ライフサイエンスコーパス: sweat gland

1 into the lumen of the secretory coil of the sweat gland.

2 ransition to unipotency after developing the sweat gland.

3 expressed only in the pons of the brain and sweat glands.

4 epithelial cords of both hair follicles and sweat glands.

5 arently identical defects in teeth, hair and sweat glands.

6 ermis; and of substance P innervation of the sweat glands.

7 idermis and papillary dermis, and around the sweat glands.

8 reased innervation and/or involvement of the sweat glands.

9 was correlated with decreased innervation of sweat glands.

10 mal morphogenesis of teeth, hair and eccrine sweat glands.

11 developing hair follicles, and sebaceous and sweat glands.

12 rmal development of teeth, hair, and eccrine sweat glands.

13 on in the sympathetic neurons that innervate sweat glands.

14 mice possess the normal complement of active sweat glands.

15 ures of hypoplastic hair, teeth, and eccrine sweat glands.

16 ulate development of adrenergic receptors in sweat glands.

17 in the duct and proximal tubules of eccrine sweat glands.

18 olaterally in the reabsorptive duct of human sweat glands.

19 and intact macrocyclic GBCA was detected in sweat glands.

20 enhance fluid and salt loss via the eccrine sweat glands.

21 mpaired chloride secretion by primary murine sweat glands.

22 s including the airways, colon, pancreas and sweat glands.

23 ommodate pressure built-up, when interfacing sweat glands.

24 In skin, SVV was found primarily in sweat glands.

25 in a subset of cells in the bone and eccrine sweat glands.

26 hidrosis, but morphologically normal eccrine sweat glands.

27 haracterised by over-activity of the eccrine sweat glands.

28 nt inflammatory skin disease of the apocrine sweat glands.

29 s lacrimal, mammary, salivary, sebaceous and sweat glands.

30 BCC11 is expressed and localized in apocrine sweat glands.

31 genes remained at elevated levels in mature sweat glands.

32 a-A1 expression level than did guard hair or sweat glands.

33 ppendages, such as hair follicles, teeth and sweat glands.

34 esentations of cardiac action potentials and sweat gland activity.

35 investigation of conditions with disordered sweat gland activity.

36 tors are also expressed on the human eccrine sweat gland, although it remains unclear whether ET-1 mo

37 ed human epidermal fragments and the eccrine sweat glands amplified the cystic fibrosis transport reg

38 utations who exhibit CF-like features in the sweat gland and lung.

39 the same labeled unit dose (1:1 U) comparing sweat gland and muscle activity.

40 AMP-mediated ion and fluid transport in the sweat gland and nasal epithelium demonstrated the presen

41 o measure the extent of CFTR function in the sweat gland and nasal epithelium.

42 Virtually all of the sweat gland and vascular innervation is peptidergic, whe

43 We find that Eda-A1 restores sweat glands and all hair subtypes in Tabby, but each re

44 macrocyclic agents, gadolinium was found in sweat glands and confirmed to be intact chelate.

45 embryogenesis: (1) determinative effects on sweat glands and hair follicles.

46 roteins cause dysplasia or absence of teeth, sweat glands and hair follicles.

47 ave defects in hair follicle induction, lack sweat glands and have malformed teeth.

48 testinal tract, male reproductive tract, and sweat glands and is caused by loss-of-function mutations

49 r is characterized by sparse hair, a lack of sweat glands and malformation of teeth.

50 e restoration of hair growth, dermal ridges, sweat glands and molars.

51 c changes in sympathetic neurons in vitro as sweat glands and periosteum do in vivo, raising the poss

52 the sympathetic innervation of two targets, sweat glands and periosteum, changes the neurotransmitte

53 on that occurs in sympathetic innervation of sweat glands and periosteum.

54 and KCTD15 in keratinocytes have diminished sweat glands and sebaceous glands as well as progressive

55 g its vital role in the development of hair, sweat glands and teeth.

56 mal dysplasia (HED) and Tabby (Ta) mice lack sweat glands and there is compelling evidence that these

57 fine-caliber innervation is affiliated with sweat glands and with the vasculature and is especially

58 ta 2 receptors are localized specifically to sweat glands, and alpha 2 receptors also are expressed i

59 -green birefringence within dermal collagen, sweat glands, and arrector pili that engulfed axons.

60 The two sympathetic targets in footpads, sweat glands, and blood vessels lacked substantial inner

61 ge organ class, which includes hair, eccrine sweat glands, and mammary glands.

62 confined to the epidermis, sebaceous glands, sweat glands, and outer root sheath of the hair follicle

63 en the sympathetic neurons first contact the sweat glands, and P21.

64 ized by poor development of hair, teeth, and sweat glands, and results from lesions in the X-linked E

65 moderate immunostaining, and hair follicles, sweat glands, and sebaceous glands were moderately immun

66 's corpuscles, as well as in hair follicles, sweat glands, and smooth muscle and endothelial cells of

67 haracterized by defective formation of hair, sweat glands, and teeth in humans and in a mouse model,

68 in ectodysplasin-A (EDA) cause loss of hair, sweat glands, and teeth in man and mouse.

69 It is characterized by loss of hair, sweat glands, and teeth.

70 ical syndrome characterized by loss of hair, sweat glands, and teeth.

71 When Foxc1 was specifically ablated in skin, sweat glands appeared mature, but the mice were severely

72 Sweat glands are abundant in the body and essential for

73 his method has made it possible to show that sweat glands are capable of sustaining near maximal acti

74 Sweat glands are critical for thermoregulation.

75 Eccrine sweat glands are essential for sweating and thermoregula

76 Eccrine sweat glands are indispensable for human thermoregulatio

77 Eccrine sweat glands are skin-associated epithelial structures (

78 nalyses and functional studies, we show that sweat glands are specified by mesenchymal-derived bone m

79 ultimately form new epidermis; (ii) eccrine sweat glands are the most abundant appendages in human s

80 lls and a framework for the further study of sweat gland biology.

81 nerves supplying autonomic adnexa, including sweat glands, blood vessels, arrector pili muscles, and

82 of organs such as the pancreas, airways and sweat glands, but the function of CFTR in salivary gland

83 Mucin-producing sweat gland carcinoma pathologically represents a contin

84 identified 16 patients with mucin-producing sweat gland carcinoma.

85 d carcinoma," and "endocrine mucin-producing sweat gland carcinoma." STUDY SELECTION: Articles descri

86 enocarcinoma of the skin," "primary mucinous sweat-gland carcinoma," and "endocrine mucin-producing s

87 of immunohistochemical subtyping of mucinous sweat gland carcinomas.

88 CaTAr inhibits Cl- secretion in sweat gland cells and reduces sweating in vivo in mice,

89 Orai1K14Cre and Stim1/2K14Cre mice and human sweat gland cells lacking ORAI1 or STIM1 expression.

90 e induced in cultured sympathetic neurons by sweat gland cells or by one of the following cytokines:

91 obial hyperresponsiveness in fibroblasts and sweat gland cells, respectively.

92 In human sweat gland cells, SOCE mediated by ORAI1 was necessary

93 , BH4 levels dropped significantly in murine sweat gland-containing footpads during the time period w

94 cultured sympathetic neurons by extracts of sweat gland-containing footpads or by leukemia inhibitor

95 Furthermore, extracts from sweat gland-containing footpads suppressed BH4 in cultur

96 In human and mouse eccrine sweat glands, corin and ANP are expressed in the luminal

97 r bodies and have by far the highest eccrine sweat gland density among primates.

98 gether, these results suggest that the mouse sweat gland-derived cholinergic differentiation factor f

99 Thus, the sweat gland-derived differentiation activity uses the sa

100 None of these is the sweat gland-derived differentiation activity.

101 To maintain body temperature, sweat glands develop from embryonic ectoderm by a poorly

102 Thus, sweat gland development shows a relay of regulatory step

103 tions, similar to those in hair follicle and sweat gland development, the structures found to be defe

104 sorder resulting in abnormal tooth, hair and sweat gland development.

105 tim1/2K14Cre) failed to sweat despite normal sweat gland development.

106 Blockade of LIFRbeta inhibited the sweat gland differentiation activity in neuron/gland co-

107 oma are distinctive skin adnexal tumors with sweat gland differentiation and potential for malignant

108 moregulatory organ, comprised of 2-4 million sweat glands distributed over the body, can secrete up t

109 ontains an approved drug to activate eccrine sweat glands, electrodes and a simple circuit and batter

110 In those wounds where only sweat gland elements remained, an epithelium formed that

111 Those sympathetic fibers present in sweat glands expressed an abnormal dual catecholaminergi

112 ibers in both epidermis/papillary dermis and sweat gland fields; of calcitonin gene-related peptide i

113 eviously unrecognized functional role in the sweat gland for the C-terminus of CFTR.

114 eciation of the unique importance of eccrine sweat glands for epidermal repair may be exploited to im

115 s of end-organs (i.e. skin blood vessels and sweat glands) for heat dissipation.

116 , hair, mammary glands, salivary glands, and sweat glands form branches, allowing much-increased surf

117 ortions started at postnatal day 1 (P1), and sweat gland formation was essentially completed by P5.

118 c reagents for conditions affecting hair and sweat gland formation.

119 temporal cascade of regulation during mouse sweat gland formation.

120 h mixed tumor formation arising from eccrine sweat glands found only in the foot pads of mice, ischio

121 uction in sweat secretion, and evaluation of sweat glands from Itpr2-/- animals revealed a decrease i

122 SOCE was absent in agonist-stimulated sweat glands from Orai1K14Cre and Stim1/2K14Cre mice and

123 vely evaluating it is essential for studying sweat gland function and mechanisms, particularly in ant

124 studies of the pharmacological regulation of sweat gland function in humans have administered agonist

125 aquaporin 5 (AQP5), and other regulators of sweat gland function was normal in the absence of SOCE.

126 The genetic basis for sweat gland function, however, is largely unknown.

127 and defects in dental enamel production and sweat gland function.

128 More specifically, (i) eccrine sweat glands generate keratinocyte outgrowths that ultim

129 In WT footpads, sweat gland germs were detected at E17.5.

130 binds to EDAR and plays an important role in sweat gland, hair, and tooth development; mutations in E

131 s characterized by reduced or absent eccrine sweat glands, hair follicles and teeth, and defective fo

132 The single tubular structure of sweat glands has a lower secretory portion and an upper

133 (malabsorption), liver (biliary cirrhosis), sweat glands (heat shock), and vas deferens (infertility

134 lia, and in vivo in the nasal epithelium and sweat gland highlights the complexity of genotype-phenot

135 n used to identify SCs in hair follicles and sweat glands; however, whether a quiescent population ex

136 The gain of eccrine sweat glands in hairy body skin has empowered humans to

137 esis and hyperplasia of sebaceous glands and sweat glands in mature mice, leading to exacerbated sebu

138 al membrane of secretory epithelial cells in sweat glands in mouse paw skin.

139 Our data demonstrate a key role for eccrine sweat glands in reconstituting the epidermis after wound

140 holinergic in the sympathetic innervation of sweat glands in rodent footpads.

141 re, we show that SVV antigens are present in sweat glands in skin and in macrophages and dendritic ce

142 ed SVV ORF63 protein at the following sites: sweat glands in skin; type II cells in lung alveoli, mac

143 We observed that autonomic innervation of sweat glands in the footpads was significantly reduced i

144 isolated nonperfused ducts of human eccrine sweat glands in vitro to investigate basolateral acid-ba

145 other major skin appendage controlled by EDA-sweat gland induction and initial progression were accom

146 Sweat gland induction failed completely when canonical W

147 A-A1 is a key regulator of hair follicle and sweat gland initiation; its soluble ligand form could ai

148 VMAT2 levels did not decrease as the sweat gland innervation became cholinergic, indicating t

149 and during VAChT acquisition, the developing sweat gland innervation contains vesicular stores of cat

150 his type of change occurs in the sympathetic sweat gland innervation during development and can be in

151 analyzed the neurotransmitter properties of sweat gland innervation in mice lacking CNTF or CNTF and

152 Although the sweat gland innervation in the adult mouse is cholinergi

153 noreactivity disappeared from the developing sweat gland innervation in vivo as it acquired cholinerg

154 arker, followed by quantitation according to sweat gland innervation index (SGII) for PGP 9.5 (SGIIPG

155 e intraepidermal nerve fiber (IENF) density, sweat gland innervation index of structural protein gene

156 urotransmitter properties that occurs in the sweat gland innervation occurs more generally in sympath

157 c skin response of the foot was impaired and sweat gland innervation was reduced.

158 During the development of sweat gland innervation, interactions with the target ti

159 duced footpads, and trans-differentiation of sweat glands into hairs.

160 te that regulation of receptor expression in sweat glands is complex, and suggest that the innervatio

161 a2+ release by InsP3R2 in clear cells of the sweat glands is important for eccrine sweat production.

162 idrosis, excessive sweating from the eccrine sweat glands, is caused by overactivity of the sympathet

163 genital disorder of teeth, hair, and eccrine sweat glands, is usually inherited as an X-linked recess

164 tive development of hair, teeth, and eccrine sweat glands, is usually inherited as an X-linked recess

165 ct clearly inhibits the absorption of Na+ in sweat glands, it is widely accepted that Na+ absorption

166 Diminished substance P innervation of the sweat glands may affect their secretory activity.

167 els is required for HF, sebaceous gland, and sweat gland morphogenesis and HF cycling.

168 Despite continued sweat gland morphogenesis, ablation of FoxA1 in mice res

169 II plays a critical role in tooth, hair, and sweat gland morphogenesis, whereas the biological signif

170 Sweat gland morphology was similar in wild-type and AQP5

171 Surprisingly, NET simultaneously appeared in sweat gland myoepithelial cells.

172 inant form of ectodermal dysplasia affecting sweat glands, nails, teeth, and skin.

173 Intra-epidermal and sweat-gland nerve fiber densities were measured for each

174 components of skin, such as hair follicles, sweat glands, nerves and blood vessels.

175 lohydrolase (GCH) became undetectable in the sweat gland neurons during this phenotypic conversion, s

176 ctable in either the axons or cell bodies of sweat gland neurons until several days after target inne

177 pad; cholinergic sympathetic axons innervate sweat glands, noradrenergic sympathetic axons innervate

178 etic neurons, including those that innervate sweat glands, occurs prior to and does not require targe

179 orm is sufficient for the formation of hair, sweat glands or teeth has remained unclear.

180 channel protein with a possible function in sweat gland outflow, was associated (P = 1.13 x 10(-07))

181 sion of keratinocyte outgrowths from eccrine sweat glands parallels the rate of reepithelialization.

182 Similarly, sweat gland pegs require Eda-A1 at an early stage to for

183 be exploited to advance our knowledge of the sweat gland physiology and the secretion process.

184 Sweat glands play a fundamental role in thermal regulati

185 cells of other secretory epithelia, such as sweat glands, potentially shedding light on other Orai1

186 Wnt signaling was still active and nascent sweat gland pre-germs were still seen in Eda-null mice,

187 The few sweat glands present within the biopsies had had reduced

188 Rat sweat glands provide an interesting model system for a d

189 this phenotypic conversion, suggesting that sweat glands reduce BH4 levels by suppressing GCH expres

190 ults suggest that periosteum, in addition to sweat glands, regulates the neurotransmitter properties

191 e in the density and distribution of eccrine sweat glands relative to other mammals and a concomitant

192 n, possibly due to reduced blood flow to the sweat gland resulting in a lack of tissue perfusion.

193 In sweat glands, salt excretion and reabsorption are regula

194 ectodermal appendages, such as hair, teeth, sweat glands, sebaceous glands, and mammary glands, requ

195 e results indicate the expression of AQP5 in sweat gland secretory epithelium, but provide direct evi

196 During the further development of sweat gland secretory portions, Foxa1 and Foxi1, not at

197 Intraepidermal (IENFD), sweat gland (SGNFD), and pilomotor nerve fiber densities

198 driven by the secretion of moisture from the sweat glands, since increased hydration in stratum corne

199 Genes that determine sweat gland structure and function are largely unidentif

200 here was inflammatory infiltrate and loss of sweat gland structure.

201 regulator mRNA in both the epidermis and the sweat gland to a similar extent.

202 owed prolonged or steady-state activation of sweat glands to be examined.

203 produced by sympathetic neurons, stimulates sweat glands to produce a factor that then induces the p

204 resenting the ANS activation that causes the sweat glands to produce sweat.

205 re, we report an unexpected role of corin in sweat glands to promote sweat and salt excretion in regu

206 tant regulatory function of corin in eccrine sweat glands to promote sweat and salt excretion.

207 lopment, the sympathetic neurons innervating sweat glands undergo a neurotransmitter switch from nora

208 ment, sympathetic neurons innervating rodent sweat glands undergo a target-induced change in neurotra

209 The sympathetic innervation of sweat glands undergoes a developmental change in transmi

210 The sympathetic innervation of sweat glands undergoes a target-induced noradrenergic to

211 re methacholine-induced direct activation of sweat glands was affected, there was inflammatory infilt

212 unting of droplets, the number of functional sweat glands was not affected by AQP5 deletion.

213 An analysis of mutant mice that lack sweat glands was undertaken to determine whether VAChT e

214 e, by taking advantage of the ear's exocrine sweat glands, we describe an in-ear integrated array of

215 anding upon the integrate-and-fire nature of sweat glands, we hypothesized that the amplitude of an E

216 the model of Eda mutant Tabby mice, in which sweat glands were not formed, with wild-type (WT) mice.

217 port regulator as densely as did the eccrine sweat gland when three monoclonal antibodies for R (regu

218 n the reabsorptive duct of the human eccrine sweat gland, which most likely represents a sodium:hydro

219 ate from a variety of sources, including the sweat gland, which produces lactate from the glucose rec

220 lves delivery of stimulating agonists to the sweat glands with the aid of an electrical current.

221 ty in the sympathetic neurons that innervate sweat glands with the time that axons contact this targe