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1 e, but it does represent a potential site of perinatal acquisition of S. agalactiae, a major cause of
4 nd after adjustment for sociodemographic and perinatal adversities and IQ, psychotic experiences at a
5 follicle assembly in the mouse occurs during perinatal ages and largely determines the ovarian reserv
6 DA) neurons of the VTA in rat pups following perinatal alcohol and joint nicotine-alcohol exposure.
11 stakeholders to inform strategies to reduce perinatal and childhood mortality in sub-Saharan Africa
12 bit sustained GI colonization following both perinatal and postnatal exposure to GBS, with 21% and 27
15 National registries provided information on perinatal and sociodemographic characteristics, on psych
16 In line with this, we identified an altered perinatal and/or postnatal expression of genes involved
17 al, and behavioral consequences of prenatal, perinatal, and adolescent exposure to cannabis/delta-9-t
20 tal exposure to testosterone proprionate, 3) perinatal androgen exposure guides bone marrow MC progen
21 n postnatal day 4, shortly after a transient perinatal androgen surge in males that could play an org
22 s is linked with the naturally high level of perinatal androgens and can be recapitulated in females
26 the intestinal microbiome but the effects of perinatal antibiotics on gut microbiome in vaginally del
30 the present work is to analyze the effect of perinatal asphyxia on different subpopulations of GABAer
31 common underlying causes of stillbirth were perinatal asphyxia or hypoxia (130 [72%] of 180 stillbir
32 ications (187 [42%] of 449 neonatal deaths), perinatal asphyxia or hypoxia (98 [22%]), and neonatal s
36 ors in offspring, but how it interplays with perinatal brain injury (especially birth asphyxia or hyp
37 /A >= 1.0 mol:mol were equally predictive of perinatal brain injury (sensitivity 100%, specificity 93
38 e and survival time of newborns, and reduces perinatal brain injury in cases of intrauterine inflamma
39 5%] of 222; excepting cases with evidence of perinatal brain injury) than in those with combined (19
41 epigenetic misregulation in animal models of perinatal cannabinoid exposure (using synthetic cannabin
43 The prevalence of detrimental outcomes of perinatal cannabis exposure is likely to increase in tan
47 or extremely preterm infants with suboptimal perinatal care or major antenatal events that cause seve
48 World Health Organization (WHO)-recommended perinatal care outputs assessed in the intervention grou
49 of prematurity are to optimize prenatal and perinatal care, improve diagnostic acumen worldwide and
51 iated with an increase in infant deaths from perinatal causes (1.214 [1.156, 1.275; p < 0.001]) and f
52 had more chronic diseases, experienced more perinatal complications, and utilized more acute care po
53 during pregnancy causes severe maternal and perinatal complications, despite a lack of vertical tran
57 verse events were pregnancy, puerperium, and perinatal conditions (in 255 [10%] of 2530 women in the
59 onstrated the importance of the link between perinatal cytokines and abnormal behaviors in offspring,
63 erience adverse perinatal outcomes including perinatal death, admission to a neonatal unit, resuscita
66 ssociated with a severe rhythm phenotype and perinatal death: 9 (82%) showed signature LQTS rhythms,
72 sociated with a lower likelihood of onset of perinatal depression (pooled risk ratio [RR], 0.61 [95%
73 ts and harms of preventive interventions for perinatal depression in pregnant or postpartum women or
74 sual care (EUC; so-called because, in India, perinatal depression is not typically treated) only (con
75 ses clinical evidence showing the effects of perinatal depression on offspring physical and behaviour
77 tween physical activity during pregnancy and perinatal depression, and it is limited for different ph
82 in TH expression levels, specifically during perinatal development compared to mice raised under Long
83 d masculinization of the rat amygdala during perinatal development produces higher levels of juvenile
87 g, feeding, and swallowing from birth onward-perinatal dysphagia-is often associated with several neu
88 ions varies considerably with factors in the perinatal environment and the genetic background of the
92 s the cellular and molecular consequences of perinatal exposure (mostly in rodents) to representative
93 loping infant oral microbiome, the effect of perinatal exposure (without infection) appears transient
97 offspring in a sex-specific manner following perinatal exposure to nicotine in only the F0 gestation,
98 ogens and can be recapitulated in females by perinatal exposure to testosterone proprionate, 3) perin
99 st study to evaluate the association between perinatal exposure to UFPs and the incidence of childhoo
100 ltered following alcohol or nicotine-alcohol perinatal exposure when compared to saline control.
101 shed rat model for both nicotine and alcohol perinatal exposure, we investigated miRNA and mRNA expre
103 tigated the association between in-utero and perinatal factors and suicide, suicide attempt, and suic
105 fter preterm birth in combination with other perinatal factors is a strong risk factor for LRD, sugge
112 terventions with public health education and perinatal healthcare service improvement could have impl
115 ssical monocytes determine susceptibility to perinatal hepatic inflammation in late gestation fetuses
116 In this mathematical modelling study of perinatal hepatitis B transmission and disease progressi
118 Disruption of Ezh1 and Ezh2 in livers caused perinatal hepatocytes to differentiate prematurely and t
119 tal characteristics, quality of family life, perinatal history, cardiometabolic health, cognition, an
121 We observed age-stratified associations of perinatal HIV exposure on community composition, with HE
122 acterial communities, however, the impact of perinatal HIV exposure on the oral microbiota remains un
123 ions in mothers and infants, irrespective of perinatal HIV exposure or infant CMV status at 6 months
124 and middle-income countries where the higher perinatal HIV exposure rates result in cotrimoxazole pro
126 pression during pregnancy, women living with perinatal HIV infection have a high risk of post-partum
127 a on pregnancy history for women living with perinatal HIV infection in the Pediatric HIV/AIDS Cohort
131 artum outcomes among young women living with perinatal HIV infection who are now ageing into adulthoo
132 2017, we enrolled 323 women, of whom 234 had perinatal HIV infection, and reported age at sexual debu
134 ly a preferred regimen for the prevention of perinatal HIV transmission with raltegravir recommended
135 and middle-income countries where the higher perinatal HIV-exposure rates result in cotrimoxazole pro
137 in type I interferon signaling that promotes perinatal HPC expansion and sensitizes progenitors to th
139 e neurodevelopmental effects of maternal and perinatal hypothyroxinemia and that we need to develop m
147 included prematurity, respiratory disorders, perinatal infections, and retinopathy of prematurity (RO
148 irthweight infants and those identified with perinatal infections, candidemia, bacteremia, respirator
149 sed on multivariate logistic regression were perinatal infections, candidemia, bacteremia, very low b
151 matrix protein cyclophilin D (CypD) prevents perinatal KET-induced increases in ROS and the resulting
152 important implications as they suggest that perinatal Klotho deficiency contributes to BPD-PH risk a
153 ant genes PROC, PROS1 and SERPINC1 result in perinatal lethal thrombosis in homozygotes and markedly
154 ause of p53 activation, p53(KQ/KQ) mice were perinatal lethal, yet this lethality was averted in p53(
155 esults in placenta and heart over-growth and perinatal lethality (>90%) due to raised extra-cellular
157 in mice during fetal development resulted in perinatal lethality associated with structural and genom
158 ient to rescue Ripk1 (mRHIM/mRHIM) mice from perinatal lethality caused by ZBP1-driven cell death and
159 scular specific knockout of Lztr1 results in perinatal lethality due to cardiovascular dysfunction.
160 tion and survival remains unclear because of perinatal lethality exhibited by knockout mice lacking a
161 of endogenous ligands induces ZBP1-mediated perinatal lethality in mice expressing RIPK1 with mutate
162 nza A virus-induced PANoptosis and underlies perinatal lethality in mice in which the RIP homotypic i
165 lation of TRADD rescues Ripk1(-/-) mice from perinatal lethality when RIPK3-mediated necroptosis is d
166 al deletion of both Crk and CrkL resulted in perinatal lethality with defects in desmosome morphology
168 (NCCs) causes severe conotruncal defects and perinatal lethality, thus providing mouse genetic eviden
175 hat Ly6c(Lo) monocytes promote resolution of perinatal liver inflammation in the late gestation fetus
178 ence of clock synchrony and functionality in perinatal lung development, and the possibility of lung
179 ck biology is also likely to be important in perinatal lung development, where it has received far le
180 re screening, cyanotic heart disease, active perinatal lung disease, and preparation or recovery from
183 re more likely than those without to develop perinatal mental illness (18.1% vs. 16.0%; adjusted rela
189 secting mechanistic interactions between the perinatal microbiota, immune system, and nervous system
192 growth restriction (IUGR) is associated with perinatal morbidity and increased risk of lifelong disea
197 s (CS) translate into reduced maternal/child perinatal morbidity or mortality, CS have been increasin
199 , we also observed significant reductions in perinatal mortality (0.86 [0.73-1.00], p=0.048), fetal l
201 the risk of overestimation of the effect on perinatal mortality due to early stopping of the largest
202 each chart achieved similar sensitivity for perinatal mortality in small infants (29% for all charts
205 easing wealth (OR 1.09, 1.03-1.14) and lower perinatal mortality with increasing distance from childb
206 2008), whereas there was evidence for higher perinatal mortality with increasing wealth (OR 1.09, 1.0
217 lted overall in a decrease of severe adverse perinatal outcome (0.4% [10/2,281] versus 1.0% [23/2,280
219 imary outcome was a composite of maternal or perinatal outcome (either maternal, fetal, or neonatal d
220 ound that, overall, IOL at 41 weeks improved perinatal outcome compared with expectant management unt
222 cases and were significantly associated with perinatal outcome, including hydrops, respiratory distre
224 igated the association between cirrhosis and perinatal outcomes and evaluated perinatal liver-related
226 term births, factors associated with poorer perinatal outcomes and related management interventions.
227 age restrictions, for studies on maternal or perinatal outcomes following caesarean sections in LMICs
228 easing, although population-based data about perinatal outcomes following in utero exposure remain li
229 atabase inception to June 1, 2018, reporting perinatal outcomes for women with intrahepatic cholestas
230 tional study established in 2006 to evaluate perinatal outcomes in pregnant women exposed to omalizum
231 ., same- or mixed-sex) of litters influences perinatal outcomes in the common marmoset monkey (Callit
232 im to estimate the frequency of maternal and perinatal outcomes in women with different categories of
233 ursodeoxycholic acid does not reduce adverse perinatal outcomes in women with intrahepatic cholestasi
234 whether ursodeoxycholic acid reduces adverse perinatal outcomes in women with intrahepatic cholestasi
237 I 1.8-4.8, p < 0.001) and experience adverse perinatal outcomes including perinatal death, admission
239 ds associated with increased risk of adverse perinatal outcomes using population, customised, and Int
240 The strength of association with adverse perinatal outcomes was different between infants below t
243 sPTB and pi-PTb were associated with poorer perinatal outcomes, as well as late sPTB, late pi-PTB an
244 asis of pregnancy is associated with adverse perinatal outcomes, but the association with the concent
250 ry outcome was a composite of severe adverse perinatal outcomes: mortality and severe neonatal morbid
251 xpressed in the same subset of germ cells in perinatal ovaries and Figla ablation dramatically disrup
252 analyzed global gene expression profiles in perinatal ovaries from wildtype, FiglaNull, Lhx8Null and
254 ne biceps femoris skeletal muscle during the perinatal period and examined the role of thyroid hormon
255 that mitochondrial function matures over the perinatal period and is dependent on thyroid hormones, w
257 he mother and infant dyad may present in the perinatal period from 20 weeks of gestation to 28 days o
259 p8(C362A/C362A)Mlkl(-/-) mice die during the perinatal period(5), whereas Casp8(-/-)Mlkl(-/-) mice ar
260 eydig and peritubular myoid cells during the perinatal period, allowing us to identify candidate sign
261 ess can have a devastating effect during the perinatal period, and has a profound impact on the care
262 environmental exposure, particularly during perinatal period, can have a life-long impact on organis
264 portance of proper choline intake during the perinatal period, especially when the fetus is known to
265 that early-life adversity, especially in the perinatal period, influences the maturation of brain cir
274 l long-term effects when administered during perinatal periods, increasing the risk to develop anxiet
275 uire analysis by a multidisciplinary team of perinatal practitioners and laboratory specialists.
276 se cellular immunoreactivity was assessed in perinatal, prepubertal, and adult female and male rats.
280 Here we tested the hypothesis that human perinatal stem cell derived extracellular matrix (ECM) p
281 iabetes could benefit from preconception and perinatal strategies to reduce their mental illness risk
282 lity to abnormal lentiform development after perinatal stress and are associated with neuroanatomic c
284 ficant relevance to pediatrics, in utero and perinatal stressors may alter the lifelong health trajec
285 wn to reduce preterm birth (PTB) and improve perinatal survival, but no trial evidence exists for wom
288 We find that clonal expansions during a perinatal time window leave a long-lasting imprint on th
290 addition, there is evidence that over time, perinatal transmission has decreased among women and inf
291 ntify HBV-infected pregnant women at risk of perinatal transmission in countries where HBV DNA quanti
292 birth intervals, key strategies to eliminate perinatal transmission of HIV and promote maternal and c
293 n of HBV vaccine-based strategies to prevent perinatal transmission, safe injection practices and HCV
300 izoxanide is a promising agent in preventing perinatal Zika transmission as well as other RNA viruses