Background: Purulent meningitis (PM) is an important cause of mortality and morbidity in the newborn population throughout the world. The subtle of specific clinical signs and low success rates of lumbar puncture make diagnosis of PM more difficult in preterm than in older children. The objective of this study was to establish a predict model for preterm PM in hopes of helping clinicians develop new diagnostic and treatment strategies. Methods: Premature infants who were admitted to The First Affiliated Hospital of Zhengzhou University from September 2017 to March 2020 were enrolled in this study. All the patients underwent lumbar puncture. We collected data encompassing maternal diseases and neonatal clinical features. Cerebrospinal fluid (CSF) culture is the gold standard for diagnosing meningitis. The PM was diagnosed according to the diagnostic criteria. All statistical analyses were performed using R 3.63 (https://www.r-project.org/). Logistic regression and least absolute shrinkage and selection operator (LASSO) regression analyses were used to establish a risk prediction model of PM. The Brier score, calibration slope, and concordance (C)-index were used to verify the accuracy of prediction model. Results: A total of 168 preterm infants were enrolled in this study, 80 boys and 88 girls, the gestational age (GA) was 26.43-36.86 weeks (32.45 +/- 2.79 weeks), the birth weight (BW) was 700-3,400 g (1,814.05 +/- 568.84 g). There were 77 preterm infants with PM while 91 without. We identified seven variables as independent risk factors for PM in preterm infants by LASSO analysis [the optimal lambda was 0.080960, and log(lambda) = -2.5138], including procalcitonin (PCT) on the 1st day after birth, prenatal glucocorticoid use, albumin, the 1-minute Apgar score, the use of non-invasive biphasic positive airway pressure, hemoglobin, and sex. These were used to construct a risk prediction nomogram and verified its accuracy. The Brier score was 0.17, the calibration slope was 0.966, and the concordance index was 0.82018. Conclusions: Our prediction model could predict the risk of PM in preterm infants. Using this prediction model, it may be able to provide reference to determine whether lumbar puncture is performed and whether antibiotics are applied as soon as possible.

1例因腹胀就诊新生儿，发现肠系膜肿物，伴凝血功能异常、血小板减少，超声及CT未能明确该肿瘤性质，腹腔穿刺放腹水，输血治疗效果差，行剖腹探查术，术中见瘤体来源于肠系膜并广泛侵犯血管及小肠肠管，难以切除，病理免疫组化诊断为卡波西型血管内皮瘤。

Neuroblastoma (NB) is a common pediatric malignancy with high mortality in childhood. Although many attentions have been gained, novel biomarkers for NB diagnosis and prognosis are still needed. microRNAs (miRNAs) played important roles in NB progression and miR-34a is a tumor suppressor in NB. However, the mechanism that underlies miR-34a regulating proliferation, migration, invasion and autophagy in NB remains poorly understood. In this study, cell proliferation was investigated by MTT and colony assay. Cell apoptosis was measured by caspase 3 activity assay. Cell migration and invasion were detected by trans-well analysis. Autophagy was measured via GFP-LC3 puncta fluorescence assay and western blots (WB). The expression of miR-34a was examined by quantitative real-time PCR (qRT-PCR). The regulatory effect of miR-34a on autophagy-related gene 5 (ATG5) was detected by qRT-PCR and WB. The interaction between miR-34a and ATG5 was probed by luciferase activity and RNA immunoprecipitation (RIP) assay. Results showed that miR-34a expression was inhibited in NB tissues and cells with low survival rate. Addition of miR-34a suppressed cell proliferation, migration, invasion and autophagy but promoted apoptosis in NB cells, whereas miR-34a deficiency played opposite roles in NB progression. Intriguingly, ATG5 was directly targeted by miR-34a. Moreover, ATG5 restoration attenuated miR-34a-mediated inhibitory effect on proliferation, apoptosis, migration, invasion and autophagy. These results indicated miR-34a suppressed proliferation, apoptosis, migration, invasion and autophagy in NB cells by targeting ATG5, providing a novel therapeutic avenue for NB treatment.

Objective To explore the relationship between renal volume and function in the preterm and term newborns at different gestational ages.Methods This study was conducted at the First Affiliated Hospital of Zhengzhou University from October 2016 to March 2018.A total of 626 newborns with different gestational ages were included and the renal volume was determined by ultrasonography.Blood samples were taken for laboratory tests to detect renal function including urea,creatinine,uric acid and estimated glomerular filtration rate.Results A total of 352 preterm and 274 full term newborns were enrolled at birth.The mean gestational age of the neonates was (36.0 ± 3.5) weeks and the mean birth weight was (2.59 ±0.77) kg.The mean renal volume of the preterm infants was (19.57 ±4.30) cm3 and estimated glomerular filtration was (21.68 ± 5.99) mL/(min · 1.73 m2);the mean renal volume of the term infants was(23.03 ± 3.80) cm3 and estimated glomerular filtration was(46.60 ± 10.21) mL/(min · 1.73 m2).The renal volume and estimated glomerular filtration of term infants was significantly greater compared to the preterm infants (t =12.96,33.10,all P ＜ 0.001).The renal volume was highly linear positively correlated with gestational age,birth weight and birth length (r =0.546,0.605,0.592,all P ＜ 0.001).The renal volume was highly linear positively correlated with estimated glomerular filtration(r =0.396,P ＜ 0.001).The renal volume was negatively correlated with urea,creatinine and uric acid(r =-0.210,-0.280,-0.176,all P ＜ 0.001).Conclusions The renal volume increases with gestational age and birth weight in neonates.Estimated glomerular filtration increases with renal volume in neonates.The preterm infants have immaturity kidney size and poor development so that they need special medical care.

Background: Pneumonia is an infectious lung inflammation in children with high mortality and morbidity rates. Small nucleolar RNA host gene 16 (SNHG16) has been verified to accelerate the progression of acute pneumonia. However, the role of SNHG16 in acute pneumonia has not yet been fully elucidated. The study was aimed to explore the regulatory mechanism of SNHG16 in LPS-induced acute pneumonia in A549 cells. Methods: The levels of SNHG16, miR-370-3p and IGF2 in serum samples and LPS-induced A549 cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability and apoptosis of A549 cells were examined by Cell Counting Kit-8 (CCK-8) assay and flow cytometer, respectively. The levels of interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) were determined by enzyme-linked immunosorbent assay (ELISA). The binding relationships among SNHG16, miR-370-3p and IGF2 were predicted by online database and verified by Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. The protein levels of IGF2 were tested by Western blot. Results: SNHG16 and IGF2 were upregulated while miR-370-3p was downregulated in serum of acute pneumonia patients and LPS-induced A549 cells. SNHG16 regulated proliferation, apoptosis and inflammatory cytokines by inhibiting miR-370-3p in LPS-induced A549 cells. MiR-370-3p targeted IGF2 and inhibited LPS-induced inflammatory injury via IGF2 in A549 cells. Furthermore, SNHG16 was verified to promote IGF2 expression by sponging miR-370-3p in A549 cells. Conclusion: SNHG16 impeded cell viability and promoted apoptosis, inflammatory injury by targeting IGF2 mediated by miR-370-3p in LPS-induced A549 cells.