Replication error phenotype and p53 gene mutation in lymphomas of mucosa-associated lymphoid tissue.

Low grade mucosa-associated lymphoid tissue (MALT) lymphomas commonly arise from a background of chronic inflammatory lesions and can transform into high grade tumors at a late stage. Because chronic inflammation is closely associated with genetic instability, which is one of the mechanisms leading to activation of oncogenes and inactivation of tumor suppressor genes, it is possible that genetic instability plays an important role in MALT lymphomagenesis. In this study, we have examined the frequency of replication error (RER+) phenotype, a newly defined manifestation of genetic instability, and its relationship to p53 mutations in 40 MALT lymphomas (16 high grade and 24 low grade). RER+ phenotype was detected in 21/40 (52.5%) MALT lymphomas (12/24, 50% in low grade; 9/16, 56.2% in high grade). Five of seven reactive lymphoid infiltrates adjacent to tumors also showed one microsatellite alteration, four of which were identified in the corresponding lymphoma lesions in the same patient. In five RER+ high grade lymphomas with low grade lesions, homogeneous and heterogeneous microsatellite alterations were observed between the two components. The same 40 cases were investigated for p53 gene mutations at exons 5 to 8 by PCR-SSCP and direct sequencing. p53 point mutations were found in 11 (27.5%) of the 40 cases. These mutations were statistically related to RER+ phenotype (P < 0.05). Our results demonstrate that the RER+ phenotype is a common genetic feature of MALT lymphomas. Genetic instability occurs throughout the spectrum of the lymphoma development and may be related to the accumulation of genetic aberrations such as p53 mutations. The observation of identical microsatellite alterations between the adjacent lymphoid infiltrates and their corresponding lymphomas provides genetic evidence for evolutionary link of the two lesions. The homogeneous and heterogeneous microsatellite alterations observed between low and high grade components indicate their clonal lineage and genetic diversity.     

Alpha-smooth muscle actin as a marker for soft tissue tumours: a comparison with desmin

The immunoreactivity of a range of vascular and non-vascular smooth muscle tumours, rhabdomyosarcomas, and non-myoid lesions has been examined with the use of a monoclonal antibody to smooth muscle-specific actin and the muscle intermediate filament, desmin. In all cases of smooth muscle-derived tumours, the alpha-actin antibody yielded superior results. Staining of the myofibroblasts of fibromatoses was also seen. In contrast to desmin, immunoreactivity was not exhibited by rhabdomyosarcomas. We propose that this monoclonal antibody to alpha-smooth muscle actin is a useful addition to the panel of reagents used for the characterization of soft tissue proliferations and tumours. The technical aspects of the application of this monoclonal antibody to immunohistochemistry are discussed.     

低温保存内生致热原对其致热活性的影响

本实验用家兔全血加精制大肠杆菌内毒素，体外培养提取粗制家兔内生致热原。给大鼠静脉注射复制发热模型，观察了不同温度保存和不同时间保存的ＥＰ对其致热活性的影响。结果表明：４℃保存３天，－４０℃保存３天，７天，３０天和１８０天的ＥＰ与４℃保存１天的ＥＰ比较，其发热第一时相发热峰值和１小时体温反应指数均无显著性差异（Ｐ＜０．０５）。发热第二时相△Ｔ和第二时相１小时ＴＲＩ，在４℃保存３天和－４０℃保存３天，     

STAT3 couples with 14-3-3σ to regulate BCR signaling,B-cell differentiation,and IgE production

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云南省傣族G6PD一个家系的突变型研究

在调查云南少数民族Ｇ６ＰＤ缺乏症时，采用Ｇ６ＰＤ硝基四氮唑蓝纸片法筛查，按ＷＨＯ标准化方法进行生化变异型鉴定，再用错配碱基ＰＣＲ引入酶切位点法进行ＤＮＡ突变型研究，首次在傣族中发现Ｇ６ＰＤｃＤＮＡ突变型：１３８８Ｇ→Ａ。     

A novel active L1 retrotransposon subfamily in the mouse

Unlike human L1 retrotransposons, the 5' UTR of mouse L1 elements contains tandem repeats of approximately 200 bp in length called monomers. Multiple L1 subfamilies exist in the mouse which are distinguished by their monomer sequences. We previously described a young subfamily, called the T(F) subfamily, which contains approximately 1800 active elements among its 3000 full-length members. Here we characterize a novel subfamily of mouse L1 elements, G(F), which has unique monomer sequence and unusual patterns of monomer organization. A majority of these G(F) elements also have a unique length polymorphism in ORF1. Polymorphism analysis of G(F) elements in various mouse subspecies and laboratory strains revealed that, like T(F), the G(F) subfamily is young and expanding. About 1500 full-length G(F) elements exist in the diploid mouse genome and, based on the results of a cell culture assay, approximately 400 G(F) elements are potentially capable of retrotransposition. We also tested 14 A-type subfamily elements in the assay and estimate that about 900 active A elements may be present in the mouse genome. Thus, it is now known that there are three large active subfamilies of mouse L1s; T(F), A, and G(F), and that in total approximately 3000 full-length elements are potentially capable of active retrotransposition. This number is in great excess to the number of L1 elements thought to be active in the human genome.     

全髋关节置换术均衡双下肢长度的探讨

目的探讨全髋关节置换术均衡双下肢长度的临床意义和手术设计。方法回顾分析2000-2004年获得随访的单侧全髋关节置换手术病例48例,采用骨水泥型假体12髋,混合型假体36髋,术前双下肢等长30例(含股骨颈骨折患者),10例患肢长度短缩1.0-2.0cm,6例短缩2.0-4.0cm,2例短缩4.0-6.0cm。通过术前肢体长度测量及X片测量制定手术方案,选择假体、预估颈长和截骨平面;术中正确磨削髋臼,寻找最佳旋转中心,结合透视及特殊试验修正截骨平面,调节假体颈长,达到均衡双下肢长度的目的。结果全部病例采用Harris评分,优30例,良12例,中4例,差2例。术前等长30例巾术后出现5例手术侧延长1.0-2.0cm,1例延长2.5cm。术前不等长的18例中,术后恢复等长10例,6例手术侧延长1.0-2.0cm,2例术前重度短缩的先天性髋关节发育不良病人术后仍然短缩2.0-3.0cm。术后肢体等长35例Harris评分平均92.3分,术后肢体不等长13例Harris评分平均88.6分。结论全髋关节置换术的手术设计。手术技巧以及假体设计等诸多因素影响下肢长度,术后肢体不等长降低了患者的满意度。应重视术前测量及术中综合评价方法的运用,重视软组织平衡技术和肢长调节,掌握全髋置换术中均衡下肢长度的手术技术,进一步改善手术效果。     

Age-dependent and iron-independent expression of two mRNA isoforms of divalent metal transporter 1 in rat brain

The DMT1(Nramp2/DCT1) is a newly discovered proton-coupled metal-ion transport protein. The cellular localization and functional characterization of DMT1 suggest that it might play a role in physiological iron transport in the brain. In the study, we evaluated effects of dietary iron and age on iron content and DMT1 expression in four brain regions: cortex, hippocampus, striatum, substantia nigra. Total iron content in all regions was significantly lower in the low-iron diet rats and higher in the high-iron diet rats than that in the control animals, showing that dietary iron treatment for 6-weeks can alter brain iron levels. Contrary to our expectation, there was no significant alternation in DMT1(+IRE) and (-IRE) mRNA expression and protein content in all brain regions examined in spite of the existence of the altered iron levels in these regions after 6-weeks' diet treatment although TfR mRNA expression and protein level were affected significantly, as was expected. The data demonstrates that expression of DMT1(+IRE) and (-IRE) was not regulated by iron in these regions of adult rats. The lack of response of DMT1 to iron status in the brain suggests that the IRE of brain DMT1 mRNA might be not really iron-responsive and that DMT1-mediated iron transport might be not the rate-limiting step in brain iron uptake in adult rats. Our findings also showed that development can significantly affect brain iron and DMT1(+IRE) and (-IRE) expression but the effect varies in different brain regions, indicating a regionally specific regulation in the brain.     

非小细胞肺癌中p16 INK4／CDKN2基因的缺失和点突变

目的为了探讨周期素依赖性激酶４抑制因子基因（ｐ１６ＩＮＫ４）与肺癌发生的关系。方法采用双重ＰＣＲ－ＳＳＣＰ和序列分析方法，对３１例原发性非小细胞肺癌中ｐ１６ＩＮＫ４基因的存在状况进行了研究。结果３例存在ｐ１６基因缺失（３／３１），其中１例整个ｐ１６基因发生缺失，另两例则分别为外显子１和外显子２缺失；ｐ１６基因点突变２例（２／３１），外显子１和外显子２各一例；并发现在这五例基因异常样品中，４例（２例缺失和２例点突变）样品均为淋巴转移的非小细胞肺癌（４／２０）。结论提示ｐ１６基因失活和某些非小细胞肺癌（５／３１）的发生有关，并且可能发生在癌症的晚期。