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Ciao Geronimo, Non conosco ancora bene salusmaster.com per giudicarlo, ma mi sembra abbia un indirizzo e orientamento completamente diverso. Se vado a sbirciare di la', ci vado con curiosita' diverse da quelle che ho quando sto qua, quindi ... sicuramente questo forum non lo abbandono, cosi' come mi guardo sempre quello di hairsite. Poi tutto quello che c'e' in piu', se si dimostrera' valido, sara' valore aggiunto almeno spero sia cosi'....

Grazie delle info, DEP.

Androgenetic alopecia: pathogenesis and potential for therapy Justine A. Ellis, Rodney Sinclair and Stephen B. Harrap Androgenetic alopecia occurs in men and women, and is characterised by the loss of hair from the scalp in a defined pattern. Determining factors appear to be genetic predisposition coupled with the presence of sufficient circulating androgens. The prevalence of this condition is high (up to 50% of white males are affected by 50 years of age) and, although there are no serious direct health consequences, the loss of scalp hair can be distressing. Knowledge of the pathogenesis of androgenetic alopecia has increased markedly in recent years. Pre-programmed follicles on the scalp undergo a transformation from long growth (anagen) and short rest (telogen) cycles, to long rest and short growth cycles. This process is coupled with progressive miniaturisation of the follicle. These changes are androgen dependent, and require the inheritance of several genes. To date, only one of these genes, which encodes the androgen receptor (AR), has been identified. Of the many treatments available for androgenetic alopecia, only two (finasteride and minoxidil) have been scientifically shown to be useful in the treatment of hair loss. However, these therapies are variable in their effectiveness. Discovery of the involvement of the AR gene, and the identification of other genes contributing to the condition, might lead to the development of new and more effective therapies that target the condition at a more fundamental level. Expert Reviews in Molecular Medicine © Cambridge University Press ISSN 1462-3994 Author contact details Androgenetic alopecia, which in men is often referred to as male-pattern baldness, is a common form of scalp hair loss that affects most males by old age (Ref. 1). The condition can also affect females; however, this is less well characterised and it remains controversial as to whether the two conditions are the same (Ref. 2). Certainly, the pattern of hair loss is different in women and the prevalence is lower than that in men (Ref. 3). Therefore, in this review article we will focus specifically on male androgenetic alopecia. The onset of androgenetic alopecia is extremely variable, and appears to be determined by the presence of sufficient circulating androgens and the degree of genetic predisposition (Ref. 4). The condition is not a serious one from a medical perspective; however, the loss of hair is often an unwanted and stressful event for the patient (Refs 5, 6), and therefore might have considerable psychosocial consequences. Effective treatments are being developed and current research efforts, including the search for genes, are yielding much promising new information. Another common form of alopecia is alopecia areata, which is an inflammatory form of hair loss that is thought to be autoimmune in origin. Both genetic predisposition and environmental influence lead to episodes of patchy terminal hair loss. The loss might completely reverse without leaving any scarring; alternatively, it might progress and result in the total loss of scalp hair (alopecia totalis) or the total loss of body hair (alopecia universalis). Alopecia areata occurs equally in males and females, and does not appear to be androgen dependent (Refs 7, 8). Prevalence and clinical features of androgenetic alopecia By 30 years of age, ~30% of white males have androgenetic alopecia; by 50 years of age, 50% are affected (Ref. 1). White males are four times more likely to develop androgenetic alopecia than are males of African origin (Ref. 9). Hair loss follows a defined pattern, as described by the Hamilton–Norwood scale (Refs 1, 10) (Fig. 1), beginning with bitemporal recession of the frontal hairline. This is followed by diffuse thinning over the vertex (top) of the scalp, eventually leading to complete hair loss in this region. The bald patch progressively enlarges and eventually joins the receding frontal hairline. Ultimately, marginal parietal and occipital hair remains, and this might also continue to thin and be lost. Although this pattern is typical of most cases of androgenetic alopecia, the rate of hair loss in the various scalp regions can produce visual variation. For instance, rapid vertex loss coupled with slower frontal regression can appear different from faster frontal, and slower vertex, loss. Less commonly, the frontal hairline can be preserved (Ref. 11). Associations with other conditions There is some evidence to support the hypothesis that male-pattern hair loss imparts an increased risk of cardiovascular disease (CVD). It would appear that men with androgenetic alopecia are more likely to develop CVD (Ref. 12); however, there is no evidence of an increase in conventional risk factors such as blood pressure and cholesterol concentrations (Ref. 13). Recent studies have also demonstrated an increased risk of benign prostatic hyperplasia (Ref. 14) and prostate cancer (Ref. 15) in those with male-pattern baldness; however, the molecular basis for this link has yet to be evaluated. Pathogenesis of androgenetic alopecia Androgenetic alopecia is the result of step-wise miniaturisation of the hair follicle and alteration of the hair-cycle dynamics (Ref. 16). The three phases of the normal hair cycle (Ref. 17) are shown in Figure 2. Pre-programmed follicles on the scalp progress through long growth (anagen) cycles and short rest (telogen) cycles. With each passage through the hair cycle, the duration of the anagen phase decreases whereas the telogen phase elongates. Because the duration of the anagen phase is the main determinant of hair length, the maximum length of the new anagen hair is shorter than that of its predecessor. Eventually, the anagen phase is so short that the emerging hair does not reach the skin surface and the only testimony to the presence of a functioning follicle is a pore. In addition, the latency period between telogen hair shedding and anagen regrowth becomes longer, leading to a reduction in the number of hairs present on the scalp (Ref. 16). The follicular miniaturisation that accompanies these hair-cycle changes is global, affecting the papilla, the matrix and ultimately the hair shaft. The dermal papilla is fundamental to the maintenance of hair growth (Ref. 18) and is probably the target for androgen-mediated changes in the hair cycle and miniaturisation of the follicle (Refs 19, 20) (see below). Involvement of androgen and the androgen receptor Two predominant, naturally occurring androgens are the sex steroids testosterone and 5a-dihydrotestosterone (DHT). Testosterone is converted to DHT by the enzyme 5a-reductase (Fig. 3a), which exists as two isozymes: type I and type II (Ref. 21). Although the tissue distribution of the isozymes does vary, both are found in scalp follicles (Ref. 22). Androgens mediate their activities by binding to the human androgen receptor, a member of the steroid-thyroid hormone nuclear receptor superfamily. The structure of the androgen receptor includes a ligand-binding domain and a DNA-binding domain. Both testosterone and DHT can bind to the ligand domain, which activates the DNA-binding domain. The receptor–ligand complex then acts as a transcription factor, regulating the expression of androgen-sensitive genes (Fig. 3a) (Ref. 23). The androgen receptor is required for male development and, throughout adult life, for the normal functioning of organs such as the reproductive system, testes, muscles, liver, skin, nervous system and immune system (Refs 24, 25). The androgen receptor plays a role in several diseases and hereditary traits including prostate cancer, androgen insensitivity syndrome (Ref. 26) and spinal and bulbar muscular atrophy (Kennedy disease) (Ref. 27). The involvement of androgens in androgenetic alopecia has been established for some time, and is well accepted. Eunuchs, who lack androgens, do not bald (Ref. 4). Individuals who lack a functional androgen receptor are androgen insensitive and develop as females; again, these individuals do not bald (Ref. 28). Similarly, no baldness is seen in pseudohermaphrodites, who lack 5a-reductase, the enzyme that converts testosterone to the potent androgen DHT (Ref. 29). The concentration of DHT has been shown to be higher in the balding scalp than in the non-balding scalp (Fig. 3b) (Ref. 30). In addition, increased concentrations of both 5a-reductase and the androgen receptor have been detected in the balding scalp (Ref. 31), suggesting that such changes contribute to hair loss. The exact mechanism(s) through which androgens act to cause baldness remain unclear; however, given that the complex formed between the androgen receptor and androgen acts as a transcription factor, it is likely that genes controlling follicle cycling are regulated by androgen. The expression of such genes will therefore be dependent on the concentrations of androgen and androgen receptor in the follicle (Fig. 3b). Genetic models of androgenetic alopecia Androgenetic alopecia – an autosomal dominant disorder? The nature of the inheritance of genetic predisposition to androgenetic alopecia is unresolved. Although it is a popular belief that baldness is inherited from the maternal grandfather, the mode of inheritance is usually cited in the scientific literature as autosomal dominant, suggesting that the inheritance of only one autosomal gene conveys full genetic predisposition. However, there appears to be only one published comprehensive familial analysis of androgenetic alopecia, conducted by Dorothy Osborn in 1916 (Ref. 32). In this study of 22 families, it was concluded that a single autosomal gene, termed ‘B’, could account for genetic predisposition to baldness, acting in an autosomal dominant manner in men, and in an autosomal recessive manner in women. In other words, men are predisposed to baldness if they inherit either ‘BB’ or ‘Bb’; however, women are predisposed only if they inherit ‘BB’. The inheritance of androgenetic alopecia remains listed as autosomal dominant in such respected references as Victor McKusick’s Online Mendelian Inheritance in Man (OMIM: http://www.ncbi.nlm.nih.gov/Omim; entry number 109200). However, the first real test of Osborn’s hypothesis appeared in 1984, when Kuster and Happle re-assessed the inheritance of androgenetic alopecia (Ref. 33). They presented a strong argument for a more complex polygenic mode of inheritance of androgenetic alopecia, as described below. The polygenic hypothesis A trait determined by a single gene would be more likely to display two or more distinct phenotypes, rather than a continuous distribution (Ref. 34). In Kuster and Happle’s analysis, the distribution of androgenetic alopecia followed a normal distribution, representing the full range of phenotypes, from no evidence of hair loss, to fully developed baldness. This distribution is more consistent with a polygenic trait. In addition, Kuster and Happle pointed out that hereditary traits determined by a single gene rarely occur at a frequency greater than 1 in 1000. Although the exact frequency of androgenetic alopecia is difficult to ascertain, it has been estimated to be between 40% and 60% in men, further supporting a more pervasive mode of inheritance (Ref. 33). The characteristics of a polygenic trait can be illustrated using a simplified four-gene model (Ref. 35). Consider a scenario whereby predisposition to androgenetic alopecia is determined by four distinct genes, each contributing 25%. Inheritance of none of these genes obviates genetic predisposition to androgenetic alopecia. Inheritance of one gene predisposes to some hair loss later in life. Inheritance of two or three of these genes predisposes to hair loss during middle age, whereas inheritance of all four genes predisposes to hair loss at a young age. In reality, androgenetic alopecia might depend on more or fewer than four genes, each of which might contribute variably to predisposition. Father-to-son transmission A recent study of the inheritance of baldness examined fathers and sons who had participated in the Victorian Family Heart Study (VFHS) – a study of 3000 healthy Caucasian individuals belonging to 828 family groups living in the state of Victoria, Australia (Ref. 36). The VFHS was designed to examine risk factors associated with CVD that might include androgenetic alopecia. Males were surveyed for degree of baldness, and concordance was examined between 54 balding adult sons and their fathers. Under a model of autosomal dominant inheritance, sons might be expected to inherit baldness equally from their mothers and fathers. However, 81.5% of balding sons were found to have fathers with cosmetically significant baldness (type 3 or greater on the Hamilton–Norwood scale), considerably exceeding the autosomal dominant expectation (Ref. 36). These findings are consistent with a polygenic mode of inheritance, which includes a paternally inherited gene, and this polygenic model remains the most likely basis of androgenetic alopecia. Genes involved in androgenetic alopecia The identification of genes that are involved in androgenetic alopecia has been hindered by difficulties geneticists have faced when using classical genetic analysis techniques to study the condition. In general, these techniques compare the DNA sequences of unaffected and affected individuals, either from large family groups in which the presence or absence of baldness is known for all family members, or from large groups of unrelated affected and unaffected individuals. In both cases, it is vitally important that the presence or absence of baldness is correctly diagnosed. This is difficult given the variable age of onset of the condition. For example, is a 30-year-old man with a full head of hair guaranteed not to carry genetic predisposition? In recent studies, the sequences of several candidate genes were compared between groups of individuals who were considered to be most and least genetically predisposed to androgenetic alopecia (Refs 36, 37, 38). These are, respectively, young males who have a significant degree of baldness and older males who have no indication of hair loss. Candidate genes for androgenetic alopecia were chosen because of their relevance to the hypothesis that androgens are involved in this form of hair loss. Candidate genes The 5a-reductase genes As mentioned earlier, the concentrations of both DHT and 5a-reductase are increased in the balding scalp (Refs 33, 31), whereas the concentration of testosterone remains the same (Ref. 39). The involvement of DHT, rather than testosterone, in the hair-loss process implicates the genes that encode the 5a-reductase enzymes, SRD5A1 and SRD5A2, in male-pattern baldness because 5a-reductase converts testosterone to DHT. However, analyses of these genes using case–control association and familial linkage studies have shown that it is unlikely that they contribute to androgenetic alopecia (Refs 36, 40). The aromatase gene The enzyme aromatase converts androgens, such as testosterone, to oestrogens, and appears to be present at decreased concentrations in the balding scalp (Ref. 31). The autosomal gene encoding aromatase, CYP19, was compared between cases and controls but no differences were detected (Ref. 37), suggesting that it is unlikely that the aromatase gene is involved in determining predisposition to androgenetic alopecia. The Y chromosome The observed father-to-son transmission of androgenetic alopecia raises the hypothesis that a gene on the Y chromosome might contribute to the condition. In addition, the Y chromosome determines sex and the concentrations of sex steroids such as testosterone and DHT (Ref. 41). However, examination of the non-recombining region of the Y chromosome has demonstrated that it is unlikely that causative mutations occur in any genes contained in this region (Ref. 37). Although most of the Y chromosome does not recombine, it remains possible that mutations that contribute to predisposition to androgenetic alopecia occur in genes that are contained on the ends of the Y chromosome, in the so-called pseudoautosomal regions, which recombine with the X chromosome. Further study will be required to determine if this is the case. Discovery of the first gene associated with androgenetic alopecia: the AR gene Because an increased concentration of androgen receptor is associated with the balding scalp (Ref. 31), differences in the DNA sequence of the gene encoding the androgen receptor, or in the AR regulatory sequences, might lead to differences in the concentration or activity of the receptor. Such differences might increase sensitivity to DHT in balding individuals, leading to hair loss at an earlier age. On comparing the AR gene sequence found in case and control individuals, a significant difference was found between the two groups in the frequency of a single base change in the coding region (exon 1) of the gene. This polymorphism does not alter the amino acid sequence of the protein and is therefore unlikely to be functional. However, it is likely that the polymorphism is tightly linked to other functional sequence changes. All but one of the 54 young, bald men studied carried the non-functional variant of the AR gene (Ref. 38). Interestingly, 77% of non-bald men also carried this version of AR, suggesting that AR is necessary but not sufficient for causing baldness (Ref. 38). To date, AR functional mutations that are associated with androgenetic alopecia have not been located. However, the results of this study nevertheless provide good evidence for the involvement of the AR gene in androgenetic alopecia. The likely functional difference(s) will be those in the sequence of the regulatory regions that cause relatively subtle increases in androgen-receptor production and activity in the cell (Ref. 38). Further genetic research If the AR gene is necessary but not sufficient for causing baldness (Ref. 38), it is possible that other genes might be acting in conjunction with AR. For example, genes other than SRD5A1 and SRD5A2 that control DHT production remain candidates. Given that the concentration of 5a-reductase is increased in the balding scalp, candidate genes might include those encoding transcription factors that regulate the production of 5a-reductase. Such genes have yet to be identified. The many other genes, known and unknown, that are involved in androgen production, regulation and responses might also be involved. In addition to androgen-related genes, genes that are involved in patterning, signalling and hair-follicle morphogenesis are attracting much attention from researchers. All hair follicles are formed in utero. The spatial relationship of hair follicles is determined by the competing influences of follicle-inducing and follicle-repressing molecules. Interaction between the epidermis and dermis is required. Epidermal signals trigger the formation of the dermal papilla, and subsequent dermal signals direct epidermal downgrowth into the dermis that envelopes the dermal papilla and creates the hair follicle. Hair-shaft production from the follicle is regulated by signals from both the dermal papilla and lateral signalling between epithelial cells. These signalling pathways have been recently reviewed (Ref. 42). Important candidate areas include fibroblast growth factor, WNT proteins, b-catenin, LEF1, FOXN1, noggin, bone morphogenic protein 2 and 4, sonic hedgehog and its cognate receptor patched, platelet-derived growth factor A, follistatin and epidermal growth factor. Therapeutic management of androgenetic alopecia Without treatment, androgenetic alopecia is a progressive condition. Hairs decrease in number at a rate of ~5% per year (Ref. 43). Apart from various camouflage and surgical options (which are reviewed in Refs 44, 45), currently only two pharmaceutical treatments exist for the treatment of androgenetic alopecia in males: topical minoxidil and oral finasteride, both approved by the US Food and Drug Administration. Minoxidil, a vasodilator, was originally used to treat high blood pressure (Ref. 46). However, following observations that patients treated with this drug showed increased hair growth, a topical formulation was developed that arrested the progression of hair loss and promoted the regrowth of a small amount of hair in ~40% of men (4% experienced medium-to-dense regrowth) (Ref. 47). Minoxidil appears to prolong the anagen growth phase by an as yet unknown mechanism, leading to a decrease in hair shedding, but it does not inhibit the biological process. Hence, once treatment is stopped, hair shedding rapidly resumes, with the loss of all minoxidil-stimulated hair growth (Ref. 48). Finasteride is a synthetic azo-steroid that has been used for the treatment of androgenetic alopecia in males since 1997. It is a potent and highly selective 5a-reductase type-2 inhibitor (Ref. 49). It binds irreversibly to the 5a-reductase type-2 enzyme and inhibits the conversion of testosterone to DHT. Thus, although the pharmacological half-life is in the order of 8 h, the biological half-life is substantially greater. The administration of a daily dose of 1 mg reduces concentrations of scalp DHT and serum DHT by 64% and 68%, respectively (Ref. 50). The dose–response curve is non-linear, and therefore higher doses do not lead to significantly increased suppression of DHT or clinical benefit (Ref. 51). After 24 months of continuous use, 66% of patients experienced ~10–25% regrowth of their hair (Ref. 52). Most of the remainder showed no further hair loss, and only a few continued to lose hair. Continued use beyond 2 years does not appear to promote continued hair regrowth; instead the hair density stabilises with the retention of the newly acquired hairs (Ref. 52). If successful, the treatment should be continued indefinitely because the balding process continues once treatment ceases (Ref. 53). Future potential for therapy The importance of the elucidation of androgenetic alopecia genes The discovery of the genes that are involved in predisposition to androgenetic alopecia will dramatically enhance our knowledge of the mechanisms both at the molecular and cellular level that result in hair loss. For example, identifying the functional sequence change in or around the AR gene will lead to the determination of the exact differences in androgen-receptor proteins between bald and non-bald men. With this knowledge, treatments can be designed that target and reverse these differences, thereby blocking specific hair-loss mechanisms. Current pharmaceutical treatments for androgenetic alopecia do not target specific cellular mechanisms in this way. Rather, they inhibit enzymes involved in the increase of androgens in the balding scalp; thus, they are suppressive rather than curative, with variable rates of success. The use of androgen-receptor blockers Although the involvement of the AR gene in androgenetic alopecia is a recent finding, the idea of blocking the action of the androgen receptor in an attempt to prevent the action of excess DHT in the scalp is not new. However, androgen-receptor antagonists that act systemically cannot be used to treat men, owing to the potential risks of gynaecomastia (an excessive development of the male mammary glands), feminisation and impotence. Therefore, methods must be developed that block the action of the androgen receptor only in scalp follicles. Knowledge of the sequence differences between the AR gene in balding and non-balding men would allow the possibility of gene-therapy techniques that could selectively deliver the non-balding AR gene to hair follicles, preventing hair loss without any systemic effects. This possibility has been advanced by the development of a topical cream containing liposomes to deliver entrapped DNA selectively to hair follicles in mice (Ref. 54). In this study, the lacZ reporter gene was successfully targeted to the hair follicles in mice after topical application of the gene entrapped in liposomes, demonstrating the feasibility in the future of the selective and safe targeting to the hair follicles of genes relevant to androgenetic alopecia. In addition, the variability in the age of onset and severity of baldness among individuals indicates that it is likely that various numbers and combinations of predisposing genes will be identified. Assuming this proves to be the case, such treatments could be designed on a case-by-case basis to target precisely those genes involved in each individual. Conclusions Despite the recent research efforts aimed at elucidating the mechanisms behind hair loss in androgenetic alopecia, there is some way to go before a thorough understanding of this condition is achieved. Given that androgenetic alopecia is heritable, identification of the genes involved should lead to a thorough understanding of the causes of this condition. Only on the acquisition of such knowledge will it be possible to design treatments that target the causes. Current pharmaceutical treatments are suppressive rather than curative, and success is variable. The recent association of the gene encoding the androgen receptor with androgenetic alopecia might provide an incentive for the development of better treatments; however, completely effective treatments are unlikely to be developed until a thorough understanding of this condition is achieved at the genetic and molecular level.

x nocalvono e tutti gli altri interessati come me a far parte delle donazioni al progetto della doc Christiano e Jadoha, ecco il pezzo di Hairsite che descrive come fare. Bisogna mandare le donazioni all'indirizzo giusto per essere sicuri di finanziare quel progetto. -------------------------------------- The Steven and Michele Kirsch Foundation is committed to a wide spectrum of issues and causes that reflects the broad charitable interests of its two founders. In December 2002, The Kirsch Foundation awarded a two-year collaborative grant to Drs. Christiano and Jahoda for the Catalyst For Hair Follicle Biology (CHFB) project. Readers who frequent HairSite are all familiar with the work of the world's two leading follicle biologists: Angela Christiano, Ph.D. (Columbia University, New York) and Colin Jahoda, Ph.D. (Durham University, England). The two-year program totals $230,000 in funding. Anyone interested in donating money to the two researchers for this collaborative project can do so directly. Under normal circumstances, individual donations are typically subject to administrative or overhead charges by the institution the researchers are associated with. In other words, very rarely will 100% of your donations go directly to the designated research of your choice. However, in the case of the CHFB collaborative award program that is being funded by the Kirsch Foundation, the public can now match the foundation's two-year $230,000 funding with assurance that 100% of the "matching donations" will be designated strictly for CHFB research. Please do not be confused that your donations have to match Kirsch Foundation's lump sum contribution of $230,000. Donations from the public can be as little as $5, $10 or whatever amounts you decide to pledge. Individuals from around the world are welcome to contribute to this program. While U.S. residents can send their donations (checks or money orders) to Dr. Christiano's laboratory at Columbia University, New York, residents in the U.K. or Europe can send their donations to Dr. Jahoda's laboratory at Durham University, Scotland. All donations will go to the same research program. If you feel more comfortable sending donations to one location versus another, that is totally acceptable and will not affect how the donations will be utilized. In order to be certain that your donations will NOT be subject to either university's overhead charge, it is very important that you mark clearly on your donations, eg: on your checks or money orders, that the contribution is: TO MATCH KIRSCH FOUNDATION'S CATALYST FOR HAIR FOLLICLE BIOLOGY RESEARCH (CHFB) COLLABORATIVE AWARD PROGRAM Failure to clearly earmark the purpose of the donation as noted above may defeat the purpose of your intention. Individuals are welcome to send donations to either locations. Please follow instructions below Location: England United States Check payable to: The University of Durham The Department of Dermatology, Columbia University Information to be noted on checks or money orders "To match Kirsch Foundation's Catalyst for Hair Follicle Biology Research (CHFB) Collaborative Award Program" "To match Kirsch Foundation's Catalyst for Hair Follicle Biology Research (CHFB) Collaborative Award Program" Mailing address: Dr Colin Jahoda, School of Biological and Biomedical Sciences, University of Durham, South Road, Durham, DH1 3LE United Kingdom The Department of Dermatology Columbia University 630 West 168 Street, VC 15 New York, NY 10032 Attn: Alicia Batista The following is a synopsis about the Catalyst For Hair Follicle Biology (CHFB) program according to the Kirsch Foundation. Readers are encouraged to check Kirsch Foundation's website regularly for progress reports and updates about the CHFB project. Reprint from Kirsch Foundation Website, www.kirschfoundation.com CATALYST FOR HAIR FOLLICLE BIOLOGY (CHFB) - Established in December 2002, this two-year collaboration totals $230,000 in funding, and brings together two leading hair follicle biologists. The Foundation announced the researchers and the consortium in January. The members are: Angela M. Christiano, PhD (Columbia University, New York) "We are very grateful to the Kirsch foundation for its support of hair research. It is not often that scientists in our field have the privilege of being sponsored by such a prestigious organization. We are now in a unique position to make great strides in our work, as a direct result of this commitment. Colin A. B. Jahoda, PhD (Durham University, Scotland) "This is an outstanding opportunity to tackle a human condition that is of widespread concern for individuals and poses genuinely interesting scientific challenges. The foundation has helped to fill a void in funding that will allow us to bring a direct and unfettered approach to the research. The collaborative element is crucial in bringing together distinctive but complementary skills and technologies, as well as beneficial individual interactions. This has to be a good way of doing science." This consortium funding offers the potential to build upon the results that Dr. Christiano and Dr. Colin Jahoda have achieved through their informal collaboration thus far. As a result of publicity about Dr. Jahoda’s work, there have been a number of lucrative offers to market human hair loss "cures" from commercial sources. Both Drs. Jahoda and Christiano, however, believe that developing the research for therapeutic purposes should be done on an independent scientific basis. Unfortunately, given that NIH considers this to be a 'cosmetic' problem, few, if any, federal funds are available. We hope that by encouraging and supporting an effective collaboration, we will add real value to the work being conducted in these laboratories and send a positive message that can be leveraged into funding from other sources. The CHFB consortium will apply the emerging technologies of developmental biology, stem cell biology and tissue engineering to the induction of new hair follicles. The investigators have pioneered methods for the culture of hair follicle cells, and Dr. Jahoda was the first individual to demonstrate that new hair follicles can be induced to form in adult skin by implantation of cultured cells. Up to now, work has mainly been performed in animal models, and the induction of human hair follicles poses specific challenges relating to human hair follicle biology. The major focus of the CHFB is to establish that new human hair follicles can be created from cultured cells in adult human skin using transplantation techniques. The overall goal is the unequivocal demonstration that cultured human cells can induce new follicle formation and hair growth in human skin. Ultimately the hope is that the research can be used successfully to cure such conditions as premature balding and alopecia areata and offer solutions for hair loss due to chemotherapy. Serving as an advisor to the consortium is Dr. Cheng-Ming Chuong, Professor of Pathology at the University of Southern California. "Hair is the only place in the body that continues to shed and regenerate. It has a large pool of stem cells that maintains throughout our lives. It is like the fountain of youth. We need to learn how to use it. Drs. Jahoda and Christiano make up the dream team in hair biology research. Interesting new findings will emerge from this collaboration. I am thrilled that the Kirsch Foundation can support this endeavor. I am excited to see what will come out." The researchers are eager to move forward with their joint work. Features on the work of each investigator and updates on their progress will be provided from time to time and will be announced in the "what's new" section of this website

Tempions, ti ringrazio ma non mi considero ne' un eroe, ne' nessuno, ma solo me stesso con una grande voglia di ribellarmi alla mia sfortuna. Ti aspettano momenti molto duri ma per la tua eta' stai andando molto, ma molto bene. Take care.

Ringrazio Warhola e Gavino per i loro pensieri. Non mi arrendero' mai.

http://www.hairsite2.com/misc/butterfly.htm Sono giornate molto dure, queste, per me. Cercando di essere concreto, costruttivo ed andare avanti, non posso non fermarmi a vedere cose che sono capitate, e nel tentativo di migliorare e guardare al futuro, sento un profondo dolore che vivo come sempre interiormente ed in solitudine. Tanto piu' sei forte, tanto piu' sei solo. Ma non bisogna arrendersi. Vorrei soltanto essere piu' utile agli altri, perche' la battaglia x la mia sopravvivenza mi toglie tante energie e mi cambia; mia sorella si e' tolta la vita e io non posso farla tornare indietro. Quanto vorrei morire adesso, se potessi farla tornare indietro. Lo farei subito, senza alcun dubbio. Sto lottando per recuperare il mio fisico avvelenato da farmaci senza senso, ma i miei sforzi si scontrano con un metabolismo modificato; prima correre era una gioia, ora e' uno sforzo madornale. La gente che mi e' attorno non sa nulla o quasi di tutto questo. Soffoco in me ogni dolore per andare avanti. In ottobre saranno 18 anni che lotto, sopravvivendo in qualche modo, alla alopecia androgenetica. Ricordo limpidamente i miei 15 anni macchiati e sporcati da questa maledetta esperienza. Ricordo nitidamente ogni cosa. A tutti coloro che ci stanno in mezzo da 2,3 o 5 anni, voglio dare forza, e dire che il peggio deve ancora venire: la maturita' come uomini vi aiutera', si, ma portera' via il bambino che e' in voi ... molto ma molto piu' velocemente, l'alopecia accellerera' questo processo drammaticamente. Post come quelli di Tempions o altri adolescenti intrappolati in questa brutta gabbia li conosco gia' prima di averne letto il titolo. Conosco il rimuginare ed il rimuginare cercando una soluzione che non c'e'. Perche' tutti gli adolescenti tendono al futuro, al what's next, alla sfida, alla battaglia. E una battaglia impari che ti piega e ti prende di mira a quell'eta' ti strozza e ti soffoca. Non arrendiamoci. Supportiamo la ricerca. Non vergognamoci dei nostri sentimenti, non vergognamoci di un dolore che non abbiamo MAI cercato e voluto. Non dobbiamo mai smettere di pensare e agire per migliorare. Questa deve essere la nostra decade, la decade in cui la societa' e la comunita' scientifica si deve accollare seriamente questa a.a. dal punto di vista scientifico, punto e basta. basta con le chiacchere sul se e' giusto o no curarsi o investire contro la a.a., e' giusto e basta. Credo sia venuto il momento di non chiedere piu' aiuto a nessuno, proprio a nessuno, ma organizzarci tra di noi, associarci e supportare la ricerca direttamente, acquisendo tutte le nozioni possibili che permettano un diretto controllo, documentazione e diffusione dello stato delle cose. Dobbiamo aiutarci da soli. In fondo ricordiamoci di un valore immenso che nessuno potra' portarci mai via. E ve lo dico io che e' vero, perche' a me la vita ha portato via tanto, ma l'amicizia, il sorriso di un amico, vero, quello non me lo portera' via nessuno. E' con l'amicizia, per gli altri e per me stesso, che sto sopravvivendo. Come una farfalla che lotta per uscire dal bozzolo, forse. Forse non ce la faro' mai a volare come avevo pensato e progettato da bambino, ma santo dio ci provero' fino a quando avro' da respirare ... Tanti auguri a tutti. Non molliamo. Con affetto.

Mi sa che qui lo sconforto generale sta portando ad una gran confusione e a vedere il nero e il marcio anche nei pochi casi in cui non c'e' ... x chi non lo sapesse, esistono soltanto 2 - two - due studiosi che si sono rivelati vincenti in passato nella ricerca della soluzione definitiva contro l'alopecia, che essenzialmente viene identificata o nella terapia genica o nell'hair cloning. Questi due scienziati sono: Angela Christiano - Nel 1998 per la prima volta scopre un gene associato ad una forma di alopecia, detta alopecia universalis. Genetista e pioniere, sola e unica vera speranza al mondo x la terapia genica. Anch'essa sofferente di alopecia areata: da qui e' nata la sua missione. Colin Jadoha - Primo e unico assoluto scienziato al mondo ad aver clonato un follicolo pilifero ed averlo fatto ricrescere sul braccio di un'altra persona. Unico ad aver scientificamente pubblicato la clonazione come processo ed aver provato che esso e' possibile. Tutti gli altri, per adesso, da Gho a Wmsr a streghe fattucchieri e maghi vari, non hanno provato proprio un bel ca....

Antonio1, Permettimi 2 parole. Il trapianto ed il risultato conseguente sono essenzialmente una questione numerica e legata al altri fattori. Dipendentemente dal grado di alopecia e bonta' della zona donatrice potrai avere un risultato piu' o meno buono, che richiede comunque due o piu' sessioni a distanza di 8 mesi un anno l'una dall'altra, per avere veramente il "grosso" salto. Quindi almeno 2 anni dall'inizio alla fine, diciamo in media 3; TIENI CONTO DI QUESTO SUBITO. L'area donatrice e' MOLTO limitata, al massimo 6000 UF, diciamo che 4000 le avrai di sicuro. 4000 UF sono circa 9-10.000 capelli. 1 UF e' composta da 1,2,3,4 o a volte anche 5 capelli. Il gioco consiste nel ridistribuire questo serbatoio di UF in modo uniforme nelle aree riceventi, tenendo conto di questo fondamentale gioco: FINO A QUANDO non perdi il 50% dei capelli in una zona, "sembra" che ce li hai ancora tutti. Quindi, si ridistribuiscono le UF in una densita' che e' la meta' ( o un quarto ) della densita' normale che rimane 80 UF ( ma che e' tale sono nell'area donatrice, nelle tempie ad esempio e' sempre molto meno anche in condizioni normali ). Insomma, e' una questione numerica, punto e basta: non esistono miracoli. Inoltre, GRANDE GIOCO lo fanno alcune caratteristiche come il contrasto fra colore dei capelli e cute, lo spessore del capello e infine se sono mossi, ricci o no. - I capelli ricci danno sempre piu' copertura, come effetto. - Quelli biondi su carnagione abbronzata o scura danno ( a parita' di densita' di UF ) piu' copertura dei capelli neri su scalpo bianco cadavere. - I capelli piu' grossi ( a parita' sempre di UF ) danno piu' copertura di quelli piu' sottili - Il diametro si puo' misurare con uno speciale calibro. Ora metti assieme tutti questi fattori, e capisci che il trapianto non e' affatto ne' scontato, ne' di semplice previsione come risultato ... Tieni conto che, ANCHE, in TUTTI i trapianti anche da quelli fatti da Cole, Shapiro, Seager non tutte le UF sopravvivono: statisticamente un 5% non ce la fa a ricrescere, anche con tutte le precauzioni. QUINDI LA TUA DONOR AREA E' UGUALE AL 95% DELLA STESSA. Bel casino, eh ?

Ancora una volta, la doc Angela ci sta dimostrando che la scoperta dei geni associati all'alopecia non e' impresa impossibile. Angela rimane isolata nel suo lavoro, le industrie farmaceutiche la rifiutano; soltano recentemente una fondazione ha finanziato lei e il doc Jadoha con 250.000 dollari. Angela Christiano andrebbe pubblicizzata e sponsorizzata da tutti noi. Pensate solo se ognuno di noi sofferenti di a.a. nel mondo, offrisse 10 euro: sorpasseremmo di gran lunga quella donazione. Salus, cosa ne pensi di organizzare una donazione alla Kirsch Foundation da parte di noi di salusmaster, con la semplice richiesta di essere informati direttamente sugli aspetti scientifici della loro ricerca ? ( http://www.kirschfoundation.org/flash_index.html ) Potrebbe essere un modo molto serio di partecipare attivamente alla ricerca ...

Ciao Stopardi, se vuoi saperne di piu' su Gho consulta le pagine di www.hairsite.com, hai il link in copertina. C'e' anche su questo forum nelle ricerche future una sessione a lui dedicata. Qui in olanda di Gho non sa nulla nessuno, in ogni modo x adesso pratica una tecnica denominata Follicle Transplantation similmente a Woods, Cole e Jones.

Per le battone ci potrei essere anch'io, a gennaio si vola bene ed economicamente ... seriamente ci potrei essere, tutti gli interessati si tengano in contatto.

Vacci piano Maxell ! Se proprio vuoi azzardare a buttarti fino ai 2.5 mg, fallo molto ma molto gradualmente ... mai incrementare cosi' di botto, rischi di brutto. Mi raccomando ... stai attento.

http://www.hair-restoration-info.com/6/ubb...61&m=5766058962 ... veramente sempre molto positivi di commenti sul Dr. Hasson, peccato che Vancouver sia cosi' lontano !

http://www.lipoxidil.com/dutasteride.htm Sto prendendo in esame di provare questa soluzione topica di dutasteride con veicolo liposomale; Mi interessano alcuni commenti specialmente da M.Rex, Macchianera, i docs, Dep, Docale, e chiunque sia seriamente interessato o in alternativa preparato davvero sull'argomento dutasteride; Dunque la soluzione e' al 0.15% di dutasteride, 50 ml, 126 USD di costo compreso spedizione, dura 50 giorni; Come tutti sappiamo e' il DHT nello scalpo quello che conta inibire e non quello del plasma, anche se ovviamente stroncandolo nel sangue se ne riduce anche per conseguenza il livello periferico nella cute, ma in sostanza secondo i trails: 0.5 mg duta al giorno via sistemica: DHT nel sangue - 92%, DHT nello scalpo -54% 2.5 mg duta al giorno via sistemica: DHT nel sangue - 97%, DHT nello scalpo -82% Ovunque si asserisce che dutasteride e' ideale per essere assorbita attraverso la pelle, ora mi domandavo se in assenza di altri prodotti come questo i liposomi POSSANO essere un buon modo, effettivo, per rendere effettiva dutasteride localmente; Vorrei anche se possibile, analizzando la composizione chimica di duta e/o le esperienze di agenti combinati al minox come Retin-A, Alcol, etc. quale potrebbe essere un combinazione sensata. Grazie in anticipo, fatevi sotto ...

Vorrei fare il mio in bocca al lupo a Shon67, per il suo viaggio al DHI in maggio; Mi raccomando Shon subbissali letteralmente di tutte le domande di cui hai bisogno, non risparmiarti nulla; e' chiaro che loro tenteranno di convincerti a procedere gia' da subito; Interessantissime saranno le informazioni e l'eventuale esperienza con la tecnica del prelievo diretto; Se vuoi farti operare al vertex cerca di capire come possono "prevenire" un eventuale progressione della a.a. a distanza di anni dell'intervento, se vanno a lavorare anche 1-2 cm al di fuori dei bordi x lasciare un margine futuro, come ricreano la rosa del vertex in modo naturale soprattutto, perche' pare che la naturalezza in quella zona sia non facile da ottenere, anche per il fatto che viene esercitata di meno dai chirurghi in genere. Insomma Shon vai tranquillo, watch your back, ma non credo tu abbia bisogno di queste prediche, ho amici di Napoli qui e prima di fregare un napoletano, hai voglia, devi saltare i fossi per la lunga .... salutone affettuoso Lott.

Siamo alle solite, Fino a quando Gho, o Unger, o altri non PUBBLICHERANNO scientificamente - bello e chiaro - a tutto il mondo il loro lavoro ( come ad esempio si e' degnato di fare Jadoha, l'inglese che per primo ha VERAMENTE clonato un follicolo ) tutte le speculazioni sulla HM, siano 1 anno, 10 o 100 anni, francamente non mi fanno ne' caldo ne' freddo. Stesso discorso vale per il caro Dr. Woods, che anche se fosse il migliore chirurgo al mondo come lui dice, non si degna di pubblicare il suo lavoro, ma solo di VENDERLO nei suoi seminari, con la clausola che chi volesse imparare la sua tecnica se ne deve stare zitto ... grazie tante, bell'attegiamento; come se Pasteur avesse "venduto" la Penicillina obbligando a chi la utilizzava di non parlarne in giro ... la HM puo' anche essere reale, oggi aprile 2003 - forse, ma Gho non lo vuole ufficialmente dire e spiegare; questo e' un atteggiamento egoistico, ovviamente commerciale, ma senza senso ... sempre che lui sia cosi' avanti come dice - il che equivarrebbe a dire che tutti gli altri scienziati, compreso Jadoha che ha piu' volte spiegati che la clonazione dei bulbi e' un'impresa difficilissima su scala industriale ( e lui ne ha clonato uno ), sono tutti dei deficienti ritardati mentali; Beh, a noi i commenti ...

Vorrei ringraziare Piero2 x il suo dettagliato racconto, e per il coraggio e intraprendenza mostrati per fare il grande passo. I miei piu' sinceri auguri x il massimo risultato ! Chiederei anticipatamente, a coloro che abbiano domande x Piero2 ( me compreso ), di usare il massimo tatto e educazione; che non si ripeta per cortesia l'aggressione avvenuta come quando Gekko fece il report sulla sua trasferta a Minneapolis da Shapiro. L'esperienza di Piero2 e' molto interessante e ci sono forumisti come me, Ron, Geronimo che sicuramente sono incuriositi da questa nuova moderna organizzazione europea, il DHI, quindi ... massimo rispetto x Piero2. Piero2, la piu' importante novita' nel tuo racconto e' a mio avviso la garanzia scritta di ricrescita di tutte le UF trapiantate, con eventuale aggiunta futura di tutte quelle ( speriamo poche ) che eventualmente potrebbero non ricrescere. Potresti spiegare come potresti far valere questo diritto ? Voglio dire, come fai a dimostrare che ad esempio 100 UF su 1881 non sono ricresciute ? Salutoni, lott.

Ron Ron Ron, Vecchio mattacchione non perdi mai occasione x intortare eh ? eh eh eh ... Grazie del reportage; magari ti do' un colpo di tel nel weekend x scambiarci un po' di impressioni; vorrei chiamare anche il Gero, e sentire come sta il Gekko... Insomma quando venite qui in olanda da me ? Caro Ron, qui altro che greche, qui tra tutte ste teste gialle andresti giu' di testa completamente ah ah ah ... Scherzi a parte il DHI comincia ad essere interessante... potrei anche farci un salto anch'io, magari con qualcuno disposto a venirci con me ... ma solo se mi garantiscono un incontro con PIU' DI UN Ex PAZIENTE. Saludos Lottateur

Fuori i MARONI tempions ! E' arrivato il momento anche per te ! Per me fu a 23 anni, a te a 16 ! Fuori le palle che ce le hai eccome ! Leggiti come scrivi e come parli, hai sedici 16 ma ti esprimi come un uomo ... bene, allora e' arrivato il momento: una bella SCOSSA dentro e fuori, continua a curarti, rispondi PER LE RIME a tuoi finti amici e mandali senza problemi a fare in c... se approfittano come avvoltoi di questo tuo problema x denigrarti ... tu non sei l'ultimo, un par di palle !!! Esci con quella figliola, buttati provaci, gioca a pallone, curati con fina e minox, fai TUTTO QUELLO CHE DEVI E VUOI FARE, testa alta e autostima al 1000 x 1000 !!! Ti abbraccio come un fratellone maggiore, con affetto Lott.

Grazie mille Cheveaux, sei stato molto gentile. Contattero' i siti e vi saro' sapere ... Lott.

xxxxx datemi una mano x favore, Finalmente oggi e' arrivato il primo estratto conto della mia carta di credito, cosi' ho digitato il mio codicino di Paypal.com, allo scopo di attivare il mio account su Paypal e procedere all'ordine di duta da vitaminox ma ... a questo indirizzo: http://www.privatimport.nu/avolve/avodart.htm non c'e' piu' nulla ! Che succede, non si puo' piu' fare ? Javvier, tu che hai gia' usato Paypal, che mi dici ? Lott.

Geronimo, Ti ringrazio dell'apprezzamento, ma per quel che mi riguarda vedo del tutto naturale se non doveroso condividere sul forum questo tipo di colloqui ed esperienze. Sono interessato a questo punto se ti va ad un eventuale chiaccherata telefonica, ti mandero' un mex con il mio numero e se ti va ci chiamiamo. Sono curioso di un altro parere su Shapiro e dei casi visionati da te di persona. Per l'utente Sandro, vorrei gentilmente ricordarti che prima di sparare a zero, sarebbe il caso un attimino di informarsi. L'estensore nasce appunto con l'idea di ricreare un vertex folto, proprio perche' anche se utilizzi 2000 UF sul vertex in 2-3 passate non ce la farai mai ad arrivare ad una densita' eccezzionale; per natura il vertex confina con un'area posteriore dove la densita' e' al massimo. I capelli alla Bruno Vespa te li da' invece una singola one-pass proprio come dici tu ... Il vertex e' un'area pericolosa da trattare con il trapianto a UF, in caso di progressione si noterebbe subito la differenza, anche per pochi millimetri. Ecco perche' il 90% dei chirurghi ti risponde NO o MEGLIO DI NO se vuoi fare il vertex. Poi e' inutile, e' una questione numerica, se fai UF nel vertex rischi di non averne a sufficienza per l'area frontale in futuro. Sono scelte difficili, ognuna comporta dei rischi. Ma cerca di aprire la mente, e possibilmente, di dare delle risposte un po' piu' articolate. L'extender funziona LATERALMENTE e non longitudinalmente sulla cute. Non ti trasforma in un mostro deforme. Certo, non e' una passeggiata. La prima estensione comporta una notte di dolori piuttosto forti, come temevo. Ma Frechet dice, come altro non si puo' dire, " You must be motivated ". Think about it. L'unica cosa che non mi ha convinto e' questo fatto di fare micrografts alla fine invece di pure UF ... lui sostiene questo: - Con le micrografts non si va a tagliare il tessuto in tanti piccoli pezzi cosi' come si fa con le UF; dunque si salvano tutti quei capelli in fase telogen, che con delle grafts un pochino piu' grandi rimangono " nascoste " li' in mezzo alla cute impiantata. Nel caso di UF, si beccano gli anagen e catagen, ma i telogen si buttano via. Cosa ne pensate ?

Ron2, thanx ! Frechet mi ha fatto davvero una buona impressione. Non ho potuto visionare un paziente dal vivo, cosa che faro' al 100% se decidero' di optare per lui. In effetti vedo la combinazione Dr. Frechet x il vertex + UF sul resto della testa come la migliore. Ecco perche' molti docs non toccano il vertex, perche' e' troppo soggetto a progressione, anche un allargamento di pochi millimetri si noterebbe CHIARAMENTE, e allora ridaie con sessioni di rotocco ogni due anni... Invece Frechet con l'aiuto dell'estensore rimuove non solo il vertex, ma per sicurezza va avanti un po', qualche millimetro attorno. Questo ovviamente ( anche se non me l'ha detto ) comporta la distruzione di un certo numero di capelli che diciamo " molto probabilmente " dovrebbero cadere nel giro di qualche anno. Il mio unico dubbio e' se davvero l'area don atrice non viene traumatizzata in qualche modo dall'estensione. Per il resto io non avrei dubbi. Mi prendo qualche tempo per decidere. Ma in ogni modo l'extender sul vertex, come risultato folto e soprattutto come NON UTILIZZO o POCO UTILIZZO diciamo della donor area, secondo me non ha paragoni.

Ciao xxxxx, allora, qui esempi di lavori: http://medicalhairrestoration.com/frechet_ex.htm e qui i dati salienti: http://medicalhairrestoration.com/dr_frechet.htm ---- Dunque recentemente sono stato in francia dal Dr. Frecht, ho preso appuntamento con lui, mi ha illustrato la sua tecnica relativa alla scalp extension e reduction per trattare il vertex. Allora per farla in breve, Frechet vi installa un extender sottocutaneo x 6 settimane, poi fa il primo intervento sulla linea mediana del vertex; quindi dopo aver asportato diciamo il 50% del vertex vi installa un secondo extender, piu' piccolo, per altre 6 settimane; quindi altro intervento chirurgico e il vertex viene completamente eliminato. Qui sta la novita': il problema principale della scalp extension/reduction e' la cicatrice axe-like ( a forma di ascia ) che taglia in due la testa sulla linea mediana ( perdendicolare alle spalle, per intenderci ); lui la corregge con un terzo intervento, in cui in pratica muove con delle pillole scalp-flaps, le transposition-flaps, alcuni lembi della parte inferiore della cicatrice, in modo da formare la rosa tipica del vertice maschile, insomma muove "a cerchio" i capelli in modo che l'aspetto sembra naturale, quindi i capelli non crescono in direzione opposta a "spaccatura" sulla linea mediana, ma il tutto sembra naturale come lo era prima. Mi ha mostrato i movimenti delle piccole flaps sul nuovo libro di Walter Unger & Ron Shapiro "Hair Transplantation" che uscira' a breve sul mercato - li' era davvero tutto chiaro, con schemi e immagini. Alla fine molto probabilmente bisogna fare un quarto intervento finale di UF, lui fa anche micrografts, per eventualmente coprie piccole insenature rimaste all'inizio e alla fine della cicatrice. Il Dr. Frechet mi e' apparso franco e onesto, quando ha visto che ero a conoscenza in generale di un po' di tutto sul problema non ha esitato a darmi spiegazioni tecniche. Costi: si parla di 2500 euro a intervento, quindi lavoro completo 10.000 euro. Si puo' verificare un'innalzamento dell'attacaatura sulle tempie a causa della scalp extension. Il risultato e' un vertex folto, area donatrice tutta intatta per il futuro, senza utilizzare UF. xxxxx, adesso mi staccano il collegamento internet, proseguo domani, scusate. Lott.