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 showed signs of more globular hearts with decr

5 FGR cases with postsystolic shortening had absence of a

6 FGR refers to mass recirculation of a possibly cooled fr

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

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

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

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

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

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

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

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

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

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

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

18 functional alterations, increase in MAP, and FGR.

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

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

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

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

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

24 ecreasing or increasing with temperature and FGR ratio.

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

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

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

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

29 mice had reduced fertility characterized by FGR.

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

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

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

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

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

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

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

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

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

39 proved survival among patients with elevated FGR.

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

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

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

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

44 athophysiology of the post-placental hypoxic FGR.

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

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

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

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

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

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

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

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

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

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

55 ovascular changes previously demonstrated in FGR persist into preadolescence.

56 nt discrepancies in vessel length density in FGR placentas.

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

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

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

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

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

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

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

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

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

66 mechanism for cardiovascular programming in FGR.

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

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

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

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

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

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

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

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

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

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

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

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

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

80 gamma only in the context of coexpression of FGR.

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

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

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

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

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

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

87 therefore contribute to the pathogenesis of FGR.

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

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

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

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

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

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

94 tandardized birth weight and a lower risk of FGR.

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

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

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

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

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

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

101 ve a pathophysiological role in either PE or FGR.

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

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

104 or in the pathophysiology of preeclampsia or FGR.

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

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

107 In perfused FGR placentas, vascular resistance was significantly ele

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 tum stillbirth and fetal growth restriction (FGR).

130 re associated with fetal growth restriction (FGR).

131 ose complicated by fetal growth restriction (FGR).

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

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

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

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

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

137 pregnancies and those complicated by severe FGR.

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

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

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

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

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

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

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

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

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

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

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

149 1 ms [interquartile range, 0.12-0.35] versus FGR, 0.35 ms [interquartile range, 0.20-0.46]; P=0.04).

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

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

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

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

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

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

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

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

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

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

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

161 fants with FGR compared with infants without FGR.