ライフサイエンスコーパス: FGR

1 FGR and preterm birth was the leading risk factor cluste

2 FGR and unimproved sanitation are the leading risk facto

3 FGR appears to be a complex trait, but the role of genet

4 FGR cases (N = 30), defined as birthweight below the 10(

5 FGR cases showed signs of more globular hearts with decr

6 FGR cases with postsystolic shortening had absence of a

7 FGR infants [individualised birth weight ratio (IBR) < 5

8 FGR lungs presented thicker alveolar septal walls and re

9 FGR prevalence was high (10.3%), however early-onset FGR

10 FGR rabbits had higher respiratory resistance and altere

11 FGR refers to mass recirculation of a possibly cooled fr

12 FGR was associated with impaired pulmonary function and

13 FGR was associated with significantly lower Bayley-III s

14 FGR was defined as estimated fetal weight (EFW) <10th pe

15 FGR was induced at gestational day 25 by surgically redu

16 al cells in both abnormal groups (PE P<0.01; FGR P<0.0005 vs. control group) but no differences in vi

17 nested case-control design that compared 174 FGR cases, 114 preterm births, and 399 controls.

18 bed biopsy samples (controls n=17, PE n=19, FGR n=10).

19 mmunohistochemistry (controls n=18, PE n=19, FGR n=10).

20 lacenta previa (OR 2.31, 95% CI 0.35-15.22), FGR (OR 7.22, 95% CI 0.28-188.69), or PTB (OR 3.00, 95%

21 METHODS AND A cohort study of 58 FGR (defined as birth weight below 10th centile) and 94

22 e stillbirth but when combined with having a FGR pregnancy, maternal supine position leads to 15 time

23 In addition, FGR was associated with anxiety-like behavior, impaired

24 monary function and structural changes after FGR, independent of prematurity, and beyond the neonatal

25 ppropriate weight for gestational age (AGA), FGR babies have smaller placentas with reduced activity

26 s, NCCMs occurred in, e.g., the WASF-2/AHDC1/FGR locus.

27 es in non-targeted urinary metabolites among FGR cases and non-FGR controls.

28 y SR (one or four species, with FGR = 1) and FGR (1-4 groups, with SR = 4) to assess SR and FGR effec

29 d genes include SOX5, CD11C, galectin-1, and FGR, similar to a previously described FCRL4(+) memory B

30 measured in normal pregnancies (n = 10) and FGR (n = 10) both in vivo by umbilical artery Doppler ve

31 dds ratio (aOR) 1.46, 95% CI: 1.12-1.90) and FGR (aOR 1.64, 95% CI: 1.11-2.43), whereas B-cells only

32 it hypertension, endothelial dysfunction and FGR.

33 had both normal-weight (0.51 +/- 0.11 g) and FGR (0.34 +/- 0.1 g) fetuses within the same litter.

34 sed levels of the src-family kinases HCK and FGR.

35 ynthesis of H(2)S is enhanced in hypoxic and FGR unborn offspring in both species and this acts to pr

36 ability of P. gingivalis to produce ISAR and FGR in Sprague Dawley (SD) and Wistar (WIS) rats.

37 women; similar association between LRP8 and FGR was observed in this sample.

38 functional alterations, increase in MAP, and FGR.

39 opaque plastic vessel networks of normal and FGR placentas (n = 12/group) were created by filling the

40 orts the specific requirement of HCK p59 and FGR src-family kinases for FCRL4-mediated immunomodulato

41 tal bed of pregnancies complicated by PE and FGR and matched control pregnancies.

42 ssion of HO-2 on endothelial cells in PE and FGR may be responsible for reduced placental blood flow

43 enes differentially expressed in both PE and FGR, one encodes a secreted protein FSTL3 (follistatin-l

44 nt women are predictive of subsequent PE and FGR.

45 ies complicated by the combination of PE and FGR.

46 Maternal preeclampsia and FGR in very preterm infants.

47 R (1-4 groups, with SR = 4) to assess SR and FGR effects on ecosystem N cycling and its response to e

48 ecreasing or increasing with temperature and FGR ratio.

49 ht litters containing both normal-weight and FGR fetuses, P. gingivalis DNA was detected only in the

50 e-gene association study of birth weight and FGR in two independent study samples obtained at the Bos

51 th Asian women and 63.7% in Black women) and FGR (71.7% in South Asian women and 55.0% in Black women

52 ith FGR fetuses compared to dams without any FGR fetuses.

53 rkers and putative molecular targets such as FGR, LCN2, and OLFM4.

54 transport of glutamine and glutamate between FGR and normal pregnancy is currently lacking.

55 Not all infants are protected, with both FGR and preeclampsia occurring among highland-resident A

56 mice had reduced fertility characterized by FGR.

57 eeks) and 23 with pregnancies complicated by FGR (IBR <5th percentile and abnormal Doppler ultrasonog

58 erentiation between pregnancy complicated by FGR and normal pregnancy by using DeltaPo2, baseline R1,

59 In contrast, in pregnancies complicated by FGR, the choline/lipid ratio was </=0.02 in all placenta

60 evidence that cardiac remodeling induced by FGR persists until preadolescence with findings similar

61 ary organic acids differed over pregnancy by FGR case status.

62 as inhibitory activity in cells coexpressing FGR but an activating function in cells coexpressing HCK

63 In conclusion, FGR and pre-eclampsia are associated with T-cell infiltr

64 cardiography was performed in 37 consecutive FGR (defined as birthweight <10th centile) and 37 normal

65 Compared to controls, FGR pregnancies demonstrated a 37% increase in uterine b

66 Compared with controls, FGR preadolescents had a different cardiac shape, with m

67 developed ISAR, but only WIS rats developed FGR despite both rat strains having equivalent microbial

68 wth and no markers of placental dysfunction, FGR is associated with poorer educational attainment in

69 alis-challenged dams had fetuses with either FGR (2 standard deviations below mean weight of nonchall

70 proved survival among patients with elevated FGR.

71 Males, especially FGR-prone offspring, were more affected by peri-adolesce

72 trated a 37% increase in uterine blood flow (FGR vs. control, 610.86+/-48.48 vs. 443.17+/-37.39 ml mi

73 Effective screening and intervention for FGR is an unmet clinical need.

74 hird-to-fourth order chorionic arteries from FGR pregnancies and in third-order femoral arteries from

75 Human placenta artery endothelial cells from FGR groups exhibited increased shear stress-induced NO g

76 tive enzyme was quantified in placentas from FGR and age-matched control pregnancies.

77 Human placentae were selected from FGR and matched controls and analyzed by immunohistochem

78 elivered at term were divided into 4 groups: FGR, appropriate-for-gestational age (AGA) with markers

79 eclampsia (23.2%), and 46 infants (8.7%) had FGR.

80 ie, group 4-TN: those not suspected to have FGR who were AGA).

81 ie, group 3-FN: those not suspected to have FGR who were SGA) and neonates with true negatives (TNs;

82 ght <3rd percentile) not suspected of having FGR, infants with severe SGA delivered for suspected FGR

83 s with normal growth not suspected of having FGR.

84 ants with severe SGA not suspected of having FGR.

85 In contrast, increasing SR (holding FGR constant and despite increasing total plant C and N

86 In contrast, human FGR placentae exhibited reduced BPGM levels in the syncy

87 of these pathways are dysregulated in human FGR, our findings suggest that this model may provide an

88 t of BPGM, were lower in cord serum of human FGR placentae compared to control.

89 athophysiology of the post-placental hypoxic FGR.

90 ve clinical utility in correctly identifying FGR among fetuses that are small for gestational age.

91 to 4 in placentas complicated by idiopathic FGR compared with gestation-matched controls.

92 expression of syndecans 1 to 4 in idiopathic FGR placentas compared with controls.

93 In FGR placentas, levels of MT1-MMP mRNA and of active MT1-

94 In FGR pregnancies, a reduction in N-acetylaspartate (NAA)/

95 ile cotyledon VEGF was decreased (P<0.05) in FGR placentae.

96 nt; whether transport of these is altered in FGR is unknown.

97 sels dictate fetoplacental resistance and in FGR exhibit endothelial dysfunction and reduced flow-med

98 n PECAM-1 expression in the placental bed in FGR.

99 enatal cardiac remodeling comprehensively in FGR including myocardial deformation imaging.

100 d syndecan 2 were significantly decreased in FGR samples compared with controls.

101 ovascular changes previously demonstrated in FGR persist into preadolescence.

102 nt discrepancies in vessel length density in FGR placentas.

103 of the spectrum of placental dysfunction in FGR.

104 ardial deformation has not been evaluated in FGR to date.

105 netic studies implicate KIR and HLA genes in FGR, however, linkage disequilibrium, genetic influence

106 .11-2.43), whereas B-cells only increased in FGR (aOR 1.65, 95% CI: 1.05-2.60).

107 Maternal caruncle PlGF mRNA was increased in FGR (P<0.02), while fetal cotyledon VEGF mRNA was reduce

108 zed that placental NOx would be increased in FGR vs. normal tissue, and be further increased in villi

109 in placental villous tissue are increased in FGR vs. placentas from women with normal pregnancies, pa

110 ed by placental vessels, and is increased in FGR.

111 pothesized that reduced placental MT1-MMP in FGR impairs trophoblast functions.

112 e conclude that reduced placental MT1-MMP in FGR may contribute to the impaired trophoblast functions

113 and ex vivo in normal pregnancy, but not in FGR.

114 e of the coagulation disturbance observed in FGR pregnancies is currently unknown.

115 troma that displays abnormal organization in FGR placentas.

116 men with normal pregnancies, particularly in FGR associated with pre-eclampsia.

117 fails in the small dysfunctional placenta in FGR [insulin-like growth factor 2 knockout (P0) mouse mo

118 , no studies on TGF-betas in the placenta in FGR or in the placental bed in PE or FGR.

119 hypothesis of primary cardiac programming in FGR for explaining the association between low birth wei

120 mechanism for cardiovascular programming in FGR.

121 VEGFR-1 mRNA was also reduced in FGR fetal cotyledon (P<0.001) but was not altered in car

122 show that abnormal inflammation resulted in FGR mediated by tumor necrosis factor-alpha (TNF).

123 tudy placental microRNA derangements seen in FGR.

124 her prevalence of postsystolic shortening in FGR as compared with controls.

125 ons and reduced intracellular trafficking in FGR.

126 thfd1(gt/+) dams with hypoxanthine increased FGR frequency and caused occasional neural tube defects

127 insufficiency are associated with increased FGR incidence; however, the molecular mechanisms underly

128 through higher root biomass, and increasing FGR strongly reduced mineralization rates, because of lo

129 phenomenon present in P. gingivalis-induced FGR, with relevance to human disease since dysregulation

130 ecular mechanisms of cigarette smoke-induced FGR is lacking.

131 in an ovine model of placental insufficiency-FGR, in relationship to uteroplacental oxygenation.

132 ee women with severe placental insufficiency/FGR and three matched controls.

133 gests that in severe placental insufficiency/FGR, the observed 60-fold reduction in the choline/lipid

134 ed to increased expression of the SRC kinase FGR and augmented responsiveness of MB cells to dasatini

135 (2) integrin, the Src family tyrosine kinase FGR and spleen tyrosine kinase SYK.

136 the cytoplasmic Src-family tyrosine kinases FGR and HCK and related signaling proteins.

137 UBC patients without known FGR should not be advised to undergo CPM.

138 emonstrate that P. gingivalis-induced murine FGR is associated with systemic dissemination of the org

139 urinary metabolites among FGR cases and non-FGR controls.

140 revealed a postsystolic shortening in 57% of FGR, which supports increased pressure overload as a mec

141 2% of preterm births (0.8-1.6), and 16.9% of FGR (16.1-17.8) could be attributed to ethnic inequality

142 gamma only in the context of coexpression of FGR.

143 , we described the long-term consequences of FGR in pulmonary function, structure, and gene expressio

144 ole of genetic factors in the development of FGR is largely unknown.

145 maternal inflammation and the development of FGR with features of PE.

146 s were blinded to the antenatal diagnosis of FGR.

147 ransfer was not independent of the effect of FGR.

148 cental (fetal) inflammation was a feature of FGR in WIS rats.

149 DNA was detected in placentas and fetuses of FGR and normal littermates from P. gingivalis-infected d

150 The incidence of FGR was also influenced by the genotype of the embryo, s

151 s emission control, suitable manipulation of FGR enhances WI performance under waste uncertainty, ena

152 growth factor 2 knockout (P0) mouse model of FGR].

153 linically and in many experimental models of FGR, impaired uteroplacental vascular function is implic

154 therefore contribute to the pathogenesis of FGR.

155 to determine the prevalence and phenotype of FGR in women with AMSB and test the predictive value of

156 were significantly increased in placentas of FGR fetuses, while expression of IL-10 was significantly

157 is DNA was detected only in the placentas of FGR fetuses.

158 eased expression of IL-10 in the presence of FGR or HCK p59 in response to CpG, but increased levels

159 elevated in pregnancies at increased risk of FGR and stillbirth and are associated with increase in p

160 l copy of the "A" allele reduced the risk of FGR by 33% (P<.05).

161 heir urine (>0.01 mg/L) had a higher risk of FGR than those with TCAA levels below the detection limi

162 A number of factors can increase the risk of FGR, one of which is poor maternal diet.

163 d THMs) was associated with a higher risk of FGR.

164 tandardized birth weight and a lower risk of FGR.

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

166 ractions of the autophosphorylation sites of FGR receptor 1 (FGFR1) with the SH2 domain of CRKL or a

167 and group 3-FN with group 4-TN, suspicion of FGR was independently associated with increased risk of

168 calculate a predictive model for early-onset FGR (birthweight centile < 3rd/< 10th with absent umbili

169 alence was high (10.3%), however early-onset FGR was uncommon (2.3%).

170 mance for detection/exclusion of early-onset FGR.

171 sonographic screening to predict early-onset FGR.

172 interval (CI) 0.87-1.00), but not late-onset FGR (AUC 0.70, 95% CI 0.64-0.75).

173 lical and placental arteries from control or FGR pregnancy and in vessels from near-term chicken embr

174 We show here that the SFKs LYN, HCK, or FGR are overexpressed and activated in AML progenitor ce

175 e residues in the presence of the HCK p59 or FGR.

176 found in placenta or placental bed in PE or FGR compared with normal pregnancy.

177 sion of HO-2 or HO-1 did not change in PE or FGR.

178 ve a pathophysiological role in either PE or FGR.

179 changes in HO in the placental bed in PE or FGR.

180 enta in FGR or in the placental bed in PE or FGR.

181 or in the pathophysiology of preeclampsia or FGR.

182 upport of these hypotheses, increasing SR or FGR (holding the other constant) enhanced total plant N

183 that increased plant diversity (either SR or FGR) and elevated CO2 would enhance plant N pools becaus

184 In perfused FGR placentas, vascular resistance was significantly ele

185 lfate and N1,N12-diacetylspermine) predicted FGR at term.

186 he third trimester in cases of preeclampsia, FGR, and control pregnancies.

187 vely) and a cohort who delivered for preterm FGR (< 34 weeks).

188 gated in pregnancies complicated by PE, PTB, FGR and GDM and aims to highlight areas where further re

189 Fluegas recirculation (FGR) in WI is an effective technique for reducing WI atm

190 ogs of several filamentous growth regulator (FGR) genes that also have suspected roles in pathogenesi

191 Fetal growth restriction (FGR) affects >200,000 pregnancies in the United States a

192 Fetal growth restriction (FGR) affects 5% to 10% of newborns and is associated wit

193 Fetal growth restriction (FGR) affects 5-10% of pregnancies, and can have serious

194 Fetal growth restriction (FGR) affects around 5% of pregnancies and is associated

195 resulted in severe fetal growth restriction (FGR) and impaired fertility in litters harvested from Mt

196 Fetal growth restriction (FGR) and maternal supine going-to-sleep position are bot

197 Fetal growth restriction (FGR) and pre-eclampsia are severe, adverse pregnancy out

198 Fetal growth restriction (FGR) and preeclampsia (PE) are often associated with abn

199 regnancy including fetal growth restriction (FGR) and preeclampsia.

200 on by-products and fetal growth restriction (FGR) and preterm birth in the PELAGIE cohort, a French b

201 t birth intervals, fetal growth restriction (FGR) and preterm birth, child nutrition and infection, a

202 Fetal growth restriction (FGR) and stillbirth are associated with placental dysfun

203 are susceptible to fetal growth restriction (FGR) and stillbirth.

204 ltitude-associated fetal growth restriction (FGR) and the positive selection of metabolic genes linke

205 eterm birth (PTB), fetal growth restriction (FGR) and/or macrosomia resulting from gestational diabet

206 eclampsia (PE) and fetal growth restriction (FGR) are associated with impaired trophoblast invasion a

207 s whose outcome is fetal growth restriction (FGR) are characterized by abnormal angiogenic developmen

208 eclampsia (PE) and fetal growth restriction (FGR) are serious complications of pregnancy, associated

209 es associated with fetal growth restriction (FGR) by examining early and late pregnancy differences i

210 evere, early-onset fetal growth restriction (FGR) causes significant fetal and neonatal mortality and

211 eclampsia (PE) and fetal growth restriction (FGR) compared with control third-trimester pregnancies.

212 orks in normal and fetal growth restriction (FGR) complicated pregnancies.

213 fetal hypoxia and fetal growth restriction (FGR) increases a prenatal origin of cardiovascular disea

214 Fetal growth restriction (FGR) is a common outcome in human suboptimal gestation a

215 Fetal growth restriction (FGR) is a major determinant of global morbidity and mort

216 Fetal growth restriction (FGR) is a major risk factor for stillbirth and has signi

217 Fetal growth restriction (FGR) is a pregnancy complication in which a newborn fail

218 Fetal growth restriction (FGR) is a significant risk factor for stillbirth, neonat

219 Fetal growth restriction (FGR) is associated with a suboptimal intrauterine enviro

220 Fetal growth restriction (FGR) is associated with aberrant placentation and accoun

221 Fetal growth restriction (FGR) is associated with global adverse cardiac remodelin

222 Fetal growth restriction (FGR) is associated with reduced lung function in childre

223 detection rate of fetal growth restriction (FGR) is low.

224 Fetal growth restriction (FGR) is the major single cause of stillbirth(1) and is a

225 Fetal growth restriction (FGR) is the most common risk factor associated with stil

226 was found to drive fetal growth restriction (FGR) of transgenic offspring and impaired maternal care

227 er, placentas from fetal growth restriction (FGR) pregnancies are characterized by increased fibrin d

228 Fetal growth restriction (FGR) remains one of the main obstetrical problems worldw

229 Fetal growth restriction (FGR) results from placental insufficiency to adequately

230 s complicated with fetal growth restriction (FGR) with and without villitis of unknown aetiology.

231 ventable causes of fetal growth restriction (FGR), a condition in which a fetus is unable to achieve

232 Fetal growth restriction (FGR), a major risk factor for stillbirth, and neonatal a

233 licated by PE with fetal growth restriction (FGR), and (2) suppressyn secretion is modulated in an AS

234 re associated with fetal growth restriction (FGR), but previous studies have not examined whether thi

235 utcomes, including fetal growth restriction (FGR), due in part to reductions in nitric oxide (NO) bio

236 tum stillbirth and fetal growth restriction (FGR).

237 re associated with fetal growth restriction (FGR).

238 eat and/or prevent fetal growth restriction (FGR).

239 R) with or without fetal growth restriction (FGR).

240 local ischemia or fetal growth restriction (FGR).

241 ose complicated by fetal growth restriction (FGR).

242 he pathogenesis of fetal growth restriction (FGR); however, the regulating sites and mechanisms remai

243 n preeclampsia and fetal growth restriction (FGR); these processes are not well understood.

244 Fetal growth restriction (FGR, <0.46 g) was defined as fetuses with weights 2 stan

245 richness (SR) and functional group richness (FGR) are often confounded in both observational and expe

246 atients with elevated familial/genetic risk (FGR, ie, BRCA carrier status and/or family history of br

247 pregnancies and those complicated by severe FGR.

248 l but normal placenta differs from the small FGR placenta in terms of ability to transfer nutrients t

249 ants with severe SGA delivered for suspected FGR were born earlier (mean gestation, 37.9 weeks vs 39.

250 of infants with severe SGA due to suspected FGR was associated with poorer school outcomes compared

251 infants with normal growth due to suspected FGR was not associated with poorer school outcomes compa

252 Neonates with suspected FGR had a significantly increased rate of induction of l

253 s (FPs; ie, group 1-FP: those with suspected FGR who were AGA) and neonates with true positives (TPs;

254 s (TPs; ie, group 2-TP: those with suspected FGR who were SGA) were compared with neonates with AGA a

255 Among 8711 neonates with suspected FGR, 34.9% were below the 10th percentile at birth, whil

256 stational age (wkGA) using 175 cases of term FGR and 299 controls from the Pregnancy Outcome Predicti

257 We hypothesised that FGR is associated with reduced placental glutamine and g

258 In this study, we show that FGR endothelial cells demonstrate inherently reduced mig

259 titative trait locus (QTL) that harbours the FGR gene responsible for the production of GABA.

260 n the normal group, but substantially in the FGR group.

261 ventricular wall was observed in 57% of the FGR cases and in none of controls (P<0.001).

262 (P < .0001) in the combined cohort, with the FGR group having a DeltaR1 that was generally 61.5% lowe

263 in relationship to metabolic demands in this FGR model and that the transplacental PO2 gradient is in

264 ilure of this adaptation might contribute to FGR.

265 pressed on fetal trophoblast cells, leads to FGR in a humanized mouse model.

266 irus-mediated overexpression of sFRP1 led to FGR, increased karyorrhexis in the junctional zone, and

267 gs to pregnant mice in late gestation led to FGR.

268 nal standards) were assessed with respect to FGR status using regression models adjusted for relevant

269 a potential mechanism for susceptibility to FGR and stillbirth with AMA.

270 thweight fails to differentiate between true FGR and constitutionally small infants and cannot accoun

271 however, the molecular mechanisms underlying FGR remain unknown.

272 ransport of nutrients to the baby, underpins FGR.

273 ies to the human are essential to understand FGR long-term consequences and design novel therapeutic

274 tly shorter in arterial but longer in venous FGR networks compared to normals.

275 m/s [interquartile range, 0.09-0.12] versus FGR median 0.09 m/s [interquartile range, 0.09-0.10]; P<

276 locity: controls mean 6 cm/s [SD 1.2] versus FGR 5.3 [1]) and diastolic dysfunction (isovolumic relax

277 1 ms [interquartile range, 0.12-0.35] versus FGR, 0.35 ms [interquartile range, 0.20-0.46]; P=0.04).

278 ased (control mean, -22.4% [SD, 1.37] versus FGR mean, -21.5% [SD, 1.16]; P<0.001) compensated by an

279 c relaxation time: controls 44 ms [6] versus FGR 52 [9]).

280 The leading risk worldwide was FGR, defined as being term and small for gestational age

281 nset (< 34 weeks) or late-onset (> 34 weeks) FGR; as a result there is no consensus on management.

282 n fraction was similar among groups, whereas FGR had decreased longitudinal motion (decreased mitral

283 entify placental dysfunction associated with FGR and may have clinical utility in correctly identifyi

284 or preterm births, and 19.2% for births with FGR).

285 rm births and 22 679 (2.0%) were births with FGR.

286 ed to healthy AGA (N = 1,429), children with FGR (N = 250) were at higher risk of "below national sta

287 By age 7, children with FGR were more likely to perform below standard in readin

288 els were significantly elevated in dams with FGR fetuses compared to dams without any FGR fetuses.

289 In serum of dams with FGR fetuses, tumor necrosis factor alpha levels were ele

290 as poorer long-term health for infants with FGR compared with infants without FGR.

291 and/or behavioral outcomes, but infants with FGR may be prone to developmental delays.

292 nical evaluation at admission to labor, with FGR defined as a birth weight less than the 10th percent

293 Of the eight challenged mice with FGR fetuses, three had PCR signals for P. gingivalis in

294 Placentas of mice with FGR had increased transport capacity in mid-pregnancy, b

295 Neonates with FGR are known to have an increased rate of obstetric int

296 preeclamptic placentas and preeclampsia with FGR.

297 learly links maternal cigarette smoking with FGR, insight into the molecular mechanisms of cigarette

298 pendently vary SR (one or four species, with FGR = 1) and FGR (1-4 groups, with SR = 4) to assess SR

299 , was assessed in normal mice and those with FGR.

300 fants with FGR compared with infants without FGR.