南沙参多糖对亚慢性受照小鼠的抗突变作用研究

目的：研究南沙参多糖对亚慢性受照小鼠抗突变作用。方法：用^60Cγ射线全身低剂量均匀间断照射小鼠106d，累计吸收剂量为3．25Gy，检测外周血白细胞数、血小板数、睾丸精原细胞染色体畸变率、精子畸形率和骨髓嗜多染红细胞微核率。结果：辐射损伤后，外周血白细胞数、血小板数降低；染色体畸变率、精子畸形率和骨髓嗜多染红细胞微核率均增加，南沙参多糖可促进上述指标的恢复。结论：南沙参多糖对亚慢性受照小鼠损伤具有明显的保护作用，其机制与抗氧化作用有关。     

HepG2细胞染色体着丝粒点变异的研究

背景与目的:探讨HepG2瘤细胞染色体着丝粒点(Cd)的变异与其非整倍性畸变的关系.材料与方法:用Cd-NOR同步银染分析技术研究HepG2细胞染色体Cd的变异.结果:HepG2细胞染色体Cd缺失率为2.30%、Cd迟滞复制率为1.02%、小Cd率为2.58%、Cd-NOR融合率为0.64%;与正常人胚胎绒毛细胞染色体Cd变异相比较,HepG2细胞染色体Cd缺失、Cd迟滞复制和小Cd升高,而Cd-NOR融合差异无显著性.结论:HepG2细胞染色体非整倍性畸变的途径可能主要涉及Cd缺失、Cd迟滞复制、小Cd.     

Retrospective analysis of clonality and detection of residual disease in myeloid leukemia by FISH on long-term stored bone marrow smears

Abstract Background. Fluorescence in situ hybridization (FISH) has allowed the detection of numerical chromosomal aberrations in interphase nuclei on fresh or frozen smears of leukemia.
Methods. To analyze clonality and residual disease in myeloid leukemia retrospectively, we applied FISH to bone marrow smears stored at ambient temperature for up to 9 years.
Results: When hybridization efficiency was investigated on stored control smears from patients without hematological malignancy, more than 96% of nuclei showed the expected number of signals using DNA probes specific for chromosome 7, X or Y. In combination with cell morphology, we observed much higher hybridization efficiency in blasts and granulomonocytic cells compared with lymphoid and erythroid cells. On the basis of good hybridization efficiency for old smear specimens, we applied FISH to stored bone marrow smears of myeloid leukemias, in which either loss of chromosome 7 or loss of sex chromosomes had been verified previously by conventional cytogenetics (one patient with chronic myelomonocytic leukemia (CMML) and four with acute myeloid leukemia (AML; three M2 and one M7)). As a result, the loss of chromosome was detected in blasts from all patients and was observed in mature granulocytes, except in M7. In the CMML patient and one AML (M2) patient with t(8;21), lymphoid and erythroid cells also showed the loss of chromosomes, suggesting that it should occur at stem-cell level. A high amount of residual disease was detected in the morphological remission samples in one AML (M2) patient after induction therapy. The patient eventually succumbed to relapse.
Conclusion Thus, the present FISH technique is useful to analyze the clinical significance of clonality and the residual disease in myeloid leukemia, retrospectively.     

Absence of ATM truncations in patients with severe acute radiation reactions

Purpose: Severe acute toxicity limits the effective use of radiotherapy in patients who are radiosensitive, and it is not usually possible to identify these radiohypersensitive (R-H) individuals before treatment commences. Five such R-H patients were detected over a 3-year period. We undertook this study to determine whether the severe acute radiohypersensitivity of these five individuals showed any correlation with cellular and molecular parameters known to be abnormal in radiosensitivity-related syndromes such as ataxia–telangiectasia (A-T).

Methods and Materials: Lymphoblastoid cells were isolated from fresh blood from the 5 R-H individuals who had previously demonstrated clinical R-H at least 9 months prior to sampling. Lymphoblastoid cell lines (LCLs) were established to determine the extent of postradiation chromosomal aberrations, cell cycle delay, cell proliferation, and tumor suppressor p53 protein stabilization. The polymerase chain reaction (PCR) and protein truncation (PTT) assays were used to test for the possibility of mutations in the gene mutated in A-T, termed ATM.

Results: LCLs derived from R-H subjects retained a significantly higher degree of radiation-induced chromosomal aberrations when compared to normal control LCLs. p53 stabilization by ionizing radiation appeared normal in all but one R-H subject. There was no evidence of A-T gene truncation mutations in any of the R-H subjects tested.

Conclusions: All R-H subjects in this study had their cellular radiosensitivity confirmed by the chromosomal aberration assay. Delayed p53 stabilization at 4 hours postirradiation in one R-H subject suggested that different etiologies may apply in the radiohypersensitivity investigated in this study.     

丹参对丝裂霉素C诱发小鼠生殖细胞遗传损伤的防护作用研究

本文根据动物实验模型的设计，研究了中药丹参对丝裂霉素Ｃ（ＭＭＣ）诱发雄性小鼠过生殖细胞遗传损伤的防护效应。雄性昆明小鼠随机分成８组，每组１５只，实验组分别注射高、中、低剂量丹参和ＭＭＣ，观察动物的精子畸形率、早期精细胞微核率和精原细胞染色体畸变率。结果表明，中药本身无诱变损伤作用，而对ＭＭＣ有拮抗抑制作用。提出中药丹参具有抗ＭＭＣ诱发小鼠生殖细胞遗传损伤的作用。     

Asclepion波前像差仪测量低阶像差的临床应用

目的　比较运用Asclepion波前像差仪在原瞳暗视和药物散瞳两种状态下测得的低阶像差 (lowerorderwavefrontaberration) ,并将测量结果与散瞳电脑验光的屈光值相比较 ,以探讨在应用Asclepion波前像差仪时散瞳的必要性及其测量低阶像差的可靠性。 方法　随机选取来我院接受准分子激光手术的术前检查的近视患者 76例 ( 76眼 ) ,分别于原瞳暗视和药物散瞳两种状态下 ,运用Asclepion波前像差仅测定患者的波前像差 ,记录低阶像差值并对结果进行统计分析。在散瞳状态下再用NIDEK (ARK -70 0 )验光仪对患眼进行电脑自动验光。结果　散瞳前后Asclepion波前像差仪测得的低阶像差以及散瞳电脑自动验光测得的等效球镜度分期为 -6 85± 3 0 3D ,-6 73± 2 98D ,-6 66± 3 42D。三者相比 ,球镜度、柱镜度和等效球镜度的差异经单因素方差分析均没有显著性意义(P >0 0 5 )。结论　应用Asclepion波前像差仪测量眼的低阶像差 ,调节通常可以忽略 ,检查可在原瞳暗视状态下进行而无需药物散瞳。Asclepion波前像差仪测得的低阶像差能较准确的反映眼的屈光状态。     

氟吗啉诱发V79和CHL细胞基因突变和染色体畸变的研究

目的 探讨氟吗啉的致突变性。方法 首先测定氟吗啉对V79和CHL的细胞毒性，然后在非代谢活化和代谢活化条件下，进行氟吗啉诱发V79细胞HGPRT基因突变试验和CHL细胞染色体畸变试验。结果 以氟吗啉500、100、20和4μg/mL浓度处理V79细胞，处理组诱变率与阴性对照组突变率比较，差异无显著性(P≥0．05)；以500、250、125和62．5μg／mL浓度处理CHL细胞24、48h后，在非代谢活化条件下，处理组染色体畸变均小于5％，但在代谢活化条件下，处理组染色体畸变率均大于5％，而且呈剂量．反应关系，通过G-显带发现断裂集中发生于4q上，是断裂热点。结论 可以认为应用氟吗啉100～200mg／L防治植物病害不会对人类健康造成危害，但是职业人群应注意防护。     

守宫木细胞与遗传毒性实验研究

目的：以体外试验研究野生蔬菜守宫木的细胞毒性和遗传毒性。方法：生（Ⅰ）和煮熟（Ⅱ）的守宫木匀浆液分别以40000、20000、10000、5000、2500、1250μg／ml浓度对CHL细胞染毒，每一浓度分别在24、48和72h时间点以中性红摄入方法对守宫木的细胞毒性进行评定；体外染色体畸变试验则以同样的浓度分别以生和煮熟的守宫木匀浆液染毒2h后，收获细胞制备中期相，对染色体结构畸变进行分析。结果：中性红摄入细胞毒性试验：在生的与煮熟的守宫木匀浆液细胞毒性剂量效应关系分析中，低剂量组随着染毒浓度加大细胞毒性增强，而在较高剂量组则出现随染毒浓度加大细胞毒性减弱，20000和40000μg／ml剂量组出现细胞的增殖现象；时间效应分析中有和剂量效应分析相似的现象，即在低剂量组随着染毒时间的延长细胞毒性增强，而从10000μg/ml剂量组开始随着染度时间的延长细胞毒性减弱并出现细胞的增殖现象；对生的与煮熟的守宫木细胞毒性进行比较分析，仅在染毒24h的20000μg／ml剂量组发现煮熟的守宫木匀浆液的细胞毒性有统计学意义（P〈0．05）地高于生的守宫木匀浆液。体外染色体畸变试验结果阴性。结论：守宫木在一定浓度范围内对细胞溶酶体和高尔基体有一定的损伤作用，未观察到守宫木对细胞的遗传物质染色体有损害作用，未发现不同的食用习惯对守宫木的毒性有影响。     

严重少精子症、无精子症15例的大Y遗传学分析

目的:探讨大Y与严重少精子症和无精子症的遗传学关系.方法:回顾性分析有实施单精子卵胞浆内注射意向的严重少精子症和无精子症患者为研究对象.进行染色体G带与Y染色体AZF区18个微缺失位点分析.结果:严重少精子症和无精子症患者病例共260例,其中大Y 15例(5.8%),但大Y中未发现AZF微缺失.结论:严重少精子症和无精子症中有部分患者为大Y,但没有发现大Y与Y染色体AZF微缺失相关.     

子宫内膜癌染色体不稳定性研究

目的探讨子宫内膜癌染色体不稳定性。方法取21例子宫内膜癌患者外周血淋巴细胞体外常规培养、制片、GTG显带分析染色体畸变(CAR),Brdu法分化染色分析姊妹染色单体交换(SCE)、微核(MN)、核仁组织形成区(NOR)。结果内膜癌组(21例)染色体结构畸变以出现次数的多少排列为:1、3、2、5、7、8号,染色体数目、结构畸变率分别为12.86%6、.1%,SCE频率、MN率、Ag-NOR分别为7.4±1.5次/细胞(、6.6±1.9)‰、7.1±1.6个/细胞,对照组(10例)染色体数目、结构畸变率分别为3.4%、0.4%,SCE频率、MN率、Ag-NOR分别为4.8±0.6次/细胞(、2.0±0.9)‰、4.9±1.1个/细胞,内膜癌组均明显高于对照组(P<0.01)。结论子宫内膜癌病人外周血淋巴细胞染色体数目和结构畸变率增高。