Abstracts from the 2007 European Hair Research Society Conf

[harold]

Wow I have been waiting a loooooong time for this to come out.
There were many verry interesting tidbits from the 2006 Conference which have only just been published in journals.
But we could find out about them early from looking at the list of abstracts of speakers and poster presentations etc
Stuff like the whole caffeine inhibition, DKKF in response to DHT and the ROS link were first seeen here.
Anyway I havent had time to look at it yet. The hosts were Shapiro and Cotsarelis apparently.
Here is the link - enjoy.
hh
http://www.nahrsmembers.org/home/Portal ... ristol.pdf

 

[Matt27]

Re: Abstractys from the 2007 European Hair Research Society Conf

Awesome file....here's a direct Follica reference:

"The mammalian hair follicle is a complex “miniorganâ€￾ thought to form only during development; loss of an adult
follicle is considered permanent. Here we show that, after wounding, hair follicles form de novo in genetically normal
adult animals. The regenerated hair follicles establish a stem cell population, express known molecular markers of
follicle differentiation, produce a hair shaft, and progress through all stages of the hair follicle cycle. Lineage analysis
demonstrated that the nascent follicles arise from epithelial cells outside of the hair follicle stem cell niche, suggesting
that epidermal cells surrounding the wound assume a hair follicle stem cell phenotype. Inhibition of Wnt signaling
after reepithelialization completely abrogates this wounding induced folliculogenesis, while overexpression of Wnt ligand
in the epidermis increases the number of regenerated hair follicles. These remarkable regenerative capabilities
of the adult support the notion that wounding induces an embryonic phenotype in skin, and that this provides
a window for manipulation of hair follicle neogenesis by Wnts. These findings suggest novel treatments for wounds,
hair loss and other degenerative skin disorders."

 

[FollicaLover]

Re: Abstractys from the 2007 European Hair Research Society Conf

Great!!, thank you Harold...

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

OK first abstract I'm gonna post.
I dont know if the licorice extract those guys were thinking of using contains this compound but maybe topical licorice is not the best idea...
hh

Epilatory Effect of Glycyrrhizic Acid
Zaper, Julijana;1 Kakadjanova, Aina;1 Pfeffer, Jeannette;1
Kippenberger, Stefan;1 Bereiter-Hahn, Juergen;2 Kaufmann,
Roland;1 Bernd, August;1
1. J.W. Goethe University, Dept. of Dermatology, Frankfurt/
M., Germany; 2. J.W. Goethe University, Dept. of Zoology,
Frankfurt/M., Germany
Hypertrichosis, hirsutism and giant hairy nevus are well
known examples of abnormal hair growth with some
risk of a significant negative impact on the psychosocial
development of affected people. So far, all known methods
for hair removal are more or less effective and show
partly considerable side effects like pain, skin irritation,
contact eczema, folliculitis, and hyper-pigmentation. In
co-operation with a study group of Turkmenistan we found
a new principle of painless and rapid hair removal based on
liquorice, a commonly used herbal extract of the traditional
Asian medicine. In the meantime we defined the liquorice
compound glycyrrhizic acid to be responsible for the
epilatory effect. We dissolved 15% glycyrrhizic acid in an
aqueous solution containing 10% urea and 20% ethanol
and treated wistar rats in the neck region twice a day.
After 3 days first indications for hair loss became visible.
After 6-12 days the treated skin was nearly free of hairs
without any sign of skin irritation. Even after a periodically
long term treatment over one year no abnormality of the
skin surface was visible, but a permanent reduction in
re-growing hair quantity by more than 50%. Based on
these findings Glycyrrhizic acid is a candidate molecule
for the development of a powerful agent for painless and
permanent hair removal.

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

Prostaglandin synthesis in hair follicles - more PGE2 synthase in female hair.
Still waiting to see Cotsarelis's report on the whole thing...
hh

Prostaglandin Metabolism in Hair Follicle: PGE2
and PGF2alpha Synthesis and Interconversion
Colombe, Laurent; Vindrios, A.; Michelet, J. F.; Bernard, B A.;
L’Oreal Recherche, Clichy, France
Prostaglandins regulate a wide number of physiological
functions. Recently PGF2a ananalogue such as latanoprost
was shown to have a real impact on hair regrowth. The aim
of this study was to investigate and describe the expression
profile in human hair follicle of prostaglandin (PG)
metabolism key enzymes, i.e. Carbonyl reductase-1 (CBR1),
microsomal Prostaglandin E synthase-1 (mPGES-1) and
microsomal Prostaglandin E synthase-2 (mPGES-2), cytosolic
Prostaglandin E synthase (cPGES), the aldoketoreductase
AKR1C1 and the Prostaglandin F synthase AKR1C3.
Quantitative RT-PCR evidenced i) the expression of all
these enzymes in plucked hair follicles and ii) a higher
expression of mPGES-2 and AKR1C3 in female hair follicles.
Using Western blot, PGE2 and PGF2 ELISA assays and
immunohistochemistry, we observed that most of hair
follicle cell types were able to produce PGE2 and/or PGF2a
and synthesized all PG metabolism enzymes. Moreover,
a specific distribution in hair follicle was noted for each of
these enzymes. These results demonstrated that an active
but intricate prostaglandin metabolism could take place in
human hair follicle, mainly oriented towards PGE2 synthesis
and concentrated in the bulb, including dermal papilla,
matrix and keratogenous area. Local production of PGF2a
might equally rely on PGE2 conversion and direct synthesis
through AKR1C3/PGFS.

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

Not only does DHT trigger the production of tgf-beta1 but tgf-beta -1 can in turn make the androgen receptor more sensitive. A potentially vicious cycle.

Novel Function of TGFb1 as a Key
Pathogenic Molecule in Androgenetic
Alopecia: Potentiation of Androgen
Receptor Through Smad3
Inui, Shigeki; Nakajima, Takeshi; Itami, Satoshi; Dept. of
Regenerative Dermatology, Osaka University School of
Medicine, Suitashi, Japan
We have reported the pathogenic role of TGF-b1 production
and activation by androgen in balding dermal papilla cells
(bald DPCs) using the coculture system of bald DPCs and
keratinocytes. Here, we examined the effect of TGF-b1
on androgen receptor (AR) transactivation by transient
transfection assays of MMTV-luciferase reporter vector.
TGF-b1 at 0.2 and 2.0ng/ml increased AR transactivation
to 2.5- and 2.7-fold, respectively. Because expression
of ARA55, one of AR coactivators, is increased by TGFb1,
we tested the possibility that TGF-b1 potentiates AR
through ARA55 by using dominant negative C-terminal
fragment ARA55. Rather, the dominant negative ARA55
augmented TGF-b1 (2.0ng/ml) effect on AR up to 5.1-fold.
When exogenous ARA55 was overexpressed in bald DPCs,
TGF-b1 increased AR activity only to 1.5-fold. Therefore,
we suggest that ARA55 constitutively coactivates AR but
paradoxically interferes TGF-b1 augmentation for AR. Next,
we examined whether Smad3 can mediate the signal from
TGF-b1 to AR by reporter assays. The silencing for Smad3 by
siRNA in bald DPCs reversed completely TGF-b1 potentiation
of AR, demonstrating that this signal is dependent on
Smad3. Together, in vivo situation of androgenetic alopecia,
TGF-b1 produced by androgen from bald DPCs suppresses
epithelial cell growth and causes early catagen induction
in a paracrine manner and furthermore enhance androgen
sensitivity in bald DPCs in a autocrine manner, recapitulating
the reciprocal pathomechanism between androgen
and TGF-b1.

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

Well sometimes we talk about which are the most important of the signals downstream of androgens in hair loss (the alphabet soup as Bryan calls it). Microarray analysis has been very helpful in this area. Here we see that pretty much every growth factor is downregulated and everything that keeps hairs in catagen is upregulated. Somewhat of an exaggeration but still.
hh

Comparison of Senescent and Androgenetic
Alopecia Using Microarray Analysis
Mirmirani, Paradi;1,2 Oshtory, Shaheen;1 Daoud, Shaza;1
McCormick, Tom;1 Cooper, Kevin;1 Karnik, Pratima;1
1. Case Western Reserve University, Cleveland, OH, USA ;
2. University of California, San Francisco, Vallejo, CA, USA
It has been suggested that senescent alopecia (SA) is
a different entity than androgenetic alopecia(Androgenetic Alopecia) despite
similar histopathology, since the age of onset, pattern
of hair loss and hormonal involvement differ. Microarray
analysis of pooled scalp biopsies from three groups of men
aged 60 and older was undertaken. Group 1-Controlsno
visible hair thinning. Group 2-SA-diffuse hair thinning
after age 60. Group 3-Androgenetic Alopecia: male pattern hair thinning
prior to age 40. Affymetrix Human-U133B was used and
data analyzed with GCOS and GeneSpring. In Androgenetic Alopecia, genes
required for anagen onset (Wnt-b-catenin, TGF-a, TGF-b,
Stat-3, Stat-1), epithelial signal to dermal papilla (PPARd,
IGF-1), hair shaft differentiation (Notch, Msx2, KRTs, KAPs),
and anagen maintenance (Msx2, Activin, IGF-1) were
downregulated; and genes for catagen (BDNF, BMP2, BMP7,
VDR, IL1, ER) and telogen induction and maintenance (VDR,
RAR) were upregulated. In contrast, the transcriptional
profile of SA was comparable to other aging systems. In
SA, genes involved in epithelial signal to dermal papilla
(FGF5), actin cytoskeleton (DST, ACTN2, TNNI3, and PARVB)
and mitochondrial function (JAK2, PRKD3, AK2, TRAP1,
TRIO, ATP12A, MLL4, STK22B) were downregulated,
while oxidative stress and inflammatory response genes
were upregulated. Thus, follicular downsizing in Androgenetic Alopecia is
due to decreased molecular signals of anagen onset and
maintenance and increased catagen and telogen inducers.
While SA is likely the result of decreased signals between
the dermal papilla and stem cells required for anagen onset.
These data suggest that Androgenetic Alopecia and SA are distinct clinical
disorders with a final common phenotype of follicular
downsizing.

 

[chain]

Re: Abstractys from the 2007 European Hair Research Society Conf

Guys,

I cannot understand a thing. Would you please translate in more apprehndable form.

 

[michael barry]

Re: Abstractys from the 2007 European Hair Research Society Conf

Harold,

I found this little gem in regards to donor dominance even in hair color particularily enlightening:



P-246

Donor Site Dominance in Action:

Transplanted Hairs Retain Their Original

Hair Pigmentation Long-Term

Dinh, Hope V.;1 Sinclair, Rodney;1 Martinick, Jennifer;2

1. Department of Dermatology, St Vincent’s Hospital,

Melbourne, VIC, Australia; 2. New Hair Clinic, Nedlands,

Perth, WA, Australia

The concept of ‘donor dominance’ in hair transplantation

refers to autografts which continue to maintain their

integrity and characteristics after transplantation to a new

site. Such hairs may retain their original texture and rate of

growth. Hair transplantation for patients with androgenetic

alopecia rely on this concept of donor dominance for a

successful and long-lasting result. Recently, the concept

of ‘recipient dominance’ in hair transplantation has been

debated. In a study of patterns after hair transplantation to

the scalp and eyebrows in patients affected by madarosis,

Lee et al found that the greying rate of hairs approximated

the recipient site rather than the donor site.

We report on the long-term maintenance of follicular

pigmentation in transplanted hairs. We describe two

patients affected by both androgenetic alopecia and hair

greying in the transplant recipient area. They were given

autografts of normally pigmented hair follicles harvested

from the occipital area. More than one year posttransplantation,

their donor hairs have remained pigmented

long-term, despite being implanted in scalp affected by

greying. In one patient the pigmented hairs have remained

stable for 10 years. As the process of greying usually affects

the temporal scalp .rst, then progresses onto the vertex

 

[michael barry]

Re: Abstractys from the 2007 European Hair Research Society Conf

Harold,


Concerning the licorice, it slows melanocyte activity down GREATLY------which leads to not only skin lightening (licorice is used in skin-lightening products in India where fairer skin is deemed desirable by some of the populace), but should induce hair greying much earlier.



This Harold, is why Ive come to wonder if peppermint might actually be bad for hair as Bryan has suggested. It reduced the living hell out of hair on one side of my chin...............this is true, but why then are so many Revita users dissapointed (Revita has both menthol and methyl saclicate)? Why aren't there more super-happy tricomin users (copper peptides and peppermint oil in the shampoo). I wonder if peppermint might do something that slows hair growth period, depsite being anti-androgenic. Its a concern of mine. Another reason is this...........................I put Revivogen on my right wrist for three months THREE YEARS AGO. Guess what, my right wrist still has obviously weaker, thinner, wavier hair than my left wrist. Body hair cycles are short, it should have caught back up by this great amount of time but it hasn't. Ive oft wondered why there arent more "home run" revivogen pictures. Something that both inhibits alpha five reductase type one and two and supposedly blocks androgen receptors (beta sistosterol and sterols in saw palmetto) should have better regrowth pics than what they do after all these years. Theoretically that would be like taking dutasteride and using RU58841 at the same time, but the success stories just arent' there.........................and there has been plenty of time for there to be at this point.


the main point being, perhaps some anti-androgens can still be 'bad' for hair growth due to other things in the compound or compounds that accompany the active anti-androgen within it. Red Clover and topical soy isoflavone genistein, perhaps arinica and rose hips and clove and beta sitosterol and cedarwood are the "reamining candidates" that are possibly anti-androgenic, not known to be anti-inflammatory (caffeic acid and the octyl and doctyl gallates are all very inflammatory), that are still "out there" as possibly cheap, easily available anti-androgens that occur in nature in sufficient quantities for a man to get a hold of at home. Even genistein inhbits angio-genesis........which IM not crazy about.

 

[michael barry]

Re: Abstractys from the 2007 European Hair Research Society Conf

Harold posted this:
Well sometimes we talk about which are the most important of the signals downstream of androgens in hair loss (the alphabet soup as Bryan calls it). Microarray analysis has been very helpful in this area. Here we see that pretty much every growth factor is downregulated and everything that keeps hairs in catagen is upregulated. Somewhat of an exaggeration but still.
hh

Comparison of Senescent and Androgenetic
Alopecia Using Microarray Analysis
Mirmirani, Paradi;1,2 Oshtory, Shaheen;1 Daoud, Shaza;1
McCormick, Tom;1 Cooper, Kevin;1 Karnik, Pratima;1
1. Case Western Reserve University, Cleveland, OH, USA ;
2. University of California, San Francisco, Vallejo, CA, USA
It has been suggested that senescent alopecia (SA) is
a different entity than androgenetic alopecia(Androgenetic Alopecia) despite
similar histopathology, since the age of onset, pattern
of hair loss and hormonal involvement differ. Microarray
analysis of pooled scalp biopsies from three groups of men
aged 60 and older was undertaken. Group 1-Controlsno
visible hair thinning. Group 2-SA-diffuse hair thinning
after age 60. Group 3-Androgenetic Alopecia: male pattern hair thinning
prior to age 40. Affymetrix Human-U133B was used and
data analyzed with GCOS and GeneSpring. In Androgenetic Alopecia, genes
required for anagen onset (Wnt-b-catenin, TGF-a, TGF-b,
Stat-3, Stat-1), epithelial signal to dermal papilla (PPARd,
IGF-1), hair shaft differentiation (Notch, Msx2, KRTs, KAPs),
and anagen maintenance (Msx2, Activin, IGF-1) were
downregulated; and genes for catagen (BDNF, BMP2, BMP7,
VDR, IL1, ER) and telogen induction and maintenance (VDR,
RAR) were upregulated. In contrast, the transcriptional
profile of SA was comparable to other aging systems. In
SA, genes involved in epithelial signal to dermal papilla
(FGF5), actin cytoskeleton (DST, ACTN2, TNNI3, and PARVB)
and mitochondrial function (JAK2, PRKD3, AK2, TRAP1,
TRIO, ATP12A, MLL4, STK22B) were downregulated,
while oxidative stress and inflammatory response genes
were upregulated. Thus, follicular downsizing in Androgenetic Alopecia is
due to decreased molecular signals of anagen onset and
maintenance and increased catagen and telogen inducers.
While SA is likely the result of decreased signals between
the dermal papilla and stem cells required for anagen onset.
These data suggest that Androgenetic Alopecia and SA are distinct clinical
disorders with a final common phenotype of follicular
downsizing.




Harold,
When I look at that above, it makes me think that several things downstream of DHT would have to be inhibited to have a "no-hormonal" intervention against alopecia. One would have to counteract all of those substances or supress at least the negative growth factors in the least in all probability as when any one gets high enough in the follicle, catagen will ensue......................and increasing the anagen inducers also would assuredly be helpful. The thing is man...............that a good 8-10 substances in all isn't it? Who knows if constantly increasing one of the growth factors like wnt or beta catenin wont cause cancer down the line also, or if inhibiting a negative growth factor might not also be carcinogenic over time?

But we do know that stopping androgens via the recptor site and inhibition of DHT isn't fatal if done topically for certain (and internally with type two dht). Hence why I think its still the best "base" route to follow with other things added atop it afterwards given what we know at this point.



I sure as hell wish they could just clone our damned donor hair so we could get injected with a shitload of it and we could forget about all this stuff...................

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

Interesting for Follica stuf and the new kit patents. EGF signalling interferes with hair placode formation. After that it has no effect on hair growth/development.
Perhaps they went with EGFR blockers rather than WNT antagonists to avoid any possible tumour risks?


EGF and FGF Signalling Have a Role in Mouse
Hair Follicle Morphogenesis and Patterning
Richardson, Gavin D.;1 Bazzi, Hisham;2 Jahoda, Colin;1 Waters,
James;1 Christiano, Angela M.;3 Fantauzzo, Katherine;2
Crawford, Heather;1 Hynd, Phil;4
1. Department of Biological Sciences, University of Durham,
Durham, UK; 2. Departments of Development and Dermatology,
Columbia University, New York, NY, USA; 3. Departments
of Genetics & Development and Dermatology, Columbia
University,, New York, NY, USA; 4. School of Agriculture, Food
& Wine, The University of Adelaide, Adelaide, SA, Australia
Epidermal growth factor (EGF) has previously been shown
to block hair follicle (HF) morphogenesis. However, the
mechanism underpinning this phenomenon has not been
investigated in detail, perhaps because EGF ligand is not
endogeneously expressed in skin during early HF initiation
and patterning. Keratinocyte growth factor (KGF) has also
been shown to block follicle formation in organ culture in a
manner not yet understood. In this study, we revisited the
roles of the EGF and KGF signalling pathways in normal HF
morphogenesis in mice.
first, semi-quantitive PCR was used to profile the
expression of EGF and KGF ligands and receptors within
separated epidermis and dermis of E12.5-15.5 mouse
dorso-lateral skin. This analysis discovered endogenous
expression of EGFR ligands, Heparin binding EGF and
Amphiregulin, as well as the KGFR ligand KGF. Intriguingly,
immunohistochemistry revealed a marked reduction in both
EGFR and KGFR expression in developing placodes and
subsequent hair germs. Functional studies using embryonic
skin organ cultures identified that EGFR or KGFR activation
within E13.5 skin (before placode formation) inhibited
HF development in a dose dependent manner. This was
confirmed by in situ hybridisation and immunological
detection of molecular markers specific to developing HFs.
Activation of either receptor within E14.5 skin (post placode
formation) had no effect on hair follicle development.
We propose a role for EGF and KGF signalling in which
receptor downregulation may be required for epidermal
cells to escape ligand stimulation, thus permitting placodal
cells to follow a follicular rather than an interfollicular
differentiation pathway.

 

[michael barry]

Re: Abstractys from the 2007 European Hair Research Society Conf

Interesting for Follica stuf and the new kit patents. EGF signalling interferes with hair placode formation. After that it has no effect on hair growth/development.
Perhaps they went with EGFR blockers rather than WNT antagonists to avoid any possible tumour risks?

Ive got a feeling they did this to keep the FDA away so they could go ahead and get it to market. Wnt is associated with cancer of course, and that might elicit some regulatory oversight by the FDA, but already approved drugs like getifitinib and avodart and minoxidil wouldn't, so perhaps they are going with the latter . You can take lithium chloride (used to be used as a salt) or internal garlic supplements (lithium in garlic) during these ten days or so post-wounding and probably get the same ooomph that a topical lithium or wnt would give you anyway.

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

If Androgenetic Alopecia development is due to inheriting an AR with increased sensitivity (which I am not convinced it is) then this study implies that in the not overly distant past it was evolutionarily advantageous to have this variant of the AR.
hh

Variability in the Androgen Receptor Gene:
Strong Association With Androgenetic
Alopecia, Functional Implications and
Indication For Positive Selection
Hillmer, Axel M.;1 Becker, Tim;2 Myles, Sean;3 Freudenberg,
Jan;4 Brockschmidt, Felix F.;1 Stoneking, Mark;3 Kruse, Roland;5
Nöthen, Markus M.;1
1. Dept. of Genomics, Life and Brain Center, University of Bonn,
Bonn, Germany; 2. Inst. for Medical Biometry, Informatics
and Epidemiology, University of Bonn, Bonn, Germany; 3.
Max Planck Institute for Evolutionary Anthropology, Leipzig,
Germany; 4. Dept. of Neurology, Laboratories of Neurogenetics,
UCSC, San Francisco, CA, USA; 5. Dept. of Dermatology,
University of Düsseldorf, Düsseldorf, Germany
Androgenetic alopecia (Androgenetic Alopecia, male pattern baldness) is
the most common form of hair loss. Its pathogenesis is
androgen dependent, and genetic predisposition is the
major requirement for the phenotype. We have recently
demonstrated that genetic variability in the androgen
receptor gene (AR) is the cardinal prerequisite for the
development of early-onset Androgenetic Alopecia, with an etiological
fraction estimated at 0.46. The investigation of a large
number of genetic variants covering the AR locus suggests
that a polyglycine encoding GGN repeat in exon one is
a plausible candidate for conferring the functional effect.
The polyglycine tract is located in the transactivating domain
of the androgen receptor protein (AR), suggesting an effect
of repeat length on receptor function. We compared the
functional characteristics of the two most common alleles
(23 and 24 repeats) and two extreme alleles (10 and 27
repeats) in a reporter gene assay in HeLa cells. Our data
provide evidence of functional differences between the
two most common alleles of the AR GGN repeat. The
AR haplotype with the highest frequency (0.45) in the
German population, which confers risk to Androgenetic Alopecia, seems to
be evolutionarily recent, as indicated by the low sequence
identity with the ancestral haplotype and larger extent
of haplotype homozygosity. This implies that a variant
at the AR locus may have experienced recent positive
selection that led to an increase in frequency of the Androgenetic Alopecia
susceptibility allele in the European population.

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

Trichodynia is hair/scalp pain. This study seems to indicate it is not a feature of male pattern baldness per se but one of chronic increased shedding.
hh

Trichodynia Is a Distinguishing Symptom of
Telogen Effluvium
Guarrera, Marcella; Baldari, Manuela; Montinari, Martina;
Rebora, Alfredo; University of Genoa, Genoa, Italy
Objectives: The prevalence of trichodynia is controversial.
Controversy may stem from the diagnostic confusion
between androgenetic alopecia (Androgenetic Alopecia), chronic telogen
effluvium (CTE) and their association (Androgenetic Alopecia+CTE).
Approach: With the aid of the modified wash test (WT)
(1), we surveyed10 men and 85 women complaining of
hair loss. After 5-day-abstention from shampooing, they
soaped and rinsed the hair in a basin and collected all hair
remaining in a gauze covering the basin bottom. Hair were
counted and divided into <3 cm hair (vellus hair) and into
>3 cm hair. Patients with <100 total hair and >10% vellus
hair were diagnosed as having Androgenetic Alopecia; those with >100 hair
and <10% vellus hair were diagnosed as having CTE; those
with >100 hair and >10% vellus hair as having Androgenetic Alopecia+Telogen Effluvium
and patients with >100 hair and <10% vellus hair as having
CTE in remission.
Results: Trichodynia was reported by 22 patients: 17 had
CTE, 2 Androgenetic Alopecia and 3 CTE+Androgenetic Alopecia. None has CTE in remission.
The prevalence (51%) of trichodynia in patients with
CTE and CTE+Androgenetic Alopecia was statistically highly significant
(c2 = 20.077, p <0.001).
Conclusion: Trichodynia is almost exclusive of patients with
CTE as it affects about one half of the them and may be a
marker of activity of an inflammatory peripilar process.

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

More downstream of androgen stuff.

Interaction of Androgen Receptor With Wnt
Signaling Axis in Dermal Papilla Cells
Kitagawa, Tomoko;1 Matsuda, Ken-ichi;2 Inui, Shigeki;3
Takenaka, Hideya;1 Katoh, Norito;1 Itami, Satoshi;3 Kawata,
Mitsuhiro;2 Kishimoto, Saburo;1
1. Department of Dermatology, Kyoto Prefectural University of
Medicine Graduate School of Medical Science, Kyoto, Japan; 2.
Department of Anatomy and Neurobiology, Kyoto Prefectural
University of Medicine Graduate School of Medical Science,
Kyoto, Japan; 3. Department of Regenerative Dermatology,
Osaka University of Medicine, Suita, Japan
Objective: Wnt and androgen are known to positively and
negatively affect mammalian hair growth. We hypothesized
that androgen reduces hair growth through the interaction
with Wnt signaling system. The purpose of this study is
to investigate the effect of androgen on Wnt signaling in
dermal papilla cells (DPCs).
Approach: The effect of androgen and Wnt3a on
keratinocytes (KCs) proliferation was measured using coculture
system of DPCs and KCs. Molecular mechanism
of interaction of androgen and Wnt signals in DPCs
was examined by analyzing the expression, intracellular
localization and activities of androgen receptor (AR) and
down-stream molecules of Wnt signaling. We also studied
the expression level of TGF-beta in DPCs by real-time
PCR analysis.
Results: Wnt3a stimulated the growth of KCs when cocultured
with DPCs. Wnt3a-dependent growth of KCs was
suppressed by androgen in male-derived DPCs (MDPCs)
co-culture, but not in female derived DPCs co-culture.
Androgen treatment suppressed Wnt-mediated transcription
and promoted the expression of TGF-beta in MDPCs. While
both of male- and female-derived DPCs expressed AR, the
expression level and the degree of nuclear translocation of
AR were higher in MDPCs.
Conclusion: These results strongly suggest that the inhibitory
action of androgen on KC proliferation in the co-culture is
mediated through the suppression of Wnt signaling as well
as TGF-beta production by AR in MDPCs.

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

More evidence that environmental effects can be significant in the development of male pattern baldness.

Androgenetic Alopecia: Concordance of
Hair Loss in Twin Pairs
Mirmirani, Paradi;1,2 Price, Vera;2 Ettefagh, Leila;1
1. Case Western Reserve University, Cleveland, OH, USA;
2. Universtiy of California, San Francisco, San Francisco,
CA, USA
Androgenetic alopecia is a common disorder that affects
both men and women, but its mode of inheritance has
been a contested topic. Our objective was to measure and
compare hair loss in monozygotic and dizygotic twins and
to determine concordance rates between pairs. In fraternal
twins, expected concordance is 50% for a monogenetic
simple Mendelian transmission and less than 50% for
a polygenetic trait; 100% concordance is expected for
monozygotic twins. Recruitment of twins took place at the
2004 National Twinsday Festival in Twinsburg, Ohio. Twins
filled out hair questionnaires to determine demographics
and exclusion criteria. Each participant had stereotactic
frontal/vertex/occipital scalp photographs(Canfield
Scientific). Buccal swabs were collected for zygosity
testing and were perfomed by AnaGen Technologies, Inc.
The photographs were evaluated in a blind manner by
one of the investigators(VHP) for degree of alopecia and
concordance/discordance amongst twin pairs. A total of
44 twin pairs were enrolled, 16 were excluded from the
study. Of the 28 twin pairs evaluated, 2 of the 4 dizygotic
twins were discordant(50%) and 3 of the 24 monozygotic
twins were discordant(11%). This preliminary data shows
an unexpected discordance rate of 11% amongst the
monozygotic twin pairs suggesting that environment may
have a greater influence on androgenetic alopecia than
previously recognized. Ongoing enrollment of twins in
the study will allow for larger sample size and improved
power to further evaluate the inheritance pattern of
androgenetic alopecia.

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

No surprises that the most commonly occuring disorder in male pattern baldness patients is seb dermatitis.

A Clinical Study of Androgenetic Alopecia
(2004 – 2006)
Ro, Byung In;1 Han, Tae Young;2 Cho, Sung Hyun;2
1. Dept. of Dermatology, Myongji Hospital, Kwandong
University College of Medicine, Koyang, Korea; 2. Departments
of Dermatology, College of Medicine, Chung Ang University,
Seoul, Korea
Objective: The purpose of this study was to evaluate
the family history, and clinical status of patients with
androgenetic alopecia.
Approaches: 789 patients with androgenetic alopecia were
assessed at the Alopecia Clinic, Department of Dermatology,
College of Medicine, ChungAng University Hospital over
a 3 year period from 2004 to 2006
Results: 1) Men (520 patients) are affected 1.9 times more
than are women (269 patients). Most of them are twenties
(male 223; 42.8%, female 85; 31.5%). 1.9:1.0. 2) In the
520 male patients, Norwood class IIIv was dominant (161
patients; 30.9%). In the 269 female patients, Ludwig
class I was superior (218 patients; 81%). 3) 395 patitents
(75.9%) of 520 male patients and 198 (73.6%) of 269
female patients had a family history. 4) The most common
accompanying disorder was seborrheic dermatitis (male
407; 78.2%, female 155; 57.6%). And others include
atopic dermatitis, hypertension, thyroid disease, etc. 5)
Serum testosterone level were increased in 92 (17.6%) of
520 male patients and 36 (13.3%) of 269 female patients.
Conclusion: Most of these results are compatible with our
previous study carried out in 2004. But, female andogenetic
alopecia patients are nowadays increasing in number.

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

In the future it may be possible to test if you will be a good responder to finasteride (if we are still using it) by looking at if you have one of the more sensitive types of AR. Those with male pattern baldness who had the more sensitive type of AR responded better to finasteride.

Estimation of finasteride Sensitivity of Male
Pattern Baldness Patients By Determination of
Triplet Repeat Number in Androgen Receptor
Gene and Hormone/Cytokine in Serum
Wakisaka, Nagaoki; Kobayashi, Kazuhiro; Taira, Yuichi;
Konishi, Sawako; Fukuda, Yasutaka; Taguchi, Masayuki;
Hirayama, Nobuo; Hama, Takanori; Inoue, Hajime;
Takeda, Katsuyuki; Nakamizo, Yoshio; Kawakami, Masaya;
NPO, Future Medical Laboratory, Tokyo, Japan
Objectives: finasteride is effective on male pattern baldness
(male pattern baldness) although there is a variation in the efficacy of
this drug among the male pattern baldness patients. To know any factor,
which correlates with the effectiveness of finasteride, the
polymorphism of androgen receptor (AR) gene and serum
levels of certain hormones and cytokines were analyzed.
Approach: After PCR of blood cell DNA, number of triplet
repeats (CAG+GGC) in the first exon of AR gene was
determined. Testosterone, dihydrotestosterone, IGF-1 and
TGFb-1 were determined by immunological assays before
and one month after the drug treatment. Symptoms, typed
by photographic method before and 6 months after the
drug treatment, were compared.
Results: When the number of the triplet repeats was
plotted against the degree of symptom improvement after
treatment, a broad correlation between these variables
was observed. The smaller the repeat number, the higher
the improvement.[b:jdd88ko7] finasteride was more effective on the
improvement of patient group with smaller repeat number
in AR gene@(

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

Dietary silicone improves hair thickness in women. Possibly gives some indirect credence to the use of MSM.

Effect of Oral Intake of Choline-Stabilized
Orthosilicic Acid on Hair Tensile Strength and
Morphology in Women With Fine Hair
Wickett, R. R.;1 Kossmann, E.;2 Barel, André O.;3 Demeester,
Nathalie;4 Clarys, Peter;3 Vanden Berghe, Dirk A.;4 Calomme,
Mario R.;4
1. College of Pharmacy, University of Cincinnati, Cincinnati,
OH, USA; 2. Practice of Dermatology and Cosmetic Medicine,
Holzminden, Germany; 3. Vrije Universiteit Brussel, Brussels,
Belgium; 4. University of Antwerp, Dept. of Pharmaceutical
Sciences, Antwerp, Belgium
Silicon (Si) has been suggested to have a role in the
formation of connective tissue. Choline-stabilized orthosilicic
acid (“ch-OSAâ€￾) is a bioavailable form of silicon which
was found to improve skin microrelief and skin mechanical
properties in women with photoaged skin.
The effect of ch-OSA on hair was investigated in a
randomized, double blind, placebo-controlled study. During
9 months, 48 women with thin hair were given orally either
ch-OSA (10 mg Si/day; n=24) or a placebo (cellulose; n=24).
Urinary Si excretion, hair morphology (apparent diameter,
cross sectional area), and tensile strength (elastic gradient,
break load, break stress) were analyzed.
After 9 months supplementation, urinary silicon
concentration increased in the ch-OSA group (p<0.05) but
not in the placebo group. The elastic gradient decreased
in both groups but the change was smaller in the ch-OSA
group (-4.52 %, p=0.027) compared to placebo
(-11.86 %). Break load changed in the placebo group (-
10.79 %, p<0.0001) but not in the ch-OSA supplemented
group. Break stress decreased in both groups but the
change tended to be smaller in the ch-OSA group. Both the
apparent diameter and the cross sectional area increased
in ch-OSA supplemented subjects (p<0.05, vs. baseline)
but not in the placebo group. The change in urinary silicon
excretion correlated positively with the change in apparent
diameter and cross sectional area (p=0.023).