18F-FDG PET/CT对非小细胞肺癌区域淋巴结诊断的假阴性与假阳性研究

目的探讨18^F-FDG PET／CT在检测非小细胞肺癌（NSCLC）区域淋巴结中出现假阴性和假阳性的因素。方法随机选择手术治疗的NSCLC患者48例，术前1周内行18^F—FDG PET／CT检查，同期行CT增强扫描，术后根据病理检查结果分析PET／CT诊断NSCLC区域淋巴结转移的假阴性与假阳性因素。结果48例患者共切除区域淋巴结313枚，转移淋巴结51枚，PET／CT结果7枚假阴性。8枚假阳性，阳性预测值和阴性预测值分别为85％，97％，高于CT（57％，94％；P=0．002，0．045）。3枚假阴性淋巴结内的癌灶较小；2枚淋巴结短径约为0．4mm，小于PET／CT的空间分辨率；2枚紧邻原发灶的淋巴结，图像无法区分而视为原发灶。8枚假阳性淋巴结为患者在原发病灶基础上并发不同程度的肺部疾病和淋巴结炎症，使其糖代谢率增高。结论假阳性出于（1）淋巴结的短径小于PET／CT的空间分辨率；（2）淋巴结内的小癌灶糖代谢率较低；（3）紧邻原发灶的淋巴结与原发灶无法区分。原发肿瘤合并肺部疾病是导致PET／CT出现假阳性的重要原因。     

左双腔支气管导管管端位置与吸气峰压变化的关系

目的 观测无隆突钩双腔支气管导管(DLT)管端位置与吸气峰压(Ppeak)以及肺顺应性环形状改变的关系，探讨用Ppeak和顺应性环的变化评估DLT管端位置的可行性。方法 拟行右侧剖胸手术的成年患者32例，静脉诱导后插入左Mallinckrodt DLT，吸入氧化亚氮和地氟醚维持麻醉。按纤维支气管镜(FOB)确认DLT管端位置和通气方式将观测过程分为四个阶段：第一阶段(S1)，管端位置正确的双肺通气；第二阶段(S2)，管端位置正确的左侧单肺通气；第三阶段(S3)，管端插入左下支气管(置管过深)的左侧单肺通气；第四阶段(S。)，管端处在左支气管开口(置管偏浅)的左侧单肺通气。每阶段均机械通气15min。结果 回归方程预计插管深度与FOB检查符合者占71．9％。S2时Ppeak值比S1时增加50．8％，肺顺应性(Cdyn)值减少36．2％；S3时Ppeak值比S1时增加87．4％，Cdyn值减少56．8％。PV环曲线斜率向右明显移位，环体显著延长。结论 用无隆突钩DLT行肺隔离，在无FOB定位的条件时，联合应用听诊法、回归方程预计插管深度、动态监测气道峰压和P-V环的变化综合评估，可提高DLT管端的正确到位率。单肺通气的气道峰压超过双肺通气时的1．65倍，且气道峰压超过25cm H2O．应高度怀疑DLT管端发生过深移位。     

放疗化疗联合治疗局部晚期非小细胞肺癌43例

目的 探讨以顺铂为主的化疗方案加放疗对局部晚期非小细胞肺癌的疗效。方法 86例局部晚期非小细胞肺癌患随机分为治疗组及对照组各43例，放疗方案以CAP、EP、MVP或MOP，每人至少化疗两个周期，化疗后10～14天放射治疗，放疗采用^60Co外照射。结果 治疗组有效率83．7％，中位生存期14．5个月，对照组有效率67．4％，中位生存期10个月，两组不良反应为骨髓抑制、胃肠道反应。结论 以顺铂为主的化疗方案加放疗治疗局部晚期非小细胞肺癌的疗效较高，可提高肿瘤的局部控制率和延长生存期。     

肺癌患者FLK-1、LRP和MDR1的表达与临床研究

目的:探讨血管内皮生长因子受体 (Flk 1),肺耐药蛋白 (LRP)基因以及多药耐药基因 (MDR1)蛋白与肺癌患者临床及病理指标的关系。方法:用免疫组化技术(ABC法)对原发性肺癌组织中三种基因的表达进行检测。结果: 70例肺癌中,非小细胞肺癌MDR1阳性率 49. 2% (29 /59),明显高于小细胞肺癌 (SCLC) 18. 2% (2 /11)(P<0. 05);非小细胞肺癌LRP阳性率 69. 5% (41 /59),明显高于小细胞肺癌 27. 3% (3 /11) (P<0. 05)。腺癌中MDR1与LRP的表达明显高于鳞癌(P<0. 05)。LRP与Flk 1在NSCLCs中共同表达 49. 2% (29 /59),LRP的表达与肺癌的组织学分级相关,MDR1和LRP的表达与肺癌的组织学类型有关,Flk 1与TNM分期相关,均有统计学意义(P<0. 05)。Flk 1 LRP均阳性、FLK 1 LRP MDR1均阳性、中药治疗、复发与患者的生存率有关(P<0. 05)。结论:FLK 1、LRP和MDR1基因蛋白产物的检测对肺癌患者的诊治和预后评估有积极意义。     

复方金荞麦颗粒治疗肺癌1000例临床疗效观察

目的 总结复方金荞麦颗粒治疗肺癌的疗效。方法 对1000例各种类型的肺癌患者采用复方金荞麦颗粒5g，3次·d^-1 口服，同时辅以中药汤剂治疗，3mo为1疗程，病情稳定后逐渐减量维持。结果本组1000例患者经3mo～15a以上治疗，基本治愈181例（18．1％），显效518例（51．8％），有效204例（20．4％），无效97例（9．7％），总有效率为90．3％。结论 复方金荞麦颗粒为抗肿瘤的纯中药制剂，具有明显抑制肿瘤细胞生长、增强免疫功能、提高患者生存质量等功效，尤其是对失去手术治疗机会、不能接受化疗和放疗的肺癌患者具有较好疗效。     

人工心肺机血液泵监测系统的研制

为避免人工心肺机血液泵转速失控现像的发生，特研制人工心肺机监测系统，通过对血泵转速的实时监测，判断系统是否正常，自动进行相应的处理，提高现有系统的安全性。     

Inhaled allergen-driven CD1c up-regulation and enhanced antigen uptake by activated human respiratory-tract dendritic cells in atopic asthma

Background Dendritic cells (DC) mediate inflammation in rodent models of allergic airway disease, but the role played by human respiratory‐tract DC (hRTDC) in atopic asthma remains poorly defined. Recent data suggest that CD1 antigen presentation by hRTDC may contribute to asthma pathogenesis. Objective To investigate the influence of hRTDC on the balance between atopy and allergic asthma in human subjects and to determine whether CD1 expression by hRTDC is modulated during asthmatic inflammation. Methods Sputum cells were induced from steroid‐naïve, allergen‐challenged and allergen‐naïve subjects (atopic asthmatics, atopic non‐asthmatics and non‐atopic controls). hRTDC were identified using monoclonal antibody labelling and analysis by flow cytometry. Results hRTDC stained HLA‐DR⁺ (negative for markers of other cell lineages) were predominantly myeloid and comprised ∼0.5% of viable sputum cells. Sputum cells were potent stimulators of allogeneic CD4⁺ naïve T cells and enrichment/depletion experiments correlated stimulatory potency with DC numbers. Sputum contained cells that exhibited typical dendritic morphology when analysed by electron microscopy. Myeloid hRTDC were endocytically active, but uptake of FITC‐dextran was enhanced in cells from asthmatics (P<0.001). Despite their increased endocytic capacity, asthmatic myeloid hRTDC appeared mature and expressed increased levels of maturation markers (P<0.05–P<0.001), CD1c, CD1d and langerin (P<0.05). CD1c expression by asthmatic myeloid hRTDC was enhanced upon in vivo allergen challenge (three to ninefold within 24 h; P<0.05). CD11c⁻CD123^high hRTDC were only detected in asthmatic sputum and were increased in number following allergen challenge. Conclusion Despite limited cell numbers, it proved possible to analyse human RTDC in induced sputum, providing evidence that increased antigen uptake and enhanced CD1 presentation by activated hRTDC may contribute to allergic airway disease. CD1 presentation by hRTDC in atopic asthma may therefore constitute a novel target for future intervention strategies.     

Closure of a large bronchial fistula with a latissimus dorsi myocutaneous flap

We describe a case of a large bronchial fistula and empyema after right upper lobectomy that was treated successfully with open window thoracostomy followed by a latissimus dorsi myocutaneous flap and limited thoracoplasty. A latissimus dorsi myocutaneous flap can provide immediate airtight closure of a large bronchial fistula, allowing lavage and curettage of the empyema cavity to reduce the chance of postoperative infection. An important aspect of this technique is that the deepithelialized skin side rather than muscle is sutured to an opening of the bronchus. As compared with other techniques, a latissimus dorsi myocutaneous flap is superior in that it requires a single incision and does not require an intraop-erative change of position. In addition, the technique causes little dysfunction of the chest and shoulder and preserves the vascular supply to ensure the viability of the flap even if it was divided in a previous operation.     

The Hemodynamic Mechanisms of Lung Injury and Systemic Inflammatory Response Following Brain Death in the Transplant Donor

Brain-dead donors are the major source of lungs for transplantation. Brain death is characterized by two hemodynamic phases. Initially, massive sympathetic discharge results in a hypertensive crisis. This is followed by neurogenic hypotension. Up-regulation of pro-inflammatory mediators occurs in all organs and lung injury develops; this can adversely affect graft function post-transplantation. The mechanisms of the systemic and lung inflammation are unknown. We hypothesized that the hemodynamic changes are responsible for these inflammatory phenomena. Brain death was induced by intra-cranial balloon inflation in rats. This resulted in hypertensive crisis, followed by hypotension. There was a significant increase in blood neutrophil CD11b/CD18 expression and pro-inflammatory cytokine levels in serum and bronchoalveolar lavage, compared with control animals. Rupture of the capillary-alveolar membrane was demonstrated by electron microscopy. Elimination of the hypertensive response by α-adrenergic antagonist pre-treatment prevented inflammatory lung injury, reduced the systemic inflammatory markers and preserved capillary-alveolar membrane integrity. Correction of the neurogenic hypotension with noradrenaline ameliorated the systemic inflammatory response and improved oxygenation. We conclude that the sympathetic discharge triggers systemic and lung inflammation, which can be further enhanced by neurogenic hypotension. Management of the brain-dead donor with early anti-inflammatory treatment and vasoconstrictors is warranted.