血清Ryanodine受体抗体检测对胸腺瘤并重症肌无力的诊断价值

目的 探讨血清Ryanodine受体抗体（RyR-Ab）对胸腺瘤并重症肌无力（MG）的诊断价值。方法 选择经病理检查证实为胸腺病变并MG的患者35例,其中胸腺瘤并MG患者（MGT组）17例、胸腺增生并MG患者（MGH组）12例、胸腺萎缩并MG患者（MGA组）6例,同时选择胸腺正常的MG患者（NTMG组）27例,健康对照者（NC组）50例;采用ELISA法检测其血清RyR-Ab。结果 MGT组血清RyR-Ab阳性率为76．5％,MGH组为8．3％,MGA组为16．6％,NTMG组为0,NC组为0。结论MGT患者血清RyR-Ab阳性率较高,检测血清RyR-Ab有助于MGT的诊断。     

胸腺瘤伴重症肌无力与单纯胸腺瘤的临床对比观察

目的评估胸腺瘤伴重症肌无力(MG)与单纯胸腺瘤临床及病理特征的差异,探讨MG对于胸腺瘤患者预后可能的影响。方法对1998～2007年收集的胸腺瘤伴MG(A组,47例)和单纯胸腺瘤(B组,31例)临床资料进行回顾性分析。结果无法手术的患者7例(A组2例,B组5例,P=0.002);胸腺瘤患者中有11例合并胸腺增生(A组9例,B组2例,P=0.001),1例合并微小胸腺瘤(A组1例,B组0例,P=0.000)。WHO分型中A型和C型胸腺瘤未发现胸腺瘤伴MG病例。术后A组有5例死于术后MG危象,B组有2例Ⅳ期和(或)C型患者死亡。A组与B组5年生存率分别为86.7%和88.3%,P=0.076。结论伴或不伴MG对胸腺瘤患者的远期生存率没有显著影响;MG危象是造成胸腺瘤伴MG患者死亡的主要原因,因肿瘤进展至Ⅳ期或处于C型则是单纯胸腺瘤患者死亡的重要原因;胸腺增生及微小胸腺瘤是引起患者术后MG的重要因素。     

51例重症肌无力患者的临床与胸腺病理和电镜分析

目的分析胸腺增生与伴胸腺瘤的重症肌无力患者临床表现及其胸腺病理类型和超微结构特点。方法对51例MG患者的病例资料进行回顾性分析。按照胸腺瘤组和胸腺增生组,对临床症状、MG危象发生率、胸腺瘤WHO组织学分型、胸腺超微结构特点等各项指标进行对比。结果胸腺瘤组临床症状重、MG危象发生率高、术后MG症状改善程度差。结论胸腺瘤组MG患者病情重,WHO组织学分型对于区别良恶性肿瘤及预后有指导意义,胸腺超微结构特点的研究有助于澄清MG的发病机制。     

重症肌无力患者外周血IL-17、IL-23的表达及其与发病的关系

目的探讨重症肌无力(MG)患者外周血白介素-17(IL-17)、白介素-23(IL-23)的表达水平及其与发病的关系。方法将2015年7月至2017年6月我院收治的重症肌无力患者40例设为观察组,选取同期在我院进行健康体检的健康志愿者20例为对照组。根据病情轻重和病变的分布,按改良Osserman临床分型[5]将MG患者分为眼肌型组(15例)和全身型组(25例);按照胸腺病理组织学活检结果将患者分为胸腺正常组(16例)、胸腺增生组(11例)、胸腺瘤组(13例)。采用酶联免疫法检测比较观察组与对照组,眼肌型组和全身型组,胸腺正常组、胸腺增生组、胸腺瘤组患者的外周血IL-17、IL-23水平。结果观察组MG患者外周血IL-17、IL-23水平均显著高于对照组健康志愿者,差异有统计学意义(P 0. 05)。全身型MG患者血清IL-17、IL-23水平均显著高于眼肌型MG患者,差异有统计学意义(P 0. 05)。胸腺瘤组患者的IL-23水平显著高于胸腺正常组、胸腺增生组患者,胸腺瘤组患者的IL-17水平显著高于胸腺正常组患者,差异有统计学意义(P 0. 05)。结论重症肌无力患者的外周血清IL-17、IL-23水平表达异常升高,眼肌型和全身型MG患者,胸腺正常、胸腺增生、胸腺瘤MG患者的外周血IL-17、IL-23水平存在显著差异。     

胸腺切除术对重症肌无力患者AchRb及PsmRAb的影响

用标准经胸胸腺切除术治疗重症肌无力（MG）患者，术前及术后3个月，采用酶联免疫吸附法检测其血清乙酰胆碱受体抗体（AchRAb）、抗突触前膜受体抗体（PsmRAb）滴度的变化。结果MG胸腺增生患者术后Ach-RAb滴度低于术前（P〈0．01），手术前后PsmRAb无统计学差异；MG胸腺瘤患者，手术前后AchRAb无统计学差异，但术后PsmRAb高于术前（P〈0．01）。提示胸腺切除后，MG胸腺增生患者AchRAb下降，MG胸腺瘤患者PsmRAb升高。     

39例中老年重症肌无力患者淋巴样滤泡性胸腺增生的CT表现

目的探讨中老年重症肌无力患者淋巴样滤泡性胸腺增生的发生情况和CT表现. 方法对39例经手术病理确诊为淋巴样滤泡性胸腺增生的中老年重症肌无力患者作了影像学分析,并与健康中老年人、青年重症肌无力患者淋巴样滤泡性胸腺增生作对比分析.凡无胸腺区形态正常的软组织影、无胸腺区脂肪内边缘清楚的肿块（〉3 cm）或结节（〈3 cm）和边缘模糊的斑片影者视为不典型淋巴样滤泡性胸腺增生. 结果 31例（79.5%）呈不典型表现,全部表现为胸腺区脂肪内夹杂＜5 mm的斑点和细索条影;与健康中老年人和青年重症肌无力患者比较差异均有统计学意义（分别为χ^2=4.135,P＜0.05;χ^2=9.584,P＜0.01）.其中1级7例, 2级14例, 3级8例, 4级2例,1～3级与健康中老年人比较,差异有统计学意义（P＜0.01）.仅8例（20.5%）呈典型表现, 包括胸腺区结节2例、胸腺软组织影2例和胸腺区边缘模糊的斑片致密影4例. 结论大多数中老年重症肌无力患者淋巴样滤泡性胸腺增生的CT表现不典型,以男性多见,容易漏诊.     

重症肌无力胸腺瘤的围术期处理

目的总结重症肌无力（myasthenia gravis,MG）胸腺瘤的围术期处理经验。方法回顾分析本科1990年7月～2008年6月连续手术治疗胸腺瘤合并MG65例患者的临床资料。结果危象预测积分〈12分者,无危象发生;12～17分者危象发生率50.0%;18～23分者危象发生率71.4%;≥24分者危象发生率75.0%。术前危象预测积分≥12分者,术后24h拔除气管插管和气管切开的患者分别为85.7%和61.4%,显著高于危象预测积分〈12分者的20.5%和6.8%。术后肌无力症状完全缓解23例、改善25例,有效率85.7%,改善不明显或加重8例。结论胸腺瘤切除是治疗重症肌无力胸腺瘤的一种较安全而有效的方法。围手术期治疗的重点是防治MG危象。     

手术治疗胸腺瘤合并重症肌无力34例

目的观察胸腺瘤合并重症肌无力（MG）的手术疗效。方法对34例胸腺瘤合并MG实施手术治疗,切除胸腺瘤及其周围胸腺组织。结果 31例术后恢复顺利,3例术后发生不同程度的MG危象。随访29例,症状完全缓解20例、部分缓解8例、无效1例。结论胸腺瘤合并MG手术治疗效果良好。     

重症肌无力64例心电图分析

目的：探讨重症肌无力（MG）的心脏损害，方法：对64例MG行心电检查。结果：心电异常率26．6％（17／64）。伴胸腺瘤与不伴胸腺瘤MG之间的心电异常率有显性差异（P＜0．05），眼肌型与全身型MG之间的心电异常率无显性差异（P＞0．05）。结论：MG伴有心脏损害，尤其是伴胸腺瘤，心电检查可提示其心脏损害。     

良恶性胸腺瘤的CT诊断及鉴别诊断

目的提高CT评价术前胸腺瘤的准确性。方法分析27例经手术、病理证实胸腺瘤的CT征象。结果良性胸腺瘤9例,肿瘤平均直径4.1cm,肿块呈类圆形7例,分叶状1例,不规则形1例,边缘清晰,脂肪间隙存在9例。恶性胸腺瘤18例,肿块平均直径9.2cm,肿块呈不规则17例,分叶状12例,13例肿块邻近脂肪间隙模糊、消失。10例包绕大血管,7例侵犯前胸壁,肺内浸润4例,心包积液4例,胸腔积液5例。结论 CT对良恶性胸腺瘤的诊断及鉴别诊断具有较高价值。     

脱氢表雄酮在体外对胸腺细胞的调节机制研究

目的 通过观察脱氢表雄酮(DHEA)对胸腺细胞凋亡及CD95/CD95配体(Fag/FagL)表达的影响,探讨在免疫系统中的作用.方法 四甲基偶氮唑盐比色分析法(MTT法)观察细胞的活力,用梯度状凝胶电泳观察细胞凋亡,反转录-聚合酶链反应(RT-PcR)法检测Fag与Fag-L的表达.结果 DHEA在体外降低胸腺细胞活力,促进细胞的凋亡,上调Fas/Fas-L mRNA的表达.结论 DHEA能通过Fas/FasL途径诱导胸腺细胞凋亡,提示DHEA可能在一些凋亡失调相关的自身免疫性疾病的发生发展中起作用.     

消化道恶性肿瘤手术切除同期大网膜移植胎胸腺临床观察

目的　观察消化道恶性肿瘤手术同期大网膜移植胎胸腺的疗效。方法　在胃、大肠恶性肿瘤手术切除的同时 ,将 16～ 2 4周胎龄水囊引产的胎儿胸腺移植于患者大网膜。术后观察患者临床表现及外周血 T细胞亚群的变化。结果　患者术后临床症状改善明显 ,CD3、CD4 、CD4 /CD8升高 (P均 <0 .0 5 ) ,CD8升高不显著。结论　消化道恶性肿瘤手术后同期大网膜移植胎胸腺不但简便 ,而且可显著提高患者免疫功能     

Balb/C小鼠免疫系统结构与功能的增龄性变化

目的 观察不同月龄Ｂａｌｂ／Ｃ小鼠免疫系统结构珉 改变,以增进对衰老免疫学机制报了解。方法 采用＾３Ｈ胸腺嘧核苷（＾３Ｈ－ＴｄＲ）掺入法,噻唑蓝（ＭＴＴ法）,白细胞介素２（ＩＬ－２）依赖细胞株（ＣＴＬＬ－２）测定等实验,检测１、５、１０和１９月龄小鼠脾细胞表面抗原表达及免疫功能,并用苏木精伊红（ＨＥ染色检测胸腺和脾脏的组织学变化。结果 随着增龄,小鼠胸腺皮、髓质比例砬小,界限消失,有分泌液泡形成,     

Inhibition of lymphocyte production via thymic factors

Summary A protein fraction capable of inhibiting both in vitro and in vivo lymphocyte DNA synthesis was purified, starting from a particle-free crude water extract of calf thymus and using selective precipitations with ethanol and ammonium sulphate. The semipurified T4-P2 fraction showed a preferential inhibitory activity in rat thymocyte DNA synthesis, and to a lesser extent in bone marrow and newborn rat liver cells. Non-hemopoietic cell types proved to be insensitive to T4-P2. In addition similar mouse tissue extracts (P2 fractions from testes, kidney, liver, and lung) had no effect on the spontaneous thymocyte proliferation indicating the tissue specific presence of the bioactive factor. PHA-induced T-lymphocyte proliferation was transitorily inhibited at the late G1 and S phase of the mitotic cell cycle. Also, this fraction proved to be active in decreasing the³H-thymidine incorporation into the thymus and spleen DNA time dependently after a single in vivo administration.A further purification of the bioactive factor from T4-P2 fraction was achieved using preparative isoelectric focusing.Two pH range proteins were found to be inhibitory in the short-term thymocyte assay system: pI 5.9 fraction inhibited the³H-thymidine incorporation into DNA by 80% at 10–20g per ml concentration. In contrast pI 4.3 fraction caused a lesser inhibitory effect. On a Sephadex G-100 column, under physiological ionicstrength and oxidative conditions pI 5.9 fraction was separated into a high and a low molecular weight inhibitory activity.The possible involvement of pI 5.9 factors and the thymosine like pI 4.3 factor in immune regulation is discussed.     

Thymus and aging: morphological, radiological, and functional overview

Aging is a continuous process that induces many alterations in the cytoarchitecture of different organs and systems both in humans and animals. Moreover, it is associated with increased susceptibility to infectious, autoimmune, and neoplastic processes. The thymus is a primary lymphoid organ responsible for the production of immunocompetent T cells and, with aging, it atrophies and declines in functions. Universality of thymic involution in all species possessing thymus, including human, indicates it as a long-standing evolutionary event. Although it is accepted that many factors contribute to age-associated thymic involution, little is known about the mechanisms involved in the process. The exact time point of the initiation is not well defined. To address the issue, we report the exact age of thymus throughout the review so that readers can have a nicely pictured synoptic view of the process. Focusing our attention on the different stages of the development of the thymus gland (natal, postnatal, adult, and old), we describe chronologically the morphological changes of the gland. We report that the thymic morphology and cell types are evolutionarily preserved in several vertebrate species. This finding is important in understanding the similar problems caused by senescence and other diseases. Another point that we considered very important is to indicate the assessment of the thymus through radiological images to highlight its variability in shape, size, and anatomical conformation.     

滋肾阴复方多糖对糖皮质激素诱导大鼠胸腺萎缩的保护作用及机制

目的观察滋肾阴中药复方总多糖对糖皮质激素导致的胸腺细胞凋亡及胸腺萎缩的保护作用。方法实验大鼠分为5组,对照组、模型组、模型＋总多糖低、中、高剂量组。模型组给予氢化可的松腹腔注射50mg／kg,连续7d。实验结束称体重、胸腺重量;分离胸腺细胞,进行流行细胞仪检测细胞凋亡;采用Westernblot检测各组大鼠胸腺的糖皮质激素受体α（GRα）、凋亡相关蛋白caspase8、caspase3的表达。结果糖皮质激素造模导致大鼠体重降低、肾上腺、胸腺重量降低;胸腺细胞凋亡率显著升高;胸腺组织GR、caspase8、caspase3表达显著升高。多糖应用之后,胸腺重量较模型组升高,胸腺细胞凋亡率较模型组下降,caspase8、caspase3的表达显著降低,但GR的蛋白表达未见有影响。结论提取自具滋肾阴功效复方的总多糖具有拮抗糖皮质激素诱导的胸腺萎缩、胸腺淋巴细胞凋亡的作用,其机制涉及下调caspase8、caspase3表达,但和GR的蛋白表达水平无关。     

Human bone marrow CD34+ progenitor cells mature to T cells on OP9-DL1 stromal cell line without thymus microenvironment

In this paper, we confirm data reported by the group of Zú?iga-Pflücker that human cord blood CD34(+)38(-)Lin- progenitor cells when co-cultured with the murine stromal cell line OP9-DL engineered to express the Notch ligand delta-like-1 mature into T lymphocytes with a phenotypic progression as the one seen in thymus. We show that this is also the case for human T cells starting from CD34(+) adolescent bone marrow cells. These findings offer the theoretical possibility to generate ex vivo human T cells and administer them in vivo in patients to overcome their immune deficient window period after transplantation. However, the practical and theoretical problems that this new technology has to overcome before this technique can be applied in clinic are still enormous and discussed.     

Primary solitary mediastinal mass lesions: a review of 37 cases

BACKGROUND: Primary solitary mass lesions of the mediastinum, although relatively uncommon, encompass an interesting spectrum of pathologies. METHODS: A comprehensive retrospective review was undertaken of all cases of mediastinal lesions that presented to the two major thoracic surgical centres in North Queensland, Australia, over a 7-year period. RESULTS: Thirty-seven mediastinal mass lesions were managed over the period of the review. Over one-quarter of all cases were clinically silent, the pathology having been discovered incidentally during investigation for other reasons. Malignant thymoma was the single most common pathology, being present in 13 (35.1%) cases. A variety of other pathologies were encountered, including thymic cyst, bronchogenic cyst, neurofibroma, parathyroid adenoma, and lymphoma. Expeditious surgical resection of the lesions, once discovered, afforded good medium-term survival, even for those patients with malignant pathology. CONCLUSIONS: Prompt thoracic surgical referral with view to aggressive, early resection optimizes clinical outcome in the short and medium-term for patients presenting with mass lesions of the mediastinum.     

Ethanol Increases Apoptotic Cell Death of Thymocytes in Vitro

Exposure of animals to ethanol causes thymic atrophy in adults and fetuses. Whether direct effects of ethanol contribute to thymic atrophy or whether indirect effects are entirely responsible is at present unknown. In the normal animal, large numbers of thymocytes undergo a physiological form of cell death referred to as "apoptosis." To determine if ethanol affects the process of apoptosis, studies were undertaken in which mouse thymocytes were cultured overnight in the presence or absence of ethanol. Apoptotic cell death was analyzed by flow cytometric quantitation of apoptotic nuclei, by fluorometric measurement of DNA fragments, and by gel electrophoretic analysis of DNA fragments. Ethanol in concentrations of 0.2% to 0.8% produced significantly higher levels of apoptosis than were seen in control cultures. The DNA fragmentation was characterized as apoptotic on the basis of inhibition by aurintricarboxylic acid (an inhibitor of nucleases) and by the presence of characteristic oligonucleosomal-sized fragments of DNA. The effect of ethanol on apoptosis was additive to that induced by immobilized anti-CD3 monoclonal antibody. CD4⁺CD8⁺ cells underwent apoptosis as indicated by reduction in CD4 and CD8 surface antigen expression. An inhibitor of protein kinases (H-7) reduced the DNA degradation induced by ethanol and by anti-CD3. These results suggest that direct effects of ethanol contribute to thymic atrophy in alcohol-consuming animals.