ライフサイエンスコーパス: SGA

1 SGA and LGA were determined by the sex- and gestational-

2 SGA C (OR: 2.12; 95% CI: 1.24, 3.93) and HGS (OR: 0.96;

3 SGA infants with catch-up growth in the first 3-6 mo had

4 SGA versus appropriate for gestational age infants did n

5 SGA, HGS, and food intake were independent predictors of

6 SGA, NRS-2002, and CONUT had similar capacities for scre

7 1), macrosomia (1.07; 1.06-1.08; P < 0.001), SGA (1.06; 1.02-1.10; P = 0.007), and perinatal infant d

8 pregnancy (RR, 1.22 [1.09-1.36], p < 0.001), SGA among women exposed to gabapentin early (1.17 [1.02-

9 5.6%) preterm live-births and 187,966 (9.1%) SGA live-births.

10 The NRS-2002, SGA, and CONUT tools identified nutritional risk in 67,

11 ated by bisulfite pyrosequencing (30 AGA, 21 SGA) and also analyzed in cord blood.

12 I: -4.9, -3.0 and -3.7; 95% CI: -5.0, -2.3), SGA (-1.7; 95% CI: -2.9, -0.51 and -3.8; 95% CI: -5.0, -

13 BWT (aHR, 0.81 [95% CI, .50-1.29]; P = .37); SGA (aHR, 0.92 [95% CI, .74-1.14]; P = .43).

14 Among 107,551 SGA initiators and 1,221,434 noninitiators, the risk for

15 Overall, TCI identified 634 SGAs that are predicted to cause cancer-related DEGs in

16 o define small or large for gestational age (SGA or LGA) infants.

17 who were small or large for gestational age (SGA or LGA, respectively) according to exercise during t

18 re categorized as small for gestational age (SGA) (<10th percentile) or large for gestational age (LG

19 the incidence of small for gestational age (SGA) and large for gestational age (LGA), defined as bir

20 m birth (PTB) and small for gestational age (SGA) at birth mediate the association between maternal e

21 men who delivered small for gestational age (SGA) babies (SGA, <=10th percentile), 28 who delivered l

22 preterm delivery; small for gestational age (SGA) baby; need for the neonatal intensive care unit; do

23 iction (IUGR) and small-for-gestational age (SGA) birth.

24 To distinguish small for gestational age (SGA) from intrauterine growth restriction (IUGR) as inde

25 ght gain (GWG) or small for gestational age (SGA) in IBD compared to non-IBD in the population-based

26 rd trimesters for small-for-gestational age (SGA) newborns.

27 Women with small for gestational age (SGA) offspring had 1-2 mmHg higher systolic and diastoli

28 Cases of small-for-gestational age (SGA) or pre-eclampsia were matched with healthy controls

29 live births born small for gestational age (SGA) or preterm and mean birth weight.

30 as represented by small for gestational age (SGA) status.

31 sed the effect of small-for-gestational age (SGA), a proxy for fetal growth impairment, on risk of ma

32 term birth (PTB), small for gestational age (SGA), and low birth weight (LBW) are risk factors for mo

33 term birth (PTB), small for gestational age (SGA), and neonatal intensive care unit admission (NICUa)

34 rth weight (LBW), small for gestational age (SGA), and preterm birth (PTB).

35 erm preeclampsia, small for gestational age (SGA), and women who had 2 pregnancies with preeclampsia

36 tal malformation, small for gestational age (SGA), birth injury, low Apgar score (</=8), and neonatal

37 ey determinant of small for gestational age (SGA), but some knowledge gaps remain, particularly regar

38 e associated with small for gestational age (SGA), low birth weight (LBW), and preterm birth.

39 h birth outcomes [small for gestational age (SGA), preterm birth (PTB)].In an observational study in

40 of children born small for gestational age (SGA), we measured the mRNA expression levels of p73 and

41 m birth (PTB) and small for gestational age (SGA).

42 term (LBWT), and small for gestational age (SGA).

43 microcephaly and small for gestational age (SGA).

44 ession to examine small for gestational age (SGA).

45 birth, and being small-for-gestational age (SGA).

46 cephaly and being small for gestational age (SGA).

47 preterm delivery; small for gestational age (SGA); need for neonatal intensive care unit (NICU); new

48 rol, n = 40), (b) small for gestational age (SGA, n = 34) and (c) whose mothers developed hyperglycae

49 birth, small and large for gestational age (SGA/LGA), and neonatal intensive care unit (NICU) admiss

50 (<37 weeks), small size for gestational age (SGA; <10th percentile of weight for gestational age) or

51 tional weeks) and small for gestational age (SGA; birth weight 2 standard deviations below the expect

52 Small-for-gestational-age (SGA) and preterm births were examined as secondary outco

53 dies finding that small-for-gestational-age (SGA) birth is associated with increased adiposity in chi

54 of preterm birth, small-for-gestational-age (SGA) birth, gestational diabetes, and pre-eclampsia acco

55 pre-eclampsia and small-for-gestational-age (SGA) birth, which are indicative of uteroplacental dysfu

56 Risks of small-for-gestational-age (SGA) births (<10th percentile), chorioamnionitis, preter

57 ences the risk of small-for-gestational-age (SGA) births and other aspects of fetal growth.

58 term delivery and small-for-gestational-age (SGA) births.

59 hypertension, and small-for-gestational-age (SGA) infants are complications in about 15% of all nulli

60 erentiate healthy small-for-gestational-age (SGA) infants from pathologically small infants in a huma

61 creening test for small-for-gestational-age (SGA) infants, and whether the risk of morbidity associat

62 preeclampsia; and small-for-gestational-age (SGA) neonate (birthweight below the fifth percentile).

63 onal-age (AGA) or small-for-gestational-age (SGA) to identify new genes related to fetal growth and n

64 preterm birth or small-for-gestational-age (SGA), or both--is the biggest risk factor for more than

65 [GA] at delivery, small for gestational age [SGA], multiple births, and male sex).

66 [LBW], <2500 g), small-for-gestational-age [SGA], and BW z scores [BWZ]) in HIV-exposed uninfected i

67 were active from steroidal glycol-alkaloid (SGA), lignin and flavonoid biosynthetic pathways.

68 All SGAs+LIT/VALs other than olanzapine+LIT/VAL outperformed

69 rch for a set of somatic genome alterations (SGA) that likely perturbed the signal, that is, the cand

70 well known that somatic genome alterations (SGAs) affecting the genes that encode the proteins withi

71 mainly caused by somatic genome alterations (SGAs) that perturb cellular signalling systems.

72 mainly caused by somatic genome alterations (SGAs).

73 ainly caused by somatic genomic alterations (SGAs) that perturb pathways regulating metastasis-releva

74 r (95% credible interval 6.6%, 119.1%) among SGA cases compared to AGA controls.

75 ted mean concentrations 41%-97% higher among SGA cases and 33%-39% lower among LGA cases compared to

76 tiating only SGAs, the risk was higher among SGA initiators who used antidepressants concomitantly at

77 quasispecies by single-genome amplification (SGA) and documented that a single virus variant establis

78 nd HIV envC2-V5 single-genome amplification (SGA) and T-cell receptor (TCR) repertoires assessed.

79 We used single-genome amplification (SGA) in cross-sectional and longitudinal analyses to uni

80 Single-genome amplification (SGA) was used to generate partial HIV-1 polymerase genom

81 Single-genome amplification (SGA) was used to identify full-length T/F genomes presen

82 f sampling than single-genome amplification (SGA).

83 le, and had a relative risk of delivering an SGA infant with neonatal morbidity of 17.6 (9.2-34.0, p<

84 463, 0.724).Protection against delivering an SGA neonate offered by greater preconceptional or gestat

85 Initial treatment with either an SGA or group and individual CBT.

86 f vaccinated and 8.3% of unvaccinated had an SGA birth (adjusted RR, 1.00; 95% CI, 0.96-1.06).

87 In probabilistic sensitivity analyses, SGA had a 64% to 77% likelihood of having an incremental

88 justed risk ratio [aRR] = 3.42, P = .02) and SGA (aRR = 4.24, P < .001) but not PTB (aRR = 0.88, P =

89 were observed for PM (100%), DM (100%), and SGA (42.9%) versus NSNM infants (18.3%) (p<0.001); OR 3.

90 were observed for PM (100%), DM (100%), and SGA (42.9%) vs NSNM infants (18.3%; P <.001); odds ratio

91 agreement was observed between NRS-2002 and SGA.

92 vs 17.7%; RR, 1.54; 95% CI, 1.05-2.25), and SGA status (9.2% vs 12.7%; RR, 1.51; 95% CI, 0.94-2.42).

93 pa = 0.53; CONUT/NRS-2002, kappa = 0.42; and SGA/CONUT, kappa = 0.36.

94 5% confidence interval (CI): 1.14, 1.71] and SGA (OR = 1.22, 95% CI: 1.02, 1.45), and decreased tBW (

95 in 1%, preterm delivery occurred in 9%, and SGA neonate occurred in 10%.

96 r risks for prematurity, NICU admission, and SGA status compared with longer intervals.

97 Long-term trials comparing CBT and SGA are lacking.

98 n of both preterm and term pre-eclampsia and SGA.

99 curs in normal pregnancy, pre-eclampsia, and SGA pregnancies.

100 nd increased the association between IBD and SGA with a factor of three.

101 Data on IUGR and SGA status, worst stage of and need for treatment for RO

102 , SGA B = mild or moderate malnutrition, and SGA C = severe malnutrition), Nutrition Risk Screening (

103 lation of key genes from phenylpropanoid and SGA pathways along with WRKY and MYB in WRKY1 transgenic

104 PTB and SGA may play substantial roles in the relationship betwe

105 roportions eliminated by eliminating PTB and SGA separately were, respectively, 46% and 11% for low e

106 PTB and SGA together contributed more to the association of mate

107 associations eliminated by reducing PTB and SGA together were 55% (MRRPE = 1.27, 95% CI 1.15-1.40, P

108 iminated by eliminating mediation by PTB and SGA was reported if the mortality rate ratios (MRRs) of

109 POA use during pregnancy and risk of PTB and SGA were largely due to unmeasured confounding factors,

110 ted (PE) by eliminating mediation by PTB and SGA.

111 ferential mortality risk between FGA use and SGA use in older adults is unclear.

112 erence [MD], -6.50 [CI, -8.82 to -4.18]) and SGAs (MD, -3.84 [CI, -6.55 to -1.13]) reduced binge-eati

113 ting-related obsessions and compulsions, and SGAs reduced symptoms of depression (MD, -1.97 [CI, -3.6

114 in mortality risk between users of FGAs and SGAs may develop mostly through pathways that do not inv

115 h either a second-generation antidepressant (SGA) or cognitive behavioral therapy (CBT).

116 ficacy of second-generation antidepressants (SGAs) versus most other treatments for this disorder.

117 Second-generation antipsychotics (SGAs) have increasingly been prescribed to Medicaid-enro

118 Pooled second-generation antipsychotics (SGAs) were associated with shorter TTR (SMD=-0.27) and a

119 Using synthetic genetic array (SGA) analyses in the model yeast, Saccharomyces cerevisi

120 used candidate and synthetic genetic array (SGA) approaches to more fully characterize SNARE-mediate

121 tion screens using synthetic genetic arrays (SGA) with gsk3 and amk2 as query mutants, the latter enc

122 1.2 to 5.0), mainly stillbirths assessed as SGA (IRR, 4.9; 95% CI, 2.2 to 11.0), and with preterm SG

123 Infants were categorized as SGA using the 1991 US birth weight reference, the 1999-2

124 02 (NRS-2002), Subjective Global Assessment (SGA), and Controlling Nutritional Status Index (CONUT) a

125 admission were subjective global assessment (SGA; SGA A = well nourished, SGA B = mild or moderate ma

126 ered small for gestational age (SGA) babies (SGA, <=10th percentile), 28 who delivered large for gest

127 ; -6.4, p < 0.001) decrease in odds of being SGA was observed.

128 roaches to analyzing the association between SGA birth and adiposity outcomes (skinfold thicknesses a

129 proach yielded negative associations between SGA birth and all adiposity outcomes.

130 he SGA prevalence and the risk ratio between SGA status and neonatal mortality, calculated using Pois

131 CI) to identify causal relationships between SGAs and differentially expressed genes (DEGs) within tu

132 GAs by modeling causal relationships between SGAs and molecular phenotypes (e.g., transcriptomic, pro

133 (PTB), and small for gestational age birth (SGA).

134 Children born SGA (birth weight <10th percentile) and those born large

135 Children born SGA had a significantly lower BMI, percentage body fat,

136 The 11.5-y-old Belarusian children born SGA were shorter, were thinner, and had less body fat th

137 ficantly (P < 0.001) higher in children born SGA.

138 ity measures intermediate between those born SGA without catch-up and those born AGA.

139 The incidence of both SGA and LGA significantly decreased during the study per

140 ethods-identified pathways were perturbed by SGA.

141 e (TCI) framework, which estimates causative SGAs by modeling causal relationships between SGAs and m

142 pecific aberrations resulting from causative SGAs.

143 al framework that finds the likely causative SGAs in an individual tumor and estimates their impact o

144 n HDL-C change was associated with decreased SGA odds (OR = 0.35, 95% CI: 0.19, 0.64).

145 risk factors, in addition to GA at delivery, SGA, multiple births, and male sex.

146 n maternal PHIV status and preterm delivery, SGA, or LBW were observed.

147 al-oriented framework for identifying driver SGAs.

148 e ability to find informative sets of driver SGAs that likely constitute signaling pathways.

149 Second-generation antipsychotic drugs (SGAs) are essential in the treatment of psychotic disord

150 Identifying drivers of metastasis, i.e. SGAs, sheds light on the metastasis mechanism and provid

151 decrease of 1.6% [95% CI, 1.5% to 1.7%] for SGA, 1.6% [95% CI, 1.5% to 1.8%] for LGA).

152 8.3%) (p<0.001); OR 3.4(95% CI 1.1-10.7) for SGA versus NSNM.

153 (95% confidence interval [CI], 1.1-10.7) for SGA vs NSNM.

154 (16%) (p<0.001); OR 3.9(95% CI 1.2-12.8) for SGA versus NSNM.

155 6%; (P <.001); OR 3.9 (95% CI, 1.2-12.8) for SGA vs NSNM.

156 (RRs) and 95% confidence intervals (CIs) for SGA, LBW, and preterm birth across tertiles (or categori

157 002) but was not significantly different for SGA initiators who were concomitantly using stimulants.

158 of this study is to explore risk factors for SGA in Brazil and assess potential for risk stratificati

159 concentrations were significantly higher for SGA compared with non-SGA births across the period from

160 mesters are the time windows of interest for SGA (fetal growth).

161 ORs for SGA increased (2.72, 95% CI 2.32-3.20, p < 0.001) and LG

162 for gestational age and screen positive for SGA an ultrasonographic estimated fetal weight of less t

163 t use was associated with increased risk for SGA (adjusted ORmultiple-trimester = 1.40, 95% CI 1.17-1

164 as a good biomarker of the clinical risk for SGA children to remain short in adulthood.

165 th a 2 and fourfold increase in the risk for SGA in nulliparous and multiparous, respectively.

166 egimens were associated with higher risk for SGA; ZDV-3TC-NVP was associated with higher risk of stil

167 Risk-stratification screening for SGA has been proposed in high-income countries to preven

168 allow development of risk-stratification for SGA.

169 r, we introduce a novel method to search for SGAs driving breast cancer metastasis to the lung.

170 ermethylated in placenta and cord blood from SGA newborns, whereas GPR120 (related to free fatty acid

171 We found a narrowing of disparities in SGA and LGA incidence across different maternal educatio

172 alaria during the second semester of life in SGA infants, and argue for better follow-up of these inf

173 of p73 and IGFBP3 are significantly lower in SGA children compared with controls and, in particular,

174 73 mRNA expression is significantly lower in SGA children with respect to height.

175 A reduction in SGA births, but not preterm birth or perinatal mortality

176 rved a greater-than-one-quarter reduction in SGA prevalence and no significant change in the associat

177 s and antidepressants, as well as individual SGAs.

178 acrosomia, small for gestational age infant (SGA), birth defect, and perinatal infant death.

179 llitus was increased among youths initiating SGAs and was highest in those concomitantly using antide

180 ion term IBD/PPDS was the factor that linked SGA to IBD compared to non-IBD, and increased the associ

181 nitive behavioral therapy, lisdexamfetamine, SGAs, and topiramate reduced binge eating and related ps

182 s and spontaneous abortion, PTB, macrosomia, SGA, and perinatal infant death (P for trend <0.001, <0.

183 uding spontaneous abortion, PTB, macrosomia, SGA, and perinatal infant death.

184 factors and infant's exposure to mosquitoes, SGA was associated with a 2-times higher risk of malaria

185 negative interactions than the double mutant SGA screens and uncovered additional genetic network inf

186 The triple-mutant SGA screen showed higher number of negative interactions

187 , 13 (8.3%) DM, and 116 (74.4%) were neither SGA nor had microcephaly (NSNM).

188 3%) DM, and 116 (74.4%) infants with neither SGA nor microcephaly (NSNM).

189 Neither SGAs nor CBT provides consistently superior cost-effecti

190 bined outcome (early preterm delivery, NICU, SGA).

191 l" combined outcome (preterm delivery, NICU, SGA); and "severe" combined outcome (early preterm deliv

192 hinner, and had less body fat than their non-SGA peers, irrespective of postnatal weight gain.

193 gnificantly higher for SGA compared with non-SGA births across the period from 23 to 34 wk gestation.

194 bal assessment (SGA; SGA A = well nourished, SGA B = mild or moderate malnutrition, and SGA C = sever

195 erved agreements between tools were: NRS2002/SGA, kappa = 0.53; CONUT/NRS-2002, kappa = 0.42; and SGA

196 The former group had the highest observed SGA prevalence.

197 were seen in 100% of PM and DM and 42.9% of SGA versus NSNM infants (16%) (p<0.001); OR 3.9(95% CI 1

198 re seen in 100% of PM and DM and in 42.9% of SGA vs NSNM infants 16%; (P <.001); OR 3.9 (95% CI, 1.2-

199 We 1) studied the association of SGA birth with adiposity, adjusting for baseline covaria

200 Sensitivity for detection of SGA infants was 20% (95% CI 15-24; 69 of 352 fetuses) fo

201 fetal biometry roughly tripled detection of SGA infants.

202 rth in Brazil through increased detection of SGA, appropriate management and timely delivery.

203 to estimate the controlled direct effect of SGA birth.

204 We assessed the effect of SGA on risk of malaria infection and clinical malaria fr

205 ssion levels of p73 and IGFBP3 in a group of SGA children.

206 n-related pathways were higher in mothers of SGA cases and mostly similar in mothers of LGA cases com

207 t cardiovascular risk profiles in mothers of SGA versus LGA offspring, where giving birth to SGA offs

208 PFUnDA were associated with elevated odds of SGA; and PFDeA, PFUnDA, and PFDoDA were associated with

209 reased odds of GH, and a 37% reduced odds of SGA; PTH was associated with a 45% reduction in the odds

210 ction as indicated by a composite outcome of SGA and pre-eclampsia.

211 Prevalence of SGA (<10th centile) was 10.1%, 10.0%, and 3.1%, and prev

212 rs of AEDs in monotherapy, the prevalence of SGA ranged from 7.3% for lamotrigine to 18.5% for topira

213 l growth as shown by a reduced prevalence of SGA.

214 nts were routine.In 2004, the proportions of SGA decreased with longer exposure to the new ration: no

215 to intranasal triamcinolone and the risk of SGA (OR, 1.06; 95% CI, 0.79-1.43; 50 exposed cases).

216 Higher DDS was associated with lower risk of SGA (RR highest compared with lowest quintile: 0.74; 95%

217 elines was associated with increased risk of SGA and decreased risk of LGA but only among underweight

218 The percentage of excess risk of SGA birth that was mediated was 7% in Black women, 6% in

219 D mothers is associated with reduced risk of SGA compared to non-IBD and IBD mothers with high PPDS.

220 ter were associated with an elevated risk of SGA comparing middle vs. lowest (RR, 2.34; 95% CI: 1.02,

221 re also associated with an increased risk of SGA comparing the second tertile with the first (RR, 2.6

222 S was positively associated with the risk of SGA in IBD mothers.

223 ile was associated with an increased risk of SGA of 4.5 (95% CI: 2.1, 6.8) per 100 births, and decrea

224 associated with significantly lower risk of SGA than non-IBD mothers and IBD mothers with high PPDS

225 cy were associated with an increased risk of SGA, whereas other biomarkers of DBPs examined across pr

226 regnancy was not associated with the risk of SGA/spontaneous abortions/overall malformations.

227 Next, we search for a set of SGA events that carries strong information with respect

228 ranscriptomic module, we search for a set of SGA genes (driver modules) such that genes in each drive

229 se-response effect across 2 subcategories of SGA (P < 0.001 for all comparisons).

230 fetal growth velocity identified a subset of SGA fetuses that were at increased risk of neonatal morb

231 TB appeared to be much stronger than that of SGA.

232 antidepressants concomitantly at the time of SGA initiation (OR, 1.54; 95% CI, 1.17-2.03; P = .002) b

233 data files, initiators and noninitiators of SGAs were identified in each month.

234 verall, this study highlights vital roles of SGAs as phytoalexins and phenylpropanoids along with lig

235 framework that integrates multiple types of SGAs and molecular phenotypes to estimate which genome p

236 light on how previously published studies on SGA status may be reinterpreted with the introduction of

237 There was no effect of vaccine on SGA or mean birth weight.

238 controlled for age, sex, and diagnosis, only SGA C (OR: 2.19; 95% CI: 1.28, 3.75), HGS (OR: 0.98; 95%

239 Compared with youths initiating only SGAs, the risk was higher among SGA initiators who used

240 T (HR, 1.05 [95% CI, .76-1.44]; P = .77); or SGA (HR, 0.99 [95% CI, .86-1.15]; P = .94).

241 roportional (PM) or disproportional (DM)] or SGA at birth were evaluated with anthropometric measurem

242 PM, DM, or SGA classification was based on head circumference and w

243 Classification of PM, DM, or SGA was based on head circumference and weight measureme

244 roportional [PM] or disproportional [DM]) or SGA at birth were evaluated with anthropometric measurem

245 ood samples from women with pre-eclampsia or SGA were analysed from the time of disease presentation

246 ption lipids were not associated with LGA or SGA in either group.

247 large- or small-for-gestational age (LGA or SGA) neonate by BMI group.

248 posure, a diagnosis of diabetes mellitus, or SGA use during a 1-year look-back period were ineligible

249 tensive disorders of pregnancy or preterm or SGA birth, although a small but statistically significan

250 onatal mortality not accounted for by PTB or SGA could reflect unaddressed educational disparities in

251 idual outcomes, including any PE, severe PE, SGA <10th percentile, SGA <5th percentile, preterm deliv

252 ing any PE, severe PE, SGA <10th percentile, SGA <5th percentile, preterm delivery <37 weeks, and pre

253 We also performed SGA screen with the amk2 gsk3 double mutant as a query.

254 There was a lower risk of pre-eclampsia plus SGA combined (13.6%) at 25(OH)D concentrations >75 nmol/

255 The pooled SGA prevalence was 23.7% (95% CI, 16.5%-31.0%) using the

256 4.9; 95% CI, 2.2 to 11.0), and with preterm SGA births (relative risk 3.0; 95% CI, 2.1 to 4.4).

257 y, was associated with a higher risk of PTB, SGA, and NICUa.

258 ssess associations of DDS and PDQS with PTB, SGA, LBW, and fetal loss.

259 We regarded SGA as a birthweight of less than the 10th percentile fo

260 ntion strategies should focus on both severe SGA and severe LGA pregnancies.

261 associations were stronger with more severe SGA and LGA (<5th and >95th percentile).

262 sion were subjective global assessment (SGA; SGA A = well nourished, SGA B = mild or moderate malnutr

263 pregnancy BMI or GWG and macrosomic, small- (SGA) and large- (LGA) for-gestational-age infants.

264 weeks) and small for gestational age status (SGA) among infants exposed prenatally to AEDs when used

265 ient to indicate that genes affected by such SGAs are in common pathways.

266 Babies who are term SGA low birthweight (10.4 million in these regions) are

267 In particular, our analyses revealed that SGA affecting TP53, PTK2, YWHAZ, and MED1 perturbed a se

268 Our results suggested that SGAs have a benefit for the treatment of delirium with r

269 For each study, we compared the SGA prevalence and the risk ratio between SGA status and

270 s fine details of the main feeding limb, the SGA, which are unknown in the adult of the same species.

271 A subset of the SGA cases displayed signs of FGR.

272 ight or BMI reversed (i.e., to positive) the SGA-adiposity association.

273 tlas (TCGA) and estimated for each tumor the SGAs that causally regulate the differentially expressed

274 eration antipsychotic combination therapies (SGAs) (i.e., aripiprazole, lurasidone, olanzapine, queti

275 y exhibit mutual exclusivity, in which these SGAs usually do not co-occur in a tumor.

276 percentage of neonatal death attributable to SGA.

277 f delivering prematurely and giving birth to SGA newborns.

278 versus LGA offspring, where giving birth to SGA offspring might primarily reflect adverse maternal v

279 etabolic adverse effects have been linked to SGA use in youths, estimating the risk for type 2 diabet

280 from the preceding time] and were related to SGA risk with the use of Poisson regression with confoun

281 ry DBP biomarkers examined were unrelated to SGA, LBW, or preterm birth.

282 n and HGS has a wide range of normal values, SGA is the single best predictor and should be advocated

283 risks associated with the use of FGAs versus SGAs as mediated by stroke on the risk ratio scale, as w

284 cluding very preterm birth (<32 weeks), very SGA (<3rd percentile of weight for gestational age), sti

285 the 156 ZIKV-exposed infants, 14 (9.0%) were SGA, 13 (8.3%) PM, 13 (8.3%) DM, and 116 (74.4%) infants

286 the 156 ZIKV-exposed infants, 14 (9.0%) were SGA, 13 (8.3%) PM, 13 (8.3%) DM, and 116 (74.4%) were ne

287 clampsia was 3.8%, and 10.7% of infants were SGA.

288 5.6% neonates in our study were SGA.

289 While SGA infants had fewer adverse outcomes compared with mic

290 While SGA infants had lower rates of adverse outcomes compared

291 hough short-term use was not associated with SGA (adjusted ORsingle-trimester = 0.95, 95% CI 0.87-1.0

292 nly conditional zwt+7 mo was associated with SGA and only in women with values >-0.5 (RR: 0.579; 95%

293 individual-level traits) are associated with SGA risk in rural Gambia.The sample comprised 670 women

294 eight women only and was not associated with SGA risk.

295 Factors associated with SGA were maternal lupus (OR(adj) 4.36, 95% CI [2.32-8.18

296 tic pathways were positively associated with SGA.

297 loss, and DDS was inversely associated with SGA.

298 int had a consistent nonlinear relation with SGA risk.

299 were also significantly higher in women with SGA than in controls at the time of disease detection (n

300 re generally higher in patients treated with SGAs.