References: Hair growth and hair loss
Development. 1998 Feb;125(4):557-66.
Shaker-1 mutations reveal roles for myosin VIIA in both development and function of cochlear hair cells.
Self T, Mahony M, Fleming J, Walsh J, Brown SD, Steel KP.
MRC Institute of Hearing Research, University Park, Nottingham NG7 2RD, UK.
The mouse shaker-1 locus, Myo7a, encodes myosin VIIA and mutations in the orthologous gene in humans cause Usher syndrome type 1B or non-syndromic deafness. Myo7a is expressed very early in sensory hair cell development in the inner ear. We describe the effects of three mutations on cochlear hair cell development and function. In the Myo7a816SB and Myo7a6J mutants, stereocilia grow and form rows of graded heights as normal, but the bundles become progressively more disorganised. Most of these mutants show no gross electrophysiological responses, but some did show evidence of hair cell depolarisation despite the disorganisation of their bundles. In contrast, the original shaker-1 mutants, Myo7ash1, had normal early development of stereocilia bundles, but still showed abnormal cochlear responses. These findings suggest that myosin VIIA is required for normal stereocilia bundle organisation and has a role in the function of cochlear hair cells.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9435277&dopt=Abstract
J Invest Dermatol. 2000 Aug;115(2):200-6.
Histologic and cell kinetic studies of hair loss and subsequent recovery process of human scalp hair follicles grafted onto severe combined immunodeficient mice.
Hashimoto T, Kazama T, Ito M, Urano K, Katakai Y, Yamaguchi N, Ueyama Y.
Department of Dermatology, Niigata University School of Medicine, Niigata, Japan.
To establish a model for studying human scalp hair, individually isolated hair follicles were grafted onto back skin of severe combined immunodeficient mice. Histologic changes and cell kinetics in the hair loss and subsequent recovery process were investigated. In the dystrophic stage (from day 7 to 30), all the hair shafts became dystrophic and were shed. Thickening and corrugation of vitreous membrane, apoptosis, and regression of the lower part were observed in the grafted hair follicles. 5-bromo-2'-deoxy-uridine-labeled cells were not detected in the lower end of the follicles, and keratin 19-positive cells appeared there. At the end of this stage their lower part was maximally retracted, secondary germ remained beneath the bulge, and the vitreous membrane disappeared. In the regeneration stage (from day 30 to 50), the same histologic findings as those at the end of the dystrophic stage were observed. The keratin 19-positive cells in the secondary germ, however, were replaced with keratin 19-negative and 5-bromo-2'-deoxy-uridine-labeled cells. Then, differentiation into an inner root sheath and a hair shaft began, and apoptosis was terminated. In the stable growth stage (from day 40 to at least 150), the grafted follicles were immunohistochemically and light microscopically identical with the normal anagen hair follicles except for the presence of melanin incontinence. These findings suggest that the grafted hair follicles entered into dystrophic catagen, subsequently dystrophic telogen, then returned to normal anagen follicles, and that stem cells or their close progeny in the secondary germ play an important part in the recovery process.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10951236&dopt=Abstract
Microsc Res Tech. 1997 Dec 15;39(6):479-91.
Pattern, time of birth, and morphogenesis of sensillum progenitors in Drosophila.
Younossi-Hartenstein A, Hartenstein V.
Department of Cellular, Molecular, and Developmental Biology, University of California at Los Angeles 90024, USA.
In this paper we describe the spatiotemporal pattern of sensillum progenitors (SOPs), as well as the way in which these cells segregate from the ectoderm and proliferate. The birthdate of SOPs was determined by applying short heat pulses to embryos carrying the Nintra construct [Struhl et al. (1993), Cell, 74:331-345] which allows the overexpression of the active Notch protein at defined developmental stages and thereby eliminates SOPs which would normally segregate during these stages. Our results show that sensillum progenitors appear in several waves which to some degree respect sensillum modality, as well as dorsoventral sensillum location. The four early SOPs (stage 10) give rise exclusively to multiply innervated sensilla, chordotonal organs, and some multidendritic neurons. The second wave (early stage 11) produces the remaining chordotonal organs, some multidendritic neurons, and the dorsal singly innervated mechanosensilla. The third wave (late stage 11), in a dorsal-to-ventral succession, gives rise to the lateral and ventral singly innervated hair and papilla sensilla. Labeling developing SOPs with specific markers demonstrates that only progenitors of subepidermally located chordotonal organs and multidendritic neurons delaminate, whereas progenitors of external sensilla are born and proliferate within the ectodermal layer.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9438249&dopt=Abstract
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