ライフサイエンスコーパス: SCE

1 SCE cells and TM cells exposed to isoproterenol or epine

2 SCE cells produce mucilage, a specialized secondary wall

3 SCE frequencies were measured after cells were exposed t

4 SCE-FISH also measured successful recombination in human

5 SCEs included cardiac death or arrest, ventricular arrhy

6 A low working potential (0V (SCE)), fast amperometric response (<5s), and high sensit

7 At negative potentials (-0.2V(SCE)), however, the molecules are highly mobile and can

8 At intermediate potentials (-0.2 to +0.2V(SCE)), the TPyP formed a highly ordered adlayer.

9 At positive potentials (>0.5V(SCE)), a disordered layer of TPyP is formed on the Au(11

10 Additionally, SCE oils exhibited the highest antioxidant potential (68

11 To characterize factors affecting SCE frequency, we analyzed dimer resolution at the dif s

12 lications, and approximately one-half of all SCEs are preventable.

13 rmine with great ease in which cell cycle an SCE occurred.

14 sted incidence rates (AAIRs) of EC, ACE, and SCE were calculated.

15 s important for both checkpoint function and SCE.

16 We analyzed the association between LCD and SCE for the population as a whole, and for subsets.

17 IOP-related LCD and SCE result from a complex combination of factors, includ

18 ent analysis was used to predict the LCD and SCE resulting from an increase in IOP.

19 and to determine the sensitivity of LCD and SCE to the eight factors, independently and in interacti

20 The association between LCD and SCE varied greatly depending on the properties of the la

21 tiff lamina, the association between LCD and SCE was strong and consistent with the concept of "the s

22 ctors (35% and 7% of the variance in LCD and SCE, respectively).

23 a robust structure, particularly for LCD and SCE, which is tolerant to variations in tissue geometry

24 on when interpreting measurements of LCD and SCE.

25 IOP, some cases had peculiarly large LCD and SCE.

26 analysis of the relationship between LCD and SCE.

27 suggest that simple slipped misalignment and SCE-associated misalignment intermediates are similarly

28 ore profound defect in RAD51 recruitment and SCE induced by replication fork collapse when ATR is dep

29 nd that BRCA1 promotes RAD51 recruitment and SCE induced by replication fork stalling independent of

30 t of the nascent strand and its template and SCE-associated misalignment involving both nascent stran

31 ation stress generated unrepaired breaks and SCEs at fragile sites.

32 th cellulosic rays and show that Arabidopsis SCE cells represent an excellent model in which to study

33 AD54, are required for DNA damage-associated SCE but not for spontaneous SCE.

34 hether spontaneous and DNA damage-associated SCE requires specific genes within the RAD52 and RAD3 ep

35 utant was defective in DNA damage-associated SCE when cells were exposed to either radiation or chemi

36 d for BIR, are required for X-ray-associated SCE but not for SCE stimulated by HO-induced DSBs.

37 Secondary structure-associated SCE events occur via double-strand break repair.

38 The defect in DNA damage-associated SCEs in rad51 mutants correlated with an eightfold highe

39 e that many TNR expansion mutations occur by SCE.

40 regnancies (47 of 1,315) were complicated by SCEs.

41 In contrast, SCE frequencies were significantly elevated in BLM-defic

42 After mild DNA damage, SCE was threefold higher in the knockout cells, while no

43 This newly delineated SCE-->DMP-->mMAN-->HVC/pHVC pathway is the first report

44 study, we have adapted Strand-seq to detect SCE in the yeast Saccharomyces cerevisiae.

45 gives significantly improved power to detect SCEs after in silico correction of normal tissue contami

46 lysis of CNAs and affect the power to detect SCEs in clinical samples.

47 oneal cavity at a much higher level than did SCE.

48 o T-SCE, other genomic rearrangements (i.e., SCE) were also significantly increased in mTert-/- ES ce

49 of -1.70 V vs. saturated calomel electrode (SCE) for the couple involving the neutral organic donor

50 -0.4 V vs. the saturated calomel electrode (SCE) in acetonitrile solutions.

51 -0.35 V versus saturated calomel electrode (SCE), specific to ds-ON and highly sensitive to base pai

52 - 14) mV versus saturated calomel electrode (SCE).

53 mum of 15 mV vs saturated calomel electrode (SCE).

54 l of +1.2V (vs. saturated calomel electrode [SCE]), no added nitrogen source except the lysozyme itse

55 isually guided) single-cell electroporation (SCE) and extracellular electrophysiology, and can be use

56 tes the ability of RMI2 to suppress elevated SCE.

57 d BLM protein level and rescued the elevated SCE phenotype in TopBP1-depleted cells.

58 To elucidate SCE recombination mechanisms, we determined whether spon

59 btle CT findings of centrilobular emphysema (SCE).

60 eshwork (TM) or Schlemm's canal endothelial (SCE) cells were grown on porous filter supports.

61 computing the sequence correlation entropy (SCE) using the quenched probability P(sk)(i,j) of findin

62 with PCE, the soluble form of cell envelope (SCE), which was derived from PCE by treatment with cell

63 A SUMO-conjugating enzyme (SCE) (E2, Ubc9) in C. reinhardtii was shown to be functi

64 (Arabidopsis thaliana) seed coat epidermis (SCE) to study cell wall synthesis.

65 ine the incidence of serious cardiac events (SCEs) in pregnant women with heart disease, whether they

66 ons (CNAs) and significant consensus events (SCEs) in cancer genomes is a main task in discovering po

67 tion related to the skin cancer examination (SCE) for melanoma, a relevant competency gap that influe

68 osed normal human cells, can cause excessive SCEs to an extent equivalent to that observed when the c

69 by high levels of sister-chromatid exchange (SCE) and cancer predisposition.

70 ci by combining a sister chromatid exchange (SCE) assay with fluorescent in situ hybridization (SCE-F

71 Sister chromatid exchange (SCE) can occur by several recombination mechanisms, incl

72 an be used to map sister chromatid exchange (SCE) events genome-wide in single cells.

73 tentially harmful sister chromatid exchange (SCE) events in wild-type cells but not in cells derived

74 levated levels of sister chromatid exchange (SCE) found in BLM(-/-) cells.

75 Utilizing sister chromatid exchange (SCE) frequencies as a marker of the BSE, we performed ce

76 the dependence of sister chromatid exchange (SCE) frequencies on location [i.e., genomic (G-SCE) vs.

77 we report that a sister chromatid exchange (SCE) generated by crossover-associated HR efficiently oc

78 te of spontaneous sister chromatid exchange (SCE) in Bloom syndrome (BS) cells, but not in their BLM-

79 Sister chromatid exchange (SCE) in Escherichia coli results in the formation of cir

80 ontaneous unequal sister-chromatid exchange (SCE) in vegetatively growing yeast cells.

81 ontaneous unequal sister-chromatid exchange (SCE) in yeast.

82 ells, spontaneous sister chromatid exchange (SCE) occurred with twice the frequency observed in norma

83 by adjustments in sister chromatid exchange (SCE) rate, rather than by direct selection on the number

84 NA damage-induced sister chromatid exchange (SCE) was evident by a 10-fold reduction in HO endonuclea

85 ytogenetically as sister chromatid exchange (SCE), and that this rate is dependent on genotype.

86 Spontaneous sister chromatid exchange (SCE), as monitored between truncated his3 fragments, was

87 lution mapping of sister chromatid exchange (SCE), facilitating the study of this type of genomic rea

88 te of spontaneous sister chromatid exchange (SCE), heteroallelic recombination and translocations, re

89 n is disrupted by sister chromatid exchange (SCE), the dark chromatid is always in the center, so tha

90 the frequency of sister chromatid exchange (SCE), whereas deleting both Blm and Recql5 lead to an ev

91 ncreased level of sister chromatid exchange (SCE)--the hallmark feature of Bloom syndrome cells.

92 oint response and sister chromatid exchange (SCE).

93 ogenous levels of sister chromatid exchange (SCE).

94 vel and increased sister chromatid exchange (SCE).

95 associated with sister chromosome exchange (SCE).

96 sult in elevated sister chromatid exchanges (SCE).

97 ity and increased sister chomatid exchanges (SCEs).

98 by increases in sister chromatid exchanges (SCEs) and numbers of micronuclei.

99 evated levels of sister chromatid exchanges (SCEs) and patients with Bloom's syndrome develop a broad

100 nce of excessive sister chromatid exchanges (SCEs) as an index of DNA damage in human lung fibroblast

101 uced spontaneous sister chromatid exchanges (SCEs) but this was not due to a defect in HDR-mediated c

102 the induction of sister chromatid exchanges (SCEs) by UV irradiation are greatly enhanced.

103 ized by elevated sister chromatid exchanges (SCEs), as well as chromosomal breaks, deletions, and rea

104 sociated unequal sister chromatid exchanges (SCEs), translocations, and inversions.

105 induced DSBs and sister chromatid exchanges (SCEs), two RAD51-dependent processes, are 53BP1 independ

106 reased number of sister-chromatid exchanges (SCEs).

107 displacement (LCD), scleral canal expansion (SCE), and the stresses (forces) and deformations (strain

108 al hypothalamus (stratum cellulare externum [SCE]), which may also relay information to the same dors

109 ablishment of normal databases to facilitate SCE detection.

110 equired for X-ray-associated SCE but not for SCE stimulated by HO-induced DSBs.

111 The most frequent SCEs were cardiac death or arrest, heart failure, arrhyt

112 Furthermore, SCEs were suppressed at fragile sites near centromeres i

113 E) frequencies on location [i.e., genomic (G-SCE) vs. telomeric (T-SCE) DNA] in primary human fibrobl

114 ERCC1-XPF-deficient cells, neither T- nor G-SCE frequencies differed from controls.

115 egative WRN-deficient cells, T-SCE-but not G-SCE-frequencies were significantly increased compared wi

116 s 1-1417) in BS cells can correct their high SCEs to normal levels, whereas expression of a BLM fragm

117 in both MMR- and rad1-mutant cells; however, SCE events for both IR- and non-IR-containing substrates

118 ssay with fluorescent in situ hybridization (SCE-FISH).

119 ellular stratum of the lateral hypothalamus (SCE).

120 rating the rearrangements that arise after I-SCE:I-induced double-strand breaks.

121 eatment with the rare-cutting endonuclease I-SCE:I.

122 n unexpected effect of ERCC1 deficiency on I-SCE:I-stimulated rearrangements, which are not dependent

123 We suggest that if SCEs represent homologous recombination between sister c

124 iated repair of endogenous DNA damage and in SCE formation during normal DNA replication.

125 onstrate globally increased heterogeneity in SCE subjects compared with NS and SNI subjects but demon

126 ecA mutation, reflecting the role of RecA in SCE and virtually all homologous recombination in E. col

127 nd thickness (46% and 36% of the variance in SCE, respectively).

128 that ectopic expression of FANCD2 increased SCE.

129 he complex in solution and lead to increased SCE levels in cells that are similar to those observed i

130 10-fold reduction in HO endonuclease-induced SCE and no detectable X-ray stimulation of SCE in a rad9

131 not enhanced in dun1 mutants, but UV-induced SCE and heteroallelic recombination were enhanced.

132 In contrast, UV-induced SCE is largely a product of the trimethylated state, whi

133 Interestingly, SCE produced by replication fork collapse following DNA

134 mino acids 133-1417) results in intermediate SCE levels.

135 ling the repair of double-strand breaks into SCE.

136 A short-lived, SCE-inducing factor(s) was generated in alpha-irradiated

137 In both UM and PD20 cells, low SCE was reversed by inhibiting DNA-PKcs (DNA-dependent p

138 For the class of proteins with low SCE values, there are significant numbers of mixed charg

139 Since IR-mediated SCE events are reduced in msh2 cells, we propose that TN

140 Our results also show that TNR-mediated SCE events are independent of RAD50, MRE11 and RAD51, wh

141 Most SCEs (66%) occurred in the antepartum period.

142 We use a combination of SCE and clustering based on the principle component anal

143 hibit a significantly increased frequency of SCE compared with the corresponding wild-type control.

144 d Recql5 lead to an even higher frequency of SCE.

145 ase flow through the paracellular pathway of SCE and TM cells through a beta-receptor mediated respon

146 An increase in the rate of SCE is an indicator of elevated recombination activity a

147 d SCE and no detectable X-ray stimulation of SCE in a rad9 mutant.

148 Our findings suggest that the low values of SCE and the presence of (CH) and/or (CP) may be indicati

149 that proteins with relatively low values of SCE are predominantly associated with various diseases.

150 MUS81 or SLX4 reduces the high frequency of SCEs in Bloom's syndrome cells, indicating that MUS81 an

151 Strikingly, in PML-/- cells the frequency of SCEs is increased relative to PML+/+ cells.

152 Almost one-half of SCEs (49%) were preventable; the majority of preventable

153 eral vexing questions about the induction of SCEs (genetic damage and its repair) after exposure to v

154 nd that are responsible for the induction of SCEs, persist before being repaired and thus lose their

155 se in UV sensitivity and in the induction of SCEs.

156 cation, and by demonstrating high numbers of SCEs in cultured murine Blm-/- fibroblasts.

157 High numbers of SCEs were uniformly seen in members of the panel, and se

158 his method, which permits the observation of SCEs in endoreduplicated cells, makes it possible to det

159 of amino acids 133-1417 in the reduction of SCEs was not explained by a defect in DNA helicase activ

160 A more persistent SCE-inducing factor(s), which can survive freeze-thawing

161 ere preventable; the majority of preventable SCEs (74%) were secondary to provider management factors

162 ells, indicating that MUS81 and SLX4 promote SCE formation, in events that may ultimately drive the c

163 esis that functions of proteins with similar SCE values may be linked.

164 amage-associated SCE but not for spontaneous SCE.

165 e switch pathway, play a role in spontaneous SCE.

166 quantifiable evidence that most spontaneous SCE events in wild-type cells are not due to the repair

167 parison with wild type, rates of spontaneous SCE are 10-fold lower in rad51 rad1 but not in either ra

168 e reductase in mec1-21, rates of spontaneous SCE increased 15-fold above wild-type.

169 data suggest FANCD2 may promote spontaneous SCE by influencing which double-strand break repair path

170 Therefore, reduced spontaneous SCE could be a manifestation of the same defect that cau

171 aemia patients displayed reduced spontaneous SCE formation relative to their FANCD2-complemented coun

172 involvement of p53 in regulating spontaneous SCE is BLM dependent.

173 ith the Blm helicase to suppress spontaneous SCE events.

174 Our results suggest that spontaneous SCE occurs by a template switching mechanism.

175 wed no difference in the rate of spontaneous SCEs; however, the rate of spontaneous inversions was de

176 is consistent with a model where spontaneous SCEs are the end product of endogenous recombination eve

177 AD50, MRE11 and RAD51, whereas IR-stimulated SCEs are dependent on the RAD52 epistasis-group genes.

178 analysis revealed that RMI2 and BLM suppress SCE within the same pathway.

179 TopBP1 in S phase cells in order to suppress SCE and thereby prevent genomic instability.

180 -deficient cells with mutations that cause T-SCE levels to rise.

181 n telomerase-negative WRN-deficient cells, T-SCE-but not G-SCE-frequencies were significantly increas

182 her studies, we found evidence of elevated T-SCE in telomerase-negative but not telomerase-positive b

183 Elevated T-SCE was associated with greater immortalization potentia

184 hrough telomere sister chromatid exchange (T-SCE) in murine telomere reverse transcriptase-deficient

185 lished telomere sister chromatid exchange (T-SCE), indicating that WRN normally represses T-SCEs.

186 Furthermore, T-SCE-driven premature cellular senescence may be a factor

187 elomere length but no SFEs, no increase in T-SCE was observed.

188 nto the cellular consequences of increased T-SCE frequency.

189 odel predicts that in cells with increased T-SCE, the onset of replicative senescence is dramatically

190 omologous recombination between telomeres (T-SCE).

191 tion [i.e., genomic (G-SCE) vs. telomeric (T-SCE) DNA] in primary human fibroblasts deficient in WRN,

192 In addition to T-SCE, other genomic rearrangements (i.e., SCE) were also

193 PBs), telomere sister chromatid exchanges (T-SCEs), and extrachromosomal telomeric signals (ECTSs).

194 Furthermore, T-SCEs were more often detected in ES cells than in spleno

195 at telomeres, and observed an increase in T-SCEs only in a subset of mTert-/- splenocytes or ES cell

196 E), indicating that WRN normally represses T-SCEs.

197 These findings demonstrate that SCE-FISH frequency at fragile sites is a sensitive indic

198 a therapy by promoting fluid flow across the SCE and TM cells lining tissues of the major aqueous out

199 s of instruction related to melanoma and the SCE, a description of the integrated skin examination as

200 ), and at least 1 opportunity to observe the SCE (OR, 1.95).

201 ), and at least 1 opportunity to observe the SCE (OR, 2.70).

202 and at least 4 opportunities to observe the SCE were most predictive of intent to perform an integra

203 n, and at least 1 opportunity to observe the SCE were most predictive of performance of the SCE (ORs,

204 a, and at least 1 opportunity to observe the SCE.

205 edictive of confidence in performance of the SCE (odds ratios [ORs], 15.35 and 11.48, respectively).

206 E were most predictive of performance of the SCE (ORs, 21.67, 15.48, and 9.92, respectively).

207 To augment the practice of the SCE among medical students, course directors may design

208 n examination, and actual performance of the SCE.

209 on skin cancer (OR, 2.42) and lecture on the SCE (OR, 5.04).

210 es on skin cancer (OR, 6.35), lecture on the SCE (OR, 7.54), knowledge of melanoma risk (OR, 3.71), a

211 y outcomes were confidence in performing the SCE, intent to perform an integrated skin examination, a

212 classify protein families in terms of their SCE.

213 Non-IR-associated unequal SCE events are increased in both MMR- and rad1-mutant ce

214 he rate of spontaneous IR-stimulated unequal SCE events in yeast is significantly reduced in strains

215 Using SCE-FISH, we find that endogenous and exogenous replicat

216 ntial is stepped to higher values (0.5-0.8 V(SCE)).

217 are -25(+/- 14) mV and -433(+/- 8) mV versus SCE whereas protein B' had no effect though it did alter

218 queous solution with E(1/2) = +0.41 V versus SCE at pH 4 and involves the transfer of one electron an

219 ls as negative as approximately - 3 V versus SCE by a proton-coupled electron transfer mechanism.

220 in 0.075 M Me4NBF4/CH3CN were -1.04 V versus SCE for the n-doping of P(C) and 0.40 and 0.30 V versus

221 n-doping of P(C) and 0.40 and 0.30 V versus SCE for the p-doping of P(C) and P(A), respectively.

222 based on steady-state currents at 0 V versus SCE in the presence of H2O2 were in the order horseradis

223 giving SWV peaks at approximately 1 V versus SCE that grow larger with reaction time.

224 ential in the range -1.39 to -1.58 V (versus SCE) and estimated electron affinities (LUMO levels) of

225 s can be varied from -0.05 to 0.15 V (versus SCE) by modification of the substituents on phosphorus (

226 s buffer are in the range 0.15-0.35 V versus SCE, and the rate constants for the oxidation GO(red) (w

227 le one-electron transfer waves at E(1/2) (vs SCE in MeCN) = -1.121, 0.007, and 0.329 V, and a fourth

228 nging in potential from -0.77 to +2.5 eV (vs SCE) and including thermal reductants, indirect electrol

229 wing results: FeIII/II E(1/2) at -260 mV (vs SCE), approximately 300 mV positive of the value measure

230 ave the same redox potential (ca. -180 mV vs SCE).

231 ersible one-electron reduction at -0.09 V vs SCE (MeCN), and reduced forms of DCNT have yet to be iso

232 e oxidation peaks in the region 0.6-1.1 V vs SCE after incubations with styrene oxide, DNA/AQ films g

233 (o)(1,red) = -2.02, E(o)(2,red) = -2.07 V vs SCE and E(o)(1,ox) = 1.14, E(o)(2,ox) = 1.20 V vs SCE.

234 e of DPA, which shows E(o)(red) = -2.06 V vs SCE and E(o)(ox) = 1.15 V vs SCE.

235 tion of TPrA began at approximately 0.6 V vs SCE and exhibited a broad irreversible anodic peak.

236 potential region more negative than 1.0 V vs SCE and one at more positive potentials.

237 lic voltammetric wave observed at -0.58 V vs SCE at a Pt electrode was originally proposed to corresp

238 s conductive between about 0.1 and -0.4 V vs SCE at pH 4.5.

239 p-GaP system (E(CBM) approximately -1.5 V vs SCE at pH 5) and the photochemical [Ru(phen)3](2+)/ascor

240 oxidation potentials greater than >1.7 V vs SCE do not react.

241 t 0.47 V vs SCE for (PCA)Co(2) and 0.39 V vs SCE for (BCA)Co(2).

242 ity of E(1/2) which was located at 0.47 V vs SCE for (PCA)Co(2) and 0.39 V vs SCE for (BCA)Co(2).

243 duction potential E(Br(*)/Br(-)) = 1.22 V vs SCE in acetone, which is about 460 mV less positive than

244 at potentials between -0.55 V and -0.20 V vs SCE in CH3CN.

245 ved except for some broad ones at ~-3.2 V vs SCE in THF, which is consitent with the wide highest occ

246 talytic SWV peaks at approximately 0.75 V vs SCE to increase nearly linearly over the first 10-20 min

247 rsors with oxidation potentials <or=1.7 V vs SCE undergo ready oxidative C-C bond formation with DDQ/

248 he HER or for CO(2) conversion at -1.25 V vs SCE using a glassy carbon electrode.

249 trolysis experiments, conducted at -1.2 V vs SCE using Et3NHCl as a proton source, N2O is produced se

250 tials of E(4+/3+) approximately 1.6-1.7 V vs SCE were determined for four-electron oxidation to the c

251 lues of 2.48 +/- 0.03 and 2.26 +/- 0.02 V vs SCE were obtained for benzene and toluene, respectively.

252 lectrocatalyzes H(2) generation at -0.9 V vs SCE with i(cat)/i(p) approximately 4, corresponding to a

253 rates with oxidation potentials <= +2.5 V vs SCE with pyrazole, triazole, and pyridine nucleophiles.

254 event, while ECL from luminol at +0.45 V (vs SCE) could be enhanced by the same Pt NPs, in the presen

255 ed on glassy carbon electrode at -1.25 V (vs SCE) could be quenched by closely contacted Pt nanoparti

256 s are also observed at +1.94 and +2.15 V (vs SCE) for 1 and 3.

257 between E(p) values of -1.75 and -1.93 V (vs SCE), corresponding to reductions of the alkyne units.

258 more positive than approximately -0.1 V (vs SCE).

259 reduction wave (E degrees (red) = -1.18 V vs SCE) and two nernstian one-electron oxidation waves (E d

260 ery negative reduction potential (-1.37 V vs SCE) for the formation of pyrH(*).

261 rst reduction of these compounds (-0.70 V vs SCE) occurs prior to TiO2 reduction.

262 )'s LUMO (E(0)(calc) approximately -1.3 V vs SCE) to form the solution phase PyH(0) via highly reduci

263 ly positive hole (Eox approximately 1.7 V vs SCE), which allows to drive demanding photo-oxidation re

264 arenes such as benzene (E(red) < -3.42 V vs SCE).

265 1,ox) = 1.01 V, E degrees (2,ox) = 1.24 V vs SCE).

266 rogenase mimics reported to date (-0.74 V vs SCE).

267 by electrochemical methods (up to -1.3 V vs SCE).

268 cathodic onset potential (E(cat) = -1.2 V vs SCE).

269 eroxide at low applied potentials (-0.1 V vs SCE).

270 rometric response toward glucose at 0.6 V vs SCE, demonstrating the anchoring of this enzyme via two

271 obtained by using applied voltage -0.6 V vs SCE, O(2), and 100 mM H(2)O(2).

272 with formal potentials of 0.34 and 0.76 V vs SCE, respectively.

273 ion potentials more positive than -2.21 V vs SCE, which is much higher than the thermodynamic redox p

274 O)(TBP8Cz(*+)):Zn(II) gives Ered = 0.69 V vs SCE, which is nearly +700 mV above its valence tautomer

275 /+1) = +0.99 V and E(1/2)(0/-1) = -0.45 V vs SCE.

276 IP(1-/0) processes, at -0.86 and -1.20 V vs SCE.

277 n behavior with E degrees (red) = -1.56 V vs SCE.

278 d) = -2.06 V vs SCE and E(o)(ox) = 1.15 V vs SCE.

279 nd E(o)(1,ox) = 1.14, E(o)(2,ox) = 1.20 V vs SCE.

280 the solution over the range 0.106-1.001 V vs SCE.

281 rode, over the potential range -0.4-0.5 V vs SCE.

282 (3)(-), with an onset potential of -1.1 V vs SCE.

283 owing a characteristic response at +1.5 V vs SCE.

284 on potentials ranging from -1.6 to -3.4 V vs SCE.

285 n of ADH heme proceeded at around -0.05V vs. SCE.

286 sity of 510microAcm(-2) at pH 7.0 and 0V vs. SCE.

287 ration source, a lower potential (+0.85V vs. SCE), and a platinum basket electrode.

288 gand complex of Al(3+) occurs at -1.16 V vs. SCE (500 mV overpotential).

289 ability to the reduction of FA at 0.3 V (vs. SCE) with the electron transfer rate constant (ks) of 1.

290 oxidations in the range of +0.70-1.10 V (vs. SCE).

291 ate species with oxidizing power (3.33 V vs. SCE) sufficient to oxidize benzene and halogenated benze

292 alytic activity towards the HER (-0.46 V vs. SCE) upon the 1000th cycle, such potential is the closes

293 he desired value of platinum at (-0.25 V vs. SCE).

294 pH 7.0, at low applied potentials (0.0 V vs. SCE).

295 e) with a low redox potential of -0.58 V vs. SCE.

296 ating with an applied potential of 0.3 V vs. SCE.

297 eriorly) and -12.9 mum (anteriorly), whereas SCE was between 0.5 and 15.2 mum (all expansions).

298 e to DNA polymerase III exonuclease, whereas SCE-associated events are sensitive to exonuclease I.

299 the variance in LCD, respectively), whereas SCE was most sensitive to scleral modulus and thickness

300 events were more common in pregnancies with SCEs compared with those without cardiac events (62% vs.