Diffusion-Weighted MRI of the Fetal Brain in Fetal Growth Restriction With Maternal Preeclampsia or Gestational Hypertension.

BACKGROUND: The fetal neurodevelopmental microstructural alterations of intrauterine exposure to preeclampsia (PE) or gestational hypertension (GH) remain unknown. PURPOSE: To evaluate the differences in diffusion-weighted imaging (DWI) of the fetal brain between normotensive pregnancies and PE/GH pregnancies, with a focus on PE/GH pregnancies with fetal growth restriction (FGR). STUDY TYPE: Retrospective matched case-control study. POPULATION: 40 singleton pregnancies with PE/GH complicated by FGR, and 3 paired control groups (PE/GH without FGR, normotensive FGR, normotensive pregnancies) (28-38 gestational weeks). FIELD STRENGTH/SEQUENCE: DWI with single-shot echo-planar imaging at 1.5 Tesla. ASSESSMENT: The apparent diffusion coefficient (ADC) values were calculated in the centrum semi-ovale (CSO), parietal white matter (PWM), frontal white matter (FWM), occipital white matter (OWM), temporal white matter (TWM), basal ganglia, thalamus (THAL), pons, and cerebellar hemisphere. STATISTICAL TESTS: Student t test or Wilcoxon matched test was used to reveal the difference of ADC values among the investigated brain regions. A correlation between gestational age (GA) and ADC values was determined by linear regression analysis. RESULTS: Compared with fetuses in PE/GH without FGR and those with normotensive pregnancies, fetuses in the PE/GH with FGR group had significantly lower average ADC measurements of supratentorial regions (1.65 ± 0.09 vs. 1.71 ± 0.10 10-3 mm2 /sec; vs. 1.73 ± 0.11 10-3 mm2 /sec, respectively). Regions of significantly decreased ADC values in the fetal brain included CSO, FWM, PWM, OWM, TWM and THAL in cases of PE/GH with FGR. ADC values from supratentorial regions in PE/GH pregnancies were not significantly correlated with GA (P = 0.12, 0.26); however, this trend was statistically significant in the normotensive groups. DATA CONCLUSION: ADC values may indicate fetal brain developmental alterations in PE/GH with FGR fetuses but more microscopic and morphological studies are necessary to provide additional evidence to offer a different interpretation of this trend in fetal brain. LEVEL OF EVIDENCE: 4 TECHNICAL EFFICACY STAGE: 3.

Dimethyl fumarate protects against intestine damage in necrotizing enterocolitis by inhibiting the Toll-like receptor (TLR) inflammatory signaling pathway.

OBJECTIVE: Necrotizing enterocolitis (NEC) is a severe disease in newborns, this study aimed to investigate the protective effect of dimethyl fumarate (DMF) on NEC and its possible mechanism. METHODS: In vivo, the mice were divided into the control, NEC, and NEC+DMF group. The NEC model was established by artificial feeding, hypoxic for 4 days, and lipopolysaccharide (LPS) stimulation on day 2 and day 3. DMF (25 mg/kg/d) was administered to NEC mice on day 1 and day 3. On the 11th day, the blood and intestinal tissues of mice were taken for enzyme-linked immunosorbent assay (ELISA), pathological examination, quantitative real-time PCR (RT-qPCR), Western blot, and immunohistochemical (IHC) detection. In vitro, human colorectal cells (FHC) were induced by LPS (100 ng/mL) and was divided into the control, LPS, and LPS+DMF group. The effect of DMF (20 µM) on cell viability and TLR4 signal transduction was detected by MTT and RT-qPCR, respectively. RESULTS: Compared to the NEC mice, DMF attenuated NEC-induced weight loss and abdominal distension diarrhea in mice, and alleviated NEC-induced intestinal pathological injuries. In addition, DMF reduced the expression of IL-6, IL-1ß, TNF-α, NF-κB, and TLR4 in NEC mice intestinal tissues. Furthermore, DMF inhibited NEC-induced intestinal cell apoptosis as well as the protein expression of BCL2-Associated X (BAX), caspase-3, caspase-9, and increased Bcl-2 (B-cell lymphoma-2) expression. In vitro, DMF improved cell viability, and restrained NF-κB and TLR4 expression in LPS-induced NEC cells. CONCLUSION: DMF has a protective effect against intestine damage of NEC, which is related to the inhibition of the TLR signaling pathway, alleviating the inflammatory response.

The Protective Effect of Sulforaphane on ER-induced Apoptosis and Inflammation in Necrotizing Enterocolitis Mice.

BACKGROUND: Necrotizing enterocolitis (NEC) is a neonatal intestinal necrotizing disease caused by various factors in newborns. Sulforaphane (SFN) has a strong anti-inflammatory ability and a certain protective effect on intestinal diseases. OBJECTIVE: NEC is a common developed gastrointestinal exigency in an untimely baby. SFN is a naturally originated isothiocyanate that has beneficial effects on the intestinal system.The purpose of this study is to study the protective effect of SFN on endoplasmic reticulum stress (ERS)-related NEC. METHODS: The newborn mice were randomly divided into control (n = 15), NEC (n = 20), and NEC+SFN (n = 18) groups. Mice in NEC and SFN+NEC groups were injected with 0.1 µl normal saline or 20 mg/kg/d SFN, respectively. After that, the weight and survival of the mice were recorded every day. Then the mice were sacrificed after 96 h of modeling; ileum tissue and blood samples were collected for qPCR, Western blot, ELISA, HE staining, TUNEL staining, and immunohistochemistry assays. RESULTS: SFN significantly inhibited the mRNA expression of BIP, CHOP, IL-1ß and IL-6, and protein expression of Bax, Caspase-3, Caspase-9 and CHOP, and promoted the expression of Bcl-2 in ER-induced NEC mice intestinal tissues (P<0.01). Meanwhile, SFN could suppress the serum levels of IL-8, IL-10, IL-6, TNF-α, and IL-1ß, and positive expression of TLR4 and NF-κB (P<0.01), and promote the serum levels of IL-10. HE staining showed that SFN alleviated the NEC intestinal tissue injury, and TUNNEL staining showed that SFN could reduce the rate of NEC apoptotic cells (P<0.01). Moreover, SFN treatment improved the body weight and survival rate in NEC mice. CONCLUSION: SFN could effectively protect against ERS-induced inflammation and apoptosis in NEC mice.

A phantom study of a protective trolley for neonatal radiographic imaging: new equipment to protect the operator from scatter radiation.

Chest radiography is commonly performed as a diagnostic tool of neonatal diseases. Contact-based radiation personal protective equipment (RPPE) has been widely used for radiation protection, but it does not provide full body protection and it is often shared between users, which has become a major concern during the coronavirus disease 2019 (COVID-19) pandemic. To address these issues, we developed a novel trolley to protect radiographers against X-ray radiation by reducing scatter radiation during neonatal radiographic examinations. We measured the scatter radiation doses from a standard neonatal chest radiograph to the radiosensitive organs using a phantom operator in three protection scenarios (trolley, radiation personal protective equipment [RPPE], no protection) and at three distances. The results showed that the scatter radiation surface doses were significantly reduced when using the trolley compared with RPPE and with no protection at a short distance (P<0.05 for both scenarios in all radiosensitive organs). The novel protective trolley provides a non-contact protective tool for radiographers against the hazard of scatter radiation during neonatal radiography examinations.

Sulforaphane Ameliorates the Intestinal Injury in Necrotizing Enterocolitis by Regulating the PI3K/Akt/GSK-3ß Signaling Pathway.

Objective: Necrotizing enterocolitis (NEC) is a serious neonatal disease; this study aims to investigate the role of sulforaphane (SFN) in NEC-induced intestinal injury. Methods: An animal model of NEC was established in newborn mice and intragastrically administrated with SFN; then, the general status and survival of the mice were observed. H&E staining was used to observe the pathological changes of intestinal tissues. ELISA, immunohistochemical staining, and flow cytometry assays were used to detect the levels of inflammatory factors, including TNF-α, IL-6, and IL-17, the expression of Bax, Bcl-2, TLR4, and NF-κB, and the percentages of the Th17 and Treg cells, respectively. GSK-3ß expression levels were measured by immunofluorescence. IEC-6 and FHC cells were induced with LPS to mimic NEC in vitro and coincubated with SFN; then, the inflammatory factor levels and cell apoptosis rate were detected. Finally, Western blot was used to assess the expression of PI3K/Akt/GSK-3ß pathway-related proteins in vitro and in vivo. Results: SFN improved the survival rate of NEC mice during modeling, alleviated the severity of the intestinal injury, and reduced the proportion of Th17/Treg cells. SFN could inhibit TLR4 and NF-κB levels, decrease the release of inflammatory factors TNF-α and IL-6, suppress Bax expression, increase Bcl-2 expression, and inhibit apoptosis both in in vitro and in vivo models of NEC. Meanwhile, SFN regulated the expression of PI3K/Akt/GSK-3ß pathway-related proteins in vitro and in vivo. Conclusion: SFN relieved the inflammatory response and apoptosis by regulating the PI3K/Akt/GSK-3ß signaling pathway, thereby alleviating NEC in model mice and cells.

Melatonin Alleviates Neonatal Necrotizing Enterocolitis by Repressing the Activation of the NLRP3 Inflammasome.

Objective: Necrotizing enterocolitis (NEC) is one of the commonest gastrointestinal critical diseases in newborns. Several researches have proven the efficacy of melatonin (MEL) on NEC, but the latent mechanisms were ambiguous. We designed the current research to evaluate the function and mechanism of MEL on NEC in a neonatal mouse model. Methods: The newborn mice were subjected to formula milk containing LPS and hypoxia to establish a NEC model and also intraperitoneally injected with MEL. During the experiment, all mice were closely monitored and weighed. The effect of MEL on the histopathological injury of the terminal ileum tissues, inflammation, and oxidative stress of serum in NEC mice was examined by hematoxylin-eosin (H&E) staining and ELISA. The effect of MEL on the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome was assessed via quantitative real-time PCR and Western blot. Results: MEL intensified the survival rate and body weight in NEC mice. The H&E staining illustrated that MEL improved the histopathological injury in NEC mice. Moreover, MEL repressed the IL-1ß, TNF-α, and MDA levels of serum and enhanced the SOD and GSH-Px levels of serum in NEC mice. We also discovered that MEL attenuated the mRNA and protein levels of NLRP3, Toll-like Receptor 4 (TLR4), NF-κB, and caspase-1 of the terminal ileum tissues in NEC mice. Conclusion: Our research illuminated that MEL attenuated the severity of NEC via weakening the activation of the NLRP3 inflammasome.

Alterations of brain metrics in fetuses of women with polycystic ovary syndrome : a retrospective study based on fetal magnetic resonance imaging.

BACKGROUND: Maternal polycystic ovary syndrome (PCOS) has potential detrimental effects on the neurodevelopment of offspring. This study aimed to evaluate the brain metrics in fetuses of women with PCOS based on fetal magnetic resonance imaging (MRI). METHODS: This retrospective study included 60 pregnant women with PCOS (PCOS group) and 120 pregnant non-PCOS women (control group). Fetal MRI was performed followed an ultrasound and for numerous clinical indications including known or suspected fetal pathology, history of fetal abnormality in previous pregnancy or in a family member. Fetal brain biometry and apparent diffusion coefficient (ADC) value were analysed. RESULTS: After adjusting for potential confounders, fetuses in the PCOS group showed the following characteristics compared to fetuses in the control group: (1) smaller cerebral fronto-occipital diameter (FOD), vermian height (VH) and anteroposterior diameter of the pons (APDP) (evident before 32 weeks; P = 0.042, P = 0.002 and P = 0.016, respectively); (2) larger left and right biparietal index (evident before 32 weeks; P = 0.048 and P = 0.025, respectively); (3) smaller left lateral ventricle (LV) (evident after 32 weeks; P = 0.005); (4) larger anteroposterior diameter of the vermis (APDV) and hippocampal infolding angle (HIA) (evident after 32 weeks; P = 0.003 and P < 0.001, respectively); (5) higher ADC value in frontal white matter (FWM) and in basal ganglia (BG) (evident before and after 32 weeks; all P < 0.05). CONCLUSIONS: There exist a different pattern of brain metrics in PCOS offspring in utero.

Case report of Langerhans cell histiocytosis in a fetus detected by magnetic resonance imaging.

Langerhans cell histiocytosis (LCH) is a rare disease, and the diagnosis of LCH is mainly based on clinical manifestation, imaging and pathological examinations. But during pregnancy, imaging examinations especially play an important role in the diagnosis and prognostic assessment of fetal LCH. Up to now, there has been no report about magnetic resonance imaging (MRI) features of fetal LCH. We reported a 32-year-old woman at 36 weeks' gestation took fetal MRI because of fetal anomalies diagnosed by ultrasonography. On the fetus's MR images, the thymus was slightly enlarged with smooth or lobulated contour in supra anterior mediastinum, displayed heterogeneous signals and contained multiple small cysts on T2WI. Innumerable irregular nodules and patchy shadows were present throughout both lungs. Pulmonary lesions were bilateral and diffuse with relative sparing of the costophrenic angles. The margins of these lesions were fluffy and indistinct. These lesions showed heterogeneous signals on T2WI. MRI showed no lesions in skin region. After birth, lots of round or oval skin lesions distributed all over the baby's body presenting as ulcerated or blister-like rashes. The chest computer tomography (CT) showed punctate calcification and heterogeneous enhancement in the thymus and bilateral diffuse reticular or reticulonodular opacities in both lungs with fluffy and indistinct margins. Pathological finding was consistent with LCH. Through reporting MRI features of LCH in one fetus, this study aims to improve awareness of fetal LCH in radiologists and clinicians, to improve the prenatal diagnostic rate of this disorder.

Fetal growth, fetal development, and placental features in women with polycystic ovary syndrome: analysis based on fetal and placental magnetic resonance imaging.

OBJECTIVE: Polycystic ovary syndrome (PCOS), a common endocrine-metabolic dysfunction in reproductive-aged women, may be involved in compromised pregnancy and offspring outcomes. This study aimed to investigate whether maternal PCOS affects fetal growth, fetal development, and placental features. METHODS: This retrospective case-control study included 60 pregnant women with PCOS (PCOS group) and 120 healthy pregnant women without PCOS (control group). Fetal magnetic resonance imaging (MRI) was performed followed by an ultrasound examination and indications for imaging, including known or suspected fetal pathology, history of fetal abnormality in previous pregnancy or in a family member, and concern for placenta accreta. Fetal MRI images were analyzed for head circumference (HC), abdomen circumference (AC), lung-to-liver signal intensity ratio (LLSIR, a prenatal marker of fetal lung maturity), lengths of liver and kidney diameters in fetuses, and placental relative signal intensity on T2-weighted single-shot fast spin echo (SSFSE) imaging (rSISSFSE), and placental relative apparent diffusion coefficient value (rADC). Data on height and weight of offspring were collected through telephone follow-up. RESULTS: Compared to the control group, the PCOS group showed the following characteristics: (1) smaller biparietal diameter and femur length in fetuses (P=0.026 and P=0.005, respectively), (2) smaller HC in fetuses (evident after 32 weeks; P=0.044), (3) lower LLSIR and smaller dorsoventral length of liver in fetuses (evident before 32 weeks; P=0.005 and P=0.019, respectively), and (4) smaller placental thickness (evident before 32 weeks; P=0.017). No significant differences in placental rSISSFSE or rADC were observed between the groups (all P>0.05). No significant differences in height and weight of offspring during childhood existed between the groups (all P>0.05). CONCLUSIONS: There exist alterations of fetal growth, fetal development, and placental features from women with PCOS.