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International guidelines regarding the role of intravenous immunoglobulin (IVIG) in the management of Rh- and ABO-mediated haemolytic disease of the newborn was drafted by an international panel of experts in the fields of hematology, neonatology, and blood transfusion and was published in British Journal of Haematology on March 16, 2022. The guidelines summarize the evidence-based practice of IVIG in Rh- and ABO-mediated haemolytic disease of the newborn and propose related recommendations. The guidelines recommend that IVIG should not be applied as a routine treatment regimen for Rh- and ABO-mediated haemolytic disease of the newborn in order to reduce exchange transfusion (ET), and the best time to apply IVIG remains unclear in the situations where hyperbilirubinaemia is severe (approaching or exceeding the ET threshold) or ET cannot be implemented. These guidelines are formulated with rigorous methods, but with the lower quality of evidence.

Several studies have assessed the association between cerebral palsy (CP) and assisted reproductive technology (ART), but the results remain controversial. We conducted a meta-analysis to evaluate the risk of CP after ART compared with natural conceptions and to examine CP risk separately in ART singletons, multiples and preterm births.Web-based databases (PubMed, Embase, the Cochrane Library, and Web of Science) were searched until November 22, 2020. Studies which compare CP rates after ART with natural conceptions were included. The Newcastle-Ottawa Scale was used to assess the quality of the included studies. Effect estimates were extracted and combined using the fixed-effects or random-effects model depending on the heterogeneity test.There were nine studies included in the meta-analysis. The included studies were of moderate or high quality. A significantly higher risk of CP [odds ratio (OR) = 2.17, 95% confidence interval (CI) 1.72-2.74] was found in ART children (n = 89,214) compared with naturally conceived children (n = 4,160,745). The significantly higher risk decreased when data were restricted to singletons (OR = 1.36, 95% CI 1.16-1.59) and disappeared when data were restricted to multiples (OR = 1.05, 95% CI 0.86-1.29) or preterm births (OR = 1.53, 95% CI 0.66-3.56). Subgroup and sensitivity analyses indicated that the overall results were robust.The risk of CP is increased more than two-fold after ART. This increased risk is largely due to increased rates of multiple birth and preterm delivery in ART children.

Front cover: The cover image is based on the Original Article Regulation of hippocampal neuronal apoptosis and autophagy in mice with sepsis‐associated encephalopathy by immunity‐related GTPase M1 by Rui‐Xi Zhou et al., https://doi.org/10.1111/cns.13229. [Image: see text]

OBJECTIVE: To study the effect and mechanism of action of irisin on hypoxic-ischemic brain damage in neonatal rats. METHODS: A total of 248 7-day-old Sprague-Dawley rats were randomly divided into a sham-operation group, a model group, and low-and high-dose irisin intervention groups (n=62 each). The rats in the model and irisin intervention groups were given hypoxic treatment after right common carotid artery ligation to establish a model of hypoxic-ischemic brain damage. Those in the sham-operation group were given the separation of the right common carotid artery without ligation or hypoxic treatment. The rats in the high-and low-dose irisin intervention groups were given intracerebroventricular injection of recombinant irisin polypeptide at a dose of 0.30 μg and 0.15 μg respectively. Those in the model and sham-operation groups were given the injection of an equal volume of PBS. The water maze test was used to compare neurological behaviors between groups. TTC staining, hematoxylin-eosin staining and TUNEL staining were used to observe histopathological changes of the brain. Western blot was used to measure the expression of the apoptosis-related molecules cleaved-caspase-3 (CC3), BCL-2 and BAX. RESULTS: Compared with the sham-operation group, the model group had a significant increase in latency time and a significant reduction in the number of platform crossings (P < 0.05). Compared with the model group, the high-dose irisin intervention group had a significant reduction in latency time and a significant increase in the number of platform crossings (P < 0.05). Compared with the sham-operation group, the model group had massive infarction in the right hemisphere, with significant increases in karyopyknosis and karyorrhexis. Compared with the model group, the high-dose irisin intervention group had a smaller infarct area of the right hemisphere, with reductions in karyopyknosis and karyorrhexis. The model group had a significantly higher apoptosis rate of cells in the right cerebral cortex and the hippocampus than the sham-operation group. The high-dose irisin intervention group had a significantly lower apoptosis rate than the model group (P < 0.05). At 24 and 48 hours after modeling, the sham-operation group had a significantly lower level of CC3 than the model group (P < 0.05). Compared with the model group, the high-dose irisin intervention group had a significantly lower level of CC3 and a significantly higher BCL-2/BAX ratio (P < 0.05). The low-dose irisin intervention group had similar laboratory markers and histopathological changes of the brain to the model group. CONCLUSIONS: Irisin can alleviate hypoxic-ischemic brain damage in neonatal rats in a dose-dependent manner, possibly by reducing cell apoptosis in the cerebral cortex and the hippocampus.

OBJECTIVE: To compare the effect and safety of prednisolone and adrenocorticotropic hormone (ACTH) in the treatment of infantile spasms (IS). METHODS: Cochrane Library, Embase, PubMed, China Biology Medicine Disc, CNKI, and Wanfang Data were searched for clinical studies on the comparison between prednisolone and ACTH in the treatment of IS. Literature screening, data extraction, and quality assessment were performed. Review Manager 5.3 was used for Meta analysis. RESULTS: Five clinical studies were included according to the inclusion criteria and exclusion criteria. Meta analysis showed that there was no significant difference in the spasm remission rate, spasm remission time, complicating infection rate, and irritability rate between the prednisolone and ACTH treatment groups (P > 0.05), but the disappearance rate of hypsarrhythmia in the electroencephalogram was higher in the ACTH treatment group than in the prednisolone treatment group (P < 0.05). CONCLUSIONS: The available evidence shows no difference in the clinical efficacy of prednisolone versus ACTH in the treatment of IS. However, ACTH is superior to prednisolone in stabilizing EEG. The two therapies have no difference in the incidence of adverse reactions such as infection and irritability.

OBJECTIVE: To reveal the current research status on stem cell transplantation in the treatment of neonates with hypoxic-ischemic encephalopathy (HIE), and to summarize the recent hotspots of the research in this field. METHODS: Using the key words of "stem cells" and "HIE", a computerized search was performed for the articles in English published before June 1, 2018 in PubMed, EMBASE, and Web of Science. Microsoft Office Excel 2013 was used for the statistical analysis of key words. Bicomb 2.0 and VOSviewer 1.6.6 were used for the cluster analysis of hot words and plotting of knowledge maps, respectively. RESULTS: A total of 106 articles were included and 43 high-frequency key words were extracted. The words of "cell transplantation" and "hypoxia-ischemia" were in the core position of the co-word map. The cluster analysis showed that the studies of stem cell transplantation in the treatment of neonatal HIE mainly focused on umbilical cord blood cell transplantation (32.6%), mesenchymal stem cells and neural stem cells (29.5%), perinatal brain injury (28.1%), and other topics (9.8%). CONCLUSIONS: In the current studies of stem cell transplantation in the treatment of neonatal HIE, umbilical cord blood cell transplantation, mesenchymal stem cells, neural stem cells, and perinatal brain injury are popular research topics at different levels.

White matter damage, characterized by demyelination due to the damage of oligodendrocyte precursor cells (OPCs), is the most common type of brain damage in preterm infants. Survivors are often subject to long-term neurodevelopmental sequelae because of the lack of effective treatment. In recent years, it has been found that cell transplantation has the potential for the treatment of white matter damage. OPCs are frequently used cells in cell transplantation therapy. With abilities of migration and myelinization, OPCs are the best seed cells for the treatment of white matter damage. Several studies have found that OPCs may not only replace impaired cells to reconstruct the structure and function of white matter, but also inhibit neuronal apoptosis, promote the proliferation of endogenous neural stem cells, and enhance the repairment of the blood-brain barrier. However, the clinical application of OPC transplantation therapy faces many challenges, such as the effectiveness, risk of tumorigenesis and immune rejection. With reference to these studies, this article reviewed the development of myelination, the obtainment of OPCs, the therapeutic mechanism as well as application research, and analyzed the current challenges of OPC transplantation, in order to provide a new direction for clinical treatment of white matter damage in preterm infants.

Preterm infants are a special group, and related severe neurological, respiratory, and digestive disorders have high disability/fatality rates. Allogeneic cell transplantation may be an effective method for the prevention and treatment of these diseases. At present, animal studies have been conducted for allogeneic cell transplantation in the treatment of hypoxic-ischemic encephalopathy, bronchopulmonary dysplasia, and necrotizing enterocolitis. The main difficulty of this technique is graft-versus-host reaction (GVHR), and successful induction of immune tolerance needs to be achieved in order to solve this problem. This article reviews the research advances in immune tolerance of allogeneic cell transplantation in preterm infants.

Mesenchymal stem cell (MSC) transplantation is considered one of the most promising therapeutic strategies for the repair of brain injuries and plays an important role in various links of nerve repair. Recent studies have shown that MSC-derived exosomes may dominate the repair of brain injuries and help to promote angiogenesis, regulate immunity, inhibit apoptosis, and repair the nerves, and therefore, they have a great potential in the treatment of brain injuries in neonates. With reference to these studies, this article reviews the mechanism of action of exosomes in the repair of brain injuries and related prospects and challenges, in order to provide new directions for the treatment of brain injuries in neonates with stem cells.

Cerebral palsy is a group of syndromes caused by non-progressive brain injury in the fetus or infant and can cause disabilities in childhood. Etiology of cerebral palsy has always been a hot topic for clinical scientists. More and more studies have shown that genetic factors are closely associated with the development of cerebral palsy. With the development and application of various molecular and biological techniques such as chromosome microarray analysis, genome-wide association study, and whole exome sequencing, new achievements have been made in the genetic research of cerebral palsy. Chromosome abnormalities, copy number variations, susceptibility genes, and single gene mutation associated with the development of cerebral palsy have been identified, which provides new opportunities for the research on the pathogenesis of cerebral palsy. This article reviews the advances in the genetic research on cerebral palsy in recent years.

OBJECTIVE: To investigate the effect of premature rupture of membranes (PROM) on maternal infections and outcome of preterm infants. METHODS: A total of 441 preterm infants and 387 mothers were enrolled as subjects. According to the presence or absence of PROM, the mothers were divided into non-PROM group with 104 mothers, PROM duration < 72 hours group with 90 mothers, and PROM duration ≥72 hours group with 193 mothers. The three groups were compared in terms of clinical features of mothers and infants and complications. RESULTS: Compared with the control group and the PROM duration < 72 hours group, the PROM duration ≥72 hours group had significantly higher maternal age, incidence rate of umbilical vasculitis, and rate of antibiotic use; the PROM duration ≥72 hours group had a significantly higher incidence rate of moderate-to-severe chorioamnionitis than the control group (P < 0.05), while there was no significant difference between the PROM duration ≥72 hours group and the PROM duration < 72 hours group (P > 0.05). Compared with the control group and the PROM duration < 72 hours group, the PROM duration ≥72 hours group had significantly higher incidence rates of pneumonia and intracranial hemorrhage in preterm infants; the PROM duration ≥72 hours group had a significantly higher incidence rate of congenital infection and a significantly longer mean length of hospital stay compared with the control group (P < 0.05), while there were no significant differences between the PROM duration ≥72 hours group and the PROM duration < 72 hours group (P > 0.05). The multivariate analysis showed that PROM duration ≥72 hours was an independent risk factors for pneumonia (OR=2.200, 95%CI: 1.386-3.492) and intracranial hemorrhage (OR=2.331, 95%CI: 1.420-3.827) in preterm infants. CONCLUSIONS: PROM duration ≥72 hours significantly increases the risk of placental infection in mothers and it is an independent risk factor for pneumonia and intracranial hemorrhage in preterm infants.

OBJECTIVE: To investigate the expression of autophagic gene and circadian gene in the neurons of neonatal rats after hypoxic-ischemic brain damage and the mechanism of nerve injury induced by hypoxia/ischemia. METHODS: Twelve Sprague-Dawley (SD) rats were randomly divided into hypoxic-ischemic (HI) group and sham-operation group, with 6 rats in each group. Ligation of the right common carotid artery and hypoxic treatment were performed to establish a model of hypoxic-ischemic brain damage. Western blot was used to measure the expression of the circadian protein Clock in the cortex and hippocampus. The neurons of the rats were cultured in vitro and randomly divided into oxygen glucose deprivation (OGD) group and control group. The neurons in the OGD group were treated with DMEM medium without glucose or serum to simulate ischemic state, and hypoxic treatment was performed to establish an in vitro model of hypoxic-ischemic brain damage. Western blot was used to measure the expression of autophagy-related proteins Beclin1 and LC3 and Clock protein at different time points. The changes in the expression of Beclin1 and LC3 were measured after the expression of Clock protein in neurons was inhibited by small interfering RNA technique. RESULTS: The expression of autophagy-related proteins Beclin1 and LC3 Ⅱ in neurons cultured in vitro displayed a rhythmic fluctuation; after OGD treatment, the expression of Beclin1 and LC3 Ⅱ gradually increased over the time of treatment and no longer had a rhythmic fluctuation. Compared with the sham-operation group, the HI group had a significant reduction in the expression of Clock protein in the cortex and hippocampus (P < 0.05). After OGD treatment, the neurons cultured in vitro had a significant reduction in the expression of Clock protein (P < 0.05). Compared with the negative control group, the Clock gene inhibition group had significant reductions in the expression of Beclin1 and LC3 Ⅱ (P < 0.05). CONCLUSIONS: Hypoxia/ischemia induces the disorder in the expression rhythm of autophagy-related proteins Beclin1 and LC3, and the mechanism may be associated with the fact that the circadian protein Clock participates in the regulation of the expression of Beclin1 and LC3.

To determine the therapeutic effect and protective mechanism of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) on newborn rats with hypoxia ischemic brain damage (HIBD).Umbilical cord (3-4 cm) was collected from a healthy male infant for preparation of hUC-MSCs using explants technique. The hUC-MSCs were cultured and labeled with BrdU. The differentiation function of MSCs was identified. Healthy SPF grade neonatal SD rats were randomly divided into sham (Rats in the hUC-MSCs treatment group had significant higher weight gain and lower Longa scores (at the second and the third week post transplantation) than those in the HIBD group (Transplanted hUC-MSCs can migrate brain damages through differentiating into neuron-like cells and promoting endogenous neurological differentiations.

Mitophagy is a process during which the cell selectively removes the mitochondria via the mechanism of autophagy. It is crucial to the functional completeness of the whole mitochondrial network and determines cell survival and death. On the one hand, the damaged mitochondria releases pro-apoptotic factors which induce cell apoptosis; on the other hand, the damaged mitochondria eliminates itself via autophagy, which helps to maintain cell viability. Mitophagy is of vital importance for the development and function of the nervous system. Neural cells rely on autophagy to control protein quality and eliminate the damaged mitochondria, and under normal circumstances, mitophagy can protect the neural cells. Mutations in genes related to mitophagy may cause the development and progression of neurodegenerative diseases. An understanding of the role of mitophagy in nervous system diseases may provide new theoretical bases for clinical treatment. This article reviews the research advances in the relationship between mitophagy and different types of nervous system diseases.

To analyze the differentially expressed genes (DEGs) in cerebral cortices of rats which were seven weeks after neonatal hypoxic ischemic brain damage (HIBD) and elucidate the biological significance of the DEGs.The gene expression profile of GSE37777, including 4 HI samples subjected to HIBD and 4 normal controls, was downloaded from the Gene Expression Omnibus database (GEO). DEGs were screened using the R package in HIBD groups compared with normal controls. Pathway enrichment analysis was carried out using the Cytoscape plug-in ClueGO+Cluepedia and a functionally grouped pathway network of DEGs was constructed and analyzed. Besides, the protein-protein interaction (PPI) network was constructed with the Search Tool for the Retrieval of Interacting Genes (STRING) database and visualized using Cytoscape.A total of 973 DEGs were identified in HIBD group compared with the control group, including 599 up-regulated and 374 down-regulated genes. Furthermore, a functionally grouped pathway network of DEGs was constructed and hedgehog signaling pathway were identified.Our results showed that Hedgehog and Wnt signaling pathway may be activated HIBD group. Additionally, Shh and Ret which were related to the repair process of brain damage were up-regulated. Continuous repair process may exist in the cerebral cortices of rats which were seven weeks after neonatal HIBD.

OBJECTIVE: To study the effects of maternal folate deficiency on fetal growth and development and the methylation profiles of insulin-like growth factor system in the offspring rats. METHODS: Twenty-two Sprague-Dawley female rats were randomly assigned to two groups:a folate deficient group (n=12) and a control group (n=10). They were fed with folate deficient and normal diet respectively. Dams were mated after 2 weeks of feeding. Eight female rats from each group were pregnant. On the 20th day of gestation, the fetuses were delivered by caesarean section. Thirty-two fetal rats from each group were randomly selected and the body length and weight were measured. Eight fetal rats from each group were randomly selected and ELISA was used to measure the level of folate content, IGF-1 and IGFBP-3 in the fetal brain and liver. Three fetal rats from each group were randomly selected and methylated DNA immunoprecipitation sequencing (MeDIP-Seq) was used to detect the methylation level of insulin-like growth factor system in the fetal brain and liver. ELISA was used to measure the level of IGF-1 and IGFBP-3 in the maternal serum from both groups. RESULTS: The mean fetal length and weight were lower in the folate deficient group than in the control group (P < 0.05). The levels of IGF-1 and IGFBP-3 in the maternal serum, as well as folate content and IGFBP-3 in the fetal brain and liver were significantly lower in the folate deficient group than in the control group (P < 0.05). The methylation levels of IGF-1R, IGF-2R, IGFBP-2, IGFBP-5, IGFBP-6 and IGFBP-7 in the fetal brain were higher in the folate deficient group than in the control group (P < 0.05). The methylation levels of IGF-1R, IGF-2R, IGFBP-3 and IGFBP-5 in the fetal liver were higher in the folate deficient group than in the control group. The methylation of IGF-2 gene showed a significant reduction in the folate deficient group (P < 0.05). CONCLUSIONS: Maternal folate deficiency may cause retardation of growth and development of the offspring, which is possibly associated with the changes of methylation profiles of insulin-like growth factors.

OBJECTIVE: To investigate mitophagy in an animal model of hypoxic-ischemic brain damage (HIBD) and its role in HIBD. METHODS: A total of 120 neonatal Sprague-Dawley rats aged 7 days were divided into three groups: sham-operation, HIBD, and autophagy inhibitor intervention (3MA group). The rats in the HIBD group were treated with right common carotid artery ligation and then put in a hypoxic chamber (8% oxygen and 92% nitrogen) for 2.5 hours. Those in the 3MA group were given ligation and hypoxic treatment at 30 minutes after intraperitoneal injection of 2 μL 3MA. Those in the sham-operation group were not given ligation or hypoxic treatment. Single cell suspension was obtained from all groups after model establishment. Immunofluorescence localization was performed for mitochondria labeled with MitoTracker, autophagosomes labeled with LysoTracker, and autophagy labeled with LC3 to observe mitophagy. After staining with the fluorescent probe JC-1, flow cytometry was used to measure mitochondrial membrane potential. TTC staining was used to measure infarct volume. Cytoplasmic proteins in cortical neurons were extracted, and Western blot was used to measure the expression of mitophagy-related proteins. RESULTS: Compared with the shamoperation group, the HIBD group had a significant reduction in mitochondrial membrane potential (P < 0.05), a significant increase in mitophagy (P < 0.05), a significant increase in the expression of the proteins associated with the division of the mitochondrial Drp1 and Fis1 (P < 0.05), and a significant reduction in the expression of the mitochondrial outer membrane protein Tom20 and the mitochondrial inner membrane protein Tim23 (P < 0.05). Compared with the HIBD group, the 3MA group had a significantly greater reduction in mitochondrial membrane potential (P < 0.05), but showed significantly reduced mitophagy (P < 0.05). In addition, the 3MA group had a significantly increased degree of cerebral infarction compared with the HIBD group (P < 0.05). CONCLUSIONS: HIBD can increase the degree of mitophagy, and the inhibition of mitophagy can aggravate HIBD in neonatal rats.

OBJECTIVE: To investigate the protective effect of histone acetylation against hypoxic-ischemic cortical injury in neonatal rats. METHODS: A total of 90 neonatal rats aged 3 days were divided into three groups: sham-operation, cortical injury model, and sodium butyrate (a histone deacetylase inhibitor) treatment. The rats in the model and the sodium butyrate treatment groups were intraperitoneally injected with lipopolysaccharide (0.05 mg/kg), and then right common carotid artery ligation was performed 2 hours later and the rats were put in a hypoxic chamber (oxygen concentration 6.5%) for 90 minutes. The rats in the sham-operation group were intraperitoneally injected with normal saline and the right common carotid artery was only separated and exposed without ligation or hypoxic treatment. The rats in the sodium butyrate treatment group were intraperitoneally injected with sodium butyrate (300 mg/kg) immediately after establishment of the cortical injury model once a day for 7 days. Those in the sham-operation and the model groups were injected with the same volume of normal saline. At 7 days after establishment of the model, Western blot was used to measure the protein expression of histone H3 (HH3), acetylated histone H3 (AH3), B-cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated X protein (BAX), cleaved caspase-3 (CC3), and brain-derived neurotrophic factor (BDNF). Immunofluorescence assay was used to measure the expression of 5-bromo-2'-deoxyuridine (BrdU) as the cortex cell proliferation index. RESULTS: The sodium butyrate treatment group had a significantly lower HH3/AH3 ratio than the model group ( P

OBJECTIVE: To study the effect of telomerase reverse transcriptase (TERT) on cell apoptosis in neonatal rat brains after hypoxic-ischemic brain injury (HIBD). METHODS: A total of 72 neonatal rats were divided into sham, vehicle, HIBD and TERT groups. HIBD was induced by Rice method in the later three groups. The neonatal rats in the vehicle and TERT groups were injected with plasmids containing mock or full length TERT by an intracerebroventricular injection 30 minutes after hypoxic-ischemic (HI) injury. Pathological changes of brain tissue were observed by hematoxylin and eosin (HE) staining. Western blot was used to detect the protein expression of TERT, apoptosis-inducing factor (AIF) and cleaved caspase 3 (CC3). Apoptotic cells were detected by TUNEL staining. RESULTS: Western blot showed that TERT protein was dramatically increased in the vehicle, HIBD and TERT groups compared with the sham group. Compared with the vehicle and HIBD groups, TERT protein in the TERT group was significantly upregulated. Compared with the sham group, there was a significant increase in apoptotic index and expression of AIF and CC3 proteins in the vehicle and HIBD groups (P < 0.01). The TERT group showed decreased expression of AIF and CC3 proteins and apoptotic index compared with the vehicle and HIBD groups (P < 0.01). CONCLUSIONS: TERT can inhibit cell apoptosis induced by HI and might have a neuroprotective role in developing brain with HIBD.

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Hypoxic-ischemic encephalopathy (HIE) in neonates is the brain injury caused by perinatal asphyxia or hypoxia and is a major cause of death in neonates and nervous system dysfunction in infants and young children. Although to a certain degree, mild hypothermia therapy reduces the mortality of infants with moderate to severe HIE, it cannot achieve the expected improvements in nervous system dysfunction. Hence, it is of vital importance to search for effective therapeutic methods for HIE. The search for more therapies and better preventive measures based on the pathogenesis of HIE has resulted in much research. As an important link in the course of HIE, energy failure greatly affects the development and progression of HIE. This article reviews the research advances in the treatment and prevention of energy failure in the course of HIE.

As a kind of mitochondrial membrane protein with protein kinase activity, phosphatase and tensin homolog deleted on chromosome ten induced kinase 1 (PINK1) is involved in many biological metabolic processes. Since PINK1 had been found to be associated with Parkinson's disease, researchers have been exploring its biological function. PINK1 localizes in the outer mitochondrial membrane and regulates cell function through phosphorylating proteins. PINK1 is involved in mitochondrial function, mitochondrial morphology and mitochondrial autophagy, but the regulatory pathway is not yet clear. PINK1 is expressed widely in many tissues with a variety of biological activity, especially in tissues with high energy consumption. It may therefore be involved in the development and regulation of many diseases. Mutations in PINK1 were originally discovered to cause autosomal recessive Parkinson's disease. Recently some research has revealed that PINK1 is related to the development of neonatal hypoxic-ischemic encephalopathy, cancer, diabetes and other diseases. Studying and exploring the biological functions of PINK1 will facilitate the identification of the targets for therapeutic intervention for its related diseases. This review article mainly focuses on recent studies about the biological function and related diseases of PINK1.

OBJECTIVE: To investigate the parents' compliance in non-hospital settings during the operation of expressed breast milk bank. METHODS: In September 2014, a questionnaire survey was carried out to investigate the parents' willingness about feeding the inpatient neonates with maternal expressed breast milk, to evaluate the effectiveness of the breast milk feeding supporting system, and to monitor the compliance in non-hospital settings during the delivery of maternal expressed breast milk. Improvements in education were made according to the results. A second survey was done in September 2015. RESULTS: A total of 340 questionnaires were sent out, and 338 usable questionnaires were returned. According to the time when the questionnaires were sent out, they were divided into two groups: 2014 group (n=229) and 2015 group (n=109). The age of most mothers was 20-30 years in the 2014 group and 30-40 years in the 2015 group. Most mothers delivered at the West China Second Hospital of Sichuan University in both groups, but the 2015 group had a significantly higher proportion than the 2014 group (74.3% vs 61.6%; P < 0.05). Guidance was given to mothers in the presence of insufficient breast milk production in both groups, but the 2015 group had a significantly higher proportion than the 2014 group (91.7% vs 79.9%; P < 0.05). Both groups had good family compliance in the collection, storage, and transport of breast milk. There were no significant differences in their compliance with washing hands, sterilizing instruments, and using a clean special refrigerator between the two groups. The expressed breast milk was transported strictly according to the procedure in both groups, but the 2015 group had a significantly higher proportion than the 2014 group (100% vs 87.1%; P < 0.05). CONCLUSIONS: Before and after improvements in the health education, most parents have good compliance in the collection, storage, and transport of breast milk.

To explore the possible mechanism of berberine improve insulin resistance in skeletal muscle of obese rats.Forty Wistar rats were divided into normal control group (NC group, n =10) and high fat food group (HF group, n=30). After the obese model rats established successfully, the rats of NC group (n=10) and HF group (n=10) were sacrificed. The level of fasting plasma endotoxin (ET) was detected. The expression of Toll-like receptor 4 (TLR4) mRNA in skeletal muscle were detected by real time quantitative PCR. The expression of TLR4, IkappaB kinase beta (IKKbeta), phospho-IKKbeta(Ser181) (p-IKKbeta(Ser181)), nuclear factor-kappaB (NF-kappaB), tumor necrosis factor-alpha (TNF-alpha), insulin receptor (IR), insulin receptor substrate-1 (IRS-1), phospho-IRS-1(Ser307) (p-IRS-1(ser307)) and the tyrosine phosphorylation of IR and IRS-1 (p-IR(Tyr) and p-IRS-1(Tyr)) protein in skeletal muscle were detected by Western blot. The twenty HF group rats were randomly divided into two group: the fat model control group (FC group, n=10) were fed with high fat diet and distilled water. The fat berberine group (FB group, n=10) were fed with high fat diet and berberine. All rats were sacrificed after effective interventions of eight weeks. The same indexes as the first part of experiment were detected. Results The results showed that the level of ET was increased. The TLR4/IKKneta/NF-kappaB signaling pathway is activated and the expression of TNF-alpha was increased of the skeletal muscle in obese rats. However, the insulin signaling pathways of the skeletal muscle in obese rats was inhibited. Berberine could reduce the level of ET of obese rats, down-regulate the TLR4/IKKbeta/NF- kappaB inflammation signaling pathway and improve insulin resistance of skeletal muscle in obese rats.Our study revealed that berberine could reduce the level of ET of obese rats, down-regulate the TLR4/IKKbeta/NF-kappaB inflammation signaling pathway in skeletal muscle and berberine can improve insulin resistance of skeletal muscle through inhibiting the active of the TLR4/IKKbeta/NF-kappaB signaling pathway.

To investigate the role of phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) signaling pathway for umbilical cord-derived mesenchymal stem cells (UC-MSCs) treating in neonatal rats with hypoxia-ischemia brain damage (HIBD).P10 SD rats were divided into sham group, MSCs group, inhibitor (LY 294002) group (LY group) and HIBD group randomly. To establish a neonatal rat model of HIBD, UC-MSCs labeled with Brd U were transplanted into the lateral ventricle of rats. At 24 and 48 h after transplantation, the number of apoptotic cells was detected by TUNEL, while the expression of caspase3 protein and phosphorylation of Akt (P-Akt) were quantified by Western blot.At 24 and 48 h after transplantation, both the apoptotic cells and caspase3 protein expression in MSCs group were less than those in LY group and HIBD group (P0. 05), while the expression of P-Akt was higher than those in LY group and HIBD group (P0.05), and with the passage of time after transplantation, the expression of each index showed a downward trend.The apoptotic cells of brain and the expression of caspase3 protein decrease, while the expression of P-Akt increase. PI3K/Akt signaling pathway may be an important mechanism for UC-MSCs transplantation in HIBD rats.

To study the bacterial culture results of expressed breast milk.A total of 1178 expressed breast milk samples were collected for bacterial culture. The breast milk sampled from the mothers of preterm neonates (n=615) and term neonates (n=563) who were hospitalized between May 2014 and April 2015.There was no significant difference in bacterial counts between the preterm and term sample groups (P0.05). Potential intestinal pathogens were found in 55 samples (4.63%) of the 1178 samples, with no significant difference between the preterm and term sample groups (P0.05). The second expressed milk samples from 33 mothers were cultured. Only 10 samples (30%) were found to have the same bacteria as the first time. The detection rate of bacterial load of ≥ 10⁵ CFU/mL was higher in those samples with potential intestinal pathogens, as compared with those samples without potential intestinal pathogens (43.64% vs 14.87%; P0.05). There was no correlation between the incidence of neonatal infections and potential intestinal pathogens in breast milk.Breast milk is not sterile. Bacterial loads and phylotypes are variable. Random breast milk cultures can neither describe bacterial colonies in breast milk, nor be a predictor of neonatal infection.

To investigate the role of long non-coding RNA (lncRNA) BC088414 in hypoxic-ischemic injury of neural cells.Rat adrenal pheochromocytoma (PC12) cells were divided into four groups: normoxic, oxygen glucose deprivation (OGD), siRNA-normoxic (siRNA group) and siRNA-OGD (n=3 each). Cells were incubated in glucose-free and serum-free DMEM medium under the conditions of 37℃ and 1% O2+99% N2/CO2 for 6 hours to establish an in vitro hypoxic-ischemic model. Quantitative real-time PCR was used to measure mRNA expression of lncRNA BC088414, β2-adrenoceptor (Adrb2), and caspase-6 (CASP6). siRNAs were used to inhibit BC088414 expression in PC12 cells. The TUNEL method was used to measure cell apoptosis.The OGD group had a significantly higher cell apoptotic index than the normoxic group (P0.01). After inhibition of BC088414 expression, the OGD group had a significantly reduced apoptotic index (P0.05). The OGD group had significantly higher mRNA expression levels of lncRNA BC088414, Adrb2, and CASP6 compared with the normoxic group (P0.05). The siRNA -normoxic group had significantly lower mRNA expression levels of Adrb2 and CASP6 than the normoxic group (P0.05), and the siRNA-OGD group also had significantly lower mRNA expression levels of Adrb2 and CASP6 than the OGD group (P0.05).LncRNA BC088414 may promote apoptosis through Adrb2 and CASP6 and aggravate neural cell injury induced by hypoxia-ischemia.

To study the pharmacokinetic and pharmacodynamic features of different doses of aminophylline in very low birth weight (VLBW) infants with different postmenstrual ages, weights, and ages (in days).A total of 40 VLBW infants with apnea were enrolled. After an intravenous loading dose of 5 mg/kg aminophylline, they were randomized into two groups with different maintenance doses of aminophylline (1 mg/kg and 2 mg/kg, once every 8 hours). Blood concentrations of aminophylline and liver and renal functions were monitored at 8 hours, 3 days, and 7 days after the loading dose. Attacks of apnea were documented. Pharmacokinetic data of aminophylline were compared between the two groups.The steady-state plasma concentration of aminophylline and plasma clearance in the 2 mg/kg group were significantly higher than those in the 1 mg/kg group (P0.05). However, the elimination half life was shorter in the 2 mg/kg group (P0.05). Days of apnea attacks within 7 days after birth in the 2 mg/kg group were significantly fewer than in the 1 mg/kg group (P0.05). Aminophylline plasma clearance was positively correlated with age (in days) after birth and postmenstrual age in both groups.In VLBW infants, pharmacokinetics and pharmacodynamics are different when different maintenance doses of aminophylline are given. The maintenance dose of 2 mg/kg is associated with a better effect in the treatment of apnea. Postmenstrual age and age (in days) should be considered during the adjustment of dose, and routine blood concentration monitoring should be performed.

To investigate the activity of collapsin response mediator protein 2 (CRMP-2) and its possible regulation for axonal and dendrictic injury under hypoxia-ischemia (HI).Postnatal day 10 SD rats were suffered the right common carotid artery ligation and 8% mixture of oxygen and nitrogen hypoxia 2.5 h to produce HI model. The expression of total and phosphorylated CRMP-2 and amyloid precursor protein (APP) were detected by Western blot after HI. After pretreatment of protein kinase B (Akt) inhibitor, wortmannin or LY294002, western blot and immunohistochemistry were applied to detect the expression of total and phosphorylated of CRMP-2 at 4 h and 24 h after HI. At 72 h after HI, APP was detected by Western blot and immunohistochemistry, axonal and dendrictic injury was determined by electron microscope.Total CRMP-2 was not obviously changed after HI, compared with that of sham controls. However, the phosphorylated CRMP-2 (p-CRMP-2) protein transiently increased at 0.5 h, started to decrease at 2 h, remained at a low level at the rest of the time points, compared with that of sham controls. APP protein started to increase at 2 h, remained at a high level at 4, 8, 24 h, and then progressively increased at 48 and 72 h. In wortmannin and LY294002 group, CRMP-2 protein was not obviously changed at 4 h and 24 h after HI. However, p-CRMP-2 increased at 4 h and 24 h. At 72 h, wortmannin pretreatment increased APP expression, leading to more severe ultrastructure failure of axon and dendrite.As a downstream effector of Akt pathway, CRMP-2 is involved in axonal and dendritic injury regulation after HI in neonatal rat.

Aquaporin-4 (AQP4), a water channel protein, is abundantly expressed in astrocytes and plays a key role in the development of brain edema. However, it is not clear whether AQP4 contributes to astrocytic swelling in hypoxia-ischemia (HI). To investigate the roles of AQP4 in astrocytic swelling during HI and reoxygenation, we measured AQP4 expression and astrocytic cellular volume in cultured rat astrocytes following HI and reoxygenation. RNA interference was used to knockdown AQP4 expression (AQP4(-/-)). Real-time polymerase chain reaction and Western blot analysis were used to detect the inhibitory efficiency of AQP4. We found that the maximal inhibition of AQP4 mRNA and protein in astrocytes after AQP4 siRNA transfection (AQP4(-/-)) was approximately 77 and 85%, respectively, compared to wild-type AQP4 (AQP4(+/+)) expression. Cellular volume in both AQP4(-/-) and AQP4(+/+) astrocytes was significantly increased during HI compared to cells cultured in normoxia (P

To investigate the clinical efficacy and safety of preferred use of high-frequency oscillatory ventilation (HFOV) in the treatment of neonatal pulmonary hemorrhage.The clinical efficacy of preferred use of HFOV (preferred use group) and rescue use of HFOV after conventional mechanical ventilation proved ineffective (rescue use group) in the treatment of 26 cases of neonatal pulmonary hemorrhage was retrospectively analyzed. The oxygenation index (OI), pulmonary hemorrhage time, hospitalization time, ventilation time, oxygen therapy time, complications, and outcome of the two groups were compared.Compared with the rescue use group, the preferred use group had significantly lower IO values at 1, 6, 12, 24, 48, and 72 hours after treatment (P0.05). Compared with the rescue use group, the preferred use group had a significantly lower incidence of ventilator associated pneumonia (VAP) (P0.05) and a significantly higher cure rate (P0.05). There were no statistically significant differences in the incidences of pneumothorax, intracranial hemorrhage, and digestive tract hemorrhage between the two groups (P0.05). Compared with those in the rescue use group, children who survived in the preferred use group had significantly shorter pulmonary hemorrhage time, hospitalization time, ventilation time, and oxygen therapy time (P0.05).Compared with the rescue use of HFOV, preferred use of HFOV can better improve oxygenation function, reduce the incidence of VAP, shorten the course of disease, and increase cure rate while not increasing the incidence of adverse effects.

MicroRNAs (miRNAs) are short, noncoding RNAs that function as posttranscriptional regulators of gene expression by controlling the translation of messenger RNAs. Epilepsy is a chronic and debilitating brain disorder and occurs frequently in childhood. The brain expresses several unique miRNAs which are associated with epileptogenesis. As a new layer of gene expression in the pathogenesis of epilepsy, miRNAs have shed a new light on the potential to transform an understanding of the underlying mechanisms promising novel therapeutic targets and effective antiepileptogenic medications. This article reviews the roles and mechanisms of miRNAs in the pathogenesis of seizure-damage and pathophysiology of epileptogenesis.

To examine the changes in expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN) protein, p-PTEN protein and Bim (Bcl-2 interacting mediator of cell death) mRNA in the cortex of neonate rat brains with hypoxic-ischemic brain damage (HIBD) and to explore the mechanisms of neuroprotective effects of PTEN inhibition.One hundred and twenty-eight neonate (10 days) SD rats were divided into four groups: hypoxia-ischemia (HI), sham control (Sham), bisperoxovanadium (bpv), and normal saline (NS) group. Rats in the HI group had their right common carotid arteries (CCA) exposed and ligated, and were then exposed to hypoxia in a chamber filled with 8% oxygen (balanced with nitrogen) for 2.5 h. Rats in the sham control group had their right CCA surgically exposed without ligation and exposure to hypoxia. Rats in the bpv treated group received intraperitoneal injections of bpv, 30 min before HI was induced. Instead of bpv, rats in the NS-treated group received intraperitoneal injections of NS. Cerebral cortex samples of the rats were collected 0.5 h and 24 h after hypoxia. Western blot was used to detect the protein expression of PTEN, p-PTEN and Bim. Real-Time PCR was used to detect the level of Bim mRNA. TUNEL staining was used to detect apoptotic cells.No significant changes of PTEN protein were observed in the rats exposed to HI. However, p-PTEN protein decreased in the rats exposed to HI (0.5 h and 24 h) compared with those exposed to sham surgery (P0.01). Compared with the sham controls, Bim mRNA and protein increased in the rats exposed to HI (0.5 h, P0.01) and then returned to the baseline level 24 h after HI. No significant changes of PTEN protein were observed in the bpv-treated rats. However, p-PTEN protein increased and Bim mRNA and protein decreased in the bpv-treated rats (0.5 h and 24 h, P0.01) compared with those in the HI group and NS-treated group. TUNEL positive cells also reduced in the bpv-treated rats (24 h, P0.01) compared with those in the HI group and NS-treated group.PTEN activities increase in the brains of neonate rats with hypoxic-ischemic brain damage. PTEN activity inhibition can decrease the level of pro-apoptotic protein Bim mRNA, leading to reduction of neuronal apoptosis.

Brain hypoxia-ischemia has been considered as critical factors in many human central nervous system diseases, including stroke and neonatal hypoxic-ischemic encephalopathy. In brain hypoxia-ischemia processes, inducible NO synthase (iNOS) is induced to produce excessive nitric oxide (NO) which leads to cascade reactions of inflammation and neuronal death, deteriorating primary brain injury. Inhibiting iNOS expression has opened new perspectives in the treatment of brain hypoxia-ischemia because iNOS inhibitor has been shown as a potent therapeutic agent. This reviews focus on recent research achievements regarding the relationship between iNOS and ischemic-hypoxic brain damage and the perspective of using iNOS inhibitors as therapeutic strategies for brain ischemic-hypoxic brain damage.

To study the brain protection and the possible mechanism of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) in neonatal rat model of hypoxic-ischemic brain damage (HIBD).Successfully establishing a neonatal rat model of HIBD, hUC-MSCs labeled with BrdU were transplanted into the lateral ventricle 24 hours after HIBD. The number of apoptotic cells and the expression of Caspase-3 were detected by TUNEL and Western blot respectively at 24 and 48 hours after transplantation. The neurological functions of HIBD rats were evaluated by Longa score, and the survival, differentiation and pro-differentiation effects of hUC-MSCs were identified by immunofluorescence at 1 to 3 weeks after transplantation.At 24 and 48 hours after transplantation, apoptotic cells and Caspase-3 expression in the MSCs group were less than in the HIBD group (P0.05). At 2 and 3 weeks after transplantation, the Longa score in the MSCs group was lower than in the HIBD group (P0.05). After transplantation, positive cells labeled with BrdU were seen in the brain tissue. The expression levels of glial fibrillary acidic protein (GFAP) and neuron specific esterase (NSE) in the MSCs group were higher than in the HIBD and sham-operated control groups (P0.05), and increased gradually with the transplantation time (P0.05).hUC-MSCs transplantation in HIBD rats can inhibit Caspase-3 expression and reduce apoptotic cells in the early stage, and in the later period, the survival hUC-MSCs can differentiate into neural-like cells and promote the differentiation of endogenous neural-like cells, providing protective effects to brain.

To investigate the research on neonatal jaundice in recent years by co-word analysis and to summarize the hot spots and trend of research in this field in China.The CNKI was searched with "neonate" and "jaundice" as the key words to identify the papers published from January 2009 to July 2013 that were in accordance with strict inclusion and exclusion criteria. To reveal the relationship between different high-frequency key words, Microsoft Office Excel 2013 was used for statistical analysis of key words, and Ucinet 6.0 and Netdraw were used for co-occurrence analysis.A total of 2 054 papers were included, and 44 high-frequency key words were extracted. The current hotspots of research on neonatal jaundice in China were displayed, and the relationship between different high-frequency key words was presented.There has been in-depth research on clinical manifestations and diagnosis of neonatal jaundice in China, but further research is needed to investigate the etiology, mechanism, and treatment of neonatal jaundice.

To evaluate the effect of oral administration of probiotics on intestinal colonization with drug-resistant bacteria among preterm infants in the neonatal intensive care unit (NICU).A double-blind, randomized, placebo-controlled trial was carried out in the preterm infants who were transferred to the NICU immediately after birth. These infants were stratified by whether they were breastfed and then randomized into test group and control group. The test group was given probiotics from the day when enteral feeding began, while the control group was treated conventionally without probiotics. The two groups were compared in terms of the colonization with extended-spectrum beta-lactamase-producing bacteria, as assessed by rectal swabs on days 1, 3, 7, and 14 after birth, and the incidence of diseases.Rectal colonization with drug-resistant bacteria was found in the test group (n=119) and control group (n=138) on days 1, 3, 7, and 14 after birth. There were no significant differences in the incidence of late-onset sepsis and necrotizing enterocolitis between the two groups (P0.05). Among non-breastfed infants, the test group had significantly decreased rectal colonization with drug-resistant bacteria compared with the control group on day 14 after birth (71.1% vs 88.9%; P=0.04). No probiotic-related adverse events were observed in the study.Oral administration of probiotics may reduce rectal colonization with drug-resistant bacteria in preterm infants under certain conditions and shows good safety.

To study changes in paired-immunoglobulin-like receptor B (PirB) expression after hypoxic-ischemic brain damage (HIBD) as well as the role for targeted inhibition of PirB activity in nerve regeneration in rats.Newborn Sprague-Dawleyrats rats were divided into: a sham operation group (n=30), a HIBD group (n=30), and an anti PirB antibody treatment group (n=6). In the HIBD group, HIBD was induced by right carotid artery ligature and subsequent exposure to hypoxia (8% O2) for 3 hours. In the sham operation group, right carotid artery was dissected as in the HIBD group but no ligature and hypoxic exposure was not applied. In the two groups, 6 animals were sacrificed at 0, 6, 12, 24 and 72 hours after the operation and hypoxic exposure. In the antibody treatment group, after carotid artery ligation and hypoxia exposure as in the HIBD group, an anti PirB antibody was injected intracerebrally and animals were sacrificed 72 hours after the injection. Immediately after sacrifice of the animals at designated time points, brain tissue specimens were collected. The presence and content of PirB protein were assessed by immunohistochemistry and Western blot analysis respectively, the abundance of PirB mRNA was determined by RT-PCR, and the Rho kinase (Rock) activity was determined by immunoprecipitation.At 72 hours after operation, PirB mRNA abundance and protein content in the brain were significantly increased as compared with the measurements at 0 hour after operation in the HIBD group (P0.05); ROCK activity was significantly increased in the HIBD group as compared with the sham operation and anti PirB antibody groups (P0.05).PirB might be involved in HIBD through a Rho-ROCK-dependent mechanism and antibody-mediated neutralization of PirB in the brain may offer a novel therapeutic strategy for HIBD.

To study the effect of β8 expression on transforming growth factor β1(TGF-β1) activation in astrocytes with oxygen glucose deprivation (OGD).Astrocytes were cultured and then subjected to OGD to generate hypoxia-ischemia (HI) model in vitro. Immunocytochemistry was used to detect the expression and distribution of β8 in nomoxia cultured cells. β8 protein expression was quantified by Western blot at 12 hours, 1 day and 2 days after OGD. Astrocytes and luciferase reporter cells (TMLC) were co-cultured. β8 RNA interference system was established to specifically inhibit β8 expression in cultured astrocytes. TGF-β1 activation was then detected in the co-culture system.β8 was mainly located in the cytoplasm and neurites of astrocytes. OGD resulted in increase of β8 protein expression at 12 hours after reoxygenation in astrocytes, which was peaked at 1 day after reoxygenation. TGF-β1 activation was in accordance with β8 expression in astrocyte-TMLC co-culture system after reoxygenation. After the inhibition of β8, TGF-β1 activation was significantly reduced in all time points.The highly expressed β8 plays important roles in the regulation of TGF-β1 activation in neonatal rats with hypoxic-ischemic brain damage.

Inhaled NO (iNO) has been shown to have beneficial effects on decreasing pulmonary inflammation, increasing function of surfactant and improving lung growth in prematurely born animal models. iNO has been gradually applied in the neonatal intensive care unit since its first use for persistent pulmonary hypertension (PPHN) in the early 1990's. Although many research findings have shown the benefits of iNO for hypoxic respiratory failure (HRF) of preterm infants, there is no certain evidence to support the routine use of iNO in premature infants. According to recent literature, the mechanism of iNO therapy, treatment scheme, iNO effectiveness and safety in premature infants were reviewed in this article, so as to provide bases for the clinical use of this treatment.

To observe the outcomes of hospitalized neonates who were managed with two different antibiotics strategies, namely, the risk factor based antibiotic strategy and the combination antibiotic strategy that is based on risk factors, infection screening and monitoring.A cohort study was performed on a control group of 4 406 cases of neonates hospitalized between January 2010 and May 2011 and an observed group of 4 476 neonates hospitalized between July 2011 and October 2012. The control group adopted the risk factor based antibiotic strategy and the observed group received a combination antibiotic strategy based on risk factors, infection screening and monitoring. The rate of antibiotic use, average length of stay, readmission rate and mortality rate were compared between the two groups.With the change from the risk factor based antibiotic strategy to the combination antibiotic strategy, the total rate of antibiotic use decreased from 79.6% to 50.5% (P0.01). There were no differences in the average length of stay, readmission rate, and mortality rate between the two groups.The combination antibiotic strategy based on risk factors, infection screening and monitoring can reduce antibiotic use substantially and has no adverse effects on treatment outcomes in hospitalized neonates.

To explore the role and mechanisms of FOXO3a nuclear translocation in neuronal apoptosis after hypoxia-ischemia (HI).One hundred and sixty 10-day-old Sprague-Dawly rats were randomly divided into two groups: HI and sham-operated. The right common carotid artery was ligated followed by hypoxia exposure for 2.5 hours in the HI group. The sham-operated group rats were not subjected to carotid artery ligation or hypoxia treatment. Rat cerebral cortex was collected at 0.5, 2, 4, 8 and 24 hours after hypoxia. Western blot was used to detect expression of total FOXO3a protein, pnuclear and cytoplasmic FOXO3a and Bim. TUNEL staining was used to detect apoptotic cells.The nuclear protein of FOXO3a obviously increased from 0.5 to 24 hours after HI in a time-dependent manner compared with the sham-operated group (P0.01). On the contrary, cytoplasmic protein evidently decreased from 0.5 to 24 hours in the HI group compared with the sham-operated group (P0.01). Bim protein increased from 0.5 hour, peaked at 2 hours, started to decline at 4 hours (P0.01), and returned to baseline level at 8 and 24 hours after HI in the HI group compared with the sham-operated group. TUNEL positive cells started to express at 4 hours, and peaked at 24 hours after HI (P0.01). However, TUNEL positive cells were rarely found in the sham-operated group.HI induces FOXO3a translocation from cytoplasm to nucleus, and enhances protein expression of its target gene Bim in the neonatal rat brain. The upregulation of Bim expression might be related to neuronal apoptosis.

To investigate the effect of different operation time to percutaneous balloon pulmonic valvuloplasty (PBPV) to critical pulmonary valve stenosis (CPS).Twenty-one infants (age ≤ 60 days at operating day) suffered from CPS, diagnosed by fetal echocardiogram and confirmed by echocardiography after birth, were enrolled in this case-control-study with written informed consent during April 2007 to December 2011. Of the 21 cases, 7 had prenatal diagnosis in our prenatal diagnosis center (prenatal group, Pre) and 14 were referred from other hospitals, who were divided into postpartum group A (Post A, referred within 28 days after birth) and postpartum group B (Post B, referred 29 to 60 days after birth). To Pre-group, the integrative interventional protocol was cautiously made by the consultative specialists, including intrauterine diagnosis, perinatal care and urgent PBPV soon after birth. To Post-group, emergency PBPV was preformed after the referral. Tei index of right ventricular and pressure-gradient (PG) between right ventricular and pulmonary artery were measured before and at different time points one year after PBPV.The values of SpO2 in Pre-group ranged from 82%-92% (86.57% ± 5.34%) under the state of continuous intravenous infusion of alprostadil. PBPV was successfully preformed within 3-6 days after birth. The values of SpO2 increased to 97.33% ± 1.15% post procedure. The values of PG pre- and post- procedure were (86.34 ± 11.77) mm Hg and (31.43 ± 8.46) mm Hg respectively. Preoperative RV Tei-index was 0.68 ± 0.05, it decreased rapidly after procedure, and recovered to normal one month after procedure. Only one case showed restenosis seven months after procedure and repeated PBPV. Fourteen referral cases (6 cases in Post A group and 8 cases in Post B group, accompanied in 1 and 3 cases with heart failure), the values of SpO2 ranged from 83%-91% under state of continuous intravenous infusion of alprostadil. And the operating time was 10-57 days after birth. The values of SpO2 recovered to normal post procedure, and heart failure alleviated. Increased preoperative RV pressure obviously decreased significantly post-procedure. And increased Tei-index declined gradually, at one-year follow-up, the value of Tei-index in Post A group recovered to normal, whereas that of Post B was (0.51 ± 0.06), compared to Pre and Post A groups, the difference was significant (P0.05) . One case showed restenosis nine months after procedure and repeated PBPV was performed. The hypoxic exposure durations were (4.43 ± 0.68) , (16.33 ± 4.46) , (41.25 ± 9.19) , respectively, and the difference among the three groups was significant (P0.05).To the fetuses with definite prenatal diagnosis of critical pulmonary valve stenosis, preoperative general condition can be adjusted to more suitable for emergency operation. Early PBPV can achieve shorter hypoxic exposure and better recovery of right ventricular function post procedure. Perinatal integrated intervention for CPS can significantly improve the prognosis and quality of life in this patient population.

Inadequate postnatal nutritional support is an important factor contributing to growth failure, which leads to poor neurological outcome. In this study, co-word analysis was used to investigate the research on nutrition of premature infants over the last six years in China, describe the research trend in this field in China, and provide possible directions for future research.A literature search was performed in January 2013 using the CNKI database and the key words "preterm infant" and "nutrition". A total of 772 articles were retrieved. Then high-frequency key words were extracted using Excel 2010 to create a co-occurrence matrix. Finally, a visualized network was built using Ucinet 6.0.The knowledge domain map of research on nutritional support for premature infants in China showed that the major topic of relevant research is still the combination of parenteral nutrition and enteral nutrition, with the goal of maintaining appropriate growth rates in premature infants. Researchers have paid much attention to the adverse effects of parenteral nutrition. Feeding intolerance is still the main problem in nutritional support, especially enteral nutrition, for premature infants.A visualized network of current research on nutrition of premature infants in China has been created, and a knowledge domain map has been drawn to reflect the hot topics in this field of study over the last six years.

To investigate the clinical value of mycobacterial DNA microarray technology for diagnosis of childhood tuberculosis.120 clinical specimens were collected from hospitalized child patients. Acid-fast staining, mycobacterial culture and DNA microarray assays were performed using these clinical specimens. The results of DNA microarray assays were compared with the results of acid-fast staining and mycobacterial culture.The sensitivity of DNA microarray assays for specimens from children with tuberculosis was 24.3% (17/70), of acid-fast staining 17.1% (12/70), of mycobacterial culture 20.0% (14/70), and the specificity of the three methods was all 100.0% (50/50). The difference between results of DNA microarray assays and that of acid-fast staining or mycobacterial culture was not significant.DNA microarray assay has reference value for the diagnosis of childhood tuberculosis. It provides a new way for the diagnosis of childhood tuberculosis.

To investigate the activity of protein kinase B (Akt) and its downstream protein, glycogen synthase kinase-3beta (GSK-3beta) under hypoxia-ischemia (HI), and the possible regulation for axonal density.Postnatal day 10 SD rats were suffered the right common carotid artery ligation and 8% mixture of oxygen and nitrogen hypoxia 2.5 h to produce HI model. The expression of total and phosphorylated Akt and GSK-3beta was detected by western blot after HI. After pretreatment of Akt inhibitor, wortmannin or LY294002, Western blot detect the expression of total and phosphorylated of Akt, GSK-3beta at 4 h and 24 h after HI. After pretreatment of wortmannin, axonal density was determined by Bielschowsky silver impregnation, and histological injury was evaluated by hematoxylin and eosin (HE) staining.The expression of total Akt and GSK-3beta remained unchanged after HI. p-Akt protein significantly decreased at 0.5 h, increased at 2 h and reached the highest at 4 h, returned to baseline at 8 h, declined at 24 and 48 h after HI, and finally returned to baseline again at 72 h compared with that of sham controls, p-GSK-3beta protein decreased at 0. 5 h, increased at 2 h, reached the highest at 4 h, returned to baseline at 8 and decreased at 24 h, reached the lowest at 48 h, and returned to baseline at 72 h. Wortmannin or LY294002 intervention didn't change the expression of total Akt and GSK-3beta, while decrease the p-Akt and p-GSK-3beta expression. HI cause decreased axonal density, and the histological injury of brain. Wortmannin pretreatment could aggravate the histological injury and decrease axonal density after HI.The Akt pathway is involved in axonal density and histological brain injury after HI in neonatal rat.

To study the pathogens, drug sensitivity and risk factors for ventilator-associated pneumonia (VAP) in neonates.Retrospective analysis was performed on the clinical data of 401 neonates who were admitted to the neonatal intensive care unit and received mechanical ventilation for 48 hours or longer from January 2008 to February 2012. Eighty-five of the 401 neonates suffered VAP.The main pathogens for VAP were Gram-negative bacteria (97%), including Klebsiella pneumoniae (51%), Acinetobacter baumannii (17%) and Escherichia coli (12%) as the three most frequent ones. The drug sensitivity test showed that these pathogens developed resistance to amoxicillin, amoxicillin/clavulanic acid, piperacillin, ceftazidime, cefazolin, and cefotaxime, with a susceptibility rate of below 15%, and demonstrated decreased sensitivity to imipenem and meropenem, with a susceptibility rate of below 75%. The independent risk factors for neonatal VAP included birth weight (OR=1.399, P0.05), duration of mechanical ventilation (OR=1.966, P0.01), length of hospital stay (OR=1.812, P0.01), times of tracheal intubation (OR=2.056, P0.01), and 1 min Apgar score (OR=2.146, P0.01).The incidence of neonatal VAP is influenced by many factors. The main pathogens for neonatal VAP are Gram-negative bacteria and antibacterial agents should be properly used according to drug sensitivity test results. Comprehensive prevention and control measures should be taken to reduce the incidence of VAP.