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目的　探讨小儿活动拉钩辅助单孔腹腔镜治疗鞘膜积液的临床疗效。方法　选取150例鞘膜积液患儿， 采用随机分组方法将其分为观察组和对照组各75例，观察组采用小儿活动拉钩辅助单孔腹腔镜治疗，对照组采用 硬膜外穿刺针常规腹腔镜治疗，由同一医师采取以上两种不同手术方式治疗；对比两组手术时间、术后皮下穿刺孔 并发症、术后复发等情况。结果　观察组术前诊断均为单侧，术中发现32例为双侧鞘状突未闭，予以同期处理。对 照组术前诊断均为单侧，术中发现30例为双侧鞘状突未闭，予以同期处理。患儿均顺利完成手术。观察组、对照组 双侧手术时间分别为（18. 91 ± 1. 94）、（19. 63 ± 2. 46）min，两组双侧手术时间比较差异无统计学意义（P>0. 05）；观 察组、对照组单侧手术时间分别为（10. 19 ± 1. 16）、（12. 09 ± 2. 13）min，两组单侧手术时间比较差异有统计学意义 （P<0. 05）。观察组无术后皮下穿刺孔并发症，对照组术后发生皮下穿刺孔并发症7例，两组比较差异有统计学意义 （P<0. 05）。观察组随访期间无复发，对照组2例复发，两组比较差异无统计学意义（P>0. 05）。结论　单孔腹腔镜 下使用小儿活动拉钩治疗鞘膜积液可达到常规腹腔镜治疗效果，且创伤小、术后无皮下穿刺孔并发症发生。 [ABSTRACT FROM AUTHOR]

口腔微生物可能通过炎症作用和化学致癌物质的直接代谢对癌症的发生发展起重要作用.卟啉单胞菌和具核梭杆菌是牙周炎的主要致病菌,二者参与了口腔鳞状细胞癌(OSCC)的发生发展,其可通过降低p53表达、诱导B7-H1表达、激活JAK1/AKT/STAT3信号通路、阻止P2X7嘌呤能受体与ATP结合,从而抑制细胞凋亡,增加患癌风险.致病菌的脂多糖激活宿主免疫系统,免疫细胞表达炎性细胞因子如IL-1β、IL-6、TNF-α等,IL-1β导致牙周局部炎症变化、IL-6刺激免疫抑制因子产生及激活JAK/STAT途径,促进细胞增殖和血管形成;诱导MMP-9表达、DNA损伤及激活致癌信号通路增强细胞的侵袭与转移,促进细胞增殖和血管形成,促进OSCC发生发展;致病菌可产生活性氧、活性氮和挥发性硫化合物等致癌物质,促进癌症发生发展. [ABSTRACT FROM AUTHOR]

目 的 探讨基于外周血淋巴细胞亚群及免疫球蛋自 水平建立 的 Fisher 判别模型对进展性脑梗死的诊断 价值。 方法 选择 120 例急 性脑梗死患者 ， 根据入院期间病程是否进行性加重 ，将患者分为非进展组(42 例 ） 、 进展 组 ( 78 例） 。 比较两组入院时外周血淋 巴 细胞亚群参数及免疫球蛋 自 水平，筛选出具有价值的参数指标， 并建立 Fisher 判别模型。 结果 进展组外周血 CD3 +%, CD4 +%, CD4 + % /CDS + ％ 及 lgA 水平均低于非进展组 ( P 均 < 0. 05 ) 。 CD3 +%, CD4+%, CD4 +% /CD8 + ％ 及 lgA 水平评估进展 性脑梗死价值 的 ROC 曲线下面积(AUC ) 分别为 0. 623 、0. 789 、0. 659 、0. 730 ， 尤登指数对应的最佳界值点分别为 62. 46% 、32. 93% 、1 . 40、2. 68 g/L。 Fisher 判别模型 为 凡顷嗖组 ＝ 0. 75Xl + O. 37X2 +6. 03X3 + 7. 46X4 - 50. 17, F进配且 ＝ 0. 71Xl + 0. 22X2 + 5. 75X3 + 6. 07X4 - 37. 03 （ 公 式 中 Xl 代表 CD3 + ％ 、X2 代表 CD4 +% 、 X3 代表 CD4 + %/CDS 飞仁X4 代表 lgA ) ， 该判别 函数模型诊断进展 性脑 梗死的灵敏度为 8 1 . 1 % 、特异度为 90. 5% 、准确率为 84. 5% 。 结论 成功建立了基于外周血淋巴细胞亚群及免疫 球蛋自水平建立 的 Fisher 判别模型，该模型对进展性脑梗死患者进行风险评估 ， 具有较高 的 鉴别 特异性及临 床实 用价值 。 [ABSTRACT FROM AUTHOR]

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To observe the expression of NIK-IKK binding protein (NIBP), CyclinE and CyclinD1 in the tissues of patients with colon cancer, and to explore its clinical significance. Methods We collected 130 cases of samples from surgical resection and enteroscope biopsy of digestive internal medicine, 65 cases of normal colon mucosa and 65 cases of cancer tissues in each group, all patients did not receive radiotherapy and chemotherapy. The expression of NIBP, CyclinE and CyclinD1 was detected by immunohistochemistry SP method, and then we analyzed the relationship between the positive expression of proteins and the clinicopathologic features in patients with colon cancer. The correlations between expression of NIBP, CyclinE and CyclinD1 were determined by Pearson or Spearman tests. Results The positive expression rates of NIBP in the normal colonic mucosa and colon cancer tissues were 18.46% (12 /65) and 60.00% (39 /65), respectively; the positive expression rates of CyclinD1 were 3.08% (2 /65) and 56.92% (37 /65), respectively; and the positive expression rates of CyclinE were 43.08% (28 /65) and 89.23% (58 /65), respectively. Significant differences were found in the positive expression rates of NIBP, CyclinE and CyclinD1 between these two groups (all P <0.05). The expression of NIBP, CyclinE and CyclinD1 was significantly related with the depth of tumor invasion, TNM staging, lymph node metastasis and distant metastasis in patients with colon cancer (all P <0.05). In the colon cancer tissues,the expression of NIBP was positively correlated with CyclinE and CyclinD1 expression (r =0.43,0.32, all P <0.05), and the expression of CyclinD1 and CyclinE was positively correlated (r =0.23,P <0.05). Conclusion NIBP, CyclinE and CyclinD1 is highly expressed in the human colon cancer tissues, and they may participate in the occurrence and development of colon cancer tissues. [ABSTRACT FROM AUTHOR]

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)