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References: Hair growth and hair loss

J Invest Dermatol. 1997 Feb;108(2):160-5.
Production of POMC, CRH-R1, MC1, and MC2 receptor mRNA and expression of tyrosinase gene in relation to hair cycle and dexamethasone treatment in the C57BL/6 mouse skin.

Ermak G, Slominski A.

Department of Pathology and Laboratory Medicine, Albany Medical College, New York 12208, USA.

In skin of the C57BL/6 mouse, the production of mRNA transcripts that hybridized to the coding region of the MC1 receptor (MC1-R) gene was undetectable in telogen, increased during hair growth, and, after reaching the highest values in anagen VI, decreased during the anagen-catagen transition phase. This production was associated with anagen-dependent expression of the tyrosinase gene and enzyme activity. In contrast, the production of 4.5- and 2.0-kb mRNAs hybridizable to the coding region of the MC2 receptor (MC2-R) gene was similar throughout the entire hair cycle. Previously, dexamethasone was demonstrated to induce premature catagen development accompanied by an abrupt termination of melanogenesis. Here we demonstrate that topical application of dexamethasone during anagen VI decreased the concentration of POMC, MC1-R, and tyrosinase mRNA in the skin. The decrease in tyrosinase mRNA concentration was accompanied by a decrease in tyrosinase protein concentration and enzyme activity. These results support the hypothesis that murine hair growth and attendant melanogenesis can be regulated through coordinated changes in local expression of POMC, MC1-R, and tyrosinase genes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9008228&dopt=Abstract

J Invest Dermatol. 1997 Feb;108(2):205-9.
Activation of cytoprotective prostaglandin synthase-1 by minoxidil as a possible explanation for its hair growth-stimulating effect.

Michelet JF, Commo S, Billoni N, Mahe YF, Bernard BA.

Hair Biology Research Group, L'OREAL, Clichy, France.

Data from the literature indicate that nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin, naproxen, piroxicam, or ibuprofen, induce hair loss in vivo. These NSAIDs are well-known inhibitors of both the cytoprotective isoform of prostaglandin endoperoxide synthase-1 (PGHS-1) and of the inducible form (PGHS-2). By immunohistochemical staining, we found that PGHS-1 is the main isoform present in the dermal papilla from normal human hair follicle (either anagen or catagen), whereas PGHS-2 was only faintly and exclusively expressed in anagen dermal papilla. Thus, PGHS-1 might be the primary target of the hair growth-inhibitory effects of NSAIDs. We thus speculated that activation of PGHS-1 might be a mechanism by which minoxidil (2,4-diamino-6-piperidinopyrimidine-3-oxyde) stimulates hair growth in vivo. We demonstrate here that minoxidil is a potent activator of purified PGHS-1 (AC50 = 80 microM), as assayed by oxygen consumption and PGE2 production. This activation was also evidenced by increased PGE2 production by BALB/c 3T3 fibroblasts and by human dermal papilla fibroblasts in culture. Our findings suggest that minoxidil and its derivatives may have a cytoprotective activity in vivo and that more potent second-generation hair growth-promoting drugs might be designed, based on this mechanism.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9008235&dopt=Abstract

Mycoses. 1996 Sep-Oct;39(9-10):387-92.
Human androgenic steroids affect growth of dermatophytes in vitro.

Brasch J, Flader S.

Department of Dermatology, University of Kiel, Germany.

Hormonal effects on fungal growth are of particular interest to medical mycology. In the skin, androgenic steroids metabolized within pilosebaceous units may have direct effects on dermatophytes that invade hair follicles. In this study, 10(-1) to 10(2) mg 1(-1) testosterone, 5-alpha-dihydrotestosterone, dehydroepiandrosterone, androstenedione and androstanedione were used in agar dilution assays to test their effects on thallus diameters of Trichophyton rubrum, Epidermophyton floccosum, T. tonsurans, T. mentagrophytes and Microsporum canis. All dermatophytes responded in a dose-dependent manner with reduced diameters of thalli. Growth of T. rubrum and E. floccosum was completely or strongly suppressed by 10(2) mg 1(-1) androstenedione and androstanedione. A minor inhibition of all strains was obtained with 10(1) to 10(2) mg 1(-1) testosterone, dehydroepiandrosterone and 5-alpha-dihydrotestosterone, the last being least inhibitory for all species. Trichophyton mentagrophytes and M. canis were least responsive to most hormones. The high susceptibility of T. rubrum and E. floccosum to intrafollicular androstenedione and androstanedione could be one reason why these two species are unable to cause tinea capitis. Receptor-mediated effects and an unspecific interference with fungal sterol metabolism are discussed as mechanisms of fungal inhibition by steroidal hormones.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9009664&dopt=Abstract

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