Objective To observe the effect of single kneeling position trunk intensive training on the balance of patients with stroke Pusher syndrome. Methods From January, 2014 to February, 2016, forty patients with stroke Pusher syndrome were randomly divided into observation group and control group equally. They all accepted routine rehabilitation, while the observation group added a trunk intensive training with one knee kneeled. They were assessed with Berg Balance Scale (BBS), Fugl-Meyer Assessment (FMA) of lower limb and Sheikh's Scale of Trunk Control before and after training. Results The scores of BBS, lower limb FMA and trunk control improved in both groups after eight weeks of treatment (t>1.756, P<0.05), and improved more in the observation group than in the control group (t>1.827, P<0.05). Conclusion Single kneeling trunk intensive training can effectively improve the balance in stroke patients with Pusher syndrome.

AIM: To study the roles of Toll-like receptor 4 ( TLR4 ) and TLR4 activator lipopolysaccharide ( LPS) in colonic inflammation recovery .METHODS:Normal intestinal epithelial cells were cultured with LPS in vitro. The subgroups of the intestinal epithelial cells with differential expression of TLR 4 ( low, normal and high ) were construc-ted by the technique of lentivirus transfection .The cells with normal and high expression of TLR 4 were induced by LPS for 0 h, 2 h and 4 h.Inflammatory cytokines TNF-α, IL-6 and IL-8 in the culture supernatant were detected by ELISA .The mRNA levels of TNF-α, IL-6, IL-8, IL-10 and IL-1βwere detected by qPCR .The cell mobility was also monitored by wound healing assay .RESULTS:The protein expression of TLR 4 was significantly higher after LPS treatment than that in control groups of both cells with TLR4 normal and high expression (P<0.05).The inflammatory cytokines TNF-α, IL-6, IL-8 and IL-1βat mRNA and protein levels were also significantly increased after LPS treatment compared with control group (P<0.05).The protein levels of TNF-α, IL-6 and IL-8 between the 2 groups were also different with statistical sig-nificance ( P<0.05 ) .Higher mobility was observed in the cells with TLR 4 high expression compared to control cells . CONCLUSION:LPS induction might play a role in the activation of TLR 4-mediated inflammatory pathways by up-regula-ting the expression of inflammatory cytokines at both transcriptional and translational levels .

[Objective] To investigate the evolution of inflammation under conditions and the effects of ginsenosides on macrophages subjected to the simulated weightlessness, with the aim of mitigating the inflammation. [Methods] Initially, genes related to weightlessness, inflammation, and immunity were identified in the GeneCards database. Then, Search Tool for the Retrieval of Interaction Gene/Proteins (STRING) protein network analysis was conducted to determine the core targets involved in the weightlessness-induced inflammation. Subsequently, Label-Free Quantitative (LFQ) proteomics was carried out to discern the distinctive genes within ginsenoside-treated Tohoku Hospital Pediatrics-1 (THP-1) cells. Next, utilizing the outcomes of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, the biological processes and signaling pathways in which ginsenosides predominately engaged were scrutinized, and the primary targets of ginsenosides in combating weightlessness-induced inflammation were examined. Finally, enzyme-linked immunosorbent assay (ELISA) was performed to detect the secretion levels of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α from lipopolysaccharide (LPS)-induced THP-1 cells under simulated weightlessness conditions, as well as during the weightlessness recovery period following treatment with ginsenosides. [Results] A total of 2 933 genes associated with inflammation, 425 genes linked to weightlessness, and 4 564 genes connected to immunity were retrieved from the GeneCards database. Protein-protein interaction (PPI) networks were generated to identify pivotal targets associated with weightlessness-induced inflammation such as IL-1β, IL-6, TNF, and albumin (ALB). It was found that ginsenosides primarily participated in the regulation of various inflammationrelated signaling pathways and pathways related to pathogenic microorganism infections. Moreover, it has a significant impact on the expression of proteins such as cluster of differentiation 40 (CD40), IL-1β, and poly ADP-ribose polymerase 1 (PARP1). As revealed in the simulated weightlessness cell test, ginsenosides exhibited a remarkable capacity to attenuate the secretion of inflammatory factors, specifically IL-6 and TNF-α (P < 0.000 1), in THP-1 macrophages following induction by LPS under simulated weightlessness conditions. In addition, it reduced the secretion of IL-1β, IL-6, IL-8, and TNF-α (P < 0.000 1) during the weightlessness recovery phase [Conclusion] Weightlessness can disrupt several inflammation-related signaling pathways, but ginsenosides were shown to mitigate the release of various inflammatory factors in macrophages subjected to simulated weightlessness, thereby exerting a protective role against inflammation. This study has laid a theoretical groundwork for further exploring the potential application of ginsenosides in safeguarding against LPS induced inflammation in a weightlessness environment.