Glioblastoma multiforme (GBM) is a malignant cancer with severely poor survival, and the cells continue to thrive during hypoxia and toxic stress through autophagy. To validate the oncogenic role of long noncoding RNA H19 in GBM progression and examine whether autophagy and/or miR-491-5p participate in the process. The expression of H19 and autophagy-related genes in GBM and healthy control tissues was assessed via quantitative polymerase chain reaction. In addition, cell viability, proliferation, apoptosis and autophagy were respectively determined via cell counting kit-8 assay, clone formation assay, flow cytometry, western blotting and green fluorescent protein–microtubule-associated protein 1 light chain 3 alpha fluorescence analysis in vitro. Furthermore, a rescue assay was performed using rapamycin or miR-491-5p antagomir to examine the role of autophagy or miR-491-5p in H19-mediated regulation of proliferation and apoptosis. RNA pull-down and dual-luciferase reporter assays were employed to analyze the interaction between H19 and miR-491-5p. Additionally, tumor growth in a xenograft-bearing mouse model and autophagy in tumor mass were analyzed in vivo. The expression H19 was increased in GBM and was positively correlated with LC3 or Beclin-1. Silencing H19 inhibited growth and promoted apoptosis in GBM cells both in vitro and in vivo, and miR-491-5p was identified as one of the important mediators. H19 regulated the autophagy signaling pathway at least partly via miR-491-5p. Increased H19 expression in GBM exerts oncogenic effects by sponging miR-491-5p and enhancing autophagy. Therefore, H19 may be explored as a target for GBM therapy. GRAPHICAL ABSTRACT

The research aimed to provide the most recent and comprehensive analysis and evidence update comparing outcomes in neonatal encephalopathy (NE) based on different glycemia levels. A comprehensive search of Cochrane, PubMed, Embase, Web of Science, CNKI, and Wanfang databases was conducted until September 2023. The purpose was to identify research that examined the effects of hyperglycemia, hypoglycemia, and normoglycemia on NE outcomes. The hyperglycemic, normoglycemic and hypoglycemic group were compared. Outcomes measured were mortality, abnormal MRI, hearing or visual unfavorable outcomes, neurodevelopmental delay, cerebral palsy, and all unfavorable outcomes. Thirteen literatures comprising 2,427 participants (1,233 with normoglycemia, 835 with hyperglycemia, and 359 with hypoglycemia) were considered. Pooled analysis showed more overall adverse outcomes, higher mortality and worse hearing or visual outcomes in the hyperglycemic and hypoglycemic group compared to the normoglycemic group. There was no notable distinction found in abnormal MRI and cerebral palsy among all groups. The hypoglycemic group exhibited greater neurodevelopmental delay than normoglycemia. Maintaining normal blood glucose levels in neonates with NE can help reduce the risk of adverse consequences such as hearing and visual impairment.

Escherichia coli (E. coli) causes infections in neonates admitted to neonatal intensive care units (NICUs). Although β-lactam antibiotics are commonly used for neonatal infectious diseases, E. coli has exhibited resistance to them. Therefore, we investigated the resistance of E. coli strains isolated from a NICU to β-lactam antibiotics. E. coli isolates were collected from patients admitted to a NICU from 2020–2023. The clinical characteristics of the patients were analyzed. The antimicrobial susceptibility was determined using the agar dilution method, and the distribution of β-lactamase genes was analyzed using PCR. Conjugation experiments were conducted to analyze the horizontal transferability of resistance genes on plasmids. Genomic DNA was extracted for whole genome sequencing, construction of plasmid physical maps, locating resistance genes, and analyzing flanking regions and the resistance gene-related sequences. Throughout the study period, 110 distinct E. coli strains were collected. Among these, 62 cases presented strains, which were resistant against at least one of seven ß-lactam antibiotics associated with conditions such as ventilator-associated pneumonia (35/62), catheter-associated urinary tract infection (14/62), necrotizing enterocolitis (7/62), skin infection (1/62), and neonatal septicemia (5/62). Resistance of E. coli isolates to seven β-lactam antibiotics ranged from 2.73–56.36%. In 62 strains (56.36%, 62/110), six genotypes (11 sub-genotypes) of 111 β-lactamase genes were identified. Conjugation experiments revealed two transconjugants carrying the blaKPC-2 gene and two carrying the blaOXA-1 gene, exhibiting resistance to carbapenems and other β-lactams. The plasmids of four strains were successfully conjugated and transferred to recipient E. coli C600. PCR of the transconjugant resistance genes revealed that two carried a blaKPC-2 gene with a MIC increased up to 32-fold relative to the recipients, and the other two carried a blaOXA-1 gene with a 32-fold increased MIC. For isolate ECK03 carrying blaKPC-2, blaCTX-M-64, blaCTX-M-65, and blaTEM-1, sequencing results showed that blaKPC-2, blaCTX-M-64, and blaTEM-1 were harbored on a 114-kb pECK03_KPC-2 plasmid, whereas two identical blaCTX-M-64 genes were harbored in E. coli isolate ECF13. These findings highlight the existence of E. coli β-lactam resistance within NICU populations, emphasizing the need for continual monitoring of β-lactamase isolates to facilitate effective antibiotic selection.