OBJECTIVE:To investigate the clinicopathological characteristics and the diagnosis of multilocular cystic renal cell carcinoma (MCRCC).METHODS:The clinicopathological data of 19 MCRCC cases were collected and immunohistochemical staining assays were carried out. Forty-six cases of other cystic kidney lesions within the same period were collected as controls, including extensively cystic clear cell RCC (12 cases), clear cell tubulopapillary renal cell carcinoma (6 cases), tubulocystic carcinoma (2 cases), simple cortical cysts (22 cases), multilocular cystic nephroma (1 cases) and multicystic kidney (3 cases).RESULTS:The patients included 14 males and 5 females. The ages ranged from 31 to 66 years (median age = 50 years). Most of the MCRCC cases were detected incidentally in physical examination, occasionally accompanied with hematuria, back pain or other symptoms. The follow-up period of 17 patients ranged from 6 to 170 months. All patients were alive without evidence of tumor recurrence or metastasis. Pathological findings showed that macroscopically, tumor size ranges from 1.5 to 7.0 cm in the maximum diameter, generally a entirely of various sized. The cysts contain serous, hemorrhagic or turbid fluid. Solid areas or substantially discernible mural nodules were absent; histologicallly, single layer of cuboidal and flattened epithelial tumor cells were lined in the cysts, described as clear cytoplasm, small nuclear, no nucleoli and low Fuhrman nuclear grade (I or II). Multilayer tumor cells could be observed in a few cysts, with granular cytoplasm and small intracystic papillae formed. The clear tumor cell clusters, similar as cystic lined tumor cells, were seen within pathological fibrous in almost all cases, and significant myofibroblastic proliferation was found in 14 cases. Immunohistochemically, the cysts lined epithelial cells and the clear tumor cell clusters were positive for epithelium markers, including CKpan(19/19), EMA(16/19) and CK7 (15/19); higher percentage of CAIX (17/19) and PAX8(15/19) than control groups, but lower percentage of CD10 (7/19), RCC (6/19) and AMACR(2/19); and all were negative for 34βE12, CD117 and CD68.CONCLUSIONS:Multilocular cysts, clear cells clusters of low Fuhrman grade within fibrous septa and capillary vessel proliferation under epithelium are important features of MCRCC. The united using of CAIX, CK7, CD10 and RCC is helpful for differentiating variable cystic renal tumor. MCRCC usually has an excellent prognosis, nephron sparing surgery is first recommended as a therapeutic strategy.

病人 男,26岁.胸痛,胸部CT扫描发现前上纵隔内巨大占位性病变(图1).2005年9月经胸骨正中切口行开胸手术.术中见前上纵隔肿块约10 cm×10 cm×10 cm大小,包膜不完整.右侧第2肋间胸骨旁肿物向外生长至皮下.手术完整切除肿瘤.

Objective To investigate the pathological changes of gastric antrum mucosa after Helicobacter pylori eradication.Methods Total 180 cases who suffered from epigastralgia and took the endoscopic examination were randomly divided into two groups,one was Hp eradication group which included 98 cases and given anti-Hp medication treatment,and the other was control group which included 82 cases and given an expectant treatment.At the end of the study,they took reexamination by gastroscope and tests on Hp by Giemsa dyeing rapid urase detection and on gastric antrum pathological changes by HE dyeing.Results In treatment group,atrophic gastritis as well as intestinal metaplasia decreased significantly after Helicobacter pylori eradication,but in control group,no change of atrophic gastritis was found while intestinal metaplasia aggravated.Conclusion The eradication of Helicobacter pylori is able to decrease atrophic gastritis and intestinal metaplasia.

<正>病人,男,85岁,住院号;327027。因“发现腹部包块2个月”入院,病人2个月前出现腹胀,进食后加重,无明显反酸、暖气、时伴有胸闷憋气,近期症状加重,偶有疼痛并乏力,病程中无发热、黄疸无恶心、呕吐,外院CT检查示:提示中上腹腔巨大占位性病变,性质待定。腹腔巨大包块与肝左叶有关,未经治疗收入我院。入院查体,皮肤巩膜无黄染,浅表淋巴结无肿大,上中腹部明显球形突起,未见肠型及蠕动波,扪及20 cm×l5 cm大小包块,上达剑突,下平脐,表面光滑,

目的:观察长期摄入大量葡萄糖通过抑制11β羟化固醇脱氢酶2型导致大鼠血压升高致肾脏滋养动脉损伤的病理学改变.方法:40只雄性Wister大鼠随机分为四组;对照组(10只),其它三组(各10只)分别给予葡萄糖15.0g/kg*d,25.0g/kg*d,35.0g/kg*d(分别为葡萄糖1组、葡萄糖2组和葡萄糖3组)共3个月.分别于1月、2月和3月末测尾动脉血压,3月末对大鼠肾脏滋养动脉行光镜观察摄片.结果:与对照组比较,长期摄入大量葡萄糖大鼠动脉血压水平升高(P＜0.01);肾脏滋养动脉出现平滑肌痉挛,平滑肌增生,血管壁增厚,血管腔变窄.结论:长期摄入大量葡萄糖可能通过抑制11β羟化固醇脱氢酶2型参与了高血压的发病过程.

目的:验证长期摄入高糖对大鼠血管11β2型羟化固醇脱氢酶及血压的影响并探讨其机制.方法:40只雄性Wistar大鼠随机分为4组:对照组(10只),其它3组(各10只)分别给予葡萄糖15.0g/(kg@d)(高糖1组),25.0g/(kg@d)(高糖2组)和35.0g/(kg@d)(高糖3组)共3个月.分别于1个月、2个月和3个月末测尾动脉血压,肠系膜动脉对去甲肾上腺素的加压反应,肠系膜血管网离体灌注液中皮质醇及醛固酮的含量,以及通过逆转录聚合酶链反应(RT-PCR)观察主动脉11β2型羟化固醇脱氢酶及醛固酮合酶信使核糖核酸(mRNA)表达的变化.结果:与对照组比较①长期摄入高糖大鼠动脉血压1个月时已经升高,3个月末仍升高(P＜0.01);②长期摄入高糖大鼠离体肠系膜动脉对去甲肾上腺素反应的最高灌注压升高(P＜0.01);③长期摄入高糖大鼠离体肠系膜血管网分泌醛固酮减少,分泌皮质醇增多(P＜0.01);④长期摄入高糖大鼠主动脉11β2型羟化固醇脱氢酶及醛固酮合酶信使核糖核酸表达降低.结论:长期摄入高糖抑制11β2型羟化固醇脱氢酶及醛固酮合酶信使核糖核酸表达、增高血管合成皮质醇、减低血管合成醛固酮、增加血管对去甲肾上腺素的反应并可引起血压升高,可能在高血压发病机制中起一定的作用.

目的:观察乙醇和高糖可能通过抑制11β羟化固醇脱氢酶2型导致大鼠血压升高致心肌损伤的超微结构变化.方法:70只雄性Wister大鼠随机分为七组:对照组(10只),其它六组(各10只)分别给予乙醇0.7g*kg-1*d-1,1.4g*kg-1*d-1,2.1g-1*kg-1*d(分别为乙醇1组、乙醇2组和乙醇3组)和葡萄糖15.0g*kg-1*d-1,25.0g*kg-1*d-1,35.0g*kg-1*d-1(分别为高糖1组、高糖2组和高糖3组)共3个月.分别于1月、2月和3月末测尾动脉血压,3月末对大鼠心肌行透射电镜观察摄片.结果:与对照组比较,长期摄入乙醇或高糖大鼠动脉血压水平升高(P＜0.01);心肌细胞结构紊乱,Z线变形,部分肌丝溶解,糖原减少,线粒体肿胀、嵴变少、紊乱、消失或空泡变.结论乙醇和高糖可能通过抑制11β羟化固醇脱氢酶2型参与了高血压的发病过程.

Objective To observe the influence of intravenous injection of vincristinum on marginal veins of rabbit's ear to prevent clinical phlebitis. Methods Twenty rabbits were randomly divided into four groups: control microscopic control (A1), study microscopic group(A2), control transmission electron microscopic group(A3),and study transmission electron microscopic group(A4). A1 and A3 control groups used the left ears,using the same volume of isotonic saline as control(B1 and B3). The control groups of A2 and A4 study groups used the right ears, using the usual methods as control (B2 and B4). Control groups used 60ml isotonic saline by usual methods,and study groups used the drawing-and-pushing method. Pathologic changes were observed using light microscope and transmission electron microscope. Results: Most of the endothelium disappeared in A1 and B2 groups and hyperplasia of fiber , thickened tube walls and thrombotic vasculum were observed. In A2 group,most of the endothelium was normal and there were lightly thickened tube walls and light hyperplasia of fiber. In A3 and B4 groups,dense nuclei in endothelium and some bubbles and harmed structure were observed. In A4 group,the membrane in endothelium was normal,and there was slightly dense nuclei and some mitochondria. Conclusion Compared with B2 and B4 groups, A2 and A4 groups showed lighter harm,suggesting that the drawing-and-pushing method is better than the usual one.

Objective To investigate the changes of TXB2, 6-Keto-PGF1α and TXB2/6-Keto- PGF1α (T/K) in the myocardium with relation to blood-gas after hypothermic sea water near drowning in rats. Methods The rats were put into hypothermic sea water(16-18 ℃) and let swim freely; in about 15 minutes they would be near drowned and sunk to the bottom. Then, within a few seconds of breath- ing-stop, the rats were taken out of water immediately and examined under room temperature in every 5, 15, 30, 60, 240 and 360 min groups (6 in each group ) for rectal temperature and left heart blood-gas analysis(including pH, PaO2 and PaCO2 ). Besides,4 animals of each group were examined for myocar- dial TXB2 and 6-Keto-PGF1α contents with T/K ratio and also for dry weight and wet weight ratio (D/ W) of lung tissue; while other 2 animals were observed microscopically their changes in the lung and heart. Results After near drowning the rectal temperature, pH,PaO2,TXB2 and 6-Keto-PGF1α all de- creased obviously and reached lowest level in the 5 min group(P0.01); while PaCO2 and TXB2 both increased remarkably and reached the highest level in 5 min group and 30 min group respectively. The T/K also increased significantly after near drowning. As time went by, the rectal temperature, pH, PaO2 and PaCO2 all had a tendency to recover, but TXB2, 6-Keto-PGF1α and T/K showed no obvious im- provement. Conclusions The contents of TXB2 and 6-Keto-PGF1α in the myocardium could be influ- enced by hypothermia, hypoxemia and acidosis in the experiment and lead to the increase of TXB2 and decrease of 6-Keto-PGF1α with T/K imbalance and at the same time worsen the function of heart.

传染病与寄生虫病组：　田庚善△　王爱霞△　斯崇文　汪俊韬　贾克明　崔振宇　姜素椿　林秀玉 　陈乃玲　盛瑞媛　　许炽　贺联印　程道新 呼吸病组：　罗慰慈△　刘秉锟△　朱元珏　赵鸣武　严碧涯　李继成　崔德健　张洪玉 　刘又宁　张沪生　　蔡柏蔷 心血管病组：　吴　宁△　李清朗△　汪丽蕙　胡旭东　刘国树　徐成斌　汪家瑞　高润霖 　刘国仗　朱文玲　　朱国英　陈　湛　张钧华 消化病组：　贾博琦△　潘其英△　陈寿坡　潘国宗　李益农　汪鸿志　于中麟　林三仁 血液病组：　陆道培△　虞积仁△　单渊东　楼方定　张之南　朱嘉芷　汪声恒　陈珊珊 内分泌病组：　史轶蘩△　潘长玉△　潘孝仁　白　耀　高　妍　孟迅吾　施曼珠　钱荣立 　王　　张桂元 肾脏病组：　王海燕△　毕增祺△　陈香美　谌贻璞　郑法雷　王质刚　刘惠兰　杜学海 　章友康 结缔组织病组：　董　怡△　施桂英△　蒋　明　刘　恕　吴东海　马骥良 神经系病组：　许贤豪△　袁锦楣△　王新德　朱镛连　魏岗之　张振馨　王鲁宁 职业病与地方病组：　王世俊△　赵德禄△　赵金垣　李崇正　唐学林　王云钊 　　　△为该组正、副组长

目的探讨低温海水淹溺大鼠心肌TXB2、6-Keto-PGF1α及TXB2/6-Keto-PGF1α(T/K)与血气的关系.方法将淹溺组大鼠置于低温(16～18℃)海水中,任其自由游动直至沉入水底,呼吸暂停,迅速取出置室温下观察,分别于5,15,30,60,240,360 min(每小组各6只)测大鼠肛温,取左心血行血气分析,取各小组4只检测心肌组织TXB2及6-Keto-PGF1α含量,观察T/K变化,肺组织计算干重/湿重比值(D/W),另2只光镜下观察肺脏及心脏形态改变.结果淹溺大鼠肛温、pH、PaO2及6-Keto-PGF1α明显降低,于5 min组降至最低点(P＜0.01),PaCO2及TXB2则明显上升,分别于5 min组及30min组升至最高点(P＜0.01),T/K比值明显上升;淹溺后随离海水的时间延长,肛温、pH、PaO2及Pa-CO2呈恢复趋势,心肌的TXB2、6-Keto-PGF1α及T/K比值则无明显改善.结论低温海水淹溺大鼠心肌的TXB2及6-Keto-PGF1α含量受低温、低氧血症及酸中毒的影响,造成TXB2增高、6-Keto-PGF1α降低及T/K比值失衡从而使心脏功能趋于恶化.

目的 :探讨反复脑缺血后痴呆大鼠皮质内钙分布及生长抑素含量的变化。方法 :采用 SD大鼠 4 -血管阻断、脑反复缺血再灌注方法 ,制作缺血痴呆动物模型 ,水迷宫和跳台试验观察学习、记忆的变化 ,电镜观察皮质钙颗粒的分布情况 ,放射免疫法测定丘脑和海马区生长抑素含量的变化。结果 :缺血痴呆动物脑神经元及胶质细胞均见钙颗粒分布于损伤细胞的线粒体及细胞浆空泡内 ;丘脑和海马区生长抑素含量与对照组比较明显减少 （P＜0 .0 5） .结论 :痴呆大鼠学习、记忆能力的减退可能与皮质钙内流过度 ,丘脑和海马内生长抑素含量的减少有关