戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 e, but it does represent a potential site of perinatal acquisition of S. agalactiae, a major cause of
2 rovider-initiated deliveries, and to prevent perinatal adverse outcomes.
3 this approach reduced subsequent maternal or perinatal adverse outcomes.
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.
7 ce during the infancy in rats in response to perinatal alcohol/ or nicotine-alcohol exposure.
8 ing differences in Lck transcription between perinatal and adult gammadelta T cell development.
9                              In contrast, in perinatal and adult male and female Zfpm1 mutants, a lat
10 in the skin innate immune system between the perinatal and adult periods of life.
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
13                  Using murine models of both perinatal and postnatal GBS acquisition, we assessed the
14                                         Both perinatal and postnatal murine models of GBS acquisition
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
18                        We linked laboratory, perinatal, and hospital data of 469 589 children born in
19 nal DALYs arose from communicable, maternal, perinatal, and nutritional disorders.
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
23            Thus, factors affecting levels of perinatal androgens could have a significant impact on M
24 se severity are established in early life by perinatal androgens.
25                               In conclusion, perinatal antibiotics markedly disturbed vertical transm
26 the intestinal microbiome but the effects of perinatal antibiotics on gut microbiome in vaginally del
27                                The impact of perinatal antibiotics on vertical transmission of microb
28 ) and a treatment group (10 pairs) receiving perinatal antibiotics.
29                                          The perinatal asphyxia (PA) group showed a significant decre
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
33 immersion in water (19 min) at 37 degrees C (perinatal asphyxia).
34  exposed to 10 degrees C during 30 min after perinatal asphyxia.
35                                              Perinatal brain abnormality was associated with less inc
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
40 , myelination, and functional recovery after perinatal brain injury.
41 epigenetic misregulation in animal models of perinatal cannabinoid exposure (using synthetic cannabin
42                     These results reveal how perinatal cannabinoid exposure retards an early mileston
43    The prevalence of detrimental outcomes of perinatal cannabis exposure is likely to increase in tan
44 e maturation of oxidative phosphorylation in perinatal cardiomyocytes.
45  38.3%) and +28.9% (from 13.9% to 17.9%) for perinatal care (p-value = 0.13).
46                                  Advances in perinatal care have improved survival for premature babi
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
50 in pregnancy was ascertained through routine perinatal care.
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
54            The first mode revealed traces of perinatal complications, including preterm and twin birt
55 persons has moderate net benefit in reducing perinatal complications.
56 orn after an uncomplicated pregnancy with no perinatal complications.
57 verse events were pregnancy, puerperium, and perinatal conditions (in 255 [10%] of 2530 women in the
58                         Adverse in-utero and perinatal conditions might contribute to an increased su
59 onstrated the importance of the link between perinatal cytokines and abnormal behaviors in offspring,
60                 Using data from the National Perinatal Data Collection we compared rates of preterm b
61                                  The risk of perinatal death and severe neonatal morbidity increases
62 rsisted throughout development, resulting in perinatal death of 35% of Olfml3-deficient mice.
63 erience adverse perinatal outcomes including perinatal death, admission to a neonatal unit, resuscita
64 s were also strongly associated with TdP and perinatal death.
65 nduced by cPAF, preventing preterm birth and perinatal death.
66 ssociated with a severe rhythm phenotype and perinatal death: 9 (82%) showed signature LQTS rhythms,
67                          Maternal deaths and perinatal deaths following caesarean sections are dispro
68                                              Perinatal deaths occurred in one (<0.1%) versus eight (0
69 n of Diseases, Tenth Revision application to perinatal deaths.
70                                  Prenatal or perinatal deletion of Arc/Arg3.1 alters cortical network
71  1.16], p-value 0.81) nor in other important perinatal, delivery, and maternal outcomes.
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
76 tpartum persons who are at increased risk of perinatal depression to counseling interventions.
77 tween physical activity during pregnancy and perinatal depression, and it is limited for different ph
78                                              Perinatal depression, which is the occurrence of a depre
79 ntervention recommended for the treatment of perinatal depression.
80           We enrolled 280 (84.1%) women with perinatal depression; 140 women were assigned to the THP
81  in widespread expansion of oncogenes during perinatal development but not in adults.
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
84                        These data identify a perinatal developmental period, in which neuronal GALC e
85      Some children with CVI and a history of perinatal distress have prenatal dysgenesis of the devel
86                                        Thus, perinatal dysphagia may be an early indicator of disrupt
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
89                                 The maternal perinatal environment modulates brain formation, and alt
90                    Neonatal APPs varied with perinatal environmental factors and maternal/fetal pheno
91 dren with severe CVI and clinical history of perinatal events were included.
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
94 of PBDEs, on glucoregulatory parameters in a perinatal exposure model using female C57Bl/6 mice.
95                                     However, perinatal exposure to adverse environments can also be a
96                                              Perinatal exposure to H pylori extract or its immunomodu
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
102                         Associations between perinatal factors (gestation, labour, sex, birth size),
103 tigated the association between in-utero and perinatal factors and suicide, suicide attempt, and suic
104 ngitudinal studies that account for relevant perinatal factors are required.
105 fter preterm birth in combination with other perinatal factors is a strong risk factor for LRD, sugge
106 and of how this development is influenced by perinatal factors.
107 hrough maternal immunization, a reduction in perinatal GBS disease might be possible.
108                         Here, we report that perinatal glucocorticoid exposure had long-term conseque
109                                We found that perinatal glucocorticoid exposure resulted in persistent
110             Unique to the natural history of perinatal HCMV infections is the occurrence of congenita
111 bortion but other important reproductive and perinatal health outcomes.
112 terventions with public health education and perinatal healthcare service improvement could have impl
113 varying disparities in access and quality of perinatal healthcare.
114                                              Perinatal hepatic inflammation can have devastating cons
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
117                      Most U.S. children with perinatal hepatitis C virus (HCV) exposure fail to recei
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
120               The main outcome measures were perinatal history, visual and neurologic findings, and m
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
125 rospective study of young adults living with perinatal HIV from 14 sites in the USA.
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
128                             The incidence of perinatal HIV infection in the United States peaked in 1
129                                              Perinatal HIV infection was significantly associated wit
130 end the window of opportunity for preventing perinatal HIV infection when treatment is delayed.
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
133                                              Perinatal HIV transmission has substantially decreased w
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
136            The remaining 3 trials provided a perinatal home-visiting intervention to pregnant Native
137 in type I interferon signaling that promotes perinatal HPC expansion and sensitizes progenitors to th
138                Children and adolescents with perinatal human immunodeficiency virus (HIV) infection a
139 e neurodevelopmental effects of maternal and perinatal hypothyroxinemia and that we need to develop m
140             Therefore, a clinical history of perinatal hypoxia-ischemia is nonspecific and merits neu
141                                     Although perinatal ILC2s were variably replaced across tissues wi
142 tational age infant (SGA), birth defect, and perinatal infant death.
143 eficiency virus (SHIV) in a macaque model of perinatal infection.
144 NA targeting of EMT may prevent pPROM due to perinatal infection.
145                                              Perinatal infections are a major driver of this burden b
146 ic cases were aged <18 years; congenital and perinatal infections were excluded.
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
150 re clinics at the Instituto Nacional Materno Perinatal (INMP) in Lima, Peru.
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
156         Genetic ablation of Ripk1 results in perinatal lethality arising from both RIPK3-mediated nec
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
163 activator of IFN-driven RIPK3 activation and perinatal lethality in the absence of RIPK1.
164                                              Perinatal lethality was observed in Slc7a7Lbu/Lbu and Sl
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
167                             Thm1 loss causes perinatal lethality, and Thm2 loss allows survival into
168 (NCCs) causes severe conotruncal defects and perinatal lethality, thus providing mouse genetic eviden
169 evere phenotype with reduced weight gain and perinatal lethality.
170  liver resulted in hematopoietic failure and perinatal lethality.
171 lting in intrauterine growth restriction and perinatal lethality.
172 tes, neuromuscular degenerative disease, and perinatal lethality.
173 se allele, Specc1lDeltaC510, that results in perinatal lethality.
174 romotion of influenza-induced PANoptosis and perinatal lethality.
175 hat Ly6c(Lo) monocytes promote resolution of perinatal liver inflammation in the late gestation fetus
176 tion may mitigate the detrimental effects of perinatal liver inflammation.
177 rrhosis and perinatal outcomes and evaluated perinatal liver-related events.
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
181  studies have focused on the adult lung, the perinatal lung remains unexplored.
182      Otherwise, there were no differences in perinatal, maternal, or obstetric parameters.
183 re more likely than those without to develop perinatal mental illness (18.1% vs. 16.0%; adjusted rela
184                  We examined the risk of any perinatal mental illness associated with prepregnancy di
185        Modified Poisson regression estimated perinatal mental illness risk between conception and 1 y
186        Modified Poisson regression estimated perinatal mental illness risk between conception and 1 y
187                                              Perinatal mental illness risk was elevated in all classe
188                                              Perinatal mental illness risk was elevated in all classe
189 secting mechanistic interactions between the perinatal microbiota, immune system, and nervous system
190 defined LO disease as >7 days of life in the perinatal model.
191                            Understanding the perinatal molecular clock may unravel mechanistic target
192 growth restriction (IUGR) is associated with perinatal morbidity and increased risk of lifelong disea
193 precedes preterm birth, the leading cause of perinatal morbidity and mortality worldwide.
194 orldwide and causes significant maternal and perinatal morbidity and mortality.
195 proposed in high-income countries to prevent perinatal morbidity and mortality.
196 ended pregnancy is associated with increased perinatal morbidity and mortality.
197 s (CS) translate into reduced maternal/child perinatal morbidity or mortality, CS have been increasin
198 y merit exploration as a factor impacting on perinatal morbidity.
199 , we also observed significant reductions in perinatal mortality (0.86 [0.73-1.00], p=0.048), fetal l
200  Preterm birth (PTB) is the leading cause of perinatal mortality and newborn complications.
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
203           The magnitude of risk reduction of perinatal mortality remains uncertain.
204                In the multivariable context, perinatal mortality was associated with only 3 of the 30
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
207 stically significant variation was found for perinatal mortality.
208 reterm delivery before 37 weeks, and reduced perinatal mortality.
209 that have been relayed by hospital teams and perinatal networks.
210                              In a rat model, perinatal nicotine exposure results in an epigenetically
211 f the ventral tegmental area (VTA) following perinatal nicotine exposure.
212  an overall decrease in DA neurons following perinatal nicotine exposure.
213  within the sub-regions of the VTA following perinatal nicotine exposure.
214 st protection from PVI dysfunction following perinatal NMDAR blockade.
215  1 medullar follicles during mouse fetal and perinatal oogenesis.
216                                Patients with perinatal or infantile hypophosphatasia treated with asf
217 lted overall in a decrease of severe adverse perinatal outcome (0.4% [10/2,281] versus 1.0% [23/2,280
218 rs independently associated with any adverse perinatal outcome (APO).
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
221                   The risk of severe adverse perinatal outcome was decreased for nulliparous women in
222 cases and were significantly associated with perinatal outcome, including hydrops, respiratory distre
223 ogether with a per-protocol analysis for the perinatal outcome.
224 igated the association between cirrhosis and perinatal outcomes and evaluated perinatal liver-related
225                  An under-recognition of the perinatal outcomes and its associated factors might have
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
235 d active case finding, together with data on perinatal outcomes in women with these outcomes.
236                                      Adverse perinatal outcomes included macrosomia (multiple thresho
237 I 1.8-4.8, p < 0.001) and experience adverse perinatal outcomes including perinatal death, admission
238                                              Perinatal outcomes may vary according to lots of factors
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
241                                 Maternal and perinatal outcomes were also collected according to mate
242              Aggregate data for maternal and perinatal outcomes were extracted from case-control stud
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
245 licated pregnancies at 41 weeks will improve perinatal outcomes.
246 hnologies (ARTs) are associated with adverse perinatal outcomes.
247 gnancy has not been associated with improved perinatal outcomes.
248 regnancy after bariatric surgery and adverse perinatal outcomes.
249 is is an independent risk factor for adverse perinatal outcomes.
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
253 ten requires the expertise of an experienced perinatal pathologist.
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
256                     This work highlights the perinatal period as a critical time window, especially r
257 he mother and infant dyad may present in the perinatal period from 20 weeks of gestation to 28 days o
258 ants and testicular somatic cells during the perinatal period in mice.
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
263                                       In the perinatal period, cardiomyocytes still proliferate, and
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
266  cells in a stage-specific manner during the perinatal period.
267 eonates scanned cross-sectionally across the perinatal period.
268 rm and somatic cell developmental during the perinatal period.
269 y important for brain development during the perinatal period.
270 associated with neuroanatomic changes in the perinatal period.
271 on offspring's glucose metabolism during the perinatal period.
272 diated inflammation and is lethal during the perinatal period.
273  relatively mild outcome to death during the perinatal period.
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.
277    Complimentary, we demonstrated two-phased perinatal programming after IUGR.
278 at two study sites through the Collaborative Perinatal Project.
279                             In cases without perinatal sentinel events, genomic alterations contribut
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
283             Our study thus demonstrates that perinatal stress can have long-term consequences on CD8
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
286                                              Perinatal T cells broadly access nonlymphoid tissues, wh
287 pening of anergy occurred after depletion of perinatal T reg cells.
288      We find that clonal expansions during a perinatal time window leave a long-lasting imprint on th
289       All patients had been infected through perinatal transmission and were treatment naive.
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
294 providing protective immunity and preventing perinatal transmission.
295 dentifies women whose infants are at risk of perinatal transmission.
296 on of HBV-infected pregnant women at risk of perinatal transmission.
297                                              Perinatal treatment with lopinavir boosted by ritonavir
298         This review will address the role of perinatal vascular insults in the development of late pu
299        We postulate that there is a critical perinatal window, ranging from embryonic day 18.5 to pos
300 izoxanide is a promising agent in preventing perinatal Zika transmission as well as other RNA viruses

 
Page Top