BACKGROUND: Abnormal prolongation in the QT interval or long QT syndrome (LQTS) is associated with several cardiac complications such as sudden infant death syndrome (SIDS). LQTS is believed to be linked to genetic mutations which can be understood by using animal models, such as mice models. Nevertheless, the research related to fetal QT interval in mice is still limited because of challenges associated with T wave measurements in fetal electrocardiogram (fECG). Reliable measurement of T waves is essential for estimating their end timings for QT interval assessment. RESULTS: A mathematical model was used to estimate QT intervals. Estimated QT intervals were validated with Q-aortic closure (Q-Ac) intervals of Doppler ultrasound (DUS) and comparison between both showed good agreement with a correlation coefficient higher than 0.88 (r > 0.88, P < 0.05). CONCLUSION: Model-based estimation of QT intervals can help in better understanding of QT intervals in fetal mice.

This study examines the role of autonomic control of maternal and fetal heart rate variability (MHRV and FHRV) and their heartbeats phase coupling prevalence (CPheartbeat) in mice. The subjects are divided into three groups: control with saline, cholinergic blockade with atropine, and β-adrenergic blockade with propranolol. Electrocardiogram signals of 27 anesthetized pregnant mice and 48 fetuses were measured for 20 min (drugs were administered after 10 min). For the coupling analysis, different maternal heartbeats were considered for one fetal beat. Results show that saline infusion did not produce any significant changes in MHRV and FHRV, as well as CPheartbeat. Atropine increased maternal HR (MHR) and decreased MHRV significantly without any considerable effect on fetal HR (FHR) and FHRV. Propranolol infusion did not produce any significant changes in MHR and MHRV, but significantly decreased FHR and increased FHRV. Moreover, atropine had led to a decrease in CPheartbeat when considering two and three maternal beats, and an increase for four beats; while propranolol resulted in a decrease for two heartbeats, but an increase for four and five beats. The proposed approach is useful for assessing the impact of maternal autonomic modulation activity on fetal distress and obstetric complications prevalent in pregnant mothers.

Beat-by-beat maternal and fetal heart couplings were reported to be evident throughout the fetal development. However, it is still unknown whether maternal-fetal heartbeat coupling parameters are associated with fetal development, and the potential interrelationships. Therefore, this study aims to investigate the associations of coupling parameters with fetal gestational age by multivariate regression models. Ten min abdominal lead-based maternal and fetal ECG signals were collected from 16 healthy pregnant women with healthy singleton pregnancies (19-32 weeks). Maternal and Fetal Heart Rate Variability (MHRV and FHRV) values as well as maternal-fetal heart rate coupling (strength, measured by A) parameters at various coupling ratios (associated with different Maternal:Fetal heartbeat ratios of 1:2, 1:3, 2:3, 2:4, 3:4, and 3:5) were calculated. Based on those features stepwise multivariate regression models were constructed by validating against the gold standard gestational age identified by crown-rump length from doppler echocardiogram. Among all models, the best model (Root Mean Square Error, RMSE=1.92) was found to be significantly (p<0.05) associated with mean fetal heart rate, mean maternal heart rate, standard deviation of maternal heart rate, λ[1:3], λ[2:3], λ[2:4]. Correlation coefficients and Bland Altman plots were constructed to statistically validate the results. The model developed based on coupling parameters only, showed the second-best performance (RMSE=2.50). Therefore, combining maternal and fetal heart rate variability parameters with maternal-fetal heart rate coupling values (rather than considering FHRV or MHRV parameters only) is found to be better associated with fetal development.Clinical relevance- This is a brief additional statement on why this might be of interest to practicing clinicians. Example: This establishes the anesthetic efficacy of 10% intraosseous injections with epinephrine to positively influence cardiovascular function.

INTRODUCTION: Early detection and monitoring for malignant arrhythmias is fundamental to prenatal care in long QT syndrome (LQTS). Recently, we studied the feasibility of isolating the fetal electrocardiogram (fECG) and measuring electrocardiographic intervals with a noninvasive fECG device using blind source separation with reference signal. Our aim was to evaluate the ability of fECG to diagnose LQTS. CASE PRESENTATIONS: We identified 3 cases of clinically suspected LQTS based on fetal echocardiogram (2 had sinus bradycardia, 1 had second-degree atrioventricular block with negative maternal anti-SSA/SSB antibody titers). With institutional review board approval, these patients were prospectively enrolled for fECG acquisition. Offline post-processing generated fECG waveforms and calculated QT intervals. Case 1 and 3 had a maternal history of LQTS. Two of the three fetuses with suspected LQTS had confirmed LQTS by postnatal ECG and genetic testing. FECG was able to identify a prolonged corrected QT interval in both cases. One of these also had fetal magnetocardiography (fMCG), which yielded similar findings to the fECG. The third fetus had a normal fECG; fMCG and postnatal ECG were also normal. CONCLUSIONS: In 3 cases, fECG findings corroborated the diagnosis of LQTS. Noninvasive fECG may offer a novel method for fECG that is portable and more clinically accessible.

Non-invasive fetal electrocardiography (ECG) is a promising method for evaluating fetal cardiac electrical activity. Despite advances in fetal ECG technology, its ability to provide reliable, interpretable results in a typical outpatient fetal cardiology setting remains unclear. We sought to determine the feasibility of measuring standard ECG intervals in an outpatient fetal cardiology practice using an abdominal fetal ECG device that employs blind source separation with reference, an innovative signal-processing technique for fetal ECG extraction. Women scheduled for clinically indicated outpatient fetal echocardiogram underwent 10 min of fetal ECG acquisition from the maternal abdomen using specialized gel electrodes. A bedside laptop computer performed fetal ECG extraction, allowing real-time visualization of fetal and maternal ECG signals. Offline post-processing of 1 min of recorded data yielded fetal P-wave duration, PR interval, QRS duration, RR interval, QT interval, and QTc. Fifty-five fetuses were studied with gestational age 18-37 weeks, including 13 with abnormal fetal echocardiogram findings and three sets of twins. Interpretable results were obtained in 91% of fetuses, including 85% during the vernix period and 100% of twin fetuses. PR interval and RR interval of 18-24 week gestation fetuses were significantly shorter than those with gestational age 25-31 and 32-37 weeks. Of the six fetuses with abnormal rhythms on fetal echocardiogram, fetal ECG tracing was interpretable in five and matched the rhythm noted on fetal echocardiogram. Abdominal fetal ECG acquisition is feasible for arrhythmia detection and ECG interval calculation in a routine clinical setting.

The aim of this preliminary study is to look how maternal-fetal heart rates and their coupling patterns are influenced by injection of β blocker(propranolol) into pregnant mice. Total of 6 pregnant female mice were divided into two groups [control (N=3) and β blockade (N=3)]. On 17.5-day mean heart rate of mothers and fetuses (MHR and FHR) were simultaneously measured for 20 minutes (10 minutes under normal condition and 10 minutes with saline (to control group) and propranolol (to the β blockade group) solution by using an invasive maternal and fetal electrocardiogram techniques with needle electrodes. Results show that FHR decreased and maternal-fetal heart rate coupling (λ) patterns changed with propranolol infusion (no change with saline). Statistical test showed that changes (increase/decrease from pre to post values) in mean, rmssd and power spectral density (PSD) (2~4 Hz)) of MHR, short term variability of FHR, PSD (0.0~1.0 Hz) of FHR and λ were found to be significantly associated with treatment types (saline to propranolol). The presented results and protocol allow for assessment of β adrenergic control of maternal and fetal heart, which will further enhance the value of the mouse as a model of heritable human pregnancy and hypertension.

The hypoxic microenvironment existing in vivo is known to significantly affect cell morphology and dynamics, and cell group behaviour. Collective migration of vascular endothelial cells is essential for vasculogenesis and angiogenesis, and for maintenance of monolayer integrity. Although hypoxic stress increases vascular endothelial permeability, the changes in collective migration and intracellular junction morphology of vascular endothelial cells remain poorly understood. This study reveals the migration of confluent vascular endothelial cells and changes in their adherens junction, as reflected by changes in the vascular endothelial (VE)-cadherin distribution, under hypoxic exposure. Vascular endothelial monolayers of human umbilical vein endothelial cells (HUVECs) were formed in microfluidic devices with controllability of oxygen tension. The oxygen tension was set to either normoxia (21% O2) or hypoxia (<3% O2) by supplying gas mixtures into separate gas channels. The migration velocity of HUVECs was measured using particle image velocimetry with a time series of phase-contrast microscopic images of the vascular endothelial monolayers. Hypoxia inducible factor-1α (HIF-1α) and VE-cadherin in HUVECs were observed after exposure to normoxic or hypoxic conditions using immunofluorescence staining and quantitative confocal image analysis. Changes in the migration speed of HUVECs were observed in as little as one hour after exposure to hypoxic condition, showing that the migration speed was increased 1.4-fold under hypoxia compared to that under normoxia. Nuclear translocation of HIF-1α peaked after the hypoxic gas mixture was supplied for 2 h. VE-cadherin expression was also found to be reduced. When ethanol was added to the cell culture medium, cell migration increased. By contrast, by strengthening VE-cadherin junctions with forskolin, cell migration decreased gradually in spite the effect of ethanol to stimulate migration. These results indicate that the increase of cell migration by hypoxic exposure was attributable to loosening of intercellular junction resulting from the decrease of VE-cadherin expression.

The aim of this preliminary study is to investigate if there is any evidence of maternal-fetal heart rate coupling in mice fetuses and how the coupling patterns are regulated by vagal nervous system on beat by beat. Total of 6 pregnant female mice were divided into two groups [control (N=3) and vagal blockade (N=3)]. On 17.5-day beat-to-beat heart rates of mothers and fetuses (MHR and FHR) were simultaneously measured for 20 minutes (10 minutes under normal condition and 10 minutes with saline (to control group) and atropine (to the vagal blockade group)) solution by using an invasive maternal and fetal electrocardiogram techniques with needle electrodes. Results show that occasional strong maternal-fetal heart rate coupling (strength was measured by $\lambda$) appeared and its patterns changed with atropine infusion (no change with saline). Additionally, fisher's exact test shows that changes (increase/decrease from pre to post injection values) in mean, rmssd and power spectral density (PSD) (2~4 Hz) of MHR, rmssd FHR and PSD (2~4 Hz) of${\lambda }$were found to be significantly (p<0.05) associated with treatment types (saline/ atropine). The presented results and protocol allow for the first time in the assessment of autonomic regulation of maternal and fetal heart and their interactions, which will further enhance the value of the mouse as a murine model of heritable human pregnancy and perinatal complications due to maternal conditions.

Endothelial permeability has been extensively investigated in the context of pathologies such as cancer and also in studies of drug delivery from the circulation. Hypoxia is a critical regulator of endothelial cell (EC) behavior and affects the barrier function of endothelial linings, yet its role has been little studied. This paper reveals the effect of hypoxia on the permeability of an EC monolayer by cellular experiments using a microfluidic device and a conventional cell culture dish. Human umbilical vein endothelial cells (HUVECs) were seeded into one microfluidic channel, creating an EC monolayer on each vertical surface of a collagen gel confined to a central chamber. Oxygen tension was regulated to produce normoxic (21% O2) or hypoxic (3% O2) conditions by the supply of gas mixtures of oxygen, carbon dioxide, and nitrogen at predefined ratios into channels fabricated into the device. Permeability of the EC monolayer quantified by analyzing diffusion of fluorescence-labelled dextrans into the collagen gel increases with barrier function loss by 6 hour hypoxic exposure, showing 11-fold and 4-fold increases for 70 kDa and 10 kDa dextrans, respectively, on average. Consistent with this, subsequent immunofluorescent staining and separate western blot analysis of HUVECs on a culture dish demonstrate loose cell-cell adhesion resulting from internalization of VE-cadherin under hypoxia. Thus, hypoxic stress increases endothelial permeability by altering cell-cell junction integrity.

Despite vast improvement in perinatal care during the 30 years, the incidence rate of neonatal encephalopathy remains unchanged without any further Progress towards preventive strategies for the clinical impasse. Antenatal brain injury including fetal intracranial hemorrhage caused by ischemia/reperfusion is known as one of the primary triggers of neonatal injury. However, the mechanisms of antenatal brain injury are poorly understood unless better predictive models of the disease are developed. Here we show a mouse model for fetal intracranial hemorrhage in vivo developed to investigate the actual timing of hypoxia-ischemic events and their related mechanisms of injury. Intrauterine growth restriction mouse fetuses were exposed to ischemia/reperfusion cycles by occluding and opening the uterine and ovarian arteries in the mother. The presence and timing of fetal intracranial hemorrhage caused by the ischemia/reperfusion were measured with histological observation and ultrasound imaging. Protein-restricted diet increased the risk of fetal intracranial hemorrhage. The monitoring of fetal brains by ultrasound B-mode imaging clarified that cerebral hemorrhage in the fetal brain occurred after the second ischemic period. Three-dimensional ultrasound power Doppler imaging visualized the disappearance of main blood flows in the fetal brain. These indicate a breakdown of cerebrovascular autoregulation which causes the fetal intracranial hemorrhage. This study supports the fact that the ischemia/reperfusion triggers cerebral hemorrhage in the fetal brain. The present method enables us to noninvasively create the cerebral hemorrhage in a fetus without directly touching the body but with repeated occlusion and opening of the uterine and ovarian arteries in the mother.

Objectives: This descriptive study was performed to evaluate the capability of a non-invasive transabdominal electrocardiographic system to extract clear fetal electrocardiographic (FECG) measurements from intrauterine growth restricted (IUGR) fetuses and to assess whether abdominal FECG parameters can be developed as markers for evaluating the fetal cardiac status in IUGR. Methods: Transabdominal FECG was attempted in 20 controls and 15 IUGR singleton pregnancies at 20+0-33+6 weeks gestation. Standard ECG parameters were compared between the study groups and evaluated for their correlation. Accuracy for the prediction of IUGR by cut off values of the different FECG parameters was also determined. Results: Clear P-QRST complexes were recognized in all cases. In the IUGR fetuses, the QT and QTc intervals were significantly prolonged (p = 0.017 and p = 0.002, respectively). There was no correlation between ECG parameters and Doppler or other indices to predict IUGR. The generation of cut off values for detecting IUGR showed increasing sensitivities but decreasing specificities with the prolongation of ECG parameters. Conclusion: The study of fetal electrocardiophysiology is now feasible through a non-invasive transabdominal route. This study confirms the potential of FECG as a clinical screening tool to aid diagnosis and management of fetuses after key limitations are addressed. In the case of IUGR, both QT and QTc intervals were significantly prolonged and thus validate earlier study findings where both these parameters were found to be markers of diastolic dysfunction. This research is a useful prelude to a test of accuracy and Receiver Operating Characteristics (ROC) study.

Electromechanical coupling of the fetal heart can be evaluated noninvasively using doppler ultrasound (DUS) signal and fetal electrocardiography (fECG). In this study, an efficient model is proposed using K-means clustering and hybrid Support Vector Machine-Hidden Markov Model (SVM-HMM) modeling techniques. Opening and closing of the cardiac valves were detected from peaks in the high frequency component of the DUS signal decomposed by wavelet analysis. It was previously proposed to automatically identify the valve motion by hybrid SVM-HMM based on the amplitude and timing of the peaks. However, in the present study, six patterns were identified for the DUS components which were actually variable on a beat-to-beat basis and found to be different for the early gestation (16-32 weeks), compared to the late gestation fetuses (36-41 weeks). The amplitude of the peaks linked to the valve motion was different across the six patterns and this affected the precision of valve motion identification by the previous hybrid SVM-HMM method. Therefore in the present study, clustering of the DUS components based on K-means was proposed and the hybrid SVM-HMM was trained for each cluster separately. The valve motion events were consequently identified more efficiently by beat-to-beat attribution of the DUS component peaks. Applying this method, more than 98.6% of valve motion events were beat-to-beat identified with average precision and recall of 83.4% and 84.2% respectively. It was an improvement compared to the hybrid method without clustering with average precision and recall of 79.0% and 79.8%. Therefore, this model would be useful for reliable screening of fetal wellbeing.

In this paper, a new noninvasive method is proposed for automated estimation of fetal cardiac intervals from Doppler Ultrasound (DUS) signal. This method is based on a novel combination of empirical mode decomposition (EMD) and hybrid support vector machines-hidden Markov models (SVM/HMM). EMD was used for feature extraction by decomposing the DUS signal into different components (IMFs), one of which is linked to the cardiac valve motions, i.e. opening (o) and closing (c) of the Aortic (A) and Mitral (M) valves. The noninvasive fetal electrocardiogram (fECG) was used as a reference for the segmentation of the IMF into cardiac cycles. The hybrid SVM/HMM was then applied to identify the cardiac events, based on the amplitude and timing of the IMF peaks as well as the sequence of the events. The estimated timings were verified using pulsed doppler images. Results show that this automated method can continuously evaluate beat-to-beat valve motion timings and identify more than 91% of total events which is higher than previous methods. Moreover, the changes of the cardiac intervals were analyzed for three fetal age groups: 16-29, 30-35, and 36-41 weeks. The time intervals from Q-wave of fECG to Ac (Systolic Time Interval, STI), Ac to Mo (Isovolumic Relaxation Time, IRT), Q-wave to Ao (Preejection Period, PEP) and Ao to Ac (Ventricular Ejection Time, VET) were found to change significantly ( ) across these age groups. In particular, STI, IRT, and PEP of the fetuses with 36-41 week were significantly ( ) different from other age groups. These findings can be used as sensitive markers for evaluating the fetal cardiac performance.

Ischemic reperfusion (IR) during the perinatal period is a known causative factor of fetal brain damage. So far, both morphologic and histologic evidence has shown that fetal brain damage can be observed only several hours to days after an IR insult has occurred. Therefore, to prevent fetal brain damage under these circumstances, a more detailed understanding of the underlying molecular mechanisms involved during an acute response to IR is necessary. In the present work, pregnant mice were exposed to IR on day 18 of gestation by clipping one side of the maternal uterine horn. Simultaneous fetal electrocardiography was performed during the procedure to verify that conditions resulting in fetal brain damage were met. Fetal brain sampling within 30 minutes after IR insult revealed molecular evidence that a fetal response was indeed triggered in the form of inhibition of the Akt-mTOR-S6 synthesis pathway. Interestingly, significant changes in mRNA levels for both HIF-1α and p53 were apparent and gene regulation patterns were observed to switch from a HIF-1α-dependent to a p53-dependent process. Moreover, pre-treatment with pifithrin-α, a p53 inhibitor, inhibited protein synthesis almost completely, revealing the possibility of preventing fetal brain damage by prophylactic pifithrin-α treatment.

Introduction. Prenatal programming secondary to maternal protein restriction renders an inherent susceptibility to neural compromise in neonates and any addition of glucocorticosteroids results in further damage. This is an investigation of consequent global gene activity due to effects of antenatal steroid therapy on a protein restriction mouse model. Methods. C57BL/6N pregnant mice were administered control or protein restricted diets and subjected to either 100  μ g/Kg of dexamethasone sodium phosphate with normosaline or normosaline alone during late gestation (E10-E17). Nontreatment groups were also included. Brain samples were collected on embryonic day 17 and analyzed by mRNA microarray analysis. Results. Microarray analyses presented 332 significantly regulated genes. Overall, neurodevelopmental genes were overrepresented and a subset of 8 genes allowed treatment segregation through the hierarchical clustering method. The addition of stress or steroids greatly affected gene regulation through glucocorticoid receptor and stress signaling pathways. Furthermore, differences between dexamethasone-administered treatments implied a harmful effect during conditions of high stress. Microarray analysis was validated using qPCR. Conclusion. The effects of antenatal steroid therapy vary in fetuses according to maternal-fetal factors and environmental stimuli. Defining the key regulatory networks that signal either beneficial or damaging corticosteroid action would result in valuable adjustments to current treatment protocols.

The development of the fetal cardiovascular system plays a crucial role in fetal health. The evolution of the relationship between fetal and maternal cardiac systems during fetal maturation is a characterizing feature for fetal cardiac development. This paper aims to evaluate this relationship by investigating the beat-to-beat synchronization between fetal and maternal heart rates and its variation at different stages of pregnancy. Synchronization epochs and phase locking patterns are analyzed at certain synchronization ratios (SRs) for three gestational age groups (16-26 weeks, 27-33 weeks, 34-40 weeks). Results show that the normalized synchronization epoch is significantly different for three age groups with the p-value of 6.72*10(-6) and 2.89*10(-4) at SR of 1:2 and 4:5 respectively. The variance of phase locking also shows significant difference for three groups with the p-value less than 10(-7) at four SRs. Results also suggest that synchronization may be the force behind the increase in the maternal heart rate to maintain the fetal development and provide supplies for the fetus. Overall, the findings propose new clinical markers for evaluating the antenatal development.

In this paper a new noninvasive method is proposed for automated estimation of opening and closure timings of fetal cardiac valves. These timings are obtained from Doppler Ultrasound (DUS) signal and fetal electrocardiogram (fECG) as a reference. Empirical Mode Decomposition (EMD) is first applied to the DUS signal to decompose it into different components called Intrinsic Mode Functions (IMFs). The envelope of the first IMF is then taken and its peaks are identified. The opening and closure of the valves are then automatically assigned to the IMF peaks by using Hidden Markov Model (HMM). It is shown that this new method can continuously evaluate fetal cardiac valves' (aortic and mitral) motion timings for 82.5~99.7% of cardiac cycles. The estimated timings are verified using the Pulsed Doppler images. These findings can be used as sensitive markers for evaluating the fetal cardiac performance.

Maternal undernutrition during pregnancy is a risk factor for cerebrovascular and cardiovascular diseases in adulthood. Hypoxia-inducible factor 1 alpha (HIF1α) plays an essential role in cellular hypoxic responses, and its increased expression is associated with cerebrovascular and cardiovascular diseases. However, it is not known whether maternal undernutrition influences HIF1α expression in the fetal brain. We therefore analyzed the expression levels of HIF1α and its downstream genes in the fetal brain (day 17.5 of gestation, 1-2 days before birth). Maternal undernutrition did not noticeably affect the fetal body and brain weights. Both HIF1α mRNA and protein levels were increased in the brain under maternal undernutrition, despite the absence of hypoxia, as judged by the staining profile with hypoxyprobe-1 that identifies hypoxic cells. Importantly, maternal undernutrition caused the accumulation of HIF1α protein in oligodendrocyte precursor cells at the subventricular zone, a site of neurogenesis in the fetal brain. Maternal undernutrition also increased the mRNA level of mammalian target of rapamycin (mTOR), which could increase the level of HIF1α protein under normoxia. Furthermore, microarray analysis revealed that expression levels of mRNAs for 10 HIF1α downstream targets, including enolase 1 and hexokinase 1, were increased in the fetal brain under maternal undernutrition. Thus, the biochemical consequence of maternal undernutrition is similar to that of mild hypoxia. In conclusion, maternal undernutrition induces the expression of HIF1α in oligodendrocyte precursor cells at the subventricular zone, and it also induces the expression of hypoxia-related genes in the fetal brain probably via activation of the mTOR pathway.

Maternal undernutrition during pregnancy is a risk factor that impairs fetal growth and causes cardiovascular diseases. However, the underlying mechanism is still unknown. In this study, we evaluated the effect of maternal undernutrition on the expression levels of transcription factors in the fetal heart. Female mice were given low protein or regular food from 2 weeks before mating and during their pregnancy. The fetal hearts were collected on day 17.5 of gestation, about 1-2 days before birth. Maternal undernutrition resulted in a significant increase in the relative heart weight (heart weight/body weight) in female fetuses, but not in male fetuses. Microarray analysis revealed that expression levels of mRNAs for 133 transcription factors were changed in the fetal heart under maternal undernutrition. Among them, we focused on hypoxia-inducible factor 1 alpha (HIF1α) that is involved in the pathogenesis of cardiovascular diseases on adulthood. Quantitative real-time PCR analysis showed that the expression level of HIF1α mRNA was increased about 1.3-fold in male fetal heart under maternal undernutrition, but remained unchanged in female heart. Moreover, maternal undernutrition increased the mRNA level of prolyl hydroxylase 1 (PHD1), which contributes to degradation of HIF1α, in male heart but not in female heart. Immunohistochemical analysis showed the accumulation of HIF1α protein in the fetal heart of both sexes under maternal undernutrition, without the induction of HIF1α mRNA expression in female heart. These results suggest that maternal undernutrition may induce HIF1α expression in the fetal heart through the distinct mechanisms depending on the sex.

Maternal undernutrition and infection during pregnancy may impair development of oligodendrocytes, thereby increasing risks of neuropsychiatric disorders of their children. We analyzed the effects of those risk factors on oligodendrogenesis in fetal and neonatal brains. Female mice were given low-protein or regular food for 2 weeks before their pregnancy. On the 14th day of pregnancy, they received a transvaginal injection of lipopolysaccharide to induce inflammation or control solution, consisting of four groups, depending on nutritional conditions with or without vaginal inflammation. We collected fetal brains on embryonic day (E) 17 for evaluating oligodendrocyte precursor cells (OPCs) and neonatal brains on postnatal day (P) 7 for evaluating mature oligodendrocytes. OPCs and mature oligodendrocytes were identified as positive immunostaining for oligodendrocyte-lineage transcription factor 2 and myelin basic protein, respectively. There was no difference in the number of OPCs in E17 brains among the four groups, suggesting that nutritional restriction with or without inflammation exerts no noticeable influence on the differentiation of OPCs. However, the number of mature oligodendrocytes was decreased in P7 brains obtained from nutrient-restricted mice with inflammation, suggesting that their combination impairs oligodendrogenesis in the neonatal brain. We also analyzed reactive astrocytes that express both glial fibrillary acidic protein and nestin for evaluating brain inflammation. The population of reactive astrocytes was increased in P7 brains derived from mice with LPS injection, irrespective of nutritional restriction, indicating that maternal vaginal inflammation induces neonatal brain inflammation. The maternal management of both nutrition and infection is crucial to prevent neuropsychiatric disorders of the children.