References: Hair growth and hair loss
Endocrinology. 2001 Dec;142(12):5386-9.
Targeting expression of the human vitamin D receptor to the keratinocytes of vitamin D receptor null mice prevents alopecia.
Chen CH, Sakai Y, Demay MB.
Endocrine Unit, Massachussetts General Hospital and Harvard Medical School, Boston MA. USA.
Vitamin D receptor (VDR) null mice develop hypocalcemia, hyperparathyroidism, rickets, osteomalacia and alopecia. Normalization of mineral ion homeostasis prevents all of these abnormalities except alopecia. Hair reconstitution assays, performed in athymic nude mice, demonstrate that the lack of VDR in keratinocytes leads to a defect in anagen initiation, similar to that observed in VDR null mice. Although these studies demonstrate that expression of the VDR in keratinocytes is necessary, they do not prove that it is sufficient for maintenance of the normal hair cycle. To address this hypothesis, we generated transgenic mice expressing the human VDR under the control of the keratin 14 (K14) promoter. Two highly expressing transgenic lines were mated with VDR null mice to obtain VDR null mice expressing the human VDR transgene (hVDR+/mVDR-). Expression of the transgene in the VDR null mice prevented alopecia. Furthermore, when subjected to anagen initiation, the hair follicle keratinocytes of the hVDR+/mVDR- mice demonstrated an enhanced proliferative response compared to those of control littermates. Restoration of VDR expression in the keratinocytes of VDR null mice, prevents the hair cycle defect that leads to the development of alopecia.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11713240&dopt=Abstract
Dtsch Med Wochenschr. 1999 May 14;124(19):589-92.
[Tinea capitis and corporis caused by Trichophyton soudanense in an immigrant family from Africa]
[Article in German]
Faulhaber D, Korting HC.
Dermatologische Klinik und Poliklinik, Ludwig-Maximilians-Universitat Munchen.
HISTORY AND FINDINGS: Several weeks before coming to Germany the two daughters (aged 3 and 6 years) of a family from Togo had developed desquamating skin changes over the hairy scalp. These had then spread to the trunk and limbs. The 8-weeks-old son also had discrete lesions on the hairy scalp and neck. In all of them these lesions had then spread and begun to itch markedly. When first seen as out-patients the father was free of symptoms, but the other members of the family had multiple, sharply circumscribed, partly confluent, dry and desquamating lesions, about 2-4 cm in diameter, with areas of alopecia and hair breaking off at skin level. In addition there were dry, desquamating, sharply circumscribed, partly hyperpigmented, partly infiltrated plaques, 1-3 cm in diameter, disseminated over the entire body surface, but especially the neck and limbs. INVESTIGATIONS: Typical micromorphological characteristics for T. soudanese were demonstrated in the outer zones of a primary culture and the organism was also demonstrated in culture on Sabouraud-glucose-agar. Typical colonies on Lowenstein-Jensen medium allowed differentiation from Microsporum ferrugineum. TREATMENT AND COURSE: The patients were treated systemically with griseofulvin and locally with ciclopiroxolamine. Marked clinical improvement occurred within 2 months and cultures became negative. But as fungal elements were still demonstrated in native preparations from two of the patients, treatment was continued. CONCLUSION: Efficacious treatment of tinea needs reliable diagnosis of the pathogen. Human infection with T. soudanese usually results from contact with other humans. If this infection occurs in persons not from Africa there is usually the history of indirect or direct contact with Africans. Increased international migration and tourism is likely to result in more cases of this kind: this pathogen should be considered in the differential diagnosis of tinea of scalp and body.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10365177&dopt=Abstract
J Cell Biol. 2001 Nov 26;155(5):821-32. Epub 2001 Nov 19.
Mice lacking desmocollin 1 show epidermal fragility accompanied by barrier defects and abnormal differentiation.
Chidgey M, Brakebusch C, Gustafsson E, Cruchley A, Hail C, Kirk S, Merritt A, North A, Tselepis C, Hewitt J, Byrne C, Fassler R, Garrod D.
School of Biological Sciences, University of Manchester, Manchester M13 9PT, UK.
The desmosomal cadherin desmocollin (Dsc)1 is expressed in upper epidermis where strong adhesion is required. To investigate its role in vivo, we have genetically engineered mice with a targeted disruption in the Dsc1 gene. Soon after birth, null mice exhibit flaky skin and a striking punctate epidermal barrier defect. The epidermis is fragile, and acantholysis in the granular layer generates localized lesions, compromising skin barrier function. Neutrophils accumulate in the lesions and further degrade the tissue, causing sloughing (flaking) of lesional epidermis, but rapid wound healing prevents the formation of overt lesions. Null epidermis is hyperproliferative and overexpresses keratins 6 and 16, indicating abnormal differentiation. From 6 wk, null mice develop ulcerating lesions resembling chronic dermatitis. We speculate that ulceration occurs after acantholysis in the fragile epidermis because environmental insults are more stringent and wound healing is less rapid than in neonatal mice. This dermatitis is accompanied by localized hair loss associated with formation of utriculi and dermal cysts, denoting hair follicle degeneration. Possible resemblance of the lesions to human blistering diseases is discussed. These results show that Dsc1 is required for strong adhesion and barrier maintenance in epidermis and contributes to epidermal differentiation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11714727&dopt=Abstract
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