Research on the coupling coordination relationship between the digital economy and high-quality energy development: Evidence from China.

The deep integration of the digital economy and high-quality energy development is a vital breakthrough in promoting the digital transformation and upgrading of energy, and it is also a critical path to achieving green and low-carbon development. However, the degree of integration of the two has yet to be discovered. This article measures the coupling coordination degree of the digital economy and high-quality energy development using panel data from 30 provinces in China from 2013 to 2020, explores the spatiotemporal evolution characteristics of the coupling coordination degree, and further analyzes the driving factors of the coupling coordination degree. The results show that:(1) The coupling coordination degree shows an upward trend, but there are apparent gradient differences and spatial non-equilibrium features in the coupling coordination degree among provinces. (2) The coupling coordination degree shows a "parabolic" spatial trend of "high east and low west" in the east-west direction and an "inverted U-shaped" spatial trend in the north-south direction. (3) The center of gravity of the coupling coordination degree moves to the southwest, clustering in the northeast-southwest direction and showing a spreading trend in the southeast-northwest direction. (4) The coupling coordination degree has a significant positive spatial correlation, and the cold-hot spot gradually develops into a distribution pattern with the Yangtze River Delta in China as the agglomeration center. (5) Economic development, industrial structure, government behavior, environmental regulation, urbanization, technological innovation, and external openness significantly impact the coupling coordination degree. In addition, economic development and human capital have a positive spatial spillover effect on the coupling coordination degree. Urbanization level and technological innovation have a negative spatial spillover effect on the coupling coordination degree. Accordingly, to promote the coupling and interaction between the digital economy and high-quality energy development, the government should take effective measures in optimizing the industrial structure, scientifically promoting the urbanization process, and enhancing the scientific and technological innovation capacity.

Circ-AGTPBP1 promotes white matter injury through miR-140-3p/Pcdh17 axis role of Circ-AGTPBP1 in white matter injury.

White matter injury (WMI) resulting from intracerebral hemorrhage (ICH) is closely associated with adverse prognoses in ICH patients. Although Circ-AGTPBP1 has been reported to exhibit high expression in the serum of premature infants with WMI, its effects and mechanisms in ICH-induced WMI remain unclear. This study aimed to investigate the role of circ-AGTPBP1 in white matter injury after intracerebral hemorrhage. An intracerebral hemorrhage rat model was established by injecting autologous blood into rat left ventricles and circ-AGTPBP1 was knocked down at the ICH site using recombinant adeno-associated virus, AAV2/9. Magnetic resonance imaging (MRI) and gait analysis were conducted to assess long-term neurobehavioral effects. Primary oligodendrocyte progenitor cells (OPCs) were isolated from rats and overexpressed with circ-AGTPBP1. Downstream targets of circ-AGTPBP1 in OPCs were investigated using CircInteractome, qPCR, FISH analysis, and miRDB network. Luciferase gene assay was utilized to explore the relationship between miR-140-3p and Pcdh17 in OPCs and HEK-293T cells. Finally, CCK-8 assay, EdU staining, and flow cytometry were employed to evaluate the effects of mi-RNA-140-3p inhibitor or silencing of sh-pcd17 on the viability, proliferation, and apoptosis of OPCs. Low expression of circ-AGTPBP1 alleviates white matter injury and improves neurological functions in rats after intracerebral hemorrhage. Conversely, overexpression of circ-AGTPBP1 reduces the proliferative and migrative potential of oligodendrocyte progenitor cells and promotes apoptosis. CircInteractome web tool and qPCR confirmed that circ-AGTPBP1 binds with miR-140-3p in OPCs. Additionally, miRDB network predicted Pcdh17 as a downstream target of miR-140-3p. Moreover, pcdh17 expression was increased in the brain tissue of rats with intracerebral-induced white matter injury. Furthermore, inhibiting miR-140-3p suppressed the proliferation and migration of OPCs and facilitated apoptosis through Pcdh17. Circ-AGTPBP1 promotes white matter injury through modulating the miR-140-3p/Pcdh17 axis. The study provides a new direction for developing therapeutic strategies for white matter injury.

Identification and Validation of Signature Genes and Their Correlations with Infiltrated Immune Cells in Neonatal Sepsis.

Background and Objective: There is increasing demand to identify accurate and reliable molecular biomarkers for early diagnosis of neonatal sepsis. We aimed to identify and verify signature genes in neonatal sepsis through comprehensive bioinformatics analysis. Methods: A Gene Expression Omnibus data set was used to identify differentially expressed genes (DEGs) in patients with neonatal sepsis and healthy controls by functional and disease enrichment analysis. Gene set enrichment analysis, screening of DEGs using 2 machine algorithms, analysis of receiver operating characteristic curves, and correlation analysis with infiltrating immune cells was performed. Results: We identified 433 DEGs: 144 downregulated and 289 upregulated. Gene Ontology analysis identified DEGs for T cell activation, positive regulation of cytokine production, secretory granule cavity, cytoplasmic vesicle cavity, immune receptor activity, and antioxidant activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis identified DEGs for hematopoietic cell lineage, cytokine-cytokine receptor interaction, and coronavirus disease (COVID-19). Disease Ontology analysis identified DEGs for hematopoietic system diseases, skin system diseases, and bacterial infectious diseases. We also gained understanding of the enrichment of various functions and pathways by gene set enrichment analysis. In the neonatal sepsis group, Gene Ontology analysis results were significant for coagulation, endocytosis, white cell migration, myeloid leukocyte-mediated immunity, and phagocytosis; KEGG analysis results were significant for chemokine signaling pathway, complement and coagulation cascade, leukocyte migration across endothelium, regulation of actin cytoskeleton, and toll-like receptor signaling pathway. We screened 2 signature DEGs (GSN and SEMA4B) using the least absolute shrinkage and selection operator and support vector machine recursive feature elimination algorithms and verified their diagnostic accuracy by receiver operating characteristic curves. We correlated GSN and SEMA4B expression levels with the infiltration levels of 22 types of immune cell. Conclusion: GSN and SEMA4B expression accurately predicted early-stage neonatal sepsis, which is beneficial for early clinical diagnosis and treatment.

miR-125b-5p Suppresses Leukemia Cell Proliferation by Regulating MCL1.

Leukemia threatens children's health, and leukemia cell proliferation and apoptosis participate in the regulation of leukemia. The current study aims to probe into the miR-125b-5p biological function in regulating leukemia cell proliferation and apoptosis by myeloid cell leukemia 1 (MCL1). Quantitative real-time polymerase chain reaction was conducted to quantify miR-125b-5p expression in leukemia cells. Cell transfection, cell-counting assay 8, Western blot, and flow cytometry assays were applied to assess the miR-125b-5p function in leukemia. A dual-luciferase reporter gene assay was applied to investigate the mechanism. miR-125b-5p was lessened in leukemia cells, and the increased miR-125b-5p repressed leukemia cell proliferation and boosted apoptosis. Further, miR-125b-5p could bound with the MCL1 3'-untranslated region and regulated its expression. Furthermore, the elevated expression of miR-125b-5p repressed leukemia cell proliferation and boosted apoptosis through downregulating MCL1. miR-125b-5p inhibited leukemia cell proliferation and boosted apoptosis through decreasing MCL1.

Clinical Observation of Extensively Hydrolysis Protein Formula With Feeding Intolerance in Preterm Infants.

Objective: To investigate whether feeding extensively hydrolysis protein formula during the NICU hospitalization was more beneficial for preterm infants with a gestational age (GA) ≤34 weeks when breastfeeding was not possible. Methods: In total, 587 preterm infants were randomly divided into two groups: observation groups fed with extensively hydrolyzed formula (EHF) milk and control groups fed with standard preterm formula (SPF) milk until discharge from the neonatal intensive care unit (NICU). The incidence of complications during hospitalization was recorded in both groups. Then, two groups were uniformly fed with 0-to-6-month infant formula milk and followed-up for 6 months after discharge. Results: The final study included 370 premature infants, including 185 babies in the observation group and 185 in the control group. In contrast to the SPF, feeding EHF among preterm infants of GA <34 weeks during NICU hospitalization significantly reduced the incidence of feeding intolerance (FI) (14.1 vs. 30.3%, p < 0.01). The incidence of necrotizing enterocolitis (NEC) was significantly reduced in the observation group (2.2 vs. 6.5%, p < 0.05), but there was no significant difference in the incidence of other related complications. At discharge, there was no difference in total serum protein (46.6 vs. 46.4 g/L), albumin (33.5 vs. 34.2 g/L), and calcium (2.37 vs. 2.35 mmol/L), but the serum phosphorus concentrations associated with skeletal mineralization (2.10 vs. 2.22 mmol/L, p < 0.05) was significantly reduced and alkaline phosphatase significantly rose (254 vs. 220 IU/L, p < 0.05) in the observation group. No significant difference was found in the growth rates of body weight, head circumference, or body length, either during the NICU hospitalization or during the 6-month follow-up after discharge (p > 0.05). Conclusions: Feeding premature infants of GA ≤34 weeks with EHF reduced the incidence of FI, but had no advantage in establishing whole intestinal nutrition, shortening parenteral nutrition (PN) time, or hospitalization time. It had little effect on physical growth or development during NICU hospitalization and within 6 months after discharge. However, it may increase the incidence of metabolic bone disease (MBD).

Novel Pathogenic Mutation of PNPLA1 Identified in Autosomal Recessive Congenital Ichthyosis: A Case Report.

Autosomal recessive congenital ichthyosis (ARCI) is characterized by being born as collodion babies, hyperkeratosis, and skin scaling. We described a collodion baby at birth with mild ectropion, eclabium, and syndactyly. Whole exome sequencing showed a compound heterozygous variant c.[56C>A], p.(Ser19X) and c.[100G>A], p.(Ala34Thr) in the PNPLA1 gene [NM_001145717; exon 1]. The protein encoded by PNPLA1 acts as a unique transacylase that specifically transfers linoleic acid from triglyceride to ω-hydroxy fatty acid in ceramide, thus giving rise to ω-O-acylceramide, a particular class of sphingolipids that is essential for skin barrier function. The variant was located in the patatin core domain of PNPLA1 and resulted in a truncated protein which could disrupt the function of the protein. This case report highlights a novel compound heterozygous mutation in PNPLA1 identified in a Chinese child.

Novel Pathogenic Mutation of PNPLA1 Identified in Autosomal Recessive Congenital Ichthyosis: A Case Report / 中国医学科学杂志(英文版)

Autosomal recessive congenital ichthyosis (ARCI) is characterized by being born as collodion babies, hyperkeratosis, and skin scaling. We described a collodion baby at birth with mild ectropion, eclabium, and syndactyly. Whole exome sequencing showed a compound heterozygous variant c.[56C>A], p.(Ser19X) and c.[100G>A], p.(Ala34Thr) in the PNPLA1 gene [NM_001145717; exon 1]. The protein encoded by PNPLA1 acts as a unique transacylase that specifically transfers linoleic acid from triglyceride to ω-hydroxy fatty acid in ceramide, thus giving rise to ω-O-acylceramide, a particular class of sphingolipids that is essential for skin barrier function. The variant was located in the patatin core domain of PNPLA1 and resulted in a truncated protein which could disrupt the function of the protein. This case report highlights a novel compound heterozygous mutation in PNPLA1 identified in a Chinese child.

A Narrative Review of Circular RNAs in Brain Development and Diseases of Preterm Infants.

Circular RNAs (circRNAs) generated by back-splicing are the vital class of non-coding RNAs (ncRNAs). Circular RNAs are highly abundant and stable in eukaryotes, and many of them are evolutionarily conserved. They are blessed with higher expression in mammalian brains and could take part in the regulation of physiological and pathophysiological processes. In addition, premature birth is important in neurodevelopmental diseases. Brain damage in preterm infants may represent the main cause of long-term neurodevelopmental disorders in surviving babies. Until recently, more and more researches have been evidenced that circRNAs are involved in the pathogenesis of encephalopathy of premature. We aim at explaining neuroinflammation promoting the brain damage. In this review, we summarize the current findings of circRNAs properties, expression, and functions, as well as their significances in the neurodevelopmental impairments, white matter damage (WMD) and hypoxic-ischemic encephalopathy (HIE). So we think that circRNAs have a direct impact on neurodevelopment and brain injury, and will be a powerful tool in the repair of the injured immature brain. Even though their exact roles and mechanisms of gene regulation remain elusive, circRNAs have potential applications as diagnostic biomarkers for brain damage and the target for neuroprotective intervention.

Dissecting the Roles of LncRNAs in the Development of Periventricular White Matter Damage.

Long non-coding RNA (LncRNA) has high expression in the brain. Animal studies have shown that lncRNA plays an important role in brain functions and mediates the development of many neurological diseases. However, data on the expression of lncRNAs and the clinical significance in prematurely born infants with diseases such as periventricular white matter damage (PWMD) remains scant. Here, we compared the expression of the lncRNAs in whole blood samples obtained from prematurely born infants with PWMD with samples from prematurely born infants without PWMD. Our data demonstrated differential expression of the lncRNAs between the two groups. Further, we showed that the lncRNAs play important roles in the development of PWMD. Our findings give insights into the functions of the lncRNAs in PWMD and provide evidence for the improvement of diagnostic and treatment strategies in infants with PWMD.

[Analysis of PNPLA1 gene mutation in a child with ichthyosis].

OBJECTIVE: To explore the genetic basis for a child with ichthyosis. METHODS: High-throughput sequencing was carried out to detect genomic copy number variants (CNVs) and variant of the medical exome. Candidate variant was verified by Sanger sequencing. RESULTS: No disease-related CNV was identified in the patient. High-throughput sequencing revealed that the child has carried compound heterozygous variants of the PNPLA1 gene, including a previously known pathogenic c.100G>A (p.Ala34Thr) mutation and a novel c.56C>A (p.Ser19x) variant which was predicted to be a pathogenic according to the ACMG guidelines. Sanger sequencing confirmed both variants in the child. Her father and mother were found to be heterozygous carriers for the c.56C>A (p.Ser19x) and c.100G>A (p.Ala34Thr) variants, respectively. CONCLUSION: The compound heterozygous c.100G>A and c.56C>A variants of the PNPLA1 gene probably underlay the ichthyosis in this child.

Silencing of long non­coding antisense RNA brain­derived neurotrophic factor attenuates hypoxia/ischemia­induced neonatal brain injury.

Hypoxic/ischemic (HI) brain damage (HIBD) is a major cause of acute neonatal brain injury, leading to high mortality and serious neurological deficits. The antisense RNA of brain­derived neurotrophic factor (BDNF­AS) is transcribed from the opposite strand of the BDNF gene. The aim of the present study was to investigate the role of BDNF­AS in HI­induced neuronal cell injury in vivo and in vitro. Reverse transcription­quantitative PCR (RT­qPCR) assays indicated that BDNF­AS expression was significantly upregulated in HI­injured neonatal brains and hippocampal neurons. However, BDNF expression was downregulated in HI­injured neonatal brains and hippocampal neurons. Cell Counting Kit­8 assays, Hoechst staining, calcein­AM/PI staining, immunostaining, water maze tests and rotarod tests demonstrated that BDNF­AS silencing protected against hypoxia­induced primary hippocampal neuron injury in vitro and HI­induced brain injury in vivo. Mechanistically, RT­qPCR assays and western blotting indicated that BDNF­AS silencing led to increased expression of BDNF and activated the BDNF­mediated signaling pathway, as demonstrated by increased expression levels of BDNF, phosphorylated­Akt and phosphorylated­tropomyosin receptor kinase B. Collectively, the present study provides important insights into the pathogenesis of HIBD, and it was indicated that BDNF­AS silencing may be a promising approach for the treatment of neonatal HIBD.

Circular RNA expression alteration in whole blood of premature infants with periventricular white matter damage.

Circular RNAs (circRNAs) are evolutionarily conserved and tissue-specific types of non-coding RNA and can serve as potential diagnostic biomarkers for disease. However, the clinical significance and levels of expression of circRNAs for whole blood samples of prematurely born infants afflicted by diseases such as periventricular white matter damage (PWMD) are largely unknown. Therefore, we sought to identify measures of expression of circRNAs in whole blood samples obtained from prematurely born infants afflicted by PWMD and comparatively in samples from prematurely born infants without PWMD. We found the expression levels of circRNAs which from premature with PWMD has changed. Further analysis suggests that these circRNAs have important roles in PWMD. This study can improve the understanding for the potential of the circRNAs to serve as biomarkers in PWMD. Moreover, these circRNAs may provide evidence for improving diagnosis and treatment for infants afflicted by PWMD, and merits continued research.

[Safety and efficacy of caffeine use started at different time in preterm infants: a multicenter study in Jiangsu Province, China].

OBJECTIVE: To study the efficacy and safety of caffeine used in the early (≤72 hours after birth) and late (>72 hours after birth) stage in preterm infants with a gestational age of ≤31 weeks. METHODS: A retrospective analysis was performed for 640 preterm infants (with a gestational age of ≤31 weeks) who were admitted to the neonatal intensive care unit of eight hospitals in Jiangsu Province, China. Of the 640 preterm infants, 510 were given caffeine in the early stage (≤72 hours after birth; early use group) and 130 were given caffeine in the late stage (>72 hours after birth; late use group). The clinical data were compared between the two groups. RESULTS: There were no significant differences in birth weight, Apgar score, sex, gestational age, and age on admission between the two groups (P>0.05). Compared with the late use group, the early use group had a significantly younger age at the beginning and withdrawal of caffeine treatment (P<0.05) and a significantly shorter duration of caffeine treatment (P<0.05). There was no significant difference in respiratory support on admission between the two groups (P>0.05). Compared with the late use group, the early use group had significantly lower incidence rate of apnea (P<0.05) and significantly shorter oxygen supply time and length of hospital stay (P<0.05). There were no significant differences between the two groups in the incidence rates of neonatal intracranial hemorrhage, periventricular leukomalacia, necrotizing enterocolitis, retinopathy of prematurity, and patent ductus arteriosus at discharge and NBNA score at the corrected gestational age of 40 weeks (P>0.05). However, significant differences were found in the incidence of bronchopulmonary dysplasia and the rate of home oxygen therapy, but there was no significant difference in the mortality rate between the two groups (P>0.05). CONCLUSIONS: Early use of caffeine can shorten the duration of caffeine treatment, oxygen supply time, and length of hospital stay, with little adverse effect, in preterm infants with a gestational age of ≤31 weeks.

Long non-coding RNA Snhg3 protects against hypoxia/ischemia-induced neonatal brain injury.

Hypoxic-ischemic brain damage (HIBD) is a major cause of morbidity and mortality in the preterm and term infant. However, the precise mechanism of HIBD remains largely elusive. As a newly discovered long non-coding RNA, small nucleolar RNA host gene 3 (Snhg3) has shown its important roles in cell apoptosis, proliferation, and disease development. In this study, we determined the role of Snhg3 in the pathogenesis of HIBD. Snhg3 expression was significantly down-regulated in the neonatal brain and primary hippocampal cells response to hypoxic/ischemic stress. Snhg3 overexpression protected against hypoxic/ischemic-induced brain injury in vivo and hippocampal cell injury in vitro. Snhg3 acted as the sponge of miR-196 in the hippocampal cells by regulating the expression of miR-196 target genes, XIAP and CAAP1. Moreover, Snhg3 overexpression decreased brain infarct size and ameliorated hypoxic-ischemic neonatal brain damage. This study suggests that Snhg3 is a potential target for the treatment of HIBD.

Risk factors and outcomes of acute kidney injury in ventilated newborns.

Purpose: This study aimed to investigate the occurrence and risk factors of acute kidney injury (AKI) in ventilated newborns.Methods: In total, 139 newborns receiving mechanical ventilation (MV) were reviewed in this retrospective study. The demographic and clinical data were collected. Then, the independent risk factors for AKI were evaluated using univariate and multivariate logistic regression analyses.Results: The incidence rate of AKI was 15.11% (21/139) in ventilated newborns. Univariate analysis showed significant differences in gestational age, birth weight, Apagar scores, the highest oxygen concentration, serum creatinine levels at admission and 48 h after MV, history of asphyxia, urine output at 48 h after MV, invasive MV, noninvasive MV, and outcomes between AKI and non-AKI groups (all p < .05). The lower gestational age (odd ratio (OR): 1.194, 95% confidence interval (CI): 1.013-1.407, p = .035), the increased use of invasive mechanical ventilation (IMV) (OR: 4.790, 95% CI: 1.115-20.575, p = .035), and lower birth weight (OR: 0.377, 95% CI: 0.178-0.801, p = .011) were independent risk factors for the occurrence of AKI. Additionally, higher stage of AKI was significantly associated with poor prognosis of AKI (p = .018).Conclusion: In this retrospective study, it was found that lower gestational age, birth weight, and increased use of IMV were independent risk factors for AKI in ventilated newborns. The poor prognosis might be indicated by the higher AKI stage.

Long noncoding RNA ROR1-AS1 enhances lung adenocarcinoma metastasis and induces epithelial-mesenchymal transition by sponging miR-375.

PURPOSE: The vital role of long noncoding RNAs (lncRNAs) in tumor progression have been identified in numerous studies. In this research, lncRNA ROR1-AS1 was explored to verify its function during the development of lung adenocarcinoma (LAC). METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) was utilized to measure ROR1-AS1 expression of LAC tissues. Function assays including wound healing assay and transwell assay were conducted to detect the effect of knockdown of ROR1-AS1 on the metastasis of LAC, and luciferase assays and RNA immunoprecipitation assay (RIP) were also performed to explore the underlying mechanism. RESULTS: ROR1-AS1 expression level was significantly higher in LAC samples compared with that in adjacent tissues, which was associated with patients' prognosis. Knockdown of ROR1-AS1 inhibited cell migration and cell invasion of LAC cells via suppressing epithelial-mesenchymal transition (EMT) process. Furthermore, it was discovered that ROR1-AS1 acted as a competing endogenous RNA via sponging miR-375 in LAC. CONCLUSIONS: These results suggested that ROR1-AS1 could act as a sponge for miR-375 and promo//e cell migration and invasion through suppressing the process of EMT in LAC, which may offer a potential therapeutic target in LAC.

Analysis of curative effects of human gamma globulin on bacterial pneumonia in pediatric patients.

The main aim of this study was to investigate the effects of human gamma globulin (HGG) on inflammation targets in children. A total of 80 children were randomly divided into observation and control group with 40 cases in each group. The control group was given comprehensive treatment while the observation group was treated with HGG. The time of disappearance of clinical signs and symptoms, time of improvement of pulmonary iconography, inflammatory indices, time and degree of improvement of lung function and adverse reactions were observed. The total effective rate in the observation group was 97.5% and significantly higher than control group (77.5%). The time of fever clearance, imaging improvement as well as cough and pulmonary rales disappearance in the observation group was shorter than control group. After treatment, the levels of inflammatory indicators such as erythrocyte sedimentation rate (ESR) and C-reaction protein (CRP) in the observation group were lower than control group. No obvious abnormalities of urea nitrogen, creatinine, serum alanine amino transferase (ALT) and aspartate amino transferase (AST) were found in the two groups. Overall, HGG effectively shortened the course of RMPP, improved the cure rate, reduced the inflammatory reaction and promoted the recovery of lung function without obvious adverse reaction.

Genomics of neonatal sepsis: has-miR-150 targeting BCL11B functions in disease progression.

BACKGROUND: Neonatal sepsis is an inflammatory systemic syndrome, which is a major cause of morbidity and mortality in premature infants. We analyzed the expression profile data of E-MTAB-4785 to reveal the pathogenesis of the disease. METHODS: The expression profile dataset E-MTAB-4785, which contained 17 sepsis samples and 19 normal samples, was obtained from the ArrayExpress database. The differentially expressed genes (DEGs) were analyzed by the Bayesian testing method in limma package. Based on the DAVID online tool, enrichment analysis was conducted for the DEGs. Using STRING database and Cytoscape software, protein-protein interaction (PPI) network and module analyses were performed. Besides, transcription factor (TF)-DEG regulatory network was also constructed by Cytoscape software. Additionally, miRNA-DEG pairs were searched using miR2Disease and miRWalk 2.0 databases, followed by miRNA-DEG regulatory network was visualized by Cytoscape software. RESULTS: A total of 275 DEGs were identified from the sepsis samples in comparison to normal samples. TSPO, MAPK14, and ZAP70 were the hub nodes in the PPI network. Pathway enrichment analysis indicated that CEBPB and MAPK14 were enriched in TNF signaling pathway. Moreover, CEBPB and has-miR-150 might function in neonatal sepsis separately through targeting MAPK14 and BCL11B in the regulatory networks. These genes and miRNA might be novel targets for the clinical treatment of neonatal sepsis. CONCLUSION: TSPO, ZAP70, CEBPB targeting MAPK14, has-miR-150 targeting BCL11B might affect the pathogenesis of neonatal sepsis. However, their roles in neonatal sepsis still needed to be confirmed by further experimental researches.

Circular RNA Expression in the Brain of a Neonatal Rat Model of Periventricular White Matter Damage.

BACKGROUND/AIMS: Periventricular white matter damage (PWMD) is the predominant neurologic lesion in preterm infants who survive brain injury. In this study, we assessed the global changes in and characteristics of the transcriptome of circular RNAs (circRNAs) in the brain tissues of rats with PWMD. METHODS: We compared the expression profiles of circRNAs in brain samples from three rats with PWMD and three paired control tissues using deep RNA sequencing. Bioinformatics analysis was applied to investigate these differentially expressed circRNAs, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis was performed to confirm the results. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to predict associated cell signaling pathways and functions. Network analysis was performed to predict circRNAs-microRNAs, and target genes related to PWMD. RESULTS: A total of 2151 more reliable circRNAs were dysregulated in the brain tissues of rats with PWMD, indicating a potential role in the condition. Of the 98 circRNAs significantly differentially expressed in rat brains with PWMD (P< 0.05), 52 were significantly over-expressed and 46 were significantly under-expressed. The expression profiles of seven of 10 randomly selected circRNAs were confirmed by qRT-PCR analysis. The glutamatergic synapse pathway and the VEGF signaling pathway, both associated with hypoxia/ischemia induced brain damage, were inriched. Relationship between miRNA (rno-miR-433-3p and rno-miR-206-3p) and HIF-1α were evident and potential associations between chr6: 48820833|48857932 and their target genes (rno-miR-433-3p and rno-miR-206-3p) were identified. CONCLUSION: The distinct expression patterns of circRNAs in the brain tissues of rats with PWMD suggest that circRNAs actively respond to hypoxia-ischemia. These findings could assist the development of novel diagnostic and therapeutic targets for PWMD therapy.

GAS5 silencing protects against hypoxia/ischemia-induced neonatal brain injury.

Hypoxic/ischemic brain damage (HIBD) leads to high neonatal mortality and severe neurologic morbidity. However, the molecular mechanism of HIBD in the neonatal infant is still elusive. Long non-coding RNAs are shown as important regulators of brain development and many neurological diseases. Here, we determined the role of long noncoding RNA-GAS5 in HIBD. GAS5 expression was significantly up-regulated in hypoxic/ischemic-injured neonatal brain and hippocampal neurons. GAS5 silencing protected against hypoxic/ischemic-induced brain injury in vivo and primary hippocampal neuron injury in vitro. Mechanistically, GAS5 regulated hippocampal neuron function by sponging miR-23a. Intracerebroventricular injection of GAS5 shRNA significantly decreased brain GAS5 expression, reduced brain infarct size, and improved neurological function recovery. Collectively, this study suggests a promising therapeutic approach of GAS5 inhibition in the treatment of neonatal HIBD.