References: Hair growth and hair loss
Endocrinology. 1997 Jan;138(1):356-61.
Inhibition of hair growth by testosterone in the presence of dermal papilla cells from the frontal bald scalp of the postpubertal stumptailed macaque.
Obana N, Chang C, Uno H.
Regional Primate Research Center, University of Wisconsin, Madison 53715-1299, USA.
Hair-follicle regression in the bald scalps of stumptailed macaques develops after puberty, which corresponds to an elevation of serum testosterone and dihydrotestosterone. Using the cultured cells from the pre- and postpubertal macaques, we examined the role of dermal papilla cells in testosterone-induced inhibition of outer root sheath cell proliferation. Testosterone showed no effects on proliferation of either dermal papilla cells or outer root sheath cells cultured alone. Testosterone-induced inhibition of outer root sheath cell proliferation occurred only in coculture with dermal papilla cells derived from the bald scalps of adult macaques but not with dermal papilla cells from the hairy occipital scalps of adult macaques or the prebald frontal scalps of juvenile macaques. Furthermore, RU 58841, an androgen receptor blocker, antagonized this testosterone-elicited inhibition. Together our data indicate that the inhibitory effect of testosterone on proliferation of epithelial cells is age dependent, and androgen may play an essential role in hair growth either by inducing repressor(s) from dermal papilla cells, which may then inhibit the growth of epithelial cells of the hair follicle, or by inducing growth factor(s) from dermal papilla cells, which, in turn, may trigger the induction of some repressors in epithelial cells, thereby inhibiting the epithelial cell growth. Our animal studies also showed that RU 58841 has a dramatic effect on hair regrowth in the bald frontal scalp of the stumptailed macaque, which may further support our in vitro culture studies showing that antiandrogens can antagonize testosterone-elicited hair growth. In summary, our studies may provide a model for further isolation of androgen-regulated repressor(s)/growth factors, which may help control hair growth and baldness.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8977424&dopt=Abstract
Support Care Cancer. 1997 Mar;5(2):139-43.
Changes in self-concept and body image during alopecia induced cancer chemotherapy.
Munstedt K, Manthey N, Sachsse S, Vahrson H.
Department of Gynaecological Oncology and Radiotherapy, Justus Liebig University, Giessen, Germany.
Alopecia as a result of cancer chemotherapy has been reported to cause changes to the self-concept and body image. In a prospective longitudinal study, self-concept and body image were analysed in 29 patients after histological confirmation of gynaecological malignancy, mainly ovarian cancer, who were assigned to receive a complete-alopecia-inducing PEC combination chemotherapy (cisplatin 50 mg/m2, epirubicin 60 mg/m2, and cyclophosphamide 500 mg/m2 in 1 day every 28 days). The analysis was performed before the commencement of treatment and repeated when alopoecia was complete and after completion of therapy when patients had already experienced regrowth of hair, using the Frankfurt self-concept scales (FSKN) and Frankfurt body concept scales (FKKS). Significant differences were observed in the various evaluation scales FSAP (general ability to solve problems), FSSW (general self-esteem), SGKB (state of health), and SKEF (physical fitness). For all scales the results worsened during chemotherapy but did not return to normal or improve when patients experienced regrowth of hair. It was found that 73.3% of the patients did not feel as self-confident as before treatment and that for 46.6% alopecia was the most traumatic side effect of chemotherapy. Since there is no chemotherapeutic regimen or any other effective treatment that can prevent alopecia, either of the following conclusions can be drawn: the observed differences may not be related exclusively to alopecia, but also associated with coping processes initiated by chemotherapy and perhaps enhanced by alopecia; or the changes persist even after the discontinuation of chemotherapy. Regrowth of hair and other adaptive processes do not normalize or improve the impaired body image and self-concept.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9069615&dopt=Abstract
Brain Res. 1997 Feb 21;749(1):109-19.
Protein kinase C may be involved in synaptic repair of auditory neuron dendrites after AMPA injury in the cochlea.
Lerner-Natoli M, Ladrech S, Renard N, Puel JL, Eybalin M, Pujol R.
INSERM U254 and Universite de Montpellier I, CHU Hopital St Charles, France.
A suitable model of sudden deafness occurring after acoustic trauma or ischemia, is obtained in guinea pigs by an acute intracochlear perfusion of 200 microM alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), a glutamate analog. By overloading the AMPA/kainate receptors, located post-synaptically to inner hair cells (IHCs), it induces a massive swelling of primary auditory neuron dendrites, which disconnects the IHCs. This synaptic uncoupling and the resulting hearing loss are followed by a progressive regrowth of dendrites, which make new synapses with IHCs, leading to a functional recovery of auditory responses that is completed after 5 days. Knowing the role of protein kinase C in neuroplastic events, we studied the expression of its isoforms alpha,beta(I,II) and gamma, respectively pre- and post-synaptic, in auditory neurons at various times after AMPA administration. In untreated cochleas, we observed an expression of PKC alpha,beta(I,II) and gamma in cell bodies of primary auditory neurons. After the intracochlear administration of AMPA, both isozymes were transiently overexpressed, with a peak at 3-6 h, followed by a decrease after about 24 h. At this point in time immuno-electron microscopy revealed some regrowing dendrites immunoreactive for PKCgamma. Five days after AMPA, when the auditory responses were restored, PKCgamma levels were still elevated in ganglion cell bodies.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9070634&dopt=Abstract
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