Objective To investigate the effect of microcatheter in chemoembolization of HCC. Methods Using 4-F ～ 5-F Yashiro/Kouno and 5-F Hook catheters as guiding catheter,3-F microcatheter was put into segmental hepatic artery or tumor feeding artery and chemoembolization was carried out. Results All 35 cases had 50 times chemoembolizations totally, of them, 16 cases with small HCC had segmental TAE and 19 cases with large but localized HCC had right/left hepatic artery or anterio/posterio brtaneh of right hepatic artery embolization,1 ～2 year survial rates were 100% ,87.5% and 52.6% ,42. 1% respectively after TAE. Liver function damage after TAE was slight and no complications occurred. Conclusion Improving embolization precision by using microcatheter is valuable in the cases with small HCC or large but localized HCC with tortuous hepatic artery,hepatic artery stenosis after injury and variations.

Objective: To investigate the effect of microcatheter in chemoembolization of HCC. Methods Using 4 - F - 5 - F Yashiro/Kouno and 5 - F Hook catheters as guiding catheter,3 - F microcatheter was put into segmental hepatic artery or tumor feeding artery and chemoembolization was carried out. Results All 35 cases had 50 times chemoembolizations totally, of them, 16 cases with small HCC had segmental TAE and 19 cases with large but localized HCC had right/left hepatic artery or anterio/posterio brtanch of right hepatic artery embolization, 1-2 year survial rates were 100%, 87. 5% and 52. 6%,42. l% respectively after TAE. Liver function damage after TAE was slight and no complications occurred. Conclusion Improving embolization precision by using microcatheter is valuable in the cases with small HCC or large but localized HCC with tortuous hepatic artery,hepatic artery stenosis after injury and variations.

Objective To research a new type of gastrointestinal anastomat -- anastomosis device with three rows of staples (Pa-tent No .2012200583213) ,and clarify its associated functions through esophagogastric anastomosis operations on pigs ,so that we could provide experiences for its clinical application in future .Methods Compared with domestic anastomat with two rows of sta-ples ,we designed and manufactured a new type of anastomat with three rows of staples and researched its function .Choosing 12 do-mestic pigs ,about 60 kg ,gastroesophageal anastomosis was taken twice with each case by anastomat with three or two rows of sta -ples randomly in sequence .According to the different types of anastomats ,cases were divided into two groups :group A ,used anas-tomat with three rows of staples ,including 12 cases of anastomosis ;group B ,used anastomat with two rows of staples ,including an-other 12 cases of anastomosis .Results Compared with group B ,cases of group A have less bleeding sites (t = 7 .00 ,P < 0 .01) . Without reinforcement and with 0 .5 kg of tension ,fewer of outermost staples exposed(t= 6 .17 ,P< 0 .01) .And the shape of used staples of group A is double circles ,which has bigger mechanical strength than that of group B (t= 6 .57 ,P < 0 .01) .Conclusion The function of anastomat with three rows of staples surpasses that of traditional anastomat with two rows of staples in pig esopha -gogastrostomy surgery .

Objective:To investigate the influence of all-trans-retinoic acid (ATRA) on the proliferation and invasion of osteosarcoma 143B cells and its possible regulatory mechanism.Methods:Different concentrations of ATRA were used to treat human osteosarcoma 143B cells, and the optimal concentration and treatment time those affected cell proliferation were selected. The MTS method, Transwell migration and invasion experiments were used to detect the changes in the proliferation, migration and invasion of 143B cells after ATRA treatment. The real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot were used to detect the expression changes of miRNA-34a (miR-34a), E2F1 and Eag1 in osteosarcoma 143B cells after ATRA treatment. Then miR-34a was interfered and E2F1 was overexpressed, and the abilities of cell proliferation, invasion and migration abilities as well as the expression changes of miR-34a, E2F1 and Eag1 in 143B cells were detected.Results:The proliferation inhibition of 143B cells was most obvious when 143B cells were treated with 10 μmol/L ATRA for 72 h. The cell migration and invasion numbers when 143B cells were treated with 10 μmol/L ATRA for 72 h were lower than those in the negative control group [(73±3) cells vs. (182±5) cells, t = 21.46, P<0.01; (94±3) cells vs. (203±7) cells, t = 13.70, P<0.01]. 10 μmol/L ATRA could promote the expression of miR-34a in 143B cells and inhibit the expressions of Eag1 and E2F1 (all P<0.01). Compared with ATRA group, the ability of cell proliferation in ATRA+miR-34a interference group was restored after 72 h of treatment [cell survival rate (41.0±2.2)% vs. (25.0±3.6)%, t = 108.68, P<0.01]. Compared with ATRA group, the abilities of cell migration and invasion in ATRA+miR-34a interference group were restored [(122±14) cells vs. (64±10) cells, t = 21.06, P<0.01; (103±10) cells vs. (59±8) cells, t = 24.27, P<0.01), and the mRNA and protein expressions of Eag1 and E2F1 in cells were promoted (both P<0.01). Compared with ATRA group, the ability of cell proliferation in ATRA+E2F1 overexpression group was restored [cell survival rate (40.0±3.4)% vs. (24.0±3.1)%, t = 108.74, P<0.01]; the abilities of cell migration and invasion in ATRA+E2F1 overexpression group were restored [(78±12) cells vs. (29±8) cells, t = 13.52, P<0.01; (75±12) cells vs. (49±10) cells, t = 6.28, P<0.01], and the mRNA and protein expressions of Eag1 and E2F1 in cells were promoted (both P<0.01). Conclusion:ATRA inhibits the proliferation and invasion of osteosarcoma cells via regulating miR-34a-E2F1-Eag1 signaling pathway, and it may become one of the effective treatment drugs for osteosarcoma.

Objective To detect the effect and regulatory mechanism of human ether à go?go related gene 1 ( Herg 1) knockdown on the proliferation and invasion of osteosarcoma ( OS). Methods We constructed a recombinant adenovirus vector ( Ad5?Herg1?shRNA) expressing short hair RNA ( shRNA) against Herg1 and tested the knockdown efficiency. Then, the effects of Herg 1 knockdown on the proliferation, growth and invasion of osteosarcoma were measured by using cell counting kit?8 (CCK?8), wound healing assay, Transwell assay and xenograft model of nude mice, respectively. Tandem affinity purification, mass spectrometry and dual luciferase reporter assay were used to find out the molecules interacted with Herg1. Western blot was used to detect the expressions of large tumor suppressor gene (LATS1), p?LATS1, Yes?associated protein ( YAP ) and p?YAP in cells after infection of Ad5?Herg1?shRNA. Results Compared to Ad5?control?shRNA, Ad5?Herg1?shRNA dramatically inhibited the expression of Herg1 in OS cells. The result of CCK8 array demonstrated that 143B cell vitalities of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were ( 65.47 ± 3.90)% and ( 79.90 ± 1.52)%, significantly lower than (100.00±6.14)% of Ad5?control?shRNA group. Meanwhile, U2OS cell vitality of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were (69.69±1.36)% and (76.72±2.75)%, significantly lower than (100.00± 3.01)% of Ad5?control?shRNA group (all P＜0.001). The results of wound healing array showed that 143B cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were (33.03± 2.88)% and (36.47±4.16)%, significantly lower than (97.78±2.28)% of Ad5?control?shRNA group. Meanwhile, U2OS cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were ( 68.07 ± 0.90 )% and (73.97±1.25)%, significantly lower than (96.50± 1.12)% of Ad5?control?shRNA group ( all P＜0.001). The results of Transwell showed that 143B cell invasion numbers of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were 36.50±12.15 and 44.83±7.62, significantly lower than 195.33±19.68 of Ad5?control?shRNA group. Meanwhile, U2OS cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were 21.83±7.99 and 22.85±7.08, significantly lower than 83.33±12.36 of Ad5?control?shRNA group ( all P＜0.001). The results of xenograft model of OS showed that the tumor volume and weight of Ad5?Herg1?shRNA group were significantly smaller than of Ad5?control?shRNA group after 14 days and 5 weeks of inoculation, respectively (P＜0.001).Moreover, knockdown of Herg1 inhibited the metastasis of OS cells.In mechanism, Herg1 protein interacted with NF2 protein. Knockdown of Herg1 significantly suppressed the expression levels of LATS1 and YAP protein, and promoted the phosphorylation of LATS1 and YAP in OS cells ( all P＜0.001). Conclusion Our findings suggest that Herg1 participates in the proliferation and motility of OS cells and may serve as a potential therapeutic target for osteosarcoma patients.

Objective To detect the effect and regulatory mechanism of human ether à go?go related gene 1 ( Herg 1) knockdown on the proliferation and invasion of osteosarcoma ( OS). Methods We constructed a recombinant adenovirus vector ( Ad5?Herg1?shRNA) expressing short hair RNA ( shRNA) against Herg1 and tested the knockdown efficiency. Then, the effects of Herg 1 knockdown on the proliferation, growth and invasion of osteosarcoma were measured by using cell counting kit?8 (CCK?8), wound healing assay, Transwell assay and xenograft model of nude mice, respectively. Tandem affinity purification, mass spectrometry and dual luciferase reporter assay were used to find out the molecules interacted with Herg1. Western blot was used to detect the expressions of large tumor suppressor gene (LATS1), p?LATS1, Yes?associated protein ( YAP ) and p?YAP in cells after infection of Ad5?Herg1?shRNA. Results Compared to Ad5?control?shRNA, Ad5?Herg1?shRNA dramatically inhibited the expression of Herg1 in OS cells. The result of CCK8 array demonstrated that 143B cell vitalities of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were ( 65.47 ± 3.90)% and ( 79.90 ± 1.52)%, significantly lower than (100.00±6.14)% of Ad5?control?shRNA group. Meanwhile, U2OS cell vitality of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were (69.69±1.36)% and (76.72±2.75)%, significantly lower than (100.00± 3.01)% of Ad5?control?shRNA group (all P＜0.001). The results of wound healing array showed that 143B cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were (33.03± 2.88)% and (36.47±4.16)%, significantly lower than (97.78±2.28)% of Ad5?control?shRNA group. Meanwhile, U2OS cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were ( 68.07 ± 0.90 )% and (73.97±1.25)%, significantly lower than (96.50± 1.12)% of Ad5?control?shRNA group ( all P＜0.001). The results of Transwell showed that 143B cell invasion numbers of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were 36.50±12.15 and 44.83±7.62, significantly lower than 195.33±19.68 of Ad5?control?shRNA group. Meanwhile, U2OS cell migration rates of Ad5?Herg1?shRNA1 and Ad5?Herg1?shRNA2 group were 21.83±7.99 and 22.85±7.08, significantly lower than 83.33±12.36 of Ad5?control?shRNA group ( all P＜0.001). The results of xenograft model of OS showed that the tumor volume and weight of Ad5?Herg1?shRNA group were significantly smaller than of Ad5?control?shRNA group after 14 days and 5 weeks of inoculation, respectively (P＜0.001).Moreover, knockdown of Herg1 inhibited the metastasis of OS cells.In mechanism, Herg1 protein interacted with NF2 protein. Knockdown of Herg1 significantly suppressed the expression levels of LATS1 and YAP protein, and promoted the phosphorylation of LATS1 and YAP in OS cells ( all P＜0.001). Conclusion Our findings suggest that Herg1 participates in the proliferation and motility of OS cells and may serve as a potential therapeutic target for osteosarcoma patients.

Objective: To detect the effect and regulatory mechanism of human ether à go-go related gene 1 (Herg 1) knockdown on the proliferation and invasion of osteosarcoma (OS). Methods: We constructed a recombinant adenovirus vector (Ad5-Herg1-shRNA) expressing short hair RNA (shRNA) against Herg1 and tested the knockdown efficiency. Then, the effects of Herg 1 knockdown on the proliferation, growth and invasion of osteosarcoma were measured by using cell counting kit-8 (CCK-8), wound healing assay, Transwell assay and xenograft model of nude mice, respectively. Tandem affinity purification, mass spectrometry and dual luciferase reporter assay were used to find out the molecules interacted with Herg1. Western blot was used to detect the expressions of large tumor suppressor gene (LATS1), p-LATS1, Yes-associated protein (YAP) and p-YAP in cells after infection of Ad5-Herg1-shRNA. Results: Compared to Ad5-control-shRNA, Ad5-Herg1-shRNA dramatically inhibited the expression of Herg1 in OS cells. The result of CCK8 array demonstrated that 143B cell vitalities of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were (65.47±3.90)% and (79.90±1.52)%, significantly lower than (100.00±6.14)% of Ad5-control-shRNA group. Meanwhile, U2OS cell vitality of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were (69.69±1.36)% and (76.72±2.75)%, significantly lower than (100.00±3.01)% of Ad5-control-shRNA group (all P<0.001). The results of wound healing array showed that 143B cell migration rates of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were (33.03±2.88)% and (36.47±4.16)%, significantly lower than (97.78±2.28)% of Ad5-control-shRNA group. Meanwhile, U2OS cell migration rates of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were (68.07±0.90)% and (73.97±1.25)%, significantly lower than (96.50±1.12)% of Ad5-control-shRNA group (all P<0.001). The results of Transwell showed that 143B cell invasion numbers of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were 36.50±12.15 and 44.83±7.62, significantly lower than 195.33±19.68 of Ad5-control-shRNA group. Meanwhile, U2OS cell migration rates of Ad5-Herg1-shRNA1 and Ad5-Herg1-shRNA2 group were 21.83±7.99 and 22.85±7.08, significantly lower than 83.33±12.36 of Ad5-control-shRNA group (all P<0.001). The results of xenograft model of OS showed that the tumor volume and weight of Ad5-Herg1-shRNA group were significantly smaller than of Ad5-control-shRNA group after 14 days and 5 weeks of inoculation, respectively (P<0.001). Moreover, knockdown of Herg1 inhibited the metastasis of OS cells. In mechanism, Herg1 protein interacted with NF2 protein. Knockdown of Herg1 significantly suppressed the expression levels of LATS1 and YAP protein, and promoted the phosphorylation of LATS1 and YAP in OS cells (all P<0.001). Conclusion Our findings suggest that Herg1 participates in the proliferation and motility of OS cells and may serve as a potential therapeutic target for osteosarcoma patients.