The oncogene ABL1 plays an important role in various cancers, while its roles remain unclear in pneumonia. This study aims to investigate the roles of ABL1 in pneumonia and the underlying mechanisms. RNA sequencing was used to determine the expressions of multiple kinases in the PBMCs. A series of overexpression and knockout cell lines were constructed. Besides, an intranasal lung infection mouse model was pre-treated with asciminb. ELISAs and qPCR were used to determine the levels of target genes. In addition, STRING Interaction Network and Immunoblotting assays were used to determine the interaction between target proteins. An elevation in ABL1 was observed in the infant with Ecoli pneumonia. ABL1 was positively correlated to the levels of inflammatory cytokines and the activation of the NF-kB pathways. In vivo data demonstrated that the inhibition of ABL1 suppressed the inflammatory cytokines, reduced the lung bacterial burden, and ameliorated the lung injury score. ABL1 inhibited the phosphorylation of IκBα and p38 and regulated the ubiquitination of TRAF6. ABL1 regulates the inflammatory response in pneumonia in part by the regulation of MAPK and NF-κB pathways and TRAF6 ubiquitination.

Bronchial pneumonia in children is a common infectious disease in toddlers and infants, which may cause hyperpyrexia, pulmonary moist rales, and even respiratory failure. Traditional drugs for bronchial pneumonia in children often lead to drug resistance and side effects. Recently, naringenin has been reported to be a potential treatment for several airway inflammatory diseases due to its anti-inflammatory and anti-microbial activities. The current clinical study aimed to evaluate the safety and therapeutic effect of naringenin in treating bronchial pneumonia in children. A total of 180 eligible patients were randomly assigned into naringenin (NAR) group and azithromycin (AZI) group. All participants were required to follow a 5-day oral administration, and their serum cytokine levels were measured during the clinical intervention. After the treatment, the disappearance time of clinical symptoms, and the incidences of complications and adverse reactions were compared between the two groups. Naringenin was able to inhibit inflammation, shorten the disappearance time of clinical symptoms, reduce the incidences of bronchial pneumonia complications and related adverse reactions, and improve the health conditions of the patients. Our results suggested that naringenin was safe and beneficial to children with bronchial pneumonia, providing new insights into the clinical application of naringenin.

目的 观察鼠神经生长因子(mNGF)对新生大鼠缺氧缺血性脑损伤(HIBD)后巢蛋白(nestin)表达水平的影响,研究内源性神经干细胞增殖情况,探讨mNGF可能的神经保护机制.方法 新生7 d龄Wistar大鼠108只按完全随机法分为对照组、HIBD组和治疗组,每组36只.结扎大鼠左侧颈总动脉和8％低氧暴露2 h,制作新生大鼠HIBD模型.对照组仅暴露游离左侧颈总动脉,不结扎左侧颈总动脉和低氧暴露.治疗组大鼠于左侧股二头肌部位肌肉注射mNGF(10μg/kg),1次/d,连用3 d.HIBD组大鼠于相同部位注射等量生理盐水3 d.每组随机取12只大鼠分别于术后4 d、7 d、14 d处死后,制备大鼠海马部位脑组织HE及免疫组化切片.利用计算机图像分析技术检测各组nestin阳性细胞计数.结果 对照组海马部位椎体细胞排列整齐,HIBD组海马部位椎体细胞排列紊乱,可见较多凋亡神经细胞,治疗组可见海马部位椎体细胞排列较整齐,可见少量凋亡神经细胞;对照组、HIBD组及治疗组大鼠术后4 d nestin阳性细胞个数分别为(15.25±3.02)个、(24.67±3.37)个、(40.33±2.68)个,差异有统计学意义(P<0.05);对照组、HIBD组及治疗组大鼠术后7 d nestin阳性细胞个数分别为(17.33±2.71)个、(30.58±4.03)个、(48.75±2.99)个,差异有统计学意义(P<0.05);对照组、HIBD组及治疗组大鼠术后14 d nestin阳性细胞个数分别为(14.58±1.83)个、(22.75±2.05)个、(32.17±2.52)个,差异有统计学意义(P<0.05).结论 新生HIBD大鼠经mNGF干预后位于海马齿状回nestin表达增加,提示可能促进内源性神经干细胞的增殖、再生,在HIBD后神经再生、修复中可能发挥一定保护作用.

•Geniposide attenuates HI-induced brain injury.•PI3K/Akt signaling pathway is involved in the protection of Geniposide.•Geniposide may be used for HI treatment.

目的:针对简易鼻塞式持续气道正压呼吸器治疗新生儿呼吸窘迫的临床效果进行分析.方法:本次选取2017年1月-2019年1月期间来我院就医的94例呼吸窘迫的新生儿患者进行研究,分为对照组(n=47例)和研究组(n=47例),其中对照组采用肺表面活性物质治疗,研究组采用简易鼻塞式持续气道正压呼吸器给养治疗,对两组患者治疗前后的血气动脉值进行对比.结果:两组患者在治疗前的血气动脉值没有对比意义,但是在治疗后对照组血气动脉值相比研究组明显较低,数据有对比意义,P<0.05.结论:使用简易鼻塞式持续气道正压呼吸器给养治疗对患者的治疗具有十分积极的效果,治疗后患儿不良反应方面的情况影响较小,值得在临床上进行应用.