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1 S appears to be a primary abnormality in the pilosebaceous-apocrine unit.
2 of triglyceride hydrolysis within the normal pilosebaceous apparatus, despite high rates of triglycer
3  Nrf2 specifically promoted the expansion of pilosebaceous cells expressing markers of junctional zon
4                              The increase in pilosebaceous cells provided a larger pool of keratinocy
5 ychia congenita type 2; (ii) the presence of pilosebaceous cysts following puberty is the best indica
6 icular keratosis, and cysts (steatocysts and pilosebaceous cysts).
7  by hypertrophic nail dystrophy and multiple pilosebaceous cysts.
8 sociated with focal keratoderma and multiple pilosebaceous cysts.
9 er root sheath of the hair follicle, and the pilosebaceous duct.
10         Cytokine and chemokine expression by pilosebaceous epithelial cells (i.e., sebocytes and foll
11 nflammatory gene expression in acne-involved pilosebaceous epithelial cells are still unknown because
12 lgaris is a common cutaneous disorder of the pilosebaceous follicle.
13 caspase-1 and NLRP3 were detected around the pilosebaceous follicles and colocalized with tissue macr
14  isolates are present on and around the skin pilosebaceous follicles, the finding of multiple subtype
15  the cell surface of macrophages surrounding pilosebaceous follicles.
16                          The human sebaceous pilosebaceous infundibulum was isolated and maintained i
17 rically to differentiate into cycling mature pilosebaceous structures.
18 GATA6 is involved in regulation of the upper pilosebaceous unit and may be an actionable target in th
19 e to amyloid deposition primarily around the pilosebaceous unit but also within the papillary and ret
20 sorders affecting the hair follicle (HF) and pilosebaceous unit impose psychosocial and financial bur
21  process of follicular keratinization in the pilosebaceous unit leading to inflammatory acne lesions,
22 e sebaceous gland is an integral part of the pilosebaceous unit of mammalian skin, which produces and
23  that GATA6, which is expressed in the upper pilosebaceous unit of normal human skin, is down-regulat
24 nocycline and the retinoid tazarotene to the pilosebaceous unit of the dermis.
25 e vulgaris is an inflammatory disease of the pilosebaceous unit of the skin that primarily involves t
26       Enhanced proliferation of cells of the pilosebaceous unit peripheral to the wound and a concomi
27 cne is a chronic inflammatory disease of the pilosebaceous unit resulting from androgen-induced incre
28 in contrast to their epidermal counterparts, pilosebaceous unit stem cells depend on a functional ETC
29 ynthesize knowledge about the biology of the pilosebaceous unit that has been derived from GWASs of h
30 ostasis, regeneration and disease within the pilosebaceous unit, an integral structure of the epiderm
31 als that Lrig1(+ve) cells maintain the upper pilosebaceous unit, containing the infundibulum and seba
32         We provide an up-to-date view of the pilosebaceous unit, encompassing the heterogeneity and p
33 l model, was designed to be delivered to the pilosebaceous unit, the site of action, preferentially b
34 stochemically to this affected region of the pilosebaceous unit, was specifically up-regulated by ME1
35 indings might be due to abnormalities of the pilosebaceous unit, we carried out three-dimensional mor
36 rentiation, and stem cell maintenance in the pilosebaceous unit, which are all essential for the home
37 mmatory cells followed by destruction of the pilosebaceous unit.
38 factors underlying acne as a disorder of the pilosebaceous unit.
39 which is implicated in acne pathogenesis and pilosebaceous-unit inflammation, are the main targets of
40 uggest that PPARgamma is crucial for healthy pilosebaceous units and it is the loss of this function
41 al examination of serial sections of labeled pilosebaceous units demonstrated a complex cell lineage.
42                    Development of incomplete pilosebaceous units in chimeric hair corresponded with u
43 cells in the basal epithelial cell layer and pilosebaceous units of healing tissue.
44 normalities, Acbp is highly expressed in the pilosebaceous units of mouse skin as determined by North
45 s and 52 healthy individuals by sampling the pilosebaceous units on their noses.
46 ogic changes and protoporphyrin synthesis in pilosebaceous units were observed from skin biopsies.
47 promotes collagen organization, formation of pilosebaceous units, and proliferation of cells in the b
48 f uncertain etiology in skin regions rich in pilosebaceous units.
49 rentiation, thus preventing the formation of pilosebaceous units.
50 ved the conversion of nipple epithelium into pilosebaceous units.