ライフサイエンスコーパス: preeclampsia

1 ated STBEVs and oxidized LDL levels (such as preeclampsia).

2 n of endothelial dysfunction associated with preeclampsia.

3 the pathogenesis of the maternal syndrome of preeclampsia.

4 in in the regulation of maternal outcomes in preeclampsia.

5 ith a potential for therapeutic targeting in preeclampsia.

6 ated to pregnancy-related disorders, such as preeclampsia.

7 egulated by ACTN4 is impaired in early onset preeclampsia.

8 men in the study group, 64 (3.6%), developed preeclampsia.

9 n implicated in the pathogenesis of IUGR and preeclampsia.

10 against prolonged placental hypoxia seen in preeclampsia.

11 oration of placental function in early-onset preeclampsia.

12 the fetus - a process which is deficient in preeclampsia.

13 isk of pregnancy complications, e.g., severe preeclampsia.

14 on placental ischemia and the progression of preeclampsia.

15 reported to contribute to pathophysiology of preeclampsia.

16 companying proteinuria, classic hallmarks of preeclampsia.

17 y increased at time of disease in women with preeclampsia.

18 12 weeks' gestation to minimize the risk of preeclampsia.

19 s dysregulated in placentas from early onset preeclampsia.

20 est risk of ESKD compared with women with no preeclampsia.

21 vels of perfluoroalkyl substances (PFAS) and preeclampsia.

22 blood (but not amniotic fluid) of women with preeclampsia.

23 apitulated a number of the features of human preeclampsia.

24 cations such as fetal growth restriction and preeclampsia.

25 ular risk factors in women with a history of preeclampsia.

26 view findings from multiple animal models of preeclampsia.

27 turity, because prematurity is an outcome of preeclampsia.

28 atients with PPCM that is not complicated by preeclampsia.

29 vailable in 10 survivors with and 16 without preeclampsia.

30 f DLX5 might help explain certain aspects of preeclampsia.

31 nary soluble nephrin levels (nephrinuria) in preeclampsia.

32 ontrol analysis among women with and without preeclampsia.

33 Maternal asthma increased the risk of preeclampsia.

34 l outcomes in women with PPCM complicated by preeclampsia.

35 ts and harms of treatment of screen-detected preeclampsia.

36 to predict biological processes affected in preeclampsia.

37 verse maternal and fetal outcomes, including preeclampsia.

38 3.7% (n = 62,728) were born to mothers with preeclampsia.

39 organs, contributing to the pathogenesis of preeclampsia.

40 whether disturbed imprinting contributes to preeclampsia.

41 Seventeen of 39 women (44%) with PPCM had preeclampsia.

42 idence, that imprinted genes are involved in preeclampsia.

43 rce (USPSTF) recommendation on screening for preeclampsia.

44 ular disease, stroke, and stroke death after preeclampsia.

45 s that additional factors modify the risk of preeclampsia.

46 risk score for hypertension associates with preeclampsia.

47 res also observed in women with a history of preeclampsia.

48 and for their potential physiologic role in preeclampsia.

49 t IVF procedures could increase the risk for preeclampsia.

50 reased further in pregnancies complicated by preeclampsia.

51 thway is regarded as a promising therapy for preeclampsia.

52 stage and may be used for the prediction of preeclampsia.

53 as a placental tissue specific biomarker for preeclampsia.

54 elevated in placenta samples from women with preeclampsia.

55 preexistent cardiac conditions or history of preeclampsia.

56 , including spontaneous preterm delivery and preeclampsia.

57 t were not associated with preterm birth and preeclampsia.

58 ated pathologies including preterm birth and preeclampsia.

59 f gestation were shown to be associated with preeclampsia.

60 developmental dysregulations associated with preeclampsia.

61 ependently associated with the occurrence of preeclampsia.

62 Moderate agreement was observed for preeclampsia (0.51) and hypertension (0.46).

63 men also have case fatality rates related to preeclampsia 3 times higher than rates among white women

64 f intrauterine growth restriction (IUGR) and preeclampsia 3-fold, augmenting perinatal morbidity and

65 oprevention (eg, aspirin therapy) to prevent preeclampsia, a disease that affects 2% to 8% of pregnan

66 An exception to this is preeclampsia, a leading cause of pregnancy-associated mo

67 Endothelial dysfunction is a hallmark of preeclampsia, a life-threatening complication of pregnan

68 Although the cause of preeclampsia, a pregnancy complication with significant

69 centa actively produces transthyretin and in preeclampsia, a significant amount is extruded into the

70 compared with mothers without asthma without preeclampsia (adjusted hazard ratio, 2.18; 95% confidenc

71 or children born to mothers with asthma with preeclampsia (adjusted hazard ratio, 4.73; 95% confidenc

72 Women who had preterm preeclampsia (adjusted HR = 9.19; 95% CI 5.16-15.61, p <

73 ciated with adverse pregnancy outcomes (e.g. preeclampsia, adjusted Odds Ratio 1.17 (95% Confidence I

74 ssociated with a clinically relevant risk of preeclampsia, adjusting for established confounders.

75 een hypertensive disorders of pregnancy, and preeclampsia alone (term and preterm), with 12 cardiovas

76 Preeclampsia also led to a higher number of C-sections a

77 ate adjustment were applied to relate ROP to preeclampsia among the full cohort and in a subcohort of

78 There was no higher risk of preeclampsia among women exposed to gabapentin after adj

79 today that there are two different types of preeclampsia: an early-onset or placental type and a lat

80 nd nervous systems, and increase the risk of preeclampsia and adverse perinatal outcomes.

81 io-demographic and clinical risk factors for preeclampsia and associated maternal and perinatal adver

82 We studied associations between preeclampsia and asthma, allergy, and eczema in Copenhag

83 pathways of dysregulated decidualization in preeclampsia and endometrial disorders revealed by micro

84 analysis to examine the association between preeclampsia and ESKD adjusting for several potential co

85 There was an association between preeclampsia and ESKD in the unadjusted analysis (hazard

86 d risk of pregnancy complications, including preeclampsia and fetal adverse outcomes.

87 t of pregnancy-associated disorders, such as preeclampsia and fetal growth restriction.

88 sociated with reduced risk of HDP, including preeclampsia and gestational hypertension.

89 predict the overall risk of developing early preeclampsia and indicate distinct subtypes of pathophys

90 dyads from the Prediction and Prevention of Preeclampsia and Intrauterine Growth Restriction cohort,

91 from the PREDO (Prediction and Prevention of Preeclampsia and Intrauterine Growth Restriction) study

92 ciated with pregnancy complications, such as preeclampsia and intrauterine growth restriction.

93 ance understanding of the pathophysiology of preeclampsia and its subtypes.

94 The present findings suggest that women with preeclampsia and no major comorbidities before their fir

95 egnant women's risk of complications such as preeclampsia and non-vaginal deliveries.

96 lammasome is involved in the pathogenesis of preeclampsia and other pregnancy syndromes associated wi

97 h symptomatic COVID-19 complicated by severe preeclampsia and placental abruption.METHODSWe analyzed

98 drome, and during pregnancy, it is linked to preeclampsia and preterm birth.

99 rs such as intra uterine growth restriction, preeclampsia and preterm birth.

100 ify the evidence on the relationship between preeclampsia and the future risk of cardiovascular disea

101 We aimed to examine the association between preeclampsia and the risk of ESKD in healthy women, whil

102 o confirm association between imprinting and preeclampsia and to predict biological processes affecte

103 parent on coronary computed tomography after preeclampsia and to what extent modifiable cardiovascula

104 placental genetic and epigenetic markers of preeclampsia and validated our findings in an independen

105 ed with aberrant placentation (cases who had preeclampsia and/or intrauterine growth restriction) and

106 composite maternal (gestational diabetes or preeclampsia) and composite offspring (stillbirth, small

107 f all pregnancies) singleton live births had preeclampsia, and 410 women developed ESKD with an incid

108 s, including diabetic complications, sepsis, preeclampsia, and atherosclerosis, is summarized.

109 disease as a risk factor for preterm birth, preeclampsia, and fetal growth restriction.

110 reeclampsia, late preterm preeclampsia, term preeclampsia, and gestational hypertension.

111 th preeclampsia, mothers with asthma without preeclampsia, and mothers with asthma with preeclampsia,

112 Antenatal factors, such as chorioamnionitis, preeclampsia, and postnatal injury, are associated with

113 o cell adhesion and migration, angiogenesis, preeclampsia, and stress.

114 pertensive disorders, in particular, preterm preeclampsia, and the need for an increased focus on int

115 ic cardiovascular dysfunction in early-onset preeclampsia, and thus sharing the pathophysiology of ca

116 sthma with preeclampsia, with asthma without preeclampsia, and with asthma with preeclampsia during t

117 Vascular complications in pregnancy (e.g. preeclampsia) are a major source of maternal and foetal

118 hypertension, gestational hypertension, and preeclampsia-are uniquely challenging as the pathology a

119 the harms of screening for and treatment of preeclampsia as no greater than small.

120 d beta peptide (Abeta) that is implicated in preeclampsia as well as with Alzheimer's disease.

121 Furthermore, renal injury in preeclampsia associated with an elevated urinary podocin

122 However, we identified infant sex-specific preeclampsia-associated differentially methylated region

123 onstrate the biological pathways involved in preeclampsia at the pre-clinical stage and may be used f

124 The primary outcome was delivery with preeclampsia before 37 weeks of gestation.

125 ies was not associated with preterm birth or preeclampsia but with the risk of delivering large-for-g

126 ept that the pathophysiological processes of preeclampsia can be regarded as the gestational manifest

127 and proteinuria during the third trimester, preeclampsia can progress rapidly to serious complicatio

128 in the placenta from an independent study of preeclampsia cases and controls and constructed the pree

129 erse maternal and neonatal outcomes, such as preeclampsia, cesarean delivery, preterm delivery, macro

130 Half of the association was mediated through preeclampsia, cesarean section delivery, and preterm del

131 livery, preterm delivery, poor fetal growth, preeclampsia, chorioamnionitis, postpartum hemorrhage, s

132 ulation would be altered under conditions of preeclampsia compared to normal pregnancy.

133 ver, women with r-AKI had increased rates of preeclampsia compared with controls (23% versus 4%; P<0.

134 children born to mothers with asthma without preeclampsia, compared with mothers without asthma witho

135 r the vasculopathy typically associated with preeclampsia.CONCLUSIONThis case demonstrates SARS-CoV-2

136 ensive disorders of pregnancy, while preterm preeclampsia conferred slightly further elevated risks.

137 cluded in-hospital arrhythmias, eclampsia or preeclampsia, congestive heart failure (CHF), length of

138 Preeclampsia, coronary artery calcification (CAC), and a

139 ngest in offspring from pregnancies in which preeclampsia developed during late gestation and offspri

140 rlie the pathogenic mechanism of early-onset preeclampsia developing secondary to molar pregnancies.

141 ma is also associated with increased risk of preeclampsia development.

142 Chronic inflammation during pregnancy (e.g., preeclampsia, diabetes) is linked to increased risk for

143 Patients with preeclampsia displayed early up-regulation of neutrophil

144 en born to mothers with asthma who developed preeclampsia during pregnancy (adjusted hazard ratio, 2.

145 a without preeclampsia, and with asthma with preeclampsia during their pregnancy.

146 changes associated with endothelial damage (preeclampsia, eclampsia, and HELLP syndrome), and postop

147 a previous C-section, gestational diabetes, preeclampsia/eclampsia or be in the third trimester (P <

148 However, only 77% of women with severe preeclampsia/eclampsia received magnesium sulphate and 6

149 alternative disorders with features of TMA (preeclampsia/eclampsia; hemolysis elevated liver enzymes

150 We describe a model for early onset preeclampsia (EOPE) that uses induced pluripotent stem c

151 of any cardiovascular disorder according to preeclampsia exposure.

152 tpartum follow-up of those with a history of preeclampsia, gestational diabetes mellitus, or preterm

153 ence of 1 or more of the following outcomes: preeclampsia, gestational hypertension, gestational diab

154 ific EVs, was significantly decreased in the Preeclampsia group (p = 2.8 x 10(-11)).

155 he etiology of their preterm birth: Group 1, preeclampsia; Group 2, spontaneous preterm labor; Group

156 ticle analysis, EV profiles from Control and Preeclampsia groups showed similar total plasma EV quant

157 en who had 1 or more pregnancies affected by preeclampsia had a hazard ratio of 1.9 (95% confidence i

158 Women with preeclampsia had smaller mean LV end-diastolic diameters

159 Preeclampsia has been suggested to increase the risk of

160 lls and that high levels of soluble CORIN in preeclampsia have a placental origin.

161 pertensive disorders of pregnancy, including preeclampsia, have a similar pattern of increased risk a

162 Women with a preeclampsia history maintained greater advancement of C

163 d more severely in early- than in late-onset preeclampsia; however, some very specific dysfunctions e

164 k of ESKD compared with parous women with no preeclampsia; however, the absolute risk of ESKD among w

165 aimed to investigate the association between preeclampsia, hypertensive disorders of pregnancy, and s

166 an extremely high risk of severe early-onset preeclampsia if left untreated.

167 iomyopathy (PPCM), but it is unknown whether preeclampsia impacts clinical or left ventricular (LV) f

168 Decreased LIN28B in preeclampsia impairs human trophoblast differentiation a

169 11.4%, gestational hypertension in 9.5%, and preeclampsia in 12.1% of women.

170 CI 5.16-15.61, p < 0.001) and women who had preeclampsia in 2 pregnancies (adjusted HR = 7.13, 95% C

171 contribute to poor outcomes associated with preeclampsia in African American women.

172 (SGA), and women who had 2 pregnancies with preeclampsia in both.

173 positively associated with increased risk of preeclampsia in human studies.

174 plicated in causing the maternal symptoms of preeclampsia in humans.

175 od vessel constriction, triggers symptoms of preeclampsia in pregnant mice.

176 The USPSTF recommends screening for preeclampsia in pregnant women with blood pressure measu

177 he occurrence of ROP was related to maternal preeclampsia in the full cohort and in a subcohort of P-

178 entify sequence variants that associate with preeclampsia in the maternal genome at ZNF831/20q13 and

179 ensitive and 95.6% specific for diagnosis of preeclampsia in this cohort (area under curve = 0.975 +/

180 Preeclampsia, in particular, is one of the most feared c

181 nearby variant, rs12050029, associated with preeclampsia independently of rs4769613.

182 several common gestational diseases such as preeclampsia, intrauterine growth restriction, and gesta

183 Preeclampsia is a complex and common human-specific preg

184 Preeclampsia is a dangerous hypertensive disorder of pre

185 We first aimed to confirm that preeclampsia is a disease of the placenta by generating

186 Preeclampsia is a hypertensive disorder of pregnancy.

187 Preeclampsia is a major cause of maternal and fetal morb

188 Preeclampsia is a multisystemic disorder leading to the

189 Preeclampsia is a pregnancy-related hypertensive disorde

190 Preeclampsia is a risk factor for the development of per

191 Preeclampsia is a serious complication of pregnancy, aff

192 Preeclampsia is a shared prenatal risk factor for asthma

193 Preeclampsia is a syndrome with diverse clinical present

194 PPCM with concomitant preeclampsia is associated with increased morbidity and

195 Preeclampsia is associated with increased risk of early

196 uced uterine perfusion pressure rat model of preeclampsia is hypoxic, and that this hypoxia is mainta

197 Preeclampsia is known to be associated with significant

198 Preeclampsia is one of the leading causes of maternal an

199 Preeclampsia is one of the most serious complications du

200 e exaggerated innate immune response seen in preeclampsia is provoked by dysfunctional mitochondria.

201 While the cause of preeclampsia is still debated, clinical and pathological

202 Preeclampsia is the most common placental pathology in p

203 Preeclampsia is the most frequent pregnancy-related comp

204 New criteria to diagnose preeclampsia, judicious reliance on measurement of ADAMT

205 ng congenital heart defects or early preterm preeclampsia, late preterm preeclampsia, term preeclamps

206 Preeclampsia leads to adverse outcomes for pregnant wome

207 These preeclampsia-like features correlated with increased ret

208 We investigated whether BPA exposure causes preeclampsia-like features in pregnant mice and the asso

209 ol A exposure alters placentation and causes preeclampsia-like features in pregnant mice involved in

210 ng, both of which lead to the development of preeclampsia-like features in pregnant mice.

211 In pregnant mice, BPA-exposed mice exhibited preeclampsia-like features including hypertension, disru

212 Preeclampsia - maternal hypertension and proteinuria - i

213 Therefore, women who experienced preeclampsia might benefit from regular cardiovascular s

214 mpsia cases and controls and constructed the preeclampsia module using protein-protein interaction ne

215 ut preeclampsia, mothers without asthma with preeclampsia, mothers with asthma without preeclampsia,

216 e born to mothers without asthma and without preeclampsia, mothers without asthma with preeclampsia,

217 sion was noted in samples from patients with preeclampsia (n = 8).

218 emopexin, which were decreased in women with preeclampsia, negatively correlated with proteinuria, ur

219 he increased aggregation of transthyretin in preeclampsia occurs at the post-transcriptional level an

220 and ages 45 to 50 in women with a history of preeclampsia (odds ratio, 4.3 [95% CI, 1.5-12.2] versus

221 e, was associated with an increased risk for preeclampsia of about 38-53% respectively.

222 ny vs no HDP, 1.54 (95% CI, 1.39-1.70) after preeclampsia or eclampsia, 1.51 (95% CI, 1.27-1.80) afte

223 ospital maternal mortality, fetal mortality, preeclampsia or eclampsia, caesarean sections, non-deliv

224 nancy complications, such as severe forms of preeclampsia or intrauterine growth restriction, are tho

225 nal hypertension (OR 1.7; 95% ICI, 1.3-2.2), preeclampsia (OR 2.7; 95% ICI, 2.5-3.0), placental abrup

226 nd that increased levels of soluble CORIN in preeclampsia originate from placenta.

227 in 80% of survivors with versus 25% without preeclampsia (P=0.014).

228 at diagnosis (29.6 with versus 27.3 without preeclampsia; P=0.5).

229 of the molecular mechanisms, which underlie preeclampsia pathophysiology.

230 low vitamin D status with increased risk of Preeclampsia (PE) development.

231 Preeclampsia (PE) is a common cause of maternal morbidit

232 Preeclampsia (PE) is a dangerous complication of pregnan

233 Preeclampsia (PE) is a hypertensive disease of pregnancy

234 Preeclampsia (PE) is a placental disorder with different

235 Preeclampsia (PE) is a pregnancy specific hypertensive d

236 Preeclampsia (PE) is characterized by poor placentation,

237 tification of patients at risk of developing preeclampsia (PE) would allow providers to tailor their

238 ng the first trimester (T1), and the risk of preeclampsia (PE), preterm birth (PTB), small for gestat

239 During the pregnancy associated syndrome preeclampsia (PE), there is increased release of placent

240 ls of sENG contribute to the pathogenesis of preeclampsia (PE).

241 placental adenosine signaling contributes to preeclampsia (PE).

242 rosine kinase-1 (sFLT1) in a baboon model of preeclampsia portends the development of effective thera

243 Manipulation of key clinical preeclampsia processes in these models (e.g., placental

244 In severe preeclampsia, PZP-positive extravillous trophoblasts are

245 evidence that urinary EVs are reflective of preeclampsia-related altered podocyte protein expression

246 feration/invasion which might be mediated by preeclampsia-related genes, suggesting a possible associ

247 , the absolute risk of ESKD among women with preeclampsia remains small.

248 r in vitro model might fill a vital niche in preeclampsia research.

249 t preeclampsia, and mothers with asthma with preeclampsia, respectively.

250 ate antenatal models of chorioamnionitis and preeclampsia, respectively.

251 F found adequate evidence that screening for preeclampsia results in a substantial benefit for the mo

252 ng micro particle (CMP) proteins will define preeclampsia risk while identifying clusters of disease

253 Evidence to estimate benefits and harms of preeclampsia screening and the test performance of diffe

254 pregnancies at increased risk of developing preeclampsia secreted significantly more STC-1 than norm

255 Preeclampsia should be considered as an important risk f

256 severe burns, the antiphospholipid syndrome, preeclampsia, sickle cell disease, and biomaterial-induc

257 ormed subgroup analyses according to preterm preeclampsia, small for gestational age (SGA), and women

258 Information on pregnancy complications (preeclampsia, small for gestational age, and spontaneous

259 tal biopsies from pregnancies complicated by preeclampsia, specifically targeting AT1-B2 heteromeriza

260 Preeclampsia status was determined by chart review, obst

261 in cumulative incidence curves, according to preeclampsia status, were apparent within 1 year of the

262 rmed in maternal plasma EVs from Control and Preeclampsia subjects by Western blot, and overall, lowe

263 ome type V is consistent with the process of preeclampsia superimposed upon clinical cardiovascular a

264 ng evaluation for the potential to influence preeclampsia susceptibility in women.

265 Women with preeclampsia sustained a higher incidence of adverse mat

266 ensitivity, which could explain the onset of preeclampsia symptoms at late-stage pregnancy as mechani

267 or early preterm preeclampsia, late preterm preeclampsia, term preeclampsia, and gestational hyperte

268 Any CAC was more prevalent after preeclampsia than after a normotensive pregnancy (20% ve

269 otential benefits and harms of screening for preeclampsia, the effectiveness of risk prediction tools

270 t morbidity and mortality, as is the case of preeclampsia, the main cause of maternal deaths globally

271 curacy of screening and diagnostic tests for preeclampsia, the potential benefits and harms of screen

272 of the pathological effects present in human preeclampsia, these models often do not represent the ph

273 nces made in the diagnosis and management of preeclampsia, this syndrome remains a leading cause of m

274 GF5/4q21 and SH2B3/12q24 also associate with preeclampsia through the maternal genome.

275 on of the maternal circulation in late-onset preeclampsia, thus sharing the pathophysiology of cardio

276 om the past several decades linking prenatal preeclampsia to altered neurodevelopment.

277 regnancies who were at high risk for preterm preeclampsia to receive aspirin, at a dose of 150 mg per

278 In preeclampsia, Tregs are fewer and display aberrant pheno

279 Among the cases of preeclampsia, two phenotypic sub clusters distinguished

280 inal changes in placental oxygenation during preeclampsia using spectral photoacoustic imaging.

281 The incidence of preeclampsia was 7.5%.

282 Preeclampsia was associated with an increased risk of de

283 Children born to mothers with preeclampsia were analyzed regarding risk of asthma, all

284 Associations between individual PFAS and preeclampsia were assessed, adjusting for parity, age, w

285 at median 10 gestational weeks and cases of preeclampsia were postnatally identified from registers.

286 Importantly, symptoms of preeclampsia were prevented by transgenic ARRB1 expressi

287 tween 1982 and 2012, including those who had preeclampsia, were identified.

288 tant, exposure is positively associated with preeclampsia which can result from aberrant trophoblasts

289 tion of an innate immune response evident in preeclampsia which may possibly be initially triggered b

290 Preeclampsia, which affects approximately 5% of pregnanc

291 such as intrauterine growth restriction and preeclampsia, which are characterized by uteroplacental

292 predict adverse pregnancy outcomes, such as preeclampsia, which can lead to mother and neonatal morb

293 relevant to cell proliferation/invasion and preeclampsia, while Western Blot data showed the activat

294 comprehensively examines the pathogenesis of preeclampsia with a specific focus on the mechanisms und

295 al and pathophysiological characteristics of preeclampsia with fetal growth restriction.

296 s are features of preeclamptic placentas and preeclampsia with FGR.

297 men of ~11.5 gestational weeks who developed preeclampsia with severe features (sPE; PE-CVS) revealed

298 ma without preeclampsia, without asthma with preeclampsia, with asthma without preeclampsia, and with

299 ynamic dysfunctions between the two types of preeclampsia, with special emphasis on the interorgan in

300 h mother, with values without asthma without preeclampsia, without asthma with preeclampsia, with ast