套细胞淋巴瘤的临床及病理学特征分析

目的探讨套细胞淋巴瘤的临床及病理组织学特征。方法回顾性分析15例套细胞淋巴瘤的临床表现、病理组织学特点，采用免疫组化SP法检测套细胞淋巴瘤免疫表型情况。结果15例套细胞淋巴瘤均为中老年患者，中位年龄57岁，临床Ⅱ-Ⅲ期患者多见；镜下15例套细胞淋巴瘤均有不同程度的淋巴结结构破坏，出现形态较为单一的淋巴样细胞增生，5例呈套区分布生长，7例呈模糊结节状生长，3例呈弥漫生长；15例的肿瘤细胞均表达CD20、Bcl-2、CD5和cyclinDl，12例表达CD79a，所有病例均不表达CD45RO、CD3、CD23和CD10。结论套细胞淋巴瘤有特征性临床、病理学改变，根据典型的临床表现、病理形态学改变、免疫表型特点可作出明确诊断。

Quick to remember, slow to forget： rapid recall responses of memory CD8^＋ T cells

The functional roles of memory B and T lymphocytes underlie the phenomenal success of prophylactic vaccinations, which have decreased morbidities and mortalities from infectious diseases globally over the last 50 years. However, it is becoming increasingly appreciated that memory cells are also capable of mediating the pathology associated with autoimmune disorders and transplant rejection, and may pose a significant barrier to future clinical advancement in immunoregulation. Therefore, understanding the unique properties of memory lymphocytes （as compared to their naive precursors） is a major area of investigation. Here, we focus on one of those singular properties of memory T cells （TM）-rapid recall. As will be discussed in more detail, rapid recall refers to the ability of quiescent TM cells to efficiently and robustly express‘effector functions＇ following stimulation. Studies that have advanced our understanding of TM cells＇ rapid recall using CD4^＋ T cells have been expertly reviewed elsewhere, so we will focus primarily on studies of CD8^＋ T cells. We will first review the different ways that CD8^＋ TM cells can be generated, followed by discussing how this influences their functional properties in the settings of immune protection and pathology. Then, rapid recall ability will be discussed, with emphasis placed on what is currently known about the mechanisms that underlie this unique property of TM cells.

Antiviral innate immunity pathways

Recent studies have uncovered two signaling pathways that activate the host innate immunity against viral infection. One of the pathways utilizes members of the Toll-like receptor （TLR） family to detect viruses that enter the endosome through endocytosis. The TLR pathway induces interferon production through several signaling proteins that ultimately lead to the activation of the transcription factors NF-kB, IRF3 and IRFT. The other antiviral pathway uses the RNA helicase RIG-Ⅰ as the receptor for intracellular viral double-stranded RNA. RIG-Ⅰ activates NF-kB and IRFs through the recently identified adaptor protein MAVS, a CARD domain containing protein that resides in the mitochondrial membrane. MAVS is essential for antiviral innate immunity, but it also serves as a target of Hepatitis C virus （HCV）, which employs a viral protease to cleave MAVS off the mitochondria, thereby allowing HCV to escape the host immune system.

Alteration of chaperonin60 and pancreatic enzyme in pancreatic acinar cell under pathological condition

AIM： To investigate the changes of chaperonin60 （Cpn60） and pancreatic enzymes in pancreatic acinar cells, and to explore their roles in the development of experimental diabetes and acute pancreatitis （AP）. METHODS： Two different pathological models were replicated in Sprague-Dawley rats： streptozotocininduced diabetes and sodium deoxycholate-induced AP. The contents of Cpn60 and pancreatic enzymes in different compartments of the acinar cells were measured by quantitative immunoo/tochemistry. RESULTS： The levels of Cpn60 significanUy increased in diabetes, but decreased in AP, especially in the zymogen granules of the pancreatic acinar cells. The elevation of Cpn60 was accompanied with the increased levels of pancreatic lipase and chymotrypsinogen in diabetes. However, a decreased Cpn60 level was accompanied by high levels of lipase and chymotrypsinogen in AP. The amylase level was markedly reduced in both the pathological conditions. CONCLUSION： The equilibrium between Cpn60 and pancreaUc enzymes in the acinar cells breaks in AP, and Cpn60 content decreases, suggesting an insufficient chaperone capacity. This may promote the aggregation and autoactivation of the premature enzymes in the pancreatic acinar cells and play roles in the development of AR

Cryoablation Combined with TACE for Treating Large Hepatocellular Carcinoma： Tumor Load and Cellular Immunity

OBJECTIVE To study the effectiveness on the tumor load and cellular immune function of percutaneous cryoablation （argon-helium cryoablative system, AHCS） combined with transarterial chemoembolization （TACE） for treating large hepatocellular carcinomas （HCCs） with diameters over 10 ca. METHODS A total of 48 HCC patients were treated with AHCS after TACE. Tumor sizes ranged from 10 to 14 cm. All cases were a hypervascular type. There were 38 Child A cases and 10 Child B cases. Forty were AFP positive and 8 negative. The patients were randomized with therapy group consisting of 26 cases and the control group 22 cases. The therapy group received AHCS 4 weeks following TACE treatment. Reexamination included pathology, tumor markers, T-lymphocyte subgroup levels and computed tomography or MRI. The necrosis rate of the tumor load was calculated by Cavalieri＇s theory. EORTC QLQ-C30 was used in quality of life evaluation. RESULTS The average tumor-load reduction rate （necrosis rate） was 8.07% after TACE, and 28.65% after AHCS. Coagulation necrosis was produced in the target area. The tumor markers deceased significantly after AHCS. Tumor-load reduction after AHCS was more significant than after TACE. Suppression of cellular immunity after TACE was significant. In contrast, CD3^＋, CD4^＋ and NK increased after AHCS and an abnormal T-lymphocyte distribution was corrected. Quality of life after AHCS increased according to the EORTC QLQ-C30 evaluation. No severe complications occurred. CONCLUSION Percutaneous AHCS cryoablation after TACE reduced the tumor load in the short term. At the same time, cellular immune function was increased after AHCS. TACE was critical in increasing the therapeutic efficacy of AHCS because of its embolisation of blood vessels preventing a Flow Effect. Reduction of the tumor load in the short term may conduce to increase cellular immunity. Percutaneous AHCS cryoablation combined with TACE can reduce the tumor load, improve cellular immunity and increase quality of life of HCC patients. This type of therapy deserves to be studied further research.

Morphological observation of tumor infiltrating immunocytes in human rectal cancer

AIM： To investigate the morphological characterization of tumor infiltrating dendritic cells （TIDCs） and tumor infiltrating lymphocytes （TILs） in human rectal cancer. METHODS： Light and electron microscopy as well as immunohistochemistry were used to observe the distributive and morphological changes of TIDCs and TILs. RESULTS： TIDCs were mainly located in tumor-surrounding tissue. The number of TIDCs in the earlier stage was higher than that in the later stage （P〈 0.01）. TILs were mainly seen in adjacent tissue of cancers and tumor-surrounding tissue. There were more TILs in the earlier stage than that in the later stage （P〈0.01）. Under electron microscope, TIDCs were irregular in shape and exhibited many dendritic protrusions. It isn＇t obvious that cancer cells perforated the basement membrane and TILs were arranged along the basement membrane in the earlier stage. In the later stage, it is explicit that cancer cells perforated the basement membrane and surrounded by TILs. There were contacts among TIDCs, TILs and tumor cell. One IIDCs contacted one or several TILs which clustered around TIDCs. Glycogen granules were seen between TIDCs and Tits. CONCLUSION： The number of TIDCs and TILs is related with tumor progression There exist close relationships among TIDCs, TILs and tumor cell.

Serum-free culture of H pylori intensifies cytotoxicity

AIM： To perform a long culture passage of H pylori without serum, taking into account its cytotoxicity and the presence of the probable new cytotoxic factor. METHODS： One sample of H pylon 60190 （ATCC 49503） was grown on Brain Heart Infusion （BHI） agar containing 0.5% 2,6-di-O-methyl-β-cyclodextrin without any serum, being passaged 70-100 times every 3-4 d for approximately 2 h, while another sample of H pylori contained 70 mL/L fetal calf serum without 2,6-di-O- methyl-β-cyclodextrin. Their supernatant and extract after 16 h in culture were evaluated for changes in cell morphology and for cell viability using HeLa cells. Furthermore, the characteristics of the probable cytotoxic factor in the extract were examined on partial purification studies and its oytotoxicity was evaluated in various human cells. RESULTS： The supernatant and the extract of the bacterium grown on serum-free medium had strong cytotoxicity compared with those grown on serumcontaining medium. They irreversibly damaged HeLa cells without vacuolation that was altogether different from that of the bacterium when grown with serum. Their cytotoxicity was easily measured by cell viability assay. The probable cytotoxic factor partially purified and detected by chromatography had characteristics difference from that of vacuolating toxin and a broad cytotoxicity toward various cell lines. CONCLUSION： Serum-free long culture method of H pylorl makes its supernatant and its extract cytotoxic enough to be easily measured by cell viability assay. The probable cytotoxic factor has a unique characteristic and might be a new cytotoxin.

Changes of CD8+CD28-T regulatory cells in rat model of colitis induced by 2,4-dinitrofluorobenzene

AIM:To determine the changes of CD8+ T subsets especially CD8+CD28-T regulatory cells in rat model of experimental colitis induced by 2,4-dinitrofluorobenzene (DNFB). METHODS:The rat model of experimental colitis was induced by enema with DNFB.Ten days later,colonic intraepithelial and splenic lymphooltes were isolated from colitis animals (n=16) and controls (n=8).The proportion of CD8+ T cells,CD8+CD28+ T cells and CD8+CD28-T regulatory cells were determined by flow cytometry. RESULTS:The model of experimental colitis was successfully established by DNFB that was demonstrated by bloody diarrhea,weight loss and colonic histopathology.The proportion of CD8+ T cells in either splenic or colonic intraepithelial lymphocytes was not significantly different between colitis animals and controls (spleen:34.6±7.24 % vs 33.5±9.41%, colon:14.0±8.93 % vs 18.0±4.06 %,P>0.05).But CD8+CD28- T regulatory cells from colitis animals were significantly more than those from controls (spleen:11.3±2.26 % vs 5.64±1.01%, colon:6.50±5.37 % vs 1.07±0.65 %,P<0.05).In contrast, CD8+CD28+ T cells from colitis animals were less than those from controls (spleen:23.3±6.14 % vs 27.8±9.70 %,P=0.06; colon:7.52±4.18 % vs 16.9±4.07 %,P<0.05).The proportion of CD8+CD28-T regulatory cells in splenic and colon intraepithelial CD8+ T cells from colitis animals was higher than that from controls (spleen:33.3±5.49 % vs 18.4±7.26 %, colon:46.0±14.3 % vs6.10±3.72 %,P<0.005). CONCLUSION:Experimental colitis of rats can be induced by DNFB with simplicity and good reproducibility.The proportion of CD8+CD28-T regulatory cells in rats with experimental colitis is increased,which may be associated with the pathogenesis of colitis.

Renal Collecting Duct Cancer： a Report of 2 Cases

Renal collecting duct cancer is a rare malignant tumor, which accounts for 1% to 2% of epithelial kidney tumors. Its pathologial appearance has been easily misdiagnosed as a mammilliform renal cell carcinoma or as other tumors. The malignancy of renal collecting duct cancer is high, with early metastasis and poor prognosis. The clinical data for 2 cases of the tumor are discussed in this report, including reports on the histopathology and the changes in immunohistochemistry.

硝酸钇对成年雌性小鼠免疫毒性研究

目的探究硝酸钇对成年雌性小鼠的免疫毒性。方法100只雌性BALB/c小鼠随机分为5组,每组20只,分别灌胃硝酸钇溶液0、0.2、2.0、20.0和200.0 mg/kg·bw,每日1次,连续30 d。染毒结束后,各组随机选取10只小鼠,麻醉后处死,分离胸腺和脾称重并计算脏器系数,测定脾淋巴细胞增殖能力、脾NK细胞活性以及外周血、胸腺和脾主要免疫细胞表型。其余小鼠,用抗原生成细胞试验(PFC)和足跖增厚法(DTH)检测体液和细胞免疫功能。结果200.0 mg/kg·bw组小鼠体重和脾脏系数低于对照组(P<0.05)。与对照组相比,0.2、2.0、20.0和200.0 mg/kg·bw组小鼠脾B细胞增殖能力降低(P<0.05)。200 mg/kg·bw组小鼠溶血空斑数目少于对照组(P<0.05)。免疫细胞病理学结果表示,与对照组相比,200 mg/kg·bw组小鼠外周血和脾B细胞比例降低(P<0.05),外周血中性粒细胞、Th细胞和NK细胞,脾T细胞、Th细胞、NK细胞和巨噬细胞,胸腺Th细胞比例均较对照组增高,差异有统计学意义(P<0.05)。结论经口摄入200.0 mg/kg·bw硝酸钇能抑制成年雌性小鼠脾B淋巴细胞增殖,降低外周血和脾B细胞比例,抑制体液免疫功能,产生明显的体液免疫毒性作用。脾是硝酸钇免疫毒性作用的敏感靶器官,脾B细胞增殖能力是其免疫毒性的敏感指标。