ライフサイエンスコーパス: pre-eclampsia

1 affinity-purified AT(1)-AAs from women with pre-eclampsia.

2 ntribute to some of the maternal symptoms of pre-eclampsia.

3 membranes (PPROM), placental abruption, and pre-eclampsia.

4 ion could result in the maternal syndrome of pre-eclampsia.

5 ow-frequency, large-effect risk variants for pre-eclampsia.

6 precede and contribute to the development of pre-eclampsia.

7 abour, small for gestational age infants, or pre-eclampsia.

8 of the immune system in the pathogenesis of pre-eclampsia.

9 ing plasma extravasation in diseases such as pre-eclampsia.

10 evated in pregnancy-induced hypertension and pre-eclampsia.

11 lacental insufficiency and the occurrence of pre-eclampsia.

12 as been implicated in the pathophysiology of pre-eclampsia.

13 ms of circulating inhibin A and activin A in pre-eclampsia.

14 ther evidence for trophoblast dysfunction in pre-eclampsia.

15 nancies could be helpful in the diagnosis of pre-eclampsia.

16 indicated by a composite outcome of SGA and pre-eclampsia.

17 n identified in people with hypertension and pre-eclampsia.

18 omeric KIR B genes protect Europeans against pre-eclampsia.

19 te the risks of gestational hypertension and pre-eclampsia.

20 rthweight, pregnancy loss or miscarriage, or pre-eclampsia.

21 iodontitis was significantly associated with pre-eclampsia.

22 his is accentuated by multiple gestation and pre-eclampsia.

23 in corin and ANP function may contribute to pre-eclampsia.

24 ystemic angiogenic imbalance, accentuated by pre-eclampsia.

25 pressure and proteinuria, characteristics of pre-eclampsia.

26 maternal blood to the placenta, but fails in pre-eclampsia.

27 cluding intra-uterine growth restriction and pre-eclampsia.

28 stream molecular defect(s) may contribute to pre-eclampsia.

29 are significantly lower in women with severe pre-eclampsia.

30 r more units during an average 2 years were: pre-eclampsia, 1.78 (95% CI 1.52-2.08); gestational hype

31 .4]), preterm delivery (1.8 [1.3--2.5]), and pre-eclampsia (2.0 [1.5--2.5]).

32 m and postpartum haemorrhage (70% each), and pre-eclampsia (56%).

33 cated in the hypertension that characterises pre-eclampsia, a condition where tissue oedema is also o

34 Remodeling is impaired during pre-eclampsia, a disease of pregnancy that results in ma

35 uring normal pregnancy, is down regulated in pre-eclampsia, a human pregnancy disorder associated wit

36 al artery remodelling has been implicated in pre-eclampsia, a major complication of pregnancy, for a

37 One-third of the deaths are caused by pre-eclampsia, a syndrome arising from defective placent

38 Pre-eclampsia affects 2% to 8% of all pregnancies worldw

39 Pre-eclampsia affects 3-5% of pregnancies and is traditi

40 Pre-eclampsia affects approximately 5% of pregnancies an

41 eterm birth, PPROM, placental abruption, and pre-eclampsia aggregate in families, which may be explai

42 risk of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin

43 r more than a century of intensive research, pre-eclampsia and eclampsia remain an enigmatic set of c

44 thologic conditions include entities such as pre-eclampsia and eclampsia, along with conditions that

45 en 62 000 and 77 000 women die annually from pre-eclampsia and eclampsia.

46 r calcium-channel antagonists, magnesium for pre-eclampsia and eclampsia; and short-term parenteral a

47 associated with gestational hypoxia such as pre-eclampsia and fetal growth restriction.

48 is review is to determine the association of pre-eclampsia and future cardiovascular risk and to expl

49 ause placental structural changes leading to pre-eclampsia and impaired nutrient transport causing lo

50 mplicated in pathological conditions such as pre-eclampsia and intra-uterine growth retardation.

51 re of the feto-maternal interface results in pre-eclampsia and intrauterine growth retardation.

52 treatments will hasten our understanding of pre-eclampsia and is an effort much needed by the women

53 is impaired in women who eventually develop pre-eclampsia and it occurs before the development of th

54 ses a threat to cardiac homeostasis, and why pre-eclampsia and multiple gestation are important risk

55 a) and activin A (> 100 kDa) were similar in pre-eclampsia and normal pregnancy.

56 ns, and activin A in the serum of women with pre-eclampsia and of healthy matched control pregnant wo

57 c women to test the association of them with pre-eclampsia and quantitative traits relevant for the d

58 e in the prediction of both preterm and term pre-eclampsia and SGA.

59 pregnancy and investigated associations with pre-eclampsia and small-for-gestational-age (SGA) birth,

60 r studies identify a genetic mouse model for pre-eclampsia and suggest that 2-ME may have utility as

61 diagnosis, risk factors, and pathogenesis of pre-eclampsia and the present status of its prediction,

62 The clinical presentation of pre-eclampsia and toxic effects of antiretroviral therap

63 and it occurs more frequently in women with pre-eclampsia and/or multiple gestation.

64 The presence or absence of mHTN (e.g., pre-eclampsia) and infant factors (birthweight, gestatio

65 tcome of human pregnancy (ie, development of pre-eclampsia) and that, by the time delivery becomes ne

66 o had to have terminations because of severe pre-eclampsia, and 23 spontaneously aborted (<24 weeks'

67 n from 20 women in hospital with established pre-eclampsia, and from 20 control pregnant women attend

68 which is a potential contributory factor for pre-eclampsia, and is associated with endothelial dysfun

69 Our primary endpoint was pre-eclampsia, and our main secondary endpoints were low

70 rriage, intrauterine growth restriction, and pre-eclampsia, and raises new possibilities for interven

71 B concentrations occurs in normal pregnancy, pre-eclampsia, and SGA pregnancies.

72 ancy may be an indicator of hypertension and pre-eclampsia, and that treatment with certain neurokini

73 related immune deficiency with a low rate of pre-eclampsia, and the restoration of this rate in women

74 Oxidative stress could play a part in pre-eclampsia, and there is some evidence to suggest tha

75 t intrauterine growth restriction (IUGR) and pre-eclampsia are associated with a greater degree of tr

76 Women with a history of pre-eclampsia are at increased risk of future cardiovasc

77 Although algorithms to predict pre-eclampsia are promising, they have yet to become val

78 DPs), including gestational hypertension and pre-eclampsia, are common obstetric complications associ

79 growth restriction of the fetus (IUGR), and pre-eclampsia arose in ten (23%).

80 The patient was admitted with pre-eclampsia at 31 full weeks and 5 days, and 16 h late

81 mplications include gestational diabetes and pre-eclampsia, both of which are associated with long-te

82 lial dysfunction is a feature of established pre-eclampsia but whether this is a cause or consequence

83 ring pregnancy have not shown a reduction in pre-eclampsia, but the effect in women with diabetes is

84 ere identified as being at increased risk of pre-eclampsia by abnormal two-stage uterine-artery doppl

85 lt-1 expression by decidual cells to promote pre-eclampsia by interfering with local vascular transfo

86 When left untreated, pre-eclampsia can be lethal, and in low-resource setting

87 In pre-eclampsia, deficient HB-EGF signalling during placen

88 Rates of pre-eclampsia did not differ between vitamin (15%, n=57)

89 However, pre-eclampsia does not develop in all women with high sF

90 egnancy, and one mother with SPKTx developed pre-eclampsia during both pregnancies.

91 Pre-eclampsia/eclampsia are leading causes of maternal m

92 T, previously implicated in hypertension and pre-eclampsia, exhibits a similar geographic distributio

93 In pre-eclampsia, expression of the Notch ligand JAG1 was a

94 lure of transformation has been described in pre-eclampsia, fetal growth restriction, and miscarriage

95 icated in adverse obstetric outcomes such as pre-eclampsia, fetal growth restriction, and preterm bir

96 410 women identified as at increased risk of pre-eclampsia from 25 hospitals.

97 eight gain and subsequently increase risk of pre-eclampsia, gestational diabetes mellitus, hypertensi

98 Pre-eclampsia, gestational hypertension, and small-for-g

99 Women who developed pre-eclampsia had significantly lower flow-mediated dila

100 Low birthweight, pre-term birth and pre-eclampsia have been associated with maternal periodo

101 urological symptoms are often diagnosed with pre-eclampsia; however, a range of other causes must als

102 However, the rate of pre-eclampsia in HIV-1-positive women on treatment did n

103 in supplementation affects the occurrence of pre-eclampsia in low-risk women and to confirm our resul

104 g antiplatelet agents, for the prevention of pre-eclampsia in pregnancy.

105 and E may be beneficial in the prevention of pre-eclampsia in women at increased risk of the disease.

106 ith vitamin C and vitamin E does not prevent pre-eclampsia in women at risk, but does increase the ra

107 with vitamins C and E did not reduce risk of pre-eclampsia in women with type 1 diabetes.

108 n with vitamins C and E reduced incidence of pre-eclampsia in women with type 1 diabetes.

109 We show here that key features of pre-eclampsia, including hypertension, proteinuria, glom

110 completed using data from 1,300 women in the Pre-eclampsia Integrated Estimate of RiSk (fullPIERS) da

111 ce localization on placental tissue, that in pre-eclampsia invasive cytotrophoblasts fail to properly

112 nce of curative treatment, the management of pre-eclampsia involves stabilisation of the mother and f

113 Pre-eclampsia is a common pregnancy disorder that is a m

114 Pre-eclampsia is a disorder of pregnancy associated with

115 Pre-eclampsia is a major cause of maternal mortality (15

116 Pre-eclampsia is a multisystem placentally mediated dise

117 Pre-eclampsia is a principal cause of maternal morbidity

118 The pregnancy disease pre-eclampsia is associated with shallow cytotrophoblast

119 Pre-eclampsia is associated with significant morbidity a

120 In conclusion, the genetic risk for pre-eclampsia is likely complex even in a population iso

121 nificance, as the downregulation of HBEGF in pre-eclampsia is likely to be a contributing factor lead

122 An effective treatment of pre-eclampsia is unavailable owing to the poor understan

123 resistance placental circulation at risk of pre-eclampsia, IUGR, or both have raised concentrations

124 receptor 1 secreted from the placenta causes pre-eclampsia-like features by antagonizing vascular end

125 2-ME ameliorates all pre-eclampsia-like features without toxicity in the Comt

126 g in female mice lacking eNOS aggravates the pre-eclampsia-like phenotype induced by increased sFlt-1

127 n catechol-O-methyltransferase (COMT) show a pre-eclampsia-like phenotype resulting from an absence o

128 S/nitric oxide exacerbates the sFlt1-related pre-eclampsia-like phenotype through activation of the e

129 Thus, our studies indicate that pre-eclampsia may be a pregnancy-induced autoimmune dise

130 who were matched for duration of gestation (pre-eclampsia mean 29.15 [SD 3.75] weeks; controls 29.30

131 Variants predisposing to pre-eclampsia might be under negative evolutionary selec

132 -term birth (<37 weeks), growth restriction, pre-eclampsia, miscarriage and/or stillbirth.

133 1-39.8] vs 16.9 [10.4-19.1], p=0.04; preterm pre-eclampsia n=11, 23.1 [11.2-30.9] vs 17.2 [9.8-19.1],

134 ls at the time of disease presentation (term pre-eclampsia n=14, median 22.2 ng/mL [IQR 15.1-39.8] vs

135 In the intention-to-treat cohort, pre-eclampsia occurred in 24 (17%) of 142 women in the p

136 dividuals, particularly when associated with pre-eclampsia or acute glomerulonephritis.

137 reasons for indicated preterm births include pre-eclampsia or eclampsia, and intrauterine growth rest

138 iethylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors.

139 lts in excessive dNK inhibition, the risk of pre-eclampsia or growth restriction is increased.

140 nts are correlated with low birth weight and pre-eclampsia or high birth weight and obstructed labor,

141 e fetus and required delivery as a result of pre-eclampsia or hypertension were randomly assigned (1:

142 sation for induction of labour in women with pre-eclampsia or hypertension.

143 Blood samples from women with pre-eclampsia or SGA were analysed from the time of dise

144 tcomes associated with maternal asthma were: pre-eclampsia (OR = 2.18; 95% CI, 1.68 to 2.83), placent

145 infertility therapies (p = 0.0004), and had pre-eclampsia (p = 0.001).

146 eles encoding the C2 epitope associates with pre-eclampsia [P = 0.0318, odds ratio (OR) = 1.49].

147 Pre-eclampsia (PE) and gestational diabetes mellitus (GD

148 ) literature and determine the prevalence of pre-eclampsia (PE) in women with PPCM.

149 Pre-eclampsia (PE) is a leading cause of maternal and fe

150 The primary outcome was a composite of pre-eclampsia (PE), birth of a small-for-gestational-age

151 Placental RAS is increased in pre-eclampsia (PE), characterised by placental dysfuncti

152 Pre-eclampsia (PE), which affects approximately 8% of fi

153 normal pregnancy and in increased amounts in pre-eclampsia (PE), which have proinflammatory and antia

154 imbalance has not been fully investigated in pre-eclampsia (PE).

155 hanisms that facilitate the emergence of the pre-eclampsia phenotype in women are still unknown.

156 r endotheliosis (a classical renal lesion of pre-eclampsia), placental abnormalities and small fetus

157 There was a lower risk of pre-eclampsia plus SGA combined (13.6%) at 25(OH)D conce

158 lice site variants that were enriched in the pre-eclampsia pools compared to reference data, and geno

159 us recent studies have shown that women with pre-eclampsia possess autoantibodies, termed AT(1)-AAs,

160 Because pre-eclampsia predisposes mothers to cardiovascular dise

161 ding increased risk of gestational diabetes, pre-eclampsia, preterm birth, instrumental and caesarean

162 the group of women who eventually developed pre-eclampsia (r=-0.8, p=0.005).

163 risk factors, but the diagnostic criteria of pre-eclampsia remain unclear, with no known biomarkers.

164 ology of PPCM, and why it is associated with pre-eclampsia, remain unknown.

165 eterm birth, PPROM, placental abruption, and pre-eclampsia, respectively).

166 eterm birth, PPROM, placental abruption, and pre-eclampsia, respectively).

167 ypothesis has obvious implications regarding pre-eclampsia screening, diagnosis and therapy.

168 Pooled samples of control (n = 3) and pre-eclampsia serum (n = 3) subsequently underwent fast

169 ived no antiretroviral therapy had a rate of pre-eclampsia significantly lower (none of 61) than thos

170 ependently adjudicated severe or early-onset pre-eclampsia, small-for-gestational-age infant (birthwe

171 nta-mediated pregnancy complications (severe pre-eclampsia, small-for-gestational-age infants, and pl

172 and pro alpha C were significantly higher in pre-eclampsia than in control normal pregnancy (inhibin

173 hibin A, pro alpha C, and total activin A in pre-eclampsia than in control pregnancies could be helpf

174 PBB concentrations were higher in women with pre-eclampsia than in controls at the time of disease pr

175 NK-B was implicated in pregnancy-associated pre-eclampsia, the regulation of NK-B synthesis and func

176 -bridged form in the maternal circulation in pre-eclampsia-the hypertensive crisis of pregnancy that

177 In patients with pre-eclampsia, uterine Corin messenger RNA and protein l

178 group, 79 vitamin group), the odds ratio for pre-eclampsia was 0.24 (0.08-0.70, p=0.002).

179 The prevalence of pre-eclampsia was 3.8%, and 10.7% of infants were SGA.

180 Pre-eclampsia was assessed by the development of protein

181 Toxemia of pregnancy or pre-eclampsia was observed in 23% of pregnancies postKTx

182 The incidence of pre-eclampsia was similar in treatment placebo groups (1

183 ariants in individuals with hypertension and pre-eclampsia were defective in PCSK6-mediated activatio

184 tect sub-Saharan Africans and Europeans from pre-eclampsia, whereas in both populations, the KIR AA g

185 The primary endpoint was pre-eclampsia, which we defined as gestational hypertens