CT导向经皮肺肿瘤射频消融术的监护

目的探讨CT导向经皮穿刺肺肿瘤射频消融术的监护.方法对37例肺癌患者行CT导向经皮穿刺肺肿瘤多极针射频消融过程监护.结果本组病人手术顺利,均获手术成功.结论本手术是一种微创安全有效的治疗手段,在有计划的监护下有助于病人更好配合手术治疗,及早发现并发症及处理.     

CT导向经皮肺肿瘤射频消融术的监护

目的　探讨CT导向经皮穿刺肺肿瘤射频消融术的监护 .方法　对 37例肺癌患者行CT导向经皮穿刺肺肿瘤多极针射频消融过程监护 .结果　本组病人手术顺利 ,均获手术成功 .结论　本手术是一种微创安全有效的治疗手段 ,在有计划的监护下有助于病人更好配合手术治疗 ,及早发现并发症及处理     

一种智能化的多极射频消融治疗仪的研制

介绍了一种基于射频原位灭活原理的智能化的多极射频消融治疗仪的研制.仪器为上、下位机结构,上位机为PC机,下位机以89C52单片机为核心的测温控温装置,上、下位机通过RS232串行口通信实现数据传送.仪器有两种功率控制模式:手动控制和自动控制,自动控制采用改进PID控温算法,确保对肿瘤病灶进行均匀、平稳的射频加热.智能化的病历数据库管理系统实现对病历数据的有效管理.动物实验证明,仪器工作稳定可靠,疗效好,具有较高的临床应用价值.     

人工胸水辅助超声引导下射频消融治疗肝肿瘤的初步研究

目的探讨人工胸水辅助下冷循环射频消融治疗位于膈面肝脏肿瘤的可行性与安全性。方法2005年1月至7月在南京大学医学院附属鼓楼医院接受射频消融治疗方法的9例患者，均为男性，平均年龄53．2岁（25～83岁）；Chdd—Pugh分级均为A级，肿瘤位于肝Ⅳ段1例，肝Ⅶ段6例，肝Ⅷ段2例。采用人工胸水的方法，以显露肿瘤全貌，然后进行超声引导下冷循环射频消融治疗。结果人工胸水后，射频消融治疗均顺利完成，没有发生与手术相关的死亡。手术后8例患者存活，1例患者死亡。结论人工胸水辅助超声引导下射频消融是治疗肝脏肿瘤的．一种安全方法，有助于拓展射频消融治疗的适应证。     

术中超声在冷循环射频治疗肿瘤中的应用

目的 探讨术中超声(10US)在冷循环射频治疗肿瘤中的临床应用价值。方法 48例肝癌患者，5例胰体尾癌患者。将术中探头直接置于脏器表面，首先观察肿瘤的部位、大小、数量和周围血管的毗邻关系，取活检后在超声引导下将射频电极针穿刺入肿瘤内部，多点分次进行治疗。结果 53例患者全部在超声引导下完成治疗。5例患者经术中超声检查发现新病灶。术中观察到治疗后肿瘤颜色变暗，瘤体变瘪凹陷，声像图上肿瘤呈高回声改变。术后随访2—12个月，46例存活。结论 开腹下应用术中超声引导冷循环射频治疗，定位准确，安全性高，可多点多次对肿瘤进行射频灭活，坏死区域大。并且术中超声能够弥补术前影像学的不足，发现术前漏诊的病灶而使患者及时得到治疗。     

射频热毁损治疗肝脏恶性肿瘤

射频热毁损 (radiofrequency therm al ablation,RFA)是国内外近几年来开展的一项治疗肝脏恶性肿瘤的新技术 ,具有快速毁损肝脏肿瘤而且安全性高、并发症少、患者易接受、可重复治疗等诸多优点 ,具有良好的应用前景 〔1～ 4〕。1　射频治疗仪和射频热毁损原理射频 (RF)是一种频率在 30 HHz- 30 0 MHz的高频电磁波 ,电流高度集中 ,随高频发生离子振荡而产生 90～ 12 0℃的高温。射频治疗仪主要由射频发射器、针式治疗电极、弥散电极板及 B超监视系统等部分组成〔1 ,2〕。目前使用的主流机型为 RF2 0 0 0 TM型治疗仪 ,其发射器频率为 46…     

射频治疗鼻衄疗效的临床与病理96例报告

作者采用射频技术治疗96例鼻衄，治疗有效率达94.7％，治疗痊愈率达84.3％．文章对鼻衄的发病率、鼻衄的部位、儿童鼻衄的年龄特征、分析了射频治疗的机理与治疗效果并推荐射频治疗为鼻衄治疗的一种安全有效方法．     

血清甲胎蛋白对多电极射频治疗肝癌近期疗效的监测

血清甲胎蛋白(AFP)检测在肝细胞癌诊断及判断疗效中具有十分重要的意义.我院自1999年6月至2000年3月首先采用由意大利科学家Rossi发明的多电极射频治疗肝癌,并对其中31例AFP阳性者以AFP值监测多极射频治疗肝癌近期疗效,现将初步结果报道如下.     

留置针在肝癌射频消融术围手术期中的运用价值

肝癌是一种恶性程度高，严重威胁人类健康的肿瘤性疾病。手术一直是传统的首选治疗方案。然而，多数病人发现该病后均属中、晚期，无手术指征，仅有10％～20％的患者可以接受以手术为主的综合治疗。近年来，随着微创外科技术的发展，肝癌的治疗方式也发生了较大的改变，射频消融是近几年兴起的一种新的肿瘤局部间质消融方法，其机理是在超声、     

经皮多极射频消融治疗老年肝脏恶性肿瘤的临床观察

目的：探讨经皮多极射频消融治疗老年肝脏恶性肿瘤的临床价值。方法42例老年MHC患者行PRFA治疗，观察近期有效率，并发症和1、2、3年生存率。结果近期有效率为90.48%，消融术后1、2、3年生存率分别为92.85%、78.57%、45.23%，所有患者术后均无严重并发症发生。结论 PRFA治疗老年MHC安全、高效、微创、可重复性强，值得进一步研究和推广。     

Segmentation and visualization of nasopharyngeal carcinoma using MRI

In this study, a semi-automatic system was developed for nasopharyngeal carcinoma (NPC) tumor segmentation, volume measurement and visualization using magnetic resonance imaging (MRI). Some novel algorithms for tumor segmentation from MRI and inter-slice interpolation were integrated in this medical diagnosis system. This system was applied to 10 MR image data sets of NPC patients and satisfactory results were achieved. This system can be used as a clinical image analysis tool for doctors or radiologists to obtain tumor location from MRI, tumor volume estimation, and 3D information.     

The plasminogen activator inhibitor "paradox" in cancer

Proteolysis in general and specifically the plasminogen activating system regulated by urokinase (uPA) its specific receptor, the GPI membrane anchored urokinase receptor (uPAR) and the specific plasminogen activator inhibitor 1 (PAI-1) plays a major role in tumorigenesis, tumor progression, tumor invasion and metastasis formation. This is exemplified by a body of published work showing a positive correlation between the expression of uPA or uPAR in several tumors and their malignancy. It is generally assumed that such a "pro-malignant" effect of the uPA-uPAR system is mediated by increased local proteolysis thus favoring tumor invasion, by a pro-angiogenic effect of this system and also by uPA-uPAR signaling towards the tumor thereby shifting the tumor phenotype to a more "malignant" one. However, when tumor patients are analyzed for long term survival, those with high levels of the inhibitor of the system, PAI-1 have a much worse prognosis than those with lower PAI-1 levels. This indicates that increased overall proteolysis alone cannot be made responsible for the adverse effects of the plasminogen activating system in tumors. Moreover, it becomes increasingly evident that components of the fibrinolytic system secreted by the tumor cells themselves are not solely responsible for a correlation between the plasminogen activating system and tumor malignancy; components of the plasminogen activating system secreted by stroma cells or cells of the immune system such as macrophages contribute also to the impact of fibrinolysis on malignancy. This review summarizes the evidence for the role of plasminogen activator inhibitor-1 in mediating the malignant phenotype and possible mechanism thereby trying to explain the "PAI-1 paradox in cancer" on a molecular level.     

Host–tumor interactions during the regression of a rat histiocytoma, AK-5

Summary: An efficient immune response comprises a highly intricate, integrated circuitry involving both the cellular and the humoral arms of the immune system of the host interacting with the rapidly proliferating microcosm of the tumor. The mechanism of tumor rejection involving multiple arms of the immune system was reviewed in a spontaneously regressing rat histiocytoma, AK-5, an autologous tumor–host system. Intraperitoneal tumor transplantation leads to death in all animals, whereas subcutaneously (s.c.) transplanted tumor undergoes regression in 70% of animals. Regression of the tumor occurs by both apoptosis and necrosis, and natural killer (NK) cells were identified as the chief effectors mediating tumor cell death in vivo . A type 1 helper T cell (Th1)-driven cytokine cascade played a crucial role in enhancing cellular functions at the tumor site and obtaining a sufficient immune response for tumor rejection. The s.c. tumor-bearing hosts were shown to produce a factor which induced apoptosis in tumor cells, mediating tumor rejection. This review emphasizes the daunting complexities and interesting liaisons between the host immune system and the tumor, highlighting the work from our laboratory, and stressing that it is the interaction of several factors in concert or antagonizing each other that is responsible for the spontaneous regression of a tumor.     

肿瘤免疫编辑研究进展

在肿瘤发生发展的过程中,机体免疫系统与肿瘤细胞相互作用,相互编辑.免疫系统的监视作用可清除肿瘤或抑制肿瘤的发生发展,同时免疫系统又可对肿瘤细胞进行重塑,使肿瘤发生免疫逃逸.而肿瘤可诱发机体抗肿瘤的固有及获得性免疫应答,同时也可改变免疫系统的抗肿瘤效应.了解肿瘤免疫编辑的相关研究进展可以为肿瘤防治提供参考.     

肿瘤免疫编辑研究进展

在肿瘤发生发展的过程中,机体免疫系统与肿瘤细胞相互作用,相互编辑。免疫系统的监视作用可清除肿瘤或抑制肿瘤的发生发展,同时免疫系统又可对肿瘤细胞进行重塑,使肿瘤发生免疫逃逸。而肿瘤可诱发机体抗肿瘤的固有及获得性免疫应答,同时也可改变免疫系统的抗肿瘤效应。了解肿瘤免疫编辑的相关研究进展可以为肿瘤防治提供参考。     

Tumor budding in colorectal carcinoma: An institutional interobserver reliability and prognostic study of colorectal adenocarcinoma cases

BackgroundColorectal carcinomas are one of the most commonly diagnosed malignancies. There are many prognostic factors relating to clinical course and disease progression, including tumor stage, metastasis, and tumor budding. In 2016, the International Tumor Budding Consensus Conference (ITBCC) created a system to uniformly assess tumor budding. This system includes a 3-tier system for the grading of tumor budding. In the past, there lacked uniform consensus, however the general grading practice was based on a 2-tiered system. Given that tumor budding is considered to have prognostic value, the accuracy and reproducibility of its assessment is vital. Our study aims to look at interobserver agreement in the scoring of tumor budding.DesignA total of 233 cases of colorectal carcinoma diagnosed in our health system were retrospectively analyzed and routine H&E stained slides of these cases were collected. A representative slide for tumor budding was selected per case. Four investigators with different levels of experience and expertise evaluated the selected slide of each case for tumor budding. Scoring was based on the ITBCC protocol. Clinico-pathological data was collected for each case and analyzed with tumor budding scores. Tumor budding scores per individual investigator and consensus tumor budding score were compared to patient and tumor characteristics including patient survival, tumor grade, tumor stage, and lymph node status.ResultsInter-observer agreement was calculated using Gwet's Agreement Coefficient (AC₁) and associated 95% confidence intervals was used to compare the ratings made by 4 pathologists. Overall, there was variation among pathologists in tumor budding score (Gwet's agreement coefficient = 0.25 and 0.326 for 3-tier and 2-tier grading system, respectively). Results show higher reliability with the 2-tier system compared to the 3-tier system. Tumor stage was significantly associated with budding score for all individual investigators and the consensus value (p value < 0.001).ConclusionThere is low inter-observer agreement in the assessment of tumor budding in colorectal carcinoma. This suggests that it is difficult to uniformly grade tumor budding and that our classification system needs improvement. We found that the older 2-tier system (Hase et al.) results in slightly higher inter-observer agreement than the recently proposed 3-tier grading system (ITBCC, 2016), though both systems lead to suboptimal agreement. Worth noting is that observers with subspecialty GI training and more work experience had higher inter-observer agreement. Our results showed that subspecialty training tends to increase agreement more than overall work experience. In addition, our exploratory results showed that there is an association of tumor budding score to tumor stage. While increasing refinement in classification, the 3-tiered system resulted in decreased agreement in tumor budding assessment. Clearly, there is more work to be done in the identification and quantification of tumor buds.     

肿瘤免疫编辑研究进展

在肿瘤发生发展的过程中,机体免疫系统与肿瘤细胞相互作用,相互编辑.免疫系统的监视作用可清除肿瘤或抑制肿瘤的发生发展,同时免疫系统又可对肿瘤细胞进行重塑,使肿瘤发生免疫逃逸.而肿瘤可诱发机体抗肿瘤的固有及获得性免疫应答,同时也可改变免疫系统的抗肿瘤效应.了解肿瘤免疫编辑的相关研究进展可以为肿瘤防治提供参考.     

肿瘤免疫编辑研究进展

在肿瘤发生发展的过程中,机体免疫系统与肿瘤细胞相互作用,相互编辑.免疫系统的监视作用可清除肿瘤或抑制肿瘤的发生发展,同时免疫系统又可对肿瘤细胞进行重塑,使肿瘤发生免疫逃逸.而肿瘤可诱发机体抗肿瘤的固有及获得性免疫应答,同时也可改变免疫系统的抗肿瘤效应.了解肿瘤免疫编辑的相关研究进展可以为肿瘤防治提供参考.     

肿瘤免疫编辑研究进展

在肿瘤发生发展的过程中,机体免疫系统与肿瘤细胞相互作用,相互编辑.免疫系统的监视作用可清除肿瘤或抑制肿瘤的发生发展,同时免疫系统又可对肿瘤细胞进行重塑,使肿瘤发生免疫逃逸.而肿瘤可诱发机体抗肿瘤的固有及获得性免疫应答,同时也可改变免疫系统的抗肿瘤效应.了解肿瘤免疫编辑的相关研究进展可以为肿瘤防治提供参考.     

肿瘤免疫编辑研究进展

在肿瘤发生发展的过程中,机体免疫系统与肿瘤细胞相互作用,相互编辑.免疫系统的监视作用可清除肿瘤或抑制肿瘤的发生发展,同时免疫系统又可对肿瘤细胞进行重塑,使肿瘤发生免疫逃逸.而肿瘤可诱发机体抗肿瘤的固有及获得性免疫应答,同时也可改变免疫系统的抗肿瘤效应.了解肿瘤免疫编辑的相关研究进展可以为肿瘤防治提供参考.