API2-MALT1融合基因变异体在粘膜相关淋巴组织结外边缘区B细胞淋巴瘤中的分布及凋亡的关系

目的探讨API2-MALT1融合基因变异体在粘膜相关淋巴组织结外边缘区B细胞淋巴瘤(extranodal marginal zone B—cell lymphoma of mucosa—associated lymphoid tissue，MALT)中的分布特点及其转录与肿瘤凋亡的关系。方法将逆转录-聚合酶链反应和巢式聚合酶链式反应结合，检测62例不同部位MALT淋巴瘤中API2-MALT1融合基因的多种变异体；通过TdT介导脱氧核苷酸缺口末端标记技术进行肿瘤细胞的原位凋亡检测；通过逆转录-聚合酶链反应和免疫组化染色检测API2的mRNA和蛋白水平。结果62例MALT淋巴瘤中28例检出API2-MALT1融合基因(45．16％)，为变异体A1446-M1123或A1446-M814，但未检出A1446-M541和A1446-M1150。A1446-M1123(18／28)的检出明显多于A1446-M814(10／28)。融和基因转录在甲状腺MALT淋巴瘤中检出最低，在其它部位的分布无差异。在API2-MALT1^ 组(API2-MALT1mRNA表达阳性组)肿瘤凋亡水平明显高于API2-MALT1^-组(API2-MALT1mRNA表达阴性组)，API2的mRNA和蛋白水平低于阴性组。A1446-M1123^ 与A1446-M814^ 病例之间凋亡和API2的变化无差异。结论MALT淋巴瘤中t(11；18)(q21；q21)的发生有部位差异，A1446-M1123可能是中国人MALT淋巴瘤中API2-MALT1融合基因变异体的主要类型。API2-MALT1融合基因转录与MALT淋巴瘤的凋亡水平和API2的变化有关。     

妇产科常见疾病与染色体核型异常的关系分析

目的 分析染色体核型异常与妇产科常见疾病的关系，探讨流产、死胎、畸胎、不孕、月经不调及青春期发育异常的遗传病因。方法 532例病例，每例行外周血培养，细胞收获，制片及G显带，并行染色体核型分析。结果 532个病例中，共检出异常核型25例，检出率为4．7％，其中异常孕产史和不孕16例，占64％，月经不调和发育异常7例，占28％，其它2例，占8％。结论 染色体核型异常是导致流产、死胎、畸胎及不孕的重要原因之一；染色体核型异常与月经不调、青少年发育异常有密切关系。     

肺淋巴管平滑肌瘤病临床病理学观察

目的 探讨肺淋巴管平滑肌瘤病临床、病理特征。方法 对5例肺淋巴管平滑肌瘤病临床资料进行收集分析,HE切片观察,采用免疫组织化学(SP法)检测平滑肌肌动蛋白(SMA)、HMB45、基质金属蛋白酶(MMP)2、孕激素受体(PR)、雌激素受体(ER),并进行文献复习。结果 肺淋巴管平滑肌瘤病是原因不明的肺部疾病,只发生在女性,特别是绝经前妇女。临床表现为呼吸困难,咯血,气胸和乳糜胸等。病理学检查显示不同成熟度平滑肌细胞在细支气管壁、肺泡壁、淋巴管壁和血管壁周围增生,肺实质呈囊性变。增生的平滑肌细胞免疫组织化学5例SMA、HMB45、MMP2均阳性;1例的ER和PR均阳性,1例仅ER阳性,1例仅PR阳性,1例的ER和PR均阴性。结论 育龄期妇女如反复出现自发性气胸、咯血、活动后呼吸困难应考虑肺淋巴管平滑肌瘤病的可能,病理检查可确定肺淋巴管平滑肌瘤病的诊断。     

体外免疫法抗MG7人源性单抗的研制及其意义

本文建立了人淋巴细胞体外致敏技术,用本文作者既往制备的鼠抗人胃癌单抗MG7作为免疫原,在体外致敏人淋巴细胞获得成功。经与本文作者在建立的人鼠种间骨髓瘤细胞系FMC-1进行人鼠人双杂交,获得一株能与鼠源性抗体反应,但不与人、羊、马、兔等其他种属动物产生的抗体相反应的人源性单抗HMG7。本文讨论了HMG7可能的应用价值,以及在人淋巴细胞体外致敏过程中应注意的几个环节。     

White matter damage precedes that in gray matter despite similar magnetic resonance imaging changes following cerebral hypoxia-ischemia in neonatal rats

We hypothesized that the cerebral injury produced by hypoxia-ischemia (HI) in neonatal rats would differ in white compared with gray matter as detected histologically or with magnetic resonance (MR) imaging methods. Maps of T₂ and the apparent diffusion coefficient (ADC) of water were acquired in 1-week-old rats at times prior to cerebral HI (right carotid artery occlusion plus 1.5 h of hypoxia), within the last 5–10 min of HI, and 1 h or 24 h after HI. Near the end of HI, ADC decreased and T₂ increased in both cortical gray and subcortical white matter within the cingulum of the HI hemisphere. One hour after HI, ADC partially recovered, but T₂ remained increased and then increased further by 24 h post-HI. In contrast to the similar MR responses in white and gray matter, histological evidence for irreversible cell damage occurred in white matter earlier than in gray matter within the HI hemisphere. At 1 h post-HI, rarefied or disrupted nerve fibers and an increase in TUNEL-positive cells were observed within white matter in the cingulum, whereas neurons within the cortical gray matter appeared normal. By 24 h post-HI, damage was apparent in both white and gray matter. Thus, MR imaging detected acute tissue edema following cerebral HI in both gray and white matter but did not distinguish between the early irreversible tissue injury detected histologically in white but not gray matter in this rather severe model of neonatal encephalopathy.     

Screening of human anti-TNF-alpha scFv from large phage library

AIM: To clone human anti-TNF-alpha scFv from large phage antibody library. METHODS: Panning of large phage library against TNF-alpha was conducted to select specific antibodies. The antigen binding activity and DNA sequence were determined and analyzed by ELISA, restriction enzyme map. RESULTS: After 4 rounds of panning, 62 positive clones were obtained and 27 clones had specific binding ability to TNF-alpha. DNA fingerprinting of the 27 clones showed 7 different stripes indicated 7 different positive clones. 5 of the 7 clones expressed soluble anti-TNF-alpha activity. DNA sequence analysis showed that the variable regions of these scFvs belonged to different subgroups. CONCLUSION: Human TNF-alpha scFv have been successfully obtained from large phage antibody library.     

纤维蛋白原Bβ链基因-1420G/A、-993C/T和-854G/A多态性与冠状动脉粥样硬化性心脏病的关联研究

目的调查健康人和冠状动脉粥样硬化性心脏病(简称冠心病)患者的纤维蛋白原B(fibrino-genB,FGB)β基因-1420G/A、-993C/T和-854G/A的基因多态性频率分布,以及与血浆Fg水平的关系。方法应用等位基因特异性PCR扩增技术和限制性片段长度多态性技术对186例冠心病患者和149名健康对照者进行分析。比浊法测定血浆Fg浓度。结果等位基因频率-1420A在冠心病组为0.33,在对照组为0.26,冠心病组明显比对照组升高,两者比较差异有统计学意义(P<0.05)。等位基因频率-993T和-854A在两组之间无差别。Logistic回归分析显示β-1420G/A与冠心病相关(OR=1.922,P=0.003)。冠心病组血浆Fg水平(3.87±1.75)g/L较健康人组(3.10±0.77)g/L明显升高,且差异有统计学意义(P<0·05)。结论纤维蛋白原Bβ-1420G/A可能与冠心病发病相关联。     

The critical role of ocular-infiltrating macrophages in the development of choroidal neovascularization

Choroidal neovascularization (CNV) is directly related to visual loss in some eye diseases, such as age-related macular degeneration. Although several human histological studies have suggested the participation of macrophages in CNV formation, the precise mechanisms are still not fully understood. In this study, we elucidated the role of ocular-infiltrating macrophages in experimental CNV using CCR2 knockout (KO) mice, wild-type mice, and C57BL/6 (B6) mice. CCR2 is the receptor of monocyte chemoattractant protein-1, and the number of infiltrating macrophage and the area of CNV were significantly reduced in CCR2 KO mice. Enriched ocular-infiltrating macrophages from B6 mice actually showed angiogenic ability in a dorsal air sac assay. Moreover, their expression of class II, CD40, B7-1 and B7-2 molecules, and the mRNA for potential angiogenic factors, such as vascular endothelial growth factor, basic fibroblast growth factor, and tumor necrosis factor alpha, was also observed. Collectively, we conclude that ocular-infiltrating macrophages play an important role in CNV generation.     

老年人脑白质疏松症血液流变性及血液成分的改变

对３８例老年脑白质疏松症（ＬＡ）患者进行了部分血液流变性和血液成分指标的测定。结果：与健康者比较，ＬＡ患者全血粘度、血浆粘度、ＲＢＣ刚性指数和聚集指数、纤维蛋白原显著增高，ＲＢＣ变形能力明显降低，血Ｈｂ、ＭＣＶ、ＭＣＨ、ＭＣＨＣ、ＲＤＷ－ＣＶ显著增高。提示：血液流变性异常和红细胞老化参与了ＬＡ的发生。设法纠正患者高粘和高凝状态、提高红细胞变形能力有益于阻止该病的进展     

单侧外周伤害性刺激诱发大鼠脊髓中转录因子CREB的双侧磷酸化(英文)

c AMP反应成分结合蛋白 (c AMP response elem ent-binding protein,CREB)是一种转录因子 ,它在磷酸化之后可调节靶基因的转录。 CREB在 13 3位置的丝氨酸的磷酸化 ,与脊髓中伤害性传入的处理有关 ,本文作者等用特殊抗体对此进行了免疫细胞化学研究。在正常大鼠 ,虽然几乎所有脊髓神经元的核中都可见 CREB的轻度着色 ,但磷酸化的 CREB仅见于双侧腰段脊髓的 ～ 层 (75± 15 vs60± 18)和 层 (9± 3 )。用福尔马林注射引起一侧后脚掌出现炎症时 ,可在双侧腰段脊髓看到磷酸化CREB细胞核的快速 (小于 5 min)和节段性的显著增多 ;它们主要分布在双侧背角表层 ～ 层 (2 5 4± 2 0 vs 2 62± 2 3 )、 层(115± 13 )和双侧 ～ 层 (3 46± 2 0 vs3 2 8± 2 6) ;而在对照和炎症组大鼠的胸段脊髓中均未见磷酸化 CREB的增加。在注射CFA诱发一侧炎症或切断一侧坐骨神经的实验组大鼠 ,也可看到至少延续到第三天的强而双侧性的 CREB的磷酸化。这种由一侧后肢伤害性传入引致腰段脊髓中镜像式双侧 CREB磷酸化的出现 ,与一般看到的损伤传入只在同侧脊髓背角引起某些神经化学改变的结果不同 ,可能是人神经损伤后或在实验动物中出现对侧镜像式疼痛过敏现象的基础