The role of rhIGF-1/BP3 in the prevention of pulmonary hypertension in bronchopulmonary dysplasia and its underlying mechanism.

BACKGROUND: This study aimed to determine whether postnatal treatment with recombinant human IGF-1 (rhIGF-1)/binding peptide 3 (BP3) ameliorates lung injury and prevents pulmonary hypertension (PH) in bronchopulmonary dysplasia (BPD) models. METHODS: We used two models of BPD in this study: one model that was associated with chorioamnionitis (CA), stimulated by intra-amniotic fluid and exposure to lipopolysaccharide (LPS), whereas the other was exposed to postnatal hyperoxia. Newborn rats were treated with rhIGF-1/BP3 (0.2 mg/Kg/d) or saline via intraperitoneal injection. The study endpoints included the wet/dry weight (W/D) ratio of lung tissues, radial alveolar counts (RACs), vessel density, right ventricular hypertrophy (RVH), lung resistance, and lung compliance. Hematoxylin and eosin (H&E) and Masson staining were used to evaluate the degree of lung injury and pulmonary fibrosis. IGF-1 and eNOS expression were detected using western blotting or quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). The levels of SP-C, E-cadherin, N-cadherin, FSP1, and Vimentin in the lung tissues were detected by immunofluorescence. RESULTS: LPS and hyperoxia treatment increased lung injury and pulmonary fibrosis, enhanced RVH and total respiratory resistance, and decreased RAC, pulmonary vascular density and pulmonary compliance in young mice (all p < 0.01). Simultaneously, LPS and hyperoxia induced an increase in epithelial-mesenchymal transition (EMT) in airway epithelial cells. However, rhIGF-1/BP3 treatment reduced lung injury and pulmonary fibrosis, decreased RVH and total respiratory resistance, and enhanced RAC, pulmonary vascular density and pulmonary compliance, as well as inhibited EMT in airway epithelial cells in LPS and hyperoxia treated mice. CONCLUSION: Postnatal rhIGF-1/BP3 treatment relieved the effects of LPS or hyperoxia on lung injury and prevented RVH, providing a promising strategy for the treatment of BPD.

Pathogenic bacteria distributions and drug resistance analysis in 96 cases of neonatal sepsis.

BACKGROUND: This study aimed to summarize common pathogens and associated drug resistance in neonatal sepsis (NS). METHODS: Blood culture and drug sensitivity results from 96 NS cases treated from January 2010 to August 2014 were retrospectively analyzed. RESULTS: A total of 97 pathogenic bacteria were detected from these 96 NS cases; Gram-positive cocci accounted for 76.3% of the cases, among which 70.1% involved coagulase-negative staphylococcus (CONS), whereas Gram-negative bacilli and fungi accounted for 19.6% and fungi 4.1% of cases, respectively. Gram-positive cocci exhibited a higher penicillin resistance rate and full vancomycin sensitivity, whereas Gram-negative bacilli exhibited a higher cephalosporin resistance rate, low meropenem resistance rate (6.7%), and no resistance to amikacin. CONCLUSIONS: The main causative pathogens of NS in our hospital were Gram-positive cocci, among which coagulase-negative Staphylococcus spp such as S. epidermidis and S. haemolyticus were the main conditional pathogens; among Gram-negative pathogens, Klebsiella pneumoniae were most frequently isolated and showed widespread resistance to penicillins and cephalosporins.

[A randomized controlled study of nasal intermittent positive pressure ventilation in the treatment of neonatal respiratory distress syndrome].

OBJECTIVE: To compare the clinical effects of nasal intermittent positive pressure ventilation (NIPPV) and nasal continuous positive airway pressure (NCPAP) in the treatment of neonatal respiratory distress syndrome. METHODS: A prospective, randomized, controlled, single-center study was performed on 67 premature infants with NRDS between March 2011 and May 2012 and selected according to the inclusion and exclusion criteria. These premature infants were randomly assigned to receive NIPPV and NCPAP. Oxygenation index (OI), pH, PaCO2, duration of respiratory support, complications, success rate, hospital mortality, and incidence of bronchopulmonary dysplasia (BPD) were compared between the two groups. RESULTS: Sixty-two patients were finally enrolled in the study, including 32 cases in the NIPPV group and 30 cases in the NCPAP group. After one hour of non-invasive ventilation, OI in the NIPPV group was higher than the NCPAP group (P<0.05), but there were no significant differences in pH and PaCO2 between the two groups (P>0.05 for both). A significantly lower proportion of infants needed mechanical ventilation via endotracheal tube (MVET) when they were treated initially with NIPPV than when they were treated initially with NCPAP (P<0.05). The NIPPV group had a significant higher success rate than the NCPAP group (P<0.05), but there was no significant difference in duration of respiratory support between the two groups (P>0.05). In addition, no significant differences in incidence of pneumothorax, hospital mortality and incidence of BPD were seen between the two groups (P>0.05 for all). CONCLUSIONS: Compared with NCPAP, NIPPV can significantly decrease the proportion of premature infants with NRDS in need of MVET. However, there is no evidence that NIPPV can significantly reduce hospital mortality and incidence of BPD in premature infants with NRDS.

Prediction Effect of Amplitude-Integrated EEG on the Brain Damage and Long-Term Nervous System Development of Late Preterm Infants.

In order to explore the prediction effect of amplitude-integrated EEG on the brain damage and long-term nervous system development of late preterm infants, this paper uses the hospital's late preterm infants as the research object and analyzes the prediction effect of amplitude-integrated EEG on the brain damage and long-term nervous system development of late preterm infants through controlled trials. Among them, the test group used amplitude-integrated EEG for prediction analysis, and the control group used traditional clinical prediction methods. Furthermore, the real-time monitoring and short-term prediction effects of amplitude-integrated EEG on brain damage in late preterm babies and the prediction impact on long-term nervous system development are evaluated in this study. It incorporates statistical techniques to evaluate the findings statistically. In addition, a nonparametric rank-sum test is used in this work, and a chi-square test is used to compare enumeration data across groups. Through experimental research, it can be seen that the amplitude-integrated EEG has a pronounced prediction effect on the brain damage and long-term nervous system development of late preterm infants, and the effect is higher than that of the traditional clinical prediction methods.

18q22.1-qter deletion and 4p16.3 microduplication in a boy with speech delay and mental retardation: case report and review of the literature.

BACKGROUND: Deletions involving the long arm of chromosome 18 have been associated with a highly variable phenotypic spectrum that is related to the extent of the deleted region. Duplications in chromosomal region 4p16.3 have also been shown to cause 4p16.3 microduplication syndrome. Most reported patients of trisomy 4p16.3 have more duplications, including the Wolf-Hirschhorn critical region (WHSCR). Here, we present a patient with speech delay and mental retardation caused by a deletion of 18q (18q22.1-qter) and terminal microduplication of 4p (4p16.3-pter) distal to WHSCR. CASE PRESENTATION: The patient was a 23-month-old boy with moderate growth retardation, severe speech delay, mental retardation, and dysmorphic features. Single nucleotide polymorphism (SNP) array analysis confirmed an 11.2-Mb terminal deletion at 18q22.1 and revealed a 1.8-Mb terminal duplication of 4p16.3. Our patient showed clinical overlap with these two syndromes, although his overall features were milder than what had been previously described. Some dosage-sensitive genes on the 18q terminal deleted region and 4p16.3 duplicated region of the present case may have contributed to his phenotype. CONCLUSIONS: This is the first report of a patient with combined terminal deletion of 18q22.1 and duplication of 4p16.3. In this report, we provide clinical and molecular evidence supporting that the microduplication in 4p16.3, distal to WHSCR, is pathogenic. The coexistence of two chromosome aberrations complicates the clinical picture and creates a chimeric phenotype. This report provides further information on the genotype-phenotype correlation of 18q terminal deletion and 4p microduplication.

Changes in the cytokine expression of peripheral Treg and Th17 cells in children with rotavirus enteritis.

The aim of the present study was to investigate the changes in the cytokine expression of peripheral regulatory T cells (Treg) and T helper 17 (Th17) cells in children with rotavirus (RV) enteritis. In total, 102 children with RV enteritis were recruited for the observation group, while 30 healthy cases were included in the control group. Peripheral blood samples were collected from the individuals in the two groups, after which flow cytometry was conducted to detect the proportion of Treg and Th17 cells. In addition, ELISA was used to determine the levels of the cytokines, interleukin (IL)-10, transforming growth factor (TGF)-ß, IL-17 and IL-6. When compared with the control group, the proportion of Treg cells and level of TGF-ß in the peripheral blood of the children with RV enteritis were significantly decreased (P<0.05); however, the proportion of Th17 cells and the serum levels of IL-17 and IL-6 in the peripheral blood of children with RV enteritis were significantly increased (P<0.05). In conclusion, the present study identified an imbalance in the proportion of peripheral blood Treg/Th17 cells, and subsequently in the expression of cytokines, in children with RV enteritis. Thus, detecting the proportion of peripheral blood Treg/Th17 cells in children with RV enteritis, or the changes in the levels of serum cytokines, is of clinical significance for further investigation into the pathogenesis of RV enteritis.