Objective To investigate the clinical efficacy of purging fu-organs traditional Chinese medicine (TCM)therapy for treatment of patients with severe pneumonia and sthenia-heat. Methods According to random number table method,71 patients with sthenia-heat of severe pneumonia were divided into a treatment group (35 cases)and a control group(36 cases). Conventional basic treatment was given to both groups,and additionally, small chengqi decoction was applied nasogastrically for the therapy in treatment group for 2 weeks. The clinical pulmonary infection score(CPIS),Marshall score,integration score of TCM syndromes and the mortalities in 28 days and 60 days were used to compare the clinical efficacy of the two groups. Results With the prolongation of treatment,the CPIS,Marshall score and integration score of syndromes in the two groups were gradually decreased. In treatment group,CPIS and Marshall scores were lower than those of control group on the 4th day ,and there were statistically significant differences(CPIS score:5.8±1.7 vs. 6.8±1.9,Marshall score:5.3±2.3 vs. 6.6±2.7,both P<0.05);the above 2 scores in treatment group were also lower than those of control group on the 7th and 14th day after treatment(7th day CPIS score:5.3±1.5 vs. 5.6±1.4,Marshall score:5.1±1.9 vs. 5.7±1.8;14th day CPIS score:3.9±1.7 vs. 4.4±2.3,Marshall score:4.2±1.9 vs. 4.9±2.5),but there were no statistically significant differences(all P>0.05). In addition,the integration scores of syndromes were significantly decreased on the 4th, 7th and 14th day in the treatment group significantly lower than those in the control group(4th day:7.6±2.3 vs. 10.6±2.7,7th day:7.4±2.5 vs. 9.2±2.1,14th day:6.1±1.9 vs. 8.3±2.4,all P<0.05). However,there were no statistically significant differences in mortality rates in 28 days and 60 days respectively between control group and treatment group(28 days:16.7% vs. 11.4%,60 days:25.0% vs. 20.3%,both P>0.05). Conclusion Purging fu-organs therapy not only can decrease the CPIS and Marshall scores of patients with sthenia-heat of severe pneumonia,but also can improve their syndromes.

Objective :To explore rehabilitative effect of low—frequency (1Hz ,LF) repetitive transcranial magnetic stimulation (rTMS) combined functional electrical stimulation (FES) on lower limb spasm and motor function in pa—tients with subacute ischemic stroke (SAIS).Methods : A total of 92 SAIS patients with lower limb spasm and motor dysfunction hospitalized in our department were randomly divided into sham stimulation + FES group (sham stimu—lation group ,n＝45) and low—frequency rTMS + FES group (LF—rTMS group ,n＝47) ,both groups were continu—ously treated for three weeks .Lower limb motor function and spasm severity were assessed by Fugl—Meyer motor as—sessment (FMA) and modified Ashworth scale (MAS) respectively before and after treatment ,and motor evoked potential (MEP) was detected .Results : Compared with before treatment ,there was significant rise in FMA score , and significant reductions in MAS score and MEP in two groups after three—week treatment , P＝ 0.001 all ;com—pared with sham stimulation group ,there was significant rise in FMA score [16. 0 (13.0 ,23. 5 ) scores vs. 19. 0 (16.0 ,27.0) scores] ,and significant reductions in MAS score [1. 5 (1. 3 ,1.5) scores vs. 1. 0 (0. 5 ,1. 5) scores] and MEP [ (24.64 ± 0. 39) ms vs. (24.43 ± 0.31) ms] in LF—rTMS group after treatment , P＜0.05 or ＜ 0. 01 . Conclusion : Compared with sham stimulation + FES ,LF—rTMS + FES can more significantly improve lower limb spasm and motor function in patients with subacute ischemic stroke .

Objective:To explore the molecular mechanism through which repetitive transcranial magnetic stimulation (rTMS) promotes nerve regeneration after ischemic stroke.Methods:The miRNA expression profile in rats after rTMS was downloaded from the GEO database. Differentially-expressed miRNAs were identified using R software, and their corresponding mRNAs were predicted using the online database in order to construct miRNA-mRNA regulatory networks and identify the key miRNAs. The protein interaction network encoded by each gene was constructed by functional enrichment analysis, and the core mRNAs in the network were identified. Twenty-four male Sprague-Dawley rats of a specific pathogen-free grade were randomly divided into a sham operation group, a model group and a magnetic stimulation group, each of 8, and a stroke model was induced in the model and magnetic stimulation groups. The magnetic stimulation group then received rTMS for 7 consecutive days, while the other 2 groups did not. Modified neural function scores (mNSSs) were used to quantify neural function deficits before the experiment and 1, 3 and 7 days after the modeling. Eight days after the modeling, brain tissues were sampled for hematoxylin-eosin and Nishin staining to observe tissue loss and neuron morphology. Real-time fluorescence quantitative polymerase chain reactions were employed to verify the differential gene expression in the ischemic cortex.Results:A total of 167 different miRNAs were screened, and 25 mRNAs were predicted. Enrichment analysis showed that those genes are related to the positive regulation of cell migration and the positive regulation of neurotrophic factor receptor signaling pathways, including adenylate-activated protein kinase, the neurotrophic factor pathway, and rat sarcoma signaling pathways. The miRNA-mRNA regulatory network highlighted miR-206-3p, miR-378a-3p, miR-107-3p, miR-92a-3p and miR-29b-3p as key miRNAs. Integrin subunit β1, aquaporin 4, brain-derived nerve growth factor (BDNF), and member 4 of solutes vector family 2 were identified as key mRNAs by the protein interaction network analysis. Seven days after the modeling, the average mNSS score of the magnetic stimulation group was significantly lower than the model group′s average. Compared with the model group, the expression of miR-206-3p in the right cortex of the magnetic stimulation group had decreased significantly, while BDNF expression had increased significantly.Conclusions:miR-206-3p-BDNF pathways play an important role in neural repair promoted by rTMS.