ライフサイエンスコーパス: high-salt

1 sin II, L-NG-nitroarginine methyl ester, and high salt).

2 oes peeling exhibiting hysteresis at low and high salt.

3 tion of stable pre-RCs that are resistant to high salt.

4 ormotensive but become hypertensive when fed high salt.

5 us proteins are significantly less stable in high salt.

6 increased from 32 nm in low salt to 38 nm in high salt.

7 sed into the native state by the addition of high salt.

8 d by GB in the medium and 60-fold by GB plus high salt.

9 60-fold higher in cells grown in media with high salt.

10 alloprotease FtsH as well as the presence of high salt.

11 ing requires special digestion conditions in high salt (0.3 M KCl) or in Ni2+ buffer.

12 cyanobacterium Synechocystis sp. PCC 6803 in high-salt (0.7 m NaCl) stress but not in mild heat stres

13 of the C-rich RNA in low salt (10 mm KCl) or high salt (100 mm KCl) was typical of mixed sequence RNA

14 iet (percentage of lung: control = 44 +/- 6, high salt = 12 +/- 3, P < 0.05), without reducing primar

15 ter from 8% to 25% in all buffers except for high salt (250 mM NaCl).

16 processing temperatures (25-35 degrees C) or high salt (30%) concentration are needed, such as in fis

17 In vivo, in a high-salt administration experiment, male and female Dah

18 High salt also impairs Treg function by inducing IFNgamm

19 ght-activated rhodopsin is less sensitive to high salt and appears to release retinal faster.

20 esponse of N. thermophilus to external pH at high salt and elevated temperature and identify mechanis

21 MeCP2 was found to be monomeric in low and high salt and over a nearly 1000-fold concentration rang

22 ed with the known tolerance of B. villosa to high salt and the calcium-rich natural habitat of this w

23 The kinase in this fraction was resistant to high salt and Triton X-100 extraction at pH 6.5.

24 intron RNAs self-splice in vitro but only at high salt and/or Mg2+ concentrations and have been thoug

25 n has the least segmental mobility under the high-salt and low-anionic lipid condition, which has the

26 : high-salt, low-iron, or a combination of a high-salt and low-iron diet.

27 tory environments (rich medium, low glucose, high salt, and a nonfermentable carbon source).

28 se environmental conditions, including cold, high salt, and drought.

29 ignificantly more susceptible to drought and high salt, and have increased rates of water loss.

30 < 90% for >12% of the night) were studied in high-salt balance pre- and post-CPAP therapy (>4 h CPAP

31 k contrast to Th17 cells and M1 macrophages, high salt blunted the alternative activation of BM-deriv

32 Exposure of these pellets to a high-salt buffer caused release of the vp13 to the super

33 e (ELP), which reversibly self-associates in high-salt buffers at temperatures above 30 degrees C; an

34 BA levels in Arabidopsis exposed to cold and high salt by differentially controlling NCED3 and NCED5

35 In line with these findings, a moderate high-salt challenge in a pilot study in humans reduced i

36 Given the relatively high salt concentration of urine, marine bacteria would

37 ic size, and tolerance to a wide pH range or high salt concentration over time.

38 Strict nuclear localization and high salt concentration required for Suv4-20h1 extractio

39 of GTP-FtsZ polymers previously observed at high salt concentration was maintained in all KCl concen

40 more, upon mutation of the salt bridge or at high salt concentration, an additional kinetic phase was

41 nd activity remain unchanged, or increase at high salt concentration, and that the L. quadripunctata

42 s, the relative populations of conformers at high salt concentration, and the inter-duplex angle (IDA

43 The 600- and 300-kD complexes were stable at high salt concentration, suggesting that hydrophobic eff

44 was found more resistant to dissociation by high salt concentration.

45 uence effects determine the conformations at high salt concentration.

46 ustatory neurons led to the specific loss of high-salt concentration avoidance in larvae, whereas the

47 stability over a wide pH range (4-12) and at high salt concentrations (>100 mM Na(+) or Mg(2+)), brig

48 Dialysates containing high salt concentrations (>150 mM) were directly assayed

49 rticle crystals can be obtained at extremely high salt concentrations and in a divalent salt environm

50 lyplexes containing siRNA in the presence of high salt concentrations and serum proteins.

51 rsion to a random coil structure; whereas at high salt concentrations both dissociation processes occ

52 n suppression often observed in samples with high salt concentrations can be overcome by preparing sa

53 substantial acidification of pI and require high salt concentrations for cooperative folding.

54 For example, high salt concentrations hamper disulfide bond reduction

55 Plant adaptation to high salt concentrations involves integrated functions,

56 of H. pylori cagA expression in response to high salt concentrations may be a factor that contribute

57 In this study, we tested the hypothesis that high salt concentrations might alter gene expression in

58 s accomplished using alkaline solutions with high salt concentrations or deionized (DI) water.

59 High salt concentrations together with anaerobic conditi

60 ression of the genes encoding the pathway by high salt concentrations was established by transcriptom

61 High salt concentrations were used to establish the elec

62 ibited long-term stability in solutions with high salt concentrations without aggregation or silver e

63 showed attenuated antimicrobial activity at high salt concentrations, as well as lower membrane disr

64 row pH operating range, limited tolerance to high salt concentrations, or/and high cost.

65 m soluble species in atmospheric waters with high salt concentrations, such as aerosols.

66 ese proteins on membranes are insensitive to high salt concentrations, suggesting a nonelectrostatic

67 At high salt concentrations, the AmPrbetaCD blockage of the

68 lized as adsorbed 3D-projected coils; (c) at high salt concentrations, the polymer coils reexpand and

69 However, at medium to high salt concentrations, this trend is reversed, and ne

70 attractive potential well at intermediate-to-high salt concentrations, which demonstrates that electr

71 that NCBD undergoes a charge reversal under high salt concentrations.

72 issolution and was facilitated in media with high salt concentrations.

73 hat glyoxal uptake is kinetically limited at high salt concentrations.

74 eatest increase in expression in response to high salt concentrations.

75 xternal stimulus set by exposure of cells to high salt concentrations.

76 n solution but forms dimers and tetramers at high salt concentrations.

77 Target DNA is incubated with the plate in high salt concentrations.

78 an inability to initiate growth at low pH or high salt concentrations.

79 itro interaction with mTORC1 is disrupted by high salt concentrations.

80 e evident at low salt concentrations than at high salt concentrations.

81 vibacter smithii) are leaky and aggregate at high salt concentrations.

82 I, a betaFP that forms beta-sheet fibrils at high salt concentrations.

83 often characterized by extremely low pHs and high salt concentrations.

84 ions provide an attractive stimulus, whereas high-salt concentrations are avoided.

85 d resists denaturation in strong detergents, high-salt concentrations, and ionic liquids.

86 equired for neuronal activity in response to high-salt concentrations.

87 larval gustatory organs for the detection of high-salt concentrations.

88 ion also eliminated the cellular response to high-salt concentrations.

89 k rods with the rods being most prevalent in high salt conditions and absent in low salt.

90 Because DNA is strongly charged, high salt conditions are required to enable binding betw

91 Diverse stresses such as high salt conditions cause an increase in reactive oxyge

92 epithelial cells with H. pylori grown under high salt conditions resulted in increased tyrosine-phos

93 Increased expression of cagA in response to high salt conditions was confirmed by the use of transcr

94 nds and two crossover strands, stabilized by high salt conditions.

95 High-salt conditions activate the p38/MAPK pathway invol

96 s mutation conferred increased resistance to high-salt conditions and oxidative stress.

97 The TH17 cells generated under high-salt conditions display a highly pathogenic and sta

98 Saccharomyces cerevisiae self-splices under high-salt conditions in vitro, but requires the assistan

99 High-salt conditions lowered the chlorophyll and phycobi

100 potential of the instantaneous current under high-salt conditions was essential for decreasing sodium

101 nduction of many of these stress genes under high-salt conditions was significantly lower in flp-1 my

102 n of the choline pool inhibited growth under high-salt conditions with choline as the sole carbon sou

103 a compact denatured form found under acidic high-salt conditions, as well as a kinetic intermediate

104 than in the wild type under either normal or high-salt conditions, suggesting that CBL10 mediates a n

105 holipase production and impacts growth under high-salt conditions.

106 respectively, than in the control strain in high-salt conditions.

107 DNA and that the MCM complex is stable under high-salt conditions.

108 ersensitive cell death in leaf tissues under high-salt conditions.

109 tant and acetonitrile phase separation under high-salt conditions.

110 A Western lifestyle with high salt consumption can lead to hypertension and cardi

111 Infected gerbils consuming diets with a high salt content developed gastric ulcers significantly

112 ufficiently robust to analyze samples with a high salt content.

113 lly appropriate perfusate buffers containing high salt content.

114 In vitro, high salt decreased the ability of M(IL-4+IL-13) macroph

115 On high salt diet (HS), BPs of hAS(+/-) mice were significa

116 xamined murine models of colitis on either a high salt diet (HSD) or a low salt diet.

117 In Sprague-Dawley rats, high salt diet activated c-Src and induced redistributio

118 r in VP neurons from animals that were fed a high salt diet compared with controls.

119 Moreover, mice fed a high salt diet exhibited reduced M2 activation following

120 rane potential observed in VP neurons in the high salt diet group.

121 itro and ex vivo results, Efnb1 KO mice on a high salt diet showed a statistically significant height

122 Specifically, in Dahl R rats, high salt diet significantly stimulated phosphorylation

123 m by which an environmental factor such as a high salt diet triggers TH17 development and promotes ti

124 l salt-sensitive (Dahl-S) rats were fed with high salt diet with or without 0.1% caffeine in drinking

125 -regulated in Dahl salt-sensitive rats fed a high salt diet.

126 ol rats when the rats were challenged with a high salt diet.

127 Dahl salt-sensitive rats were fed a high-salt diet (8% NaCl) from 7 weeks of age to induce H

128 pecifically, we investigated the effect of a high-salt diet (a known risk factor for gastric adenocar

129 llenged with deoxycorticosterone acetate and high-salt diet (DOCA-salt).

130 e MPS cells prevents the VEGFC response to a high-salt diet (HSD) and increases blood pressure.

131 A high-salt diet (HSD) in humans is linked to a number of

132 pertension relative to wild types (WTs) on a high-salt diet (HSD); this was attenuated by a PGI(2) re

133 development of hypertension in SS rats on a high-salt diet (n = 7-8, p < 0.05).

134 e (n=15) were fed normal chow or a high-fat, high-salt diet (WD).

135 A high-salt diet also impaired human Treg function and was

136 In a separate experiment, a high-salt diet and subcutaneous angiotensin II was admin

137 bacter pylori infection and consumption of a high-salt diet are each associated with an increased ris

138 were detected in the H. pylori-infection and high-salt diet combined group compared with the other gr

139 cagA transcription in vivo in animals fed a high-salt diet compared to those on a regular diet.

140 Moreover, mice fed with a high-salt diet develop a more severe form of EAE, in lin

141 In C57BL6/J mice, exposure to a high-salt diet exacerbated disease in both sexes, while

142 But the high-salt diet failed to reduce the impact of losartan o

143 genotype (AG vs. AA) and fed them a low- or high-salt diet for 1 week, after which they were challen

144 ificantly increased when rats had been fed a high-salt diet for 7 days (n = 6 or 9, p < 0.01).

145 thy, Dahl salt-sensitive rats were fed an 8% high-salt diet from 6 weeks of age and then were infused

146 als infected with the WT strain, those fed a high-salt diet had more severe gastric inflammation, hig

147 ate that cortical EGF levels decrease with a high-salt diet in salt-sensitive rats, promoting ENaC-me

148 model combined with H. pylori infection and high-salt diet is useful for gene expression profiling i

149 We propose a model in which a high-salt diet leads to high levels of gastric inflammat

150 Feeding these salt-sensitive rats a high-salt diet led to lower levels of EGF in the kidney

151 A high-salt diet markedly increased lupus features in MRL/

152 isolated from Mongolian gerbils fed either a high-salt diet or a regular diet for 4 months by proteom

153 e model was also reduced after exposure to a high-salt diet or induced CKD.

154 ference comparable to the changes induced by high-salt diet or saline infusion.

155 These results indicate that a high-salt diet potentiates the carcinogenic effects of c

156 diet, the output strains from animals fed a high-salt diet produced higher levels of proteins involv

157 The high-salt diet suppressed plasma and whole-kidney Ang II

158 After 7 weeks of a high-salt diet, 31 of 38 rats showed diastolic dysfuncti

159 In Dahl salt-sensitive rats that were fed a high-salt diet, a model for hypertension-induced congest

160 On a high-salt diet, all mice with D(5)(-/-) kidneys excreted

161 To assess whether a high-salt diet, as measured by urinary sodium concentrat

162 Within 10 days on a high-salt diet, BP increased similarly in ES and SS allo

163 When mice were fed with a high-salt diet, knockdown of miR-192 blunted the adaptat

164 During the first week on a high-salt diet, SS rats and SS rats with only one functi

165 Additional studies showed that, on a high-salt diet, Tmem27(Y/-) mice had lower renal blood f

166 To investigate the effects of a high-salt diet, we infected Mongolian gerbils with a wil

167 On a high-salt diet, WT mice with Tmem27(Y/-) kidneys had the

168 difference (PDamil) than control mice fed a high-salt diet.

169 insensitive, congenic SS.13(BN26) rats fed a high-salt diet.

170 oup were inoculated with H. pylori and fed a high-salt diet.

171 ed by combination of H. pylori infection and high-salt diet.

172 aintained the animals on a regular diet or a high-salt diet.

173 model combined with H. pylori infection and high-salt diet.

174 ly, developed hypertension when exposed to a high-salt diet.

175 ood pressure at baseline or in response to a high-salt diet.

176 t develop elevated blood pressure when fed a high-salt diet.

177 sive effect in individuals challenged with a high-salt diet.

178 ifferences and differences in responses to a high-salt diet.

179 n late proximal flow rate in response to the high-salt diet.

180 priate increase in sodium balance when fed a high-salt diet.

181 e versus 32.0 mmHg in WT mice (P<0.01) fed a high-salt diet.

182 xpression in the macula densa increases on a high-salt diet.

183 ce (P<0.01) but not NOS1flox/flox mice fed a high-salt diet.

184 transgenic mice, an effect accentuated by a high-salt diet.

185 noma was detected in 100% of the WT-infected/high-salt-diet animals, 58% of WT-infected/regular-diet

186 enesis and causes organismal lethality under high-salt dietary stress.

187 Epidemiological evidence links high-salt diets and Helicobacter pylori infection with i

188 ction of proinflammatory Th17 cells and that high-salt diets exacerbate experimental models of autoim

189 and potassium did not change with regular or high-salt diets or potassium loading in control or Scnn1

190 e but became hypertensive when fed normal or high-salt diets.

191 cle that is still dynamic but insensitive to high salt due to a new series of bonds that are resistan

192 is due to electroosmotic flow separation, a high-salt electrokinetic effect.

193 of UWO 241 to its unique low-temperature and high-salt environment favors the phosphorylation of a PS

194 e urine osmolarity was normal as a result of high salt excretion.

195 ow salt favoring the closed conformation and high salt favoring the open conformation in the absence

196 uninephrectomized, aldosterone-infused, and high salt-fed (ALDO) systemic GC-A KO mice with enhanced

197 reased after subtotal nephrectomy and during high-salt feeding, raising the question of whether colle

198 combinations, and possibly processed and/or high salt foods.

199 scenarios were developed: 1) substitution of high-salt foods with low-salt foods, 2) a reduction in t

200 Adding a high-salt, high-fat diet accelerates endothelial senesce

201 High salt, however, compromises prospects for label-free

202 Compared with DSS rats fed a high-salt (HS) diet (6% NaCl for 6 weeks), HS+PC was ass

203 wn that some of the deleterious effects of a high-salt (HS) diet are independent of elevated blood pr

204 study aimed to assess the effect of a 1-week high-salt (HS) diet on the role of cyclo-oxygenases (COX

205 ores were elevated 15- to 30-fold by GB plus high salt in sporulation media, GB levels did not affect

206 L-NAME/high salt increased macrophage and dendritic cell surfac

207 the grik1-2 grik2-1 mutant was sensitive to high salt, indicating that GRIKs are also involved in sa

208 y electrostatic, it could not be reversed by high salt, indicating the presence of a second, irrevers

209 ot only explain the epigenetic mechanisms of high-salt induced autoimmunity but also provide an attra

210 ies were significantly inhibited by 45%, and high salt-induced increases of nitric oxide synthase-2 a

211 We further identified a high salt-induced reduction in glycolysis and mitochondr

212 ally, in rats treated with an ODN to prevent high salt-induced up-regulation of brain Galphai(2) prot

213 The angiotensin/high-salt-induced increase in systolic blood pressure, p

214 ion of p38/MAPK, NFAT5 or SGK1 abrogates the high-salt-induced TH17 cell development.

215 Finally, chronic high-salt ingestion produces endothelial dysfunction, ev

216 Here we show that high salt intake affects the gut microbiome in mice, par

217 ypertension produced by the combination of a high salt intake and administration of angiotensin II, t

218 In decoy rats, high salt intake caused a greater positive sodium balanc

219 rt the unexpected observation that long-term high salt intake did not increase water consumption in h

220 Here we show that chronic high salt intake impairs baroreceptor inhibition of rat

221 We show that high salt intake increases the spontaneous firing rate o

222 costerone-acetate (DOCA) in combination with high salt intake induced arterial hypertension of simila

223 onstrate that osmotic balance in response to high salt intake involves a complex regulatory process t

224 High salt intake is a major risk factor for hypertension

225 aintenance of osmotic balance in response to high salt intake is a passive process that is mediated l

226 High salt intake leads to high blood pressure, even when

227 Our results connect high salt intake to the gut-immune axis and highlight th

228 , thereby influencing BP under conditions of high salt intake.

229 grally involved in the vascular responses to high salt intake.

230 mice were challenged to a normal- or chronic high-salt intake (1% NaCl).

231 o levels that may occur in human blood after high-salt intake can potentiate, in serum-free culture c

232 high blood pressure development triggered by high-salt intake through the modulation of the contracti

233 After 4 weeks of high-salt intake, ES rats still showed a lower mean seru

234 During high-salt intake, the sik1(+/+) mice exhibited an increa

235 nd DeltanW, the dominant folded structure at high salt is most likely the antiparallel stacked-X stru

236 High salt levels interfere with alternative activation o

237 s created by high light levels, rose bengal, high salt levels, and osmotic shock.

238 eased amounts of reactive oxygen species and high salt levels.

239 Further, high salt loading did not correct the hypotension in MOR

240 sociated with increased H. pylori virulence: high-salt, low-iron, or a combination of a high-salt and

241 opuABCD mutant strains are more resistant to high-salt, low-pH and -hydrogen peroxide, conditions tha

242 levels were in infected gerbils consuming a high-salt/low-iron diet.

243 High salt may additionally drive autoimmunity by inducin

244 d, in cultured dendritic cells we found that high salt media potentiates cytokine expression downstre

245 Efficient locomotion in urine samples and in high-salt media is illustrated.

246 ed molar concentrations of KCl when grown in high salt medium as detected by x-ray microanalysis and

247 decorated this residue in cells grown in the high-salt medium.

248 activators) induced rtsA-lac expression in a high-salt medium.

249 effect has been demonstrated using heat, pH, high salt mediums, and high energy ionising radiation.

250 In the L-NAME/high-salt model, memory T cells of the kidney were predo

251 The adverse effects of high salt on plants include Na(+) toxicity and hyperosmo

252 of the E1841K mutation in mice subjected to high salt or angiotensin II (Ang II) as models of hypert

253 arginine methyl ester hydrochloride (L-NAME)/high salt or repeated angiotensin II stimulation in mice

254 s and did not develop hypertension to either high salt or the second angiotensin II challenge and wer

255 o hyperosmolality, most often in the form of high salt or urea.

256 on of the Hog1 kinase, and impairs growth in high-salt or sorbitol conditions.

257 ers to solid surfaces is severely limited by high salt, pH, and hydration, yet these conditions have

258 We show that high salt recruits the two primary aversive taste pathwa

259 In contrast, hypoxia, the dauer state, and high salt reduce touch sensitivity by preventing the rel

260 lectively, this study provides evidence that high salt reduces noninflammatory innate immune cell act

261 e interactions of glass nanopipettes in this high-salt regime with a variety of surfaces and propose

262 logy applications, but their scalability and high salt rejection when in a strong cross flow for long

263 emerging water treatment technology that has high salt rejection; however, its commercialization pote

264 Formation of stable complexes, resistant to high salt, requires ATP hydrolysis.

265 In high salt, rHb (betaE6V/alphaH20R) is the only mutant th

266 In high salt, S-layer glycoprotein Asn-13 and Asn-83 are mo

267 The multivariable-adjusted odds ratio of high salt sensitivity of systolic BP was 0.66 (95% CI: 0

268 High salt sensitivity was defined as a decrease in mean

269 nd a 3.13-fold increased odds (1.80-5.43) of high salt-sensitivity during the high-sodium interventio

270 54-fold increased odds (95% CI 2.05-6.11) of high salt-sensitivity during the low-sodium and a 3.13-f

271 under challenging physiological conditions (high salts, serum, and acidic pH).

272 mildly increased albuminuria in response to high salt; severe albuminuria, nephrinuria, FSGS, and po

273 In this study, high salt (sodium chloride, NaCl), under physiological c

274 to an ATP-sepharose matrix and washed with a high salt solution followed by nicotinamide adenine dinu

275 ts on fluid balance following ingestion of a high-salt solution-rats produced significantly more urin

276 ects the nanoparticles from aggregating in a high-salt solution.

277 ong-term stability in biological buffers and high-salt solutions.

278 ATII-LCL mercuric reductase is functional in high salt, stable at high temperatures, resistant to hig

279 i.e., field-amplified stacking, sweeping, or high-salt stacking).

280 ptidergic signaling potentiates responses to high salt stimuli, which may promote ion homeostasis.

281 Exposure to a high salt stress (150 mM NaCl) triggered a rapid repress

282 Di19-2 and AtDi19-4 increased in response to high-salt stress.

283 However, it remains unclear how low- and high-salt taste perceptions are differentially encoded.

284 Unless stabilized by heparin or high salt, the active tetramer converts to an inactive s

285 inhibition by flooding and anoxia, drought, high salt, the presence of fungal and bacterial pathogen

286 4 tail deletion suppresses the attraction at high salts to a larger extent than H3 tail deletion.

287 ytes and provided good reproducibility and a high salt tolerance, underscoring the potential applicat

288 Skin macrophages from high-salt-treated mice with either genetic or pharmacolo

289 nd that macrophages isolated from kidneys of high-salt-treated WT mice have increased levels of COX-2

290 Kidneys from high-salt-treated WT mice transplanted with Cox2-/- BM h

291 ith low-salt treatment 6.6 mg/m(3) (n = 14), high-salt treatment 10.8 mg/m(3) (n = 15) or placebo 0.3

292 -associated intermediate that is stable upon high-salt treatment and other MHR mutants arrested as la

293 In the high-salt treatment group, it was 12 192 mug/l vs 11 803

294 Alkali and high-salt treatment of mycoplasma membranes and Triton X

295 e, the germination rate of gpat5 seeds under high salt was reduced, and gpat5 seedlings had lower tol

296 ge binding capacity for U sequestration from high salt water (HSW) simulant (54 mg U/g sorbent).

297 the opposing behavioral responses to low and high salt were determined largely by an elegant bimodal

298 e pool, inhibited growth under conditions of high salt with glucose as the primary carbon source.

299 onadectomized male DI rats both responded to high salt with the same spectrum of gene expression chan

300 caffeine attenuates hypertension induced by high salt without affecting sympathetic nerve activity i