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    <title>Hair regrowth</title>
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      <title>Hair regrowth</title>
      <link>http://a.gohair.com/blog/</link>
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    <item>
 <title>Hair Loss and Hair Regrowth Blogs</title>
 <link>http://a.gohair.com/blog/index.php?itemid=33</link>
<description><![CDATA[List of Hair loss treatment blogs<br />
<br />
<a href="http://b2.ce.st/">Hair loss blog</a><br />
<br />
<! a href="http://www.drproctor.com/blogb2/">Hair loss treatment blog</a><br />
<br />
<! a href="http://www.mn.st">Hair Loss treatment</a><br />
<br />
<a href="http://wp.tx.st/">Hair loss blog</a>   b2.tx.st<br />
<br />
More  hair regrowth blogs<br />
<br />
Hair loss and hair loss treatment]]></description>
 <category>General</category>
<comments>http://a.gohair.com/blog/index.php?itemid=33</comments>
 <pubDate>Mon, 19 Dec 2011 10:44:02 -0500</pubDate>
</item><item>
 <title></title>
 <link>http://a.gohair.com/blog/index.php?itemid=32</link>
<description><![CDATA[Int J Cancer. 2011 Nov 30. doi: 10.1002/ijc.27379. [Epub ahead of print]<br />
<br />
Treatment for chemotherapy-induced alopecia in mice using parathyroid hormone agonists and antagonists linked to a collagen binding domain.<br />
<br />
Katikaneni R, Ponnapakkam T, Suda H, Miyata S, Sakon J, Matsushita O, Gensure RC.<br />
<br />
Source<br />
<br />
Pediatric Endocrinology, Children's Hospital at Montefiore and Albert Einstein College of Medicine, Bronx, NY, USA.<br />
<br />
Abstract<br />
<br />
Parathyroid hormone (PTH) agonists and antagonists have been shown to improve hair growth after chemotherapy; however, rapid clearance and systemic side-effects complicate their usage. To facilitate delivery and retention to skin, we fused PTH agonists and antagonists to the collagen binding domain of Clostridium histolyticum collagenase. In-vitro studies showed that the agonist fusion protein, PTH-CBD, bound collagen and activated the PTH/parathyroid hormone-related peptide (PTHrP) receptor in SaOS-2 cells. The antagonist fusion proteins, PTH(7-33)-CBD and PTH([-1]-33)-CBD, also bound collagen and antagonized PTH(1-34) effect in SaOS-2 cells; however, PTH(7-33)-CBD had lower intrinsic activity. Distribution studies confirmed uptake of PTH-CBD to the skin at 1 hour and 12 hours after subcutaneous injection. We assessed in-vivo efficacy of PTH-CBD and PTH(7-33)-CBD in C57BL/6J mice. Animals were depilated to synchronize the hair follicles; treated on day 7 with agonist, antagonist, or vehicle; treated on day 9 with cyclophosphamide (CYP) (150 mg/kg i.p.) or vehicle; and sacrificed on day 39. Normal mice (no chemo, no treatment) showed rapid regrowth of hair and normal histology. Chemo+Vehicle mice showed reduced hair regrowth and decreased pigmentation; histology revealed reduced number and dystrophic anagen/catagen follicles. Chemo+Antagonist mice were grossly and histologically indistinguishable from Chemo+Vehicle mice. Chemo+Agonist mice showed more rapid regrowth and repigmentation of hair; histologically there was a normal number of hair follicles, most of which were in the anagen phase. Overall, the agonist PTH-CBD had prominent effects in reducing chemotherapy-induced damage of hair follicles, and may show promise as a therapy for chemotherapy-induced alopecia.<br />
]]></description>
 <category>General</category>
<comments>http://a.gohair.com/blog/index.php?itemid=32</comments>
 <pubDate>Wed, 7 Dec 2011 12:20:39 -0500</pubDate>
</item><item>
 <title>Hair regrowth and hair loss treatment</title>
 <link>http://a.gohair.com/blog/index.php?itemid=31</link>
<description><![CDATA[<H3>Medical <a href=http://www.doctorproctor.com>Hair Loss Treatment</a></H3>]]></description>
 <category>General</category>
<comments>http://a.gohair.com/blog/index.php?itemid=31</comments>
 <pubDate>Mon, 6 Sep 2010 21:47:55 -0400</pubDate>
</item><item>
 <title>Treatment of Hair Loss in Trichotillomania</title>
 <link>http://a.gohair.com/blog/index.php?itemid=30</link>
<description><![CDATA[J Behav Ther Exp Psychiatry. 2010 Jul 14.<br />
<br />
Movement decoupling: A self-help intervention for the treatment of trichotillomania.<br />
Moritz S, Rufer M.<br />
<br />
Trichotillomania (TTM) is classified as an impulse control disorder characterized by the recurrent urge to pull out one's own hair resulting in noticeable hair loss. Cognitive-behavioral therapy, involving habit reversal training, currently represents the treatment of choice. The present study assessed the feasibility and effectiveness of a novel self-help technique, entitled decoupling (DC). DC aims at attenuating TTM by performing movements that decouple the behavioral elements involved in hair pulling. A total of 42 subjects with TTM were recruited via self-help forums for TTM and were randomized either to DC or progressive muscle relaxation (PMR). After four weeks, participants were asked to fill out the same questionnaires as before and rate the effectiveness of the intervention. The completion rate was high and the reliability of the assessments at least satisfactory. The DC group showed a significantly greater decline on the Massachusetts General Hospital - Hair-Pulling Scale, which served as the primary outcome, relative to PMR indicating a medium to strong effect size. Declines on scales tapping depression and obsessive-compulsive disorder were comparable between the two groups. Despite some methodological limitations and the need for replication including follow-up and expert ratings, the present study suggests that DC may prove beneficial to a substantial number of individuals affected with TTM.<br />
]]></description>
 <category>General</category>
<comments>http://a.gohair.com/blog/index.php?itemid=30</comments>
 <pubDate>Mon, 30 Aug 2010 00:36:00 -0400</pubDate>
</item><item>
 <title>Hair loss regrowth and lamanin</title>
 <link>http://a.gohair.com/blog/index.php?itemid=29</link>
<description><![CDATA[J Dermatol Sci. 2010 Apr;58(1):43-54. Epub 2010 Feb 16.<br />
<br />
Laminin-511, inducer of hair regrowth, is down-regulated and its suppressor in hair growth, laminin-332 up-regulated in chemotherapy-induced alopecia.<br />
Imanishi H,Abstract<br />
BACKGROUND: Chemotherapy-induced alopecia (CIA) has a devastating cosmetic effect, especially in the young. Recent data indicate that two major basement membrane components (laminin-332 and -511) of the skin have opposing effects on hair growth. OBJECTIVE: In this study, we examined the role and localization of laminin-332 and -511 in CIA. METHODS: We examined the expression of laminin-332 and -511 during the dystrophic catagen form of CIA induced in C57BL/6 mice by cyclophosphamide (CYP) treatment. RESULTS: Our data indicate that both laminin-332 and its receptor alpha 6 beta 4 integrin are up-regulated (both quantitatively and spatially) after mid to late dystrophic catagen around the outer root sheath (ORS) in the lower third of hair follicles in CIA. This up-regulation also occurs at the transcriptional level. In contrast, laminin-511 is down-regulated after mid dystrophic catagen at the protein level, with transcriptional inactivation of laminin-511 occurring transiently at the early dystrophic catagen stage in both epidermal and ORS keratinocytes. Laminin-511 expression correlates with expression of alpha 3 integrin in CIA and we also demonstrate that laminin-511 can up-regulate the activity of the alpha 3 integrin promoter in cultured keratinocytes. Injection of a laminin-511 rich protein extract, but not recombinant laminin-332, in the back skin of mice delays hair loss in CYP-induced CIA. CONCLUSIONS: We propose that abrupt hair loss in CIA is, at least in part, caused by down-regulation of laminin-511 and up-regulation of laminin-332 at the transcriptional and translational levels. (c) 2010 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.<br />
]]></description>
 <category>General</category>
<comments>http://a.gohair.com/blog/index.php?itemid=29</comments>
 <pubDate>Tue, 3 Aug 2010 04:01:28 -0400</pubDate>
</item><item>
 <title>Treatment of hair loss in alopecia areata</title>
 <link>http://a.gohair.com/blog/index.php?itemid=28</link>
<description><![CDATA[Ann Dermatol. 2009 May;21(2):142.<br />
<br />
The therapeutic effect and the changed serum zinc level after zinc<br />
supplementation in alopecia areata patients who had a low serum zinc level.<br />
<br />
Park H, Kim CW, Kim SS, Park CW.<br />
<br />
Department of Dermatology, College of Medicine, Hallym University, Seoul, Korea.<br />
<br />
BACKGROUND: It has been reported that some alopecia areata patients have zinc<br />
deficiency. There have also been several reports published concerning oral zinc<br />
sulfate therapy, with encouraging results, in some alopecia areata patients.<br />
OBJECTIVE: The purpose of this study was to evaluate the therapeutic effects of<br />
oral zinc supplementation for twelve weeks in alopecia areata patients who had a <br />
low serum zinc level. METHODS: Oral zinc gluconate (50 mg/T/day) supplementation <br />
was given to alopecia areata patients without any other treatment for twelve<br />
weeks. The serum zinc level was measured before and after zinc supplementation. A<br />
four-point scale of hair regrowth was used to evaluate the therapeutic effect of <br />
oral zinc supplementation in these patients. RESULTS: Fifteen alopecia areata<br />
patients were enrolled in this study. After the therapy, the serum zinc levels<br />
increased significantly from 56.9 microg/ to 84.5 microg/dl. Positive therapeutic<br />
effects were observed for 9 out of 15 patients (66.7%) although this was not<br />
statistically significant. The serum zinc levels of the positive response group<br />
increased more than those of the negative response group (p=0.003). CONCLUSION:<br />
Zinc supplementation needs to be given to the alopecia areata patients who have a<br />
low serum zinc level. We suggest that zinc supplementation could become an<br />
adjuvant therapy for the alopecia areata patients with a low serum zinc level and<br />
for whom the traditional therapeutic methods have been unsuccessful.]]></description>
 <category>General</category>
<comments>http://a.gohair.com/blog/index.php?itemid=28</comments>
 <pubDate>Tue, 20 Jul 2010 21:29:23 -0400</pubDate>
</item><item>
 <title>Hair regrowth and vitamin D</title>
 <link>http://a.gohair.com/blog/index.php?itemid=27</link>
<description><![CDATA[Dermatol Online J. 2010 Feb 15;16(2):3.<br />
<br />
Does D matter? The role of vitamin D in hair disorders and hair follicle cycling.<br />
Amor KT, Rashid RM, Mirmirani P.<br />
<br />
Department of Dermatology, University of Texas and MD Anderson Cancer Center, Houston, Texas, USA. rashidrashid.mdphd@yahoo.com<br />
<br />
Hair regrowth and hair cycle<br />
The formation of the hair follicle during embryogenesis requires reciprocal signaling between the epithelium and mesenchymal cells. The major epithelial-derived signaling molecules involved in the early stages of hair follicle morphogenesis include fibroblast growth factors (FGF), bone morphogenic proteins (BMP), and sonic hedgehog (SHH) [9, 10].These signals result in elongation of the hair follicle in embryogenesis. The first hair cycle after birth is unique because it represents the completion of the embryological development of the hair follicle and it is not dependent on the factors required for the maintenance of the hair follicle postnatally [11]. Therefore, deficiencies in factors required for maintenance of the hair regrowth cycle are not evident until the first hair is shed.<br />
<br />
The maintenance of the hair follicle postnatally is dependent on the integrity of the dermis, epidermis, and the normal hair cycle. The hair cycle consists of three phases: anagen, catagen, and telogen. The anagen phase is the growth phase of the hair cycle. Anagen is initiated by signals from the mesodermal dermal papilla cells, which are at the base of the hair follicle, to the keratinocyte/hair follicle stem cells, which are located in the bulge of the hair follicle. These signals stimulate the follicular stem cell to proliferate and differentiate into a mature hair follicle, which consists of an outer root sheath, the inner root sheath, and the hair shaft. Approximately 85 percent of hairs are in anagen phase at one time, and this phase lasts two to six years. The catagen phase is the transition phase, which occurs when the anagen follicle receives a signal ends the growth phase. In catagen, apoptosis of the lower part of the hair follicle, located below the bulge, occurs. The dermal papilla cells also break away from the hair follicle and enter a rest stage. The catagen phase lasts one to two weeks. At the conclusion of the catagen phase, the hair follicle is one-sixth its original diameter. Telogen is the final phase of the hair cycle. It is also known as the resting phase. This phase lasts five to six weeks, until anagen is initiated again.<br />
<br />
]]></description>
 <category>General</category>
<comments>http://a.gohair.com/blog/index.php?itemid=27</comments>
 <pubDate>Sat, 1 May 2010 01:22:44 -0400</pubDate>
</item><item>
 <title>Dr Proctor treats hair loss</title>
 <link>http://a.gohair.com/blog/index.php?itemid=21</link>
<description><![CDATA[Dr Proctor treats <B><a href="http://www.drproctor.com">hair loss</A></a>]]></description>
 <category>General</category>
<comments>http://a.gohair.com/blog/index.php?itemid=21</comments>
 <pubDate>Fri, 8 Jan 2010 22:35:00 -0500</pubDate>
</item><item>
 <title>Hereditary hair loss and hair regrowth</title>
 <link>http://a.gohair.com/blog/index.php?itemid=26</link>
<description><![CDATA[Clin Genet. 2009Oct;76(4):332<br />
Hereditary hair loss and the ancient signaling pathways....<br />
<br />
Van Raamsdonk CD.<br />
<br />
....hair, teeth, and nails, begin as a thickening of the ectoderm, called a placode. The placode arises from a primary induction signal that is sent from the underlying mesenchyme.  The arrangement of hair follicles is due to the amount and distribution of signals that promote and inhibit hair placode formation. Continued development of a hair follicle after placode formation requires a complex cross-talk. Here, I will review recent studies in humans and mice that have increased our understanding of the role of these signaling pathways...in hereditary hair loss syndromes.....]]></description>
 <category>General</category>
<comments>http://a.gohair.com/blog/index.php?itemid=26</comments>
 <pubDate>Sun, 27 Dec 2009 11:40:40 -0500</pubDate>
</item><item>
 <title>Stroke,tempol, and Uric acid</title>
 <link>http://a.gohair.com/blog/index.php?itemid=25</link>
<description><![CDATA[Some of the same processes and agents that figure in hair loss and hair loss treatment also figure in stroke.   All of this is at a very basic level of pathogenesis.  E.g., see Dr proctor's paper on <a href="http://stroke.ahajournals.org/cgi/content/full/39/8/e126">uric acid and stroke</A>.    Effective in both experimental animals of neuroprotection in stroke and in preventing uric-acid-induced kidney damage, TEMPOL (e.g.,) is effective in radiation-induced hair loss.]]></description>
 <category>General</category>
<comments>http://a.gohair.com/blog/index.php?itemid=25</comments>
 <pubDate>Fri, 27 Nov 2009 15:50:33 -0500</pubDate>
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