ライフサイエンスコーパス: DBP

1 DBP concentrations were remarkably similar between the t

2 DBP exposure in pregnancy induces focal dysgenetic areas

3 DBP formation generally decreased significantly with BAC

4 DBP was lower in blacks when measured by the monoclonal

5 DBP, the DBP genotype, and the 25(OH)D3 half-life did no

6 DBP/ZCl cells exhibit open-circuit voltages of 1.33 V co

7 DBPs are generated at concentrations below their carcino

8 More than 100 DBPs were identified, including a new class of DBPs, bro

9 The concentration of the sum of 21 DBPs measured quantitatively increased from finished to

10 nfidence interval, 0.61-0.90) in the upper 4 DBP quintiles (mean baseline DBP, 82+/-9 mm Hg), with an

11 3.59; -1.21), SBP -4.29 mmHg (-5.73, -2.84), DBP -2.56 mmHg (-3.40, 1.71), HDL +0.85 mg/dL (-0.10, 1.

12 In translation, Gle1 modulates Ded1, a DBP required for initiation.

13 on, compared with a DBP of 80 to 89 mm Hg, a DBP <60 mm Hg was associated with incident CHD and morta

14 and all-cause death (1.16, 1.06-1.28) than a DBP 70-80 mm Hg (14 305).

15 In addition, compared with a DBP of 80 to 89 mm Hg, a DBP <60 mm Hg was associated wi

16 as with the circadian oscillation activator DBP and the repressor E4BP4 to modulate CREBH transcript

17 d algal bloom stage may significantly affect DBP formation in source water.

18 Compared to the unheated soil leachates, all DBP yields were higher for the leachates of soils heated

19 est risk for most outcomes compared with all DBP categories 70 mm Hg or more.

20 l of the epitopes are highly conserved among DBP alleles.

21 hydes exhibit the highest cytotoxicity among DBP classes.

22 rosis Risk In Communities) cohort, analyzing DBP and hs-cTnT associations as well as prospective asso

23 h SBP (SMD: -0.20; 95% CI: -0.37, -0.03) and DBP (SMD: -0.27; 95% CI: -0.52, -0.03) than did the cont

24 Plasma 25(OH)D3, 1,25(OH)2D, and DBP were higher in pregnancy, and calculated free-25(OH)

25 oung adulthood, SBP in black individuals and DBP in white individuals were the most robust indicators

26 , CVD, and CHD, SBP on cancer mortality, and DBP on stroke mortality.

27 Both Nb and DBP-FITC induced extensive transcriptional changes that

28 identified no shared pathways between Nb and DBP-FITC, but revealed a type-I IFN (IFN-I) signature un

29 ced the overall pooled estimates for SBP and DBP by 1.1 mm Hg (95% CI: -0.3, 2.5 mm Hg; P = 0.11) and

30 ced the overall pooled estimates for SBP and DBP by 2.0 mm Hg (95% CI: 0.2, 3.8 mm Hg; P = 0.03) and

31 Mean SBP and DBP levels were calculated for daytime (10:00 am-8:00 pm

32 n of homocysteine concentration with SBP and DBP was assessed by conventional ordinary least-squares

33 Mean baseline SBP and DBP were 139.7+/-15.6 and 78.1+/-11.9 mm Hg, respectivel

34 tion, higher cumulative exposures to SBP and DBP were associated with low early diastolic longitudina

35 Both SBP and DBP were positively associated with BMI, WC, and WHtR, r

36 stolic and diastolic blood pressure (SBP and DBP), central pulse pressure (cPP) and flow-mediated dil

37 oportional hazards models, including SBP and DBP, jointly suggested that, at Y0, SBP (hazard ratio [H

38 stolic and diastolic blood pressure (SBP and DBP, respectively) in adults with the use of Mendelian r

39 tolic and diastolic blood pressures (SBP and DBP, respectively)].

40 ere positively associated with their SBP and DBP.

41 ntation also lowered 24-h ambulatory SBP and DBP.

42 adhesion molecules and a decrease in SBP and DBP.

43 n of sVCAM-1, sICAM-1, sP-selectin, SBP, and DBP after 6 wk of hesperidin treatment.

44 triglycerides, TC:HDL cholesterol, SBP, and DBP, respectively].

45 TC:HDL cholesterol, triglycerides, SBP, and DBP; calculated overall effect sizes of change values; a

46 Analyzing mixtures of U or Pu with TBP and DBP yielded the formation of ternary complexes whose sto

47 uate the speciation of U and Pu with TBP and DBP.

48 s were determined for U complexed to TBP and DBP.

49 erol, TC:HDL cholesterol, triglycerides, and DBP, but not SBP, decreased over time (P < 0.05).

50 and autochthonous DOM as well as associated DBP formation are changed during an entire algal life cy

51 oscopy and chlorination/chloramination-based DBP formation experiments.

52 rescence spectroscopy and chlorination-based DBP-FP experiments.

53 mary outcome were not influenced by baseline DBP level (P for interaction=0.83).

54 of the SBP intervention differed by baseline DBP.

55 intensive SBP lowering differed by baseline DBP.

56 Low baseline DBP was associated with increased risk of cardiovascular

57 7) in the lowest DBP quintile (mean baseline DBP, 61+/-5 mm Hg) and 0.74 (95% confidence interval, 0.

58 in the upper 4 DBP quintiles (mean baseline DBP, 82+/-9 mm Hg), with an interaction P value of 0.78.

59 rdless of the randomized treatment, baseline DBP had a U-shaped association with the hazard of the pr

60 as well as prospective associations between DBP and events.

61 tify both the 1D- and 3D-cooperation between DBPs.

62 d previously unknown 3D-cooperations between DBPs in chromosomal loops that may be a key factor in in

63 ; P = 0.03, respectively), and diastolic BP (DBP) with stroke mortality (HR: 1.30; 95% CI: 1.02-1.66;

64 muscle SNA burst areas against diastolic BP (DBP).

65 ion (daytime systolic BP [SBP]/diastolic BP [DBP] >/=135/85 mm Hg, 24-hour SBP/DBP >/=130/80 mm Hg, a

66 scenarios to elucidate the mechanisms of Br-DBP formation.

67 entrations of the nine HAAs, Br-HAAs, and Br-DBPs.

68 This is of concern because Br-DBPs are generally more toxic than their chlorinated ana

69 ation of regulated chloro-bromo-DBPs (Cl-/Br-DBPs).

70 The total concentration of Br-DBPs was measured as adsorbable organic bromine (AOBr).

71 A brominated DBP with a relative abundance of almost 22% was identifi

72 mide), which resulted in elevated brominated DBP concentrations in the effluent.

73 ulas matched those of other known brominated DBPs, such as dibromomethane, which could be generated b

74 ling the formation of regulated chloro-bromo-DBPs (Cl-/Br-DBPs).

75 lar composition, and disinfection byproduct (DBP) formation following the addition of chlorine.

76 To control disinfection byproduct (DBP) formation in drinking water, an understanding of th

77 nsequently impacting disinfection byproduct (DBP) formation in finished water; however, it remains un

78 eting drinking water disinfection byproduct (DBP) regulations.

79 her hazardous water disinfection byproducts (DBP) is currently hampered by a limited understanding of

80 ciated formation of disinfection byproducts (DBP).

81 (-) and halogenated disinfection byproducts (DBPs) (e.g., trihalomethanes, THMs and haloacetic acids,

82 ile and hydrophilic disinfection byproducts (DBPs) and hence likely tend to underestimate biological

83 weight halogenated disinfection byproducts (DBPs) and industrial chemicals.

84 disinfection, toxic disinfection byproducts (DBPs) are formed.

85 Certain unregulated disinfection byproducts (DBPs) are more of a health concern than regulated DBPs.

86 e identification of disinfection byproducts (DBPs) formed in spas.

87 gulated halogenated disinfection byproducts (DBPs), 8 N-nitrosamines, and bromate.

88 Throughout the entire experiment, C-DBP precursors in the control ranged from 2.41 to 3.09 m

89 n the treatment with 10% BE, the amount of C-DBP precursors decreased from 6.8 to 3.0 mmol/mol-C at i

90 rsor of both N-DBPs and carbonaceous DBPs (C-DBPs) upon chloramination.

91 ssuming toxicity is additive, the calculated DBP-associated toxicity of the O3/BAC-treated chloramina

92 a precursor of both N-DBPs and carbonaceous DBPs (C-DBPs) upon chloramination.

93 xamined nine CVDs in relation to categorical DBP exposures including bromoform, chloroform, dibromoch

94 persion compensation (EDC) and multi-channel DBP (MC-DBP).

95 During the bonne chauffe, DBP and DEHP accumulated in the secondes more than in th

96 were identified only for SBP because clinic DBP was not associated with the outcome.

97 (Br-HAAs) (r = 0.98) and nitrogen-containing DBPs (N-DBPs) (r = 0.97) and the least with Br-trihalome

98 halonitromethanes, these nitrogen-containing DBPs were the driving agents of the predicted genotoxici

99 In contrast DBP, U-DBP, and Pu-DBP complexes were observed in both p

100 eventing nitrification are needed to control DBP precursor release in storage facilities.

101 female rats were administered 750 mg/kg/day DBP in three different time windows: full window (FW; e1

102 to WT offspring, systolic (SBP), diastolic (DBP) and mean (MAP) BP progressively increased from KOP,

103 aromatic fragments, such as in syn-dibenzo- (DBP) and syn-dinaphthoporphyrins (DNP), lowers the symme

104 We found that soft electrophile DBPs could be an important predictor of common mechanism

105 nd additive toxicity among soft electrophile DBPs.

106 ovel findings have implications for elevated DBP formation during transportation of chlorinated water

107 and one noninhibitory mAb (3D10) that engage DBP.

108 By using novel engineered DBP immunogens, we validate that the prime targets of pr

109 (*)OH rate constants predicted experimental DBP loss in a lab-scale UV/H2O2 AOP well.

110 For DBP, there were no significant differences between the i

111 Further adjustment for DBP did not alter this association.

112 for SBP and regression-derived approach for DBP, the following definitions for daytime, 24-hour, and

113 formation for making treatment decisions for DBP regulation compliance under future climate scenarios

114 effect for SBP; a significant difference for DBP (P = 0.031) existed among preintervention kerosene u

115 ctivity of fire-affected terrestrial DOM for DBP formation.

116 -3.9, 0.4 mm Hg; P = 0.01) and 0.1 mm Hg for DBP (95% CI: -1.5, 1.7 mm Hg; P = 0.24).

117 Similar patterns were observed for DBP less than 70 mm Hg, plus increased risk for myocardi

118 n for a fluorescent, DNA-binding protein (FP-DBP) that completely 'paints' entire DNA molecules, wher

119 component/vitamin D binding protein gene (GC/DBP) rs4588 functional polymorphism (AA vs. CC: -16.7 nm

120 mm Hg (95% CI -9.9 to -0.2; p=0.0414), 24-h DBP -4.4 mm Hg (-7.2 to -1.6; p=0.0024), office SBP -7.7

121 Compared with persons who had DBP between 80 to 89 mm Hg at baseline (ARIC visit 2), t

122 o increases in N-nitrosamine and halogenated DBP formation, suggesting the release of precursors from

123 r, BPC promoted the formation of halogenated DBPs while a free chlorine residual was maintained.

124 y toxic iodinated disinfection byproducts (I-DBPs) while controlling the formation of regulated chlor

125 Due to its functional importance, DBP is considered a prime vaccine candidate, but variati

126 We found no significant changes in DBP after the consumption of other nuts.

127 The more severe testis dysgenesis in DBP-MPW animals may result from the presence of basally

128 n SBP and of 1.0 (95% CI: 0.6, 1.4) mm Hg in DBP.

129 ction of 4.18 mm Hg in SBP and 2.27 mm Hg in DBP.The pooled results suggest that magnesium supplement

130 2-mmHg (95% CI: 1.69, 2.75 mmHg) increase in DBP, respectively.

131 lamina, whereas GC migration was minimal in DBP-FW animals.

132 [95% CI, -2.0 to 1.0 mm Hg]; P = .55) or in DBP (-0.2 mm Hg [95% CI, -1.6 to 1.3 mm Hg]; P = .82).

133 t this increase is associated with increased DBP concentrations.

134 onship reflects the transduction of SNA into DBP.

135 To our knowledge, this is the largest DBP and fetal growth study to date with individual water

136 Low DBP at baseline was also independently associated with p

137 Associations of low DBP with prevalent hs-cTnT and incident CHD were most pr

138 mm Hg, and thus elevated pulse pressure, low DBP was associated with subclinical myocardial damage an

139 amin D bioavailability in those with a lower DBP level.

140 gher BMI, which cannot be explained by lower DBP or the shorter half-life of 25(OH)D3 We speculate th

141 Polymorphisms associated with lower DBP level attenuated the association between low serum 2

142 onfidence interval, 0.57-1.07) in the lowest DBP quintile (mean baseline DBP, 61+/-5 mm Hg) and 0.74

143 compensation (EDC) and multi-channel DBP (MC-DBP).

144 f multi-channel digital back-propagation (MC-DBP) for compensating fibre nonlinearities in Nyquist-sp

145 Mean DBP during CPR and Utstein-style standardized cardiac ar

146 A mean DBP less than 70 mm Hg (n=5352) during treatment was ass

147 Maintaining mean DBP >/=25 mm Hg in infants and >/=30 mm Hg in children >

148 These data demonstrate that mean DBP >/=25 mm Hg during CPR in infants and >/=30 mm Hg in

149 without asthma (p = 0.03), whereas the mean DBP was higher in women with asthma than in women withou

150 At the last visit, mean DBP was 2.8 mm Hg higher in control subjects than in eth

151 ressure during wake periods (SBP, +1.6 mmHg; DBP, +1.4 mmHg).

152 during sleep opportunities (SBP, +5.6 mmHg; DBP, +1.9 mmHg) and, to a lesser extent, by raised blood

153 he first birth defect study to develop multi-DBP adjusted regression models as well as the first CVD

154 entification of cooperation between multiple DBPs and reveals cell-type-specific and -independent reg

155 he greatest DOC and had the highest C- and N-DBP precursor reactivity per unit carbon compared to the

156 On the other hand, N-DBP precursors continuously declined in all treatments.

157 Instead of DCAM, a previously unreported N-DBP, N-chloro-2,2-dichloroacetamide (N-Cl-DCAM), was con

158 indicating that it is a precursor of both N-DBPs and carbonaceous DBPs (C-DBPs) upon chloramination.

159 with Br-trihalomethanes (r = 0.29) and Br-N-DBPs (r = 0.04).

160 on of nitrogenous disinfection byproducts (N-DBPs) was investigated from the chloramination of nitrog

161 ified nitrogenous disinfection byproducts (N-DBPs) whose occurrence in drinking waters has recently b

162 ) (r = 0.98) and nitrogen-containing DBPs (N-DBPs) (r = 0.97) and the least with Br-trihalomethanes (

163 ll molecules led to the formation of known N-DBPs (e.g., dichloroacetonitrile, dichloroacetamide) wit

164 cator to predict the formation of specific N-DBPs in chlorination.

165 were conducted on resorcinol to understand N-DBPs formation mechanisms and to identify reaction inter

166 he previously reported porphyrin-based NMOF, DBP-UiO.

167 nse in mammalian cells than the nonpurgeable DBPs enriched with SPE after purging, while contribution

168 For nonvolatile DBPs, solid-phase extraction (SPE) with TELOS ENV as sol

169 D increase, 1.32; 95% CI, 1.09-1.61) but not DBP (HR, 1.05; 95% CI, 0.88-1.26) was associated with CV

170 However, these dynamic changes of C- and O-DBP precursors exhibited opposite patterns in 65% extrac

171 The same trend was observed for O-DBP precursors.

172 e hypothesized that selective association of DBP with a small population of immature reticulocytes co

173 ht to examine the independent association of DBP with myocardial damage (using high-sensitivity cardi

174 n DARC is key to the preferential binding of DBP to immature reticulocytes, which is the potential me

175 or multi-channel systems, the degradation of DBP performance due to neglecting the spectral broadenin

176 Previously, identification of DBP cooperation has been limited to those binding to nei

177 in B-cell epitopes at the dimer interface of DBP leads to induction of strain-limited immunity.

178 d by genotype at rs7041 as a proxy marker of DBP levels (low, the GT/TT genotype; high, the GG genoty

179 rucial for achieving the best performance of DBP in both single-channel and multi-channel communicati

180 differences in the sympathetic regulation of DBP and may be valuable in quantifying transduction in d

181 eceptor-binding and dimerization residues of DBP, and introduce globally conserved protective targets

182 nd the concentrations, fate, and toxicity of DBP need to be further characterized.

183 ently hampered by a limited understanding of DBP formation mechanisms.

184 Ps were identified, including a new class of DBPs, bromoimidazoles.

185 The predicted cyto- and genotoxicity of DBPs was calculated using published potencies based on t

186 ut the cellular mechanisms and regulation of DBPs are not fully defined.

187 Gle1 is a multifunctional regulator of DBPs with roles in mRNA export and translation.

188 Of the two types of DBPs, HAAs were generally present at higher concentratio

189 mm Hg (-14.0 to -1.5; p=0.0155), and office DBP -4.9 mm Hg (-8.5 to -1.4; p=0.0077).

190 ubjects were hypertensive (SBP >/=140 and/or DBP >/=90 mm Hg) versus 1.9% of ethanol users (P = 0.051

191 d epitopes important for receptor binding or DBP dimerization.

192 but ozonation was less significant for other DBPs.

193 of carbonaceous, nitrogenous, and oxygenated DBP precursors during algal growth.

194 tituents including U, Pu, dibutyl phosphate (DBP), and tributyl phosphate (TBP).

195 Administration of dibutyl phthalate (DBP) to pregnant rats causes reproductive disorders in m

196 Dibutyl phthalate (DBP) was entirely carried over into the distillate, whil

197 nd the contact sensitizer dibutyl phthalate (DBP)-FITC.

198 eatures hamper the rational design of potent DBP-based vaccines and necessitate the identification of

199 mmHg increment in diastolic blood pressure (DBP) (p < 0.001) or each 15 mmHg increment in pulse pres

200 pressure (SBP) and diastolic blood pressure (DBP) between the magnesium-supplementation group and the

201 pressure (SBP) and diastolic blood pressure (DBP) by 3.0 mmHg and 1.5 mmHg, respectively.

202 adequate arterial diastolic blood pressure (DBP) during CPR, the American Heart Association recommen

203 pressure (SBP) and diastolic blood pressure (DBP) in healthy individuals.A systematic review and meta

204 ntrast, a baseline diastolic blood pressure (DBP) less than 70 mm Hg was associated with the highest

205 180 mm Hg, office diastolic blood pressure (DBP) of 90 mm Hg or greater, and a mean 24-h ambulatory

206 The change in diastolic blood pressure (DBP) over time was significantly different between ethan

207 his low may reduce diastolic blood pressure (DBP) to levels that could compromise myocardial perfusio

208 The mean diastolic blood pressure (DBP) was lower in men with asthma than in men without as

209 ressure (SBP), and diastolic blood pressure (DBP) were assessed.

210 pressure (SBP) and diastolic blood pressure (DBP) were associated with lower longitudinal strain rate

211 /=10 mm Hg drop in diastolic blood pressure (DBP) within 3 min from postural change.

212 od pressure (SBP), diastolic blood pressure (DBP), and the prevalence of children with BP within the

213 viduals with a low diastolic blood pressure (DBP), the potential benefits or risks of intensive systo

214 pressure (SBP) and diastolic blood pressure (DBP).

215 i was selected for diastolic blood pressure (DBP).

216 ): -3.9 mm Hg; for diastolic blood pressure (DBP): -2.5 mm Hg; P = 0.050 for both)] were observed aft

217 t women exposed to disinfection by-products (DBPs) have an increased risk of delivering babies with c

218 contain regulated disinfection by-products (DBPs), mainly through contact with brine solutions prepa

219 um total 25(OH)D, vitamin D-binding protein (DBP) by 2 different immunoassays (with the use of monocl

220 The Duffy binding protein (DBP) dimerization with its cognate receptor is vital for

221 Lower vitamin D-binding protein (DBP) levels increase the biological availability of seru

222 in D metabolites, vitamin D binding protein (DBP), PTH and 25(OH)D3 half-life were measured in third-

223 acilitated by P vivax Duffy binding protein (DBP), which utilizes DARC (Duffy antigen receptor for ch

224 ay be due to low vitamin D-binding proteins (DBPs) or faster metabolic clearance.

225 is mainly mediated by DNA-binding proteins (DBPs) that bind to the interacting sites and form comple

226 DEAD-box proteins (DBPs) are required in gene expression to facilitate chan

227 In contrast DBP, U-DBP, and Pu-DBP complexes were observed in both positive and negativ

228 The purgeable DBP fraction enriched with the purge-and-trap method exe

229 37 quantified DBPs explained almost the entire AOX in the purge-and-tr

230 sed to comprehensively identify and quantify DBPs and other contaminants.

231 oclonal anti-DARC antibodies and recombinant DBP to CD71(high)/RNA(high) reticulocytes was significan

232 Ethanol cookstoves have potential to reduce DBP and hypertension during pregnancy.

233 are more of a health concern than regulated DBPs.

234 could be used to identify the most relevant DBPs that are the forcing factors of the toxicity of fin

235 As a result, DBPs and DNPs exhibit stronger 2PA into the one-photon-a

236 significantly associated with elevated SBP, DBP, and cPP, and with lower FMD, adjusting for age, BMI

237 and NTL were associated with increased SBP, DBP, and cPP, and with reduced FMD, suggesting a possibl

238 age of incident CVD events that occur at SBP/DBP <140/90 mm Hg in a pooled analysis of 3 contemporary

239 ime hypertension corresponding to clinic SBP/DBP >/=140/90 mm Hg are proposed for African American ad

240 ighttime SBP/DBP corresponding to clinic SBP/DBP of 140/90 mm Hg were 134/85 mm Hg, 130/81 mm Hg, and

241 ighttime SBP/DBP corresponding to clinic SBP/DBP of 140/90 mm Hg were 135/85 mm Hg, 133/82 mm Hg, and

242 sed for African American adults: daytime SBP/DBP >/=140/85 mm Hg, 24-hour SBP/DBP >/=135/80 mm Hg, an

243 stolic BP [DBP] >/=135/85 mm Hg, 24-hour SBP/DBP >/=130/80 mm Hg, and nighttime SBP/DBP >/=120/70 mm

244 daytime SBP/DBP >/=140/85 mm Hg, 24-hour SBP/DBP >/=135/80 mm Hg, and nighttime SBP/DBP >/=130/75 mm

245 The mean SBP/DBP was 112/69 mm Hg in blacks and 109/68 mm Hg in white

246 r SBP/DBP >/=130/80 mm Hg, and nighttime SBP/DBP >/=120/70 mm Hg) have been derived from European, As

247 r SBP/DBP >/=135/80 mm Hg, and nighttime SBP/DBP >/=130/75 mm Hg, respectively.

248 olds for daytime, 24-hour, and nighttime SBP/DBP corresponding to clinic SBP/DBP of 140/90 mm Hg were

249 olds for daytime, 24-hour, and nighttime SBP/DBP corresponding to clinic SBP/DBP of 140/90 mm Hg were

250 h systolic and diastolic blood pressure (SBP/DBP) >/=140/90 mm Hg.

251 ], systolic or diastolic blood pressure [SBP/DBP], total [TC] or HDL-cholesterol).

252 risk-reduction measures for adults with SBP/DBP <140/90 mm Hg at high risk for CVD may be warranted.

253 taking antihypertensive medication with SBP/DBP <140/90 mm Hg, 76.6% (95% CI, 75.8-77.5) were eligib

254 ident CVD events occur in US adults with SBP/DBP <140/90 mm Hg.

255 of events occurred in participants with SBP/DBP <140/90 mm Hg; 58.4% (95% CI, 47.7-69.2) and 68.1% (

256 e; sex; smoking status; alcohol intake; SBP; DBP; cholesterol:high-density lipoprotein ratio; diabete

257 lts do not support the hypothesis that serum DBP or 25(OH)D plays a protective role in pancreatic can

258 waters has recently been reported in several DBP surveys.

259 h profiles assessed using the AM only showed DBP precursor sorption occurred in each column that decr

260 A), trichloroacetic acid (TCAA), and summary DBP measures (HAA5, THMBr, THM4, and DBP9).

261 In both rat and human fetal testes, DBP exposure induced similar germ cell effects, namely,

262 analogous tetraphenyldibenzoperyflanthrene (DBP)/C60-based devices.

263 ith more ectopic SC and germ cells (GC) than DBP-FW treatment; DBP-LW induces no dysgenesis.

264 We demonstrate that DBP precursors in fire-affected forest detritus are high

265 <140 mm Hg, it may be prudent to ensure that DBP levels do not fall below 70 mm Hg, and particularly

266 We show that DBP-MPW treatment produces more extensive and severe dys

267 This study questions the classic view that DBP is more able to identify future CVD events than SBP

268 The hypothesis was that DBP >/=25 mm Hg during CPR in infants and >/=30 mm Hg in

269 d hydroxyl radical ((*)OH) reaction, so that DBPs most likely to pass through the AOP could be predic

270 The DBP and incident CHD association was strongest with base

271 DBP, the DBP genotype, and the 25(OH)D3 half-life did not differ

272 nitial reactant concentrations influence the DBP formation.

273 stigate whether polymorphisms that lower the DBP could compensate for adverse effects of low serum vi

274 data suggest that selective exposure of the DBP binding site within DARC is key to the preferential

275 Human use increased significantly the DBP concentrations and mutagenic potencies for most pool

276 he percentage of water decreased because the DBPs were concentrated in the aqueous phase of the chees

277 e difficulty associated with degrading these DBPs, at the 500-1000 mJ/cm(2) UV fluence applied in pot

278 s reflected by lower concentrations of these DBPs measured after re-establishment of a chloramine res

279 e range of chemical characteristics of these DBPs, this study developed methods to predict their degr

280 In contrast, the response to DBP-FITC was not affected by IFN-I receptor blockade, a

281 was directly related to the ratio of TBP to DBP.

282 Exposure to DBPs was associated with increased risk of bladder cance

283 A pretreatment and mean on-treatment DBP of about 75 mm Hg was associated with the lowest ris

284 C and germ cells (GC) than DBP-FW treatment; DBP-LW induces no dysgenesis.

285 Weight-averaged aggregate first-trimester DBP exposures were assigned to individuals based on resi

286 In contrast DBP, U-DBP, and Pu-DBP complexes were observed in both positive

287 onpurgeable fraction is dominated by unknown DBPs.

288 omethanes, haloacetic acids, and unregulated DBPs, and the SOS genotoxicity followed the breakthrough

289 may not control the formation of unregulated DBPs with higher genotoxicity potencies.

290 mation of regulated and selected unregulated DBPs following chlorine disinfection was evaluated.

291 he species [UO2(DBP)], [UO2(DBP)3], and [UO2(DBP)4].

292 determined for the species [UO2(DBP)], [UO2(DBP)3], and [UO2(DBP)4].

293 nstants were determined for the species [UO2(DBP)], [UO2(DBP)3], and [UO2(DBP)4].

294 ays, for extracting nonvolatile and volatile DBPs from chlorinated and chloraminated drinking water t

295 For volatile DBPs, cryogenic vacuum distillation performed unsatisfac

296 When DBP concentrations were weighted by measures of their to

297 associated with CVD risk in blacks, whereas DBP (HR, 1.74; 95% CI, 1.21-2.50) but not SBP (HR, 0.82;

298 .9 mm Hg) but was positively associated with DBP (beta = 1.1 mm Hg; 95% CI: 0.2, 1.9 mm Hg).

299 n of genetically increased homocysteine with DBP was not consistent across different SNPs.

300 at that visit was 2.2 and 1.5 in those with DBP <60 mm Hg and 60 to 69 mm Hg, respectively.