AIM: To investigate the application of phrenic nerve conduction time(PNCT) in the recovery of general anaesthesia. METHODS: Pdi (t) and PNCT were measured by cervical magnetic stimulation of phrenic nerves in 8 patients before and after the administration of muscle relaxant. RESULTS: Pdi (t) was reduced from (23.7?2.4) cmH 2O to (11.5?3.4) cmH 2O (reduction rate: 51.5%, P

Objective:To investigate the effects of acupuncture therapy on acute cerebral infarction. Methods: Eighty patients with acute cerebral infarction were randomly divided into a treatment group of 40 cases and a control group of 40 cases. Xuanzhong(GB 39)-through-Sanyinjiao(SP 6) acupuncture was performed as a main treatment. The curative effects were compared between the two groups and the sizes of cerebral infarct, between pretreatment and posttreatment after one course of treatment. Results: The total recovery rate was 88.5% in the treatment group and 57.5% in the control group after one course of treatment. There was a significant difference between the two(P<0.05). The rate of change in the infarct for the better was significantly higher in the treatment group than in the control group. There was also a significant difference(P<0.05). Conclusion: This treatment is an effective method for lowering the rate of apoplectic disability and raising the cure rate.

ObjectiveTo explore the hub genes of acute-on-chronic liver failure （ACLF） using bioinformatics methods， predict the potential traditional Chinese medicines （TCMs） against ACLF， and verify the treatment mechanism based on experiments. MethodPerl and R were used to analyze the GSE142255 dataset to obtain the differentially expressed genes （DEGs）， from which the hub genes in the protein-protein interaction of DEGs were identified by five algorithms of the CytoHubba plug-in. The receiver operating characteristic （ROC） curve and GSE168048 dataset were then used to verify the hub genes. Coremine Medical was employed to map the TCMs corresponding to the hub genes and then the natures， tastes， and meridian tropism of the TCMs were analyzed. The TCM systems pharmacology database and analysis platform （TCMSP） and DEGs were used to obtain the common targets shared by high-frequency TCMs and ACLF， and Cytoscape was used to establish the "hub gene-high-frequency TCM-active ingredient-common target" network. Furthermore， gene ontology （GO） annotation， Kyoto encyclopedia of genes and genomes （KEGG） enrichment analysis， and in vitro experiments were performed. ResultA total of 388 DEGs were obtained， in which the 7 hub genes encoded CD4 integrin subunit alpha M （ITGAM）， CD2， lymphocyte-specific protein tyrosine kinase （LCK） proto-oncogene， C-C motif chemokine ligand 5 （CCL5）， matrix metallopeptidase-9 （MMP-9）， and Fc epsilon receptor IG （FCER1G）. The TCM candidates for treating ACLF were mainly cold， bitter， and had tropism to the liver meridian， among which the high-frequency TCMs （Hedyotis Diffusae Herba， Ganoderma， and Astragali Radix） and the active ingredients （quercetin， kaempferol， and beta-sitosterol） had significant therapeutic potential. The enrichment analysis results showed that TCMs acted on multiple targets and pathways such as autophagy， oxidative stress， and inflammatory cytokines in addition to regulating hub genes. L02 cell experiments showed that the quercetin group had lower levels of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and malondialdehyde （MDA）， lower protein levels of ubiquitin-binding protein p62 and MMP-9， and higher levels of superoxide dismutase （SOD）， glutathione （GSH）， and microtubule-associated protein 1 light chain 3 Ⅱ/Ⅰ （LC3 Ⅱ/Ⅰ） than the D-galactosamine （D-GaLN） group （P<0.05， P<0.01）. In addition， the pretreatment with 3-methyladenine （3-MA） inhibited the activating effect of quercetin on the autophagy of L02 cells. ConclusionThe potential TCMs and active ingredients predicted based on the hub genes of ACLF have a great research value. Quercetin has the potential to treat ACLF by inhibiting the D-GaLN-induced oxidative stress and inflammatory response in L02 cells and regulating the expression of MMP-9， which may be associated with the activation of autophagy.