Добірка наукової літератури з теми "Hair follicle miniaturisation"

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Статті в журналах з теми "Hair follicle miniaturisation":

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Yadav, Deepika, Sujay Khandpur, Sweta Subhadarshani, and Kanika Sahni. "Congenital symmetrical circumscribed patterned non-scarring alopecia of eyebrows: a variant of congenital triangular alopecia or an anatomical variation?" BMJ Case Reports 12, no. 5 (May 2019): e227472. http://dx.doi.org/10.1136/bcr-2018-227472.

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Triangular alopecia presents as a unilateral triangular-shaped non-scarring alopecia usually involving the temporal scalp. There are few reports of occipital scalp involvement and bilateral disease. Usually it is seen at 2–3 years of age but occasionally can be present at birth. Here we present a unique case of triangular alopecia involving the eyebrows in a 23-year-old man. He had bilateral symmetrical involvement since birth. Points in favour of triangular alopecia in our case were non-scarring alopecia, oval-to-triangular shape, fringe of terminal hair at superior margin; trichoscopy showing significant decrease in hair diameter diversity with increased number of vellus and intermediate hair and histopathology showing normal hair follicle density and increased vellus and intermediate hair (miniaturisation) with absence of inflammation on histopathology. Other differential diagnoses kept were partial duplication of eyebrows, congenital alopecia areata and mild form of ectodermal dysplasia.
2

Ellis, Justine A., Rodney Sinclair, and Stephen B. Harrap. "Androgenetic alopecia: pathogenesis and potential for therapy." Expert Reviews in Molecular Medicine 4, no. 22 (November 19, 2002): 1–11. http://dx.doi.org/10.1017/s1462399402005112.

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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.
3

Wadstein, Jan, Erling Thom, and Aida Gadzhigoroeva. "Integral Roles of Specific Proteoglycans in Hair Growth and Hair Loss: Mechanisms behind the Bioactivity of Proteoglycan Replacement Therapy with Nourkrin® with Marilex® in Pattern Hair Loss and Telogen Effluvium." Dermatology Research and Practice 2020 (May 5, 2020): 1–17. http://dx.doi.org/10.1155/2020/8125081.

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Follicular proteoglycans are key players with structural, functional, and regulatory roles in the growth and cycling behaviour of the hair follicles. The expression pattern of specific proteoglycans is strongly correlated with follicular phase transitions, which further affirms their functional involvement. Research shows that bioactive proteoglycans, e.g., versican and decorin, can actively trigger follicular phase shift by their anagen-inducing, anagen-maintaining, and immunoregulatory properties. This emerging insight has led to the recognition of “dysregulated proteoglycan metabolism” as a plausible causal or mediating pathology in hair growth disorders in both men and women. In support of this, declined expression of proteoglycans has been reported in cases of anagen shortening and follicular miniaturisation. To facilitate scientific communication, we propose designating this pathology “follicular hypoglycania (FHG),” which results from an impaired ability of follicular cells to replenish and maintain a minimum relative concentration of key proteoglycans during anagen. Lasting FHG may advance to structural decay, called proteoglycan follicular atrophy (PFA). This process is suggested to be an integral pathogenetic factor in pattern hair loss (PHL) and telogen effluvium (TE). To address FHG and PFA, a proteoglycan replacement therapy (PRT) program using oral administration of a marine-derived extract (Nourkrin® with Marilex®, produced by Pharma Medico Aps, Aarhus, Denmark) containing specific proteoglycans has been developed. In clinical studies, this treatment significantly reduced hair fall, promoted hair growth, and improved quality of life in patients with male- and female-pattern hair loss. Accordingly, PRT (using Nourkrin® with Marilex®) can be recommended as an add-on treatment or monotherapy in patients with PHL and TE.
4

Rushton, D. Hugh, Gillian E. Westgate, and Dominique J. Van Neste. "Following historical “tracks” of hair follicle miniaturisation in patterned hair loss: Are elastin bodies the forgotten aetiology?" Experimental Dermatology, June 11, 2021. http://dx.doi.org/10.1111/exd.14393.

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Дисертації з теми "Hair follicle miniaturisation":

1

Rushton, D. H., Gillian E. Westgate, and Neste D. J. Van. "Following historical 'tracks' of hair follicle miniaturisation in patterned hair loss: Are elastin bodies the forgotten aetiology?" Wiley, 2021. http://hdl.handle.net/10454/18515.

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Yes
Pattern Hair Loss (PHL) is a chronic regressive condition of the scalp, where follicular miniaturisation and decreased scalp hair coverage occurs in affected areas. In all PHL cases there is a measurable progressive shortening of the terminal hair growth duration, along with reduced linear growth rates. In both genders, PHL initially shows an increase in short telogen hairs ≤30mm in length, reflecting a cycle completion of under six months in affected terminal hair follicles. To understand the miniaturisation process, we re-examine the dynamics of miniaturisation and ask the question, 'why do miniaturised hair follicles resist treatment?' In the light of recent developments in relation to hair regeneration, we looked back in the older literature for helpful clues 'lost to time' and reprise a 1978 Hermann Pinkus observation of an array of elastin deposits beneath the dermal papilla following subsequent anagen/telogen transitions in male balding, originally described by Arao and Perkins who concluded that these changes provide a "morphologic marker of the entire biologic process in the balding scalp". Thus, we have reviewed the role of the elastin-like bodies in hair pathology and we propose that alterations in elastin architecture may contribute to the failure of vellus-like hair reverting back to their terminal status and may indicate a new area for therapeutic intervention.

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