ライフサイエンスコーパス: midgestation

1 xpression resulted in embryonic lethality by midgestation.

2 lacentas, and altered placental structure at midgestation.

3 mately 25 and miR-17 approximately 92 die at midgestation.

4 nts with Diamond-Blackfan anemia, and die in midgestation.

5 ch were merely distorted in Pitx2 mutants at midgestation.

6 ient erythropoietin (Epo) production and die midgestation.

7 sed heart failure and embryonic lethality at midgestation.

8 but Gcn5(-/-) p53(-/-) embryos still die in midgestation.

9 required for in vivo FAK function until late midgestation.

10 lves inhibition of Gli3R and continues after midgestation.

11 Snx13-null mice were embryonic lethal around midgestation.

12 the medial to lateral axis, and only before midgestation.

13 cytokine-dominated mechanism operating after midgestation.

14 bors a large pool of pluripotent HSCs during midgestation.

15 and is fully compatible with development to midgestation.

16 F-3beta) in the pancreatic primordium during midgestation.

17 t, heart, lung, kidney, and limb buds during midgestation.

18 was highly expressed in endothelial cells at midgestation.

19 ion and that tetraploid cells may persist to midgestation.

20 atic precursors from the gut endoderm during midgestation.

21 yield Mrad9(-/-) pups, since embryos died at midgestation.

22 t that deficient embryos do not survive past midgestation.

23 e germ cells were developmentally delayed at midgestation.

24 mice deficient in either Mfn1 or Mfn2 die in midgestation.

25 the development of most mouse embryos beyond midgestation.

26 viable, double knockout embryos died around midgestation.

27 th a transient impairment of fetal growth in midgestation.

28 sis of the inner ear is greatly perturbed by midgestation.

29 embryos deficient in both proteins arrest at midgestation.

30 Most tbp(Delta N/Delta N) fetuses die in midgestation.

31 us progeny of homozygous females died before midgestation.

32 was markedly elevated in multiple nuclei at midgestation.

33 ty of homozygous mutant (Shp-2(-/-)) mice at midgestation.

34 yonic lethality of homozygous mutant mice at midgestation.

35 ch the eccentricity of the optic nerve until midgestation.

36 hypertrophy, peak wall stress normalized by midgestation.

37 nkeys (Macaca fascicularis) is lethal before midgestation.

38 3c double knockout (DKO) mice is arrested at midgestation.

39 he course of human retinal development up to midgestation.

40 embryo implantation that was sustained into midgestation.

41 pecifically in the lower diencephalon during midgestation.

42 e for PDPN in regulating eMk function during midgestation.

43 the expansion of the subplate region during midgestation.

44 r to clinical IUGE would be less relevant at midgestation.

45 and immunomodulation events that occur up to midgestation.

46 pitulate the tissue architecture in early to midgestation.

47 tribute to the HSC pool increase observed at midgestation.

48 death of homozygous Fbxl10-mutant embryos at midgestation.

49 2, to control their expression at and beyond midgestation.

50 BV abnormalities as Rasa1-null mice and died midgestation.

51 l embryos lack centrosomes but survive until midgestation.

52 120-catenin in the embryo proper, survive to midgestation.

53 ivors developed eye defects beginning around midgestation.

54 for sustaining proliferation of LaTP during midgestation.

55 n fetal exposure or metabolism of BPA during midgestation.

56 rm populations within the mouse embryo until midgestation.

57 hat functional synaptic contacts are rare at midgestation.

58 Twist1(-/-) embryos die at midgestation.

59 ly positioned metanephric mesenchyme (MM) in midgestation.

60 specific absence of most of the forebrain at midgestation.

61 ation, several inbred mouse strains abort at midgestation.

62 ull embryos undergo normal development until midgestation (12.5 to 13.5 days postcoitum), at which ti

63 neous depolarizations in human SP neurons at midgestation (17-23 gestational weeks) were not complete

64 e generated in the human cortical SVZ during midgestation (18-24 gw) under in vitro conditions.

65 In human brain at midgestation (19-21 weeks), huntingtin was detected in a

66 zone of the ganglionic eminences, whereas at midgestation (20 GW), they were also expressed in the te

67 embryonic death, revealing that most act at midgestation (8.5-10.5) or sooner.

68 H/PF/2013; n = 3 for PR isolate PRVABC59) at midgestation (86 to 95 days of gestation [dG]; term, 183

69 analysis of human cerebral patterning during midgestation, a critical epoch in cortical regionalizati

70 ic oxide synthase within human myometrium at midgestation, a time when the uterus is normally quiesce

71 In addition, at midgestation, aberrant nerve projection and arborization

72 r2 in the uterine deciduae of mice triggered midgestation abnormalities in decidualization that resul

73 fraction of double-mutant embryos exhibited midgestation abnormalities with perinatal lethality, via

74 gene in mice leads to embryonic lethality in midgestation accompanied by defective erythropoiesis.

75 onservation of enhancers decreases following midgestation across all tissues examined.

76 While Hb Null embryos die in midgestation, adult globin genes are not required for pr

77 In midgestation, after primary neurogenesis in compact vent

78 all regions of the human fetal brainstem at midgestation, an unexpected finding given the trophic ro

79 /- fetuses displayed transient anemia during midgestation and abnormal definitive erythropoiesis.

80 heir routine fetal ultrasound examination at midgestation and agreed to participate in the Advanced C

81 associated with maternal hemoglobin at both midgestation and at delivery (P < 0.01 for both).

82 rnal and cord blood samples were obtained at midgestation and at delivery, respectively.

83 mouse mutation chato, which causes arrest at midgestation and defects characteristic of convergent ex

84 subunit develop intracerebral hemorrhages at midgestation and die shortly after birth.

85 Although NMDA binding increased between midgestation and early infancy to moderately high adult

86 disruption of Raldh2 arrests development at midgestation and eliminates all RA synthesis except that

87 Here, we transiently induced CAErbB2 during midgestation and examined synapse restoration after indu

88 study, we show that Wdr34 mutant mice die in midgestation and exhibit open brain and polydactyly phen

89 ory component of the WAVE complex, arrest at midgestation and have defects in morphogenesis of all th

90 ng measured with 3H-LSD was observed between midgestation and infancy, and between infancy and maturi

91 binding did not change significantly between midgestation and infancy, except for an elevation in the

92 on of distal chromosome 7 (PatDup.d7) die at midgestation and lack placental spongiotrophoblast.

93 Whereas Osr1(-/-) mutant mice died at midgestation and Osr2(-/-) mutant mice had only subtle d

94 omolog1 (Disp1) mutation causes lethality at midgestation and prevents specification of ventral cell

95 per day) can prevent the death of embryos at midgestation and prevents the early embryonic abnormalit

96 sac undergoes cell death and degeneration at midgestation and the fetuses die over a range of several

97 hed the far peripheral edge of the retina by midgestation and the OPL by late gestation.

98 ic valvuloplasty can be performed for severe midgestation aortic stenosis in an attempt to prevent pr

99 primary aim was to determine whether FAV for midgestation aortic stenosis increases survival from fet

100 lvuloplasty (FAV) may prevent progression of midgestation aortic stenosis to hypoplastic left heart s

101 erwent fetal aortic valvuloplasty for severe midgestation aortic stenosis with evolving HLHS from Mar

102 ers of vitamin D and iron were determined at midgestation ( approximately 25 wk) and delivery ( appro

103 yvitamin D [1,25(OH)(2)D] were determined at midgestation ( approximately 26 wk) and at delivery in 1

104 on of LKLF by gene targeting die in utero at midgestation around day 12.5 due to severe hemorrhage, m

105 on of Rac1 results in embryonic lethality in midgestation (around E9.5), and defective development of

106 e fetal liver (FL) were also decreased after midgestation because of decreased cell proliferation and

107 These knock-in mice died in midgestation because of hemorrhaging in the central nerv

108 integrin beta8 (itgbeta8) gene die either at midgestation, because of insufficient vascularization of

109 Homozygous mutant mice died at midgestation, before embryonic day 11.5 (E11.5), with va

110 describe differences in cardiac function at midgestation between women who develop PE and those with

111 Importantly, in the absence of Etv2 at midgestation, binding of Etv2 at Ets-binding sites in th

112 ) showed normal morphological development to midgestation but died shortly thereafter.

113 Mutant embryos develop normally until midgestation but then exhibit a distinct block in the de

114 Cardiac pathology was not apparent at midgestation but was evident by day 2 of postnatal life,

115 bryos devoid of cytochrome c die in utero by midgestation, but cell lines established from early cyto

116 arly embryo inhibits vascular development at midgestation, but Edn2 overexpression in developing skin

117 l tetraploid embryos develop normally during midgestation, but encounter a secondary developmental bl

118 Mpc1 deletion was homozygous lethal in midgestation, but Mpc1 hypomorphs and tissue-specific de

119 The jaw of Pitx2 mutants was vestigial by midgestation, but significant size reductions were obser

120 hese tissues differ metabolically throughout midgestation, but we pinpointed gestational days (GD) 10

121 We show that human midgestation c-Kit(-) lineage-committed amniotic cells (

122 ablish whether routine cardiac assessment at midgestation can improve performance of screening for PE

123 eir germline Rb(-/-) counterparts, brains of midgestation chimeric embryos exhibited extensive ectopi

124 In addition, using organotypic human midgestation chorionic villous explants, we show that sy

125 In mouse, placental defects during midgestation commonly lead to embryonic lethality.

126 nsmission of anti-AAV IgG was inefficient in midgestation compared with term, suggesting that the mat

127 sues including testes were miscarried during midgestation, consistent with RTT-linked male embryonic

128 mary human RG that constitute only 1% of the midgestation cortex and classified them as ventricular z

129 o, but, in the mouse model, delivery at late midgestation could not transduce hematopoietic stem cell

130 log-like 2 (Drosophila)], and their death at midgestation could result from two inactive paternal cop

131 assayed replicated efficiently in early and midgestation cultures, and two isolates examined replica

132 n further insight, we examined the causes of midgestation death of embryos with paternal duplication

133 t in aortic arch artery smooth muscle during midgestation, despite intact neural crest cell migration

134 ne in mice results in embryonic lethality at midgestation due to hemorrhaging in the central nervous

135 AML1) gene results in embryonic lethality at midgestation due to hemorrhaging in the central nervous

136 Midgestation (e10.5) Pitx2(-/-) embryos have normally fo

137 By midgestation (e13-e16), PC5 mRNA expression in the devel

138 ., before the onset of corticogenesis, or in midgestation (E70-E81), when superficial cortical layers

139 175-350 cGy) in early gestation (E33-E42) or midgestation (E70-E90); eight nonirradiated macaques wer

140 c and vascular abnormalities, and die during midgestation (E9.5-10).

141 enchymal cells are abundantly distributed in midgestation (E9.5-12.5), and adult derivatives of the t

142 , the women were diagnosed with GD after the midgestation echocardiographic assessment (8.4%).

143 d by modified reverse transcription-PCR from midgestation embryo templates, using a degenerate consen

144 Expression of Brca2 was detected in midgestation embryos and adult testis, thymus, and ovary

145 region is less differentially methylated in midgestation embryos and, like most of the genome, is la

146 al chromosome 7 gene, Mash2, which in normal midgestation embryos exhibits spongiotrophoblast-specifi

147 een for abnormal morphological phenotypes of midgestation embryos identified five mutant lines; the p

148 d from mouse or rat prostatic epithelia from midgestation embryos or adult mice, when combined with t

149 We also observed rare gut bud structures in midgestation embryos that appear to represent murine exa

150 In midgestation embryos, Cbfbeta was expressed in populatio

151 In midgestation embryos, the most extensive expression of P

152 Ctgf is expressed in a variety of tissues in midgestation embryos, with highest levels in vascular ti

153 t is strikingly differentially methylated in midgestation embryos.

154 However, rapid DNA demethylation after midgestation erases these parental imprints, in preparat

155 e Intu null mutants are homozygous lethal at midgestation, exhibiting multiple defects including neur

156 The ALK1 homozygous embryos die at midgestation, exhibiting severe vascular abnormalities c

157 Midgestation features increasing oxygen and nutrient ava

158 phic features associated with progression of midgestation fetal AS to HLHS.

159 iation potential, were transplanted into the midgestation fetal Gunn rat liver via ultrasound-guided

160 ralipid on the adipose tissue development of midgestation fetal sheep.

161 alogously diminished ZIKV infection in human midgestation fetal- and maternal-derived tissue explants

162 Aortic stenosis in the midgestation fetus with a normal-sized or dilated left v

163 In midgestation fetuses with AS and normal LV length, rever

164 Fetal echocardiography can identify midgestation fetuses with AS who are at high risk for de

165 first evidence of detectable BPA sulfate in midgestation fetuses.

166 ples from 32 HLHS and 17 structurally normal midgestation fetuses.

167 st tbp(DeltaN/DeltaN) fetuses (>90%) died in midgestation from an apparent defect in the placenta.

168 Brg1(fl/fl):Tie2-Cre(+) embryos die at midgestation from anemia, as mutant primitive erythrocyt

169 a hypoplastic ventricular chamber and die in midgestation from cardiac insufficiency.

170 , approximately 50% Tgfb1-/- conceptuses die midgestation from defective yolk sac vasculogenesis.

171 owed that >99% of Bright(-/-) embryos die at midgestation from failed hematopoiesis.

172 s for an AML1-ETO allele (AML1-ETO/+) die in midgestation from haemorrhaging in the central nervous s

173 etinoic acid receptor gene RXR(alpha) die in midgestation from hypoplastic development of the myocard

174 als regulate myocardial proliferation during midgestation heart development.

175 sed in the embryonic mouse epicardium during midgestation heart development.

176 MET mRNA expression in the midgestation human fetal cerebral cortex is strikingly r

177 oding the major surfactant protein, SP-A, in midgestation human fetal lung (HFL) is dramatically indu

178 d in the brain and peripheral tissues of the midgestation human fetus.

179 Here we transcriptomically profiled the midgestation human spinal cord with single-cell resoluti

180 we used Nestin-cre to ablate beta-catenin at midgestation in developing CNS precursors to investigate

181 of Shp-2 leads to an embryonic lethality at midgestation in homozygous mutant mice.

182 programmes in the placenta and embryo during midgestation in mice.

183 emporarily expressed in neural tissue during midgestation in mice.

184 ressed abundantly in the proximal CCS during midgestation in mice.

185 carboxylic acid (TCA) cycle rises throughout midgestation in the embryo but not in the placenta.

186 hortly after it becomes a distinct tissue at midgestation in the mouse: slowly dividing self-renewing

187 lso associated with impaired fetal growth in midgestation independent of fetal genotype, indicating p

188 children born to GDM mothers and exposed to midgestation infections have an increased vulnerability

189 d forward genetic screen we discovered a new midgestation lethal mouse mutant, called trex, which dis

190 e loss of PKA activity in the mouse leads to midgestation lethality and a completely ventralized neur

191 Complete loss of Gpr161 in mouse causes midgestation lethality and increased Shh signaling in th

192 ng one copy each of Smad2 and Smad3 suffered midgestation lethality due to liver hypoplasia and anemi

193 recessive allele of Axin2, canp, that causes midgestation lethality in homozygotes.

194 N1ICD(+) embryos showed midgestation lethality with defects in angiogenic remode

195 Consistent with a midgestation lethality, UTX-null male and female ES cell

196 entified a mutation in Wdr35 as the cause of midgestation lethality, with abnormalities characteristi

197 However, loss of endogenous TAK1 causes midgestation lethality, with defective yolk sac and intr

198 lts in placental defects and frequent (>90%) midgestation lethality.

199 to an underdeveloped ventricular chamber and midgestation lethality.

200 re, block Sonic hedgehog signaling and cause midgestation lethality.

201 Protein abundance of TfR1 was related to midgestation maternal serum ferritin (SF) (beta = -0.32;

202 of prothrombin-deficient embryos die during midgestation, mice lacking both PAR4 and fibrinogen deve

203 and vitelline and umbilical arteries of the midgestation mouse embryo.

204 ent of a variety of embryonic tissues in the midgestation mouse embryo.

205 loss of CCBE1 also confers severe anemia in midgestation mouse embryos due to defective definitive e

206 viously uncharacterized gene is expressed in midgestation mouse embryos in the branchial arches and l

207 rom aorta/gonad/mesonephros (AGM) regions of midgestation mouse embryos revealed a robust innate immu

208 and in the forebrain, face, and limb buds of midgestation mouse embryos.

209 test these possibilities by producing cloned midgestation mouse fetuses from three different donor so

210 frequency and spectrum of point mutations in midgestation mouse fetuses produced by either natural re

211 d at understanding how specific genes in the midgestation mouse placenta are regulated.

212 econd-trimester human NPC markers aligned to midgestation murine NPCs.

213 elivery, we did yolk sac vessel injection at midgestation of mouse embryos.

214 ECA as well as SBA are already present from midgestation onward.

215 rsely associated with erythropoietin at both midgestation (P <0.05) and delivery (P <0.001).

216 In contrast, during midgestation perforin was no longer required for pregnan

217 However, c-jun-null mice die at midgestation, precluding critical investigation.

218 mice remained susceptible to alphaGalCer at midgestation, pregnant BALB/cJ mice were resistant to it

219 emonstrate that somatic gene transfer to the midgestation rat placenta may be efficiently accomplishe

220 In contrast, exposure to x-rays at midgestation reduced cortical thickness, mainly due to e

221 Furthermore, disruption of Rasa1 in midgestation resulted in LEC apoptosis in developing LV

222 /3cDKO) prevented inner ear morphogenesis at midgestation, resulting in indiscernible cochlear and ve

223 Surprisingly, mostly during midgestation, SP cells become secondarily displaced and

224 expressed in the mouse placenta beginning at midgestation, specifically in the spongiotrophoblasts.

225 wn-regulated in Gpr48-/- fetal livers during midgestation stage through the cAMP-PKA-CREB pathway, su

226 Homozygous Wnt7b mutant mice die at midgestation stages as a result of placental abnormaliti

227 pha(-/-) embryos to proceed normally through midgestation stages of development.

228 mbers that regulate the postimplantation and midgestation stages of pregnancy.

229 s are colocalized in the cribriform plate at midgestation, suggesting that Ark is expressed in migrat

230 tic females to exogenous testosterone during midgestation, suggesting that early exposure to androgen

231 nt temporally limited neurogenesis defect at midgestation that correlates with long-lasting effects o

232 After midgestation, the highest level of mRNA is in the mammil

233 ies in the Hs2st(-/-) mice occurs only after midgestation, the most dramatic being the complete failu

234 helial expression of the Etv2 gene ceases at midgestation; therefore, vascular development past this

235 bunits in human white matter and cortex from midgestation through early childhood.

236 o their intra- and subcortical targets, from midgestation through infancy.

237 Homozygous mGATA-3 mutant embryos die at midgestation, thus complicating the analysis of its cont

238 creased from 5.19 mm at Fwk 8 to 20.92 mm at midgestation to 32.88 mm just after birth.

239 in a large-animal model, ASOs were delivered midgestation to fetal sheep by IA or intracranial inject

240 ith the increase in plasma free choline from midgestation to late gestation (P < 0.001).

241 spiratory function in the human medulla from midgestation to maturity.

242 000 postsynaptic density (PSD) proteins from midgestation to young adulthood, we find that PSD matura

243 long-acting anandamide in wild-type mice at midgestation triggered premature decidual senescence uti

244 At midgestation, TWH expression identifies subsets of spina

245 SoxC triple-null embryos die at midgestation unturned and tiny, with normal patterning a

246 In vivo, ZnT1 mRNA was abundant in the midgestation visceral yolk sac and placenta.

247 Higher prenatal PM2.5 exposure at midgestation was associated with asthma development by a

248 Pregnancy loss during midgestation was correlated with dramatically higher ser

249 t with the loss of a perforin requirement at midgestation was the emergence of strain-dependent varia

250 zygous male mice with Nsdhl mutations die by midgestation, we generated a conditional targeted Nsdhl

251 ersely associated with PM2.5 exposure during midgestation (weeks 12-25 for cord blood and weeks 15-27

252 e, nucleated EryPs begin to circulate around midgestation, when connections between yolk sac and embr

253 By midgestation, when invasion is complete, MMP levels are

254 ominant populations in uteri during early to midgestation, whereas T and B cells were constrained.

255 gamma-aminobutyric acid) neurogenesis around midgestation, which coincides with an onset of oligodend

256 FOG-2(-/-) embryos die at midgestation with a cardiac defect characterized by a th

257 Mutants, however, die at midgestation with cardiovascular and skeletal defects, d

258 ssion is blocked briefly in mouse embryos at midgestation with citral (a general alcohol dehydrogenas

259 Murine embryos nullizygous for Rb die midgestation with defects in cell cycle regulation, cont

260 Rb(-/-) mouse embryos die at midgestation with defects in cell cycle regulation, cont

261 Mice deficient in Shp-2 die at midgestation with defects in mesodermal patterning, and

262 Piezo1-deficient embryos die at midgestation with defects in vascular remodeling, a proc

263 We find that Adm(-/-) embryos die at midgestation with extreme hydrops fetalis and cardiovasc

264 TKO mice died at midgestation with major defects in the circulatory syste

265 d glomeruli fail to form, and animals die at midgestation with neural tube closure and placental defi

266 expressed isoforms (JNK1 and -2) die during midgestation with neural tube closure defects and brain

267 ale embryos for several Nsdhl alleles die in midgestation with placental insufficiency.

268 Strip1-null mutants arrest development at midgestation with profound disruptions in the organizati

269 the O(2)-regulated HIF-1alpha subunit die at midgestation with severe cardiac malformations and vascu

270 T mutant Brachyury mice die in midgestation with severe defects in posterior mesodermal

271 acking protein O-fucosyltransferase 1 die at midgestation with severe defects in somitogenesis, vascu

272 myoglobin-deficient embryos die in utero at midgestation with signs of cardiac failure.

273 ce homozygous for the Shp-2 mutation died at midgestation with similar phenotype to FAK and fibronect

274 l embryonic development, as null mice die in midgestation with widespread unscheduled cell proliferat

275 port here that UBR1-/-UBR2-/- embryos die at midgestation, with defects in neurogenesis and cardiovas

276 t of integrin beta8-deficient embryos die at midgestation, with evidence of insufficient vascularizat

277 Most Dmap1(+/+) progeny died during midgestation, with loss of DNA methylation on imprinted

278 for a null allele at the Hif1a locus die at midgestation, with multiple cardiovascular malformations

279 and Ets2 resulted in embryonic lethality at midgestation, with striking defects in vascular branchin

280 ial hemozoin accumulation in the placenta at midgestation, with the latter associated with induction