References: Hair growth and hair loss
Am J Vet Res. 1977 Apr;38(4):521-4.
Clinical investigation of doxorubicin, daunomycin, and 6-thioguanine in normal cats.
Henness AM, Theilen GH, Lewis JP.
Cats frequently develop a variety of spontaneous hemolymphatic noeplasias. Long-term remissions in the nonlymphatic leukemic cat are difficult to obtain; therefore, more successful chemotherapeutic agents are sought for disease control. The purpose in the present study is to describe the clinical investigation of 3 antineoplastic drugs given to 23 normal cats. The cats tolerated doxorubican given at the dose level of 30 mg/m2 of body surface area once every 3 weeks; daunomycin, 15 to 30 mg/m2 once every 3 weeks; and 6-thioguanine, 25 mg/m2 for 5 days every 20 to 30 days.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=851285&dopt=Abstract
Am J Hum Genet. 1999 May;64(5):1323-9.
Identification of a genetic defect in the hairless gene in atrichia with papular lesions: evidence for phenotypic heterogeneity among inherited atrichias.
Sprecher E, Bergman R, Szargel R, Friedman-Birnbaum R, Cohen N.
Department of Dermatology, Rambam Medical Center, Technion-Israel Institute of Technology, Haifa 31096, Israel.
Recently, we showed that atrichia with papular lesions (APL), a rare inherited form of alopecia, is transmitted as an autosomal recessive trait in a large inbred kindred of Israeli-Arab origin. Furthermore, we mapped the APL locus to a 5-cM region of chromosome 8p12 in this family. The human "hairless" gene is a candidate target gene for the disease mutation because it maps to the APL locus and because it was recently found to be mutated in a related but clinically distinct form of alopecia known as "alopecia universalis" or "congenital alopecia." In the present study, the coding sequence of the hairless gene was compared by reverse transcription-PCR in fibroblast cell lines derived from an affected patient and an unrelated individual. We identified a single-base deletion (3434delC) in the hairless gene that cosegregated with the disease phenotype in the family. This deletion is predicted to cause a frameshift mutation in the highly conserved C-terminal part of the hairless protein, a region putatively involved in the transcription factor activity of the hairless gene product. The present results are indicative of phenotypic heterogeneity in inherited atrichias caused by mutations in the hairless gene, suggesting different roles for the regions mutated in APL and in other forms of congenital atrichia during hair development.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10205263&dopt=Abstract
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