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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.
Clin Exp Dermatol 2003 Jan;28(1):25-7
Postmenopausal frontal fibrosing alopecia.
Recently a new entity, postmenopausal frontal fibrosing alopecia, was added to the established subtypes of scarring alopecias affecting postmenopausal women. This condition is characterized by a progressive frontal hairline recession associated with scarring. We studied the clinical and histopathologic features in four women with this disorder. Of note, a history of bilateral oophorectomy in two of them appears to be a new association. All four cases had frontoparietal recession of the hairline and two of them also had loss of their eyebrows. None of our four patients had any mucous membrane or other skin lesions. Histological examination showed perifollicular fibrosis and lymphocytic inflammation around the isthmus and infundibular areas of the follicles. No effective treatments have emerged for this type of postmenopausal alopecia, but progression of the hair loss and scarring appears to be self-limiting. We believe that this condition is a distinct clinicopathological variant of lichen planopilaris.
Clin Exp Dermatol 2002 Jul;27(5):389-5
Telogen effluvium.
The term telogen effluvium, first coined by Kligman in 1961, refers to the loss of club (telogen) hair in disease states of the follicle. Kligman's hypothesis was that whatever the cause of hair loss, the follicle tends to behave in a similar way, namely the premature termination of anagen. "The follicle is precipitated into catagen and transforms into a resting stage that mimics telogen." Ipso facto the observation of telogen hair loss does not infer a cause. To establish the cause of the hair loss, one requires a history to identify known triggers, biochemical investigations to exclude endocrine, nutritional or autoimmune aetiologies and in many cases histology to identify the earliest stages of androgenetic alopecia. The duration of the hair loss at presentation helps predict those patients in whom further investigation will have the greatest yield. "It is unfortunate that baldness has been approached with an eye toward "regrowing" or "restoring hair", and thus with a tendency toward commercialism. Locked within the metamorphosing hair follicles in the balding scalp are all the secrets of growth and differentation. Searching for these secrets should transcend the eagerness to "regrow" hair on a bald scalp, an achievement which is of no great consequence. When we know these answers, we shall have the key, not to hair growth alone, but to all growth, which is, after all, the basis of all biological phenomena." William Montagna, 1959.
Australas J Dermatol. 2003 Feb;44(1):62-6.
Androgenetic alopecia in a postmenopausal woman as a result of ovarian hyperthecosis.
A 65-year-old woman presented with an 8-year history of progressive frontotemporal alopecia and hirsutism. She had elevated serum levels of testosterone, androstenedione and estradiol. Ultrasound and computed tomography imaging suggested a right ovarian mass, while bilateral ovarian venous sampling demonstrated increased testosterone levels originating from both ovarian veins. Histology obtained following bilateral oophorectomy demonstrated bilateral ovarian hyperthecosis. Six months after surgery, the patient remains well with no progression of the alopecia. Ovarian hyperthecosis is a rare cause of androgenetic alopecia in postmenopausal women. The role of hyperthecosis and its relationship to androgenetic alopecia is reviewed.
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