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1 s of the natural pigment called melanin from hair.
2 e ratios or quantities of amino acids in the hair.
3 very short primary roots and elongated root hairs.
4 ent atrichoblast cells that do not form root hairs.
6 ecurity with levels of ART concentrations in hair among women living with human immunodeficiency viru
11 wth that occurs during the formation of root hairs and pollen tubes or de novo formation of cell plat
16 ajor actin-bundling proteins in bristles and hairs are known, this information on scales is unknown.
18 sing hydroxamic acids immobilized on resins (HAIRs) as stable and versatile building blocks for the p
20 lead (Pb), copper (Cu), and chromium (Cr) in hair, blood, urine, nails, and saliva from 635 Italian a
22 genically-active melanocytes from the anagen hair bulbs of affected human scalp remains unclear, oxid
24 mediates this effect by changing location of hair bundle establishment or positions of HCs since daug
25 eld maps, and sensitivity curves that show a hair bundle is desensitized by efferent stimulation.
29 ey stereociliary proteins involved in normal hair bundle morphogenesis, such as CDC42, RAC1, EPS8 and
31 acid substitutions consistent with abnormal hair bundle morphology and reduced hearing sensitivity.
34 owed that transcription factor Emx2 reverses hair bundle orientation and its expression in the mouse
36 I-BAR protein family, is a newly identified hair bundle protein that is localized to the tips of the
38 recovery of mechanoelectrical transduction, hair bundle stiffness, and spontaneous bundle oscillatio
44 ant larvae retain normal gross morphology of hair bundles and proper trafficking of known MET compone
45 econds after Ca(2+) chelation, especially if hair bundles are deflected toward their short edges.
48 r from criticality suggested that individual hair bundles may be regarded as nonisochronous oscillato
49 ation to the ankle-link region in developing hair bundles moreover depends on the presence of PCDH15-
50 ly on the capacity of mechanically sensitive hair bundles to transduce vibrations into electrical sig
51 ely disrupt the tip links of individual frog hair bundles with displacement clamping to control hair
52 echnique of mechanically coupling two active hair bundles, enabling us to probe the dynamics of the c
54 ng conditions requires infection of the root hairs by soil symbiotic bacteria, collectively referred
57 (ARHL) is associated with the loss of inner hair cell (IHC) ribbon synapses, lower hearing sensitivi
60 eft ([K(+) ](c) ) contributes to setting the hair cell and afferent membrane potentials; the potassiu
61 anscription factors that serve dual roles in hair cell and neuronal development (e.g. Neurod1, Atoh1
62 ) modules mediate planar polarization of the hair cell apical cytoskeleton, including the kinocilium
63 tores harmonin protein expression in sensory hair cell bundles, prevents hair cell loss, improves hea
68 rs protection against aminoglycoside-induced hair cell death via paracrine signaling that requires ex
71 opose a dual mechanism for GFI1 in promoting hair cell development, consisting of repression of neuro
72 ant FGF ligands may contribute to vestibular hair cell differentiation and supports a developmental m
73 rgic signaling in supporting cells regulates hair cell excitability by controlling the volume of the
75 ting from acoustic pressure and active outer hair cell force to the inner hair cells that synapse on
78 e-related cochlear synaptic degeneration and hair cell loss in mice with enhanced alpha9alpha10 choli
79 ture cochlea, prior to the onset of hearing, hair cell loss stimulates neighboring supporting cells t
80 ssion in sensory hair cell bundles, prevents hair cell loss, improves hearing sensitivity, and amelio
83 sed to function as a motor that tensions the hair cell mechanotransduction (MET) complex, but conclus
84 MC1 has been shown to constitute the pore of hair cell mechanotransduction channels, but little is kn
87 sults suggest that fluid motion due to outer hair cell motility can help maintain longitudinal homeos
89 nt advances, we propose a unifying theory of hair cell MT that may reconcile most of the functional d
91 d mouse cochleas, we demonstrated that inner hair cell stereocilia developed in specific stages, wher
92 pses between auditory nerve fibers and their hair cell targets without destroying the hair cells them
94 auditory-nerve terminals extend towards the hair cell's apical end to re-establish contact with them
95 emonstrated at large appositions such as the hair cell-calyx afferent synapses present in central reg
100 al-associated genes as well as activation of hair cell-specific genes required for normal functional
102 onses, vestibular-induced eye movements, and hair-cell activity as assessed with FM dye labeling and
115 mice, outer hair cells (OHCs), but not inner hair cells (IHCs), began to lose their third row of ster
116 al ganglion neurons (SGNs) on cochlear inner hair cells (IHCs), resulting in loss of synapses, a proc
117 day 7 (P7), before the primary sensory inner hair cells (IHCs), which become competent at about the o
125 tional RBF mutants that produced ectopic non-hair cells and determined that this cell fate switch is
127 of spontaneous correlated activity in inner hair cells and spiral ganglion neurons, which begins at
128 -pass transmembrane proteins are enriched in hair cells and underlie nonsyndromic human deafness.
130 or destructive, which implies that the outer hair cells can either amplify or reduce vibrations in th
131 elopmental model in which Type-I and Type-II hair cells develop in parallel rather than from an inter
132 icles were sufficient to improve survival of hair cells exposed to the aminoglycoside antibiotic neom
133 ure striolar region of the utricle, labeling hair cells following EdU birthdating, and demonstrates t
138 t the development of low- and high-frequency hair cells is differentially regulated during developmen
139 t the development of low- and high-frequency hair cells is differentially regulated during pre-hearin
143 Hearing loss caused by the death of sensory hair cells of the inner ear is an unfortunate side effec
144 d to tonotopic variations in the constituent hair cells or cytoarchitecture of the organ of Corti.
145 e copy signal acted with high selectivity on hair cells polarized to be activated by posterior deflec
147 We show that burst firing of mouse inner hair cells prior to hearing onset requires P2RY1 autorec
150 potentials; the potassium efflux from type I hair cells results from the interdependent gating of thr
151 eriments reveal that, in developing cristae, hair cells stratify into an upper, Tmc2a-dependent layer
155 IO23 (APUM23), which caused prospective root hair cells to instead adopt the non-hair cell fate.
158 The maturation of high-frequency (basal) hair cells was also affected in Ca(V) 1.3(-/-) mice, but
164 nsitize the channel to PIP(2) depletion from hair cells, and alter the channel's unitary conductance
165 phibians, and birds which readily regenerate hair cells, are responsible in part for the mammalian ea
167 n triggers K(+) efflux and depolarization of hair cells, as well as osmotic shrinkage of supporting c
168 er scale-between internal structures such as hair cells, basilar membrane (BM), and modiolus with ext
169 and post-synaptic markers on cochlear inner hair cells, in guinea pigs surviving from 1 day to 6 mon
170 membrane currents in low-frequency (apical) hair cells, such as I(K,n) (carried by KCNQ4 channels),
171 t the tips of the tall stereocilia in mature hair cells, together with PCDH15 isoforms CD1 and CD2; L
172 ng in mammals uses somatic motility of outer hair cells, underpinned by the membrane protein prestin,
173 correlate with synaptic position on sensory hair cells, we combined patch clamping with fiber labeli
189 processes produces the diversity of skin and hair color among human populations, and defects in these
190 tability; these sets ranged in size from 28 (hair color) to 3,400 (height) to 2 million (number of ch
191 s meta-analysis with GWAS of nevus count and hair color, and transcriptome association approaches, un
192 cted link between puberty timing and natural hair colour, possibly reflecting common effects of pitui
194 related to cumulative glucocorticoid levels (hair cortisol), parenting stress, and performance on mem
195 stress did not significantly correlate with hair cortisol, and there was no evidence to suggest that
198 ations were as follows: hair Mn, 0.08 mug/g; hair Cu, 9.6 mug/g; hair Cr, 0.05 mug/g; and blood Pb, 1
200 e data suggest that LGR4 promotes the normal hair cycle by activating HF stem cells and by influencin
202 Through recurrent bouts synchronous with the hair cycle, quiescent melanocyte stem cells (McSCs) beco
205 hesis of ethylene to fine-tune root and root hair development, which are important for seedling estab
209 ous structure, the removal of free lipids in hair does not lead to an increase of water permeability.
210 e (PPD) is a strong contact allergen used in hair dye that is known to cause allergic contact dermati
211 urthermore, in Arabidopsis, KAR-induced root hair elongation depends on ACS7 Thus, we reveal a connec
216 ion, MC and keratinocyte precursors from the hair follicle bulge of untreated vitiligo skin and vitil
217 iligo, the melanocyte (MC) precursors in the hair follicle bulge proliferate, migrate, and differenti
219 D to regulate epidermal differentiation and hair follicle cycling and, in so doing, to promote barri
220 HH gene correlates with chemotherapy-induced hair follicle damage or the degree of CIA, respectively.
221 mouse interfollicular epidermal, mammary and hair follicle epithelia that genotoxicity does not promo
223 te resembles transit-amplifying cells of the hair follicle matrix, with AP-1 and TGFB cooperativity d
224 e key role of ATM in the protection of human hair follicle melanocytes from oxidative stress/damage w
227 nerves form "synapse-like" connections with hair follicle stem cells to promote hair regeneration in
230 n skin microenvironment, these cells express hair-follicle lineage markers and contribute to hair fol
234 mpathetic nerves, arrector pili muscles, and hair follicles form a tri-lineage unit to cause piloerec
235 ilization of stem cells to regenerate anagen hair follicles in AA and intraepidermal melanocytes in v
236 replication forks was altered in ORSCs from hair follicles of HS patients, leading to activation of
237 tent skin competence explaining why aberrant hair follicles or sebaceous glands are sometimes observe
239 ied epidermis, fat-rich dermis and pigmented hair follicles that are equipped with sebaceous glands.
241 hance skin repair, including regeneration of hair follicles with arrector pili muscles in healed woun
243 bundles that target Merkel cells in organoid hair follicles, mimicking the neural circuitry associate
244 r-follicle lineage markers and contribute to hair follicles, sebaceous glands and/or epidermis renewa
245 using spatiotemporal gene ablation in murine hair follicles, we uncover a critical role for the trans
251 oss of BMP signaling in the lineage leads to hair graying due to a block in melanocyte maturation.
254 report that, in mice, acute stress leads to hair greying through the fast depletion of melanocyte st
260 o truncatula requires repolarization of root hairs, including the rearrangement of cytoskeletal filam
261 role for one ROS, H(2)O(2), in driving root hair initiation and demonstrated that localized synthesi
264 particular, twitching-mode motility employs hair-like pili to transverse moist surfaces with a jitte
269 ves both MeSCs and melanocytes of the anagen hair matrix of proinflammatory signals required for full
271 Median metal concentrations were as follows: hair Mn, 0.08 mug/g; hair Cu, 9.6 mug/g; hair Cr, 0.05 m
273 cid-specific isotope ratio analysis of scalp hair of American individuals to predict soft biometric t
275 simulate contamination of uncovered skin and hair of health care workers wearing personal protective
277 he role of Wnt ligands in the orientation of hairs of Drosophila wings, an established system for the
278 of-function lines phenocopy the stunted root hair phenotype of other Atget lines, its heterologous ex
280 mpaired movement of basal progenitors during hair placode morphogenesis and diminished migration of m
281 hortness of breath, fear of progression, and hair problems) of the five multi-item scales showed resp
282 g, shortness of breath, fear of progression, hair problems, and surgery-related symptoms) plus 15 sin
283 ptomics with genetics, we show that emerging hair progenitors produce both WNTs and WNT inhibitors.
286 ower with 4% chlorhexidine soap, appropriate hair removal, adequate preoperative systemic antibiotic
288 72 weeks, and concentrations of tenofovir in hair samples from individuals reporting HIV risk and adh
289 sease, characterized by severe skin disease, hair shaft defects, atopic diathesis, and increased susc
290 red for severity of skin condition, specific hair shaft defects, atopy, and recurrent infections.
291 gh performance for analysis of these dyes in hair shampoo and an orange juice as real samples with ac
292 associated with lower ART concentrations in hair, suggesting that food insecurity may be associated
293 Most angiosperms produce trichomes-epidermal hairs that have protective or more specialized roles.
298 subcellular distribution of lipids in human hair was investigated to better understand their role in