References: Hair growth and hair loss
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In this study the optic nerve changes in zinc (Zn)-deficient rats are examined. Zinc is one of the essential trace elements and is known to be related to optic nerve diseases such as ethambutol neuropathy. However, the effect of Zn on the optic nerve has not been studied experimentally in animals. We used 3 week old weanling male Wistar Kyoto rats weighing 40-50 g. Rats were fed a Zn-deficient diet containing 0.007 mg of Zn per 100 g, all other nutrients and distilled and deionized water. The same water supplemented with 3 mg Zn per 100 g was given to the control group. After 4 or 7 weeks on a Zn-deficient diet, the optic nerve was examined with an electron microscope. A recovery group was fed a Zn-containing diet for 5 weeks after 7 weeks on the Zn-deficient diet. The serum Zn levels of the deficient group were significantly decreased at both 4 and 7 weeks. Most of the Zn-deficient rats showed hair loss around the eyes and on the extremities. Ultrastructural findings were as follows. The number of myelinated axons of Zn-deficient rats at 4 and 7 weeks were significantly decreased and the myelin sheaths were significantly thinner in the Zn-deficient groups and in the recovery group. Unmyelinated axons were more numerous than in the control rats. Destruction of myelin and proliferation of glial cells were found in the optic nerves of Zn-deficient rats. This study suggests that the optic nerve needs Zn for the maintenance of its cell structure and even if Zn is supplied to the Zn-deficient rats, destruction of the myelin structure may continue. Zn-deficiency induce a decrease of myelinated nerve fibers, and it is thought that optic neuropathy in patients treated with some drugs such as ethambutol may be a secondary change due to Zn-deficiency following drug administration.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11273664&dopt=Abstract
Plast Reconstr Surg. 1997 Jul;100(1):257-61.
Sideburn reconstruction with an expanded supraauricular trapezoidal flap.
Giraldo F, Gonzalez C, Garnica I, Ferron M, Rus JA.
Plastic and Reconstructive Surgery Unit, Regional Hospital Carlos Haya, Malaga, Spain.
Although loss of the sideburn and temporal scalp with subsequent alopecia is relatively frequent as a consequence of traumatic, surgical, and iatrogenic processes, not many techniques of sideburn reconstruction have been reported. We present a two-stage technique to correct the long-sideburns when there is an associated temporal alopecic defect due to trauma or surgery by means of an expanded supra-auricular trapezoidal flap. The method can achieve not only a satisfactory appearance of the sideburn but also a normal capillary line from the occipital to the frontal region.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9207684&dopt=Abstract
Am J Med Genet. 1997 Jul 11;71(1):80-6.
The gene for autosomal dominant hidrotic ectodermal dysplasia (Clouston syndrome) in a large Indian family maps to the 13q11-q12.1 pericentromeric region.
Radhakrishna U, Blouin JL, Mehenni H, Mehta TY, Sheth FJ, Sheth JJ, Solanki JV, Antonarakis SE.
Department of Genetics and Microbiology, Geneva Medical School, Cantonal Hospital, Switzerland.
Hidrotic ectodermal dysplasia (HED), Clouston syndrome (MIM No. 129500), is an autosomal dominant disorder affecting the skin and its derivatives. It is characterized by alopecia, dysplastic nails in hands and feet, and hyperkeratosis of the palms and soles. We have studied a large Indian pedigree (UR005), from Gujarat region, consisting of a total 127 individuals including 41 affected (12 males and 29 females). The phenotype in this family ranged from atrichosis to hypotrichosis, sparsity or absence of eyebrows, and thickening of palms and soles. In order to map the disease locus by linkage analysis, DNA polymorphisms were used in DNAs from 23 affected and 8 normal individuals. While genotyping was in progress, Kibar et al. [1996] reported mapping of the locus of a similar disease in French-Canadian families to 13q around marker D13S141. We then utilized markers on 13q to genotype the members of the Indian family. Linkage with 13q11-12.1 markers was confirmed with a maximum lod score of 3.27 (theta=0.00) with locus D13S1316. Multipoint linkage analysis yielded a lod score of 5.04 at theta=0.00 with D13S1316; haplotype analysis indicated that the gene for the Clouston syndrome in this family is localized proximal to D13S292. These data suggest that the gene for the Clouston syndrome in this Indian pedigree is probably the same as that described in the French Canadian families. The combination of data from all available families linked to 13q11-12.1 will make it possible to narrow the critical region and facilitate the positional cloning of the elusive gene.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9215774&dopt=Abstract
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