ライフサイエンスコーパス: I2

1 I2(II) is 4.565(2) A from the hydroxyl group with an occ

2 I2(II) is located interstitially between two phenyl ring

3 ed with heparin was 0.88 (95% CI, 0.77-1.00; I2 = 0%; 2,477 patients; six trials; moderate strength o

4 ents; RR, 1.97; 95% CI, 1.71-2.27; P < .001, I2 = 0%).

5 ess (OR, 2.27; 95% CI, 1.54-3.35) (P < .001, I2 = 24%).

6 ity (OR, 1.79; 95% CI, 1.39-2.31) (P < .001, I2 = 64%), poor sleep quality (OR, 1.53; 95% CI, 1.11-2.

7 tically heterogeneous (Q = 203.50, P < .001, I2 = 65.60).

8 ents; RR, 1.96; 95% CI, 1.67-2.31; P < .001, I2 = 74%).

9 atio [RR],1.79; 95% CI, 1.47-2.18; P < .001, I2 = 85%); when SMR was qualitatively graded, the incide

10 io [OR], 2.17; 95% CI, 1.42-3.32) (P < .001, I2 = 90%), poor sleep quality (OR, 1.46; 95% CI, 1.14-1.

11 irst patient-controlled analgesia; P < .001; I2 = 19%).

12 ity (OR, 1.46; 95% CI, 1.14-1.88) (P = .003, I2 = 76%), and excessive daytime sleepiness (OR, 2.72; 9

13 n a visual analog scale at 2 days; P = .003; I2 = 0%).

14 ligrams per kilogram per 48 hours; P = .004; I2 = 17%) and that acupuncture delayed opioid use (mean

15 s ratio, 1.57; 95% CI, 1.14-2.15; p = 0.006; I2 = 37%), microbiological eradication (odds ratio, 1.61

16 ess (OR, 2.72; 95% CI, 1.32-5.61) (P = .007, I2 = 50%).

17 ity (OR, 1.53; 95% CI, 1.11-2.10) (P = .009, I2 = 74%), and excessive daytime sleepiness (OR, 2.27; 9

18 e as follows: aHR = 1.04 (95% CI 0.54-2.01), I2 = 0%, p = 0.910; aHR = 0.73 (95% CI 0.26-2.06), p = 0

19 ds ratio, 1.61; 95% CI, 1.11-2.35; p = 0.01; I2 = 0%), and infection-related mortality (odds ratio, 0

20 ression (SMD, -0.54; 95% CI, -1.08 to -0.01; I2=68%) and depressive symptoms (SMD, -0.27; 95% CI, -0.

21 ymptoms (SMD, -0.27; 95% CI, -0.53 to -0.01; I2=68%).

22 ated treatment (RR, 0.71; 95% CI, 0.49-1.02; I2 = 49.0%) (n = 876) showed no significant risk reducti

23 g ORR (RR, 1.31; 95% CI, 1.05-1.64; P = .02; I2 = 0%) in 5 studies.

24 k ratio, 0.87 [95% CI, 0.76-0.99]; p = 0.03; I2 = 0%) but no significant reduction in hospital mortal

25 tality (risk ratio, 0.93; 95% CI, 0.84-1.03; I2 = 0%).

26 an OR of death of 3.71 (95% CI, 1.25-11.03; I2 = 0%).

27 lligrams per kilogram per 48 hours; P = .03; I2 = 86%) and in pain improvement (mean difference, -0.5

28 95% CI, 17.5%-24.7%, Q = 14.4, tau2 = 0.04, I2 = 79.2%) to 43.2% for the 2-item PRIME-MD (1349/2891

29 ds ratio, 0.58; 95% CI, 0.34-0.96; p = 0.04; I2 = 46%) was observed with the addition of aerosolized

30 o -0.02 on the visual analog scale; P < .05; I2 = 62%).

31 ds ratio, 0.74; 95% CI, 0.54-1.01; p = 0.06; I2 = 25%) or nephrotoxicity (odds ratio, 1.18; 95% CI, 0

32 lecoxib (SMD, -0.29; 95% CI, -0.49 to -0.08; I2=73%) on remission (OR, 7.89; 95% CI, 2.94 to 21.17; I

33 95% CI, 37.6%-49.0%, Q = 45.6, tau2 = 0.09, I2 = 84.6%).

34 ax = 640 nm), and an eta(1) species [(eta(1)-I2)BiI4](3-) (lambdamax = 750 nm).

35 Interestingly, [(eta(1)-I2)BiI5](4-) decayed to ground state products with a fir

36 ted with 1 equiv of iodide to yield [(eta(1)-I2)BiI5](4-).

37 sk ratio, 0.84 [95% CI, 0.66-1.05]; p = 0.1; I2 = 16%) associated with a critical care transition pro

38 95% CI, 1.19-1.50]; No. of studies [K] = 10, I2 = 7.9%) compared with usual care, with absolute incre

39 eatment orders (RR, 0.95; 95% CI, 0.81-1.10; I2 = 0.0%) (n = 742), compliance enhancement (RR, 0.52;

40 identical genotype constellations (G10-P[11]-I2-R2-C2-M2-A1-N1-T1-E2-H3), the same as those of the pr

41 dds of MS (95% CI: 1.7-2.5; p = 7.7 x 10-12; I2 = 63%, 95% CI: 0%-88%).

42 e in age was -0.24 cm (95% CI: -0.34, -0.14; I2 = 30%), reflecting a compositional change (lower dens

43 09; 95% confidence interval [CI], 0.06-0.15; I2 = 0.60, P < .01; 15 trials).

44 reased (risk ratio, 0.79; 95% CI, 0.53-1.17; I2 = 0%; 2,392 patients; three trials).

45 remission (OR, 7.89; 95% CI, 2.94 to 21.17; I2=0%) and response (OR, 6.59; 95% CI, 2.24 to 19.42; I2

46 ratio for death was 1.30 (95% CI, 0.78-2.18; I2 = 0%; 160 patients; three trials; low strength of evi

47 K antagonists (RR, 0.84; 95% CI, 0.59-1.19; I2 = 35%; 5 RCTs), and no increased risk was identified

48 turn is modulated by endogenous inhibitor 2 (I2 (PP2A)).

49 bitals as an eta(2) ligated I2(*-), [(eta(2)-I2)BiI4](3-) (lambdamax = 640 nm), and an eta(1) species

50 The [(eta(2)-I2)BiI4](3-) subsequently reacted with 1 equiv of iodide

51 n K antagonist (RR, 0.67; 95% CI, 0.37-1.20; I2 = 0%; 5 RCTs) was identified.

52 zard ratio [aHR] = 0.73 [95% CI 0.44, 1.21], I2 = 0%, p = 0.228), in the risk of stillbirth (artemisi

53 its (odds ratio [OR] 2.92, 95% CI 2.02-4.22; I2 = 63.7%, 95% CI 4.4%-86.2%), use of a sterile blade t

54 for neonatal death, 1.15 (95% CI, 1.07-1.23; I2 = 78.5%; n = 12 studies); and for infant death, 1.18

55 49%; nine population-based studies (n=2408); I2=27%) and 5-year survival was 29% (95% CI 26% to 33%;

56 g ORR (RR, 1.17; 95% CI, 0.89-1.53; P = .26; I2 = 0%) in 9 studies.

57 d for infant death, 1.18 (95% CI, 1.09-1.28; I2 = 79%; n = 4 studies).

58 ula of this compound is thus (CH3NH3)PbI3-2x(I2)x where x approximately 0.007 at room temperature.

59 difference, -0.57 d; 95% CI, -2.44 to 1.30; I2 = 0%), ventilator-associated events (risk ratio, 0.97

60 s); for stillbirth, 1.24 (95% CI, 1.18-1.30; I2 = 80%; n = 18 studies); for perinatal death, 1.16 (95

61 pioid consumption at 1 and 2 weeks (P = .32, I2 = 87%), and for preoperative exercise, the mean diffe

62 difference, -0.16 d; 95% CI, -0.64 to 0.33; I2 = 0%), ICU length of stay (weighted mean difference,

63 radicalPD (-0.38 cm [95% CI: -0.44, -0.33]; I2 = 30%) was additionally driven by increasing breast a

64 for fetal death was 1.21 (95% CI, 1.09-1.35; I2 = 77.6%; n = 7 studies); for stillbirth, 1.24 (95% CI

65 or perinatal death, 1.16 (95% CI, 1.00-1.35; I2 = 93.7%; n = 11 studies); for neonatal death, 1.15 (9

66 igoanuric HUS (OR, 2.38 [95% CI, 1.30-4.35]; I2 = 2%), renal replacement therapy (OR, 1.90 [95% CI, 1

67 ce enhancement (RR, 0.52; 95% CI, 0.11-2.37; I2 = 55.7%) (n = 250), and integrated treatment (RR, 0.7

68 ildren were vaccinated: 22% (95% CI, 1%-38%; I2 = 0%; N = 1903) against acute respiratory infections

69 -study heterogeneity (Q = 1247, tau2 = 0.39, I2 = 95.8%, P < .001).

70 110/954 individuals; 95% CI, 10.2% to 23.4%, I2 = 70.1%).

71 issed (95% confidence interval: 15.3%-35.4%; I2 = 0%).

72 d response (OR, 6.59; 95% CI, 2.24 to 19.42; I2=0%).

73 to 0.93]; P = 0.030; heterogeneity P = 0.45; I2 = 0%), and increases in the serum creatine kinase lev

74 ds ratio, 1.18; 95% CI, 0.76-1.83; p = 0.45; I2 = 0%).

75 on (risk ratio, 0.29 [95% CI, 0.17 to 0.49]; I2 = 0%).

76 OR]: 1.41, 95% CI 1.20-1.66, p = 2.7 x 10-5, I2 = 0%, 95% CI 0-29).

77 tricted to studies of widespread pain (n = 5,I2 = 82.3%) MRR1.22(95%CI 0.93-1.60).

78 ',5'-R2C6H3)2C6H3-N horizontal lineC(H)-(3,5-I2-2-O-C6H2)}]NiCH3(pyridine)] (1a-pyr, R = Me; 1b-pyr,

79 [OR] = 1.7, 95% CI: 1.3-2.2; p = 2.3 x 10-5; I2 = 47%, 95% CI: 0%-85%) and including only SNPs involv

80 eight heparin (RR, 2.13; 95% CI, 0.22-20.50; I2 = 0%; 5 RCTs).

81 ), and death (OR, 5.13 [95% CI, 1.50-17.57]; I2 = 55%).

82 x 109 cells/L (RR, 1.05 [CI, 0.68 to 1.61]; I2 = 56%).

83 to 0.86]; P = 0.015; heterogeneity P = 0.63; I2 = 0%) and cardiovascular mortality (OR, 0.50 [CI, 0.2

84 to 0.96]; P = 0.026; heterogeneity P = 0.65; I2 = 0%).

85 tion (4 trials; RR, 1.47; 95% CI, 1.30-1.66; I2 = 42%; absolute risk difference, 24%; 95% CI, 12%-37%

86 rates (risk ratio, 0.58; 95% CI, 0.51-0.67; I2 = 0%), but there were no significant differences betw

87 33%; three population-based studies (n=699); I2=6%).

88 43/21002 individuals; 95% CI, 9.0% to 13.7%, I2 = 95.8%).

89 es using comparable outcome measures (n = 7)(I2 = 78.8%) and a modest but non-significant pooled esti

90 infarction (RR, 0.64 [95% CI, 0.57 to 0.71]; I2 = 0%; ARD, -0.81% [95% CI, -1.19 to -0.43%]), and com

91 60% (95% confidence interval [CI], 41%-72%; I2 = 0%; N = 2326) against laboratory-confirmed influenz

92 e to FOLFOXIRI-Bev was 69% (95% CI, 65%-72%; I2 = 25%).

93 nsitivity was low (64% [95% CI, 55% to 72%]; I2 = 95.7%; P < 0.001) but specificity was high (96% [CI

94 peanut allergy (RR, 0.29; 95% CI, 0.11-0.74; I2 = 66%; P = .009).

95 o 0.25) on the visual analog scale (P = .74; I2 = 52%) and 6.58 (95% CI, -6.33 to 19.49) opioid consu

96 Universities Arthritis Index Scale (P = .78, I2 = 65%).

97 to 1.10]; P = 0.084; heterogeneity P = 0.78; I2 = 0%).

98 r outcomes (RR, 0.70 [95% CI, 0.63 to 0.78]; I2 = 36%; ARD, -1.39% [95% CI, -1.79 to -0.99%]).

99 r (199.2-202.1), iodine value (104.8-125.7kg I2/kg) and cetane number (43.8-48.8), confirmed that the

100 ]), stroke (RR, 0.71 [95% CI, 0.62 to 0.82]; I2 = 0; ARD, -0.38% [95% CI, -0.53% to -0.23%]), myocard

101 an delayed ART (RR, 2.31 [CI, 1.87 to 2.86]; I2 = 19%).

102 y (risk ratio [RR], 0.56; 95% CI, 0.36-0.87; I2 = 36%; P = .009).

103 mortality (RR, 0.69 [95% CI, 0.54 to 0.88]; I2 = 54%; ARD, -0.43% [95% CI, -0.75% to -0.11%]), strok

104 /122356 individuals; 95% CI, 24.7% to 29.9%, I2 = 98.9%).

105 ement therapy (OR, 1.90 [95% CI, 1.25-2.90]; I2 = 17%), and death (OR, 5.13 [95% CI, 1.50-17.57]; I2

106 x 109 cells/L (RR, 0.71 [CI, 0.54 to 0.93]; I2 = 0%).

107 isk ratio [RR], 0.86 [95% CI, 0.80 to 0.93]; I2 = 0%; absolute risk difference [ARD], -0.40% [95% CI,

108 difference, +0.17 d; 95% CI, -0.62 to 0.95; I2 = 0%), hospital length of stay (weighted mean differe

109 specificity was high (96% [CI, 93% to 97%]; I2 = 96.3%; P < 0.001).

110 ignificant 23% (RR, 0.77; 95% CI, 0.60-0.98; I2 = 2.2%) (n = 1102) risk reduction in compulsory admis

111 tive risk [RR], 0.81 [95% CI, 0.66 to 0.99]; I2 = 0%).

112 Heterogeneity was assessed using an I2 statistic.

113 ply from readily available benzoic acids and I2.

114 enhanced ClNO3 formation for higher Br2 and I2 emission flux.

115 e crystalline channels, which absorb CO2 and I2 vapors at low pressure.

116 The transition states from both I1 and I2 to the native state are plastic and change with mutat

117 Both of the intermediates, I1 and I2, showed a propensity to self-associate under stirring

118 e and proceeds via two intermediates, I1 and I2.

119 mprehensive understanding of the host-I2 and I2-I2 binding interactions at a molecular level.

120 igating the voltammetric response of ICl and I2 under these conditions).

121 nal analyses using random-effects models and I2 to assess heterogeneity were performed in the subset

122 y decompose yielding methylamine, PbI2 , and I2 as products.

123 study-specific ORs using the Q statistic and I2 statistic.

124 geneity was assessed using the chi2 test and I2 statistic.

125 CO2(-) ligand exchange to generate 1-TFA and I2 as a soluble byproduct.

126 sient species assigned as the diiodide anion I2(*-) directly ligated to Bi, [Bi(I2(*-))Ix](n).

127 Here we present Arctic atmospheric I2 and snowpack iodide (I(-)) measurements, which were c

128 NLS and the mechanistic relationship between I2 (PP2A)-induced inhibition of PP2A and hyperphosphoryl

129 ide anion I2(*-) directly ligated to Bi, [Bi(I2(*-))Ix](n).

130 and the corresponding aldehydes followed by I2-mediated oxidative C-O/C-S bond formation.

131 tor dynamics could be switched off and on by I2 absorption/desorption, showing remarkable change of m

132 d in vivo, including human chondrocytes (C28/I2), human hepatic epithelial cells (L-02) and human tub

133 showed a similar antagonistic effect in C28/I2, L-02 and HK-2 cells.

134 Fractions were added to C28/I2 chondrocytes, grown in micromasses, ions with or with

135 3I, CH3OH, BrCH2Cl, CH3CH2OH, CH3CN, CH3NO2, I2), and a propyne clathrate (CH3CCH@Me,H,SiMe2.2CHCl3),

136 Under the same experimental conditions, I2(*-) in CH3CN rapidly disproportionates with a tremend

137 L(-) with CuI formed the unique, neutral Cu2 I2 (L(.) ) complex of a ligand-centered radical, whereas

138 e, reducing the surface concentration of dye-I2 complexes.

139 A highly efficient I2-catalyzed Povarov-type reaction of methyl ketones, ar

140 Knockdown of endogenous I2-containing SAP102 isoforms differentially affect NMDA

141 significant heterogeneity between estimates (I2 = 90.7%).

142 ty was observed for PR+ and HER2+ estimates (I2>80%, in all instances).

143 packing of I2 molecules with an exceptional I2 storage density of 3.08 g cm(-3) in MFM-300(Sc).

144 e to replicate in cells that did not express I2.

145 ed a cell line that constitutively expressed I2 and allowed construction of the VACV I2L deletion mut

146 al hyperphosphorylation of Tau by expressing I2 (PP2A) in which the NLS was inactivated by (179)RKR(1

147 velopment of a PET radioligand selective for I2-imidazoline binding sites (I2BS) would enable, for th

148 pharynx revealed evidence for synapses from I2 onto muscle that were missing from the published conn

149 new zeolite crystallizes in the space group I2/m, with cell parameters a = 17.511 A, b = 17.907 A, c

150 izes in a monoclinic structure (space group: I2/a; a = 5.7048(1)A, b = 5.1610(1)A, c = 12.2285(2)A, b

151 tent with a four-step pathway U <--> I1 <--> I2 <--> I3 <--> F where U and F represent unfolded and f

152 mation of I2 molecules, suggesting a 2I(-)-->I2+2e(-) redox couple.

153 ption, binding domains and dynamics of guest I2 molecules within these hosts have been achieved using

154 (95% CI=1.56-1.76), with high heterogeneity (I2=83, 95% CI=80-84).

155 ations of this review include heterogeneity (I2 > 50% for most analysis) and variation in quality amo

156 5% CI, 0.72-0.95) with little heterogeneity (I2 = 0%; tau2 <.0001).

157 % CI, 0.55-0.85) with minimal heterogeneity (I2 = 0%).

158 omes trials revealed moderate heterogeneity (I2 = 44.9, P = .16).

159 CI, 0.57-0.89), with moderate heterogeneity (I2 = 47%).

160 imited due to the presence of heterogeneity (I2 = 82.65%, p < 0.001) and evidence of possible publica

161 41), with high between-sample heterogeneity (I2 = 98%).

162 ant between-study statistical heterogeneity (I2 = 99.5%; tau2 = 182.5; P < .001).

163 8.7%-45.5%), with substantial heterogeneity (I2 = 68%).

164 of these factors resolved the heterogeneity (I2 = reduced from 78% to 45% and 0%, respectively) and p

165 ross population groups due to heterogeneity (I2) was 16.5%.

166 ons with type 2 diabetes were heterogeneous (I2 = 77.2%; P = .002), indicating gene-specific associat

167 Significantly, at high I2 loading an unprecedented self-aggregation of I2 molec

168 Here, we report high I2 adsorption in a series of robust porous metal-organic

169 HMS-I1 and HMS-I2 bear no resemblance to known inhibitors of chromatin-

170 tro HDAC assays revealed that HMS-I1 and HMS-I2 inhibit Clr3 HDAC activity.

171 ease in methylation caused by HMS-I1 and HMS-I2 was observed at all loci regulated by histone methyla

172 cturally unrelated compounds, HMS-I1 and HMS-I2, alleviated kanMX silencing and decreased repressive

173 al a comprehensive understanding of the host-I2 and I2-I2 binding interactions at a molecular level.

174 In this study, the electrochemistry of I(-), I2, and ICl has been investigated by cyclic voltammetry

175 In summary, the I(-)/I2/I(+) processes in nonhaloaluminate ILs involve a comp

176 be strongly electrophilic, and thus the I(-)/I2/I(+) redox processes are sensitive to the presence of

177 lassified into 9 known superfamilies (A, I1, I2, M, O1, O2, S, T, Z), and identified 16 new superfami

178 and folded conformational ensembles and I1, I2, and I3 are intermediates.

179 ng rise to two resolved I(-)/I3(-) and I3(-)/I2 processes, as per previous reports.

180 s at potentials less positive than the I3(-)/I2 process, which corresponds to the oxidation of I3(-)

181 h good to excellent yields using inexpensive I2 as a catalyst.

182 t-compete the well-established PP1-inhibitor I2 in vitro.

183 variant that possesses a C-terminal insert (I2) between the SH3 and GK domains is highly enriched at

184 3bp to form a short-lived open intermediate (I2).

185 tration of the transiently generated iodine (I2 ) as I3 (-) , this approach precludes undesired I2 -m

186 o previous measurements of molecular iodine (I2) have been reported in the Arctic.

187 dobenzene diacetate (PIDA)/molecular iodine (I2), under mild reaction conditions.

188 IYIY-I2-BODIPY alone and in combination with PDT modulates th

189 IYIY-I2-BODIPY binds TrkC similar to neurotrophin-3 (NT-3), a

190 e the immunological impacts mediated by IYIY-I2-BODIPY in pre- and post-PDT conditions.

191 osuppressive conventional chemotherapy, IYIY-I2-BODIPY can act as an immune-stimulatory chemotherapeu

192 ruct, IYIY-diiodo-boron-dipyrromethene (IYIY-I2-BODIPY) and its scrambled counterpart YIYI-I2-BODIPY

193 Adoptive transfer of immune cells from IYIY-I2-BODIPY-treated survivor mice that were photoirradiate

194 PDT effects (drug-light interval 1 h), IYIY-I2-BODIPY induced stronger responses.

195 Only IYIY-I2-BODIPY enhanced the IFN-gamma(+) and IL-17(+) T-lymph

196 Moreover, photoirradiated IYIY-I2-BODIPY treated mice had high levels of effector T-cel

197 We demonstrated that IYIY-I2-BODIPY (strong response) and YIYI-I2-BODIPY (weak res

198 dine molecular orbitals as an eta(2) ligated I2(*-), [(eta(2)-I2)BiI4](3-) (lambdamax = 640 nm), and

199 In this model, the mutant NLS (mNLS)-I2 (PP2A) (I2 (PP2A)AA-AAA) was retained in the cell cyt

200 Expression of mNLS-I2 (PP2A) activated CAMKII and GSK-3beta, which are Tau

201 ssed in a specific coefficient in the model (I2, describing the angular change of the backscattering

202 ng hydroxyl group of the [ScO4(OH)2] moiety [I2(I)...H-O = 2.263(9) A] with an occupancy of 0.268.

203 (II)-catalyzed C-H iodination with molecular I2 as the sole oxidant.

204 ough a redox reaction with iodine molecules (I2 ), which formed vacancies accompanied by a localized

205 henyl rings of neighboring ligand molecules [I2(II)...phenyl ring = 3.378(9) and 4.228(5) A].

206 An efficient NaNO2 /I2 -mediated one-pot transformation of Morita-Baylis-Hil

207 The neutral (I2) and positive (I(+)) oxidation states of iodine are k

208 -BODIPY (weak response) at 10 mg/kg, but not I2-BODIPY control, increased the levels of IL-2, IL-4, I

209 A novel I2-promoted direct conversion of arylacetic acids into a

210 Modeling shows that observed I2 levels are able to significantly increase ozone deple

211 e was no significant heterogeneity observed (I2 = 4.8%, P = .40).

212 trate the viability of oxidative addition of I2 to Pd(II).

213 king does not occur prior to the addition of I2 to the reaction mixture.

214 loading an unprecedented self-aggregation of I2 molecules into triple-helical chains within the confi

215 nding benzamides using a catalytic amount of I2 and TBHP as the green oxidant via the C-H bond cleava

216 d acid catalysis by partial decomposition of I2 to HI and suggest a halogen bond activation instead.

217 In addition, expression of I2-containing SAP102 isoforms is regulated developmental

218 at lengths consistent with the formation of I2 molecules, suggesting a 2I(-)-->I2+2e(-) redox couple

219 experiments showed the direct interaction of I2 (PP2A) with PP2A and GSK-3beta but not with CAMKII.

220 on, leading to a highly efficient packing of I2 molecules with an exceptional I2 storage density of 3

221 ion signal (NLS) in the C-terminal region of I2 (PP2A) containing a conserved basic motif, (179)RKR(1

222 letely unperturbed upon inclusion/removal of I2.

223 The initial binding site of I2 in MFM-300(Sc), I2(I), is located near the bridging h

224 The CD spectrum of I2 is characteristic of an antiparallel quadruplex that

225 nstrate that the HPA can reduce the oxidized I2 back into I(-), and our results indicate that this fa

226 e; however, the effect of prostaglandin (PG) I2 on ILC2 function is unknown.

227 on in this convergent approach involves Ph3P-I2-mediated formation of amidine upon condensation of an

228 N-acylbenzotriazoles in the presence of Ph3P-I2 as a dehydrating agent.

229 c and cyclic guanidines mediated by the Ph3P/I2 system is described.

230 tor, GKT137831, a NOX1/4 inhibitor, and Phox-I2, a NOX2 inhibitor.

231 this model, the mutant NLS (mNLS)-I2 (PP2A) (I2 (PP2A)AA-AAA) was retained in the cell cytoplasm, whe

232 hough statistical heterogeneity was present (I2 = 52%), and 1 trial found high-intensity statins asso

233 1) while sparing EP2, EP3, and prostaglandin I2 receptors (IPs); Kb values (in nanomoles) are given i

234 ts, indicating a role for both prostaglandin I2 and E2 Activation of ERKs and p38, but not JNKs, by C

235 the counteracting eicosanoids prostaglandin I2, E1, E2, and A2, while in HRGEC only more prostagland

236 but not anti-inflammatory EP2, prostaglandin I2, or EP3 receptors.

237 d A2, while in HRGEC only more prostaglandin I2 was detected.

238 hanced autocrine production of prostaglandin I2 (PGI2, also called prostacyclin) in Cav-1 KO EC, and

239 , but not absent, formation of prostaglandin I2 (prostacyclin; control 956 +/- 422 pg/ml vs. patient

240 ells depressed biosynthesis of prostaglandin I2 and prostaglandin E2, elevated blood pressure, and ac

241 pharmacological agonism of the prostaglandin I2 (IP) receptor in pancreatic beta-cells and in glomeru

242 t to activation by exposure to prostaglandin I2 (PGI2) or forskolin, both of which increase platelet

243 ggers the rapid production of prostaglandins I2 and E2 through cyclooxygenase (COX)-1 and regulates g

244 f the primary photoproduct, diiodide radical I2(*)(-), indicates that I4(*)(-) was formed via a secon

245 ion using a series of iodine-based reagents [I2, ICl, ICl3, I(TFA)3, I2O4, I2O5, (IO2)2S2O7, (IO)2SO4

246 eneity in the ER+ estimates in both regions (I2>90%), with the majority reporting proportions between

247 erogeneity (P = 0.82 and 0.52, respectively; I2= 0%).

248 heterogeneity = 0.69 and 0.88, respectively; I2 = 0%).

249 MFM-300(Sc) exhibits fully reversible I2 uptake of 1.54 g g(-1), and its structure remains com

250 r reduction in coronary artery disease risk (I2 = 0% for heterogeneity in genetic associations; P = .

251 e initial binding site of I2 in MFM-300(Sc), I2(I), is located near the bridging hydroxyl group of th

252 nd medium or high flow velocities (mean [SD] I2, 0.3 [5.3], 20.4 [6.4], and 21.7 [4.0], respectively)

253 Heterogeneity for sensitivity (I2 = 87%) and specificity (I2 = 82%) was observed across

254 for sensitivity (I2 = 87%) and specificity (I2 = 82%) was observed across studies.

255 Using chemical ionization mass spectrometry, I2 was observed in the atmosphere at mole ratios of 0.3-

256 ll statistical heterogeneity across studies (I2, 3.5%).

257 of heterogeneity was observed among studies (I2 = 60.1%).

258 was substantial heterogeneity among studies (I2 = 74%).

259 o [OR], 1.56; 95% CI, 1.25-1.94; 14 studies; I2, 39%) and low birth weight (OR, 1.96; 95% CI, 1.24-3.

260 est (OR, 2.50; 95% CI, 1.70-3.67; 5 studies; I2, 0%), studies not reporting such conflicts showed mor

261 o: -0.86 (95% CI, -1.44 to -0.29; 6 studies; I2 = 0%) for metformin and -0.50 to -0.94 for orlistat.

262 -4.0 mm Hg (95% CI, -5.6 to -2.5; 6 studies; I2 = 17%) for diastolic blood pressure.

263 -6.4 mm Hg (95% CI, -8.6 to -4.2; 6 studies; I2 = 51%) for systolic blood pressure and -4.0 mm Hg (95

264 ght (OR, 1.96; 95% CI, 1.24-3.10; 8 studies; I2, 48%), with a trend toward higher risks for exposure

265 lts (OR, 1.34; 95% CI, 1.08-1.66; 9 studies; I2, 30%).

266 rophile for the C(sp(2))-H halogenation than I2.

267 We concluded that I2 is required for virion morphogenesis, release of the

268 racycline-inducible mutant demonstrated that I2-deficient virions are defective in cell entry.

269 ctic atmospheric composition, and imply that I2 is likely a dominant source of iodine atoms in the Ar

270 orescence microscopy experiments showed that I2 colocalized with a major membrane protein of immature

271 The I2 pharyngeal neurons increase calcium in response to li

272 The I2 protein is conserved in all poxviruses that infect ve

273 The I2 state is more unfolded, but it retains some residual

274 S and study heterogeneity as measured by the I2 statistic.

275 ion or entry that is affected by loss of the I2 protein.

276 he SH3 and GK domains in SAP102 but that the I2 splicing does not influence SH3-GK interaction.

277 IgD1 reveals that it actually belongs to the I2 set of IgSF folds.

278 We assessed heterogeneity using the I2 index.

279 odel (and quantified inconsistency using the I2 statistic).

280 analyses, quantified heterogeneity using the I2 statistic, and explored it with subgroup analyses by

281 First, light inhibits pumping via the I2 neuron monosynaptic circuit.

282 Heterogeneity was assessed with the I2 test.

283 and the remaining two haplotypes belonged to I2 haplogroup.

284 The current study shows that I1 converts to I2 with a relaxation time tau1=0.1s at 25 degrees C in 2

285 For example, charge transfer from I(-) to I2 gives rise to the linear, symmetrical [I-I-I](-) anio

286 erall one electron per iodide ion process to I2 via an I3(-) intermediate, giving rise to two resolve

287 skeletal muscle genes troponin T3, troponin I2, and myosin light chain 1.

288 the allylnitro intermediate which undergoes I2 -catalyzed oxidative alpha-CH nitration of the nitrom

289 s I3 (-) , this approach precludes undesired I2 -mediated decomposition which can otherwise limit syn

290 double decarboxylative activations that use I2 as the terminal oxidant.

291 ity and publication bias were assessed using I2 and Begg and Egger tests.

292 mido cyclization of the sp(3) C-H bond using I2-TBHP as the catalytic system.

293 nes and primary nitroalkanes simply by using I2 and K2 CO3 under O2 .

294 ), with significant between-study variation (I2 = 96.8%; P < .001).

295 Groebke-Blackburn-Bienayme MCR combined with I2-promoted electrophilic cyclization.

296 thiol was oxidized to disulfide groups with I2, a mixture of cyclic oligomers (a library) was obtain

297 P(III) /P(V) hexameric rings or reacted with I2 to give trimeric P(V) variants.

298 rms more crowded complexes in reactions with I2, PhCl, and Al2Me6, which generate (C5Me5)3ThI, (C5Me5

299 at IYIY-I2-BODIPY (strong response) and YIYI-I2-BODIPY (weak response) at 10 mg/kg, but not I2-BODIPY

300 2-BODIPY) and its scrambled counterpart YIYI-I2-BODIPY have been prepared.