No abstract available

Objective To explore the clinical efficacy of intratracheal instillation of pulmonary surfactant (PS) combined with budesonide for preventing bronchopulmonary dysplasia (BPD) in very low birth weight (VLBW) infants. Methods Thirty VLBW infants with gestational age < 32 weeks who developed neonatal respiratory distress syndrome (NRDS) (grade Ⅲ-IV) suffering from intrauterine infection were randomly assigned into a PS+budesonide group and a PS alone group. The changes were compared between the two groups in arterial blood gas indexes, oxygenation index (OI), duration of mechanical ventilation, duration of oxygen supplementation, incidence of BPD, mortality rate at 36 weeks corrected gestational age and incidences of other complications except BPD. Results Compared with the PS alone group, the PS+budesonide group had a lower incidence of BPD, shorter duration of mechanical ventilation and oxygen supplementation (P < 0.05). On the 2nd to 6th day after treatment, the PS+budesonide group had higher pH value of arterial blood gas and OI and lower carbon dioxide partial pressure compared with the PS alone group (P < 0.05). There were no significant differences in the mortality rate at 36 weeks corrected gestational age and the incidences of other complications except BPD between the two groups (P > 0.05). Conclusions Intratracheal instillation of PS combined with budesonide can effectively reduce the incidence of BPD in VLBW premature infants with severe NRDS.

Objective To investigate the early intellectual developmental outcome of late preterm infants. Methods A total of 106 late preterm infants with a gestational age of 34-36⁺⁶ weeks who were admitted to the neonatal ward between January 2012 and January 2015, cured, discharged, and regularly followed up at the outpatient service for high-risk children were enrolled as the preterm group. A total of 120 healthy full-term infants during the same period were randomly selected as the term group. Neonatal behavioral neurological assessment (NBNA) was performed for late preterm infants at a corrected gestational age of 40 weeks and full-term infants at a gestational age of 40 weeks. The Gesell Developmental Scale was used for late preterm infants at a corrected age of 3, 6, and 12 months and full-term infants at an age of 3, 6, and 12 months. Results The preterm group had an NBNA score of < 37 and a significantly lower NBNA score than the term group (P < 0.05). At the corrected age of 3 months, the preterm group had significantly lower scores of gross motor, fine motor, and social competence than the term group (P < 0.05). At the corrected age of 6 months, the preterm group had significantly lower scores of adaptability, gross motor, and fine motor than the term group (P < 0.05). At the corrected age of 12 months, the preterm group had significantly lower scores of adaptability, gross motor, and social competence than the term group (P < 0.05). Conclusions Late preterm infants have early intellectual developmental delay. It is necessary to perform neurodevelopmental monitoring for late preterm infants.

Objective To investigate the neurodevelopmental level of preterm infants at the corrected age of 1 year and the effect of complications on neurodevelopment. Methods The clinical data and follow-up data of hospitalized preterm infants were retrospectively studied. The Bayley Scales of Infant Development was used to assess the neurodevelopmental level. Preterm infants were divided into groups according to gestational age, birth weight, and the presence or absence of complications. The mental development index (MDI) and psychomotor development index (PDI) were compared between groups. Results At the corrected age of 1 year, compared with the late preterm infants, the early preterm infants had significantly lower MDI and PDI (P < 0.05) and significantly higher rates of retarded intellectual and psychomotor development (P < 0.01). Compared with the normal birth weight group, the low birth weight group had significantly lower MDI and PDI (P < 0.01) and significantly higher rates of retarded intellectual and psychomotor development (P < 0.01). The preterm infants with hyperbilirubinemia, birth asphyxia or neonatal respiratory distress syndrome (NRDS) had significantly lower MDI and PDI than those without such complications (P < 0.05). Conclusions Lower gestational age and birth weight are associated with worse intellectual and psychomotor development in preterm infants. Complications, such as hyperbilirubinemia, birth asphyxia and NRDS, have adverse effects on neurodevelopment of preterm infants.

Objective To investigate the mortality rate and the cause of death of hospitalized neonates. Methods The clinical data of 480 neonates who died between January 2008 and December 2014 were collected. The mortality rates of neonates with different gestational ages, birth weights, sexes, and ages in days were analyzed. The abnormal perinatal factors, cause of death, and death grade were summarized. Results Among the 41 910 hospitalized neonates, 480 (1.1%) died, and the mortality rates of preterm infants and full-term infants were 1.7% and 0.7%, respectively. The mortality rate of hospitalized neonates decreased from 1.4% in 2008 to 1.1% in 2014, and the decrease was more apparent in the preterm infants with a gestational age of < 32 weeks and the neonates with a birth weight of < 1 000 g. Among preterm infants and full-term infants, those with a lower gestational age tended to have a higher mortality rate, but post-term infants had an increased mortality rate. The infants with a lower birth weight tended to have a higher mortality rate. Male neonates had a significantly higher mortality rate than female neonates (1.31% vs 0.92%; P < 0.05).Among the neonates who died, 61.3% had definite abnormal perinatal factors, including abnormal amniotic fluid (29.4%), premature rupture of membranes (16.9%), placental abnormality (16.9%), fetal intrauterine distress (14.0%), and abnormal umbilical cord (12.3%). Among the 480 neonates who died, 57 (11.9%) died within 24 hours after birth, 181 (37.7%) died within 2-7 days, and 242 (50.4%) died within 8-28 days. The three most common causes of death were infection, birth defect, and respiratory distress syndrome. The most common cause of death was respiratory distress syndrome in 2008-2011 and infection in 2012-2014. Respiratory distress syndrome was the most common cause of death in preterm infants with a gestational age of < 32 weeks, neonates with a birth weight of < 1 500 g, and neonates who died with 24 hours; infection was the most common cause of death in neonates with a gestational age of 32-42 weeks, neonates with a birth weight of 1 500-4 000 g, and neonates who died within 8-28 days. Neonatal asphyxia was the major cause of death in post-term infants. Inevitable deaths (grade 1) accounted for 54.4%, deaths that could be avoided under certain conditions (grade 2) accounted for 23.3%, and deaths caused by concerns about prognosis or economic reasons (grade 3) accounted for 22.3%. Conclusions In recent years, the treatment of neonates has gradually improved, and the mortality rate of neonates is gradually decreasing, especially in neonates with low gestational age and birth weight. Important measures for reducing the mortality rate in neonates include enhancing perinatal management, reducing abnormal perinatal factors, preventing infection, and increasing parents’ confidence in treatment.

Objective To investigate the risk factors for poor prognosis of severe adenovirus pneumonia (SAP) in children. Methods The clinical data of 189 children with SAP were retrospectively analyzed. Univariate logistic regression analysis was performed to assess the risk factors for poor prognosis. Results The univariate logistic regression analysis showed that the patients with hemoglobin < 90 g/L, plasma albumin < 30 g/L, C-reactive protein > 30 mg/L, procalcitonin > 10 ng/mL, alanine aminotransferase > 100 U/L, or aspartate aminotransferase > 100 U/L had poor prognosis (P < 0.05), and that those with congenital dysplasia of the airway, acute respiratory distress syndrome, circulatory complications, electrolyte and acid-base disturbance, or more than three complications also had poor prognosis (P < 0.05). Conclusions Poor prognosis of severe adenovirus pneumonia in children is associated with anemia, low serum albumin, inflammatory response, concurrent multiple complications and underlying lung diseases.

Objective To investigate the effect of atopy on the expression of glucocorticoid receptors in children with bronchiolitis. Methods ELISA was used to measure the changes in the serum levels of glucocorticoid receptor α (GRα) and glucocorticoid receptor β (GRβ) in the bronchiolitis group (77 children, including 34 children with atopy) and pneumonia group (68 children). Thirty-eight children who were prepared to undergo surgeries for non-infectious diseases and had no atopy or family history of allergic diseases were enrolled as the control group. Results The bronchiolitis group and the pneumonia group had significant increases in the serum levels of GRα and GRβ compared with the control group (P < 0.01), and the bronchiolitis group had significant increases in these levels compared with the pneumonia group (P < 0.01). Compared with the control group and the pneumonia group, the bronchiolitis group had a significant increase in the GRα/GRβ ratio (P < 0.01). Compared with the control group, the children with or without atopy in the bronchiolitis group had significant increases in the serum levels of GRα and GRβ (P < 0.01). The non-atopic children in the bronchiolitis group had a significant increase in the serum level of GRβ compared with the atopic children (P < 0.01). The atopic children in the bronchiolitis group had a significant increase in the GRα/GRβ ratio compared with the control group and non-atopic children in the bronchiolitis group (P < 0.01). Conclusions Children with bronchiolitis have increased serum levels of GRα and GRβ. The children with atopy have an increased GRα/GRβ ratio, suggesting that the atopic children with bronchiolitis are highly sensitive to glucocorticoids.

Objective To investigate the association between the serum level of brain-derived neurotrophic factor (BDNF) and the severity of asthma in children. Methods A total of 60 children with acute exacerbation of asthma were enrolled and divided according to the severity of the disease into mild group (n=18), moderate group (n=25), and severe group (n=17). Sixty healthy children were enrolled as controls. ELISA was used to measure the serum BDNF level in each group and the association between serum BDNF level and the severity of asthma was analyzed. Results The asthmatic children at the acute exacerbation and remission stages had significantly higher serum BDNF levels than healthy controls (P < 0.05). The serum BDNF level was significantly reduced in the remission stage compared with that in the acute exacerbation stage in asthmatic children (P < 0.05). The children with varying degrees of severity at the acute exacerbation stage had different serum BDNF levels: the severe group had the highest serum BDNF level and the mild group had the lowest level (P < 0.05). Conclusions BDNF may play an important role in the pathogenesis of childhood asthma and is related to the severity of the disease.

Objective To investigate the clinical features of Diamond-Blackfan anemia (DBA) and related pathogenic genes. Methods A retrospective analysis was performed for the clinical data of two children with DBA, and related literature was reviewed. Results The two children with DBA (2-3 months old) manifested with severe normochromic normocytic anemia, decreased reticulocyte count, and increased serum iron and serum ferritin. Normal white blood cell and platelet counts were noted in the two patients. Bone marrow examination showed a decreased percentage of erythrocytes and rare normoblasts in the two patients. Gene screening showed a reported pathogenic heterozygous mutation in RPS19 gene, c.212G >A (p. Gly71Glu), in one patient, and there were no mutations in his parents. In the other patient, gene screening showed a heterozygous mutation in RPL5 gene, c.740T > C (p.I247L), which had not been reported in literature, and there were no mutations in her parents. A bioinformatic analysis showed that this might be a pathogenic mutation. Conclusions The onset age of DBA is early infancy in most children, with a manifestation of erythroid deficiency. RPS19 and RPL5 gene mutations are common causes of this disease. Molecular detection helps with the early diagnosis of DBA.

Objective To investigate the infections occurring in the induction period of childhood acute lymphoblastic leukemia (ALL), the pathogens of the infections, and drug resistance of isolated strains. Methods A retrospective analysis was performed for the clinical data of 130 children with newly-diagnosed childhood ALL. Infections occurring during the induction chemotherapy, pathogenic strains, and drug-resistance spectrum were analyzed. Results The incidence rate of clinical infection and/or microbial infection reached 76.2%. The lungs were the most common infection site (46.2%). The children with severe infection accounted for 52.3%, among whom 60 had pulmonary infection and/or 21 had sepsis. A total of 50 pathogenic strains were detected, which consisted of 29 bacterial strains and 21 fungal strains. Of all the children, 28.5% experienced infections caused by at least one microbe. Among the 29 bacterial strains, there were 19 (65.5%) Gram-negative bacteria and 10 (34.5%) Gram-positive bacteria. The most common Gram-negative bacteria were Klebsiella pneumoniae, Escherichia coli, and Pseudomonas aeruginosa, which were 100% sensitive to imipenem. The most common Gram-positive bacterium was Streptococcus viridans, which was 100% sensitive to vancomycin. The infections caused by fungi accounted for 16.2%, with Candida albicans as the most common fungus. Compared with those with non-severe infections, the children with severe infections had a significantly shorter time to the occurrence of agranulocytosis, a significantly longer duration of agranulocytosis,significantly higher incidence of fever and C-reactive protein (CRP) level, and a significantly longer length of hospital stay (P < 0.05). Conclusions Pulmonary infections are common in the induction period of childhood ALL. Gramnegative bacteria are the most common pathogenic bacteria. Severe infections can be controlled by carbapenems combined with vancomycin and antifungal agents.

Objective To study the value of serum S100B protein and neuron-specific enolase (NSE) levels in predicting the severity of hand, foot and mouth disease (HFMD). Methods Ninety children with HFMD were classified into three groups: common type, severe type, and critical type (n=30 each). Thirty healthy children were randomly selected as the control group. ELISA was used to measure serum levels of S100B protein and NSE before and at 7 days after treatment. The receiver operating characteristic (ROC) curve was used to evaluate the prediction efficiency of S100B protein and NSE for the severity of HFMD. Results The critical type group had significant increases in the serum levels of S100B protein and NSE compared with the other three groups (P < 0.01). The severe type group had significant increases in serum levels of S100B protein and NSE compared with the common type and control groups (P < 0.01). The critical type and severe type groups had significant reductions in serum levels of S100B protein and NSE after treatment (P < 0.05). Serum S100B protein had the highest Youden value of 0.611 at the cut-off value of 0.445 μg/L, with a sensitivity of 61% and a specificity of 100%, in the prediction of serious HFMD (including severe type and critical type HFMD). Serum NSE had the highest Youden value of 0.533 at the cut-off value of 5.905 μg/L, with a sensitivity of 80% and a specificity of 73%, in the prediction of serious HFMD. Combined measurements of these two parameters had a sensitivity of 86% and a specificity of 73% and had the highest predictive value for serious HFMD. Conclusions The serum levels of S100B protein and NSE help to predict the severity and treatment outcomes of HFMD. Combined measurements of these two parameters has a higher predictive value for serious HFMD.

Objective To study the clinical and laboratory features of macrophage activation syndrome (MAS) at the early stage of diagnosis, and to explore a method for early identification of MAS. Methods A retrospective analysis was performed for the demographic data, clinical and laboratory features, and treatment outcomes of 21 MAS patients. Results Of the 21 MAS patients, 14 had systemic juvenile idiopathic arthritis, 5 had Kawasaki disease (KD), and 2 had connective tissue disease (CTD) as primary diseases. The median time of MAS onset was 19 days. The KD patients had the shortest time of MAS onset, while the CTD patients had the longest onset time (P=0.009). The top 10 clinical symptoms were fever (95%), rash (86%), lymph node enlargement (67%), hemophagocytic phenomenon in bone marrow (63%), pulmonary disease (62%), serous effusion (62%), hepatomegaly (52%), cerebrospinal fluid abnormalities (50%), central nervous system damage (43%), and splenomegaly (38%). The median of hemoglobin level was lower than the normal value. The medians of C-reactive protein level and erythrocyte sedimentation rate were higher than the normal values. There were significant increases in serum ferritin, glutamic-pyruvic transaminase, aspartate aminotransferase, lactate dehydrogenase, and triglyceride. The median of fibrinogen level was lower than the normal value. There were significant increases in D-dimer, interleukin-6 (IL-6), interleukin-10 (IL-10), and interferon-γ (IFN-γ). Of the 21 patients, 20 were improved and discharged. Conclusions If patients with rheumatic disease have persistent fever, hepatic dysfunction, coagulation disorders, multiple organ impairment, significantly increased IL-10 and IFN-γ, and a persistent increase in serum ferritin, the development of MAS should be considered.

Objective To investigate the clinical features and prognosis of acute renal failure (ARF) caused by rhabdomyolysis (RM) in children. Methods A retrospective analysis was performed for the clinical data, laboratory examination, and prognosis of 26 RM children with ARF. Results The causes for all 26 RM children with ARF were non-traumatic diseases, and the three most common causes were infection (69%), diabetes (12%), and metabolic disease (8%). In the RM children with ARF, the five most frequent clinical manifestations were fever (69%), multiple organ dysfunction syndrome (69%), convulsion (46%), oliguria or anuria (35%), and tea-colored urine (27%). All 26 children had a serum creatine kinase (CK) level of >1 000 IU/L, among whom 26 had increased aspartate aminotransferase, 25 had increased alanine aminotransferase, 25 had increased creatine kinase isoenzyme, and 23 had increased lactate dehydrogenase. Serum myoglobin (Mb) was measured in 22 children and was found to increase in all these children. The mean time for CK to decrease to below 1 000 IU/L was 10±5 d. There was no significant difference in the time to CK recovery between the 10 children who were treated with conventional treatment as well as continuous venous-venous hemofiltration and those who were not treated with blood purification (P > 0.05). Of all 26 RM children with ARF, 7 were withdrawn from the treatment, and 19 had normal renal function after treatment. Conclusions ARF and multiple organ dysfunction syndrome are major complications in RM children. The major primary disease for RM children with ARF is infectious disease. CK is the major marker for the diagnosis of RM. Early diagnosis and appropriate treatment may reverse ARF and improve prognosis.

Objective To investigate the clinical effect of postural correction training and helmet therapy in the treatment of moderate-severe positional head deformity defined as asymmetric head shape in infants. Methods A total of 31 infants who were diagnosed with moderate-severe plagiocephaly and/or brachiocephaly were enrolled. According to the different treatment methods, the infants were divided into helmet therapy group with 11 infants and postural correction training group with 20 infants. The cranial vault asymmetry index (CVAI), cephalic ratio (CR), and head circumference growth were compared between the two groups before and after treatment. Results Compared with the postural correction training group, the helmet therapy group had significantly lower CVAI and CR after treatment. The helmet therapy group had significantly better improvements in CVAI and CR after treatment compared with the postural correction training group (CVAI difference: 6.0±1.9 vs 0.7±0.8, P=0.001; CR difference: 0.047±0.009 vs 0.008±0.005, P < 0.001). There was no significant difference in head circumference growth between the two groups (P=0.55). Conclusions Helmet therapy has a significantly better effect in the treatment of moderate-severe positional head deformity than postural correction training in infants. Helmet therapy does not limit head circumference growth.

The infant (a girl aged 6 months) was admitted to the hospital because of oliguria and acute renal dysfunction. The laboratory examination results showed serious metabolic acidosis and increased blood urea nitrogen and serum creatinine levels. The patient continued to be anuric after 10 days of treatment with continuous renal replacement therapy (CRRT). she died a day later. The family history showed that the patient's sister died of acute renal failure 6 months after birth. The genomic sequencing results showed AGXT mutation in the patient and confirmed the diagnosis of primary hyperoxaluria type 1 (PH1). Her parents were heterozygous carriers. PH1 should be considered when the children have abnormal renal function or recurrent renal calculi or have a family history of these symptoms. AGXT gene analysis is an important method for PH1 diagnosis.

Objective To study the effect of calcium-sensing receptor (CaSR) agonists and antagonists on the expression of CaSR in neonatal mice with persistent pulmonary hypertension (PPHN), and to clarify the role of CaSR in neonatal mice with PPHN. Methods Forty-nine neonatal mice were randomly divided into four groups: control (n=10), hypoxia (PPHN; n=11), agonist (n=13), and antagonist (n=15). The mice in the PPHN, agonist, and antagonist groups were exposed to an oxygen concentration of 12%, and those in the control group were exposed to the air. The mice in the agonist and antagonist groups were intraperitoneally injected with gadolinium chloride (16 mg/kg) and NPS2390 (1 mg/kg) respectively once daily. Those in the PPHN and the control groups were given normal saline daily. All the mice were treated for 14 consecutive days. Hematoxylin and eosin staining and immunohistochemistry were used to observe the changes in pulmonary vessels. Laser confocal microscopy was used to observe the site of CaSR expression and measure its content in lung tissues. qRT-PCR and Western blot were used to measure the mRNA and protein expression of CaSR in lung tissues. Results Compared with the control group, the PPHN group had significant increases in the pulmonary small artery wall thickness and the ratio of right to left ventricular wall thickness (P < 0.05), which suggested that the model was successfully prepared. Compared with the control group, the PPHN group had a significant increase in the mRNA and protein expression of CaSR (P < 0.05), and the agonist group had a significantly greater increase (P < 0.05); the antagonist group had a significant reduction in the mRNA and protein expression of CaSR (P < 0.05). Conclusions CaSR may play an important role in the development of PPHN induced by hypoxia in neonatal mice.

Objective To investigate the expression of long non-coding RNA NANCI in lung tissues of neonatal mice with hyperoxia-induced lung injury and its regulatory effect on NKX2.1. Methods A total of 48 neonatal C57BL/6J mice were randomly divided into an air group and a hyperoxia group, with 24 mice in each group. Each group was further divided into 7-day, 14-day, and 21-day subgroups, with 8 mice in each subgroup. The mice in the air group were fed in the indoor environment (FiO₂=21%) and those in the hyperoxia group were fed in a high-oxygen box (oxygen concentration: > 95%). The mice were sacrificed at each time point and lung tissue samples were collected. Hematoxylin and eosin staining was used to observe pathological changes in lung tissues. RT-qPCR and Western blot were used to measure the mRNA and protein expression of NANCI and NKX2.1. Results The air group had the highest mRNA expression of NANCI and NKX2.1 at 7 days and the same level of mRNA expression at 14 and 21 days. Compared with the air group, the hyperoxia group had significant reductions in the degree of alveolarization and radial alveolar count (RAC) in lung tissues (P < 0.05), and in the hyperoxia group, RAC gradually decreased over the time of hyperoxia exposure (P < 0.05). The hyperoxia group had significantly lower mRNA and protein expression of NANCI and NKX2.1 than the air group at all time points (P < 0.05). In both groups, the relative mRNA and protein expression of NANCI and NKX2.1 gradually decreased over the time of hyperoxia exposure (P < 0.05). The expression of NKX2 was positively correlated with that of NANCI (r=0.585, P=0.003), and the expression of NKX2 and NANCI was positively correlated with RAC in the hyperoxia group (r=0.655 and 0.541 respectively, P < 0.05). Conclusions NANCI may be involved in the development of immature lung tissues. Lung injury is gradually aggravated over the time of hyperoxia exposure. The levels of NANCI and NKX2.1 are associated with the severity of lung injury, suggesting that the NANCI/NKX2.1 target gene signaling pathway might be involved in the development of hyperoxia-induced lung injury in neonatal mice.

Objective To investigate the effect of heat shock factor 1 (HSF1) on airway hyperresponsiveness and airway inflammation in mice with asthma and possible mechanisms. Methods A total of 36 mice were randomly divided into four groups: control, asthma, HSF1 small interfering RNA negative control (siHSF1-NC), and siHSF1 intervention (n=9 each). Ovalbumin (OVA) sensitization and challenge were performed to induce asthma in the latter three groups. The mice in the siHSF1-NC and siHSF1 groups were treated with siHSF1-NC and siHSF1, respectively. A spirometer was used to measure airway responsiveness at 24 hours after the last challenge. The direct count method was used to calculate the number of eosinophils. ELISA was used to measure the serum level of OVA-specific IgE and levels of interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-13 (IL-13), and interferon-γ (IFN-γ) in lung tissues and bronchoalveolar lavage fluid (BALF). Quantitative real-time PCR was used to measure the mRNA expression of HSF1 in asthmatic mice. Western blot was used to measure the protein expression of HSF1, high-mobility group box 1 (HMGB1), and phosphorylated c-Jun N-terminal kinase (p-JNK). Results The asthma group had significant increases in the mRNA and protein expression of HSF1 compared with the control group (P < 0.05). The siHSF1 group had significantly reduced mRNA and protein expression of HSF1 compared with the siHSF1-NC group (P < 0.05). The knockdown of HSF1 increased airway wall thickness, airway hyperresponsiveness, OVA-specific IgE content, and the number of eosinophils (P < 0.05). Compared with the siHSF1-NC group, the siHSF1 group had significantly increased levels of IL-4, IL-5, and IL-13 and significantly reduced expression of IFN-γ in lung tissues and BALF (P < 0.05), as well as significantly increased expression of HMGB1 and p-JNK (P < 0.05). Conclusions Knockdown of HSF1 aggravates airway hyperresponsiveness and airway inflammation in asthmatic mice, and its possible mechanism may involve the negative regulation of HMGB1 and JNK.

Objective To investigate the effect of telomerase activation on biological behaviors of neural stem cells after hypoxic-ischemic insults. Methods The neural stem cells passaged in vitro were divided into four groups: control, oxygen-glucose deprivation (OGD), OGD+cycloastragenol (CAG) high concentration (final concentration of 25 μM), and OGD+CAG low concentration (final concentration of 10 μM). The latter three groups were subjected to OGD. Telomerase reverse transcriptase (TERT) expression level was evaluated by Western blot. Telomerase activity was detected by telomerase repeat amplification protocol (TRAP). Cell number and neural sphere diameter were measured under a microscope. The activity of lactate dehydrogenase (LDH) was examined by chemiluminescence. Cell proliferation rate and apoptosis were detected by flow cytometry. Results After OGD insults, obvious injury of neural stem cells was observed, including less cell number, smaller neural sphere, more dead cells, lower proliferation rate and decreased survival rate. In CAG-treated groups, there were higher TERT expression level and telomerase activity compared with the control group (P < 0.05). In comparison with the OGD group, CAG treatment attenuated cell loss (P < 0.05) and neural sphere diameter decrease (P < 0.05), promoted cell proliferation (P < 0.05), and increased cell survival rate (P < 0.05). Low and high concentrations of CAG had similar effects on proliferation and survival of neural stem cells (P > 0.05). In the normal cultural condition, CAG treatment also enhanced TERT expression (P < 0.05) and increased cell numbers (P < 0.05) and neural sphere diameter (P < 0.05) compared with the control group. Conclusions Telomerase activation can promote the proliferation and improve survival of neural stem cells under the state of hypoxic-ischemic insults, suggesting telomerase activators might be potential agents for the therapy of hypoxic-ischemic brain injury.

Objective To investigate the effect of ulinastatin (UTI) for early drug intervention on the serum levels of tumor necrosis factor-α (TNF-α), P-selectin, and thrombin-antithrombin complex (TAT) in young rats with sepsis. Methods A total of 120 male rats aged 4 weeks were randomly divided into normal control group, shamoperation group, sepsis group, low-dose UTI group (50 000 U/kg), and high-dose UTI group (200 000 U/kg), with 24 rats in each group. Modified cecal ligation and puncture was performed to establish a rat model of sepsis, and the rats in the low- and high-dose UTI groups were given caudal vein injection of UTI after model establishment. ELISA was used to measure the serum levels of TNF-α, P-selectin, and TAT at 6, 12, and 24 hours after model establishment. Results The sepsis group had significant increases in the serum levels of TNF-α, P-selectin, and TAT at 6 hours, and the serum levels of TNF-α and TAT continued to increase by 24 hours (P < 0.05); P-selectin reached the peak at 12 hours and decreased slightly at 24 hours (P < 0.05). The UTI groups had similar change patterns in the levels of P-selectin and TAT as the sepsis group. The UTI groups had significant increases in the level of TNF-α at 6 hours, but gradually decreased over time. The changes in serum levels of TNF-α, P-selectin, and TAT in the UTI groups were significantly smaller than in the sepsis group (P < 0.05). The high-dose UTI group had significantly smaller changes in serum levels of TNF-α, P-selectin, and TAT than the low-dose UTI group (P < 0.05). Conclusions Early intervention with UTI can significantly improve coagulation function and inhibit the production of TNF-α, P-selectin, and TAT in young rats with sepsis. High-dose UTI has a significantly greater effect than low-dose UTI.

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.

No abstract available

Discharge against medical advice (DAMA) conflicts with the purpose of disease treatment in children. Some research has shown that there are high proportions of extremely preterm infants and infants with asphyxia or congenital malformation in neonates with DAMA. This suggests that the sustainable development of neonatology needs cooperation and co-development with obstetrics, neonatal surgery, and radiology to reduce the rate of DAMA. With reference to the current status of research in both China and other countries, this article reviews the causes for DAMA and the strategies for reducing the rate of DAMA, in order to provide a theoretical basis for effectively reducing the rate of DAMA from the neonatal intensive care unit, improving treatment outcomes of the neonates, and increasing hospitals’ comprehensive benefits.