Objective To investigate the influence of benzopyrene on extracellular matrix(ECM) protein deposition of human airway smooth muscle cells(HASMC) and the related pathway mechanism.Methods HASMC were primarily cultured and the 2-6 generations cells were applied in this experiment.The expression amount of ECM gene and protein was detected by real time PCR and Western Blot the phosphorylation level was analyzed by using the Western Blot method.Results Benzopyrene could to increase the expression of HASMC collagen Ⅰ α1 protein (P＜0.01) and ECM protein (including collagen Ⅰ α1,versican,fibronectin,laminin α2) mRNA(P＜0.05).Benzopyrene could induce the rapid increase of ERK1/2 phosphorylation level (P＜0.01).Furthermore,the ERK pathway inhibitor PD98059 could significantly inhibit the increase of benzopyrene-induced collagen Ⅰ α1 (P＜0.01)and ECM protein(including collagen Ⅰ α1,versican,fibronectin,laminin α2) mRNA expression(P＜0.01).Conclusion Benzopyrene induces the ECM protein deposition of HASMC by activating the ERK1/2 pathway,blocking the ERK1/2 signal pathway can inhibit the benzopyrene-induced airway remodeling.

Objective To investigate of the effect and mechanisman of SERCA2 on the phenotype modulation of HASMCs. Methods HASMCs were starved for 5 days and divided into different groups ,then we observed morphology change of the cells from the microscope and detected a-actin、SERCA2 and p-ERK by Western Blot,cells proliferation was observed by CCK-8 method. Results Compared with the control group,PDGF could reduce a-actin of HASMCs and increased the cells proliferation ability ,TSG could significantly inhibit the effect (P<0.01), PDGF could also significantly inhibit SERCA2 protein and increased the expression p-ERK (P<0.01), while U0126 significantly inhibited the effect (P < 0.01). Conclusion PDGF may induce HASMCs phenotype modulation through the regulation of SERCA2 and p-ERK.

Objective:To explore any effect of repeated transcranial magnetic stimulation (rTMS) on the upper limb motor function and cerebral cortex activation of stroke survivors.Methods:Sixty stroke survivors were randomly divided into an intervention group and a control group, each of 30. In addition to routine rehabilitation training (including drug therapy, comprehensive hemiplegic limb training and physical factor therapy), the intervention group received 15 minutes of rTMS daily, five days a week for 4 weeks while the control group was given false rTMS. Upper limb motor function was evaluated before and after the treatment using the Fugl Meyer upper limb motor function rating scale (FMA-UE). Functional near-infrared spectroscopy was used to detect and compare the activation (β values) of the prefrontal cortex, the motor cortex and the primary somatosensory cortex in the 2 groups. The correlation between the FMA-UE scores and the β values was quantified.Results:①There was no significant difference in the average FMA-UE scores between the two groups before the treatment. Afterward, though both groups′ average scores had increased significantly, there was significantly greater improvement in the treatment group. ②There was also no significant difference in average β value between the two groups before the experiment, but afterward the average βs of channels 27 and 13 in the intervention group were significantly higher than in the control group. Moreover, in patients with lesion in the left brain, the β-values of CH27 and CH13 were also significantly higher than the control group ( P<0.05). ③The FMA-UE scores of the intervention group were moderately correlated with the CH27 and CH13 β values, but those of the control group were only weakly correlated with the β values of CH27. Conclusion:Transcranial magnetic stimulation activates a lesioned left brain region, improving upper limb motor function. The improvement is correlated with the activation of the left prefrontal cortex and the left primary somatosensory cortex.