Rates of reoperation and nonoperative intervention within 30 days of bariatric surgery

BackgroundComplications arising from laparoscopic Roux-en-Y gastric bypass (LRYGB) and laparoscopic sleeve gastrectomy (LSG) are not insignificant and can necessitate additional invasive interventions or reoperations.ObjectivesIn this study, we identify early complications that result in nonoperative and operative interventions after LSG and LRYGB, the timeframe within which to expect them, and factors that influence the likelihood of their occurrence.SettingMulti-institutional database from across North America.MethodsData for this study were obtained from Metabolic and Bariatric Accreditation and Quality Improvement Program participant use files for 2015 and 2016. Statistical analysis was performed using STATA 15. Univariate analysis using Χ² for categoric data and independent t test for continuous data was performed to determine between group differences. Multivariable logistic regression analysis was used to identify predictors of operative and nonoperative reinterventions.ResultsIn 2015 and 2016, 243,747 underwent LRYGB or LSG, of which 3013 (1.24%) required a second operative procedure and 1536 (0.63%) required an invasive but nonoperative intervention. Complications occurred in 5.48% of LRYGB patients and 2.28% of LSG patients, the most common of which was bleeding. LSG was associated with far fewer nonoperative and operative interventions (.85% versus 2.2%, respectively) than LRYGB (.67% versus 2.5%). Renal insufficiency, including dialysis dependency, was an important predictor of reoperations among bariatric surgery patients. This was also true of nonoperative interventions; however, history of pulmonary embolism, and use of therapeutic anticoagulation were marginally stronger predictors.ConclusionsIn a representative, multinational sample, operative and nonoperative interventions were half as likely among LSG patients compared with LRYGB; however, overall rates still remained low. These findings, in conjunction with new efficacy data demonstrating comparable long-term weight loss between LRYGB and LSG, provide further support for the safety, effectiveness, and cost efficiency of LSG.     

Cryo-thermal therapy inducing MI macrophage polarization created CXCL10 and IL-6-rich pro-inflammatory environment for CD4+ T cell-mediated anti-tumor immunity

Purpose: We previously developed a novel cryo-thermal therapy to treat malignant mammary carcinoma and melanoma in a mouse model; long-term survival and CD4⁺ T cell orchestrating anti-tumor immune memory response were achieved. Moreover, cryo-thermal-induced CD4⁺ T cell differentiation into Th1 and CD4⁺CTL sub-lineages, in which M1 macrophage polarization played a direct, important role. In particular, cryo-thermal therapy triggered M1 macrophage polarization with up-regulated expression of C–X–C motif ligand 10 (CXCL10) and Interleukin 6 (IL-6). But whether CXCL10 and IL-6 contribute to CD4⁺ T cell-mediated anti-tumor immunity remains unclear. In this study, the role of cryo-thermal-induced CXCL10 and IL-6 in anti-tumor immunity was determined.

Methods: The level of CXCL10 and IL-6 in spleen and serum was determined by RT-PCR and ELISA on day 14 after cryo-thermal therapy. Splenic dendritic cells (DCs) and macrophages were isolated from cryo-thermal-treated mice on day 5 and 14, and the level of CXCL10 and IL-6 in macrophages and DCs was determined by ELISA. The transwell migration assay was performed to study immune cell migration. In vivo neutralization of CXCL10 or IL-6 was performed to investigate the phenotypic changes of immune cells.

Results: Cryo-thermal therapy induced M1 macrophage polarization with up-regulation of CXCL10 and IL-6 expression in spleen. CXCL10 and IL-6 promoted DCs migration and maturation, and subsequently promoted CD4⁺ T cell migration and differentiation into Th1 and CD4⁺ CTL, moreover, reduced myeloid-derived suppressor cells (MDSCs) accumulation.

Conclusions: Cryo-thermal-induced CXCL10 and IL-6 created acute inflammatory environment to initiate a systemically cascading innate and adaptive anti-tumor immunity, which was more permissive for tumor eradication.     

黄芪汤加减治疗急性加重期慢性阻塞性肺疾病疗效研究

摘 要 目的:探讨黄芪汤加减治疗慢性阻塞性肺疾病急性加重期（AECOPD）的临床疗效。方法:采用随机数字表法将166例AECOPD患者随机分为常规组和观察组各83例。常规组采用常规西医方法治疗，观察组在常规组的基础上给予黄芪汤加减治疗。观察两组治疗前后第1秒用力呼气量（FEV1）、用力肺活量（FVC）、FEV1占FVC的百分比（FEV1/FVC％）、动脉血氧分压（PaO2）、动脉血二氧化碳分压（PaCO2）、肿瘤坏死因子 α（TNF α）、白细胞介素 1β（IL 1β）、白细胞介素 6（IL 6）水平。结果:两组治疗后FEV1、FEV1/FVC、PaO2水平与治疗前相比较均显著升高（P＜0.05），且观察组与同期常规组相比较均显著升高（P＜0.05）；两组治疗后PaCO2、TNF α、IL 1β、IL 6水平与治疗前相比较均显著降低（P＜0.05），且观察组与同期常规组相比较均显著降低（P＜0.05）。结论:黄芪汤加减治疗AECOPD可降低患者炎症反应水平，改善动脉血气和肺功能，提高治疗效果，值得临床应用。     

芪苈强心胶囊配合保元汤加减治疗慢性心力衰竭临床研究

目的:观察芪苈强心胶囊配合保元汤加减用于慢性心力衰竭的治疗效果。方法:选取收治的慢性心力衰竭患者104例作为研究对象,运用随机数字表法将其分为观察组(52例)和对照组(52例),两组患者均接受常规治疗,对照组采用保元汤治疗,观察组同时应用芪苈强心胶囊联合保元汤治疗。观察患者治疗前及治疗后6个月的6 min步行试验的步行距离(6MWD)及纽约心脏病学会心功能分级(NYHA)、血清学指标N末端B型利尿钠肽原(NT-proBNP)、半乳糖凝集素3(Galectin-3)及白介素6(IL-6)、超敏C反应蛋白(hs-CRP)、肿瘤坏死因子α(TNF-α)、心脏指数(CI)、左室射血分数(LVEF)、左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)、左室重量指数(LVMI)和室壁运动指数(WMI)、左室间隔厚度(IVST)变化情况。结果:治疗前后,两组患者比较心功能指标、Galectin-3、炎性因子指标、心室重构指标差异有统计学意义(P<0.05); 观察组与对照组患者相比,6 min步行距离、CI、LVEF、升高更为显著(P<0.05); 观察组患者NYHA分级、NT-proBNP、Galectin-3、IL-6、hs-CRP、TNF-α、LVEDD、LVESD、LVMI、WMI、IVST降低更为显著(P<0.05)。结论:芪苈强心胶囊辅助保元汤加减能够有效改善慢性心力衰竭患者心脏功能,有利于患者体内炎性因子及Galectin-3水平降低,抑制心室重构进展,患者心脏舒缩功能改善效果更佳。     

新生儿高胆红素血症的临床治疗分析

目的探讨布拉氏酵母菌散治疗对新生儿高胆红素血症的临床疗效。方法在2018年1月—2019年1月期间,将医院诊治的110例新生儿高胆红素血症患儿纳入研究对象,按照治疗方法的不同,将患儿分成两组,采用常规蓝光照射治疗的患儿定为对照组,55例,在蓝光治疗基础上增加布拉氏酵母菌散治疗的患儿定为观察组,55例,对比两组患儿治疗的临床效果。结果观察组和对照组治疗的有效率分别为98.18%和87.27%,有统计学意义(P<0.05);治疗后3 d和1周,两组患儿的胆红素水平明显下降,且观察组患儿下降更加明显,与对照组相比差异有统计学意义(P<0.05);观察组患儿黄疸消退时间为(5.12±1.21)d,对照组患儿黄疸消退时间为(7.21±1.22)d,有统计学意义(P<0.05);观察组不良反应发生率为5.45%,明显低于对照组的12.73%,有统计学意义(P<0.05)。结论对新生儿高胆红素血症患儿在常规蓝光治疗的基础上增加布拉氏酵母菌散进行治疗,可以显著提高临床治疗效果。     

穴位埋线治疗卒中后肩关节半脱位疗效及对血清TNF-α、IL-6的影响

目的观察穴位埋线治疗卒中后肩关节半脱位临床疗效及对血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)因子水平的影响,探讨抑制炎症反应的相关机制。方法将92例卒中后肩关节半脱位患者按1:1:1随机分3组,共剔除2例,最终每组30例。埋康组采用康复训练加穴位埋线;针康组采用康复训练加针刺治疗;康复组采用单纯康复治疗。分别于治疗前后采用Fugl-Meyer(FMA)上肢运动能力、视觉模拟评分(VAS)及血清TNF-α、IL-6炎性因子水平进行评价。结果治疗后3组患者Fugl-Meyer及VAS评分比较差异有统计学意义(P<0.05);血清TNF-α、IL-6炎性因子水平降低(P<0.05);3组中埋康组疗效最优;且3组治疗前后组内比较差异均有统计学意义(P<0.05)。结论穴位埋线能改善卒中肩关节半脱位患者上肢肩痛及运动功能,降低机体炎症性应激反应。     

CCR6通过上皮间质转化促进结直肠癌肝转移的机制研究

目的检测人趋化因子受体6(CCR6)、人趋化因子配体20(CCL20)、E-钙黏着蛋白和波形蛋白在结直肠癌及肝转移组织中的表达,探讨CCR6参与结直肠癌肝转移的可能机制。方法选取山西医科大学第一医院及山西省肿瘤医院2009至2017年资料齐全的62例原发性结直肠癌患者(结肠癌54例、直肠癌8例)手术切除存档蜡块,其中包含同期切除结直肠癌伴肝转移病灶的标本20例。采用免疫组织化学法检测结直肠癌及肝转移组织中CCR6、CCL20、E-钙黏着蛋白和波形蛋白的表达情况,分析CCR6、E-钙黏着蛋白和波形蛋白的表达与患者临床病理特征之间的关系,采用logistic多因素回归分析肝转移与患者临床病理特征及CCR6、E-钙黏着蛋白和波形蛋白表达的关系,采用Spearman相关分析CCR6与E-钙黏着蛋白和波形蛋白的相关性。结果CCR6在结直肠癌组织中的阳性表达率为66.1%(41/62);在伴有肝转移的结直肠癌组织中的阳性表达率为85.0%(17/20),在肝转移组织中的阳性表达率为70.0%(14/20)。CCL20在结直肠癌中的阳性表达率为83.9%(52/62);在伴有肝转移的结直肠癌组织中的阳性表达率为90.0%(18/20),在肝转移组织中的阳性表达率为90.0%(18/20)。E-钙黏着蛋白在结直肠癌中的阳性表达率为67.7%(42/62);在伴有肝转移的结直肠癌组织中的阳性表达率为50.0%(10/20),肝转移组织中的阳性表达率为65.0%(13/20)。波形蛋白在结直肠癌组织中阳性表达率为79.0%(49/62);在伴有肝转移的结直肠癌组织中的阳性表达率为85.0%(17/20),在肝转移组织中的阳性表达率为90.0%(18/20)。CCR6的表达与淋巴结转移(χ^2=11.142,P=0.001)、肝转移(χ^2=4.694,P=0.030)、TNM分期(χ^2=21.785,P<0.001)密切相关;E-钙黏着蛋白的表达与患者淋巴结转移(χ^2=4.694,P=0.030)、肝转移(χ^2=4.253,P=0.039)、TNM分期(χ^2=7.867,P=0.005)密切相关;波形蛋白的表达与患者淋巴结转移(χ^2=7.293,P=0.007)、TNM分期(χ^2=5.712,P=0.017)密切相关。CCR6、E-钙黏着蛋白、波形蛋白均与结直肠癌患者的性别、年龄、肿瘤部位、肿瘤大小及分化程度无关(均P>0.05)。logistic多因素回归分析发现,CCR6(OR=6.812,95%CI为1.206~38.474,P=0.030)、E-钙黏着蛋白(OR=0.256,95%CI为0.069~0.945,P=0.041)是结直肠癌患者肝转移的独立影响因素。Spearman相关分析显示,在20例晚期结直肠癌患者肝转移组织中,CCR6与E-钙黏着蛋白表达(r=0.454,P=0.044)、波形蛋白表达(r=0.509,P=0.022)相关。结论CCR6可能通过上皮间质转化机制促进结直肠癌的进展和肝转移。     

Experimental identification of cancer driver alterations in the era of pan‐cancer genomics

Rapidly accumulating data from large‐scale cancer genomics studies have been generating important information about genes and their somatic alterations underlying cell transformation, cancer onset and tumor progression. However, these events are usually defined by using computational techniques, whereas the understanding of their actual functional roles and impact typically warrants validation by experimental means. Critical information has been obtained from targeted genetic perturbation (gene knockout) studies conducted in animals, yet these investigations are cost‐prohibitive and time‐consuming. In addition, the 3R principles (replacement, reduction, refinement) have been set in place to reduce animal use burden and are increasingly observed in many areas of biomedical research. Consequently, the focus has shifted to new designs of innovative cell‐based experimental models of cell immortalization and transformation in which the critical cancer driver events can be introduced by mutagenic insult and studied functionally, at the level of critical phenotypic readouts. From these efforts, primary cell‐based selective barrier‐bypass models of cell immortalization have emerged as an attractive system that allows studies of the functional relevance of acquired mutations as well as their role as candidate cancer driver events. In this review, we provide an overview of various experimental systems linking carcinogen exposure‐driven cell transformation with the study of cancer driver events. We further describe the advantages and disadvantages of the currently available cell‐based models while outlining future directions for in vitro modeling and functional testing of cancer driver events.     

MOB1A regulates glucose deprivation-induced autophagy via IL6-STAT3 pathway in gallbladder carcinoma

MOB kinase activator 1A (MOB1A) plays an important role in many diseases and cancers. Here, we observed that MOB1A was substantially overexpressed in gallbladder carcinoma (GBC) tissues compared with nontumor tissues. The high expression of MOB1A was closely associated with poor survival in patients with GBC at advanced TNM stages. Furthermore, our study indicated that MOB1A promoted autophagy by activating the IL6/STAT3 signaling pathway and regulating the chemosensitivity to gemcitabine under glucose deprivation conditions both in vitro and in vivo. In conclusion, these findings suggested that MOB1A is critical for the development of GBC via the MOB1A-IL6/STAT3-autophagy axis.