ライフサイエンスコーパス: sweat

1 thies, including anhidrosis (an inability to sweat).

2 physiological range for tear, saliva, and/or sweat.

3 ysiologically relevant doses of EtG in human sweat.

4 ion limit suitable for analysis of undiluted sweat.

5 e monitoring of lactate content in undiluted sweat.

6 sol (8.16 to 141.7 ng/mL) in perspired human sweat.

7 es over prolonged and continuous exposure to sweat.

8 r materials for the detection of chloride in sweat.

9 egrated sensing for on-body testing of human sweat.

10 em have never been reported to be present in sweat.

11 She denied having a fever or night sweats.

12 ryness but no significant reduction in night sweats.

13 ature of 38.8 degrees C, and drenching night sweats.

14 l symptoms (VMSs), ie, hot flushes and night sweats.

15 s unclear whether ET-1 modulates cholinergic sweating.

16 s responses of cutaneous blood flow, but not sweating.

17 timate the amount of water left on skin when sweating.

18 supply is continuous which simulates profuse sweating.

19 ydrated (2.2-5.8% B(m)) via thermoregulatory sweating.

20 s COX-dependent cutaneous vasodilatation and sweating.

21 y delayed the mean body temperature onset of sweating (+1.24 +/- 0.18 vs. +1.60 +/- 0.18 degrees C, P

22 Injecting 5 nmol of dansylated sweat, 3908 +/- 62 peak pairs or metabolites were detect

23 ), stool (29 days), vaginal fluid (33 days), sweat (44 days), urine (64 days), amniotic fluid (38 day

24 tract dysfunction, orthostatic hypotension, sweating abnormalities, or erectile dysfunction.

25 ave provided evidence of viscerally-mediated sweating alterations in humans during exercise brought a

26 phoresis interface, integrated in a wearable sweat analysis platform.

27 Finally, lactate in sweat and blood samples was determined in a sport test u

28 followed by increased glucose levels in both sweat and blood.

29 CA12(E143K) mutation causes salt wasting in sweat and dehydration in humans.

30 the "Brett character" (stable, manure, horse sweat and phenolic notes) due to 4-ethylphenols was eval

31 Of the liquid media, sweat and urine yielded the highest amount of silver rel

32 n-flush changes in cutaneous vasodilatation, sweating and cerebral blood flow.

33 During each condition, sweating and cutaneous vascular conductance were measure

34 perosmolality delays the onset threshold for sweating and cutaneous vasodilatation by inhibiting effe

35 , plasma hyperosmolality delays the onset of sweating and cutaneous vasodilatation during heat stress

36 rmal infusion of hyperosmotic saline affects sweating and cutaneous vasodilatation during passive hea

37 Effects of blanching, sweating and drying on these characteristics were assess

38 The "wet process", including blanching, sweating and drying, had the largest impact on the compo

39 g the regulation of cutaneous blood flow and sweating and infer that ET-1 may attenuate the heat loss

40 Symptoms, heart rate, blood pressure, sweating and skin temperature were compared between NKB

41 ness and attenuate cutaneous vasodilatation, sweating and the reductions in cerebral blood flow durin

42 Eccrine sweat glands are essential for sweating and thermoregulation in humans.

43 nd the patient had begun to experience night sweats and fevers.

44 thermoregulatory responses, both autonomic (sweating) and behavioral (peeling off a layer of clothin

45 body fluids, including blood, urine, saliva, sweat, and milk.

46 range juice, milk formula, synthetic saliva, sweat, and urine (1:50 product to liquid mass ratio); in

47 sturbances, drowsiness or tiredness, nausea, sweating, and being restless or overactive) did not diff

48 e elevations in cutaneous vasodilatation and sweating, and reduced brain blood flow.

49 ss responses of cutaneous vasodilatation and sweating, and this may be mediated by prostacyclin-induc

50 nopathy, progressive dyspnea, fatigue, night sweats, and an unintentional weight loss of 25 pounds.

51 is, fever, chronic cough, weight loss, night sweats, and poor appetite).

52 Hot flashes, night sweats, and vaginal dryness.

53 HO) 4-symptom screening (fever, cough, night sweats, and weight loss), a rapid test detecting mycobac

54 stress in humans; therefore, an inability to sweat (anhidrosis) results in heat intolerance that may

55 eased by skin (primarily the constituents of sweat) are collected into hydrogel (agarose) micropatche

56 ajor thermoregulatory defences in humans are sweating, arteriovenous shunt vasoconstriction, and shiv

57 t sweat samples, thereby allowing the use of sweat as another human biofluid for comprehensive and qu

58 ET-1 does not modulate methacholine-induced sweating at any of the administered concentrations.

59 detection of viral RNA in urine (day 30) and sweat (at the last assessment on day 40) by means of pol

60 Previously reported sweat-based and other non-invasive biosensors either can

61 ene, sufficient to form a wearable patch for sweat-based diabetes monitoring and feedback therapy.

62 metabolome as health indicators, discovering sweat-based disease biomarkers, and metabolomic mapping

63 olites, proteins, etc.) stability in complex sweat buffer with varying pH levels and composition over

64 since it can be noninvasively collected from sweat, but its detection has been limited by poor sensit

65 ommercially available textiles to artificial sweat by an experimental setup that simulates wear-and-t

66 Successful detection of lactate in human sweat by means of the poly(3-APBA) based sensor has been

67 Human sweat can be noninvasively collected and used as a media

68 orm is designed such that continuous flow of sweat can pass through an array of flexible microneedle

69 igration of ENPs from the textile into human sweat can result in dermal exposure to these nanoobjects

70 factor, FoxA1, is required to generate mouse sweating capacity.

71 years; abnormal nasal potential difference; sweat chloride >40 mmol/L; forced expiratory volume in 1

72 lted in significant treatment differences in sweat chloride (-24.0 mmol/L, 95% CI -28.01 to -19.93; p

73 improvements from baseline were observed in sweat chloride (-24.8 mmol/L; 95% CI, -29.1 to -20.5; P

74 , symptom questionnaires, CFTR genetics, and sweat chloride analysis were obtained in smokers with an

75 ed FEV1, ivacaftor did significantly improve sweat chloride and CFQ-R respiratory domain scores and l

76 d ivacaftor 250 mg every 12 h decreased mean sweat chloride concentration by 9.1 mmol/L (p<0.001) dur

77 In cohorts 2 and 3, mean sweat chloride concentration did not decrease significan

78 mary outcomes for all cohorts were change in sweat chloride concentration during the combination trea

79 econdary analyses, a significant decrease in sweat chloride concentration occurred in the treatment g

80 Sweat chloride concentration provides an in vivo assessm

81 For the key secondary endpoint of sweat chloride concentration, the least squares mean dif

82 for phe508del CFTR, with a modest effect on sweat chloride concentration.

83 tcomes were absolute change from baseline in sweat chloride concentrations and bodyweight, body-mass

84 dary outcomes included safety and changes in sweat chloride concentrations and Cystic Fibrosis Questi

85 enlargement in both cohorts and had elevated sweat chloride concentrations in the derivation cohort (

86 Sweat chloride decreased from baseline to 6 months (mean

87 t week 24, in patients for whom we had data, sweat chloride had changed from baseline by a mean of -4

88 Sweat chloride is of interest as a biomarker for cystic

89 with COPD (25.07 +/- 10.92 mEq) had elevated sweat chloride levels compared with normal control subje

90 oride and a diffusion-limited response time; sweat chloride levels corresponded to measurable changes

91 Elevated sweat chloride levels, failure to thrive (FTT), and lung

92 test precision and accuracy can be improved, sweat chloride measurement could be a valuable biomarker

93 e a relatively simple technology for on-body sweat chloride measurement, however, equilibration betwe

94 A total of 2,639 sweat chloride measurements were obtained in 1,761 twins

95 Predictions were within the measured sweat chloride range for seven of eight variants, and ca

96 From these results, we show a sweat chloride sensor can be designed to provide accurat

97 F specific clones that correlate highly with sweat chloride test, BMI, and FEV1% predicted values.

98 d 11 additional CFTR variants using clinical sweat chloride testing, two functional assays, or all th

99 were found to be the primary determinant of sweat chloride variability (56.1% of variation) with con

100 e degree to which CFTR mutations account for sweat chloride variation.

101 in the CFTR gene is the predominant cause of sweat chloride variation; most of the non-CFTR variation

102 For an individual with CF, variation in sweat chloride was primarily caused by variation over ti

103 line through Week 48 in the concentration of sweat chloride, a measure of CFTR activity, with ivacaft

104 ous Omani family, two children with elevated sweat chloride, infantile FTT, and recurrent hyponatremi

105 Improvements in lung clearance index, sweat chloride, nutritional status, and health-related q

106 ican adult diagnosed with CF due to elevated sweat chloride, recurrent hyponatremia, infantile FTT an

107 sease biomarkers, and metabolomic mapping of sweat collected from different areas of skin with and wi

108 Thus, the combination of noninvasive sweat collection and CIL LC-MS is a robust analytical to

109 e report a simple and inexpensive method for sweat collection over a defined period (e.g., 24 h) base

110 adapted HR, SO(2), ECG, NIBP, exCO(2), NICO, sweat conductance measurement, OAA/S, and the Aldrete sc

111 The patient denied fevers, night sweats, contact with sick individuals, occupational expo

112 or Stim1 and Stim2 (Stim1/2K14Cre) failed to sweat despite normal sweat gland development.

113 ith and without CF, demonstrating convenient sweat diagnostics with reliable detection of cystic fibr

114 The rate of sweat droplet formation was significantly slower and the

115 t formation was significantly slower and the sweat droplet size larger and more variable in db/db mic

116 nally, db/db mice formed significantly fewer sweat droplets compared to controls as early as 6 weeks

117 n factor, Foxc1, is obligate for appreciable sweat duct activity in mice.

118 In summary, Foxc1 regulates sweat duct luminal cell differentiation, and mutant mice

119 ainly plays a major role in the occlusion of sweat ducts and leads to inflammation and pruritus.

120 fine structures inside the mouse pinna, and sweat ducts and Meissner's corpuscle in the human finger

121 elia lining the intestines, lungs, pancreas, sweat ducts and vas deferens, among others.

122 tions by Sulzberger et al on the blockage of sweat ducts in AD.

123 earlier investigators about the blockage of sweat ducts in miliaria, showing eosinophilic material i

124 Morphologic analysis revealed that sweat ducts were blocked by hyperkeratotic or parakerato

125 Occlusion of sweat ducts with periodic acid-Schiff-positive and Congo

126 D lesional skin (immediately proximal to the sweat ducts), which likely led to the initiation of prot

127 les, sebaceous glands, taste buds, nails and sweat ducts.

128 phylococci and their biofilms, which occlude sweat ducts.

129 dds either cough, sputum, fever/chills/night sweats, dyspnea or pleuritic chest pain) or with Pneumon

130 With our platform, we detected the elevated sweat electrolyte content of cystic fibrosis patients co

131 ducted using a metabolite expressed in human sweat, Ethyl Glucuronide.

132 was seen with urticaria and associated night sweats, fevers, and polyarticular arthritis.

133 easuring chloride levels in artificial human sweat for potential cystic fibrosis diagnostic use.

134 erface that can extract sufficient amount of sweat for robust sensing, without electrode corrosion an

135 or higher were fatigue (five vs one), night sweats (four vs one), and anaemia (one vs three).

136 Clinical validation was performed with sweat from individuals with and without CF, demonstratin

137 activity based on chloride concentrations in sweat from patients with cystic fibrosis, patients admit

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

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

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

141 Mucin-producing sweat gland carcinoma pathologically represents a contin

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

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

144 of immunohistochemical subtyping of mucinous sweat gland carcinomas.

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

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

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

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

149 temporal cascade of regulation during mouse sweat gland formation.

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

151 Sweat gland induction failed completely when canonical W

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

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

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

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

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

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

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

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

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

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

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

163 Sweat glands are critical for thermoregulation.

164 Eccrine sweat glands are essential for sweating and thermoregula

165 Eccrine sweat glands are skin-associated epithelial structures (

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 olaterally in the reabsorptive duct of human sweat glands.

191 mpaired chloride secretion by primary murine sweat glands.

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

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

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

195 hidrosis, but morphologically normal eccrine sweat glands.

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

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

198 s and preliminary investigation of the blood/sweat glucose correlation.

199 t sampling/analysis methods, the analysis of sweat has not become very popular in the clinical settin

200 t medical history experienced fatigue, night sweats, hoarseness of voice, and dry cough, which were f

201 e regulation of cutaneous vasodilatation and sweating; however, the mechanism(s) underpinning this re

202 of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in re

203 ain, anorexia, lethargy, weakness, and night sweats; imaging revealed generalized lymphadenopathy.

204 nterleukin-6 (IL-6) and Cortisol, from human sweat in RTILs.

205 The inherent inaccessibility of sweat in sedentary individuals in large volume (>/=10 mi

206 that, although prostacyclin does not mediate sweating in young and older males, it does modulate cuta

207 Short-term adverse events-acne, night sweats, increased weight, and altered mood and libido-ar

208 eveloping wearable sensors for biomarkers in sweat is a major technological challenge.

209 Human sweat is an excellent biofluid candidate for metabolomic

210 Chloride in sweat is an important diagnostic marker for cystic fibro

211 profiling of skin metabolites excreted with sweat is proposed.

212 Due to the high rate of secretion, eccrine sweating is a vital regulator of body temperature in res

213 ependent mechanism, and methacholine-induced sweating is not altered by ET-1.

214 that, although prostacyclin does not mediate sweating, it modulates cutaneous vasodilatation to a sim

215 jects for real-time continuous monitoring of sweat lactate dynamics during prolonged cycling exercise

216 Based on these data, the validity of the sweat lactate for the determination of the lactate thres

217 rofiles reflect changes in the production of sweat lactate upon varying the exercise intensity.

218 perties in sequential contact with synthetic sweat, laundry detergent solutions, and freshwater, simu

219 In our approach, the content present in the sweat left behind-namely the amino acids-can be used to

220 olome, offering a possibility of mapping the sweat metabolic differences according to skin locations.

221 hich simultaneously and selectively measures sweat metabolites (such as glucose and lactate) and elec

222 e of large variations in the total amount of sweat metabolites in individual samples, sample amount n

223 etection and relative quantification of 3140 sweat metabolites with 84 metabolites identified and 271

224 s, simultaneous and selective measurement of sweat metabolites, electrolytes and temperature was achi

225 plications including daily monitoring of the sweat metabolome as health indicators, discovering sweat

226 , demonstrating the possibility of using the sweat metabolome to reveal biological variations among d

227 a location-dependence characteristic of the sweat metabolome, offering a possibility of mapping the

228 Significant differences in male and female sweat metabolomes could be detected, demonstrating the p

229 rations of endogenous metabolites present in sweat, metabolomic analysis of sweat with high coverage

230 nd CIL LC-MS is a robust analytical tool for sweat metabolomics with potential applications including

231 follicles, mammary ducts, and glands such as sweat, mucous and sebaceous glands, are initiated in dev

232 fusion of hyperosmotic saline did not affect sweating or cutaneous vasodilatation.

233 us OFS were more affected by hot flushes and sweats over 5 years than were those on exemestane plus O

234 rmal infusion of HYPER saline did not affect sweating (P = 0.99).

235 icles (Ag-NPs) from textiles into artificial sweat, particularly considering the functionalization te

236 h) based on the use of a nonocclusive style sweat patch adhered to a skin.

237 Leaching from a blanket into sweat plateaued within 5 min, with less silver released

238 atment groups but not in the number of night sweats (pooled mean difference of changes, -2.14 [95% CI

239 Like the smart human sweating pores, the flaps can close automatically after

240 There are 3 major sweat-producing glands present in skin; eccrine, apocrin

241 Plasma hyperosmolality delays the onset for sweat production and cutaneous vasodilatation during hea

242 for CaCC activation, chloride secretion, and sweat production in humans and mice.

243 sP3R inhibitors have the potential to reduce sweat production in hyperhidrosis.

244 of the sweat glands is important for eccrine sweat production.

245 rable system is used to measure the detailed sweat profile of human subjects engaged in prolonged ind

246 The components of sweat provide an array of potential biomarkers for healt

247 emia and no symptoms of early satiety, night sweats, pruritus, or erythromelalgia.

248 tes the changes in cutaneous vasodilatation, sweat rate and cerebral blood flow during a hot flush.

249 Local sweat rate and/or forearm blood flow differed as a funct

250 Following training, mean hot flush sweat rate decreased by 0.04 mg cm(2) min(-1) at the che

251 No effect on sweat rate was observed in either group (all concentrati

252 Cutaneous vascular conductance (CVC) and sweat rate were assessed in three protocols: in Protocol

253 p), cutaneous vascular conductance (CVC) and sweat rate were evaluated at four intradermal forearm sk

254 Sweat rate, cutaneous vasodilatation, blood pressure, he

255 tion and transport properties of fabrics are sweat rate-dependent.

256 ter supply is adjustable to simulate varying sweat rates with reference to the specific end-use condi

257 e and glycopyrrolate increased and decreased sweating, respectively, in 6 month-old controls, db/db m

258 henotype was strikingly similar to the human sweat retention disorder miliaria.

259 7 unique metabolites were detected across 54 sweat samples collected from six individuals with an ave

260 LC-MS for mapping the metabolome profiles of sweat samples collected from skins of the left forearm,

261 Chloride concentrations increased in sweat samples from patients who acutely abused alcohol b

262 Three 24-h sweat samples were collected at three different days fro

263 to reveal metabolic differences in different sweat samples, thereby allowing the use of sweat as anot

264 porting for the presence of EtG in the human sweat samples.

265 bolite standards and labeled human urine and sweat samples.

266 uated mucociliary clearance, beta-adrenergic sweat secretion rate, gastrointestinal pH, and sputum in

267 tpr2-/- mice exhibited a marked reduction in sweat secretion, and evaluation of sweat glands from Itp

268 Given the complexity of sweat secretion, simultaneous and multiplexed screening

269 report on a wearable potentiometric chloride sweat sensor.

270 organic compounds emitted from their breath, sweat, skin, and other biological excretes were continuo

271 The real-time sweat sodium concentration was transmitted wirelessly vi

272 nstrated its ability to continuously monitor sweat sodium dynamics.

273 incubation in alkaline and acidic artificial sweat solutions we experimentally realized a worst case

274 he dissolution behavior of the Ag-NPs in the sweat solutions.

275 te, and chloride in human urine, plasma, and sweat specimens.

276 h-performance method for profiling the human sweat submetabolome based on chemical isotope labeling (

277 d described can be used to profile the human sweat submetabolome with high metabolomic coverage and h

278 olites showed significant differences in the sweat submetabolomes between male and female, as well as

279 onitoring of electrolytes and metabolites in sweat, tears, or saliva as indicators of a wearer's heal

280 ic reflex screens (77%) and thermoregulatory sweat test (67%) confirmed sudomotor dysfunction.

281 small fibers; 29 patients (60%) had abnormal sweat test results, 21 (42%) had abnormal pain threshold

282 s autonomic (heart rate, blood pressure, and sweat testing) and subjective testing of pain.

283 l elevations in cutaneous vasodilatation and sweating that are accompanied by reduced brain blood flo

284 tes cholinergic cutaneous vasodilatation and sweating through a nitric oxide synthase (NOS)-dependent

285 tes cholinergic cutaneous vasodilatation and sweating through a nitric oxide synthase (NOS)-dependent

286 irectly mediate cutaneous vasodilatation and sweating through nitric oxide synthase (NOS) and calcium

287 idity increases, as might occur during human sweating thus permitting air flow and reducing both the

288 eries of olfactory cues emanating from human sweat to select humans as their source for a blood meal.

289 Limit of detection of IL-6 in human sweat was 0.2 pg/mL for 0-24 hours and 2 pg/mL for 24-48

290 Detection of EtG from human sweat was achieved through chemiresistive sensing mechan

291 Sweat was collected using a gauze sponge style patch, ex

292 etection of IL-6 over 0.2-200 pg/mL in human sweat was demonstrated for a period of 10 hours post-ant

293 rial detection of IL-6 and Cortisol in human sweat was established with minimal cross-talk for 0-48 h

294 te fraction determined within the artificial sweat was negligible for most textiles, meaning that the

295 patient was asymptomatic and denied fevers, sweats, weight loss, shortness of breath or dyspnea on e

296 In the analysis of human sweat where the sample amount could be limited, nLC-MS o

297 Sampling human sweat, which is rich in physiological information, could

298 es present in sweat, metabolomic analysis of sweat with high coverage is difficult, making it less wi

299 Analysis of human sweat with poly(3-APBA) based sensor is possible due to

300 This interface can be programmed to induce sweat with various secretion profiles for real-time anal