Curly bare (cub), a new mouse mutation on chromosome 11 causing skin and hair abnormalities, and a modifier gene (mcub) on chromosome 5.

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Genomics 2003 Jan;81(1):6-14

Curly bare (cub), a new mouse mutation on chromosome 11 causing skin and hair abnormalities, and a modifier gene (mcub) on chromosome 5.

In the outcrossing of a new recessive mouse mutation causing hair loss, a new wavy-coated phenotype appeared. The two distinct phenotypes were shown to be alternative manifestations of the same gene mutation and attributable to a single modifier locus. The new mutation, curly bare (cub), was mapped to distal Chr 11 and the modifier (mcub) was mapped to Chr 5. When homozygous for the recessive mcub allele, cub/cub mice appear hairless. A single copy of the dominant Mcub allele confers a full, curly coat in cub/cub mice. Reciprocal transfer of full-thickness skin grafts between mutant and control animals showed that the skin phenotype was tissue autonomous. The hairless cub/cub mcub/mcub mice show normal contact sensitivity responses to oxazolone. The similarity of the wavy coat phenotype to those of Tgfa and Egfr mutations and the map positions of cub and mcub suggest candidate genes that interact in the EGF receptor signal transduction pathway.

Zhonghua Zheng Xing Wai Ke Za Zhi 2002 Jul;18(4):219-20

Dense-packing hair grafting technique for restoration of cicatricial alopecia

OBJECTIVE: To investigate the possibility of using dense-packing hair grafting technique for restoration of cicatricial alopecia. METHODS: Under local anesthesia, a scalp strip was harvested from the back of the head. A series of micro-grafts with 1-3 hairs and mini-grafts with 4-6 hairs were created from this strip. In the scarring recipient area, micro-slots were made with a 18 G needle for the micro-grafts and mini-slits were made with a No. 64 mini-blade for the mini-grafts. The grafts were then implanted into these holes. RESULTS: Ninety-six patients with 128 bald scarring areas, resulted from burn, trauma or infection, were treated with the above-mentioned technique from April. 1998 to February. 2000. All of the patients were satisfied with the appearance. In the micro-graft area, the graft density reached 10-15 mini-grafts/cm2 per session. In the micro-graft area, the graft density reached 16-19 micro-grafts/cm2 per session. Postoperative following-up for more than 1 year showed that the grafted hairs were growing well with 90%-95% survival of the hair. One third of the patients obtained satisfactory results with only one session. Two thirds of the patients needed the second session to improve the appearance. CONCLUSIONS: The dense-packing hair grafting technique is a simple, safe and effective method for hair restoration surgery. It is not only used for male pattern baldness, but could also be applied for restoration of cicatricial alopecia.

J Pract Nurs 2001 Winter;51(4):18-21; quiz 22-3

Can stress make you lose your hair?

Many individuals are frightened by hair loss and are hesitant to speak about it. Many are unaware that stressors can causes hair loss and that hair care practices and habits can aggravate a hair loss situation. Intervention by the nurse in encouraging a person to have an adequate assessment and work-up can facilitate an accurate diagnosis. Supportive and appropriate therapy can then be arranged. The hair tells a story and can be associated with good health.

Br J Dermatol. 2003 Mar;148(3):553-7.

Compound heterozygosity for mutations in the hairless gene causes atrichia with papular lesions.

BACKGROUND: Congenital atrichias represent a complex and heterogeneous group of genodermatoses, which have been shown in several consanguineous families to result from homozygous mutations in the hairless gene (HR). OBJECTIVES: To identify the molecular basis of congenital atrichia in a non-consanguineous family. METHODS: Genetic analysis was carried out in a two-generation family with two children with congenital atrichia and one healthy child. RESULTS: We established a diagnosis of atrichia with papular lesions based on clinical and histopathological data. We identified a heterozygous 11-bp deletion (189-199del) in the two affected children and their mother. In addition, the two affected children and their father were shown to carry a non sense mutation (Q478X), which has previously been described in a Pakistani family. Haplotype analysis revealed that mutation Q478X occurred independently in the two families. CONCLUSIONS: We have identified the first case of compound heterozygosity for mutations in HR as well as the first instance of a recurrent mutation in this gene. These data further expand our understanding of the molecular pathomechanisms underlying congenital atrichias.

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