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 olaterally in the reabsorptive duct of human 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 mpaired chloride secretion by primary murine sweat glands.

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

12 developing hair follicles, and sebaceous and sweat glands.

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

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

15 on in the sympathetic neurons that innervate sweat glands.

16 mice possess the normal complement of active sweat glands.

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

18 ulate development of adrenergic receptors in sweat glands.

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

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

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

22 hidrosis, but morphologically normal eccrine sweat glands.

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

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

25 BCC11 is expressed and localized in apocrine sweat glands.

26 genes remained at elevated levels in mature sweat glands.

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

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

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

30 investigation of conditions with disordered sweat gland activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 Sweat glands are abundant in the body and essential for

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

66 Sweat glands are critical for thermoregulation.

67 Eccrine sweat glands are essential for sweating and thermoregula

68 Eccrine sweat glands are skin-associated epithelial structures (

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

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

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

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

73 Mucin-producing sweat gland carcinoma pathologically represents a contin

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

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

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

77 of immunohistochemical subtyping of mucinous sweat gland carcinomas.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 temporal cascade of regulation during mouse sweat gland formation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 Sweat gland induction failed completely when canonical W

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 Sweat glands play a fundamental role in thermal regulati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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