ライフサイエンスコーパス: ANS

1 ANS (8-anilino-1-napthalene sulfonic acid) was used to p

2 ANS binding experiments and analysis of the CD data show

3 ANS binding to anastellin dramatically increased its emi

4 ANS complexation by cyclodextrins or bovine serum albumi

5 ANS fluorescence is enhanced by [14-38](Abu) and by both

6 ANS interaction with BSA reflects the existence of a lar

7 ANS support of BP is altered with age in healthy men due

8 ANS, neuroendocrine, and metabolic counterregulatory res

9 ANS-green fluorescence protein and ANS-beta-galactosidas

10 Intensive therapy reduced (P < 0.05) ANS and metabolic counterregulatory responses during hyp

11 o evaluate cavity accessibility, rate of 1,8-ANS binding was assessed between the portal and wild-typ

12 unts of ligand and protein at 4 degrees, 1,8-ANS bound within the cavity to 95% saturation (t0.95) in

13 1,8-ANS displacement assays revealed that the binding affini

14 be 1-anilinonaphthalene-8-sulfonic acid (1,8-ANS) as a surrogate ligand.

15 artial (odds ratio, 0.77; 95% CI, 0.63-0.95) ANS courses were associated with lower rates of death or

16 ATH to 1,8-anilinonaphthalenesulfonic acid (ANS) causes a large increase in quantum yield and a pron

17 R, and 8-anilino-1-naphthalenesulfonic acid (ANS) fluorescence experiments.

18 red by 8-anilino-1-naphthalenesulfonic acid (ANS) probe (p<0.05).

19 nts of 8-anilino-1-naphthalenesulfonic acid (ANS) were monitored to examine the folding of these prot

20 ies of 8-anilino-1-naphthalenesulfonic acid (ANS).

21 with 1-anilino naphthalene-8-sulfonic acid (ANS) confirm that the highly alpha-helical N-terminal tw

22 ted by 1-anilinonaphthalene-8-sulfonic acid (ANS) fluorescence.

23 ted with 8-amino-1-naphthol-5-sulfonic acid (ANS) is used as the collection/sensor element.

24 ce of 8-anilino-1-naphthalene-sulfonic acid (ANS) or Congo Red (CR), perturbants that inhibit protein

25 ed to 8-anilino-1-naphthalene sulfonic acid (ANS), a commonly used hydrophobic probe; HPsensors show

26 ce of 8-anilino-1-naphthalene sulfonic acid (ANS), we show that RBP populates a state with molten-glo

27 using 1-anilino-8-napthalene sulphonic acid (ANS) binding, near-UV CD and 1D (1)H NMR demonstrate fur

28 er than from the generation of an additional ANS-binding site.

29 ate is not obviously associated with altered ANS support of BP in healthy young men.

30 Furthermore, although ANS did not bind appreciably to the WT holoenzyme, incub

31 istration of the SSRI fluoxetine can amplify ANS and metabolic counterregulatory mechanisms during mo

32 pport the conclusion that benzyl alcohol and ANS interact hydrophobically with partially unfolded agg

33 103 is essential for the binding of BITC and ANS.

34 Far-UV CD and ANS fluorescence experiments demonstrate that under thes

35 Circular dichroism and ANS fluorescence data suggest that Ca (2+) binding provo

36 and better mapping abilities between ENS and ANS.

37 the latter, as demonstrated by intrinsic and ANS fluorescence studies.

38 lude that despite reduced neuroendocrine and ANS responses, antecedent hypoglycemia results in greate

39 ANS-green fluorescence protein and ANS-beta-galactosidase chimeras were both expressed excl

40 easurements obtained by NMR spectroscopy and ANS binding studies are consistent with a globular and c

41 e protein translation inhibitors anisomycin (ANS) and puromycin (PUR).

42 rylamide quenching, fluorescence anisotropy, ANS binding, dynamic light scattering, and FTIR were emp

43 salt reduces the rate of association between ANS and ALBP while simultaneously increasing the dissoci

44 To explore the associations between ANS administration-to-birth interval and survival and mo

45 ic anatomic context for interactions between ANS neural fibers and replication of SIV in lymphoid tis

46 studies have reported a causal link between ANS tasks and mathematics performance, implicating the A

47 h conformation as determined by CD, and bind ANS strongly, and these oligomers rapidly form dead-end

48 and R345A ovalbumins in the intact form bind ANS with equilibrium dissociation constants of 116 and 1

49 produce a near-UV signal, and does not bind ANS.

50 30-fold increase in K(m) for BITC and binds ANS poorly, whereas Y103F has a normal K(m) for BITC and

51 Bis-ANS binding to betaL-crystallin treated with oxidized be

52 Bis-ANS binding to VWF was reduced when the sheared protein

53 Bis-ANS inhibited in vitro capsid assembly induced by ionic

54 Bis-ANS, which blocks surface hydrophobicity, abrogated the

55 lino) naphthalene-5,5'-disulphonic acid (bis-ANS) and also possesses significant beta-sheet and rando

56 nilino)naphthalene-5,5'-disulfonic acid (bis-ANS) binding as compared to the wild-type protein, sugge

57 no-1,1'-binaphthyl-5,5'-disulfonic acid (bis-ANS) to examine unfolding intermediates associated with

58 no-1,1'-binaphthyl-5,5'-disulfonic acid (bis-ANS) to hydrophobic pockets in the blood protein von Wil

59 1,1'-binaphthalene-5,5'-disulfonic acid (Bis-ANS), were used to characterize the native and glutathio

60 e, bis-anilinonaphthalene sulfonic acid (bis-ANS).

61 This intermediate binds additional bis-ANS molecules.

62 Although bis-ANS itself did not alter the conformation of VWF, it sta

63 ed intrinsic tryptophan fluorescence and bis-ANS binding without significant alterations in either th

64 ectroscopy, tryptophan fluorescence, and bis-ANS dye binding.

65 tering, viscosity, refractive index, and bis-ANS fluorescence of lens proteins isolated from the alph

66 ange in hydrophobicity was determined by bis-ANS (4,4'-dianilino-1,1' binaphthyl-5,5' disulfonic acid

67 larity of empty capsids was indicated by bis-ANS binding, something not seen for DNA-containing capsi

68 conformation changes in VWF reported by bis-ANS correlate well with the normal function of the prote

69 nilino-1,1'-binaphthyl-5,5'-disulfonate (Bis-ANS) dye (a probe commonly used for detecting surface hy

70 4-,4'-bis(naphthalene)-8,8'-disulfonate (bis-ANS) to hydrophobic pockets exposed in the sheared prote

71 his study introduces the fluorescent dye bis-ANS as a tool that may be useful in studies of shear-ind

72 a mixture of two extrinsic fluorophores, bis-ANS and a styrylquinoxalin derivative, enabled one to mo

73 suggesting that the residues involved in Bis-ANS binding are also involved in protein aggregation.

74 bis-ANS demonstrated marked increase in bis-ANS binding at G > 2300/s.

75 gs indicate that the observed changes in bis-ANS spectroscopic properties could originate from the in

76 Photo-labeled bis-ANS alphaB-crystallin fluorescence studies confirmed the

77 We show that a small molecule, bis-ANS, binds to capsid protein, inhibiting assembly of nor

78 could originate from the interactions of bis-ANS and GuHCl and the aggregation of the dye at higher G

79 Although a total of seven molecules of bis-ANS bind cooperatively to this minichaperone, most of th

80 r spectroscopic measurements, the use of bis-ANS emission alone to monitor protein conformations can

81 The binding energy of bis-ANS for capsid protein calculated from assembly inhibiti

82 The spectral changes of bis-ANS in the presence of Atp11p indicate that the probe bi

83 brium dialysis to investigate binding of bis-ANS to free capsid protein, we found that only one bis-A

84 The binding of bis-ANS to multimeric VWF, but not dimeric VWF or control pr

85 alterations in fluorescence emission of bis-ANS to quantify the population of "molten globule" state

86 e capsid protein, we found that only one bis-ANS molecule binds per capsid protein dimer, with an ass

87 Binding of the hydrophobic probe bis-ANS and limited proteolysis demonstrate CII proteins und

88 with the hydrophobic fluorescence probe bis-ANS showed a pronounced increase in fluorescence yield u

89 lizing the fluorescent hydrophobic probe bis-ANS suggest that the D145E mutation dramatically reduced

90 ng to the hydrophobic fluorescence probe Bis-ANS were used to characterize the wt and truncated alpha

91 We propose that bis-ANS acts as a molecular "wedge" that interferes with nor

92 detected denaturation demonstrated that bis-ANS can destabilize the apical domain.

93 sids is inhibited, our data suggest that bis-ANS leads to formation of noncapsid polymers.

94 ta indicate that capsid protein bound to bis-ANS did not participate in assembly; this mechanism of a

95 ing NMR spectroscopy in conjunction with Bis-ANS binding, we identify three residues (Y16, D21, and Y

96 Studies with bis-ANS demonstrated marked increase in bis-ANS binding at G

97 The densities of both ANS innervation and SIV replication differed across cort

98 Clusterin bound ANS in a manner that was very similar to that of molten

99 focused on the common effects of stress, but ANS responses in different body systems are dissociable

100 The effect was partly mediated by ANS-associated reductions in rates of severe intracrania

101 o respiratory patterns that are modulated by ANS fluctuations and that the temporal structure of ANS

102 d enhances SOD1 hydrophobicity, as probed by ANS fluorescence emission.

103 Here, we examined whether changes in cardiac ANS activity (HRV) during a daytime nap were related to

104 of central and autonomic nervous system (CNS/ANS) signs.

105 approach to simultaneously model all the CNS/ANS outcomes as a function of cocaine exposure and other

106 t, it implicitly recognizes that all the CNS/ANS outcomes may together constitute one syndrome.

107 rment associated with exposure to a complete ANS course may be mediated through a reduction in rates

108 of patients in the no, partial, and complete ANS groups, respectively.

109 Among the no, partial, and complete ANS groups, there were significant differences in the ra

110 partial ANS group, and 3692 in the complete ANS group; the mean (SD) birth weights were 725 (169), 7

111 ut the effects of antenatal corticosteroids (ANS) on extremely preterm multiples.

112 irth intervals of antenatal corticosteroids (ANS) vary.

113 development of the area postrema, a crucial ANS structure that regulates temperature, breathing, and

114 the presence of the aggregation disruptants ANS and CR.

115 e (CHS) and the two most downstream enzymes (ANS and UFGT) is explained almost entirely by difference

116 circular dichroism, tryptophan fluorescence, ANS binding, and NMR spectroscopy.

117 ignal, and binds the hydrophobic fluorophore ANS.

118 103F has a normal K(m) for BITC and K(d) for ANS.

119 rm previously ascribed in vivo functions for ANS and ANR.

120 We discovered that, although a well-formed ANS scaffold exists early in embryonic development, the

121 hronic decompensated HF, and the hyperactive ANS will continue to push the heart to work at a level m

122 n cleavage primarily arises from a change in ANS binding rather than from the generation of an additi

123 ed to interfere with CNO-mediated changes in ANS function, locomotor activity or motor coordination.

124 ve center loop insertion, show a decrease in ANS fluorescence on cleavage with porcine pancreatic ela

125 Presumably, the increase in ANS emission observed in the presence of unliganded ATH

126 Both proteins exhibit a major increase in ANS fluorescence and identical rates for this early fold

127 An increase in ANS fluorescence, which accompanied Als-dependent cellul

128 Also, increases in ANS activity during waking, as measured by heart rate va

129 thalene-1-sulfonate (ANS) markedly increases ANS emission.

130 direct effects of photoperiod on integrated ANS function.

131 ation significantly (P < 0.05) increased key ANS (epinephrine, norepinephrine, and MSNA), metabolic (

132 nd insulinemia during all clamp studies, key ANS (epinephrine, norepinephrine, and MSNA but not sympt

133 We conclude that key ANS structures show unexpected dynamic developmental cha

134 LAR, ANS, and ANR proteins were localized to the cytosol in t

135 of the thiol-reactive fluorophore, maleimide-ANS (MIANS), inhibit the structural transition and prote

136 go awry in chronic HF, methods of measuring ANS activity in HF, the molecular alterations in heart p

137 rbamoyl)glutathione or S-methylglutathione + ANS protects completely.

138 degrees C, neither benzyl alcohol nor 4.2 mM ANS enhanced aggregation.

139 of 0.9% (w/v) benzyl alcohol or 4.2 or 21 mM ANS at 25 and 37 degrees C.

140 With 21 mM ANS, rhIL-1ra aggregation was accelerated at both temper

141 ave now identified a novel 41-residue motif (ANS) in the auxiliary domain of ACF that functions as an

142 e-detected 8-anilino-1-naphthalenesulfonate (ANS) binding.

143 ehavior of 8-anilino-1-naphthalenesulfonate (ANS) reflects a blue-shift and fluorescence enhancement

144 orescence, 1-anilino-8-naphthalenesulfonate (ANS) binding, circular dichroism (CD), and nuclear magne

145 ments with 1-anilino-8-naphthalenesulfonate (ANS), the WT and N78D mutant showed relatively more solv

146 preserve a wide range of key neuroendocrine, ANS, and metabolic counterregulatory homeostatic respons

147 pread blunting (P < 0.05) of neuroendocrine, ANS, and metabolic counterregulatory responses during su

148 by near- and far-UV CD, two-dimensional NMR, ANS binding experiments, pK(a) measurements, and analyti

149 Results: There were 848 infants in the no ANS group, 1581 in the partial ANS group, and 3692 in th

150 evelopmental impairment compared with the no ANS group.

151 of extremely premature infants exposed to no ANS or partial or complete courses of ANS.

152 sulted in significant blunting (P < 0.05) of ANS (epinephrine, norepinephrine, muscle sympathetic ner

153 Administration of ANS was associated with an immediate and rapid decline i

154 ese results support prompt administration of ANS, with the goal of a complete course prior to deliver

155 these linkages to calculate the affinity of ANS for the denatured state of ALBP and its dependence o

156 The binding of ANS to a protein is diagnostic of the presence of access

157 are significant physiological correlates of ANS support of BP in this population.

158 to no ANS or partial or complete courses of ANS.

159 omalies and unexposed to repeated courses of ANS.

160 study evaluates the dose-dependent effect of ANS on rates of neonatal morbidities and early childhood

161 The sulfonate group of ANS interacts strongly with the nonconserved intracavita

162 ANS indicates that the naphthalene group of ANS is proximate to Leu105 in the cavity.

163 c linkage analysis of the salt inhibition of ANS binding shows a nearly 1:1 reciprocal linkage: i.e.

164 Time from first injection of ANS to delivery in hours and days.

165 At 25 degrees C, the interaction of ANS with rhIL-1ra was electrostatic, but at 37 degrees C

166 nsitions, slow hydrogen exchange and lack of ANS binding.

167 rough the aniline or naphthalene moieties of ANS with cyclodextrins.

168 aneously increasing the dissociation rate of ANS from the protein.

169 ophysiology, the mechanisms of regulation of ANS activity and how they go awry in chronic HF, methods

170 Antisense down-regulation of ANS in M. truncatula resulted in reduced anthocyanin and

171 However, the role of ANS in sleep-dependent memory consolidation has never be

172 timing of ANS and mortality, a simulation of ANS administered 3 hours before delivery to infants who

173 site, which is also near the binding site of ANS.

174 RI fluoxetine can amplify a wide spectrum of ANS and metabolic counterregulatory responses during hyp

175 ctuations and that the temporal structure of ANS fluctuations is perinatally influenced.

176 n of a causal relationship between timing of ANS and mortality, a simulation of ANS administered 3 ho

177 e investigated the effects of photoperiod on ANS endpoints, this study examined the direct effects of

178 From that point on, ANS hyperactivity becomes a major problem in HF, conferr

179 Critically, only ANS improvement induced by parietal tRNS + Training tran

180 In contrast, CHX or ANS treatment of MCF10A cultures induced AhR loss and en

181 ps offer an alternative mechanism when other ANS pathways are blocked.

182 sport of some (pyronin, EtBr) but not other (ANS, Leu-Nap) substrates of the pump.

183 nts in the no ANS group, 1581 in the partial ANS group, and 3692 in the complete ANS group; the mean

184 t with these findings, the hydrophobic probe ANS bound wild-type StAR (K(app) = 8.1 x 10(5) M(-1)) to

185 and in the binding of the hydrophobic probe, ANS, implied that CBM-1 does undergo Ca(2+) sensorlike c

186 fore delivery to infants who did not receive ANS showed that their estimated decline in mortality wou

187 , 6094 (88%) were born to women who received ANS.

188 frequently among infants of women receiving ANS included severe intraventricular hemorrhage (aRR = 0

189 nscripts encoding dihydroflavonol reductase, ANS, and anthocyanidin reductase (ANR), the enzyme respo

190 lower tonic sympathoadrenal activity-related ANS support of BP and less effective BRB of BP than men

191 nate (ANS) binding to cCSQ closely resembles ANS binding to flavine or nucleotide binding sites.

192 rmer relies on the approximate number sense (ANS) which we share with animals and preverbal infants,

193 ht to rely on an "approximate number sense" (ANS) associated with parietal lobes.

194 ear magnetic resonance spectra, pH sensitive ANS binding and reversible folding into soluble structur

195 lated through a dominant targeting sequence (ANS) contained within ACF.

196 ion of the scheme to the Alaska North Slope (ANS) crude oil and analysis of fractions by comprehensiv

197 S, and (3) potential subsystems for specific ANS responses to different stimuli/tasks.

198 ed spectroscopy, UV absorbance spectroscopy, ANS extrinsic fluorescence, turbidity, right angle stati

199 born without exposure to antenatal steroids (ANS) or with incomplete courses.

200 olution of 8-anilinonaphthalene-1-sulfonate (ANS) markedly increases ANS emission.

201 lcohol and 8-anilinonaphthalene-1-sulfonate (ANS) were used.

202 s containing 1-aminonaphthalene-5-sulfonate (ANS) attached to their gamma-phosphate were synthesized

203 hobic dye 1-anilino-naphthalene-8-sulfonate (ANS) between pH 7 to 5.0, whereas appreciable binding oc

204 tophan and 1-anilinonaphthalene-8-sulfonate (ANS) fluorescence was used to monitor structure formatio

205 cent lipid 1-anilinonaphthalene-8-sulfonate (ANS) to the protein and induces direct displacement of t

206 that both 1-anilino-8 naphthalene sulfonate (ANS) and the covalent attachment of the thiol-reactive f

207 thermore, 8-anilino-1-naphthalene sulfonate (ANS) binding to cCSQ closely resembles ANS binding to fl

208 hione and 8-anilino-1-naphthalene sulfonate (ANS) each yield partial protection against inactivation

209 itored by 8-anilino-1-naphthalene sulfonate (ANS) fluorescence.

210 1-Anilino-8-napthalene sulfonate (ANS) binding and size-exclusion chromatography results s

211 hroism and 2-anilino-6-napthaline-sulfonate (ANS) fluorescence show that 3D(pol) has a melting temper

212 vonoid-related genes anthocyanidin synthase (ANS) and dihydroflavonol reductase (DFR) genes and also

213 the single Medicago anthocyanidin synthase (ANS; EC 1.14.11.19) and leucoanthocyanidin reductase (LA

214 show a variety of autonomic nervous system (ANS) abnormalities and mouse models show similar problem

215 neuroendocrine and autonomic nervous system (ANS) and metabolic counterregulatory responses during ne

216 tine would amplify autonomic nervous system (ANS) and neuroendocrine counterregulatory mechanisms dur

217 at activity of the autonomic nervous system (ANS) can stimulate lentivirus replication.

218 mined if the tonic autonomic nervous system (ANS) contribution to arterial blood pressure (BP) mainte

219 tine would amplify autonomic nervous system (ANS) counterregulatory responses to hypoglycemia in indi

220 Autonomic nervous system (ANS) dysfunction has been correlated with fasting insuli

221 crine pathways and autonomic nervous system (ANS) functioning which, in turn, influence the immune sy

222 he function of the autonomic nervous system (ANS) in mediating the flight-or-fight response was recog

223 thetic arms of the autonomic nervous system (ANS) in six healthy subjects (five male, one female; mea

224 The autonomic nervous system (ANS) is of paramount importance for daily life.

225 luctuations of the autonomic nervous system (ANS) mediated by vocal biomechanics.

226 The autonomic nervous system (ANS) plays a critical role in BP regulation.

227 l stressors induce autonomic nervous system (ANS) responses in multiple body systems that are linked

228 <7.0% would blunt autonomic nervous system (ANS) responses to hypoglycemia, and 2) antecedent hypogl

229 Neuroendocrine and autonomic nervous system (ANS) responses were also blunted by repeated hypoglycemi

230 The autonomic nervous system (ANS) shows strong variation across sleep stages.

231 ith changes in the autonomic nervous system (ANS), but the functional significance of these changes f

232 ll neuroendocrine, autonomic nervous system (ANS), metabolic, and symptom counterregulatory responses

233 adrenergic (or sympathetic) nervous system (ANS), whose activity and outflow are enormously elevated

234 cant change in the autonomic nervous system (ANS).

235 physiology is the autonomic nervous system (ANS).

236 c component of the autonomic nervous system (ANS).

237 controlled by the autonomic nervous system (ANS).

238 d not assume that approximate number system (ANS) tasks harness an innate sense of number.

239 e existence of an Approximate Number System (ANS) which allows individuals to represent and manipulat

240 by relying on an approximate number system (ANS).

241 ympathetic nervous component of the systemic ANS.

242 These results demonstrate that ANS fluorescence change is an indicator of the loop-inse

243 We tested the hypothesis that ANS support of BP is altered in healthy older humans.

244 t the first evidence, to our knowledge, that ANS activity may be one potential mechanism driving slee

245 These findings suggest that ANS dysfunction may be associated with the development o

246 alf by the addition of III3, suggesting that ANS and III3 share a common hydrophobic binding site on

247 The ANS on the plate reacts to form brown and pink colored p

248 The ANS-labeled BSGK displayed a modest 25% decrease in the

249 ed in HF treatment that target or affect the ANS and its effects on the failing heart.

250 c insult persists over time, chances are the ANS will not be able to maintain cardiac function, the h

251 hat catecholamine neurotransmitters from the ANS can increase lentiviral replication by identifying a

252 and catecholaminergic varicosities from the ANS were mapped by sucrose phosphate glyoxylic acid chem

253 However, the ANS neurotransmitter norepinephrine enhanced replication

254 and mathematics performance, implicating the ANS in the development of numerical skills.

255 ults in a approximately 200% increase in the ANS fluorescence, the rWT protein exhibits a approximate

256 sults in a 1.6- and 2.6-fold increase in the ANS-binding affinity.

257 nt WT or mutant SOD1s with ANS increased the ANS fluorescence and shifted its peak toward shorter wav

258 imeras or an ACF deletion mutant lacking the ANS were cytoplasmic.

259 s shown that performance on a measure of the ANS (a dot comparison task) is related to mathematics ac

260 The 2 branches of the ANS are key regulators of immune responses, thermoregula

261 of the ANS binding at pH 4.5 but none of the ANS binding at pH 4.0.

262 Nucleotide inhibits 70% of the ANS binding at pH 4.5 but none of the ANS binding at pH

263 weeks post-training) of the precision of the ANS compared with cognitive training in absence of stimu

264 The present review discusses the role of the ANS in cardiac physiology and in HF pathophysiology, the

265 heart works properly, this activation of the ANS will promptly restore cardiac function.

266 athetic and parasympathetic divisions of the ANS, and (3) potential subsystems for specific ANS respo

267 nfluence of high level math education on the ANS and the ENS.

268 Similarly, the ANS (8-anilino-1-naphthalenesulfate) binding showed gene

269 In the hematopoietic system, the ANS regulates stem cell niche homeostasis and regenerati

270 Another line of research suggests that the ANS is part of a larger, more general system of magnitud

271 These data indicate that the ANS of Siberian hamsters undergoes profound changes foll

272 hich has led researchers to suggest that the ANS plays a critical role in mathematics learning.

273 led that transportin 2 binds directly to the ANS motif.

274 on in adults shows little influence on their ANS, but it seems to be associated with a better anchore

275 ased on binding to a hydrophobic dye akin to ANS, which fluoresces upon binding to molten globules an

276 t significantly lower among those exposed to ANS vs no exposure (aRR = 0.93; 95% CI, 0.84-1.03).

277 ity was lower among infants with exposure to ANS vs no exposure (aRR = 0.87; 95% CI, 0.78-0.96).

278 Subgroup analyses indicated that exposure to ANS was associated with a lower risk of mortality and a

279 Compared with no exposure, exposure to ANS was associated with a lower risk of mortality in ext

280 Binding energies of TL to ANS and its analogues reveal contributions from electros

281 tants, resonance energy transfer from Trp to ANS indicates that the naphthalene group of ANS is proxi

282 ity for the 662 infants (14.4%) unexposed to ANS was 20.6% (136 of 661).

283 Tonic ANS support of BP was approximately 50% to 65% lower in

284 t the hypothesis that women have lower tonic ANS support of BP (reduction in intra-arterial BP during

285 The lower tonic ANS support of BP could contribute to the lower chronic

286 Tb(3+) luminescence energy transfer, ANS fluorescence, and NMR studies show biphasic metal-bi

287 These data provide a basis for understanding ANS dysfunction and disease predisposition in premature

288 conformational changes were monitored using ANS binding.

289 tion shell has been ignored in studies using ANS to sense the microenvironment of proteins, micelles,

290 When ANS bound, all the mutant proteins exhibited fluorescenc

291 When ANS is exhaustively washed from the particles, the matur

292 age: i.e. one ion is released from ALBP when ANS binds, and vice versa.

293 a synchronous way in solvent mixtures where ANS senses a homogeneous solvation shell.

294 near the glutathione binding region, whereas ANS decreases modification of Tyr(103), suggesting this

295 osis Risk In Communities study (n=8185) with ANS dysfunction, estimated by high heart rate (HR) and l

296 outcomes, the risk reduction associated with ANS was transient, with increasing mortality and risk fo

297 This increased interaction with ANS was greater for the mutant SOD1s and could be revers

298 exposing apolar surface for interaction with ANS.

299 in, as seen by its failure to interfere with ANS binding to anastellin.

300 n of metal-deficient WT or mutant SOD1s with ANS increased the ANS fluorescence and shifted its peak