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1 activation zone during the quiescence phase (telogen).
2 egression (catagen) and relative quiescence (telogen).
3 gression (catagen), and relative quiescence (telogen).
4 volution (catagen), and relative quiescence (telogen).
5 er detectable in follicles at resting stage (telogen).
6 ession (catagen), and relative "quiescence" (telogen).
7 th (anagen), regression (catagen), and rest (telogen).
8 lready entered the subsequent resting phase (telogen).
9 ring anagen and decreases during catagen and telogen.
10 ched-off in catagen to remain absent through telogen.
11 he onset of anagen when the follicles are in telogen.
12 rtens anagen phase, but prolongs catagen and telogen.
13 d in the club hair sheath during catagen and telogen.
14 ollicles during catagen but not in anagen or telogen.
15 r follicles in the control group remained in telogen.
16               Hair follicles failed to enter telogen (a resting period) and remained continuously in
17 nsitioning through a morphologically typical telogen after Gsdma3 mutation.
18 hway within the dermal papilla regulates the telogen-anagen follicle transition and suggest that diff
19 g hair follicle generation and regeneration, telogen-anagen reentry, and extra-follicular macro-envir
20                    NF-kappaB participates in telogen-anagen transition in awl and zigzag HFs, and is
21  serves as a crucial proximal signal for the telogen-anagen transition.
22 ermis (Ctip2(ep-/-) mice) leads to a shorter telogen and a premature entry into anagen during the sec
23 sitive fibroblasts from neonatal skin, adult telogen and anagen skin and adult skin in which ectopic
24              The circadian transcriptomes of telogen and anagen skin are largely distinct, with the f
25 n at two different stages of the hair cycle, telogen and anagen.
26  detected in the secondary hair germ of late telogen and early anagen HFs, suggesting a potential rol
27 modulator, which is highly expressed in late telogen and early anagen.
28 ntagonist, caused the hair follicles to exit telogen and enter anagen, thereby initiating hair growth
29 ated by Atoh1 induction during anagen versus telogen and following disruption of Notch signaling by c
30 rsal skin of mice arrested hair follicles in telogen and produced a profound and prolonged inhibition
31 of null skin did not progress from anagen to telogen and scanning electron micrografts revealed wavy,
32 behavior through regression (catagen), rest (telogen), and regeneration (anagen) during postnatal lif
33         In mature follicles, transition from telogen back into anagen involves the activation, prolif
34 ved hair follicle stem cells residing in the telogen basal bulge.
35 gen) and finally a relative quiescent phase (telogen) before returning to anagen.
36 zed cyclin D1 to the suprabasal cells of the telogen bulge and anagen outer root sheath (ORS).
37 Moreover, ablation of Dlx3 expression in the telogen bulge stem cells is associated with a loss of BM
38 ession of miR-148a markedly increases during telogen (bulge and hair germ stem cell compartments).
39  TOPGAL expression ceased during catagen and telogen, but reappeared at the start of the postnatal ha
40 n (Dsg)3-/- (knockout) mice lose hair during telogen, but their anagen hairs remain anchored to the f
41 e the increased survival of ORS cells during telogen delays the initiation of a new hair cycle.
42 re was an increase in the size of anagen and telogen DP, but the proportion of tdTomato-labeled cells
43 nylalanine hydroxylase activities during the telogen/early anagen stage (days 0-1).
44    The mean ferritin levels in patients with telogen effluvium (50.1 [33.9, 66.33]) and alopecia area
45                     We studied patients with telogen effluvium (n = 30), androgenetic alopecia (n = 5
46                                              Telogen effluvium may present suddenly or insidiously se
47  common forms of alopecia in adolescence are telogen effluvium, androgenetic alopecia, and alopecia a
48 tation (e.g., chemotherapy-induced alopecia, telogen effluvium, androgenetic alopecia, cicatricial al
49 tal fibrosing alopecia, lichen planopilaris, telogen effluvium, etc), and 32 unaffected scalps withou
50 ristics of alopecia were similar to those of telogen effluvium, which indicates that stress is one of
51 poral and vertex scalp skin, associated with telogen effluvium.
52  androgenetic alopecia, alopecia areata, and telogen effluvium.
53 xcoriation) mouse skin rescues hair follicle telogen entry and significantly decreases the Wnt10b-med
54            Overexpression of Wnt10b inhibits telogen entry by increasing epithelial strand cell proli
55 agen hair follicle with weak staining in the telogen follicle and epidermis; iii) epidermal cornifin-
56 nagen hair follicle and weak staining of the telogen follicle and the suprabasal layers of the epider
57                                   Irradiated telogen follicle survival data were consistent with that
58 est levels of expression associated with the telogen follicle.
59 ions form colonies; however, stem cells from telogen follicles formed more total colonies, and more c
60 ng hair follicles and ranged from 2.6% above telogen follicles to 7.0% above early anagen follicles.
61 ath cells directly abutting the club hair in telogen follicles.
62 S-phase cells as the control epidermis above telogen follicles; however, the number of BrdUrd S-phase
63 e of hK14 in the epithelial sac to which the telogen hair fiber is anchored.
64 nduced 99 +/- 4.5% (mean +/- SEM) of resting telogen hair follicles into a proliferative (anagen) sta
65 ar keratinocyte proliferation and reentry of telogen hair follicles into anagen.
66 anisms responsible for re-entry of quiescent telogen hair follicles into the hair-producing anagen st
67 dermis and the epithelium of both anagen and telogen hair follicles.
68 ronic activation of beta-catenin in resting (telogen) hair follicles resulted in changes consistent w
69 sentation in settings with HF growth arrest (telogen), HF loss, and nonregenerative wound areas in mo
70 air follicle (HF) buds, whereas in postnatal telogen HFs Lhx2(+) cells reside in the stem cell-enrich
71 C1 receptor (MC1-R) gene was undetectable in telogen, increased during hair growth, and, after reachi
72 atenin cycle, thus dividing the conventional telogen into new functional phases: one refractory and t
73                    Transition from anagen to telogen involves an intermediate stage, catagen, consist
74                The transition from anagen to telogen is marked by downregulation of hair cortical spe
75 ing pathway and that morphologically typical telogen is not essential for the initiation of a new hai
76  HF dystrophy, pigmentary abnormalities, and telogen-like condensed dermal papillae.
77 closely resembled neonatal dermis than adult telogen or anagen dermis.
78                                       During telogen or resting phase and in early anagen, the GFP-po
79 ure) during the time period corresponding to telogen phase in WT mice.
80 ng ability, and premature hair loss at early telogen phase of the hair cycle, resulting in cyclic alo
81                                       In the telogen phase of the hair growth cycle, PAI-2 was limite
82  function has been assumed to be part of the telogen phase, using a laboratory mouse model and newly
83 cally in the hair follicle epithelium during telogen phase.
84 ng the involution (catagen) and the resting (telogen) phase.
85 the outer root sheath results in a shortened telogen-phase length and elevated number of hair follicl
86  in FP during anagen, but not in catagen and telogen phases of the hair cycle.
87 iR-148a inhibitor into mouse skin during the telogen phases of the postnatal hair cycle results in ac
88 f anagen (growth), catagen (regression), and telogen (quiescence).
89  CD34KO hair follicles typically remained in telogen rather than transitioning into anagen growth, co
90               Furthermore, anagen to catagen/telogen ratios were lower in individuals with alopecia (
91 od, establishing a growth cycle in 3 phases: telogen (resting), anagen (growth), and catagen (regress
92 r papilla, AP-2alpha was weakly expressed in telogen, significantly upregulated in early anagen, then
93 n induces new hair growth phase in postnatal telogen skin in vivo.
94 nds on anagen skin heal faster than those on telogen skin, suggesting that hair cycle stages may infl
95  and S-phase are antiphasic to each other in telogen skin.
96 ode ruby laser exposure, whereas catagen and telogen stage hair follicles were resistant to laser irr
97 HFSC activation, suggesting that the resting telogen stage is actively maintained by the hair follicl
98 in epithelium causes a rapid transition from telogen (the resting phase of the hair follicle cycle) t
99                            A prolongation in telogen, the resting phase of the hair cycle, was also o
100 of growth (anagen) and metabolic quiescence (telogen) throughout life.
101 id growth (anagen) and metabolic quiescence (telogen) throughout life.
102 n stimulate the transition from the resting (telogen) to the growth (anagen) stage of the hair cycle
103  shown that JAK-inhibition is able to induce telogen-to-anagen transition in wild-type mice.
104 r, it has become increasingly clear that the telogen-to-anagen transition is controlled jointly by at
105 iescent state of HFSCs in the process of the telogen-to-anagen transition.
106 lar pigmentary unit during HF anagen-catagen-telogen transition and may be used for the establishing
107 that Gsdma3 has an important role in catagen-telogen transition by balancing the Wnt signaling pathwa
108 hether there is a switch controlling catagen-telogen transition remains largely unknown.
109 e induction of macrophage apoptosis in early telogen, we identify a novel involvement of macrophages
110 keratin 6-positive (K6) inner bulge cells in telogen, which regulate the quiescence of adjacent hair
111  old mutant skin show follicles in prolonged telogen with hyperplastic sebaceous glands.

 
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