ライフサイエンスコーパス: hypertonic

1 High NaCl is hypertonic.

2 multicenter, randomized, controlled trial of hypertonic (7%) versus isotonic (0.9%) saline inhaled tw

3 Whereas acute hypertonic activation of OVLT neurons critically depends

4 hotobleaching experiments indicate that both hypertonic and hypotonic conditions reduce the mobility

5 drug retention in colorectal tissue, whereas hypertonic and isotonic enemas provided markedly reduced

6 eover, reducing tension by exposing cells to hypertonic buffer shifts the onset of contraction to occ

7 an cell types are routinely exposed to acute hypertonic challenge and shrink.

8 We investigated the effects of acute hypertonic challenge on AQP2 (aquaporin-2) water channel

9 d in the trans-Golgi network (TGN) following hypertonic challenge.

10 y in a variety of cell types at the onset of hypertonic challenge.

11 tilbene-disulfonic acid) but decreased under hypertonic conditions (by addition of 300 mOsm mannitol)

12 In eukaryotes, exposure to hypertonic conditions activates a MAPK (Hog1 in Saccharo

13 uid in the pseudocoelomic space, exposure to hypertonic conditions did not significantly affect growt

14 Both hypo-and hypertonic conditions impose an increased curvature, whe

15 lyte, taurine synthesis was stimulated under hypertonic conditions in neurons.

16 ition of clathrin-mediated endocytosis using hypertonic conditions or the small molecule inhibitor, P

17 ing Nup88 in IMCD3 cells acutely stressed to hypertonic conditions reduces nuclear retention of TonEB

18 activity in oocytes under both isotonic and hypertonic conditions to the same level as in water-inje

19 kidney cells were treated under isotonic or hypertonic conditions with the nitric oxide donor S-nitr

20 s stably silenced for MUPP1 expression under hypertonic conditions, a significant decrement in Cldn4

21 this nucleus during isotonic and short-term hypertonic conditions, is an example of a modulator that

22 tical micellar concentration, and even under hypertonic conditions.

23 orter-A reporter activity under isotonic and hypertonic conditions.

24 bstantial reduction in AQP1 expression under hypertonic conditions.

25 ion in the inner medulla of the kidney under hypertonic conditions.

26 of different levels of gene expression under hypertonic conditions.

27 pressing SDH transcriptional activity during hypertonic conditions.

28 duct (IMCD3) cells grown under isotonic and hypertonic conditions.

29 rmed on NP cells with TonEBP knockdown under hypertonic conditions.

30 caspase-1 is activated in macrophages under hypertonic conditions.

31 r basis of a new mechanism for responding to hypertonic conditions.

32 e was admitted to hospital with weight loss, hypertonic dehydration, and metabolic acidosis.

33 Hypertonic dextrose injections (prolotherapy) is an emer

34 ) cells are recruited to the skin, sense the hypertonic electrolyte accumulation in skin, and activat

35 We found that strongly hypotonic and hypertonic enemas caused rapid systemic drug uptake, whe

36 chanism in teleost fish naturally exposed to hypertonic environments.

37 ncrease their chances of survival to another hypertonic episode.

38 stress by exposure to hypoxia, hypothermia, hypertonic feedings, and lipopolysaccharide, with some p

39 Hypertonic fluids restore cerebral perfusion with reduce

40 cular veins: 0.2% polidocanol diluted in 70% hypertonic glucose (HG) (group 1) vs 75% HG alone (group

41 f Saccharomyces cerevisiae vacuoles, whereas hypertonic gradients cause vacuoles to fragment on a slo

42 Water-loss dehydration (hypertonic, hyperosmotic, or intracellular dehydration)

43 ic site in the CCL2 promoter is required for hypertonic inducibility.

44 sed with hypertonicity and was necessary for hypertonic induction of target genes IL6, TNF, and NOS2

45 ese results suggest that the skin contains a hypertonic interstitial fluid compartment in which MPS c

46 tatory and pressor response than infusion of hypertonic mannitol/sorbitol.

47 Hypertonic media significantly decreased SC cell volume

48 imulated in hypotonic media and inhibited in hypertonic media; the osmotically induced changes in act

49 s in the OMCD was significantly decreased in hypertonic medium (a normal milieu for the medulla) but

50 ansepithelial reabsorption of water into the hypertonic medullary interstitium mediated by collecting

51 inA 500 U or 1000 U or placebo into the most hypertonic muscle group among the elbow, wrist, or finge

52 urons display an increased discharge to both hypertonic NaCl (+7.5 mm) and mannitol (+15 mm).

53 sthetized rats that graded concentrations of hypertonic NaCl (1.5 and 3.0 osmol kg(-1)) elicit graded

54 ICA infusions of hypertonic NaCl and mannitol each significantly (P < 0.0

55 ABSTRACT: Systemic or central infusion of hypertonic NaCl and other osmolytes readily stimulate th

56 rotid or intracerebroventricular infusion of hypertonic NaCl evokes a greater increase in OVLT neuron

57 tricular infusion or local OVLT injection of hypertonic NaCl increases lumbar sympathetic nerve activ

58 ng directly to the PVN (i.e. CTB-ir), graded hypertonic NaCl infusions again produced graded increase

59 es that expressed Fos-ir in responses to ICA hypertonic NaCl infusions was greater in the DC (P < 0.0

60 atment of HNF-1beta mutant mIMCD3 cells with hypertonic NaCl inhibited the induction of osmoregulated

61 e majority of OVLT neurons are responsive to hypertonic NaCl or mannitol.

62 ings revealed that intracarotid injection of hypertonic NaCl produced a concentration-dependent incre

63 In contrast, central infusion of hypertonic NaCl produces a greater increase in arterial

64 l osmoreceptor; however, central infusion of hypertonic NaCl produces a greater sympathoexcitatory an

65 RBC were exposed to hypertonic NaCl solution (1.5-3%) to induce crystallizat

66 However, hypertonic NaCl stimulates a greater increase in dischar

67 bsets of OVLT neurons respond differently to hypertonic NaCl versus osmolarity and subsequently regul

68 neurons may sense or respond differently to hypertonic NaCl versus osmolarity.

69 8) displayed a greater discharge response to hypertonic NaCl vs mannitol.

70 d shape changes in response to extracellular hypertonic or hypotonic challenges.

71 vity from electrophysiological recordings in hypertonic P18 kits decreased only in unmyelinated fiber

72 nce studies revealed increased urine volume, hypertonic plasma, polydipsia, and impaired urinary conc

73 us intravenous infusion of 0.9% saline or 3% hypertonic saline (1.5 mL/kg/hr) for 48 hr.

74 Clinically relevant concentrations of hypertonic saline (20 mM) significantly augmented CD69 e

75 greater increase measured using 23.4% or 30% hypertonic saline (23.4%, 365.0 +/- 8.8 mosm/L, p < .05

76 out the 300-min period by all but the lowest hypertonic saline (4.2% NaCl).

77 Animals were treated with hypertonic saline (7.5% NaCl, 4 mL/kg) before or after c

78 Hypertonic saline (7.5%) treatment significantly attenua

79 sphere of wildtype mice was attenuated after hypertonic saline (79.9% +/- 0.5%; mean +/- SEM) but not

80 irway dehydration could be reversed, we used hypertonic saline (HS) as an osmolyte to rehydrate ASL.

81 urrent evidence is unclear about the role of hypertonic saline (HS) for the acute treatment of bronch

82 Two previous meta-analyses of nebulized hypertonic saline (HS) on hospital length of stay (LOS)

83 n, have found a limited benefit of nebulized hypertonic saline (HS) treatment in the pediatric emerge

84 produced by a rehydrating treatment based on hypertonic saline (HS), a current CF clinical treatment.

85 Hypertonic saline (HTS) is an accepted treatment for tra

86 Three percent hypertonic saline (HYS) has been suggested as a means of

87 uced in rats by episcleral vein injection of hypertonic saline (N = 30).

88 S + VH + VEH) or 80 mL/kg normal saline with hypertonic saline (RESUS + VH + HTS).

89 atients received 4 mL of 3% sodium chloride (hypertonic saline [HS group]) or 0.9% sodium chloride (n

90 ular action principle in mechanistic detail: Hypertonic saline acts via metalloproteinase 9 (MMP9).

91 After 60 mins, hypertonic saline administered at 50 mosm/kg resulted in

92 The use of therapeutic interventions such as hypertonic saline administration and decompressive crani

93 easured over 4 h and again at 24 h following hypertonic saline administration.

94 ce remained only 50% regardless of timing of hypertonic saline administration.

95 e lung injury in wild-type mice treated with hypertonic saline after cecal ligation and puncture was

96 Osmotherapy with hypertonic saline ameliorates cerebral edema associated

97 ere treated with different concentrations of hypertonic saline and endotoxin of Escherichia coli O111

98 ng advantageous resuscitative fluids such as hypertonic saline and hemoglobin-based oxygen carriers a

99 arch has demonstrated an association between hypertonic saline and hyperchloremia, limited data exist

100 ce secondary brain injury through the use of hypertonic saline and induced hypothermia.

101 Hypertonic saline and mannitol are used less in infants

102 outcome was hospital billing for parenteral hypertonic saline and mannitol use, by day of service.

103 n Brown Norway rats (N = 26) by injection of hypertonic saline and monitored for 5 weeks.

104 mber of studies show the cellular effects of hypertonic saline and no studies, to our knowledge, have

105 fibrillary acidic protein immunostaining in hypertonic saline and normal saline treated rats, and un

106 active treatment group (n = 158) received 7% hypertonic saline and the control group (n = 163) receiv

107 emic encephalopathy and early treatment with hypertonic saline are critical for successful outcomes.

108 studied whether these protective effects of hypertonic saline are related to improved gammadeltaT ce

109 We used perineurial injection of hypertonic saline as a tool to open the perineurial barr

110 Treatment with 7.5% hypertonic saline attenuated blood-brain barrier disrupt

111 ries of experiments (n = 32), treatment with hypertonic saline attenuated postischemic blood-brain ba

112 via the perivascular pool of aquaporin-4, 2) hypertonic saline attenuates blood-brain barrier disrupt

113 ical role in water egress from brain; and 3) hypertonic saline attenuates blood-brain barrier disrupt

114 tested the hypothesis that osmotherapy with hypertonic saline attenuates cerebral edema following ex

115 Inhaled hypertonic saline attenuates postshock acute lung injury

116 ly higher (88%) than in animals treated with hypertonic saline before cecal ligation and puncture (50

117 of human polymorphonuclear neutrophils with hypertonic saline before stimulation with formyl methion

118 23.4% hypertonic saline bolus administration.

119 These data indicate that hypertonic saline can modulate gammadeltaT cell function

120 Hypertonic saline causes increased hydraulic conductivit

121 to 116 traits assessed through blood tests, hypertonic saline challenge tests, questionnaires, and s

122 ars with cystic fibrosis, the use of inhaled hypertonic saline compared with isotonic saline did not

123 We investigated the hypothesis that bolus hypertonic saline decreases cerebral edema in severe hep

124 Hypertonic saline decreases intestinal edema and improve

125 Hypertonic saline did not reduce nerve density, but did

126 5.0 +/- 8.8 mosm/L, p < .05 vs. other lesser hypertonic saline doses).

127 Our findings suggest that hypertonic saline enhances the elimination of inflammato

128 se data demonstrate that 1) osmotherapy with hypertonic saline exerts antiedema effects via the periv

129 We tested the hypothesis that hypertonic saline exerts its antiedema effect by promoti

130 The effect of timing of hypertonic saline exposure on A3 receptor expression and

131 ock (shock) or traumatic brain injury (TBI), hypertonic saline failed to improve survival.

132 Hypertonic saline fluids used to resuscitate trauma pati

133 We hypothesized that aerosolized inhaled hypertonic saline given at the onset of resuscitation wi

134 Hypertonic saline given to children with bronchiolitis i

135 On average, LCI decreased in the hypertonic saline group (n = 12) by 1.19 z-scores units

136 ed in an increase in serum osmolarity in all hypertonic saline groups (p < .05 vs. normal saline), wi

137 In contrast in alpha-Syn(-/-) mice, hypertonic saline had no effect on the postischemic edem

138 randomized to receive either 7.2% saline/6% hypertonic saline hydroxyethyl starch (4 mL/kg) or vehic

139 y resuscitation, which was not influenced by hypertonic saline hydroxyethyl starch administration.

140 ing results in other models of brain injury, hypertonic saline hydroxyethyl starch failed to improve

141 This might explain why hypertonic saline hydroxyethyl starch has failed to impr

142 ocampal CA1 and neocortex with no effects of hypertonic saline hydroxyethyl starch on neuronal surviv

143 Hypertonic saline hydroxyethyl starch treatment resulted

144 Bolus 23.4% hypertonic saline improves surveillance neuromonitoring

145 er A3 receptors may diminish the efficacy of hypertonic saline in a mouse model of acute lung injury.

146 , and show potentially beneficial effects of hypertonic saline in acute cervical SCI.

147 The Efficacy of 3% Hypertonic Saline in Acute Viral Bronchiolitis (GUERANDE

148 Early and continuous infusion of hypertonic saline in patients with severe cerebrovascula

149 ing a sustained experimental pain challenge (hypertonic saline infused in the masseter muscle) with a

150 50 patients with hyponatremia who underwent hypertonic saline infusion.

151 ratio of Mean Expiratory Flow after 240s of hypertonic saline inhalation with respect to the age- an

152 (Forced Expiratory Flow Volume after 240s of hypertonic saline inhalation; p = 4.81*10(-4)) and CD14

153 Additionally, nebulized hypertonic saline inhibited matrix -metalloproteinase-13

154 ncreased saline intake after dehydration and hypertonic saline injection.

155 eurons were activated by fluid satiation and hypertonic saline injection.

156 IOP elevation was induced in rats by hypertonic saline injections into episcleral veins.

157 l IOP elevation was produced by injection of hypertonic saline into the episcleral veins.

158 was raised in brown Norway rats by injecting hypertonic saline into the limbal venous system.

159 was raised in Brown Norway rats by injecting hypertonic saline into the limbal venous system.

160 weeks following these injections we injected hypertonic saline intraperitoneally into the rat.

161 Hypertonic saline is currently being used in the treatme

162 Evidence for other treatments such as hypertonic saline is evolving but not clearly defined ye

163 We found that hypertonic saline is more effective than mannitol for th

164 Inhaled hypertonic saline is recommended as therapy for patients

165 igible trials, but our findings suggest that hypertonic saline may be superior to the current standar

166 en patients with 18 administrations of 23.4% hypertonic saline met inclusion criteria.

167 Hypertonic saline mitigates intestinal edema development

168 our findings and to evaluate the effects of hypertonic saline on functional outcomes.

169 The beneficial effects of hypertonic saline on neuronal survival and on cerebral b

170 34), alpha-Syn(-/-) mice treated with either hypertonic saline or 0.9% saline had smaller infarct vol

171 Hypertonic saline or co-loaded cargo was found to preven

172 Treating acidic ASL with hypertonic saline or heparin largely reversed the increa

173 mic shock, initial resuscitation with either hypertonic saline or hypertonic saline/dextran, compared

174 Of the 1,854 patients who received hypertonic saline or mannitol for >/= 2 days in the firs

175 umin) or crystalloids (n = 1443; isotonic or hypertonic saline or Ringer lactate solution) for all fl

176 ore fluid in response to either subcutaneous hypertonic saline or water deprivation with partial rehy

177 e interval, -1.6 to 5.7), with both favoring hypertonic saline over mannitol.

178 Nebulized hypertonic saline reduced inflammation (cytokine-induced

179 Delayed treatment of hypertonic saline resulted in the greatest reduction in

180 A3 antagonists could improve the efficacy of hypertonic saline resuscitation by reducing side effects

181 l A3 receptors expression determines whether hypertonic saline resuscitation inhibits or aggravates p

182 Hypertonic saline resuscitation may therefore protect ho

183 Hypertonic saline resuscitation reduces tissue damage by

184 he effect of A3 receptors on the efficacy of hypertonic saline resuscitation was assessed in A3 recep

185 Randomized trials have suggested that hypertonic saline solutions may be superior to mannitol

186 n (LHSS) reward if rats are denied access to hypertonic saline solutions.

187 Highly concentrated hypertonic saline such as 23.4% provides a small volume

188 ed concentrations of menthol, capsaicin, and hypertonic saline that evoked comparable levels of nocif

189 cardiopulmonary resuscitation: 1) continuous hypertonic saline therapy maintained to achieve serum os

190 Intraperitoneal administration of hypertonic saline to the rat supraoptic nucleus (SON) in

191 Effects of the timing of hypertonic saline treatment administration on tissue los

192 de values should be monitored closely during hypertonic saline treatment as moderate elevations may i

193 c arrest/cardiopulmonary resuscitation, 7.5% hypertonic saline treatment did not attenuate water cont

194 Results show that hypertonic saline treatment reduced tissue loss that cor

195 rphonuclear neutrophils are activated before hypertonic saline treatment.

196 comes Consortium multicenter out-of-hospital Hypertonic Saline Trial in patients with Glasgow Coma Sc

197 Hypertonic saline triggers polymorphonuclear neutrophils

198 ating that there is a therapeutic window for hypertonic saline use after traumatic brain injury.

199 Hypertonic saline use increased and mannitol use decreas

200 %; difference, 2.2% [95% CI, -4.5% to 9.0%]; hypertonic saline vs normal saline: 54.3% vs 51.5%; diff

201 urther increased to 31.8 +/- 3.1% when 20 mM hypertonic saline was added with lipopolysaccharide.

202 In the study group, nebulized hypertonic saline was delivered at the end of the shock

203 Volumes before and after 23.4% hypertonic saline were compared with Wilcoxon signed ran

204 were randomized to control (with and without hypertonic saline) and mesenteric venous hypertension wi

205 70 (hypertonic saline/dextran), 7.5% saline (hypertonic saline), or 0.9% saline (normal saline) initi

206 , dextran, gelatin, hydroxyethyl starch, and hypertonic saline).

207 on-directed therapies (mannitol, 56% vs 21%; hypertonic saline, 14% vs 7%; hypothermia, 24% vs 10%; p

208 nt isotonic and hypotonic challenges, and to hypertonic saline, an effective therapy for mucus hydrat

209 s: 4 followed a nebulization technique using hypertonic saline, and 2 followed a chest or abdomen mas

210 3% (2,069 of 6,238) of the patients received hypertonic saline, and 40% (2,500 of 6,238) received man

211 % with hypertonic saline/dextran, 75.7% with hypertonic saline, and 75.1% with normal saline (P = .88

212 addition, vogue methods such as hypothermia, hypertonic saline, and aggressive surgical decompression

213 nd ventricular volumes increased after 23.4% hypertonic saline, consistent with a reduction in brain

214 One of these treatments, hypertonic saline, is already in use, whereas others are

215 mL vs. 3342 +/- 859 pg/mL, shock vs. shock + hypertonic saline, p = .006).

216 luid vs. 230 +/- 19 pg/mL, shock vs. shock + hypertonic saline, p = .009) and pretreatment with a mat

217 ing treatment with continuous IV infusion 3% hypertonic saline, with moderate hyperchloremia independ

218 e, this study focused on the hypothesis that hypertonic saline-induced improvements in histological o

219 on was not different between 0.9% saline and hypertonic saline-treated wild-type mice.

220 ceptor expression and degranulation, whereas hypertonic saline-treatment after formyl methionyl-leucy

221 This aggravating effect of delayed hypertonic saline-treatment was absent in A3 receptor kn

222 ly, mortality in wild-type mice with delayed hypertonic saline-treatment was significantly higher (88

223 CH selected the nebulization technique using hypertonic saline.

224 dverse effects theoretically associated with hypertonic saline.

225 uced in rats by episcleral vein injection of hypertonic saline.

226 Continuous IV infusion 3% hypertonic saline.

227 nse after an intraperitoneal injection of 1M hypertonic saline.

228 s that may be up-regulated with edema and/or hypertonic saline.

229 IOP produced by episcleral vein injection of hypertonic saline.

230 es adopted the approach of giving a bolus of hypertonic saline.

231 urface, which was significantly augmented by hypertonic saline.

232 intracranial disease should be treated with hypertonic saline.

233 eater than in wild-type mice pretreated with hypertonic saline.

234 This response was completely abrogated by hypertonic saline.

235 nt until recently were water restriction and hypertonic saline.

236 ients treated with continuous IV infusion 3% hypertonic saline.

237 , 4 [3-6] to 7 [6-9]; p = 0.008) after 23.4% hypertonic saline.

238 of 0.9% saline or various concentrations of hypertonic saline.

239 ently with nebulized racemic epinephrine and hypertonic saline.

240 ons of patients with severe TBI (GOSE </=4) (hypertonic saline/dextran vs normal saline: 53.7% vs 51.

241 e 250-mL bolus of 7.5% saline/6% dextran 70 (hypertonic saline/dextran), 7.5% saline (hypertonic sali

242 Survival at 28 days was 74.3% with hypertonic saline/dextran, 75.7% with hypertonic saline,

243 suscitation with either hypertonic saline or hypertonic saline/dextran, compared with normal saline,

244 ine had no effect on the postischemic edema (hypertonic saline: 80.3% +/- 0.7%; 0.9% saline: 80.3% +/

245 normal saline; 2-TBI, normal saline; 3-TBI, hypertonic saline; 4-TBI, 100mM NaLac, 5-TBI, 500 mM NaL

246 have shown a potential benefit of nebulized hypertonic saline; however, its effect in the emergency

247 tes global translation levels in response to hypertonic shock.

248 moter of vWF gene, suggesting involvement of hypertonic signaling in vWF up-regulation.

249 /- 0.5 to 150.2 +/- 1.3 mmol/L and activates hypertonic signaling, evidenced from increased expressio

250 ory responses after intravenous infusions of hypertonic sodium lactate.

251 ersibly manipulate the appetitive value of a hypertonic sodium solution while measuring phasic dopami

252 they directly compared equiosmolar doses of hypertonic sodium solutions to mannitol for the treatmen

253 ster stimulation indeed affects responses to hypertonic solution in a supralinear manner.

254 Finally, we found that treatment with a hypertonic solution mimicked the effect we observed with

255 were rescued when the mutant was grown in a hypertonic solution, indicating that FTT_0924 is require

256 le to no detectable epithelial damage, while hypertonic solutions caused significant damage, includin

257 Cells shrank when superfused with hypertonic solutions to a minimum relative cell volume o

258 er train stimulation and dual application of hypertonic solutions) also reveal no abnormalities.

259 ial cells to volume regulate when exposed to hypertonic solutions, and furthermore to identify the io

260 Because of the potential benefits of hypertonic solutions, it is hypothesized that hydroxyeth

261 ial, lateral, and central-in physiologic and hypertonic solutions.

262 by the immersion of the biological tissue in hypertonic solutions.

263 state model to synaptic responses induced by hypertonic solutions.

264 The responses to equi-osmotic infusions of hypertonic sorbitol were significantly smaller.

265 found for the zinc-finger protein ZAC1 under hypertonic stress (219-fold, p < 0.001).

266 st that Nup88 is up-regulated in response to hypertonic stress and acts to retain TonEBP in the nucle

267 ngly suggest that ZAC1 is up-regulated under hypertonic stress and negatively regulates expression of

268 at coordinates the intracellular response to hypertonic stress but was not previously implicated in t

269 pithelium in the medulla of the kidney under hypertonic stress by correctly localizing Cldn4 to the t

270 A 450 mOsm hypertonic stress elicited 2-fold Ca2+ transients that w

271 We previously found that hypertonic stress increases PIP(2) by selectively activa

272 Hypertonic stress induced in inner medullary (IMCD3) cel

273 Hypertonic stress induced the eIF2alpha phosphorylation-

274 isotonic conditions involves CRM-1 but under hypertonic stress is CRM1-independent.

275 For example, hypertonic stress led to strong cleavage of HB-EGF and N

276 ropose that eIF2alpha phosphorylation during hypertonic stress promotes apoptosis by sequestration of

277 tion was higher during oxidative stress than hypertonic stress, in agreement with a dramatic decrease

278 mimic of diacylglycerol and PKC activator), hypertonic stress, lysophosphatidic acid (LPA)-induced G

279 ompare tRNA cleavage patterns in response to hypertonic stress, oxidative stress (arsenite), and trea

280 hysiological stimuli of ectodomain cleavage--hypertonic stress, phorbol ester, or activation of G-pro

281 ddition of bacterial sphingomyelinase, or by hypertonic stress, S358 is rapidly dephosphorylated.

282 the transcriptional activation of aqp1 under hypertonic stress, we examined the role of the transcrip

283 Hypertonic stress-elicited TRPV1 channel stimulation med

284 cal PKC was required for TPA-induced but not hypertonic stress-induced cleavage of all EGF family lig

285 Hypertonic stress-induced dephosphorylation is blocked b

286 response shared by all eukaryotes exposed to hypertonic stress.

287 n, but it blocked NRG release in response to hypertonic stress.

288 ase in AQP1 luciferase-driven activity under hypertonic stress.

289 lationship also occurs in kidney cells under hypertonic stress.

290 motic stabilizer and compatible solute under hypertonic stress.

291 issociation of mRNA stress granules (SGs) in hypertonic-stressed cells and the role of compatible osm

292 oked by local stimulation, or osmotically by hypertonic sucrose application, were diminished, disappe

293 Hypertonic sucrose inhibited KCa3.1 endocytosis and resu

294 mediated pathway, such as chlorpromazine and hypertonic sucrose medium.

295 on of Thr-353/354 was not affected by either hypertonic sucrose or dynasore, which prevent receptor i

296 s as measured by stimulation of release with hypertonic sucrose, or alter the rate of vesicle priming

297 asis of nucleus pulposus (NP) cells in their hypertonic tissue niche.

298 Changing from a hypertonic to isotonic medium (relative hypotonicity) de

299 n contrast, isotonic and secretion-inducing (hypertonic) vehicles led to non-uniform, poor surface co

300 expression of recombinant proteins, using a hypertonic vesiculation buffer containing chloride salts