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07/09/08 | by gohaircom [mail] | Categories: Announcements [A]

Int J Clin Exp Hypn. 2008 Jul;56(3):318-33. Links
Hypnotic approaches for alopecia areata.Willemsen R, Vanderlinden J.

Alopecia areata (AA) is an autoimmune disease leading to loss of scalp hairs. The disease seems triggered by stress. Data on the possibility of using hypnotherapy in the treatment of AA are very limited. Twenty-eight patients with extensive AA, all refractory to previous conventional treatment, were treated with hypnosis at the Academic Hospital UZ Brussel, Brussels, Belgium. This paper describes in detail the authors’ hypnotherapeutic approach combining symptom-oriented suggestions with suggestions to improve self-esteem. Twelve out of 21 patients, including 4 with total loss of scalp hair, presented a significant hair growth. All patients presented a significant decrease in scores for anxiety and depression. Although the exact mechanism of hypnotic interventions has not been elucidated, the authors’ results demonstrate that hypnotic interventions may ameliorate the clinical outcome of patients with AA and may improve their psychological well-being.

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07/09/08 | by gohaircom [mail] | Categories: Announcements [A]

Nat Med. 2008 Jul;14(7):767-72. Epub 2008 Jun 29.

Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging.

Varela I, et al

Several human progerias, including Hutchinson-Gilford progeria syndrome (HGPS),are caused by the accumulation at the nuclear envelope of farnesylated forms of truncated prelamin A, a protein that is also altered during normal aging. Previous studies in cells from individuals with HGPS have shown that farnesyltransferase inhibitors (FTIs) improve nuclear abnormalities associated
with prelamin A accumulation, suggesting that these compounds could represent a therapeutic approach for this devastating progeroid syndrome. We show herein that both prelamin A and its truncated form progerin/LADelta50 undergo alternative prenylation by geranylgeranyltransferase in the setting of farnesyltransferase
inhibition, which could explain the low efficiency of FTIs in ameliorating the phenotypes of progeroid mouse models. We also show that a combination of statins and aminobisphosphonates efficiently inhibits both farnesylation and geranylgeranylation of progerin and prelamin A and markedly improves the aging-like phenotypes of mice deficient in the metalloproteinase Zmpste24, including growth retardation, loss of weight, lipodystrophy, hair loss and bone
defects. Likewise, the longevity of these mice is substantially extended. These findings open a new therapeutic approach for human progeroid syndromes associated with nuclear-envelope abnormalities.

Prelamin A farnesylation and progeroid syndromes. [J Biol Chem. 2006]

Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes. [Proc Natl Acad Sci U S A. 2005] PMID:16129834

Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation. [Proc Natl Acad Sci U S A. 2005] PMID:16014412

Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome. [Proc Natl Acad Sci U S A. 2005]

A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation. [J Clin Invest. 2006]

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06/29/08 | by gohaircom [mail] | Categories: Announcements [A]

Exp Dermatol. 2008 Jul;17(7):630-1.

17-beta estradiol and prednisolone as potential stimulators of hair re-growth in
chemotherapy-induced human hair follicle damage via ‘dystrophic catagen’
promotion?

Bodó E, van Beek N, Naumann V, Ohnemus U, Brzoska T, Abels C, Paus R.

Department of Dermatology, University of Lübeck, Lübeck, Germany.

Chemotherapy-induced hair follicle (HF) damage and alopecia are common
side-effects of cancer therapy and constitute a major burden of disease in
clinical oncology. Although several potential treatment strategies have shown
promising effects in animal models, e.g. on cyclophosphamide-induced alopecia
(CIA) in C57BL/6 mice, these strategies remain to be transferred to human
therapy. 17-beta estradiol (E2) and glucocorticoids are potent modulators of
murine CIA in vivo: topical treatment accelerates the regrowth of normally
pigmented hair shafts by shifting HFs into the ‘dystrophic catagen’ pathway,
which is associated with greater initial alopecia, but much faster HF recovery.
In the current study, we asked whether E2 and/or prednisolon display similar
activities in the human system, using our recently established human HF dystrophy
in vitro-model (Bodó et al., Am J Pathol 2007: 171(14):1153-67). E2 and/or
prednisolon were pre- and co-administered with a key cyclophosphamide metabolite
(4-HC). Indeed, E2 shifted 4-HC-treated human HFs into the dystrophic catagen
pathway in vitro, and potentiated the 4-HC-induced pigmentary disturbances.
4-HC-induced hair growth inhibition was further enhanced by E2, associated with
an additional reduction of proliferation and increased apoptosis of matrix
keratinocytes. These effects tended to be further enhanced by co-administration
of prednisolon to the HF organ culture medium. These observations suggest that,
just as in murine CIA in vivo, E2 and glucocorticoids can force
chemotherapy-damaged human HFs into the dystrophic catagen pathway. The
preclinical data provide first indications that a combination of E2 with
prednisolone may indeed serve as an effective clinical tool for accelerating hair
re-growth in human CIA.

PMID: 18559008 [PubMed - in process]

Related Links

Topical estrogen accelerates hair regrowth in mice after chemotherapy-induced
alopecia by favoring the dystrophic catagen response pathway to damage. [J Invest
Dermatol. 2004] PMID:14962083

Dissecting the impact of chemotherapy on the human hair follicle: a pragmatic in
vitro assay for studying the pathogenesis and potential management of hair
follicle dystrophy. [Am J Pathol. 2007] PMID:17823286

Zinc as an ambivalent but potent modulator of murine hair growth in vivo-
preliminary observations. [Exp Dermatol. 2005] PMID:16232307

A new strategy for modulating chemotherapy-induced alopecia, using PTH/PTHrP
receptor agonist and antagonist. [J Invest Dermatol. 2001] PMID:11511291

Hair growth modulation by topical immunophilin ligands: induction of anagen,
inhibition of massive catagen development, and relative protection from
chemotherapy-induced alopecia. [Am J Pathol. 1997] PMID:9094998

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Treatment for hair loss

06/27/08 | by gohaircom [mail] | Categories: Announcements [A]

Biol Pharm Bull. 2008 Mar;31(3):449-53.

trans-3,4′-Dimethyl-3-hydroxyflavanone, a hair growth enhancing active component,
decreases active transforming growth factor beta2 (TGF-beta2) through control of
urokinase-type plasminogen activator (uPA) on the surface of keratinocytes.

Sasajima M, Moriwaki S, Hotta M, Kitahara T, Takema Y.

Global R&D, Biological Science, Kao Corporation, 2606 Akabane, Ichikaimachi,
Haga, Tochigi 321-3497, Japan. sasajima.michiyo@kao.co.jp

trans-3,4′-Dimethyl-3-hydroxyflavanone (t-flavanone) is a synthetic compound with
hair growth enhancing activity that is effective against male pattern alopecia.
t-Flavanone was designed as a derivative of astilbin, the active hair growth
enhancing component of Hypericum perforatum extracts. This study was designed to
elucidate the mechanism of hair growth enhancement by t-flavanone. We
investigated the effects of t-flavanone on transforming growth factor beta
(TGF-beta), a known catagen-inducing factor induced in hair papilla cells by male
hormone. When t-flavanone was added to cocultures of human hair papilla cells and
human keratinocytes, there was no change in the total level of TGF-beta2.
However, levels of active TGF-beta2 were reduced, suggesting the involvement of
t-flavanone in the activation pathway of TGF-beta2. In order to investigate the
effects of t-flavanone on TGF-beta2 activation by human keratinocytes, we
evaluated the level of active TGF-beta2 converted from the inactive form in
t-flavanone-treated human keratinocytes. The amount of active TGF-beta2 was
reduced compared with controls suggesting that t-flavanone suppresses the
TGF-beta2 activation cascade in human keratinocytes. We then examined the
activity of urokinase-type plasminogen activator (uPA), the rate-limiting enzyme
in the TGF-beta2 activation cascade, in t-flavanone-treated human keratinocytes.
We found that t-flavanone reduces uPA activity on the keratinocyte surface.
t-Flavanone is a hair growth enhancing component that has a novel mechanism of
action which suppresses TGF-beta2 activation, and thereby is expected to have
therapeutic effects on other types of alopecia in addition to male pattern
alopecia.

PMID: 18310908 [PubMed - indexed for MEDLINE]

Related Links

Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans
retinoic acid induces premature hair follicle regression (catagen) by
upregulation of transforming growth factor-beta2 in the dermal papilla. [J Invest
Dermatol. 2005] PMID:15955085

Role of TGF-beta2 in the human hair cycle. [J Dermatol Sci. 2004] PMID:15194142

Androgen-inducible TGF-beta1 from balding dermal papilla cells inhibits
epithelial cell growth: a clue to understand paradoxical effects of androgen on
human hair growth. [FASEB J. 2002] PMID:12397096

L-carnitine-L-tartrate promotes human hair growth in vitro. [Exp Dermatol. 2007]
PMID:17927577

Enhanced production of plasminogen activator activity in human and murine
keratinocytes by transforming growth factor-beta 1. [J Invest Dermatol. 1992]
PMID:1629632

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Tricotillomania as a cause of hair loss

06/27/08 | by gohaircom [mail] | Categories: Announcements [A]

Dermatol Ther. 2008 Jan-Feb;21(1):13-21.

Trichotillomania.

Sah DE, Koo J, Price VH.

Department of Dermatology, University of Calfornia, San Francisco, California
94143, USA.

Patients with trichotillomania often first present to dermatologists, as patients
may be unaware of or deny hair pulling and seek an etiology for their hair loss.
It therefore becomes the job of the dermatologist to correctly diagnose
trichotillomania as well as offer treatment options. There appear to be three
groups characterized by age of onset: preschool-age children, preadolescents to
young adults, and adults. Young children often have a self-limited course of hair
pulling. Adults frequently have psychiatric conditions associated with their
trichotillomania. Preadolescents to young adults may benefit the most from active
intervention, such as increasing awareness of hair pulling behaviors and behavior
modification training. The approach of a patient by age of onset is helpful in
guiding a dermatologist towards effective treatment options.

PMID: 18318881 [PubMed - indexed for MEDLINE]

Related Links

Diagnosis and management of trichotillomania in children and adolescents.
[Paediatr Drugs. 2005] PMID:16356024

[Trichotillomania: three cases presentation and diagnosis tests review] [Invest
Clin. 2007] PMID:17853795

Trichotillomania and self-esteem: a survey of 62 female hair pullers. [J Clin
Psychiatry. 1996] PMID:8591973

Under-diagnosed psychiatric syndrome. I: Trichotillomania. [Ann Acad Med
Singapore. 1999] PMID:10497682

Trichotillomania. Presentation, etiology, diagnosis and therapy. [Am J Clin
Dermatol. 2001] PMID:11721651

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