Objective to investigate the mapping and ablation strategy of premature ventricular contraction(PVC)originating from the free wall of tricuspid annulus.Methods With the Carto3 three-dimensional electro-anatomical mapping system and long sheath supporting,the PVC originating from the free wall of the tricuspid annulus was mapped and ablated by inverted U-shaped catheter via the femoral vein access.Results In 19 patients with PVC originating from the free wall of the tricuspid annulus,mapping and ablation with an inverted U-shaped catheter under the free wall of tricuspid annulus was carried out.The treatment was immediately successful in all the 19 patients,and no complications occurred.During the 6-month follow-up period,one patient developed recurrence of PVC.Conclusion The PVC originating from the free wall of the tricuspid annulus can be roughly judged by the features of the electrocardiogram of the body surface before operation,and the mapping and ablation treatment by using inverted U-shaped catheter is technically-simple and clinically-safe with reliable therapeutic efficacy.

Objective:To evaluate the role and molecular mechanism of laminin β1(LAMB1)in cortical neurons in regulation of glutamate receptors.Methods:Recombinant lentivirus(LV-shLamb1)-mediated knockdown of LAMB1 expression in mouse primary cortical neurons was performed,followed by immunofluorescence staining and Western blot to detect changes in F-actin,glutamate receptor subtypes(AMPA receptors GluR1/GluR2,NMDA receptors NR1/NR2A),and ERK-related protein expression in cortical neurons.Results:LV-shLamb1 significantly inhibited LAMB1 expression in mouse cortical neurons.Concurrently,LV-shLamb1 markedly increased F-actin polymerization,as well as the expression of AMPA receptor subunits GluR1 and GluR2,and NMDA receptor subunits NR1 and NR2A.Further,Western blot detection showed that the phosphorylation level of ERK was significantly increased after LV-shLamb1 infec-tion.Conclusion:LAMB1 is expressed in cortical neurons.Suppression of LAMB1 expression in mouse cortical neu-rons activates the ERK pathway,which in turn promotes the polymerization of the cytoskeletal protein F-actin and the expression of glutamate receptors.This suggests that LAMB1 may regulate F-actin homeostasis and glutamate receptor levels through the ERK pathway,thereby playing a potentially important role in neuronal function.

Objective:To evaluate the role and molecular mechanism of laminin β1(LAMB1)in cortical neurons in regulation of glutamate receptors.Methods:Recombinant lentivirus(LV-shLamb1)-mediated knockdown of LAMB1 expression in mouse primary cortical neurons was performed,followed by immunofluorescence staining and Western blot to detect changes in F-actin,glutamate receptor subtypes(AMPA receptors GluR1/GluR2,NMDA receptors NR1/NR2A),and ERK-related protein expression in cortical neurons.Results:LV-shLamb1 significantly inhibited LAMB1 expression in mouse cortical neurons.Concurrently,LV-shLamb1 markedly increased F-actin polymerization,as well as the expression of AMPA receptor subunits GluR1 and GluR2,and NMDA receptor subunits NR1 and NR2A.Further,Western blot detection showed that the phosphorylation level of ERK was significantly increased after LV-shLamb1 infec-tion.Conclusion:LAMB1 is expressed in cortical neurons.Suppression of LAMB1 expression in mouse cortical neu-rons activates the ERK pathway,which in turn promotes the polymerization of the cytoskeletal protein F-actin and the expression of glutamate receptors.This suggests that LAMB1 may regulate F-actin homeostasis and glutamate receptor levels through the ERK pathway,thereby playing a potentially important role in neuronal function.

Objective:To investigate the changes of melanin concentration hormone receptor 1(MCHR1)in dorsal root ganglion(DRG)of mice with neuropathic pain.Methods:The expression profile of MCHR1 in the DRG of mice were observed by immunofluorescent staining.Neuropathic pain model was established by spared nerve injury(SNI)in mice.Male mice(C57BL/6)were randomly divided into 2 groups:Sham-operated group and SNI group.The paw withdrawal threshold(PWT)and paw withdrawal latency(PWL)were observed by von Frey fibers and thermal radiation stimulation.The mRNA and protein levels of MCHR1 in DRG were detected by real time RT-PCR and West-ern Blot,respectively.Results:MCHR1 was widely distributed in mouse DRG and co-labeled with small and medium-sized neuronal markers calcitonin gene-related peptide(CGRP)and isolectin B4(IB4),as well as large diameter neu-ronal marker NF200.Stable mechanical hyperalgesia and heat hyperalgesia were observed in the ipsilateral hindpaw of mice at 7 days post-SNI.Real time RT-PCR and Western Blot experiments showed that mRNA and protein expression levels in DRG were both significantly up-regulated in SNI-treated mice,as compared with Sham group.Conclusion:MCHR1 was widely distributed in large,medium and small neurons of DRG.After the SNI model mice presented a sta-ble phenomenon of hyperalgesia,the transcription and protein level of MCHR1 in DRG were significantly elevated in SNI mice.These data suggest that MCHR1 in DRG may be involved in the occurrence and development of neuropathic pain.

Objective:To investigate the changes of melanin concentration hormone receptor 1(MCHR1)in dorsal root ganglion(DRG)of mice with neuropathic pain.Methods:The expression profile of MCHR1 in the DRG of mice were observed by immunofluorescent staining.Neuropathic pain model was established by spared nerve injury(SNI)in mice.Male mice(C57BL/6)were randomly divided into 2 groups:Sham-operated group and SNI group.The paw withdrawal threshold(PWT)and paw withdrawal latency(PWL)were observed by von Frey fibers and thermal radiation stimulation.The mRNA and protein levels of MCHR1 in DRG were detected by real time RT-PCR and West-ern Blot,respectively.Results:MCHR1 was widely distributed in mouse DRG and co-labeled with small and medium-sized neuronal markers calcitonin gene-related peptide(CGRP)and isolectin B4(IB4),as well as large diameter neu-ronal marker NF200.Stable mechanical hyperalgesia and heat hyperalgesia were observed in the ipsilateral hindpaw of mice at 7 days post-SNI.Real time RT-PCR and Western Blot experiments showed that mRNA and protein expression levels in DRG were both significantly up-regulated in SNI-treated mice,as compared with Sham group.Conclusion:MCHR1 was widely distributed in large,medium and small neurons of DRG.After the SNI model mice presented a sta-ble phenomenon of hyperalgesia,the transcription and protein level of MCHR1 in DRG were significantly elevated in SNI mice.These data suggest that MCHR1 in DRG may be involved in the occurrence and development of neuropathic pain.

Objective:To investigate the effect of miR-23b on the malignant phenotype and the sensitivity of lenvatinib in human hepatocellular carcinoma cells.Methods:Human hepatocellular carcinoma cell line HepG2, SMMC-7721 and QGY-7703 were transfected with miR-23b mimic and its control, respectively. CCK-8 and EdU assay were used to detect cell proliferation. Transwell assay were used to detect changes in cell migration and invasion. Tube formation assay were used to detect vasculogenic mimicry formation. The comparison of the mean between groups was analyzed by t-test.Results:CCK-8 results showed that the A values ??of human hepatocellular carcinoma cell line HepG2 and SMMC-7721 in the miR-23b mimic group were 0.325 ± 0.011 and 0.537 ± 0.026, respectively, which were significantly lower than the control group 0.430±0.017 and 0.752 ± 0.051 ( P < 0.05). Transwell assay result showed that the number of cell migration of human hepatocellular carcinoma cell line HepG2 and SMMC-7721 in the miR-23b mimic group was (517.220 ± 32.873) and (242.327 ± 20.793), respectively, which were significantly lower than that of the control group (724.130 ± 15.142) and (424.432 ± 27.212) ( P < 0.01). Simultaneously, the number of cell invasions in the miR-23b mimic group were (55.671 ± 7.514) and (64.670 ± 6.011), respectively, which were significantly lower than those in the control group (124.320 ± 11.782) and (156.204 ± 12.501) ( P < 0.01). Tube formation assay showed that the number of tube forming branches of hepatocellular carcinoma cell line QGY-7703 and SMMC-7721 in the miR-23b mimic group was (489.824 ± 42.035) and (435.201 ± 44.143), respectively, which were significantly lower than that of the control group (878.620 ± 31.618) and (785.430 ± 38.723) ( P ??< 0.01). In addition, EdU results showed that after miR-23b combined with lenvatinib, the positive rates of EdU staining of hepatocellular carcinoma cell line HepG2 and SMMC-7721 in the miR-23b mimic group were (32.905 ± 1.342)% and (24.811 ± 0.820)%, respectively, which were significantly lower than the control group (52.623 ± 2.441)% and (38.702 ± 1.312)% ( P < 0.05). Conclusion:miR-23b can inhibit the proliferation, migration, invasion and vasculogenic mimicry formation, and enhance the sensitivity of lenvatinib drug in human hepatocellular carcinoma cells.

Objective To explore the therapeutic effect of dual perfusion embolization and chemotherapy via hepatic artery and portal vein(combmation treatment) in the treatment of unresectable PHC.Methods Eighty-one cases of unresectable PHC were randomly divided into two gronps: (1) Combination treatment group.Forty-one cases,These cases received embolization and chemotherapy via hepatic artery and portal vein through a drug delivery system intraoperatively,and then embolization and chemotherapy via the drug pump were given periodically. (2) TACE group.Forty cases.These cases were treated with Seldinger's technique, the dosage of drugs were the same as used in the former group during laparotomy. After 3 times of treatment, AFP, the size of tumor, liver function, body weight, abdominal perimeter, survival time of the two groups were compared.Results The weight, AFP, decrease of tumour size in combination group were much better than those in TACE group( P 0.05). The median survival time in the two groups were 18.0 months and 11.1 months ( P =0.0001). The accumulating survival rate of 6, 9, 12, 24 months were 87.8%, 78.0% , 68.2%,31.7% in combination group, and 70.0%, 52.5%, 30.0%, 5.0% in TACE group, respectively . The factors affecting survival were therapeutic method, liver function, size of tumour.Conclusions Combination treatment is simple, convenient with less complications, and the effect is better than TACE. So it is an effective method for the unresectable hepatic carcinoma.