肺隔离症11例诊断及外科治疗体会

目的通过探讨肺隔离症的临床、影像学及手术特征,提高对肺隔离症的认识。方法对11例手术证实的肺隔离症患者的临床和肺部影像学表现及手术资料作一回顾性分析。结果临床上以反复肺部感染为特点。病变位于双下肺叶后和(或)内基底段。病变表现以囊性、实变,支气管扩张为主。手术中均见有来自体循环的异常供血,行肺叶切除术。结论对双下肺叶反复发作的肺部感染、咯血患者,应想到肺隔离症的可能,行强化胸部CT和动态扫描检查,进一步明确诊断。尽早手术切除,处理异常血管是手术的关键。     

CCR7、CXCR4在肺癌中的表达及意义

目的探讨CC族趋化因子受体7(CCR7)和CXC族趋化因子受体4(CXCR4)在肺癌组织中的表达及临床意义。方法采用免疫组织化学检测72例肺癌组织标本和30例良性肺疾病肺组织标本中CXCR4和CCR7的表达情况,并分析其不同临床病理特征中表达的差异。结果 CCR7和CXCR4在肺癌组织中的表达阳性率均明显高于正常肺组织,差异有统计学意义(P<0.01);CCR7和CXCR4表达与肺癌患者的TNM分期,纵膈淋巴结转移密切相关(P<0.01),与年龄、性别、病例组织学类型等均无关(P>0.05),并且Spearman相关分析显示,CXCR4表达与CCR7表达呈高度正相关(r=0.623,P<0.001)。结论 CXCR4和CCR7在肺癌纵膈淋巴转移中发挥重要作用。     

肺癌术后乳糜胸16例诊治体会

我院自1990年1月至2006年1月对3795例肺癌患者行肺组织切除术，其中16例并发乳糜胸，占同期手术的0．42％，采取保守治疗13例，手术治疗3例，效果满意，现报告如下。     

支气管切除术治疗慢性支气管内异物1例报告

患者男,42岁.因痰中带血3个月,于2007年1月27日入院.入院前3个月患者无明显诱因发现痰中带鲜血,无发热、盗汗、胸痛、胸闷.既往体健.查体:浅表淋巴结不大.     

VCHPM循环热灌注化疗治疗肺癌恶性胸腔积液的临床疗效观察

目的探讨体腔热灌注治疗机(visceral cavity hyperthermic perfusion machine,VCHPM)循环热灌注化疗治疗肺癌恶性胸腔积液的有效性。方法对确诊为肺癌伴恶性胸腔积液的病人80例随机分为治疗组和对照组。治疗组采用体腔热灌注治疗机(VCHPM)胸膜腔循环热灌注化疗治疗,对照组采用体腔热灌注治疗机(VCHPM)胸膜腔非循环的热灌注化疗治疗。随访地观察恶性胸腔积液的疗效。结果全组病人均完成治疗方案,治疗好转出院,无严重的并发症和治疗相关性死亡。治疗组胸腔积液的有效率为97.5%,对照组有效率为82.5%。治疗组有效率高于对照组(P<0.05)两组差异有统计学意义。结论体腔热灌注治疗机(VCHPM)循环热灌注化疗治疗肺癌恶性胸腔积液的方法是一种安全,有效的方法。     

RRM1在NSCLC患者外周血和组织中的表达及其与吉西他滨疗效相关分析

目的 探讨Ⅱ,Ⅲ和Ⅳ期非小细胞肺癌(NSCLC)患者外周血和肿瘤组织中RRM1(核糖核苷酸还原酶M1)mRNA表达水平的一致性及其与吉西他滨化疗疗效之间的关系.方法 收集49例接受吉西他滨化疗患者化疗前、化疗第1个疗程后、病情恶化或停止治疗前外周血及化疗前病理组织蜡块,应用荧光定量PCR法检测肿瘤组织及外周血中RRM1 mRNA表达水平,并分析其表达量水平和相关变化与吉西他滨化疗疗效之间关系.结果 RRM1 mRNA在病理组织和外周血中的表达水平无统计学差异(P=0.336),RRM1 mRNA在化疗前、化疗第1个疗程后、病情恶化或停止治疗前表达水平的差异无统计学意义(P=0.939;P=0.878).RRM1 mRNA低表达30例(61.2%),高表达19例(38.8%);RRM1 mRNA低表达组有效(CR+PR)为23例(76.7%);RRM1 高表达组有效(CR+PR)4例(21.1%),即RRM1 mRNA低表达组对吉西他滨化疗疗效高于高表达组(P<0.05).结论 RRM1 mRNA表达水平可用于以吉西他滨为化疗基础的NSCLC患者的疗效预测指标.     

外科治疗大气道阻塞16例临床分析

目的:探讨大气道阻塞患者的手术方法、手术径路及麻醉配合.方法:气管肿瘤采用袖式切除、晚期不能切除者采用肿瘤剔除人工气管内置及自体肋骨片移植修补术;对于局限在支气管的肿瘤单纯支气管切除成形、侵及隆突部肿瘤行隆突切除重建术.结果:全组手术均获成功,无严重并发症发生,患者存活均在1年以上.结论:该手术解除了呼吸梗阻症状,保留了健康的肺组织,提高了术后生活质量,且为晚期气管、支气管肿瘤的综合治疗提供了条件.     

胸腺瘤一例误诊为肺癌

[病例]男,62岁.因刺激性咳嗽2个月入院.2个月前无明显诱因出现咳嗽,症状较轻,以刺激性咳嗽为主.无发热及咳痰,无盗汗、乏力,无胸闷、胸痛、心慌及四肢无力,未予相应治疗.     

Targeting fibroblast activation protein inhibits endothelial-mesenchymal transition by affecting cancer-associated fibroblasts derived exosomes北大核心CSCD

Aim To investigate whether targeted inhibition of fibroblast activation protein (FAP) can inhibit the endothelial-to-mesenchymal transition (EndMT) of vascular endothelial cells by affecting exosomes (Exo) of cancer-associated fibroblasts (CAFs) and explore the underlying mechanisms. Methods Primary CAFs and peri-tumor fibroblasts (PTFs) were obtained from lung cancer and peri-cancer tissues, and CAFs-exo and PTFs-exo were collected from culture medium, respectively. Exosomes from CAFs treated with specific FAP inhibitor (3.3 nmol • L-1 SP13786) for 24 h were named as Anti-FAP-exo. HMEC-1 cells were incubated in equal volumes of RPMI 1640, PTFs-exo, CAFs-exo and anti-FAP-exo respectively and named as control group, PTF group, C AF group and anti-FAP group. The scratch assay, Transwell invasion assay and angiogenesis assay were used to detect the migration ability, invasion ability and angiogenesis ability of HMEC-1 cells. Immunofluorescence, immunohistochemistry and Western blot were used to detect EndMT-associated protein expression. Results The migration ability, invasion ability and angiogenesis ability of HMEC-1 cells of CAF group were significantly higher than those of PTF group, whereas there was no significant difference between that of anti-FAP group and PTF group. HMEC-1 cells of CAF group had higher expression of α-SMA, SM22α, p-Stat3 and Snail, and lower expression of CD31 and VE-cadherin than that of PTF group. In addition, HMEC-1 cells of Anti-FAP group had lower expression of α-SMA, SM22α, pStat3 and Snail, and higher expression of CD31 and VE-cadherin than that of CAF group. Conclusions Specific inhibition of FAP could indirectly inhibit the migration ability, invasion ability and angiogenesis ability of vascular endothelial cells via affecting CAFs-exo and Stat3-snail-EndMT pathway may be the potential mechanism. © 2023 Publication Centre of Anhui Medical University. All rights reserved.