食管癌细胞核AgNOR的定量研究

本文对３４例新近切除的食管癌组织和２２例术后随访病人（生存５年以上及半年内复发死亡各１１例）的标本进行ＡｇＮＯＲ染色，以正常食管上皮细胞作对照。结果食管癌细胞核ＡｇＮＯＲ均数显著高于正常食管上皮（Ｐ〈０．００１），３４例新近切除组织的ＡｇＮＯＲ均数随细胞分化等级的增加而增加。术后生存５年以上病人的ＡｇＮＯＲ均数显著低于术后半年内复发死亡者（Ｐ〈０．０１），提示ＡｇＮＯＲ均数与食管癌恶性程度和预后有     

食管癌化疗前后AgNORs颗粒变化与疗效的关系

本文对２２例食管鳞癌患者联合化疗前后活检或手术标本进行核仁形成区（ＡｇＮＯＲｓ）染色，比较同一患者化疗前后癌细胞ＡｇＮＯＲｓ颗粒数，分析颗粒数变化与临床化疗效果的关系。结果显示１２例化疗有效（ＣＲ＋ＰＲ）者ＡｇＮＯＲｓ颗粒数均明显减少（Ｐ＜０．００１），化疗无效（ＳＤ＋ＰＤ）者颗粒数都无明显变化（Ｐ＞０．０５）。提示同一患者化疗前后癌细胞ＡｇＮＯＲｓ颗粒数变化可做为评价疗效的一个病理学指标。     

乐胃煎逆转胃癌前病变AgNOR及细胞图像分析

目的研究乐胃煎逆转胃癌前病变不完全结肠型肠化和／或中度异型增生的疗效．方法胃镜病理证实为不完全结肠型肠化和／或中度异型增生４６例．治疗组３０例用乐胃煎，对照组１６例用德诺（Ｄｅ＿Ｎｏｌ）．治疗前后胃镜活检胃窦固定部位粘膜标本作ＡｇＮＯＲ染色及细胞图像分析．结果乐胃煎对不完全结肠型肠化及中度异型增生总有效率均高于Ｄｅ＿Ｎｏｌ，分别为７２％比２５％（Ｐ＜００５）和８９５％比４４４％（Ｐ＜００５）．乐胃煎治疗前后，ＡｇＮＯＲ计数分别为７３０±１１６和４８１±１５０（Ｐ＜００１），Ｄｅ＿Ｎｏｌ组为７７３±０９２和７０５±１０２（Ｐ＜００１）．两组治疗前后ＡｇＮＯＲ计数差值均数相比，统计学上也有显著性差异，分别为２５２±１５４和０６９±０４８（Ｐ＜００１）．乐胃煎组中２０例作细胞图像分析，治疗后各参数（长轴、短轴、核浆比、结构异型指数等）均有不同程度的降低，有显著性差异．结论乐胃煎确有较好地逆转胃癌前病变的功效．     

幽门螺杆菌阳性胃粘膜病变AgNOR和rasp21的表达

目的研究幽门螺杆菌阳性（Ｈｐ＋）不同胃粘膜病变的ＡｇＮＯＲ数量及ｒａｓｐ２１阳性表达率，探讨其生物学行为及Ｈｐ在此过程中可能的作用．方法经内窥镜病理检查证实胃粘膜病变（慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、异型增生、胃癌）共计２７８例．通过Ｈｐ检测（ＣＬＯｔｅｓｔ结合ＷａｒｔｈｉｎＳｔａｒｙ染色）证实其中１４６例阳性，１３２例阴性．分别对其粘膜标本作了ＡｇＮＯＲ定量及ｒａｓｐ２１表达的研究，比较不同胃粘膜病变中Ｈｐ阳性和阴性组间ＡｇＮＯＲ数目和ｒａｓｐ２１阳性表达率．结果除慢性浅表性胃炎外各病变中Ｈｐ＋组的ＡｇＮＯＲ数量均显著高于Ｈｐ－组（Ｐ＜００５或Ｐ＜００１）；除慢性浅表性胃炎及慢性萎缩性胃炎外各病变中Ｈｐ＋组的ｒａｓｐ２１阳性表达率均显著高于Ｈｐ－组（Ｐ＜００５）．结论Ｈｐ＋胃粘膜病变具有更多的肿瘤生物学行为，该菌可能刺激胃上皮细胞的过度增殖而启动恶性变．     

幽门螺杆菌清除前后胃粘膜增殖状态的变化

本研究以流式细胞技术对幽门螺杆菌（ＨＰ）阳性和阴性患者胃粘膜细胞周期进行对比分析，并通过银染技术对ＨＰ清除前后胃粘膜细胞核仁组成区嗜银蛋白（ＡｇＮＯＲｓ）的变化进行随访观察。结果表明，ＨＰ阳性胃粘膜Ｓ期细胞比率和增殖指数均显著高于ＨＰ阴性胃粘膜，ＡｇＮＯＲｓ数量与胃粘膜增殖指数呈显著正相关。经治疗ＨＰ转阴者其胃粘膜细胞ＡｇＮＯＲｓ数量显著下降（Ｐ＜０．０１），而ＨＰ仍为阳性者ＡｓＮＯＲｓ数量则无显著变化（Ｐ＞０．０５）。ＨＰ清除后胃粘膜炎症明显好转。结果提示ＨＰ感染的胃粘膜处于高增殖状态，ＨＰ感染可能通过刺激胃粘膜细胞的增殖加速，从而增加患胃癌的危险性。     

慢性肝病,肝细胞癌及其癌旁肝组织核仁组成区嗜银蛋白的研究

采用嗜银染色技术研究正常肝、慢性肝病、肝细胞癌及其癌旁肝组织核仁组成区嗜银蛋白（Ａｇ－ＮＯＲ）的变化。正常肝组织ＡｇＮＯＲ数低于慢性肝病和癌旁肝组织（Ｐ〈０．０５），后二者低于肝细胞癌ＡｇＮＯＲ数（Ｐ〈０．０１）。不同分化程度癌组织ＡｇＮＯＲ数无差异（Ｐ〉０．０５）。１年内死亡者与生存１年以上者癌组织ＡｇＮＯＲ计数无统计学差异。结果提示，ＡｇＮＯＲ计数有助于鉴别良恶性肝病，对肝癌预后的判断无意义。     

食管癌核基质抗体的免疫组化研究

目的研究食管癌核基质抗体的肿瘤特异性和组织学特异性．方法用人食管癌组织提取核基质抗原，制备核基质抗体，采用免疫组织化学方法对食管癌４１例（男２６例，女１５例，年龄５３岁±７２岁）、正常食管粘膜８例、食管粘膜异型增生１５例、肺鳞癌１０例、喉癌１０例、胃腺癌１０例以及大鼠食管癌５例进行免疫组化染色．结果食管癌核基质抗体在食管癌组织中表达有特异性（３２／４１，７８０％），与正常食管粘膜（１／８，１２５％）及胃腺癌（２／１０，２００％）有非常显著差异（Ｐ＜００１），与食管异常增生（７／１５，４６７％）、肺鳞癌（３／１０，３００％）、喉鳞癌（４／１０，４００％）差异明显（Ｐ＜００５），但与大鼠食管癌组织（２／５，４００％）差异不明显．食管癌核基质的表达，在不同分化程度的食管癌组织中无明显差异（Ｐ＞００５）；在淋巴结转移阳性组高于淋巴结转移阴性组（１７／１８，９４４％ｖｓ１５／２３，６５２％，Ｐ＜００５）．结论食管癌核基质抗体具有较好肿瘤和组织学特异性，对肿瘤转移有一定影响，可作为食管癌的一项新标记物．     

P53突变蛋白在胃癌及癌旁组织中的表达

应用ＡＢＣ免疫组化方法及核仁形成区银染色，对３８例手术切除的胃癌及癌旁胃粘膜组织冰冻切标本进行了Ｐ５３突变蛋白表达的检测及ＡｇＮＯＲ颗粒计数，结果：３８例胃癌标本中２４例Ｐ５３突变蛋白高表达，阳率为６３、２％；３８例癌旁胃粘膜中１０例Ｐ５３突变蛋白弱表达。伴有淋结转移的２３例胃癌标本，１８例Ｐ５３蛋白高表达。Ｐ５３表达阳性的胃癌组织，每核ＡｇＮＯＲ颗粒平均数较Ｐ５３表达阴性者明显增多，差异有显著性     

氨对大鼠胃上皮细胞凋亡和白介素1β-转化酶mRNA表达的影响

探讨幽门螺杆菌（Ｈｐ）感染诱发胃上皮细胞凋亡的机制。方法： ３０只Ｗｉｓｔａｒ大鼠随机分成实验组和正常对照组，实验组大鼠饮用氨水３个月，造成胃粘膜损伤模型。采用ＴＵＮＥＬ方法检测鼠胃上皮细胞凋亡情况；采用ＲＴ－ＰＣＲ方法检测胃粘膜白介素１β－转化酶（ＩＣＥ）ｍＲＮＡ的表达。结果：与正常对照组大鼠相比，实验组大鼠胃粘膜肉眼观察见充血、水肿，病理检查示炎症和轻度萎缩改变。实验组胃粘膜上皮细胞凋亡指数（６．９±１．３）显著高于对照组（１．２±０．５， Ｐ＜０．０１），实验组ＩＣＥ ｍＲＮＡ经ＲＴ－ＰＣＲ后的电泳条带用自动图象仪处理测得相对值为０．８３±０．２０，而正常对照组为０．４７±０．１０，差异有显著性（Ｐ＜０．０１）。结论：氨所致的胃粘膜损伤可能与其诱发ＩＣＥ ｍＲＮＡ表达，引起胃粘膜上皮细胞凋亡有关。     

AgNOR变化对地方性甲状腺肿的诊断学意义

对７０例地方性甲状腺肿病变化细胞核内ＡｇＮＯＲ进行研究。结果表明，乳头状增生结节滤泡上细胞核内ＡｇＮＯＲ颗粒均数分别与胚胎型、胎儿型、胶质潴留型结节和滤泡型结节的均数比较，均存在显著性差异（Ｐ〈０．０１）。因此，作者认为ＡｇＮＯＲ染色方法对地方性甲状腺肿各结节类型的区别和预后判断有重要意义。     

胃癌及其癌前病变中细胞凋亡与细胞增殖间关系的研究

目的　通过观察胃癌及其癌前病变中细胞凋亡与细胞增殖间的关系,探讨细胞凋亡在胃癌发生中的作用．方法　利用脱氧核糖核酸末端转移酶介导的ｄ ＵＴＰ 缺口末端标记（ＴＵＮＥＬ） 技术及增殖细胞核抗原（ ＰＣＮＡ） 免疫组织化学染色对１０ 例正常胃粘膜、１６ 例萎缩性胃炎、３６ 例肠化生、２０ 例异型增生和５３ 例胃癌中的凋亡细胞、增殖细胞进行原位观察和比较．结果　萎缩性胃炎、肠化生、异型增生中凋亡细胞指数（１１－９ ％ ;１４－７ ％ ,８－０ ％ ） 均显著高于正常胃粘膜和 胃癌（３－５ ％ ,５－８ ％ ,ｔ ＝ ２－０５８ ～７－９０１ ,Ｐ＜ ０－０１ ～Ｐ ＜ ０－０５） ;异型增生、胃癌与肠化生相比,凋亡细胞明显减少、增殖细胞明显增多（ Ｐ＜ ０－０５） ;胃癌细胞增殖指数（４７－５ ％ ） 显著高于异型增生（３０－１ ％ ,Ｐ＜ ０－０１） ． 胃癌前病变及胃癌组织中的凋亡细胞指数与 增 殖细 胞指 数 呈显 著相 关（ ｒ ＝ ０－９６６ , － ０－８９７ ,Ｐ＜ ０－０５） ．结论　胃粘膜癌变过程中不仅存在活跃的细胞增殖,而且存在细胞凋亡异常． 高增殖能力的细胞可能通过选择而占据优势,导致胃癌的发生． 细胞凋亡与细胞增殖平衡失调在胃癌发病中可能起重要作用     

胃安泰胶囊对胃癌前期病变大鼠胃黏膜细胞核仁组成区嗜银蛋白水平的影响

[目的]研究中药复方胃安泰胶囊对胃癌前病变（PLGC）大鼠胃黏膜细胞核仁组成区嗜银蛋白（Ag—NORs）水平的影响，并探讨其可能的防治PLGC作用机制。[方法]采用综合造模法建立PLGC大鼠模型。造模前，将大鼠随机分为正常组、预防组、造模组。预防组在造模的同时灌服胃安泰胶囊，最后和其他组进行比较。确认造模成功后大鼠随机分为正常组，预防组，胃安泰高、中、低剂量组，维酶素组和病理对照组，以胃安泰胶囊（不同剂量）分别对高、中、低剂量组大鼠进行灌胃，以维酶素片作为西药对照。实验结束后摘取胃，测定胃黏膜AgNORs颗粒的水平。[结果]经胃安泰胶囊治疗后，PLGC大鼠胃黏膜AgNORs颗粒数明显减少，疗效优于维霉素组（P〈0．01）；预防组大鼠胃黏膜AgNORs颗粒数明显少于病理对照组（P〈0．01）。[结论]胃安泰胶囊对胃癌前期病变有很好的预防和逆转作用。     

A case report of pleural involvement in primary macroglobulinemia

A case of primary macroglobulinemia with pleural and gastric involvement was presented. A 48-year-old female was admitted with productive cough. On physical examination neither lymphoadenopathy nor hepatosplenomegaly were found. In addition, no bleeding tendency nor disturbance of the visual acuity were detected. Her chest roentgenogram showed a moderate amount of pleural effusion in the left pleural cavity without infiltration in the lung fields and no evidence of swollen hilar or mediastinal lymphnodes. A monoclonal M-band of to IgM-kappa type was observed in her serum and the pleural effusion. The diffuse ulcerative lesion in the gastric mucosa was detected by gastrofiberscopy. The lymphoid cells taken from the pleural effusion and the gastric mucosa stained positively with fluorescein-conjugated antiserum to u or the kappa chain. Pleural effusion and gastric infiltration of lymphoid cells improved remarkably following ACOP therapy.     

A New Classification System for Early Carcinomas of the Esophagus

Abstract: Carcinomas of the esophagus have a higher degree of malignancy than gastric carcinomas. Likewise, the therapeutic response of esophageal cancer patients to radical surgery has been poor because a thoracotomy and/or laparotomy are required. Since the advent of the iodine staining technique for the detection of esophageal carcinoma, the diagnosis of small, thin lesions limited to the mucosa ha become endoscopically possible. Progress in diagnostic techniques has thus resulted in the detection of increasing numbers of early carcinomas. Recent advances in techniques for the endoscopic mucosectomy of early esophageal carcinomas have similarly contributed to an increasing trend towards early detection and endoscopic resection. As mucosectomy is indicated for the treatment of small, thin lesions without lymh node metastases, a new endoscopic classification system has become necessay, to insure improved diagnostic accuracy.     

Features of early gastric cancer and gastric adenoma by enhanced-magnification endoscopy

Background Changes to the mucosal surface of early gastric carcinomas and gastric adenomas as viewed by enhanced-magnification endoscopy with acetic acid have not been investigated thoroughly. Using this technology, we investigated the appearance of the gastric surface patterns of neoplastic and surrounding nonneoplastic mucosa. Methods Forty-seven consecutive patients with early gastric carcinomas or gastric adenomas underwent enhanced-magnification endoscopy following 1.5% acetic acid instillation. All biopsy specimens were taken from the area at which the enhanced-magnified endoscopic image was obtained. Results Surface patterns of gastric tumors and the surrounding mucosa were classified into five types: type I, small round pits of uniform size and shape; type II, slit-like pits; type III, gyrus and villous patterns; type IV, irregular arrangements and sizes of pattern types I, II and III; type V, destructive patterns of types I, II and III. The predominant pattern of the surrounding mucosa was type III, and most type III mucosa had characteristics of intestinal metaplasia. Although all elevated adenomas showed type II or type III surface patterns, both depressed adenomas showed type IV. Elevated carcinomas showed type III (42.9%) or type IV (57.1%) surface patterns, while depressed carcinomas showed type IV (70%) or type V (30%). Although differentiated tubular adenocarcinomas showed type III (10.3%), type IV (86.2%), or type V (3.5%) surface patterns, all of the signet-ring cell carcinomas and poorly differentiated tubular adenocarcinomas showed type V. Conclusions Enhanced-magnification endoscopy may be useful for identifying gastric tumors and determining the extent of horizontal spread, especially in tumors of the depressed type.     

Immunoperoxidase study of the secretory immunoglobulin system and lysozyme in normal and diseased gastric mucosa.

Using an immunoperoxidase technique the distribution of secretory component, IgA, and lysozyme has been investigated in normal, inflamed, dysplastic, and carcinomatous gastric mucosa. Apart from pyloric glands which contain lysozyme, normal gastric mucosa stains negatively for all three antigens. In gastric mucosa neck cells appear to adapt by synthesising secretory component and lysozyme and transporting IgA. Intense staining for the three antigens is seen in dysplastic gastric epithelium and in well-differentiated intestinal type carcinomas. With progressive de-differentiation the tumours lose the ability to synthesise secretory component and lysozyme. Carcinomas of the diffuse type stain positively for secretory component and lysozyme and individual cells appear to take up IgA even in the absence of surrounding IgA containing plasma cells. These functional properties are retained in lymph node metastases. It is suggested that secretory component synthesising malignant cells might take up circulating dimeric IgA and that this could be a reflection of an important physiological mechanism.     

癌相关成纤维细胞与食管鳞状细胞癌淋巴转移及淋巴管生成的相关性研究

目的探讨食管鳞状细胞癌中癌相关成纤维细胞浸润与淋巴转移及淋巴管生成的关系。方法本研究中收集53例手术切除并病理确诊的食管鳞状细胞癌新鲜组织,25例距癌灶>5 cm的正常食管黏膜新鲜组织,并统计患者性别、年龄、病理级别、浸润深度、淋巴结是否转移等临床病理资料,应用免疫组织化学染色法检测癌相关成纤维细胞标记蛋白α-SMA以及淋巴管内皮细胞标记蛋白D2-40。采用SPSS 21.0统计学软件对数据进行分析。结果食管鳞状细胞癌组织中癌相关成纤维细胞数量与微淋巴管密度均高于正常食管黏膜组织(P<0.05)。食管鳞状细胞癌组织中癌相关成纤维细胞数量与临床分期、浸润深度、肿瘤淋巴结转移密切相关(P<0.05),与性别、年龄无关。食管鳞状细胞癌组织中癌相关成纤维细胞数量与微淋巴管密度呈正相关(P<0.05)。结论癌相关成纤维细胞可能通过促进淋巴管生成参与食管鳞状细胞癌的浸润和转移,这可能为食管鳞状细胞癌的早期预防和靶向治疗提供新方向。     

Usefulness of contrast-enhanced EUS in the diagnosis of upper GI tract diseases.

BACKGROUND: We evaluated the usefulness of contrast-enhanced endoscopic ultrasonography (EUS) in the diagnosis of upper gastrointestinal (GI) tract diseases. METHODS: The subjects were 42 patients with upper GI tract diseases: 4 esophageal carcinomas, 30 gastric carcinomas, 5 gastric myogenic tumors, and 3 gastric ulcers. After the lesion was observed by EUS, air-filled albumin (0.22 mL/kg) was intravenously injected at a rate of 1 mL/sec into the right cubital median vein, and observation was continued for 10 minutes. RESULTS: Enhancement of the third and fifth layers was observed in all normal esophageal and gastric walls. No esophageal carcinomas were enhanced. Enhancement was observed in 5 gastric carcinomas that had abundant, enlarged, and winding vascular beds. In all esophageal and the other 25 gastric carcinomas, although the tumors per se were not enhanced, enhancement of the third and fifth layers around the lesions clearly demarcated the tumor boundaries. As a result, accuracy for detection of the depth of gastric carcinoma improved from 76.7% for EUS to 90% for contrast-enhanced EUS. All gastric myogenic tumors were enhanced, and irregularly shaped sonolucent areas within these tumors became clear, but we could not distinguish between leiomyoma and leiomyosarcoma. CONCLUSIONS: Contrast-enhanced EUS is a noninvasive, useful diagnostic method for assessment of the depth of invasion of esophageal and gastric carcinomas.     

Epidermal growth factor in the oesophagus.

Epidermal growth factor (EGF) has been implicated in mitogenesis and oncogenesis in the gastrointestinal tract. To determine the role of EGF in oesophageal disease, its quantity and distribution in the oesophageal mucosa of control subjects and patients with oesophageal disease were studied. Oesophageal biopsy specimens, taken 20-40 cm from the incisors in 72 patients, were graded histologically and adjacent specimens were taken for immunohistochemical analysis of the distribution of EGF. In patients with Barrett's columnar lined oesophagus, specimens were also taken from the gastric cardia for comparison. Twenty two biopsy specimens showed oesophagitis, 20 Barrett's mucosa, and 30 were histologically normal. EGF was found in the capillary endothelium of the normal oesophageal papillae and basal mucosa. Significantly more EGF positive papillae were found in the normal mucosa (81%) than in the inflamed mucosa (42%) (p < 0.001). The 20 patients with Barrett's mucosa showed abnormal expression of EGF in 25% of the isthmus and superficial epithelial cells. This study has shown that EGF is found only in the endothelial cells of the capillaries of the normal oesophageal mucosa and that the peptide is detectable significantly less frequently than normal in the inflamed oesophageal mucosa. EGF is also abnormally present, in large quantities, in the cytoplasm of the epithelial cells of Barrett's mucosa compared with gastric mucosa.