Preterm neonates undergo many painful procedures as part of their standard care in the neonatal intensive care unit. However, pain treatment is inadequate in many of these routine procedures. In the present study, we investigated the impact and mechanism of combined music and touch intervention (CMT) on the pain response in premature infants. Sixty-two preterm neonates (gestational age of 0.05). After 2 weeks, the Premature Infant Pain Profile scores were significantly higher in the control group than experimental group (13.000 ± 0.461 vs 10.500 ± 0.850, respectively; P < 0.05). The cortisol concentration was not significantly different between the control and experimental groups either at the beginning of hospitalization (131.000 ± 18.190 vs 237.200 ± 43.860, respectively; P > 0.05) or 2 weeks later (162.400 ± 23.580 vs 184.600 ± 21.170, respectively; P > 0.05). However, the serum β-endorphin concentration was higher in the experimental group than in the control group both at the beginning of hospitalization (1.640 ± 0.390 vs 1.179 ± 0.090, respectively; P < 0.05) and 2 weeks later (2.290 ± 0.740 vs 1.390 ± 0.410, respectively; P < 0.05). CMT might decrease the pain response of preterm neonates by significantly improving the β-endorphin concentration, but not the blood cortisol concentration. Current Controlled Trials ISRCTN14131492 . Registered on 01 Aug 2016.

Objectives. To reveal the effect of microRNA-210 on cell apoptosis caused by HIE.Methods. Postnatal day 7 rats after HI injury were intraventricularly injected with microRNA-210 mimic, microRNA-210 inhibitor, or physiological saline. 72 h after the injection, rats were sacrificed and the left hemispheres were collected. The expression level of microRNA-210 was identified by quantitative real-time PCR analysis. Apoptosis in brain sections was investigated by TUNEL assay. Apoptosis-related protein expressions were studied by Western blot analysis.Results. The results showed that microRNA-210, whose expression was downregulated in the brain 72 h after HI injury, suppressed neuronal apoptosis by inhibiting caspase activity and regulating the balance between bcl-2 and bax levels.Discussion. Recent study demonstrated that microRNA-210 has neuroprotective effects through inhibiting apoptosis in a murine model of HIE. It represents a potential novel therapeutic approach for the treatment of HIE.

Previous studies on the mortality rate of omphalocele are limited. The risk of death of non-isolated omphalocele and that of cases of omphalocele that are diagnosed prenatally by ultrasound are unclear. This study aimed to estimate the perinatal mortality of pregnancies with omphalocele. This study also examined the potential risk of death of non-isolated omphalocele and that of cases that are prenatally diagnosed by ultrasound.

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Hypoxic-ischemic brain damage (HIBD) is a relatively common malignant complication that occurs in newborn infants, but promising therapies remain limited. In this study, we focused on the role of miR-326 and its target gene δ-opioid receptor (DOR) in the pathogenesis of neonatal HIBD. The expression levels of miR-326 and DOR after hypoxic-ischemic injury were examined both in vivo and in vitro. The direct relationship between miR-326 and DOR was confirmed by a dual-luciferase reporter assay. Further, effects of miR-326 on cell viability and apoptosis levels under oxygen glucose deprivation (OGD) were analyzed. The expression levels of miR-326 were significantly lower and DOR levels were significantly higher in the HIBD group than the control group both in vivo and in vitro. Overexpression of miR-326 downregulated the expression of DOR, while suppression of miR-326 upregulated the expression of DOR. The dual-luciferase reporter assay further confirmed that DOR could be directly targeted and regulated by miR-326. MiR-326 knockdown improved cell survival and decreased cell apoptosis by decreasing the expression levels of Caspase-3 and Bax and increasing Bcl-2 expression in PC12 cells after exposure to OGD. Moreover, DOR knockdown rescued the effect of the improved cell survival and suppressed cell apoptosis induced by silencing miR-326. Our findings indicated that inhibition of miR-326 may improve cell survival and decrease cell apoptosis in neonatal HIBD through the target gene DOR.

Hypoxic-ischemic brain injury (HIBD) causes neonatal death and serious neurological disability; however, there are currently no promising therapies for it excepting cooling. Therefore, in this study, we used peptidome analysis to identify differentially expressed peptides in cerebrospinal fluid (CSF) of neonates with HIBD or controls, which may give a foundation for finding new promising drugs of neonatal HIBD. CSF samples were collected from neonates with HIBD (n = 4) or controls (n = 4). ITRAQ LC–MS/MS was used to identify differentially expressed peptides between two groups. A total of 35 differentially expressed peptides from 25 precursor proteins were identified. The 2671.5 Da peptide (HSQFIGYPITLFVEKER), one of the down-regulated peptides in neonatal HIBD, is a fragment of heat shock protein 90-alpha (HSP90α/HSP90AA1). Results of bioinformatics analysis showed that HSP90α/HSP90AA1 was located in the protein–protein interaction (PPI) network hub and was involved in the NOD-LIKE receptor (NLR) signaling pathway. This peptide, we named it Hypoxic-Ischemic Brain Damage Associated Peptide (HIBDAP), is a hydrophilic peptide with high stability and has a long half-life of 3.5 h in mammalian reticulocytes. It was demonstrated that TAT-HIBDAP could successfully enter PC12 cells and further into the nucleus. After HIBDAP pretreatment and 6 h of OGD treatment, low concentrations of HIBDAP increased the survival rate of cells, except 40 μM had a toxic effect. Safe concentrations of HIBDAP reduced pyroptosis of PC12 cells under OGD, except 20 μM had no effect, by suppressing expressions of NLRP3, ASC and Caspase-1 except NLRP1. The results of our study identified the characterization and expression profiles of peptides in CSF of neonatal HIBD. Several meaningful peptides such as HIBDAP may play significant roles in neonatal HIBD and provide new therapeutic targets for neonatal HIBD.