To study the biological characteristics and mutations of influenza A(H1N1)pdm09 virus isolated from one case of pneumonia of unknown etiology (PUE),which would provide references for clinical treatment and disease control,the throat swab specimen from the PUE case was isolated in the Madin-Darby Canine Kidney (MDCK) cells,and then the antigenicity,pathogenicity and drug resistance of influenza A (H1N1) pdm09 virus were analyzed after sequencing.As a result,one influenza virus strain was isolated from the specimen and named as A/FujianGulou/SWL64/2016(H1N1).The similarities of nucleotide sequences and amino acids sequences compared with the vaccine strain A/California/07/2009 (H1N1) were 96.9％-98.9％ and 96.7％-99.5％,respectively.Eighteen amino acids had mutated in the HA and 4 mutations,K163Q,S185T,S203T and D222N,were involved in 3 different epitopes,which indicated that the antigenic drift had occurred in the influenza virus.The D222N mutation associated with receptor binding site made the virus infect lower respiratory tract more easily.The virus was still amantadine-resistance and oseltamivir-sensitive.In conclusion,the influenza A (H1N1) pdm09 virus in this study have occurred antigenic drift and has the molecular characterization of causing severe pneumonia,so further surveillance should be performed to prevent and control the influenza epidemic.

Post-stroke cognitive impairment (PSCI) is a common complication after stroke, which has high disability rate and mortality rate, and can affect the patient′s daily living ability and quality of life. Non-invasive brain stimulation (NIBS) has the advantages of non-invasiveness, safety, and ease of operation, and is easily accepted by patients. NIBS has a good application prospect in the treatment of PSCI, especially the representative treatment repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) such as have good clinical application effects. At present, there is no standardized treatment plan for NIBS, and there are large individual differences in therapeutic effects. This study reviewed the mechanism and clinical application of NIBS in the treatment of PSCI, and discussed the future application direction of NIBS.

Objective To investigate the genetic characteristics and mutations in hemagglutinin ( HA) genes of influenza A subtype H3N2 viruses isolated in Fujian province during 2014—2016. Methods HA gene fragments of 44 randomly selected influenza A (H3N2) viruses were amplified by RT-PCR and then sequenced by Sanger sequencing. Obtained sequences were analyzed by bioinformatics software and on-line websites. Results Pair-wise similarity among HA genes of the 44 strains was between 97. 3%-100. 0% at nucleotide level. The average variations between epidemic strains and corresponding vaccine strains in the year of 2014, 2015 and 2016 were 0. 012, 0. 008 and 0. 009, respectively. The genotype of epidemic strains in 2014 was 3C. 3a rather than 3C. 1 of the vaccine strain. Notably, variations at some antigenic sites, re-ceptor binding sites ( RBSs) and N-Glycosylation sites were identified despite the fact that the genotypes were identical between epidemic and vaccine strains in 2015 and 2016. Conclusion Variations at the HA genes of influenza A (H3N2) viruses in Fujian province occurred during the year of 2014—2016, reflecting the ability of circulating strains to escape the vaccine-induced immunity. Sustainable influenza surveillance and prompt identification of viral variants would benefit influenza prevention and control.

[This corrects the article DOI: 10.1016/j.apsb.2021.09.017.].

Pulmonary endothelial barrier dysfunction is a hallmark of clinical pulmonary edema and contributes to the development of acute lung injury (ALI). Here we reported that ruscogenin (RUS), an effective steroidal sapogenin of Radix Ophiopogon japonicus, attenuated lipopolysaccharides (LPS)-induced pulmonary endothelial barrier disruption through mediating non-muscle myosin heavy chain IIA (NMMHC IIA)‒Toll-like receptor 4 (TLR4) interactions. By in vivo and in vitro experiments, we observed that RUS administration significantly ameliorated LPS-triggered pulmonary endothelial barrier dysfunction and ALI. Moreover, we identified that RUS directly targeted NMMHC IIA on its N-terminal and head domain by serial affinity chromatography, molecular docking, biolayer interferometry, and microscale thermophoresis analyses. Downregulation of endothelial NMMHC IIA expression in vivo and in vitro abolished the protective effect of RUS. It was also observed that NMMHC IIA was dissociated from TLR4 and then activating TLR4 downstream Src/vascular endothelial cadherin (VE-cadherin) signaling in pulmonary vascular endothelial cells after LPS treatment, which could be restored by RUS. Collectively, these findings provide pharmacological evidence showing that RUS attenuates LPS-induced pulmonary endothelial barrier dysfunction by inhibiting TLR4/Src/VE-cadherin pathway through targeting NMMHC IIA and mediating NMMHC IIA‒TLR4 interactions.