BackgroundWhen thyroid cancer invades the trachea, tumor resection and trachea reconstruction are required. Although the traditional way of anesthesia and tracheal intubation can maintain the necessary ventilation function during the operation, tracheal intubation affects the surgical field of vision and is not conducive to the protection of the recurrent laryngeal nerve beside the trachea during the operation.Case presentationExtracorporeal membrane oxygenation (ECMO) is used to replace traditional tracheal intubation in the process of resection and end-to-end anastomosis of tracheal tumors, and complete tracheal tumor resection and trachea reconstruction are achieved.ConclusionUsing ECMO for thyroid carcinoma resection, invaded trachea resection, and trachea reconstruction is safe and effective, which reduces the obstruction of endotracheal intubation on the operative field, guarantees the rapid and efficient end-to-end anastomosis in the upper trachea, and clearly avoids laryngeal recurrent nerve injury in the process of anastomosis.

Background Postoperative lung cancer patients belong to the high-risk group for venous thromboembolism (VTE). The standardized preventive measures for perioperative VTE in lung cancer are not perfect, especially for the prevention and treatment of catheter-related thrombosis (CRT) caused by carried central venous catheters (CVCs) in lung cancer surgery. Patients and methods This study included 460 patients with lung cancer undergoing video-assisted thoracic surgery (VATS) in our center from July 2020 to June 2021. Patients were randomized into two groups, and intraoperatively-placed CVCs would be carried to discharge. During hospitalization, the control group was treated with low-molecular-weight heparin (LMWH), and the experimental group with LMWH + intermittent pneumatic compression (IPC). Vascular ultrasound was performed at three time points which included before surgery, before discharge, and one month after discharge. The incidence of VTE between the two groups was studied by the Log-binomial regression model. Results CRT occurred in 71.7% of the experimental group and 79.7% of the control group. The multivariate regression showed that the risk of developing CRT in the experimental group was lower than in the control group (Adjusted RR = 0.889 [95%CI0.799–0.989], p = 0.031), with no heterogeneity in subgroups (P for Interaction > 0.05). Moreover, the fibrinogen of patients in the experimental group was lower than control group at follow-up ( P = 0.019). Conclusion IPC reduced the incidence of CRT during hospitalization in lung cancer patients after surgery. Trial registration No. ChiCTR2000034511.

Supplementary Tables S1-S2. Table S1. Baseline characteristics of the lung adenocarcinoma patients Table S2. Incidence of lung metastasis in nude mice subcutaneously injected ARHGEF5 knock-down (RNAi) or control (Par) A549 or H1650 cells.

目的 探讨分层递进式教学法在胸外科住院医师规范化培训 日常教学活动中的实施效果.方法 选取2021年11月至2022年6月在该院胸外科轮转的30名住院医师规范化培训(以下简称"住培")学员作为分层递进式教学组,另选取2020年11月至2021年6月接受传统培训的住培学员34名作为传统教学组.分层递进式教学组学员入科后明确不同阶段的培训 目标和要求,带教老师明确对不同阶段学员的教学方法,进行分层递进式教学.出科后对分层递进式教学组学员和老师进行满意度调查,并比较分层递进式教学组与传统教学组学员的理论和技能成绩.结果 分层递进式教学模式下,学员与带教老师满意度均达到100％;分层递进式教学组学员技能成绩和理论成绩均高于传统教学组,差异有统计学意义(P＜0.05).结论 分层递进在胸外科的临床实践教学中体现出明显的优越性,值得在临床教学中推广.

目的 探讨miR-451a通过调控PI3K/Akt通路对食管鳞状细胞癌顺铂(cisplatin,DDP)耐药的作用及其可能机制.方法 人正常食管鳞状上皮细胞系Het-1A、人食管鳞状细胞癌细胞系Eca109、人食管鳞状细胞癌顺铂耐药细胞系Eca109/DDP,采用实时荧光定量PCR法检测3种细胞miR-451a相对表达量,采用Western blot法检测3种细胞KIF2A蛋白相对表达量.对数生长期Eca109/DDP细胞分为空白对照组(不进行转染操作)、miR-NC组(转染miR-NC)、miR-451a模拟物组(转染miR-451a模拟物),采用实时荧光定量PCR法检测3组细胞miR-451a相对表达量,采用Western blot法检测3组细胞KIF2A蛋白相对表达量.采用荧光素酶报告实验检测miR-451a和KIF2A的靶向关系.对数生长期Eca109/DDP细胞再分为对照组(不进行转染操作)、miR-NC+ oe-NC组(转染miR-NC+ oe-NC)、miR-451a模拟物+oe-NC组(转染miR-451a模拟物+oe-NC)、miR-451a模拟物+oe-KIF2A组(转染miR-451a模拟物+ oe-KIF2A),4组细胞分别加入不同浓度DDP,采用CCK-8实验检测细胞活力及DDP对细胞的半数抑制浓度,确定DDP在后续实验中的浓度.采用实时荧光定量PCR法检测4组细胞miR-451a相对表达量,采用Western blot法检测4组细胞KIF2A、p-PI3K、PI3K、p-Akt、Akt蛋白相对表达量,比较p-PI3K/PI3K、p-Akt/Akt,采用EdU实验检测4组细胞增殖情况,采用流式细胞术检测4组细胞凋亡率.结果 Eca109/DDP细胞miR-451a相对表达量(0.32±0.06)低于Het-1A细胞(1.00±0.09)、Eca109细胞(0.62±0.07)(P＜0.05),KIF2A蛋白相对表达量(0.65±0.10)高于Het-1A细胞(0.21±0.05)、Eca109细胞(0.41±0.08) (P＜0.05);Eca109细胞miR-451a相对表达量低于Het-1A细胞(P＜0.05),KIF2A蛋白相对表达量高于Het-1A细胞(P＜0.05).miR-451a模拟物组细胞miR-451a相对表达量(2.47±0.13)高于miR-NC组(0.96±0.04)、空白对照组(1.00±0.03) (P＜0.05),KIF2A蛋白相对表达量(0.21±0.03)低于miR-NC组(0.74土0.06)、空白对照组(0.76土0.05)(P＜0.05);miR-NC组细胞miR-451a和KIF2A蛋白相对表达量与空白对照组比较差异均无统计学意义(P＞0.05).荧光素酶报告实验结果显示,miR-451a靶向调控KIF2A.DDP在后续实验中的浓度为90μmol/L.miR-451a模拟物+oe-NC组、miR-451a模拟物+oe-KIF2A组细胞miR-451a相对表达量高于miR-NC+ oe-NC组、对照组(P＜0.05),miR-451a模拟物+oe-NC组与miR-451a模拟物+oe-KIF2A组比较差异无统计学意义(P＞0.05);miR-451a模拟物+oe-NC组细胞KIF2A蛋白相对表达量低于对照组、miR-NC+ oe-NC组、miR-451a模拟物+oe-KIF2A组(P＜0.05),对照组、miR-NC+ oe-NC组低于miR-451a模拟物+oe-KIF2A组(P＜0.05).miR-451a模拟物+oe-NC组不同浓度DDP作用下的细胞活力、DDP对细胞的半数抑制浓度、EdU阳性细胞数、p-PI3K/PI3K、p-Akt/Akt均低于对照组、miR-NC+oe-NC组、miR-451a模拟物+oe-KIF2A组(P＜0.05),miR-451a模拟物+oe-KIF2A组均低于对照组、miR-NC+ oe-NC组(P＜0.05);miR-451a模拟物+oe-NC组细胞凋亡率高于对照组、miR-NC+ oe-NC组、miR-451a模拟物+oe-KIF2A组(P＜0.05),miR-451a模拟物+oe-KIF2A组高于对照组、miR-NC+oe-NC组(P＜0.05);以上指标对照组与miR-NC+oe-NC组比较差异均无统计学意义(P＞0.05).结论 miR-451a通过抑制KIF2A表达,从而抑制PI3K/Akt通路,增加食管鳞状细胞癌耐药细胞对DDP的敏感性,发挥抗肿瘤作用.

目的:探讨肺挫伤患者血清可溶性髓系细胞触发受体-1(sTREM-1)、白细胞介素-8(IL-8)的动态变化及其对患者预后的预测价值.方法:分别将肺挫伤、单纯肋骨骨折及健康体检者设为肺挫伤组(n=98)、肋骨骨折组(n=70)和对照组(n=68);比较三组对象第1天、第3天、第7天血清sTREM-1、IL-8水平及其在肺挫伤患者血清中的动态变化情况.肺挫伤组再依据病情分为轻度组(n=30)、中度组(n=45)和重度组(n=23);根据1个月后愈合情况分为预后良好组(n=80)和预后不良组(n=18),比较不同病情及不同预后肺挫伤患者第1天、第3天、第7天血清sTREM-1、IL-8水平,分析其对患者预后评估的价值.结果:肺挫伤组及肋骨骨折组患者不同时间点血清sTREM-1、IL-8水平均高于对照组(P＜0.05),且肺挫伤组高于肋骨骨折组(P＜0.05),第3天及第7天低于第1天,第7天低于第3天(P＜0.05);肺挫伤中度组及重度组不同时间点血清sTREM-1、IL-8水平高于轻度组(P＜0.05),且重度组高于中度组(P＜0.05),第3天及第7天低于第1天,第7天低于第3天(P＜0.05);预后不良组不同时间点血清sTREM-1、IL-8水平高于预后良好组(P＜0.05),且第3天及第7天低于第1天,第7天低于第3天(P＜0.05);血清sTREM-1、IL-8单独及联合评估肺挫伤预后的AUC分别为0.761、0.751、0.860(P＜0.05).结论:肺挫伤患者血清sTREM-1、IL-8明显上调,且水平越高,肺挫伤越重,预后越差,二者均可作为评估患者预后的重要指标之一.

目的 观察中晚期食管鳞癌患者血清肿瘤坏死因子受体相关蛋白1 (tumor necrosis factor receptor associated protein 1,TRAP1)水平、癌组织癌胚抗原(carcinoembryonic antigen,CEA)表达变化,探讨其与中晚期食管鳞癌患者化疗效果的相关性.方法 中晚期食管鳞癌患者147例,均行紫杉醇+顺铂方案化疗2个周期,化疗结束时行CT检查评估化疗疗效,完全缓解及部分缓解者为缓解组,稳定及进展者为未缓解组.比较2组年龄、性别、病程、发病部位、分化程度、临床分期;取2组化疗前内镜活检食管癌组织,采用免疫组织化学染色法评估癌组织CEA阳性表达情况;化疗前1d采用ELISA法检测2组血清TRAP1水平;多因素logistic回归分析中晚期食管鳞癌患者化疗后未缓解的影响因素;绘制ROC曲线,评估血清TRAP1、癌组织CEA阳性表达预测中晚期食管鳞癌患者化疗后未缓解的价值.结果 147例患者化疗未缓解率为56.46％(83/147).未缓解组血清TRAP1水平[(55.51土5.17)ng/L]及癌组织CEA阳性表达率(65.06％)均高于缓解组[(48.62±4.39)ng/L、46.88％](P＜0.05),年龄、性别、病程、发病部位、分化程度、临床分期与缓解组比较差异均无统计学意义(P＞0.05).多因素logistic回归分析结果显示,血清TRAP1(OR=1.357,95％CI:1.228～1.501,P＜0.001)、癌组织CEA阳性表达(OR=9.540,95 ％CI:4.245～21.441,P＜0.001)是中晚期食管鳞癌患者化疗后未缓解的影响因素.ROC曲线分析结果显示,血清TRAP1以52.60 ng/L为最佳截断值,预测中晚期食管鳞癌患者化疗后未缓解的AUC为0.712(95％CI:0.774～0.907,P＜0.001),灵敏度为75.0％,特异度为83.1％;CEA阳性表达预测中晚期食管鳞癌患者化疗后未缓解的AUC为0.591(95％CI:0.498～0.684,P=0.049),灵敏度为53.1％,特异度为65.1％.结论 中晚期食管鳞癌化疗未缓解患者血清TRAP1水平及癌组织CEA阳性表达率升高,血清TRAP1预测中晚期食管鳞癌患者化疗效果有一定价值.

住院医师规范化培训制度对培养合格临床医师至关重要.通过总结既往思政建设方面存在的问题,探索将"医学人文-思政教育"纳入医科大学附属教学医院胸外科专业基地住院医师规范化培训工作中,对于年轻规培医师的思想觉悟、道德水准和知识技能提升有很大的帮助.以"医学人文-思政教育"为特色的住院医师规范化培训教学改革是响应新时期住院医师规范化培训乃至医学人文教育改革的必经之路,将为培养符合人民需求的德才兼备的医师起到积极作用.

Objective . To investigate the clinical significance of the mRNA expression of RRM 1, TUBB 3, and ERCC 1 in non-small-cell lung cancer (NSCLC) tissues for the selection of adjuvant/postoperative chemotherapy regimens. Methods . Patients diagnosed with stage Ib-IIIa NSCLC were enrolled and randomly divided into a control group (undetected group) and an experimental group (detected group) after radical operation. The control group randomly received chemotherapy with gemcitabine plus cisplatin or paclitaxel plus cisplatin. The mRNA expression of RRM 1, TUBB 3, and ERCC 1 was detected in the experimental group before chemotherapy, and based on the detected expression, the chemotherapy regimen of cisplatin plus gemcitabine or cisplatin plus paclitaxel was chosen. The disease-free survival (DFS) of the control group and experimental group was compared. Results . Pathological type, stage, gene expression detection, and treatment method were not significantly correlated with DFS ( P > 0.05). In the subgroups treated with gemcitabine, the median DFS was 17 months in the detected group and 10.5 months in the undetected group (hazard ratio = 0.2147, 95% confidence interval: 0.07909–0.5827, P = 0.0025). Multivariate regression analysis was performed to analyse whether gene expression detection was independently correlated with DFS in the subgroups treated with gemcitabine ( P = 0.025). In the detected group, the prognosis of patients with low expression of RRM 1 was better than that of patients with high expression of RRM 1 after paclitaxel treatment ( P = 0.0039). Conclusions . The selection of chemotherapy regimen based on mRNA expression of the RRM 1, TUBB 3, and ERCC 1 genes may improve selection of candidate patients to receive clinical chemotherapy. However, large-scale prospective clinical studies are needed for in-depth investigation.

目的 对比经剑突肋缘下与经肋间胸腔镜手术治疗前纵隔肿瘤的临床效果.方法 回顾性分析陆军军医大学第一附属医院胸外科2017年12月至2020年1月收治的41例前纵隔肿瘤患者及重庆市中医院胸外科收治的4例前纵隔肿瘤患者的临床资料,根据手术方式不同分为经剑突肋缘下胸腔镜手术(SS-VATS组,26例)和经肋间胸腔镜手术(I-VATS组,19例),对比2组患者手术时间、术中出血量、术后住院时间、术后3个月疼痛评分、术后并发症的差异,SS-VATS组术后不留置胸管,仅记录I-VATS组术后置管时间、胸引液总量.结果 患者的手术时间及术中出血量组间比较,差异无统计学意义(P>0.05).SS-VATS组患者术后住院时间明显短于I-VATS组,差异有统计学意义(P<0.05).SS-VATS组术后3个月疼痛评分明显低于I-VATS组,差异有统计学意义(P<0.05).2组患者术后并发症发生率比较,差异无统计学意义(P>0.05).结论 经剑突肋缘下胸腔镜手术治疗前纵隔肿瘤术中有更充足的手术视野,术后远期疼痛明显较轻,住院时间明显缩短,与经肋间胸腔镜手术比较更具优势.

Multidrug resistance is a major obstacle to the effective treatment of esophageal carcinoma. It occurs more readily in hypoxia and acidosis microenvironment. TTLL6 is one of Tubulin tyrosine ligase-like family members. In this study, the effect of TTLL6 on the regulation of cisplatin (CDDP) sensitivity was evaluated in CDDP-resistant esophageal carcinoma (EC) cells both in vitro and in vivo. In hypoxia/acidosis condition, overexpression of TTLL6 in EC109/CDDP cells significantly lowered the IC50 of CDDP and increased the CDDP-induced apoptosis; while knockdown of TTLL6 expression in EC109/CDDP cells exhibited the opposite effects. Further study showed that, mechanistically, TTLL6 was inversely correlated with ERBB2 and TOPOIIA, and positively correlated with apoptosis-associated factor Caspase 9. Furthermore, animal model confirmed that TTLL6 negatively regulated the growth of xenograft tumor after chemotherapy. Alternated expression of TTLL6 also regulated the expression of ERBB2, TOPOIIA and Caspase 9 in EC109/CDDP cells in vivo. In conclusion, our results suggest that TTLL6 could reverse the drug resistant of EC109/CDDP cells, it might provide a potential treatment strategy for the clinical reversing the chemotherapy resistance.

Background How to maximally improve the drainage of intracranial and upper body venous and to reduce neurological complications during thoracic tumor‐causedsuperior vena cava replacement are still clinical problems to be solved. Methods We have innovatively used the bilateral jugular vein‐left femoral vein ECMO shunting to perform mediastinal tumor resection and superior vena cava replacement in a 50‐year‐old woman. Results During the operation, this technique maintained the patient's hemodynamic stability, improved the cerebral oxygen saturation and reduced the cerebral ischemia, hypoxia as well as the neurological complications. Conclusion It is indicated for patients with superior vena cava replacement who are unable to perform venous bypass (such as innominate vein to right atrial bypass) or venous shunting (such as differential pressure drainage from internal jugular vein to femoral vein).

Carina resection and reconstruction is required when a tracheal tumor invades the tracheal carina. It is a relatively complicated surgical procedure that requires complex reconstruction to maintain airway continuity. The technical difficulty lies in minimizing the influence of anesthetic endotracheal intubation and maintaining good ventilation function during surgery by establishing appropriate ventilation channels, which are contradictory in many cases. Therefore, in order to achieve the optimal surgical outcome, we performed intratracheal tumor resection and carina reconstruction with the help of extracorporeal membrane oxygenation.

Multidrug resistance (MDR) often leads to chemotherapy failure of lung cancer and has been linking to the cellular expression of several DNA transcription- and repair-related genes such as Trps1 and MGMT. However, their roles in the formation of MDR are largely unknown. In this study, overexpression/knockdown, luciferase assay and ChIP assay were performed to study the relationship between Trps1 and MGMT, as well as their roles in MDR formation. Our results demonstrated that Trps1 and MGMT expression both increased in drug-resistant lung cancer cell line (H446/CDDP). Silencing of Trps1 resulted in downregulation of MGMT expression and decrease in the multidrug sensitivity of H446/CDDP cells, while Trps1 overexpression exhibited the opposite effects in H446 cells. Ectopic expression of MGMT had no effect on Trps1 expression, but enhanced the IC50 values of H446 cells or rescued the IC50 values of Trps1-silenced H446/CDDP cells in treatment of multidrug. Our data further showed that, mechanistically, Trps1 acted as a transcription activator that directly induced MGMT transcription by binding to the MGMT promoter. Taken together, we consider that upregulation of Trps1 induces MGMT transcription contributing to the formation of MDR in lung cancer cells. Our findings proved potential targets for reversing MDR in clinical chemotherapy of lung cancer.

The underlying molecular mechanism of lung cancer drug resistance is poorly understood. The mediator of endoplasmic reticulum stress CHOP (DNA damage inducible transcript 3) promotes stress-induced apoptosis and appears to function as a transcription factor in multiple diseases. However, its potential contributions to multidrug resistance in solid tumors is unknown. Here, we investigated CHOP expression in tumor tissues form 69 lung cancer patients, finding that deficient CHOP expression is associated with poor prognosis. Cisplatin-resistant lung cancer cells exhibited lower expression of CHOP compared to that in sensitive lung cancer cells, and silencing or augmenting CHOP expression enhanced or impaired cisplatin resistance, respectively. Mechanistic investigations revealed that CHOP is directly associated with the regulation of autophagy or apoptosis-regulatory genes including LC3-II, death receptor 5 (DR5), and telomere repeat-binding factor 3. Notably, CHOP was identified as a target of miR-146a, and increased miR-146a expression in lung cancer cells was suggested to be responsible for CHOP mRNA down-regulation. Further, animal models confirmed that abnormally expressed miR-146a in lung cancer cells does not affect growth, but rather alters chemotherapy sensitivity. Together, CHOP is a useful prognostic marker and miR-146a is a potential therapeutic target for multidrug-resistant lung cancer.

BACKGROUND:Thoracic wall tumors can leave large defects in the thoracic wall after tumor resection. Currently, the shape of the materials commonly used for thoracic wall repair, including dacron mesh and titanium alloy mesh, cannot readily conform to the shapes of defect sites. In this study, we aimed to retrospectively review and evaluate the outcomes of applying three-dimensional (3D) printing technology in assisting in thoracic wall tumor resection and thoracic wall construction.METHODS:Six patients with thoracic wall tumors underwent thin-slice CT scanning. We 3D reconstructed pleural tumors and adjacent structures with Amira software and 3D printed them. Preoperative simulation, surgical rehearsal, and surgical planning were performed, and 3D conformal titanium plates were created based on 3D reconstruction models and sutured to the defect sites of the thoracic wall. We also retrospectively reviewed 10 patients who underwent this surgery with conventional methods. All of the demographic data, clinical data, and laboratory findings (non-normally distributed variables) were compared between these two groups.RESULTS:3D reconstructions of the tumors and their adjacent structures were successfully performed, and 3D printing physical models and conformal titanium plates were also successfully obtained. The plate afforded accurate matching, less bleeding, fewer postoperative complications, and less pain.CONCLUSIONS:This 3D printing technology can aid in preoperative rehearsal, surgical planning, and the manufacturing of 3D implants. The 3D titanium plate has such advantages over traditional implants as having good fit and hardness, improving the surgical accuracy and curative effect, and reducing complications, such as bleeding and pain.

Abstract We sought to elucidate the role of Rho guanine nucleotide exchange factor 5 (ARHGEF5) in tumorigenesis of lung adenocarcinoma cells. ARHGEF5 protein levels were assessed in 91 human lung adenocarcinoma specimens, and A549 and NCI-H1650 cells, by IHC and Western blotting. In addition, ARHGEF5 mRNA expression was evaluated by quantitative reverse transcriptase-PCR. Furthermore, ARHGEF5 long and short isoform coexpression was detected by immunofluorescence. Finally, flow cytometry; CCK8 and wound-healing assays; cell invasion, migration and adhesion; and xenografts were used to evaluate the biologic significance of ARHGEF5. ARHGEF5 was significantly increased in lung adenocarcinoma tissues and cell lines. Interestingly, ARHGEF5 levels were significantly associated with tumor grade and pathologic stage, but not age, gender, T stage, or lymph node metastasis status. ARHGEF5 knockdown by RNAi resulted in dramatically reduced proliferation, adhesion, invasion, and migratory capability of A549 and NCI-H1650 cells. Likewise, protein levels of p-Src, p-Akt, and NF-κB were significantly decreased after ARHGEF5 knockdown. In parallel, increased S-phase population and MMP-2/cyclin D1 expression were observed in the cancer cells, which were not apoptotic. In addition, ARHGEF5 knockdown A549 and NCI-H1650 cells injected s.c. and i.v. into nude mice exhibited decreased xenograft volume and overtly reduced metastasis. Conversely, ARHGEF5 overexpression in A549 and NCI-H1650 cells increased their tumorigenicity in vitro. ARHGEF5 acts as a proto-oncogene in human lung adenocarcinoma cell tumorigenesis. Mol Cancer Ther; 14(7); 1671–9. ©2015 AACR.