Hair follicle development

Molecular Control of Hair Follicle Development and Cycling. 127... 

Millar SE (2002) Molecular mechanisms regulating hair follicle development J Invest Dermatol 118(2) 216-225... 

DasGupta R, Fuchs E (1999) Multiple roles for activated LEF/TCF transcription complexes during hair follicle development and differentiation. Development 126(20) 4557 568... 

Karlsson L, Bondjers C, Betsholtz C (1999) Roles for PDGF-A and sonic hedgehog in development of mesenchymal components of the hair follicle. Development 126(12) 2611-2621... 

Vauclair S et al (2005) Notchl is essential for postnatal hair follicle development and... 

Kizawa K, Tsuchimoto S, Hashimoto K, Uchiwa H. 1998. Gene expression of mouse S100A3, a cysteine-rich calcium-binding protein, in developing hair follicle. J Invest Dermatol 111(5) ... 

Kam, E. and Hodgins, M. B. (1992) Communication compartments in hair follicles and their implication in differentiative control. Development 114 389-393... 

On normal skin NaOH erosions first develop at hair follicles and orifices of sweat gland ducts, usually after 4 to 5 min. They are small and circular in appearance. However, erosions on xerotic leg skin look different, they often develop along cracks in the SC, revealing the weak spots of xerotic skin. Erosion times are significantly reduced, on severely dry skin erosions develop within the first minute. 

Developments in this application of cationic surfactants follow the developments in the fabric softener field since traditionally fabric softener surfactants have been employed in hair conditioners. The use of ester-based cationics is drawing attention [68]. Again, the selection of the hydrophobe is seen to control the performance of the cationic surfactant. The conditioning performance of the ester-based cationic is excellent and, additionally, improved static control is demonstrated. This is potentially due to the improved hydration of the hair follicle as a consequence of the more polar nature of the ester-based cationics. 

Hair follicles also have calcitriol receptors and type 11 vitamin D-resistant rickets (Section 3.4.2), which is caused hy lack of calcitriol receptor function, is associated with total alopecia, suggesting that calcitriol has a role in their development. 

Biotin deficiency and the functional deficiency associated with lack of holo-carboxylase synthetase (Section 11.2.2.1), or biotinidase (Section 11.2.3.1), causes alopecia (hair loss) and a scaly erythematous dermatitis, especially around the body orifices. The dermatitis is similar to that seen in zinc and essential fatty acid deficiency and is commonly associated with Candida albicans infection. Histology of the skin shows an absence of sebaceous glands and atrophy of the hair follicles. The dermatitis is because of impaired metabolism of polyunsaturated fatty acids as a result of low activity of acetyl CoA carboxylase (Section 11.2.1.1). In biotin-deficient experimental animals, provision of supplements of long-chain 6 polyunsaturated fatty acids prevents the development of skin lesions (Mock et al., 1988a, 1988b Mock, 1991). 

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