Archive for the ‘Uncategorized’ Category

Hairloss treatment

Monday, September 6th, 2010

Hair loss treatment at the Proctor clinic.

Hair loss treatment and hair regrowth formulations.

interferon signature in the scalp lesions of hair loss due to alopecia areata

Monday, August 23rd, 2010

Br J Dermatol. 2010 Jul;163(1):57-62.

Type 1 interferon signature in the scalp lesions of hair loss due to alopecia areata.
Ghoreishi M, et al

Abstract
BACKGROUND: Autoimmune attack of the bulbar region of anagen phase hair follicles by CD8+ T cells and Th1 cytokines has been proposed to result in hair loss in alopecia areata (AA). The initiating stimuli are unknown. As interferon-alpha therapy may trigger AA, we propose that type 1 interferons are involved in the induction of disease.

OBJECTIVES: To compare lesional scalp from patients with AA with scalp lesions of cutaneous diseases associated with local type 1 interferon-related protein expression.

METHODS: Lesional scalp of patients with AA, discoid lupus erythematosus, lichen planopilaris and androgenetic alopecia ( male pattern hair loss ) was examined by immunohistochemistry for expression of the type 1 interferon-inducible myxovirus protein A (MxA), the chemokine receptor CXCR3, and the cytotoxic proteins granzyme B (GrB) and T-cell intracytoplasmic antigen 1 (TiA-1).

RESULTS: MxA was expressed in the intradermal and subcutaneous compartments of the hair follicle including sebaceous glands in inflammatory AA similar to lesions of cicatricial alopecia (discoid lupus erythematosus, lichen planopilaris) but not in the epidermal compartment of AA, and not at all in noninflammatory AA or androgenetic alopecia. The location of CXCR3-expressing cells correlated with MxA expression. The inflammatory cells around the hair follicle in AA included a lower number of GrB+ and TiA-1+ cells compared with cicatricial alopecia and demonstrated predominant TiA-1+ expression.

CONCLUSIONS: We demonstrate the expression of type 1 interferon-related proteins in the inflammatory lesions of hair loss due to AA. The distribution pattern of the interferon signature and cytotoxicity-associated proteins in AA differs from cicatricial alopecia.

edited for hair loss treatment blog

Hair Loss Treatment at the Proctor Clinic

Friday, July 9th, 2010

Hair Loss Treatment at the Proctor Clinic

Hair loss treatment with melatonin

Thursday, July 8th, 2010

Can Vet J. 2009; 50(5): 511–514.

“… To increase hair regrowth, melatonin was prescribed in association with shampoo therapy, as described in previous studies on dogs with alopecia X, recurrent flank alopecia, and pattern baldness. Administration of melatonin was suspended after 3 mo, when no improvement in overall hair regrowth was noted. However, the secondary bacterial infections and pruritus were effectively controlled with the biweekly shampoo therapy….”

Hair loss hair loss treatment

Chemotherapy-induced hair loss

Tuesday, January 26th, 2010

Cell Stress Chaperones. 2008;13:31

Prevention of chemotherapy-induced alopecia in rodent models.
Jimenez JJ, et al

…..Next, we tested whether the same protective mechanism could also mitigate or suppress the alopecic effects of anthracyclines, alkylating agents, and taxanes. Groups of (typically four) animals were subjected to heat treatment to the nape of the neck or were not heat-treated. After a delay of 7 h, the groups were administered alopecia-causing doses of cyclophosphamide or a combination of cyclophosphamide and adriamycin. Because no alopecia-causing, sublethal i.p. dose of taxol could be identified, amounts sufficient to cause local hair loss were injected s.c. in the region that had previously been subjected to heat treatment. Results summarized in Table 2 indicated that hair in heat-treated areas was effectively protected against the latter antineoplastic agents. No protection was observed in unheated, drug-exposed animals. Subcutaneous injection of GA also prevented hair loss caused by cyclophosphamide and taxol. Following standard practice in the field, we had observed and recorded protective effects at the time animals had lost most of their body hair, which occurred about 1 week after exposure to chemotherapeutic agents. Anticipating a potential future use of the same preventative method in human patients, we investigated whether the observed protective effects were long-lasting. We followed-up heat-preconditioned, chemotherapeutic drug-treated (etoposide, cyclophosphamide, or cyclophosphamide/adriamycin) animals for longer periods, in some cases, until they had acquired a new fur coat about 3 weeks after chemotherapy. We observed that a majority of animals, and in some groups, all animals exposed to 48–48.5°C heat for 20 min retained their patches of protected hair. However, at lower heat doses, animals tended to gradually lose their patches.

Edited for Hair regrowth blog use.

Antiandrogens for hair loss treatment

Wednesday, December 30th, 2009

J Steroid Biochem.1986;25:885

Edited for hair loss treatment blog

Pharmacology of antiandrogens.
Neumann F, Töpert M.

Principally, antiandrogens affect all androgen-dependent organs and functions as for instance accessory sexual glands, spermatogenesis, skin and skin appendages, libido and potency, male sexual differentiation, longitudinal bone growth and bone maturation. Pharmacologically, it is important to distinguish between the steroidal antiandrogens of the cyproterone acetate type and the nonsteroidal pure antiandrogens. For the clinical use of cyproterone acetate and similar antiandrogens in both men and women the three main properties are important: Cyproterone acetate is antiandrogenic, it is a quite potent progestogen and it is antigonadotrophic. Based on pharmacological and biochemical backgrounds cyproterone acetate is used in the following indications: Androgen mediated disorders of the skin such as acne, seborrhoea, hirsutism, hair loss treatment, prostatic carcinoma, precocious puberty and male hypersexuality. In order to avoid undesired systemic side effects local application of antiandrogens, e.g. of cyproterone acetate, has been tried several times.snip.. 17 alpha-propylmesterolone is active when given topically (hamster ear model) and has no systemic antiandrogenic effects. This antiandrogen is highly lipophilic and does penetrate preferentially through the hair follicle as has been shown by autoradiography.

The hair regrowth cycle

Wednesday, December 2nd, 2009

“..Recent reports have shown that apoptosis contributes to the hair cycle of regrowth and loss. It is now firmly established that apoptosis is regulated by an intracellular proteolytic cascade, primarily mediated by members of the caspase family of cysteine proteases, which cleave one another and various key intracellular target proteins to destroy the cell. Two prototypical signalling pathways for the induction of apoptosis have been described. One pathway involves ligation of death receptors that activate procaspase 8 and possibly other initiator caspases. The other pathway is controlled by the mitochondrion and involves the apoptosis protease inducing factor-1. Once activated by cytochrome c,, together with cofactor nucleotide triphosphates, they then bind and activate procaspase 9, which in turn cleaves and activates caspase 3 and other downstream caspases. Therefore, caspase 8 and 9 represent the pinnical caspases in the death receptors and cytochrome c/Apap-1 pathways respectively….”

incomplete hair regrowth in bone marrow transplants

Tuesday, November 24th, 2009

Bone Marrow Transplant. 1991 Jan;7(1):43-7.

Busulphan/cyclophosphamide conditioning for bone marrow transplantation may lead to failure of hair regrowth.
Baker BW, et al

Following the introduction of bulsulphan and cyclophosphamide, patients noted incomplete scalp hair regrowth following bone marrow transplantation (BMT). snip.. Six patients had experienced incomplete hair regrowth of varying severity 7-27 months following BMT. snip.. None of the patients had evidence of graft-versus-host disease. No laboratory test abnormalities distinguished the affected from the unaffected patients. … our.. results suggest that BUCY has caused permanent damage to the hair follicles of the affected patients. Prolonged hair loss may markedly impair the quality of life for long-term survivors of BMT and this unexpected complication also has significant medicolegal implications.

Hair loss blog

Sunday, November 15th, 2009

Hair regrowth blog

Dr Proctor treats hair loss

Hair loss regrowth

Tuesday, November 10th, 2009

hair loss regrowth

Dr Proctor treats hair loss

Hair care tips

Sunday, November 8th, 2009

Hair tips:

“If hair is healthy and plentiful, there’s no reason to chop it into a conservative crop just to make it more age-appropriate,” says Thom Priano, a hairstylist at Garren New York in New York City. Even as they move into their 40s and 50s, plenty of women still look better with long hair.

Instead: If you do go short, keep it slightly shaggy — think Sharon Stone’s crop. You’ll look more modern, and the maintenance will be easier without blunt lines. “You should soften things up as you get older,” says Jason Stanton, a hairstylist in Los Angeles and London. Use a pomade on the ends (more will be too slick) to give your cropped cut shine. ” article of MSN

A hereditary cause of hair loss

Wednesday, November 4th, 2009

Can Med Assoc J. 1979 Aug 18;121(4):428-30, 433-4.

Familial hypogonadotropic hypogonadism with hair loss.
Slti IS, Salem Z.

In one family several male and female members had hypogonadism and frontoparietal hair loss, whereas other members with normal sexual development had normal scalp hair. Clinical and laboratory evaluation of three affected young men (two brothers and their cousin) revealed that the hypogonadism was the result of decreased serum concentrations of follicle stimulating and luteinizing hormones. There was no evidence of a deficiency of any other pituitary hormone. snip…

Hair Loss Treatment Clinic

Thursday, October 29th, 2009

Hair loss treatment at the Proctor clinic.

Male pattern hair loss

Tuesday, October 27th, 2009

edited for hair loss blog

Hair follicle in normal scalp and male pattern hair loss.
The number of cell nuclei in the matrix and the papilla of balding scalp was found to be 30% and 50% smaller, respectively, than those of normal scalp. Finally, a morphometric study revealed enlarged nuclei in the matrix and papilla, as shown by their increased areas, perimeters, and maximal diameters.

hair loss blog

Dendritic cells in hair loss due to alopecia areata

Friday, October 23rd, 2009

Dermatologica. 1985;171(5):327

Increased number of OKT6-positive dendritic cells in the hair follicles of patients with alopecia areata.

Kohchiyama A, et al

edited
In 6 patients with untreated hair loss secondary to alopecia areata in the progressive stage, 6 in the stationary stage, and 6 normal individuals as controls, an in situ analysis of OKT6-positive dendritic cells in hair follicles, and peribulbar and intrabulbar infiltrates was performed using the avidin-biotin-peroxidase method with monoclonal antibodies. …snip… This indicates that the number of OKT6-positive dendritic cells increases in the hair follicles of progressive alopecia areata and that these cells may play an important role in cooperation with T cells in the pathogenesis of alopecia areata.

Protection against radiation-induced hair loss

Wednesday, October 21st, 2009

Cancer Res. 1982;42(5):1888

Protective effects of S-2-(3-aminopropylamino)ethylphosphorothioic acid against radiation damage of normal tissues and a fibrosarcoma in mice.Milas L, Hunter N, Reid BO, Thames HD Jr.

S-2-(3-Aminopropylamino)ethylphosphorothioic acid (WR-2721) was investigated for its protective effect against radiation-produced damage of jejunum, testis, lung, hair follicles, and a fibrosarcoma of C3Hf/Kam mice. Most of these tissues were radioprotected, and the degree of radioprotection depended on the dose of WR-2721 and the time interval between administration of WR-2721 and radiation treatment. WR-2721 increased resistance of jejunal epithelial cells and spermatogenic cells to single doses of gamma-rays by factors of 1.64 and 1.54, respectively. Protection against hair loss was less pronounced; the dose-modifying factor here was 1.24. ..snip..

edited

hair loss blog

A hairloss mutant in Rats

Tuesday, October 20th, 2009

J Hered. 1976;67(5):284

Fuzzy, a hypotrichotic mutant in linkage group I of the Norway rat.

Palm J, Ferguson FG.

A new recessive hypotrichosis gene in the rat designated fuzzy (fz) is described. Fuzzy is linked to albino (c) in linkage group I with a 18.13 +/- 3.05 percent recombination. After an initial sparse hair coat, the fuzzy animals rapidly become devoid of hair. Histologically the skin of these animals has poorly developed, and often cystic hair follicles that contain accumulations of keratinacious material.

Loose anagen hair

Thursday, October 15th, 2009

Arch Dermatol. 1997 Sep;133(9):1089-93.

Loose anagen hair.

Tosti A, et al

OBJECTIVE: To review clinical and pathologic features and the long-term follow-up of patients with loose anagen hair (LAH). DESIGN: Clinical evaluation and long-term follow-up. … snip…. RESULTS: In 4 children and 1 adult the condition remained stable; in 2 children and 1 adult, a considerable improvement in hair density was noticed. The pathologic study of hair from 5 patients did not reveal morphological abnormalities of the hair follicles except for a high incidence of fragmentations of the inner root sheath. CONCLUSIONS: Analysis of our patients with LAH reveals that the condition does not develop exclusively during childhood but can occasionally manifest itself later in life. The development of LAH may be sporadic, occur in association with developmental or acquired conditions, or, less commonly, be a familial disorder. While adult-onset LAH may not be exceptional, it can be easily misdiagnosed as telogen hair loss. The pathologic findings of LAH do not demonstrate any specific features and are of little value in the diagnosis of this condition.

Antiandrogens in hirsuitism

Monday, October 12th, 2009

Fertil Steril. 1994 Feb;61(2):281-7.Links

Comparison of flutamide and spironolactone in the treatment of hirsutism: a randomized controlled trial.
Cusan L, et al

OBJECTIVE: To compare the clinical efficacy and safety of the pure antiandrogen flutamide and the steroidal derivative spironolactone in the treatment of hirsutism in women. DESIGN: Fifty-three premenopausal women suffering from moderate to severe hirsutism were randomized into two groups and received either flutamide or spironolactone in association with a triphasic oral contraceptive (OC) pill. Hirsutism, acne, seborrhea, alopecia, and side effects were monitored monthly for a treatment period of 9 months and a follow-up after treatment period of 6 months. Blood samples were taken at each visit for assessment of endocrine, biochemical, and hematologic parameters. RESULTS: After only 6 months of therapy, flutamide caused a maximal reduction in the hirsutism score to a value within almost normal range; during the same period, spironolactone caused only a 30% reduction of the hirsutism score. Whereas flutamide caused a dramatic (80%) decrease in total acne, seborrhea, and hair loss score after only 3 months of therapy, spironolactone caused only a 50% reduction in acne and seborrhea, with no significant effect on the hair loss score. Four patients in the spironolactone group but only one in the flutamide group stopped the medication because of adverse side effects. CONCLUSION: The present data obtained in a randomized prospective study clearly demonstrate that the pure antiandrogen flutamide is superior to spironolactone in the treatment of female hirsutism and its related androgen-dependent symptoms and signs in women.

hair loss blog

An in vitro model for the study of human hair growth

Friday, October 9th, 2009

Ann N Y Acad Sci. 1991 Dec 26;642:148-64; discussion 164-6.

An in vitro model for the study of human hair growth.
Philpott MP, et al

Human anagen hair follicles were isolated by microdissection from human scalp skin. Isolation of the hair follicles was achieved by cutting the follicle at the dermosubcutaneous fat interface using a scalpel blade. Intact hair follicles were then removed from the fat using watch makers’ forceps. Isolated hair follicles maintained free floating in supplemented Williams E medium in individual wells of 24-well multiwell plates showed a significant increase in length over 4 days. The increase in length was seen to be attributed to the production of a keratinized hair shaft, and was not associated with the loss of hair follicle morphology. [Methyl-3H]thymidine autoradiography confirmed that in vitro the in vivo pattern of DNA synthesis was maintained; furthermore, [35S]methionine labeling of keratins showed that their patterns of synthesis did not change with maintenance. Serum was found to inhibit hair follicle regrowth in vitro; and when follicles were maintained in serum-free medium, they grew for up to 10 days, suggesting that in vitro the hair follicles are able to regulate their own growth, possibly by the production of relevant growth factors. This may prove useful in identifying the autocrine/paracrine mechanisms that operate in the hair follicle. The importance of this model to hair follicle biology is further demonstrated by the observations that TGF-beta 1 has a negative growth regulatory effect on hair follicles in vitro and that EGF and its other receptor ligand TGF-alpha mimic the in vivo depilatory effects of EGF that have been reported for sheep and mice.