在霍奇金病患者淋巴结中检测巨细胞病毒基因

60 %的霍奇金病 (ＨＤ)患者淋巴组织ＲＳ和ＨＤ细胞中可检测到ＥＢ病毒 (ＥＢＶ) [1 ] ,甚至有人报道可高达 93% [2 ] 。但ＥＢＶ可能不是ＨＤ的唯一病因。我们利用聚合酶链反应(ＰＣＲ)及原位杂交的方法直接检测了ＨＤ淋巴组织中的ＨＣ ＭＶ。材料和方法1　材料1.1　标本来源及ＤＮＡ提取 :5 3例ＨＤ患者淋巴结及 1例尸检涎腺巨细胞包涵体病的涎腺组织来自第四军医大学病理教研室 ,其中混合细胞型 37例 ,淋巴细胞减少型 5例 ,结节硬化型 10例及滤泡间ＨＤ 1例。 1例结节硬化型同时留取冰冻组织块及患者全血。 5 μｍ贴胶连续切片后 ,进行原…     

TC/HDL与Ⅱ型糖尿病视网膜病变的关系

目的 比较Ⅱ型糖尿病视网膜病变（ＤＲ）中ＴＣ／ＨＤＬ与其它脂代谢指标关系。方法测定了 Ⅱ型糖尿病有 ＤＲ组 ４０例,无ＤＲ组７０例及正常对照５０例病人的血脂、载脂蛋白Ａ１及Ｂ。结果 Ⅱ型糖尿病人血脂,载脂蛋白 Ａ１及 Ｂ较高于对照组（Ｐ＜０．０５）,有ＤＲ组ＴＣ／ＨＤＬ明显高于无ＤＲ组（Ｐ＜０．０５）。结论ＴＣ／ＨＤＬ在糖尿病视网膜病变发生中是一种较敏感的指标。     

301例B—ALL细胞表面抗原检测结果分析

目的 探讨Ｂ淋巴细胞相关抗原在急性Ｂ细胞型淋巴细胞白血病（Ｂ－ＡＬＬ）细胞表面的表达及其与细胞形态和治疗的关系。方法 采用ＡＢＣ－ＡＰ免疫组化法结合选用多种Ｂ淋巴细胞相关抗原的克隆性抗体对３０１例初发（Ｂ－ＡＬＬ）患者的白血病细胞进行细胞表面抗原检测。结果 Ｂ－ＡＬＬ患者的白血病细胞ＣＤ１９、ＨＬＡ－ＤＲ呈高阳性率表达；而ＣＤ２０的阳性表达率较低。阳性表达率与ＦＡＢ分类分型有一定关系。其中Ｌ１型Ｃ     

108例霍奇金病患者多因素预后分析

我们用Ｃｏｘ回归模型对１０８例霍奇金病（ＨＤ）患者进行多因素预后分析，以提高对本病预后的预见性。临床资料１　病例　１９７６年１月～１９９７年４月我院收治的１０８例可评价病例。全部ＨＤ患者均经病理组织学诊断。男６９例，女３９例，中位年龄３０岁（６～７９岁），＜６５岁９７例，≥６５岁１１例。组织学亚型分布：淋巴细胞为主型（ＬＰ）１８例，结节硬化型（ＮＳ）３７例，混合细胞型（ＭＣ）４８例，淋巴细胞削减型（ＬＤ）５例。临床分期：Ⅰ期３例，Ⅱ期４１例，Ⅲ期３８例，Ⅳ期２６例。Ａ组（无发热、盗汗、消瘦）３２…     

人类疱疹病毒6型、EB病毒与霍奇金病关系的研究

新近发现的人类疱疹病毒６型（ＨＨＶ６）在白血病、淋巴瘤中有较高的抗体滴度［１］,与淋巴瘤关系密切。长期以来人们发现ＥＢ病毒（ＥＢＶ）不仅嗜Ｂ淋巴细胞,还发现与Ｔ细胞淋巴瘤和霍奇金病（ＨＤ）有关［２］。为了解ＨＤ中ＨＨＶ６、ＥＢＶ的感染情况、ＨＤ与ＨＨ...     

增殖细胞核抗原／周期素在恶性淋巴瘤与淋巴结反应性增性中…

应用增殖细胞核抗原／周期素单克隆抗体（ＰＣＮＡ／ｃｙｃｌｉｎ ｐｃ１０ ｍｃＡｄ）对非霍奇金淋巴瘤（ＮＨＬ）３０例［低恶组（ＬＭ）１４例，高恶组（ＨＭ）１６例］，淋巴结反应性增生（ＲＨ）１６例及霍奇金病（ＨＤ）１４例标本石包埋组切片进行免疫组化（ＡＢＣ法）染色。用半定量计阳性细胞均数，并观察阳性细胞分布的规律。结果显示：ＮＨＬ中阳性细胞呈弥漫分布，阳性细胞数与恶性高低呈正相关。ＨＭ组与ＬＭ组，ＬＭ     

胆固醇酯转移蛋白基因taqIB多态性与胆囊结石病关系的临床实验研究

目的：揭示胆囊结石病与遗传因素的关系。方法：运用多聚酶链反应技术（ＰＣＲ）和基因限制性片段长度多态性分析法（ＲＦＬＰｓ）对１０４例胆囊结石病人和６８例健康人进行调查研究。结果：发现胆囊结石组Ｂ１等位基因，Ｂ１Ｂ１基因型，Ｂ２等位基因，Ｂ２Ｂ２基因型频率与对照组相应等位基因及基因型频率比较有差异（０５２３０ｖｓ０３４６００２８８０ｖｓ０１１７６０４７７０ｖｓ０６５４００２４２０ｖｓ０４２６４Ｐ＜００１）。Ｂ１Ｂ１基因型ＨＤＬｃｈ和ＨＤＬ２ｃｈ水平降低，与Ｂ２Ｂ２基因型的ＨＤＬｃｈ、ＨＤＬ２ｃｈ比较有差异（Ｐ＜００１）。结论：Ｂ１等位基因和Ｂ１Ｂ１基因型与低ＨＤＬｃｈ、ＨＤＬ２ｃｈ水平相关。Ｂ１等位基因是部分中国汉族人胆囊结石病人的遗传易感因素。     

四川地区间变性大细胞淋巴瘤的临床病理与免疫组化研究

目的 观察四川地区间变性大细胞淋巴瘤（ａｎａｐｌａｓｔｉｃ ｌａｒｇｅ ｃｅｌｌ ｌｙｍｈｏｍａ,ＡＬＣＬ）的临床病理和免疫组化特征。方法 搜集临床资料并随访,应用免疫组化（ＡＢＣ法）,对１９例ＡＬＣＬ的临床病理和免疫组化进行研究。结果 记均阳性）。１１例为ＣＤ４５阳性,１０例ＥＭＡ阳性,１４例ＴＩＡ１阳性。ＣＤ１５及ＣＤ６８均为阴性。形态学上瘤组织表现为窦、滤泡间侵犯,瘤细胞形态多样,可见胚胎样     

非诺贝特治疗高脂血症40例疗效观察

目的：观察非诺贝特对高脂血症的疗效。方法：对４０例高脂血症患者使用非诺贝特，每日３００ｍｇ，疗程６个月；治疗前后检测血清总胆固醇（ＴＣ）、甘油三酯（ＴＧ）、低密度脂蛋白胆固醇（ＬＤＬＣ）、高密度脂蛋白胆固醇（ＨＤＬＣ）和载脂蛋白Ａ１（ａｐｏＡ１）、载脂蛋白Ｂ（ａｐｏＢ）等。结果：ＴＧ平均降低了４５．２％，ＴＣ平均降低了２０．５％，ＨＤＬＣ平均上升了１５．４％，ＬＤＬＣ平均降低了２５．５％，ａｐｏＡ１平均上升了２．０％，ａｐｏＢ平均下降了３０．０％。结论：非诺贝特具有降低ＴＧ、ＴＣ、ＬＤＬＣ、ａｐｏＢ和升高ＨＤＬＣ、ａｐｏＡ１作用，从而可减少冠状动脉粥样硬化性心脏病的发病率和病死率     

异基因外周血干细胞移植治疗恶性血液病的临床研究

目的 评价异基因外周血干细胞移植（ａｌｌｏＰＢＳＣＴ） 治疗恶性血液病的疗效。方法 用异基因外周血干细胞移植治疗恶性血液病１６ 例,其中急性淋巴细胞白血病５ 例（ＣＲ１ ４ 例,ＣＲ２ １ 例） , 急性非淋巴细胞白血病２ 例（ＣＲ１） ,慢性粒细胞白血病８ 例（ＣＰ５ 例,ＡＰ３ 例） ,非霍奇金淋巴瘤１ 例（ＰＲ） 。中位年龄３３（１８ ～４９） 岁。预处理方案：ＴＢＩ９ ～１０ Ｇｙ（ 分２ 次照射） ＋ ＣＴＸ １２０ ｍ ｇ／ｋｇ 或ＴＢＩ１０Ｇｙ ＋ＣＴＸ１２０ ｍｇ／ｋｇ ＋ Ｖｐ１６ ５００ ｍｇ 。预防移植物抗宿主病（ ＧＶＨＤ） 方案：ＣｓＡ＋ 短程ＭＴＸ。供者年龄中位数３２（１４ ～５２） 岁, 用ＧＣＳＦ５μｇ ·ｋｇ － １ ·ｄ － １ ×５ ～６ 天进行造血干细胞动员, 分离单个核细胞中位数９ ×１０８／ｋｇ［５ ．７９ ～１３ ．７０） ×１０８／ｋｇ］ ,ＣＤ３４ ＋ 细胞中位数１３ ．９ ×１０６／ｋｇ［５ ．６９ ～４９ ．００） ×１０６／ ｋｇ］ 。结果全部患者移植后均重建造血,仅１ 例（ＡＢＯ 血型不合） 红系延迟重建。粒细胞＞ ０ ．５ ×１０９／ Ｌ 中位数１２（１０ ～１５） 天,血小板＞ ３０ ×１０９／Ｌ 中位数１３（８ ～２４） 天     

CD4+ T cells that express high levels of CD45RB induce wasting disease when transferred into congenic severe combined immunodeficient mice. Disease development is prevented by cotransfer of purified CD4+ T cells

Purified CD4+ lymph node T cells were sorted into two populations on the basis of their expression of CD45RB (CD45RBhi and CD45RBlo) and injected into congenic severe combined immunodeficient (SCID) mice. After a period of time that was dependent on the number of cells injected, the SCID mice that received CD45RBhi/CD4+ T cells developed a wasting disease that was not seen in SCID mice that received the CD4+/CD45RBlo cells or whole lymph node cells. At death, SCID mice that received the CD4+/CD45RBhi cells had increased spleen and lymph node cellularity compared with normal SCID mice and SCID mice that received the CD4+/CD45RBlo T cells. The spleen and lymph node contained CD4+ cells and neither CD8+ nor surface immunoglobulin M-positive cells, plus a population of cells that did not express any of those markers. At necropsy, the SCID mice that received the CD4+/CD45RBhi cells had significant hyperplasia of the intestinal mucosa with significant lymphoid cell accumulation in the lamina propria. Interestingly, mice that received mixtures of whole lymph node or purified CD4+ cells with CD4+/CD45RBhi cells did not develop weight loss, indicating that the unseparated CD4+ population contained cells that were capable of regulating the reactivity of the CD4+/CD45RBhi cells.     

An Assessment of Laparotomy in the Management of Patients with Hodgkin's Disease

Planned laparotomy and splenectomy has been a safe investigationfor sixty patients with clinical Stage I, II or III Hodgkin'sdisease. Twenty-four of the 60 patients (40 per cent) changedstage and 18 patients had their treatment altered as a consequenceof the procedure. Forty-three per cent of patients without apalpably enlarged spleen had unsuspected disease when the organwas examined pathologically, although a false positive spleenwas uncommon. Eight of 55 patients (14·5 per cent) hadintra-abdominal disease which was not detected by lymphangiography.Intra-abdominal disease occurred with all histological sub-typesand was found in two patients who had clinical Stage I diseaseand lymphocyte predominance in their node histology. Sarcoid-like granulomata were found in ten patients, seven inthe spleen, one in the liver and spleen, one in the skin andone in the original node biopsy. In the majority of patients,granulomata were associated with nodular sclerosing or mixedcellular histology. In all ten patients the Hodgkin's diseasewas suppressed by appropriate chemotherapy and disease has notrecurred. No patient has shown any clinical evidence of sarcoidosisand the Kveim test done in three patients was negative. Our experience encourages us to recommend staging laparotomyfor all adult patients with Hodgkin's disease which does notshow obvious generalized spread beyond lymph nodes.     

Nodular sclerosing Hodgkin's disease with giant Reed-Sternberg cells

A 70-year-old woman with multiple symptoms and extensive lymphadenopathy had a lymph node biopsy specimen that contained highly pleomorphic, giant Reed-Sternberg cells that resembled cells from other malignant giant cell neoplasms. The cells were strongly positive for Leu-M1, alpha 1-antitrypsin, S-100 protein, kappa light chain, and lambda light chain. With five courses of chemotherapy for pathologic stage IV-B Hodgkin's disease, the patient achieved a complete remission, and remains free of disease 85 months after diagnosis.     

霍奇金淋巴瘤的免疫表型与鉴别诊断

目的　研究霍奇金淋巴瘤 (HL)的免疫表型和鉴别诊断。方法　采用SP免疫组化法检测 5 6例HL患者瘤细胞及背景细胞的免疫表型 ,根据WHO 2 0 0 0淋巴瘤新分类重新评价。结果　HL患者 47例 ,其中结节性淋巴细胞为主型HL(NLPHL) 2例 ,经典型HL(CHL) 4 3例 ,未分类 2例 ;富于T细胞的B细胞淋巴瘤 (TCRBCL) 6例 ,间变性大细胞淋巴瘤 (ALCL) 2例以及转移性肿瘤 1例。NLPHL中L&H细胞呈CD2 0 (+) ,CD1 5(- ) ,CD3 0 (- ) ;背景细胞中TIA 1阳性细胞稀少 ,CD57阳性细胞多见。CHL中诊断性R S细胞及变异型R S细胞呈CD1 5(+) (81% ) ,CD3 0 (+) (10 0 % ) ,其中 3例共同表达CD2 0 呈弱阳性 ;背景细胞中TIA 1阳性细胞多见 ,而CD57阳性细胞稀少。TCRBCL中瘤细胞呈CD2 0(+) ,CD1 5(- ) ,CD3 0 (- ) ;背景细胞中TIA 1阳性细胞增多 ,CD57阳性细胞少见。ALCL中瘤细胞呈CD3(+) ,CD3 0 (+) ,ALK 1(+) ,CD1 5(- ) ,CD2 0 (- ) ,背景细胞中TIA 1阳性细胞多见 ,CD57阳性细胞少见。结论　石蜡免疫组化检测瘤细胞CD2 0 、CD3 、CD1 5、CD3 0 以及背景细胞TIA 1、CD57、CD2 0 和CD45RO 的表达 ,有助于HL的诊断和鉴别诊断     

Lymphocyte subsets show marked differences in their distribution between blood and the afferent and efferent lymph of peripheral lymph nodes

The surface phenotypes (CD1, CD4, CD5, CD8, SBU-T19, MHC class I, MHC class II, and sIg) of cells in blood, lymph nodes, and lymph were determined to examine simultaneously the distribution of lymphocyte subsets circulating in blood, afferent lymph, and efferent lymph of a peripheral lymph node. Marked differences in the percentage of certain lymphocyte subsets were apparent within the compartments examined, suggesting that lymphocyte subsets leave the blood with differing efficiencies. Lymphocyte subsets also appeared to be extracted from the blood at different rates by lymph node as opposed to subcutaneous vascular endothelium. Endothelial cells in different vascular beds may express different numbers of molecules complementary to a set of migration-related cell surface molecules specific for each lymphocyte subset. Accordingly, the vascular endothelium would be the key factor in regulating nonrandom cell migration.     

Utility of flow cytometry in subtyping composite and sequential lymphoma.

Composite lymphoma (CL) is defined as more than one distinct lymphoma variant occurring in the same anatomic site, and sequential lymphoma (SL) is defined as different lymphoma variants occurring at different sites or at different times in the same patient. The utility of flow cytometry immunophenotyping in evaluating CL and SL has only been investigated in a few single-case studies. To further define the utility of flow cytometry in evaluating these tumors, records were searched at two institutions. Cases representing high-grade progression of low-grade lymphoma were excluded. For each CL/SL, clinical data was obtained and morphology was evaluated in routinely processed H&E-stained tissue sections. Tumor components were subtyped using revised European-American classification (REAL) criteria. Follicle center components were graded using modified Rappaport criteria. Immunophenotype was determined using two-color flow cytometry and paraffin-section immunostains. Four cases were identified. Case 1, nodal follicle center, follicular, grade III plus marginal zone CL, showed two discrete populations of monoclonal B-cells that differed in their expression of CD10. Case 2, cutaneous lymphoplasmacytoid lymphoma followed by mesenteric non-Hodgkin's lymphoma (lymphoplasmacytoid plus follicle center, follicular, grade III) plus Hodgkin's disease CL, showed CD5-/CD10-/CD19+/kappa+ cells by flow cytometry in both tissue samples. The Hodgkin's disease component showed CD3-/CD15-/CD20-/CD30+ Reed-Sternberg cell variants in paraffin-section immunostains. Case 3 represented nodal follicle center lymphoma, follicular, grade I (CD3-/CD5-/CD10-/CD19+/kappa+) followed by cutaneous anaplastic large T-cell lymphoma (CD2+/CD4+/CD5+/CD19- cells with partial expression of CD3 and CD7). Case 4 represented cutaneous follicle center lymphoma, follicular, grade I (CD5-/CD10+/CD19+/CD23+/lambda+) followed by bone marrow B-cell small lymphocytic lymphoma (CD5+/CD10-/CD19+/CD23+/kappa+). Results show that flow cytometry is a potentially useful adjunct in characterizing CL and SL.     

Memory/effector (CD45RB(lo)) CD4 T cells are controlled directly by IL-10 and cause IL-22-dependent intestinal pathology

The role of direct IL-10 signaling in different T cell subsets is not well understood. To address this, we generated transgenic mice expressing a dominant-negative IL-10 receptor specifically in T cells (CD4dnIL-10Rα). We found that Foxp3-depleted CD45RB(lo) (regulatory T cell [T(reg) cell]-depleted CD45RB(lo)) but not CD45RB(hi) CD4(+) T cells are controlled directly by IL-10 upon transfer into Rag1 knockout (KO) mice. Furthermore, the colitis induced by transfer of T(reg) cell-depleted CD45RB(lo) CD4(+) T cells into Rag1 KO mice was characterized by reduced Th1 and increased Th17 cytokine messenger RNA levels in the colon as compared with the colitis induced by transfer of CD45RB(hi) T cells. In contrast to the CD45RB(hi) transfer colitis model, in which IL-22 is protective, we found that T cell-derived IL-22 was pathogenic upon transfer of T(reg) cell-depleted CD45RB(lo) T cells into Rag1 KO mice. Our results highlight characteristic differences between colitis induced by naive (CD45RB(hi)) and memory/effector (T(reg) cell-depleted CD45RB(lo)) cells and different ways that IL-22 impacts inflammatory bowel disease.     

Flow fluorimetry in differential diagnosis of diffuse large B-cell lymphoma

AIM: To analyse immunophenotype of diffuse large B-cell lymphoma (DLBCL) with flow cytometry. MATERIAL AND METHODS: Combinations of antibodies against the following antigens were used: CD3/ CD19/CD45, CD5/CD19/CD38, CD19/CD10/CD23, CD4/CD8/CD3, kappa/lambda/CD19, CD25/CD20/FMC7; CD43/CD22/CD20; CD79a/Ki-67/CD3; cytoplasmic kappa/lambda. The analysis was made on flow fluorimeter FacsCalibur using computer program CellQuest (Beckton Dickenson, USA). RESULTS: Specific coexpression of markers is not detectable in DLBCL, in the greatest degree the phenotype corresponds to lymphoma from the cells of the marginal zone. The study of cells with maximal direct light diffusion provides more precise assessment of clonality and proliferative potential of tumor cells than the analysis of the whole lymphocytic polygon. The proliferative index in 33 cases of DLBCL varied in the range 10-60%. CONCLUSION: Flow cytometry in most DLBCL cases allows identification of B-cell clonality, more precise assessment of a proliferative potential of the tumor.     

Nonlymphocyte-derived tumor necrosis factor is required for induction of colitis in recombination activating gene (RAG)2(-/-) mice upon transfer of CD4(+)CD45RB(hi) T cells

In this study, we addressed the role of tumor necrosis factor (TNF)-alpha and lymphotoxin (LT)-alpha in the development of colitis and defined the cellular sources (T cells versus non-T cells) of TNF (TNF-alpha and LT-alpha) relevant to disease development. After adoptive transfer of TNF(+/+) CD4(+)CD45RB(hi) splenocytes into TNF(+/+) recombination activating gene (RAG)2(-/-) mice, the recipients develop massive inflammation of the large intestinal mucosa concurrent with massive weight loss. In contrast, clinical signs of disease are completely absent in TNF(-/-)RAG2(-/-) recipients of TNF(-/-) CD4(+)CD45RB(hi) T cells, although elevated numbers of interferon-gamma-producing cells are present in the colonic mucosa. Surprisingly, upon transfer of TNF(-/-)CD4(+)CD45RB(hi) T cells into TNF(+/+)RAG2(-/-) recipients, colitis develops with kinetics similar to those upon transfer of TNF(+/+)CD4(+)CD45RB(hi) donor cells. In contrast, no clinical signs of colitis are observed in TNF(-/-)RAG2(-/-) recipients of TNF(+/+)CD4(+)CD45RB(hi) T cells. This protection from colitis is not a consequence of the absence of LT-alpha, as TNF-alpha(-/-)RAG2(-/-) recipients of TNF-alpha(-/-) CD4(+)CD45RB(hi) T cells are also protected from colitis induction. These results demonstrate the importance of TNF production by non-T cells of the colonic mucosa in the pathogenesis of colitis and provide direct evidence for a nonredundant role of TNF-alpha in this mouse model of colitis.     

The Hodgkin's cell in nodular sclerosis does not release interleukin-1

Cell cultures were established from lymph nodes from eight patients with nodular sclerosing Hodgkin's disease and 12 controls. The patient cultures were demonstrated to produce a transforming growth factor for fibroblasts; none of the control cultures produced this transforming growth factor. The serum-containing and serum-free conditioned media were also tested for interleukin-1 activity produced by these cultures. Two nodular sclerosing Hodgkin's disease cell cultures produced measurable levels of interleukin-1 activity, and one had persistent levels of interleukin-1 activity after depletion of normal macrophages. However, nonspecific esterase stains confirmed the persistence of many normal macrophages. Two alveolar macrophage cultures had measurable interleukin-1 but did not induce fibroblast colony formation in soft agar. These data suggest that the Hodgkin's cell does not produce measurable levels of interleukin-1 and that interleukin-1 derived from the Hodgkin's cell is not the mediator responsible for the fibroblast hyperplasia and agar colony formation produced by cell cultures from nodular sclerosing Hodgkin's disease.