胆道镜辅助Glission蒂横断法在腹腔镜左半肝切除治疗左肝内胆管结石的应用

目的：　探讨腹腔镜下胆道镜辅助Glisson蒂法解剖性左半肝切除治疗左肝内胆管结石的可行性。方法：　回顾性分析2016年12月至2020年2月中国人民解放军西部战区总医院全军普外中心采用腹腔镜下胆道镜辅助Glisson蒂法解剖性左半肝切除处置的10例左肝内胆管结石患者的临床资料。结果：　10例患者中男性4 例,女性6 例;年龄45~68 岁;10例患者均手术成功,手术时间245（200,320） min,术中出血300（200,650） mL,术中左肝蒂在胆道镜引导下采用一次性切割吻合器离断,离断位置良好,无一例出现保留侧胆管损伤,无一例出现大出血和胆漏;无一例出现中转开腹;术后不良事件轻微,1例患者出现轻微漏胆,1例出现少量胸腔积液,Clavien-Dindo并发症分级均为Ⅱ级,经保守治疗后痊愈;恢复流质饮食时间90~102 h,术后住院时间8~13 d,住院费用为（4.02±0.36）万元。结论：　腹腔镜下胆道镜辅助Glisson蒂法解剖性左半肝切除治疗左肝内胆管结石在器械、技术保障下是安全、可行的,且不会增加患者住院费用。     

初发Graves病患者外周血调节性T细胞及滤泡调节性T细胞检测的临床研究

目的：　检测Graves病（Graves'' disease,GD）患者外周血调节性T细胞（regulatory T cells,Tregs）、滤泡调节性T细胞（follicular regulatory T cells,Tfrs）、滤泡辅助性T细胞（follicular helper T cells,Tfhs）数量及其表面分子肿瘤坏死因子受体超家族成员4（tumor necrosis factor receptor superfamily member 4,OX40）、程序性死亡因子1（programmed-death 1,PD-1）的表达。方法：　纳入初发GD患者23例（GD组）和健康对照者22例（NC组）,通过流式细胞术检测2组外周血Tregs（CD3⁺CD4⁺CD25⁺Foxp3⁺）、Tfrs（CD4⁺Foxp3⁺PD-1⁺CXCR5⁺）及Tfhs（CD4⁺Foxp3^-PD-1⁺CXCR5⁺）细胞比例及其表面分子OX40、PD-1表达,分析GD发病与Tregs、Tfrs、Tfhs及其OX40、PD-1表达的关系,同时分析各检测指标与临床指标的相关性,初步探讨其临床意义。结果：　与NC组相比,GD组Tregs数量明显升高,Tregs上PD-1表达降低,Tregs上PD-1表达与TRAb水平呈显著负相关;初发GD患者Tfrs数量明显降低,且Tfrs上OX40表达上调,Tfrs数量与TRAb呈显著负相关。结论：　PD-1在Tregs上的低表达可能通过影响Tregs功能参与GD发病,GD患者体内Tfrs数量明显减少,且其OX40表达明显升高,OX40可能通过影响Tfrs与Tfhs稳态参与GD发病,这为临床上关于GD的治疗提供了新思路。     

二次电切在降低非肌层浸润性膀胱癌初次电切术后复发率中的临床价值

目的探讨经尿道膀胱肿瘤二次电切术（Re-TURBT）在降低T_a和T₁期非肌层浸润性膀胱癌（NMIBC）电切术后肿瘤复发率的临床价值。 方法回顾性分析2015年2月至2018年11月我院86例诊断为T_a和T₁期的NMIBC患者。患者接受单次经尿道膀胱肿瘤电切术为对照组（40例）,接受二次经尿道膀胱肿瘤切除术为观察组（46例）,两组患者首次电切术中均联合了吉西他滨即刻膀胱灌注化疗。统计观察组二次电切的阳性率及肿瘤分期分级变化情况,同时比较两组患者术后2年内的肿瘤复发及进展情况。 结果两组患者年龄、性别、吸烟史、肿瘤最大径、肿瘤个数、首次电切病理分期比较差异无统计学意义（P>0.05）。观察组二次电切术后的病理结果显示,11例（23.91%）检出残余癌,5例出现临床分期升级,4例病理分级升级。观察组术后2年总复发率低于对照组（P<0.05）。两组术后2年总进展率差异无统计学意义（P>0.05）。 结论Re-TURBT可明显降低T_a和T₁期NMIBC电切术后肿瘤复发率,同时可获得更准确的肿瘤分期,具有一定的临床价值。     

Overexpression of BCLXL in Osteoblasts Inhibits Osteoblast Apoptosis and Increases Bone Volume and Strength

The Bcl2 family proteins, Bcl2 and BclXL, suppress apoptosis by preventing the release of caspase activators from mitochondria through the inhibition of Bax subfamily proteins. We reported that BCL2 overexpression in osteoblasts using the 2.3 kb Col1a1 promoter increased osteoblast proliferation, failed to reduce osteoblast apoptosis, inhibited osteoblast maturation, and reduced the number of osteocyte processes, leading to massive osteocyte death. We generated BCLXL (BCL2L1) transgenic mice using the same promoter to investigate BCLXL functions in bone development and maintenance. Bone mineral density in the trabecular bone of femurs was increased, whereas that in the cortical bone was similar to that in wild‐type mice. Osteocyte process formation was unaffected and bone structures were similar to those in wild‐type mice. A micro‐CT analysis showed that trabecular bone volume in femurs and vertebrae and the cortical thickness of femurs were increased. A dynamic bone histomorphometric analysis revealed that the mineralizing surface was larger in trabecular bone, and the bone‐formation rate was increased in cortical bone. Serum osteocalcin but not TRAP5b was increased, BrdU‐positive osteoblastic cell numbers were increased, TUNEL‐positive osteoblastic cell numbers were reduced, and osteoblast marker gene expression was enhanced in BCLXL transgenic mice. The three‐point bending test indicated that femurs were stronger in BCLXL transgenic mice than in wild‐type mice. The frequency of TUNEL‐positive primary osteoblasts was lower in BCLXL transgenic mice than in wild‐type mice during cultivation, and osteoblast differentiation was enhanced but depended on cell density, indicating that enhanced differentiation was mainly owing to reduced apoptosis. Increased trabecular and cortical bone volumes were maintained during aging in male and female mice. These results indicate that BCLXL overexpression in osteoblasts increased the trabecular and cortical bone volumes with normal structures and maintained them majorly by preventing osteoblast apoptosis, implicating BCLXL as a therapeutic target of osteoporosis. © 2016 American Society for Bone and Mineral Research.