescence, and the intensity increased significantly in fully differentiated thecal cells. Distinct EGFR protein was localized in the nucleus of the oocytes and granulosa cells. FSH significantly stimulated EGFR expression in the GC, especially the mural GC, theca, and interstitial cells in hypophysectomized hamster. Estrogen stimulated EGFR expression in preantral GC as well as in interstitial cells. Progesterone and hCG effect was limited to theca and interstitial cells. EGFR expression correlated well with EGFR activation following endogenous or exogenous gonadotropin exposure. Receptor mRNA expression closely followed the protein expression, with increased mRNA expression in mural GC of antral follicles. These results suggest that low levels of EGF signal as a consequence of low levels of receptors in preantral GC may be critical for cell proliferation, but higher receptor density may evoke increased signal intensity due to activation of other intracellular signal pathways, which activate cellular processes related to granulosa, theca, and interstitial cell differentiation. The spatiotemporal cell type and follicle stage-specific expression of receptor mRNA and protein and EGFR activation is critically regulated by gonadotropins and ovarian steroids, primarily estradiol.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12390893&dopt=Abstract



Biol Reprod. 2002 Nov;67(5):1621-7.
Transcription and translation of the salmon gonadotropin-releasing hormone genes in brain and gonads of sexually maturing rainbow trout (Oncorhynchus mykiss).

Gray SL, Adams BA, Warby CM, Von Schalburg KR, Sherwood NM.

Department of Biology, University of Victoria, Victoria, British Columbia, Canada V8W 3N5.

Rainbow trout sexually mature at the end of Year 3. The form of GnRH that controls gonadotropin release in trout is salmon GnRH (sGnRH). In the tetraploid rainbow trout, two genes encode an identical sGnRH peptide. The sGnRH gene-1 produces one mRNA, whereas sGnRH gene-2 can produce more than one. This study asks whether the transcripts and their protein products are expressed in the brain and gonads and whether the pattern correlates with sexual maturity over the final year leading to first spawning. Brain sGnRH mRNA and protein were continuously present throughout the third year. We show for the first time that the long sGnRH-2 mRNA transcript is expressed in neural tissue and not exclusively in gonadal tissue. Expression of the long sGnRH-2 mRNA in the brain coincides with high levels of sGnRH peptide in the brain during a time of increased gonadal growth. Thus, the long sGnRH-2 mRNA in the brain may act to regulate sGnRH production in a stage-specific rather than a tissue-specific manner. In gonads, local sGnRH is thought to play an autocrine/paracrine role in regulating gonadal maturation and spawning. In the maturing gonads, sGnRH gene-1 and -2 are expressed intermittently. Strikingly, sGnRH peptide was not detected in the gonads at any time during Year 3. These results suggest that either the sGnRH transcripts in the gonads are not translated into protein or, if translated, the protein is rapidly released, resulting in gonadal content below 1 fM per fish.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12390896&dopt=Abstract



J Appl Physiol. 2003 Jan;94(1):285-94. Epub 2002 Sep 20.
Effects of oral contraceptives on glucose flux and substrate oxidation rates during rest and exercise.

Suh SH, Casazza GA, Horning MA, Miller BF, Brooks GA.

Exercise Physiology Laboratory, Department of Integrative Biology, University of California, Berkeley, 94720-3140, USA.

We examined the effects of oral contraceptives (OC) on glucose flux and whole body substrate oxidation rates during rest (90 min) and two exercise intensities [60-min leg ergometer cycling at 45 and 65% peak O(2) uptake (Vo(2 peak))]. Eight healthy, eumenorrheic women were studied during the follicular and luteal phases before OC and the inactive and high-dose phases after 4 mo of a low-dose, triphasic OC. Subjects were studied in the morning 3 h after a standardized (308 kcal) breakfast. There were significant reductions in glucose rates of appearance and disappearance during exercise of both intensities with OC but not rest. There were no phase effects on substrate oxidation during rest or exercise. These results are interpreted to mean that, in women fed several hours before study, 1) OC decreases glucose flux, but not overall carbohydrate and lipid oxidation rates during moderate-intensity exercise; and 2) synthetic ovarian hormone analogs in the doses contained in OC have greater metabolic effects on glucose metabolism during exercise than do endogenous ovarian hormones.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12391078&dopt=Abstract








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