ライフサイエンスコーパス: intrauterine

1 nferred by (+)-naloxone administration after intrauterine administration of heat-killed E. coli.

2 The intrauterine and early life environments have been linke

3 Nutritional status during intrauterine and early postnatal life impacts the risk o

4 observations support previous findings that intrauterine and perinatal factors can have long-lasting

5 Intrauterine and systemic infection and inflammation cau

6 Nutritional status during intrauterine and/or early postnatal life has substantial

7 use of effective contraception (hormonal or intrauterine) at 4 months.

8 We hypothesized that intrauterine bacterial infection induces changes in micr

9 tion that replicates the in utero fetus, but intrauterine body composition reference charts for prete

10 uestions abound as to the sensitivity of the intrauterine brain to environmental programming, to wind

11 The amnion membrane that lines the human intrauterine cavity is composed of amnion epithelial cel

12 e placenta restricts microbial access to the intrauterine compartment.

13 cal factors including age, prematurity, sex, intrauterine complications, and postnatal adversity.

14 variability and carries a memory of adverse intrauterine conditions experienced during the last thir

15 Furthermore, modeling of intrauterine conditions has indicated a substantially gr

16 A better understanding of intrauterine conditions that influence offspring disease

17 sparing response may be affected by adverse intrauterine conditions, this area of research has been

18 ous embryos from 43.9 mm to 117.4 mm and the intrauterine content of the maternal recognition of preg

19 We compared gVL, plasma VL (pVL), and intrauterine contraceptive (IUC) continuation between th

20 taining the pubertal milestones according to intrauterine cumulative (weeks) and trimester-specific a

21 Intrauterine death was observed in 1 fetus (<1%) in the

22 o group: abortion, n=22; blighted ovum, n=1; intrauterine death, n=2; early neonatal death, n=1; and

23 oup: abortion, n=20; blighted ovum, and n=2; intrauterine death, n=2; placebo group: abortion, n=22;

24 men had a miscarriage, and three fetuses had intrauterine death.

25 measure of adverse maternal-fetal outcomes (intrauterine death/stillbirth, poor fetal growth, aborti

26 CHDs with univentricular outcome (P<0.0001), intrauterine deaths (P=0.01), and terminations of pregna

27 stores in the KO fetus, suggesting that this intrauterine deficiency might have deleterious consequen

28 CHDs with univentricular outcome (P<0.0001), intrauterine demise (P=0.036), and early termination (P<

29 Rationale: Exposure to air pollution during intrauterine development and through childhood may have

30 ronic gestational hypoxia (13%) during their intrauterine development had decreased ovarian primordia

31 ble to a high vulnerability to stress during intrauterine development of a maturing organism.

32 rel intrauterine system (LNG-IUS) and copper intrauterine device (C-IUD) in Cape Town, South Africa.

33 ntrauterine system (LNG-IUS, n = 11), copper intrauterine device (cu-IUD, n = 13) or levonorgestrel-c

34 ce data from women in the United States with intrauterine device (IUD) insertions during 2011-2018, t

35 esterone Acetate (DMPA), implant, pills, and intrauterine device (IUD)) were promoted and provided to

36 distinguish those reporting use of (1) LARC (intrauterine device or implant), (2) oral contraceptives

37 ould select birth control pills; condoms; an intrauterine device or implant; injection, patch, or rin

38 Dislodgement of an intrauterine device was reported in 13 women who used th

39 een 1 week and 13 months of insertion of the intrauterine device.

40 Contraceptive implants and intrauterine devices (IUDs) are long-acting reversible c

41 The contraceptive effectiveness of intrauterine devices (IUDs) has been attributed in part

42 nsdermal patches, intravaginal rings (IVRs), intrauterine devices (IUDs), injectables and subdermal i

43 rm selecting condoms, oral contraception, or intrauterine devices (IUDs).

44 methods (OCP 28% versus injectable/implants/intrauterine devices [IUDs] 18%; p = 0.06).

45 eversible contraception (LARC), specifically intrauterine devices and implants, offers an unprecedent

46 sing other contraceptive methods, except for intrauterine devices and permanent methods, had 3.1-4.1

47 -acting reversible contraceptives (implants, intrauterine devices) are associated with low failure ra

48 as modern contraceptive methods: oral pills, intrauterine devices, injectables, male and female steri

49 e little evidence to support a strong causal intrauterine effect of incrementally greater maternal BM

50 However, we found evidence for acausal intrauterine effect of maternal BMI on newborn methylati

51 h maternal diabetes, suggesting sex-specific intrauterine effects on adult metabolic health.

52 owever, it is unclear whether this is due to intrauterine effects.

53 f insanity could arise from psychological or intrauterine effects.

54 ies of human subjects exposed to an abnormal intrauterine environment (e.g., individuals with a low b

55 transgenic animals lacking NOS3 that adverse intrauterine environment alters fetal programming of vas

56 c animals, we previously showed that adverse intrauterine environment alters vascular reactivity in a

57 mechanisms of bacterial translocation to the intrauterine environment and immune responses to the pre

58 Perturbations in the intrauterine environment can result in lifelong conseque

59 Our study indicates that adverse intrauterine environment contributes, along with multipl

60 rozygous NOS3(+/-) (KOM: mother with adverse intrauterine environment from NOS3 deficiency), paternal

61 The role of the intrauterine environment in mediating this effect is sti

62 evidence supports an important role for the intrauterine environment in shaping fetal development an

63 The intrauterine environment is particularly vulnerable to e

64 It is well known that the intrauterine environment plays an important role in medi

65 t-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it ca

66 The intrauterine environment provides a key interface betwee

67 gs suggest that adaptation to the suboptimal intrauterine environment underlying chronic causes of pr

68 Our results suggest that the maternal intrauterine environment, as proxied by maternal SNPs th

69 lead to the translocation of bacteria to the intrauterine environment, eliciting an inflammatory resp

70 that supports prenatal growth in the hypoxic intrauterine environment, to the postnatal state wherein

71 stational age, parental characteristics, and intrauterine environment.

72 wth and lung function and prevents RVH after intrauterine ETX exposure.

73 These results support the notion that intrauterine exposure to a major psychological maternal

74 for further studies examining the effects of intrauterine exposure to antidiabetic agents on longitud

75 ion (MR) to investigate the causal effect of intrauterine exposure to greater maternal body mass inde

76 nd obesity in early life in association with intrauterine exposure to maternal hyperglycemia, a commo

77 Following intrauterine exposure to metformin for treatment of mate

78 her causes included hereditary factors (4%), intrauterine factors (2.0%) and perinatal factors (4.4%)

79 n maternal reproductive tract tissues and in intrauterine fetal compartments.

80 sions (one pregnancy resulted in p-aHUS, one intrauterine fetal death occurred, and seven pregancies

81 y, major fetal neurologic abnormalities, and intrauterine fetal death).

82 There were 3 intrauterine fetal deaths (1 woman had used LMWH); 9 cas

83 Of the 872 terminations of pregnancy and intrauterine fetal deaths, 189 fetopsies were available:

84 The mother from the family with recurrent intrauterine fetal demise exhibited the CALM3-E141K muta

85 births were normal with the exceptions of an intrauterine fetal demise owing to acrania and a molar p

86 There were eight spontaneous abortions, 18 intrauterine fetal demise, 672 pregnancy terminations an

87 ffected offspring or multiple occurrences of intrauterine fetal demise.

88 Intrauterine fetal growth restriction (IUGR) is often as

89 e pregnancies; and previous pre-eclampsia or intrauterine fetal growth restriction.

90 Early diagnosis offers an opportunity for a intrauterine fetal intervention in potentially lethal ca

91 natal ultrasound scan showed a single, live, intrauterine foetus corresponding to a gestational age o

92 nd whose mothers have chorioamnionitis or an intrauterine foreign body.

93 rly pathogenesis, safety and efficacy of AAV-intrauterine gene transfer (IUGT) requires assessment.

94 owing adeno-associated viral vector-mediated intrauterine gene transfer in early-gestation fetal maca

95 natal ultrasound scan showed a single, live, intrauterine gestation corresponding to a gestational ag

96 reased risk of spontaneous abortion and poor intrauterine growth although the underlying mechanisms r

97 impaired DLK1 expression and to predict poor intrauterine growth and complications of pregnancy.

98 between 1997 and 2014, indicating increased intrauterine growth and population health improvements.

99 Plasmodium falciparum exposure had retarded intrauterine growth between gestational ages of 212 and

100 supporting the growing body of evidence that intrauterine growth has a lifelong impact on cardiovascu

101 It is unclear whether abnormal intrauterine growth influences arterial morphology durin

102 Intrauterine growth of all investigated UCDs and postnat

103 These results indicate that the intrauterine growth of fetal arterial LD and wall layer

104 examined the extent to which information on intrauterine growth patterns improved prediction of chil

105 different brain areas between two groups of intrauterine growth restricted (IUGR) foetuses and contr

106 of membranes (aOR, 1.42; 95% CI, 1.08-1.86), intrauterine growth restriction (aOR, 1.17; 95% CI, 1.01

107 Placental insufficiency causes intrauterine growth restriction (IUGR) and disturbances

108 OINTS: Maternal nutrient restriction induces intrauterine growth restriction (IUGR) and leads to heig

109 Intrauterine growth restriction (IUGR) and low birth wei

110 ltitude (HA) residence increases the risk of intrauterine growth restriction (IUGR) and preeclampsia

111 Race/ethnicity is associated with intrauterine growth restriction (IUGR) and small-for-ges

112 igh altitude (HA) increases the incidence of intrauterine growth restriction (IUGR) approximately thr

113 inguish small for gestational age (SGA) from intrauterine growth restriction (IUGR) as independent pr

114 Intrauterine growth restriction (IUGR) enhances risk for

115 Fetuses with intrauterine growth restriction (IUGR) have lower muscle

116 Fetuses with intrauterine growth restriction (IUGR) have reduced musc

117 Previous studies in fetuses with intrauterine growth restriction (IUGR) have shown that a

118 complications such as preeclampsia (PE) and intrauterine growth restriction (IUGR) in 20% of patient

119 KEY POINTS: Intrauterine growth restriction (IUGR) increases offspri

120 Intrauterine growth restriction (IUGR) is a pathology of

121 Intrauterine growth restriction (IUGR) is associated wit

122 Intrauterine growth restriction (IUGR) is associated wit

123 Intrauterine growth restriction (IUGR) leads to offsprin

124 Placental insufficiency and intrauterine growth restriction (IUGR) of the fetus affe

125 We hypothesized that intrauterine growth restriction (IUGR) offspring hearts

126 duced skeletal muscle mass in the fetus with intrauterine growth restriction (IUGR) persists into adu

127 KEY POINTS: Rodent models of intrauterine growth restriction (IUGR) successfully iden

128 Rodent models of intrauterine growth restriction (IUGR) successfully iden

129 KEY POINTS: Adults who were affected by intrauterine growth restriction (IUGR) suffer from reduc

130 med MIRAGE syndrome that is characterized by intrauterine growth restriction (IUGR) with gonadal, adr

131 TRACT: Maternal nutrient restriction induces intrauterine growth restriction (IUGR), increasing later

132 BSTRACT: Maternal nutrient reduction induces intrauterine growth restriction (IUGR), increasing risks

133 Metabolic syndrome (MetS), following intrauterine growth restriction (IUGR), is epigeneticall

134 t is one of the main etiological factors for intrauterine growth restriction (IUGR).

135 as not been shown to prevent preeclampsia or intrauterine growth restriction (IUGR).

136 down-regulated in placentas of infants with intrauterine growth restriction (IUGR).

137 High-altitude hypoxia causes intrauterine growth restriction and cardiovascular progr

138 often leads to abortion, premature delivery, intrauterine growth restriction and low birth weight.

139 ads to devastating fetal outcomes, including intrauterine growth restriction and microcephaly.

140 tion and placental development, resulting in intrauterine growth restriction and perinatal lethality.

141 ctor to poor placental perfusion, leading to intrauterine growth restriction and preeclampsia, is the

142 associated with pregnancy disorders such as intrauterine growth restriction and preeclampsia, which

143 ic membranes of placentas from newborns with intrauterine growth restriction and underlying congenita

144 rediction and Prevention of Preeclampsia and Intrauterine Growth Restriction cohort, multiple serial

145 ging mosquito-borne virus recently linked to intrauterine growth restriction including abnormal fetal

146 Intrauterine growth restriction is associated with a nep

147 Intrauterine growth restriction is associated with short

148 dence from preclinical studies suggests that intrauterine growth restriction is protective against la

149 dies have evaluated the effect of malaria on intrauterine growth restriction on the basis of the feta

150 ome (3 women had used LMWH); and 11 cases of intrauterine growth restriction or placental insufficien

151 with normal outcomes (N = 29) and those with intrauterine growth restriction or preeclampsia (N = 12)

152 results of these meta-analyses suggest that intrauterine growth restriction protects against allergi

153 priate management of pregnancies at risk for intrauterine growth restriction relies on accurate ident

154 ommon pregnancy complication associated with intrauterine growth restriction that may influence respi

155 centation (cases who had preeclampsia and/or intrauterine growth restriction) and 2 cases that could

156 rediction and Prevention of Preeclampsia and Intrauterine Growth Restriction) study were followed up

157 ization defects can cause poor placentation, intrauterine growth restriction, and early parturition l

158 ternal morbidity, stillbirth, preterm birth, intrauterine growth restriction, and fetal congenital an

159 ing miscarriage, fetal death, preterm birth, intrauterine growth restriction, and fetal microcephaly,

160 n gestational diseases such as preeclampsia, intrauterine growth restriction, and gestational diabete

161 a, congenital transmission, pup viral loads, intrauterine growth restriction, and pup mortality compa

162 ons, such as severe forms of preeclampsia or intrauterine growth restriction, are thought to arise fr

163 rm included placental growth retardation and intrauterine growth restriction, evidence of placental a

164 ognitive impairment, behavioral alterations, intrauterine growth restriction, feeding problems, and v

165 neutrophils at the fetal-maternal interface, intrauterine growth restriction, impaired placental deve

166 trate that ZIKV(BR) infects fetuses, causing intrauterine growth restriction, including signs of micr

167 condition is characterized by short stature, intrauterine growth restriction, lipoatrophy and a facia

168 n papillomavirus may also be associated with intrauterine growth restriction, low birth weight, and f

169 l outcomes for the fetus and newborn include intrauterine growth restriction, low birth weight, and s

170 DNA in amniotic fluid and/or newborn saliva, intrauterine growth restriction, preterm deliveries, and

171 a single First Nations population and causes intrauterine growth restriction, severe microcephaly, cr

172 us (ZIKV) infection in pregnant women causes intrauterine growth restriction, spontaneous abortion, a

173 rlying placental pathologies associated with intrauterine growth restriction, which is a significant

174 including pre-term birth, pre-eclampsia, and intrauterine growth restriction-are common interrelated

175 ancy complications, such as preeclampsia and intrauterine growth restriction.

176 with structural malformations and linked to intrauterine growth restriction.

177 xy for the pathological process of interest, intrauterine growth restriction.

178 or gestational age and those with pathologic intrauterine growth restriction.

179 actor and placental growth factor levels and intrauterine growth restriction.

180 tarting on gestational day 14.5 that induced intrauterine growth restriction.

181 ding microcephaly, spontaneous abortion, and intrauterine growth restriction.

182 y represent a useful therapeutic approach to intrauterine growth retardation due to placental vascula

183 and congenital anemia accompanied by either intrauterine growth retardation or neutropenia.

184 es, including the risk of status dystonicus, intrauterine growth retardation, and endocrinopathies.

185 ients from 4 kindreds, all of whom displayed intrauterine growth retardation, chronic neutropenia, an

186 was characterized by ID, ASD, microcephaly, intrauterine growth retardation, febrile seizures in inf

187 n (IFN) during pregnancy are associated with intrauterine growth retardation, preterm birth, and feta

188 ramming of offspring phenotype by suboptimal intrauterine growth.

189 ontribute to the clinical outcomes following intrauterine HCMV infection.

190 .5-2-fold increased female susceptibility to intrauterine HIV infection.

191 tal intermediary responsible for maintaining intrauterine homeostasis.

192 le of O-T1D suggests that factors other than intrauterine hyperglycemia may contribute to the decreas

193 Exposure to chronic intrauterine hypoxia has major short- and long-term cons

194 Intrauterine hypoxia is a reason for impaired kidney dev

195 velopment and to derive from a disruption in intrauterine immune homeostasis, though the exact origin

196 e role of B cells in preconception and early intrauterine immune priming.

197 bacterium nucleatum, a bacterium linked with intrauterine infection and preterm birth.

198 gest that there is currently no evidence for intrauterine infection caused by vertical transmission i

199 Intrauterine infection is a major detriment for maternal

200 Chorioamnionitis is caused by intrauterine infection with microorganisms including Can

201 the hydrosalpinx induction in CBA/J mice by intrauterine infection with plasmid-free C. muridarum a

202 f preterm births are attributed to ascending intrauterine infection, and Ureaplasma parvum (UP) is co

203 s in infants born with microcephaly and ZIKV intrauterine infection.

204 ng from preterm labor, is commonly caused by intrauterine infection/inflammation.

205 dity, often triggered by chorioamnionitis or intrauterine inflammation (IUI) with or without infectio

206 ociation between prenatal PM2.5 exposure and intrauterine inflammation (IUI), an important risk facto

207 Intrauterine inflammation and maternal exposure to ambie

208 hat male but not female offspring exposed to intrauterine inflammation demonstrated impaired performa

209 Prior work has described induction of intrauterine inflammation in mice with a single injectio

210 Intrauterine inflammation is an etiological factor that

211 ion and prevent pulmonary hypertension after intrauterine inflammation is controversial.Objectives: T

212 Lastly, we overview the effects of intrauterine inflammation on neurodevelopment.

213 /-)) mice exhibited a greater sensitivity to intrauterine inflammation, as indicated by decreased tim

214 Histologic chorioamnionitis (HCA) reflects intrauterine inflammation, can trigger a fetal inflammat

215 Here, we used the established mouse model of intrauterine inflammation-induced PTB to determine wheth

216 Towards this goal, we used a maternal intrauterine inflammation-induced rabbit model of CP to

217 mer nanoparticle (DNAC), in a mouse model of intrauterine inflammation.

218 rly relevant in the context of pregnancy and intrauterine inflammation.

219 d reduces perinatal brain injury in cases of intrauterine inflammation.

220 Maternal intrauterine inflammation/infection is a major risk fact

221 Histological chorioamnionitis (HCA) is an intrauterine inflammatory condition that increases the r

222 O128:B12) were administered to CD1 mice via intrauterine injection at gestational day 16.

223 eterm delivery than wild type mice following intrauterine injection of 1 mug of LPS, and this is acco

224 tion-induced labour, where ultrasound guided intrauterine injection of lipopolysaccharide (LPS) at E1

225 (-)) or high dose fluoride (HF(-)) and given intrauterine injections of lipopolysaccharide (LPS) or p

226 Intrauterine inoculation at embryonic day (E) 10, but no

227 The intrauterine inoculation of the CBA/J mice with plasmid-

228 anism ascension to the oviduct following the intrauterine inoculation.

229 developmental domain for ovulation induction/intrauterine insemination (aOR, 1.00; 95% CI, 0.57-1.77

230 We identified 47,628 live-births after intrauterine insemination (n = 24,962) and in-vitro fert

231 ration is critical to achieving a successful intrauterine insemination and requires the processing of

232 allowing satellite doctor's offices to offer intrauterine insemination as an option for patients with

233 conceived through in-vitro fertilization or intrauterine insemination.

234 expectant management or the women underwent intrauterine insemination.

235 categorized into ART and ovulation induction/intrauterine insemination.

236 sfer), with no recent exposure to disruptive intrauterine instrumentation (e.g., hysteroscopy).

237 In many mammals, intrauterine interactions between brothers and sisters l

238 Such intrauterine interactions often are mediated by sex ster

239 er, over the last 3 decades, improvements in intrauterine interventions and perinatal intensive care

240 ant mice to control or HFD during pregnancy (intrauterine [IU]) and lactation (L).

241 Undernutrition during intrauterine life and early childhood is hypothesised to

242 ergenerational transmission may begin during intrauterine life via the effect of maternal CT exposure

243 smission that may operate as early as during intrauterine life.

244 BL/6J wild-type PTB mouse model of IUI given intrauterine LPS, an IRAK1 inhibitor significantly decre

245 reduced the incidence of PTB in a validated intrauterine LPS-induced PTB mouse model, decreased uter

246 y genetic or lifestyle factors than a causal intrauterine mechanism.

247 ar dysfunction in rat offspring, however the intrauterine mechanisms involved remain unknown.

248 mic cardio-metabolic profile are causal, via intrauterine mechanisms, or due to shared familial facto

249 so, whether this association is causal, via intrauterine mechanisms, or explained by shared familial

250 amilial lifestyle confounding rather than to intrauterine mechanisms.

251 fects lifelong risk of offspring fatness via intrauterine mechanisms.

252 l perinatal and childhood outcomes following intrauterine metformin exposure.

253 Since the intrauterine milieu plays a critical role in childhood g

254 studies; information on important sequelae, intrauterine mortality, and termination of pregnancy; an

255 are amongst the most common complications of intrauterine omega-6 PUFA excess, cellular underpinnings

256 umans, parturition is currently viewed as an intrauterine outbreak of inflammation, accompanied by a

257 ndings emphasize the relevance of sufficient intrauterine oxygenation for normal renal stroma differe

258 The intrauterine period is a critical time wherein developme

259 this effect may originate during the child's intrauterine period of life, which may have downstream n

260 hat this effect may start during the child's intrauterine period of life.

261 sion that can occur during pregnancy, in the intrauterine period, during labour or even breastfeeding

262 The intrauterine phase (embryonic day 21) is earmarked by a

263 Experimental IUGR identifies an intrauterine phase with inhibition of angiogenic signali

264 Serial fetal blood sampling (FBS) and intrauterine platelet transfusions (IUPT), as well as we

265 s have been shown to depend, in part, on the intrauterine position during development of female fetus

266 etinal ganglion cells reserve is affected by intrauterine processes that affect birth weight.

267 e mass in wild-type offspring, suggesting an intrauterine programming effect.

268 attributable to genetic effects, and not to intrauterine programming.

269 elicited after cPAF administered by i.p. or intrauterine routes.

270 ome (CRS) includes disorders associated with intrauterine rubella infection.

271 disease" hypothesis, which suggests that the intrauterine signals that compromise fetal growth also a

272 cending GBS infection from the vagina to the intrauterine space is associated with preterm birth, sti

273 IUC) continuation between the levonorgestrel intrauterine system (LNG-IUS) and copper intrauterine de

274 rom women using the levonorgestrel-releasing intrauterine system (LNG-IUS, n = 11), copper intrauteri

275 urrently or recently used the progestin-only intrauterine system also had a higher risk of breast can

276 I, 1.55-1.69); and users of a levonorgestrel intrauterine system, 1.4 (95% CI, 1.31-1.42).

277 long-term anticoagulation, a levonorgestrel intrauterine system, tranexamic acid (during menstrual f

278 acting (e.g. 3-5 years) levonorgestrel (LNG) intrauterine systems (IUSs), such as Mirena(R), is chall

279 These products include implants, intrauterine systems, and vaginal rings.

280 able cases, we find evidence to suggest that intrauterine therapy provides benefits during the perina

281 Information on the intrauterine trajectory through which birth weight was a

282 However, the mechanism of intrauterine transmission and the cell types involved re

283 mmune women during pregnancy and the rate of intrauterine transmission in these women are yet to be d

284 Our results suggest a mechanism for intrauterine transmission in which ZIKV gains access to

285 eading to nonprimary maternal infections and intrauterine transmission is not well defined.

286 ates that can modify maternal infections and intrauterine transmission, the source of virus leading t

287 of odorant binding protein six in the gut of intrauterine tsetse larvae.

288 Brain damage was confirmed through intrauterine ultrasonography and was complemented by mag

289 uch as repeated spontaneous abortion, sudden intrauterine unexpected foetal death syndrome and stillb

290 noxynol-9, 24 h pre-inoculation, facilitates intrauterine UP infection, upregulates pro-inflammatory

291 aracterized by sequential colonisation of i) intrauterine/vaginal birth associated taxa, ii) skin der

292 acteristics of COVID-19 in pregnancy and the intrauterine vertical transmission potential of COVID-19

293 Evidence of intrauterine vertical transmission was assessed by testi

294 here is sufficient evidence to conclude that intrauterine Zika virus infection is a cause of microcep

295 nfants with presumed or laboratory-confirmed intrauterine Zika virus infection.

296 s with microcephaly associated with presumed intrauterine ZIKV infection in Salvador, Bahia, Brazil.

297 nd neurological anomalies observed following intrauterine ZIKV infection.

298 -be-described outcomes to be associated with intrauterine ZIKV infection.

299 ng on brain tissue from a 20-week fetus with intrauterine ZIKV infection.

300 d for a variety of anomalies associated with intrauterine ZIKV infection.