Med Image Comput Comput Assist Interv. 2011;14(Pt 1):113-20.
Robotic hair harvesting system: a new proposal.
Lin X, et al
Abstract
Follicular Unit Extraction (FUE) has become a popular hair transplanting method for treating hair loss in male-pattern baldness. Manually harvesting hairs one by one, however, is a tedious and time-consuming job to doctors. We design an accurate hair harvesting robot with a novel and efficient end-effector which consists of one digital microscope and a punch device. The microscope is first employed to automatically localize target hairs and then guides the punch device for harvesting after shifting. The end-effector shows average bias and precision of 0.014 mm by virtue of a rotary guidance design for the motorized shifting mechanism.
Edited.
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Ned Tijdschr Geneeskd. 2011;155(45):A3768.
Scalp cooling for chemotherapy-induced alopecia.
[Article in Dutch]
Komen MM,et al
Abstract
Hair loss is a very common side effect of cytostatic therapy and is considered one of the most emotionally distressing effects.- To prevent hair loss scalp cooling is currently used in some indications in medical oncology in 59 hospitals in the Netherlands.- The success of scalp cooling depends on various factors such as type of chemotherapy, dose, infusion time, number of treatment cycles and combinations of drugs.- In general, scalp cooling is well tolerated. The reported side-effects are headache, coldness, dizziness and sometimes claustrophobia. An increase in the risk of scalp metastases has not been demonstrated. Proceeding from the South Netherlands Comprehensive Cancer Centre a national working group is put together in order to draw up a national guideline for chemotherapy-induced hair loss.
Edited for hair loss blog use.
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Waardenburg Syndrome Type I
PMID: 20301703
Jeff Mark Milunsky, MD
Co-Director, Center for Human Genetics
Director, Clinical Genetics
Associate Director, Molecular Genetics
Center for Human Genetics
Boston University School of Medicine
Summary
Disease characteristics. Waardenburg syndrome type I (WS1) is an auditory-pigmentary disorder comprising congenital sensorineural hearing loss and pigmentary disturbances of the iris, hair, and skin, along with dystopia canthorum (lateral displacement of the inner canthi). The hearing loss in WS1 observed in approximately 60% of affected individuals is congenital, typically non-progressive, either unilateral or bilateral, and sensorineural. Most commonly, hearing loss in WS1 is bilateral and profound (>100 d
. The majority of individuals with WS1 have either a white forelock or early graying of the scalp hair before age 30 years. The classic white forelock observed in approximately 45% of individuals is the most common hair pigmentation anomaly seen in WS1. Affected individuals may have complete heterochromia iridium, partial/segmental heterochromia, or hypoplastic or brilliant blue irides. Congenital leukoderma is frequently seen on the face, trunk, or limbs.
Diagnosis/testing. The diagnosis of WS1 is established by clinical findings in most individuals: sensorineural hearing loss, pigmentary changes in the hair and eyes, and dystopia canthorum identified by calculation of the W index. PAX3 is the only gene known to be associated with WS1; molecular genetic testing by sequencing and deletion/duplication analysis of the PAX3 gene detects more than 90% of disease-causing mutations. Such testing is available clinically.
Management. Treatment of manifestations: Management of the hearing loss depends on its severity.
Testing of relatives at risk: If the family-specific PAX3 mutation is known, molecular genetic testing of relatives at risk allows for early screening of those at risk for hearing loss.
Other: Folic acid supplementation in pregnancy is recommended for women at increased risk of having a child with WS1 because of possibly increased risk of neural tube defects in association with WS1.
Genetic counseling. Waardenburg syndrome type I (WS1) is inherited in an autosomal dominant manner. The majority of probands have an affected parent. A minority of probands do not have an affected parent and are presumed to have a de novo mutation. Offspring of an individual with WS1 have a 50% chance of inheriting the disease-causing mutation. Prenatal testing is possible for pregnancies at increased risk if the PAX3 mutation in the family is known.
Diagnosis
Clinical Diagnosis
Diagnostic criteria for Waardenburg syndrome type I (WS1) have been proposed by the Waardenburg Consortium [Farrer et al 1992]. An individual must have two major criteria or one major plus two minor criteria to be considered affected.
Major Criteria
•Congenital sensorineural hearing loss
•White forelock, hair hypopigmentation
•Pigmentation abnormality of the iris:
◦Complete heterochromia iridum (irides of different color)
◦Partial/segmental heterochromia (two different colors in same iris, typically brown and blue)
◦Hypoplastic blue irides, or brilliant blue irides
•Dystopia canthorum, W index >1.95 *
•Affected first-degree relative
Minor Criteria
•Skin hypopigmentation (congenital leukoderma)
•Synophrys/medial eyebrow flare
•Broad/high nasal root, prominent columella
•Hypoplastic alae nasi
•Premature gray hair (before age 30 years)
* W index: The measurements necessary to calculate the W index (in mm) are as follows: inner canthal distance (a), interpupillary distance (b), and outer canthal distance (c).
Calculate X = (2a – (0.2119c + 3.909))/c
Calculate Y = (2a – (0.2479b + 3.909))/b
Calculate W = X + Y + a/b
An abnormal W index result is greater than 1.95. Previously, a W index of greater than 2.07 was necessary to diagnose WS1 in an individual meeting all of the other diagnostic criteria. With molecular analysis, a family previously classified clinically as having WS2 based on the W index was found to have a PAX3 mutation and was reclassified as having WS1 [Tassabehji et al 1993]. Hence, the W index threshold was reduced to its current value of greater than 1.95.
Hair Loss Treatment at the Proctor Clinic
A history of Redox signaling.
Redox cell signaling is important in hair loss, hair regrowth, and in hair loss treatment.
Nat Prod Res. 2009 Sep 16:1-12
Effect of Citrullus colocynthis Schrad fruits on testosterone-induced hair loss.
Dhanotia R,.
Hair loss is a psychologically distressing phenomenon. Androgenetic alopecia (AGA) is the most common form of Hair loss, which affects millions of men and women worldwide, and is an androgen driven disorder. Here, the Citrullus colocynthis Schrad fruit is evaluated for hair regrowth activity in androgen-induced alopecia. Petroleum ether extract of C. colocynthis was applied topically for its hair regrowth-promoting activity. Alopecia was induced in albino mice by testosterone administration intramuscularly for 21 days. Its inhibition by simultaneous administration of extract was evaluated using follicular density, anagen/telogen (A/T) ratio and microscopic observation of skin sections. Finasteride (5alpha-reductase inhibitor) solution was applied topically and served as positive control. Petroleum ether extract of C. colocynthis exhibited promising hair growth-promoting activity, as reflected from follicular density, A/T ratio and skin sections. The treatment was also successful in bringing a greater number of hair follicles in anagenic phase than the standard finasteride. The result of treatment with 2 and 5% petroleum ether extracts were comparable to the positive control finasteride. The petroleum ether extract of C. colocynthis and its isolate is useful in the treatment of androgen-induced alopecia.
Arch Dermatol.1984;120:457.
Alopecia areata treated with topical minoxidil.
Weiss VC, et al
edited for hair loss blog
A minoxidil topical solution was used to treat 48 patients with hair loss due to alopecia areata, ie, 24 patients with patchy disease and 24 patients with total hair loss or alopecia universalis. Twenty-five patients had terminal hair regrowth"; in 11 of the 25 patients, it was cosmetically acceptable. No clinical features of the disease seemed to indicate the likelihood of hair regrowth. Hair regrowth began two months after start of treatment and was not uniformly well maintained after the treatment was terminated. One patient had an allergic contact dermatitis reaction to the minoxidil solution; no systemic side effects were seen. No notable systemic absorption was found in 18 adult patients. Effects on cutaneous blood flow or the immune system or some direct effect on hair follicles are possible mechanisms by which minoxidil therapy might stimulate hair regrowth.
...Studies demonstrate that loss of hair follicles involves distinct patterns of expression of active caspases. Active caspase 8, an initiator of the death receptor pathway, was predominately found in the isthmic and upper lower portion of the shaft. This pattern of expression suggests that the death receptor pathway is activated during hair regrowth and is initiated by toxic substances that bind to death receptors, i.e., TNF-alpha. Interestingly, activated caspase 3, a downstream effector caspase, was higher in catagen hair then in other phases of the hair cycle, indicating a role in the terminal stage of the apoptotic pathway. Activated caspase 1 was also found in the hair bulb and hair shaft. This study suggests an important role of the infundibular area of the hair shaft where inner and outer root sheath are abruptly changing and that this area may play a role in the regulation of normal hair apoptosis. Caspase 3 seems to be playing the key role in the apoptotic pathway during the catagen phase of the hair cycle in these areas. Finasteride may exhibit its influence by selectively inhibiting DHT, which affects a multitude of "androgen responsive genes", such as the caspase pathway, which affects programmed cell death in the hair regrwothcycle
This is Dr Proctor's paper on the relationship between uric acid and stroke. The same processes modulating hair loss also likely figure in stroke. Similarly, many agents that are effective in hair loss treatment are also effective in experimental models of stroke.
Singh G.Indian J Dermatol Venereol Leprol 2002;68:40
Androgenic alopecia ( hair loss ) genetically-determined., The exact mode of inheritance is unknown. The shortening of the anagen phase of the hair cycle leads to the consequent increase in the proportion of telogen hairs. Autosomal dominant inheritance with increased penetrance in males had been suggested, but there are reports of multifactorial inheritance as well. The role of androgen along with their interaction with genetic factors is demonstrated in men, but in women baldness is often associated with elevated levels of circulating androgens, the factor determining Pattern hair loss is how the follicles of the scalp react to the circulating androgens.
Dermatologica. 1987;175 Suppl 2:36-41.
Topical minoxidil in extensive alopecia areata, including 3-year follow-up.
Price VH.
Kaiser Permanente Medical Center, San Francisco, Calif.
Perhaps the most intriguing aspect of topical minoxidil is the fact that this drug can promote hair regrowth in two unrelated conditions: alopecia areata (AA) and androgenetic alopecia (male pattern hairloss ). snip... In androgenetic alopecia, genetically marked hair follicles undergo progressive, androgen-mediated miniaturization; antiandrogens have been conventionally sought to intercept this process. It is not known how minoxidil promotes hair regrowth except that living follicles capable of stimulation and hypertrophy are required. It may be that minoxidil influences some fundamental signal for regrowth to the follicular apparatus, ...snip... While topical minoxidil is not very effective for those with 100% scalp hair loss, it is an effective, easy and safe treatment for those with AA affecting 25-99% of the scalp.
Dermatologica. 1987;175 Suppl 2:29-35.
Immunohistochemical characterization of the cellular infiltrate in severe alopecia areata before and after minoxidil treatment.
Fiedler VC,
The mechanism of minoxidil-induced hair regrowth in the treatmen of alopecia areata hair loss (AA) is unknown. In vitro studies suggest that pharmacologic tissue levels of minoxidil may have both epithelial and T cell effects.snip...Nonresponders (that is peoe with no hair regrowth) showed none of these changes. Biopsies from 34 patients subsequently treated with oral minoxidil 5 mg q. 12 h showed no further changes in perifollicular total T, helper-inducer T or suppressor-cytotoxic T cell counts; they did, however, demonstrate significant decreases in perifollicular Langerhans cell and activated T cell counts, and nearly significant decreases in perifollicular monocyte counts. It is possible that minoxidil may be altering a presumed follicular chemoattractive stimulus to a variety of cell types. Decreases in activated T cell counts suggest the possibility of direct immunomodulatory effects of minoxidil on T cells which might contribute to a hair regrowth response in AA.
Geburtshilfe Frauenheilkd.1988;48:203
Hormonal diagnosis in so-called androgenetic alopecia (pattern hair loss) in the female
Moltz L.
Androgenetic alopecia or pattern hair loss occurs quite frequently. Up to 79% of women suffer at least temporarily from varying degrees of intermittent diffuse hair loss in the centro-parietal and/or fronto-temporal regions. A.A. is caused by an androgen excess acting on the hair follicle for prolonged periods of time in the presence of a genetic predisposition. However, often hyperandrogenemia cannot be demonstrated in such patients. 125 women with clinically typical a.A. were investigated prospectively under standardized conditions. Patient age ranged from 18 to 68 years. Atypical uterine bleeding such as menorrhagia, hypermenorrhea and polymenorrhea were found in 69 women. The hair loss varied between 50 and 400 hairs per day. Additional signs of hyperandrogenism, i.e. seborrhea, acne and hirsutism, were often observed. snip.. Treatment was directed at normalizing the disturbed estrogen-androgen-balance. Using low-dose antiandrogens, estrogens, prolactin suppressants, corticoids, iron-II-preparations as well as estrogen-containing hair lotions hair loss was arrested in 74 of 104 treated women, while regrowth of hair was accomplished in 16 patients. 14 women did not respond to therapy.
edited for use in hairloss blog
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