Objective To review and summarize the experiences of transcatheter closure of left ventricular-right atrium communication,and discuss the feasibility of interventional therapy for this kind of cardiac abnormalitis.Methods 22 patients who suffered from left ventricular-right atrium communication underwent transcatheter interventional therapy with ventricular septal defect(VSD) occluder.The operating procedures were performed as like as the transcatheter closure of VSD:established the pathway from femoral artery to femoral vein through left ventricle,VSD,right atrium (or from left ventricle to right atrial through the communication) and inferior vena cava,then inserted the polysheath from femoral vein,introduced by the pathway to left ventricle,and implanted VSD occluder through the polysheath to close the shunt.Results The operation succeeded in 21 patients.The cardiac murmur was disappeared in all patients,and there was no residual shunt or aortic regurgitation that conformed by postoperative ventriculography and echocardiography in follow up phase,and the tricuspid regurgitation was lessened than preoperative.The operation abort in 1 patient because of aortic regurgitation after implanting occluder.Conclusions Transcatheter closure of left ventricular-right atrium communication is feasible as the selected occluder is accordant,and atrioventricular block,aortic regurgitation and tricuspid regurgitation can be avoided.

Objective: To explore clinicopathological and ultrasound characteristics of extranodal extension in metastatic papillary thyroid carcinoma patients. Methods: 176 patients with papillary thyroid carcinoma who were diagnosed in Tianjin Medical University Cancer Institute and Hospital between March 2011 and March 2016 were identified and recruited in the study. Among the 176 patients, 59 patients were diagnosed with regional lymph nodes metastasis accompanied with extranodal extension (extranodal extension positive group), 117 patients were regional lymph nodes metastasis without extranodal extension (extranodal extension negative group). The clinicopathological and ultrasound characteristics between extranodal extension positive group and extranodal extension negative group were also discussed in this article. Results: 59 patients were diagnosed with regional lymph nodes metastasis accompanied with extranodal extension (extranodal extension positive group). Single lymph node region of extranodal extension was identified in 40 patients, while 19 patients were confirmed with more than 2 regions of extranodal extension. The most frequent extranodal extension were detected in region Ⅵ lymph nodes(32 cases), following by Ⅲ(25 cases), Ⅳ(16 cases), Ⅱ(11 cases). In the aspect of ultrasound characteristics, metastatic papillary thyroid carcinoma with extranodal extension showed a higher incidence of node matting[13.6%(8/59) vs 3.4%(4/117), P=0.022], micro-calcification[66.1%(39/59) vs 46.2%(54/117), P=0.016], cystic[28.8%(17/59) vs 12.8%(15/117), P=0.013], aspect ratio(L/S)<2[88.1%(52/59) vs 75.2%(88/117), P=0.032] and larger diameter(1.95±1.01 cm vs 1.63±0.94 cm, P=0.028). Logistic multivariate analysis demonstrated that node matting (P=0.025) and cystic (P=0.026) were independent risk factors for extranodal extension. Conclusion Node matting, micro-calcification, cystic, aspect(L/T)>2 and larger diameter were associated with extranodal extension in metastatic papillary thyroid carcinoma patients, especially node matting and cystic, which might help topre-operative ultrasound diagnosis of extranodal extension.

BACKGROUND: Small cell lung cancer (SCLC) with high c-Myc expression is prone to relapse and metastasis, leading to extremely low survival rate. Cyclin-dependent kinases 4 and 6 (CDK4/6) inhibitor Abemaciclib plays a key role in the treatment of tumors, but the effects and mechanisms on SCLC remain unclear. This study was to analyze the effect and molecular mechanism of Abemaciclib in inhibiting proliferation, migration and invasion of SCLC with high c-Myc expression, with a view to expanding a new direction for reducing the recurrence and metastasis. METHODS: Proteins interacting with CDK4/6 were predicted using the STRING database. The expressions of CDK4/6 and c-Myc in 31 cases of SCLC cancer tissues and paired adjacent normal tissues were analyzed by immunohistochemistry. The effects of Abemaciclib on the proliferation, invasion and migration of SCLC were detected by CCK-8, colony formation assay, Transwell and migration assay. Western blot was used to detect the expressions of CDK4/6 and related transcription factors. Flow cytometry was used to analyze the effects of Abemaciclib on the cell cycle and checkpoint of SCLC. RESULTS: The expression of CDK4/6 was associated with c-Myc by STRING protein interaction network. c-Myc can directly modalize achaete-scute complex homolog 1 (ASCL1), neuronal differentiation 1 (NEUROD1) and Yes-associated protein 1 (YAP1). Moreover, CDK4 and c-Myc regulate the expression of programmed cell death ligand 1 (PD-L1). Immunohistochemistry showed that the expressions of CDK4/6 and c-Myc in cancer tissues were higher than those in adjacent tissues(P<0.0001). CCK-8, colony formation assay, Transwell and migration assay verified that Abemaciclib could effectively inhibit the proliferation, invasion and migration of SBC-2 and H446OE(P<0.0001). Western blot analysis further showed that Abemaciclib not only inhibited CDK4 (P<0.05) and CDK6 (P<0.05), but also affected c-Myc (P<0.05), ASCL1 (P<0.05), NEUROD1 (P<0.05) and YAP1 (P<0.05), which are related to SCLC invasion and metastasis. Flow cytometry showed that Abemaciclib not only inhibited the cell cycle progression of SCLC cells (P<0.0001), but also significantly increased PD-L1 expression on SBC-2 (P<0.01) and H446OE (P<0.001). CONCLUSIONS Abemaciclib significantly inhibits the proliferation, invasion, migration and cell cycle progression of SCLC by inhibiting the expressions of CDK4/6, c-Myc, ASCL1, YAP1 and NEUROD1. Abemaciclib can also increase the expression of PD-L1 in SCLC.
Humans ; Small Cell Lung Carcinoma ; B7-H1 Antigen ; Sincalide ; Lung Neoplasms ; Neoplasm Recurrence, Local ; Transcription Factors ; Adaptor Proteins, Signal Transducing ; Cell Proliferation