Background: The aim of this study was to investigate the clinical features of neonatal sepsis caused by Citrobacter freundii as well as the current status and treatment strategy for multi-drug resistance of infection with this bacterium. Methods: Nine newborns were diagnosed with C. freundii sepsis between January 2014 and December 2017. We collated and analyzed a range of data for these nine patients, including general information, laboratory tests during infection, blood culture and treatment. Results: One of the patients died after only 7 h of infection. In the remaining eight cases, three patients developed meningitis, although none had brain abscess. A reduction of white blood cells (WBC) was detected <24 h after the start of infection, compared with at 48-72 h, when WBC count had increased and platelets progressively decreased. In all nine cases the infection was susceptible to tigecycline and was resistant to cephalosporins, carbapenems, and quinolones. In eight cases the infection was susceptible to co-trimoxazole and in the other case it was susceptible to amikacin. Of the eight patients who were cured, three received meropenem, two received ceftriaxone, one received amikacin, and two received tigecycline. Conclusion: Reduction in WBC could take place in the early stages of C. freundii infection in newborns. The incidence of brain abscess was not high, but multi-drug resistance was common. Some non-sensitive drugs can also treat C. freundii sepsis effectively.

Neonatal hypoxic ischemic encephalopathy (Neonatal HIE) is a common but serious disease caused by perinatal asphyxia injury in newborns. Elevated neuronal apoptosis plays an important role in the injury process post hypoxia ischemia of the brain, which accurate mechanism is still worthy to be studied. Cellular repressor of E1Astimulated genes (CREG) possesses the protective effect in ischemia-reperfusion in multiple organs, including livers and hearts. The main purpose of this work was to investigate whether CREG was involved in alleviating neonatal HIE and explore the possible mechanisms. We found that CREG expression was downregulated in the hippocampus of neonatal HIE rats as well as oxygen-glucose deprivation/reperfusion (OGD/R)-treated hippocampal neurons. Besides, CREG overexpression promoted survival while inhibited apoptosis in OGD/R-induced hippocampal neurons accompanied by AKT signaling activation, which could be reversed by CREG silence. In addition, the protective effects of CREG overexpression could be antagonized by AKT deactivation, indicating the function of CREG was attributed by regulating AKT pathway. Collectedly, we demonstrated that CREG protected hippocampal neurons from hypoxic ischemia-induced injury through regulating survival and apoptosis via activating AKT signaling pathway.

Objective This study aimed to examine the characteristics of blood lactate in neonates undergoing mechanical ventilation in Tibet. Methods We recruited 67 neonates undergoing mechanical ventilation in Naqu People’s Hospital as the plateau observation group and 94 neonates undergoing mechanical ventilation in Shengjing Hospital as the control group. We analyzed the differences in lactate levels between the two groups. Results The lactate clearance rates of neonates with asphyxia and those with respiratory distress syndrome were significantly lower in the plateau group than in the control group. Lactate levels in neonates who died in the plateau group were significantly higher and the lactate clearance rate was significantly lower than those in neonates who survived. The cut-off point for the lactate clearance rate at 6 hours for predicting mortality was 6.09% in the plateau group. Conclusion The lactate clearance rate of neonates on mechanical ventilation in the plateau area is lower than that in neonates in the non-plateau area. The lactate clearance rate at 6 hours is important for evaluating the prognoses of critical neonates in plateau areas.