封面故事：急性淋巴细胞性白血病的基因病灶

利用SNP微阵列在整个基因组范围内对DNA版本数异常进行高分辩率分析的方法,被用来识别与儿童最常见的癌症-急性淋巴细胞性白血病有关的基因病灶。对来自242位患者的白血病母细胞所做的分析显示。在40%的B-先祖细胞急性淋巴细胞性白血疾病例中,为B-淋巴细胞发育的关键调控因子编码的基因发生删除、放大、点突破和结构重排等问题,     

急性白血病患者的心理干预

了解急性白血病患者的心理状态,探讨有效的心理护理方法。针对性施以相应的心理干预,消除不良心理反应,使其积极配合治疗,取得良好的效果。     

NK淋巴细胞瘤的染色体畸变分析研究

分析了自然镣伤淋巴细胞瘤（NK淋巴细胞瘤）的染色体畸变特征，采用传统的细胞遗传学和原位杂交技术相结合，检测了10例NK淋巴细胞瘤的淋巴结内瘤细胞，细胞遗传学结果发现NK淋巴瘤常见的染色体畸变有del(6q）、－7、＋X及del(lq）等，而原位杂交发现7号、X染色体超二倍体和6号染色体低二倍体发生率较高，分别为60．0％、50．0％和40．0％。由此可见，NK淋巴瘤的发生发展与染色体畸变有关，进一步寻找这些染色体上的相关基因有助于阐明NK淋巴瘤的发生机制。     

急性白血病患者的免疫活性与预后

分析了338例急性白血病非特异性免疫指标与其预后的关系。治疗后完全缓解了患者其T淋巴转化指数与总E花环率显著高于治疗前，而血清免疫球蛋白与补体C3无此改变。治疗前总E花环率、IgG及IgM正常组的完全缓解率显著高于其减低组，T淋巴转化指数正常组的中位生存期与完全缓解期较降低线组明显延长，T淋巴转移指数、总E花环率及血清C3正常组的三年连续生存率均明显高于其降低组。治疗后T淋巴转化指数与总E花环率恢复者较未恢复者的总缓解率及三年连续生存率高、中位生存期与完全缓解期显著延长。提示急性白血病的免疫活性与其预后有关。     

白血病患者ABO变异等位基因相关研究

ABO系统是最重要血型系统,迄今用分子研究法鉴定出160多个ABO等位基因。ABO^＊001是已发现最常见等位基因,其次是ABO^＊022与ABO^＊A103等位基因。白血病患者ABO基因具有高度重组活性,展现出新的ABO变异体;在白血病患者ABO基因编码区域中,ABO变异体多位于O等位基因。     

老年急性单核细胞白血病小剂量HA方案化疗的临床观察简报

目的探讨初治老年急性单核细胞白血病的小剂量化疗效果及耐受性。方法连续2个疗程小剂量HA方案诱导:高三尖杉酯碱针1mg/d,静滴,连续6～10 d;阿糖胞苷针12.5 mg/次,皮下注射,1次/12 h,连续10～14 d;当中性粒细胞低于1.5×109/L或白细胞低于2×109/L时予粒细胞集落刺激因子5 ug/kg.d支持治疗。中性粒细胞小于0.5×109/L伴高热(体温大于38.5℃)者,或血小板小于20×109/L伴内脏出血者,或患者胃肠道反应、黏膜炎明显不愿继续化疗者均予中止化疗。每2天复查1次血常规。结果 2个疗程后12例患者中有2例达完全缓解,2例部分缓解,8例无效。全部患者坚持用完2个疗程,无严重感染、出血、黏膜炎、胃肠道反应并发症,无新增脏器功能衰竭。结论小剂量HA方案化疗对初治老年急性单核细胞白血病有较好疗效,多能耐受。     

DNA断裂修复增加基因突变风险比正常合成DNA产生的基因变异高出2800倍

据美国物理学家组织网近日报道,美国印第安纳大学与普渡大学印第安纳波利斯联合分校（IUPUI）和瑞典优密欧大学（Umea University）最近的一项联合研究显示,有一种细胞用于修复自身DNA断裂的方法（称为断裂诱导复制）,比正常合成DNA产生的基因变异要高出2800倍。     

药物阻滞白血病细胞周期的研究意义

细胞周期的循环过程是由许多基因共同协作而成的,这是一个细胞物质积累与细胞分裂的循环过程。癌变的细胞以及特定阶段的胚胎细胞常常有异常的分裂周期。外源性基因,例如p16、p21、p53、Cyclins等,使白血病K562细胞周期停滞在G1期;CDKS因子会使细胞阻滞在G2/M期;UP介导通路可能使白血病细胞细胞阻滞在G2/M期,也可能在G1期发生阻滞。不同的影响因子会使白血病细胞周期阻滞在不同时期,能为治疗白血病提供更广阔的研究前景。多路径与多靶点是我们研究药物与白血病细胞周期阻滞关系的新思路。     

王振义:白血病领域的低调破冰者

"无论获得多少荣誉,无论得到多少财富,我总觉得,一个医生能够留在人间的,只能是一些好的治疗方法。"面对2010年度国家最高科学技术奖的殊荣,王振义的淡然态度一如从前。     

急性白血病的特殊临床表现及误诊分析

报告了以髓外浸润为特殊临床表现的小儿急性白血病１３例，首发症状为：骨关节、肌肉肿痛，骨折，脊柱畸形，眼球突出，黄疸，腮腺肿大．分析了引起误诊的主要原因及如何减少及避免误诊的体会，强调了早期诊断对改善小儿急性白血病预后的重要性     

Oral Nicotine Induces Oxidative Stress and Inflammation but Does Not Subvert Tumor Suppressor and DNA Repair Responses in Mice

Nicotine, responsible for the addictive properties of tobacco, is widely used in nicotine replacement therapy for tobacco use cessation. We investigated the time-dependent effect of treatment with nicotine on the tumor suppressor, DNA repair and immune responses. Swiss Albino mice (laca strain) of both sexes received nicotine dissolved at a dose of 100 µg/ml in 2% sucrose for 24 weeks, by oral gavage, while age- and gender-matched controls received only 2% sucrose for the same period. Nicotine-treated and control mice were sacrificed 6, 16 and 24 weeks post-treatment, and their tissues evaluated for alterations in histology, oxidative stress, TNF-α levels, nitric oxide (NO) and myeloperoxidase (MPO) release, tumor suppressor response and DNA repair response. Statistical significance of results was determined using Students’ t test. The tissues of nicotine treated mice exhibited a large number of multinucleated and binucleated cells, enlarged nuclei and non-uniform distribution of cells, significant increase in expression of TNF-α gene and serum TNF-α, and time-dependent significant increase in lipid peroxidation, protein carbonylation, NO and MPO release when compared to age-and gender-matched controls. The mRNA expression of the tumor suppressor gene p53, its primary regulator Mdm2, and the DNA repair genes Brca2 and Ape1 were significantly elevated, but the corresponding protein levels remained largely unaltered. In conclusion, treatment with nicotine caused oxidative stress and inflammation which can cause widespread cellular damage from the very onset of treatment, without subverting the tumor suppressor and DNA repair responses.Electronic supplementary materialThe online version of this article (10.1007/s12291-020-00903-8) contains supplementary material, which is available to authorized users.     

一氧化氮腹膜淋巴孔调控与中药治疗腹水机理探讨

目的：研究中药与一氧化氮（NO）的腹膜淋巴孔调控，探讨中药复方的消腹水机理，方法：通过扫描电镜观察和计算机图像处理定量分析，测定腹膜淋巴孔孔径、面积和开放密度，同时测定尿钠浓度。结果：（1）中药组腹膜淋巴孔孔径，面积和开放密度均增大，尿钠排出量显著增多（P＜0．01）；（2）NO供体硝普钠组腹膜淋巴孔孔径，面积和开放密度均增加（P＜0．01或P＜0．05）；（3）在给中药时，又给NO合酶抑制剂L－硝基精氨酸，腹膜淋巴孔孔径，面积及开放密度均减小（P＜0．01）。结论：本中药复方有较好的调控淋巴孔促尿钠离子排出的作用，结果提示，中药可能是通过升高内源NO浓度，舒张腹膜淋巴孔达到消腹水作用。     

中药雷公藤对外周血淋巴细胞白细胞介素－2受体表达的影响

用荧光分光光度法和间接荧光抗体法测定雷公膝多甙和根质部水煮液对外周血淋巴细胞白细胞介素－２受体表达的影响，结果表明，两种成分均能抑制ＩＬ－２Ｒ表达，抑制程度与药物剂量有关．而相同浓度下，前者比后者对ＩＬ－２Ｒ表达的抑制作用更明显．     

浅论如何提高汽修课程教学的有效性

提高汽修专业学生的知识技能水平是我们一直追寻的教学目标,基于此,笔者针对如何提高汽修课程教学的有效性,围绕以兴趣为基点、开发菜单式课程、利用数字化资源三个方面展开论述,希望通过此举能培养出更加优秀的汽修技工。     

关于修复体断裂因素及处理方法的研究

分析了修复体断裂的原因，提出了处理的方法．材料质差、基托过薄、咀嚼硬物、保养不当等是断裂的主要原因；直接法和间接法是处理断裂的主要方法。     

Preliminary studies on the detection ofMycobacterium avium-intracellulare complex using DNA probe from a clinical isolate

Genomic DNA from a clinical isolate ofMycobacterium avium-intracellulare complex was purified and cloned in PBR 322 at the tetracycline resistance site using Bam HI restriction enzyme. A 16 kb cloned fragment was purified, radiolabeled and used as a probe. Genomic DNA isolated from nineteen MAC strains, threeM. tuberculosis strains and oneM. kansasii strain were digested with Eco RI restriction enzyme, Southern blotted and hybridized with the 16 kb cloned and labeled fragment. Twelve MAC strains showed positive hybridization although five strains gave faint signals. Positive hybridization was noted in two out of the threeM. tuberculosis strains, possibly due to shared DNA homology. No signal was received from the singleM. kansasii strain used in this study.     

牡丹江市职教中心学校区域性汽修基地建设模式的探讨

牡丹江市职教中心学校在创建示范校的过程中,不断摸索建设区域汽修基地的新模式,本文从实训基地的主导思想和具体思路、实训基地的建设目标、建设情况、校企合作情况分析以及对当前学校在汽修实训基地建设中的主要问题进行分析,试图展现本校在建设汽修实训基地模式上的成果以及不足之处。     

Evaluation of Oxidative Stress and DNA Damage in Benign Prostatic Hyperplasia Patients and Comparison with Controls

In the present study, oxidative stress and lymphocytic DNA damage in both pre-op and post-op benign prostrate hyperplasia (BPH) patients with age >50 years was evaluated and compared with normal healthy subjects (controls- without any evidence of disease) of the same sex and age group. From December 2007 to November 2009, oxidative stress in 45 BPH patients were evaluated both before (pre-op patients) and after 7 days of surgery (post-op patients) in terms of measurements of plasma levels of (1) various anti-oxidative enzymes, (2) non-enzymatic antioxidants and (3) malondialdehyde which is a product of lipid peroxidation. The lymphocyte DNA damage was also evaluated by single cell alkaline gel electrophoresis in terms of tail length migration in these patients. These values were compared with their respective control subjects of similar sex and age group. The activities of antioxidant enzymes and the levels of antioxidant, reduced glutathione were found significantly decreased (p < 0.05) in serum samples of pre-operative group of BPH patients as compared to the controls. These altered parameters increased significantly (p < 0.05) and returned to their near normal control values, but not up to baseline values, in post operative patients i.e. after the cancer load was decreased by surgery. Lymphocytic DNA damage was found to be significantly increased in pre-op group as compared to controls and was reduced after surgery in post-op group. The present study therefore, shows significantly increased levels of oxidative stress and DNA damage in BPH patients which were reduced after removal of tumour load. Thus oxidative damage plays an important role in prostate tumourogenesis and timely management of oxidative stress can be of importance in preventing the occurrence of BPH.     

Genetic Variant XRCC1 rs1799782 (C194T) and Risk of Cancer Susceptibility in Indian Population: A Meta-analysis of Case–Control Studies

X-ray repair cross-complementing group 1 (XRCC1) plays a key role in the base excision repair pathway, as a scaffold protein that brings together proteins of the DNA repair complex. Several studies have reported contradictory results for XRCC1 exon 6 C>T (rs1799782) gene polymorphism and cancer risk in Indian population has provided inconsistent results. Therefore, we have performed this meta-analysis to evaluate the relationship between XRCC1 exon 6 C>T gene polymorphism and risk of cancer by published studies. We searched PubMed and Google scholar web databases to cover all studies published on association between XRCC1 exon 6 C>T gene polymorphism and cancer risk. The meta-analysis was carried out and pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to appraise the strength of association. In order to derive a more precise estimation of the association, A total of 3197 confirmed cancer cases and 3819 controls were included from eligible seventeen case-controls studies. Results from overall pooled analysis demonstrated suggested that that variant allele (T vs. C: OR 1.301, 95% CI 1.003–1.688, p = 0.047) was associated with the risk of overall cancer. Other genetic models; heterozygous (TC vs. CC: OR 1.108, 95% CI 0.827–1.485, p = 0.491), homozygous (TT vs. CC: OR 1.479, 95% CI 0.877–2.493, p = 0.142), dominant (TT+TC vs. CC: OR 1.228, 95% CI 0.899–1.677, p = 0.196) and recessive (TT vs. TC+CC: OR 1.436, 95% CI 0.970–2.125, p = 0.071) did not reveal statistical association. Publication bias observation was also considered and none was detected during the analysis. The present meta-analysis suggested that the variant allele T of XRCC1 exon 6 gene polymorphism was associated with the risk of cancer. It is therefore pertinent to confirm this finding in a large sample size to divulge the mechanism of this polymorphism and cancer risk in Indian population.