References: Hair growth and hair loss
J Anim Sci. 1999 Jan;77(1):17-24.
The effect of bovine somatotropin treatment on production of lactating angora does with kids.
Davis JJ, Sahlu T, Puchala R, Herselman MJ, Fernandez JM, McCann JP, Coleman SW.
E. (Kika) de la Garza Institute for Goat Research, Langston University, OK 73050, USA.
Fourteen Angora does (35+/-2 kg), each with a single kid and in the first month of lactation, were used to determine ongoing (Period 1) and residual (Period 2) effects of chronic bovine somatotropin (bST) treatment. Specifically, we sought to determine whether chronic bST treatment was capable of improving milk yield, and thus kid growth, and mohair production of nursing does. The experiment consisted of a 2-wk pretreatment period, 5 wk of weekly subcutaneous treatment of slow-release bST (n = 7; Period 1), and a 4-wk posttreatment period (Period 2). The weekly dose of bST was calculated to release 100 microg/(kg BW.d(-1)). To estimate milk production, kids were separated from the does daily for 5 h, and their BW was recorded before and after suckling. The difference in BW was taken as milk production for 5 h. Fiber growth was measured by shearing does at the start of the experiment and at the end of Periods 1 and 2. Dry matter intake and BW of does were not affected by bST (P>.05). Average daily gain of kids that were suckling bST-treated does was higher (P<.05) than for kids of untreated does during Period 1 (184 vs. 139 g/d) but not during Period 2 (140 vs. 136 g/d; P>.10). Treatment with bST did not affect (P>.10) milk composition or clean fleece production in either period. Injection of bST did not affect (P>.10) plasma concentrations of glucose (mean = 49.5 mg/dL), urea N (mean = 19 mg/dL), total protein (mean = 72.5 g/d), or NEFA (mean = 122 microEq/L). During the period of bST treatment, plasma concentrations of somatotropin and IGF-I were increased (P<.05), concentrations of thyroxine and cortisol were decreased (P<.10), and plasma insulin levels were unchanged (P>.10) by bST. In conclusion, treatment of Angora dams with bST did not change DMI or mohair growth, but it improved growth of their kids.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10064023&dopt=Abstract
Cancer Res. 1999 Jul 15;59(14):3489-94.
Mouse model for the DNA repair/basal transcription disorder trichothiodystrophy reveals cancer predisposition.
de Boer J, van Steeg H, Berg RJ, Garssen J, de Wit J, van Oostrum CT, Beems RB, van der Horst GT, van Kreijl CF, de Gruijl FR, Bootsma D, Hoeijmakers JH, Weeda G.
MGC-Department of Cell Biology and Genetics, Erasmus University, Rotterdam, The Netherlands.
Patients with the nucleotide excision repair (NER) disorder xeroderma pigmentosum (XP) are highly predisposed to develop sunlight-induced skin cancer, in remarkable contrast to photosensitive NER-deficient trichothiodystrophy (TTD) patients carrying mutations in the same XPD gene. XPD encodes a helicase subunit of the dually functional DNA repair/basal transcription complex TFIIH. The pleiotropic disease phenotype is hypothesized to be, in part, derived from a repair defect causing UV sensitivity and, in part, from a subtle, viable basal transcription deficiency accounting for the cutaneous, developmental, and the typical brittle hair features of TTD. To understand the relationship between deficient NER and tumor susceptibility, we used a mouse model for TTD that mimics an XPD point mutation of a TTD patient in the mouse germline. Like the fibroblasts from the patient, mouse cells exhibit a partial NER defect, evident from the reduced UV-induced DNA repair synthesis (residual repair capacity approximately 25%), limited recovery of RNA synthesis after UV exposure, and a relatively mild hypersensitivity to cell killing by UV or 7,12-dimethylbenz[a]anthracene. In accordance with the cellular studies, TTD mice exhibit a modestly increased sensitivity to UV-induced inflammation and hyperplasia of the skin. In striking contrast to the human syndrome, TTD mice manifest a dear susceptibility to UV- and 7,12-dimethylbenz[a]anthracene-induced skin carcinogenesis, albeit not as pronounced as the totally NER-deficient XPA mice. These findings open up the possibility that TTD is associated with a so far unnoticed cancer predisposition and support the notion that a NER deficiency enhances cancer susceptibility. These findings have important implications for the etiology of the human disorder and for the impact of NER on carcinogenesis.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10416615&dopt=Abstract
Ther Umsch. 2002 May;59(5):211-6.
[Androgenetic alopecia in the man]
[Article in German]
Bader U, Trueb RM.
Dermatologische Klinik, UniversitatsSpital Zurich.
Androgenetic alopecia (AGA) occurs in approximately 40% of men at the age of 40 and 50% at 50, respectively. Especially for young men progressive hair loss can be distressing. Therefore, understanding of these patients' concerns is important for appropriate management. Current understanding of the pathophysiology of AGA mainly focuses on androgen metabolism as it affects hair growth. As a result, pharmacologic treatment has made considerable progress through the introduction of selective 5 alpha-reductase inhibition with finasteride. In placebo-controlled clinical trials in men with AGA, treatment with oral finasteride proved to be effective. Minoxidil is the only pharmacological substance for topical application with proven efficacy. So far, other treatment modalities have no proven efficacy in clinical trials, so that their use cannot be recommended. Options for advanced AGA not amenable to pharmacologic treatment are autologous hair transplantation and hair replacement, both of which have recently also made progress in terms of cosmetic appeal.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12090116&dopt=Abstract
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