下咽癌是上消化呼吸道恶性程度最高的肿瘤之一.目前对于下咽癌的治疗,首选治疗方法是以手术治疗为主的综合治疗.基于肿瘤病灶的异质性,我们选择不同治疗策略.肿瘤原发灶的位置决定手术入路;病灶不同的临床特点,如小病灶大转移、浅表扩展癌、多点多灶癌等,其治疗策略具有差异性;手术切缘的范围一直是探讨和争论的热点.本文针对于以上问题,进行经验分享及相关文献总结.针对不同类型的下咽癌,为其制定最佳的个性化的治疗策略,以改善预后,提高生存率.

医学科技进步日新月异，对于具有敏锐创新思维的多学科交叉创新型人才的需要迫在眉睫。基于已广泛应用于临床的多学科诊疗模式，我们将多学科诊疗引入教学系统，构建了一个培养多学科交叉创新型人才的新的教学体系，从单一特定学科培养模式向多学科交叉综合培养模式转变，提高了学生自主创新能力及思维，增强了学生的团结协作精神及医学人文素养，为我国医疗事业储备高层次复合型人才。

Papillary thyroid carcinoma (PTC) is the most common type of thyroid malignancy, with growing incidence every year. microRNAs (miRs) are known to regulate the physiological and pathological processes of cancers, such as proliferation, migration, invasion, survival, and epithelial-mesenchymal transition (EMT). Herein, this study aimed to investigate the effect of miR-539 on cell proliferation, apoptosis, and EMT by targeting secretory leukocyte protease inhibitor (SLPI) via the transforming growth factor β1 (TGF-β1)/Smads signaling pathway in PTC. First, PTC-related differentially expressed genes and regulatory miR were screened using bioinformatics analysis, dual luciferase reporter gene assay, and ribonucleoprotein immunoprecipitation, which identified the SLPI gene and the regulatory miR-539 for this study. We identified SLPI as a highly expressed gene in PTC tissues, and SLPI was targeted and negatively regulated by miR-539. Then, we introduced a series of miR-539 mimics, miR-539 inhibitors, and small interfering RNA against SLPI plasmids into CGTHW-3 cells to examine the effects of miR-539 and SLPI on the expression of TGF-β1/Smads signaling pathway-, EMT-, and apoptosis-related factors, as well as cell proliferation, migration, invasion, and apoptosis. The obtained results indicated that CGTHW-3 cells treated with silenced SLPI or overexpressed miR-539 suppressed the cell proliferation, migration, invasion abilities, and resistance to apoptosis of PTC cells, corresponding to increased expression of Bcl-2-associated X protein, TGF-β1, Sekelsky mothers against dpp 4, and epithelial cadherin, and decreased B cell lymphoma 2, Vimentin, and N-cadherin. Altogether, we concluded that overexpressed miR-539 could inhibit the PTC cell proliferation and promote apoptosis and EMT by targeting SPLI via activation of the TGF-β1/Smads signaling pathway.

耳鼻咽喉头颈外科学专业性强，解剖生理、影像学、疾病发展及转归知识复杂，难以直观理解，在教学上存在一定难度。根据耳鼻咽喉头颈外科学教学特点，本研究建立耳鼻咽喉科“网络化图像教学资料库”，将各种疾病的发生、发展、转归的过程以高清内镜和影像学图像表现出来，同时结合术中手术视频资料及术后病理学资料增加学生的学习兴趣和对疾病的认知。将该网络化资料库应用于临床实践教学中，丰富教学内容、加强教学的实践性和应用性，有效提升教学质量。

Tumor associated macrophage (TAMs) is one of the most important immunosuppressive cells in tumor microenvironment,which produces a variety of molecules such as growth factors,cytokines,immune suppression medium and proteolytic enzymes to have significant influence on tumor development.In this review we will explore TAMs research progress in the head and neck malignant tumor immune microenvironment.

目的：探讨体外葡萄球菌肠毒素 A（SEA）联合热疗对人喉癌细胞株（Hep－2株）生长、增殖、凋亡等生物学行为的影响。方法应用四甲基偶氮唑蓝（MTT）比色法检测不同条件下对 Hep－2细胞的增殖抑制率，流式细胞仪检测 Hep－2细胞周期进程的变化及凋亡率，透射电子显微镜检测亚细胞结构改变。结果单纯热疗组、单纯 SEA 组及联合组（SEA＋热疗）对 Hep－2细胞增殖抑制率分别16．5％、25％和45．4％，与对照组相比差别有显著意义；流式细胞仪结果显示 G0／G1期细胞增多，S 期细胞减少，G2／M 期细胞相对增多，且细胞凋亡率升高，组间比较差异显著（ P＜0．05）。结论 SEA 联合热疗能显著提高 Hep－2细胞的增殖抑制率，抑制 G1期细胞向 S 期细胞转化进程，诱导 Hep－2细胞凋亡及亚细胞结构改变。

目的：探讨斑蝥酸钠维生素B6对人喉癌细胞株（ Hep-2细胞）增殖抑制率、凋亡率及其细胞周期进程的影响。方法应用四甲基偶氮唑蓝（ MTT）比色法检测斑蝥酸钠维生素B6对Hep-2细胞增殖抑制率、流式细胞仪定量检测经斑蝥酸钠维生素 B6作用后的 Hep-2细胞周期进程变化及凋亡率。结果不同浓度的斑蝥酸钠维生素B6注射液对Hep-2细胞增殖均有抑制作用，且呈剂量依赖性。流式细胞仪结果显示，G1期细胞增多，S期细胞减少，G2/M期细胞相对增多，Hep-2细胞凋亡率升高。结论斑蝥酸钠维生素B6对人喉癌Hep-2细胞生长、增殖有明显的抑制作用，抑制Hep-2细胞G1期向S期转化进程，从而使S期细胞减少，G2/M期细胞相对增多，诱导Hep-2细胞凋亡。

OBJECTIVE:To explore the inhibitive and apoptosis inductive effect of IL-24 genes on CD133(+) laryngeal cancer cells in Hep-2 line.METHODS:Human peripheral blood monocytes were isolated. The total RNA was extracted by using Trizol method and reverse transcripted into cDNA using RT-PCR method. Primers P1 and P2 was designed for the amplification of human IL-24 genes. After confirmation of agarose gel electrophoresis tests, TA was cloned into pMD19-T simple vector. Nhe I and Xho I double digesting human IL-24 and pIRES2-ZsGreen1 and eukaryotic expression vector were used to establish the pIRES2-ZsGreen1-hIL-24 vector, and detected by enzyme digestion and gene sequencing methods. Flow cytometry (FCM) was used to isolate CD133(+) cells from Hep-2 cells. CD133(+) cells were transfected with pIRES2-ZsGreen1-hIL-24 through liposome 2000. After detection, MTT and FCM were used to observe the effect of IL-24 gene on CD133(+) laryngeal cancer Hep-2 cells.RESULTS:Lipotin mediated transfection of recombinant pIRES2-ZsGreen1-hIL-24 plasmid into CD133(+) Hep-2 could expressed IL-24 gene in cells stably. MTT results showed that IL-24 transfected group was significantly suppressed compared to empty vector group and control group (P<0.05); FCM results showed that the apoptosis rate of experimental group increased significantly compared to empty vector group and control group (P<0.05).CONCLUSIONS:IL-24 gene expressions can inhibit proliferation of CD133(+) laryngeal cells in Hep-2 line and promote their apoptosis.

目前喉癌的手术治疗以喉部分切除术为主,约占60％～80％.虽然喉部分切除术保留了喉的发声功能,而对呼吸和吞咽功能的完整保留尚有一定的难度.从某种角度来说,顺利经口进食和拔除气管套管经鼻呼吸是两个呈反比的曲线,两者在很多情况下不可兼得.而喉功能保全一般是指喉的发声、呼吸(拔除气管套管)、吞咽(没有误吸)三者缺一不可,尤以喉癌术后喉狭窄而导致的拔管困难最为多见.临床上喉癌术后放置T型管、钛金属网支架等预防及治疗喉狭窄,但其可刺激肉芽形成,尤其是老年患者黏膜修复功能较差,更易形成瘢痕,降低拔管率.

喉狭窄,也称瘢痕性狭窄,系由各种原因引起喉部瘢痕组织形成,以致喉腔变窄,影响呼吸和发声功能;以声音嘶哑、喉喘鸣、咳嗽、呼吸困难为主要症状,严重者可发生紫绀或窒息[1].医源性创伤引起的瘢痕形成是最常见的导致喉狭窄的病变,切除导致喉狭窄的增生瘢痕是治疗该类疾病的常用手术方法.目前国内外多采取喉裂开瘢痕切除术及CO2激光手术[2,3],虽然均取得了相应的治疗效果,但术后老年患者生活质量不高、生存压力较大.应用低温等离子射频消融术治疗喉癌术后喉狭窄,可以最小的创伤达到最佳的治疗效果.