Background and objectiveInfections caused by extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli (E. coli) have raised public-health concerns and are becoming a global health challenge. This study aimed to investigate changes in antimicrobial resistance of E. coli responsible for early-onset sepsis (EOS) in a perinatal center in eastern China.MethodsTwo periods, 2002 to 2008 and 2012 to 2018, were investigated. EOS was defined as the presence of a single potentially pathogenic bacterium grown from blood or cerebrospinal fluid in cultures drawn in any newborn infant within 72 hrs of birth. The changes in antimicrobial resistance of E. coli were analyzed.ResultsA total of 163 cases of EOS were identified, and E. coli continued to be the leading pathogen in our neonatal intensive care unit (NICU). Overall resistance of E. coli to third-generation cephalosporins increased from 14.3% in 2002–2008 to 46.7% in 2012–2018 (p<0.05). This resistance pattern closely parallels ESBL production. Compared to that from term infants, E. coli isolated from preterm infants had a significantly higher rate of resistance to ampicillin (93.3% vs 48.4%, p<0.01) and gentamicin (60.0% vs 9.4%, p<0.01), as well as a higher rate of ESBL production (66.7% vs 15.6%, p<0.01).ConclusionWe conclude that ESBL-producing multi-drug resistant E. coli has emerged as the major pathogen responsible for early-onset neonatal sepsis, particularly in preterm infants. Clinicians should consider this trend and attempt to select proper effective antibiotics as the empirical treatment for early-onset neonatal sepsis.

Neonatal hypoxic-ischemic (HI) brain injury is a detrimental disease, which results in high mortality and long-term neurological deficits. Nevertheless, the treatment options for this disease are limited. Thus, the aim of the present study was to assess the role of liraglutide in neonatal HI brain injury in rats and investigate the associated mechanisms. The results showed that treatment with liraglutide significantly reduced infarct volume and ameliorated cerebral edema, decreased inflammatory response, promoted the recovery of tissue structure, and improved prognosis following HI brain injury. Moreover, treatment with liraglutide inhibited apoptosis and promoted neuronal survival both in the rat model and following oxygen-glucose deprivation (OGD) insult. LY294002, an inhibitor of phosphoinositide 3-kinase (PI3K), partially reversed these therapeutic effects, suggesting that the PI3K/protein kinase B (Akt) pathway was involved. In conclusion, our data revealed that treatment with liraglutide exerts neuroprotection after neonatal HI brain injury via the PI3K/Akt/glycogen synthase kinase-3β (GSK3β) pathway and may be a promising therapy for this disease.

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Mutations in the doublecortin ( DCX) gene, which encodes a microtubule-binding protein, cause human cortical malformations, including lissencephaly and subcortical band heterotopia. A deficiency in DCX and doublecortin-like kinase 1 (DCLK1), a functionally redundant and structurally similar cognate of DCX, decreases neurite length and increases the number of primary neurites directly arising from the soma. The underlying mechanism is not completely understood. In this study, the elongation of the somatic Golgi apparatus into proximal dendrites, which have been implicated in dendrite patterning, was significantly decreased in the absence of DCX/DCLK1. Phosphorylation of DCX at S47 or S327 was involved in this process. DCX deficiency shifted the distribution of CLASP2 proteins to the soma from the dendrites. In addition to CLASP2, dynein and its co-factor JIP3 were abnormally distributed in DCX-deficient neurons. The association between JIP3 and dynein was significantly increased in the absence of DCX. Downregulation of CLASP2 or JIP3 expression with specific shRNAs rescued the Golgi phenotype observed in DCX-deficient neurons. We conclude that DCX regulates the elongation of the Golgi apparatus into proximal dendrites through microtubule-associated proteins and motors.

To evaluate the safety and efficacy of total percutaneous closure of the femoral artery access site after veno-arterial extracorporeal membrane oxygenation (VA-ECMO) with the Perclose ProGlide device.This retrospective observational study during an almost 2-year period included 21 patients who underwent VA-ECMO in whom the femoral artery puncture site was closed percutaneously with Perclose ProGlide devices. Technical success was defined as successful arterial closure of the common femoral artery, without the need for additional surgical or endovascular procedures. Access site complications were recorded at 24 hours and 30 days after arterial closure, such as major bleeding requiring transfusion or surgical intervention, minor bleeding, groin infection, pseudoaneurysm, and lymphocele.Technical success was achieved in 20 patients (95.2%). One patient required surgical repair for an access site pseudoaneurysm. Eighteen femoral arteries were closed with 2 devices each, while 3 patients required the use of a third device for femoral artery access site closure to achieve adequate hemostasis. No arterial thrombosis, arterial dissection, arterial stenosis, groin infection, or arteriovenous fistula occurred during the periprocedural period (within 24 hours of arterial closure) or during 30-day follow-up.Percutaneous closure with the Perclose ProGlide device is a feasible procedure for closing femoral arterial access sites after VA-ECMO, with a low incidence of access site complications.