早熟染色体凝聚最长染色体长宽比和最长与最短染色体长度比作为估算辐射剂量指标的研究

目的:用花萼海绵体诱癌素A(calyculin A,CA)诱导早熟染色体凝聚(premature chromosome condensation,PCC),探索将G<,2>/M-PCC细胞中最长染色体长宽比(L/B)和最长与最短染色体长度比(L/L)用于分析电离辐射损伤和作为估算辐射剂量指标的可行性.方法:分别用0、4、8、12、16和20 Gy(剂量率为1 Gy/min)的<'60>Coγ射线照射外周血,培养48 h后用50 nmol/L CA诱导PCC.分析各射线照射剂量组G<,2>/M-PCC指数,并进一步分析G<,2>-PCC、M-PCC中L/B和L/L值的变化,建立L/B和L/L值与射线照射剂量之间的剂量-效应曲线.结果:用CA可成功诱导人外周血淋巴细胞产生PCC,G<,2>/M-PCC指数随着照射剂量水平的增高而降低(P<0.05).G<,2>-PCC、M-PCC分裂相中的L/B和L/L值在8～20 Gy范围内显著增大(P<0.05或P<0.01),在同样照射剂量水平上L/L值较L/B值增加更快(P<0.05或P<0.01).结论:CA诱导淋巴细胞G<,2>/M-PCC中的L/B和L/L值可用于电离辐射损伤程度的测定和作为估算辐射剂量的指标.     

不同碳质气溶胶在线监测技术的实测比较研究

2009年10月31日-11月8日,用国际上应用较多的4种气溶胶在线监测仪同步监测了深圳大气细粒子中元素碳(EC)和有机物(OM)的浓度.比对结果显示:黑碳仪与单颗粒黑碳光度计测定EC有很高的相关度,R<'2>=0.97,斜率为1.00;在线EC/OC分析仪的EC监测结果与前两者的相关度R<'2>均大于0.95,但是其浓度水平总体偏低30%～40%;在线EC/OC分析仪测定的OC与气溶胶质谱仪测得的OM也比较吻合,相关度R<'2>=0.83,但是在OM高浓度时在线EC/OC分析仪的测量结果相对偏低.对造成不同在线仪器观测数据差异的因素进行了初步探讨,为研究者掌握这些在线仪器获得的高时间分辨率观测数据的准确性和差异性提供支撑信息.     

评价大鼠铜摄入量3种指标的比较研究

目的:筛选出对于铜摄入量敏感的指标,用于微量元素铜的健康影响评价.方法:灌胃给予大鼠不同剂量(0、0.033、0.169、0.829、4.146、20.73 mg/kg)葡萄糖酸铜,90d后测定大鼠血中铜含量、血中铜蓝蛋白活力及肝中铜含量,并进行比较研究.结果:随着铜摄入量的增加,各组大鼠血铜含量变化不明显,与正常对照组相比差异无统计学意义(P>0.05).相关性分析表明,大鼠血中铜蓝蛋白活力随着铜摄入量的增加而上升,铜蓝蛋白活力与铜摄入量之间呈对数正相关(R<'2>=0.984 5,P<0.05);大鼠肝铜含量随着铜摄入量的增加呈现直线上升趋势(R<'2>=0.989,P<0.05).结论:大鼠血中铜蓝蛋白活力水平及肝铜含量,均可以敏感反映出不同剂量组大鼠铜摄入水平,但血中铜蓝蛋白活力的测定方法简便,更适宜应用于大量样本的研究中评价铜摄入水平.     

草莓属植物染色体核型分析

[目的]分析二倍体野生种草莓的核型,为探讨草莓的起源、进化及遗传育种研究提供依据.[方法]对草莓属(Fragaria)植物4个二倍体种森林草莓(F.vesca L.)、纤细草莓(F.gracilis A.Los.)、黄毛草莓(F.nilgerrenis Schidl)和五叶草莓(F.pentaphylla A.Los.)进行了核型分析.[结果]纤细草莓的核型为2n=2x=14=10m+2sm+2m*,属1B类型;黄毛草莓为2n=2x=14=14m,属IA类型;五叶草莓为2n=2x=14=12m+2sm,属1A类型;森林草莓为2n=2x=14=14m,属lA类型.[结论]草莓二倍体及品种核型对称性为:黄毛草莓>森林草莓>五叶草莓>纤细草莓,供试草莓种的亲缘进化顺序可能为黄毛草莓、森林草莓、五叶草莓、纤细草莓.     

红缘短鼻蝗染色体C带核型研究(蝗总科:癞蝗科)

[目的]研究红缘短鼻蝗的染色体C带核型.[方法]利用BSG法进行显带处理,显微摄影后,测量染色体和C带带纹的相时长度,计算每条染色体异染色质的含量.[结果]红缘短鼻蝗的染色体组成为2n =19,性别决定机制是XO型,染色体全部为端着丝粒染色体,且仅具有着丝粒C带带纹.此外,异染色质在染色体组中的总含量为16.40%.[结论]该研究为癞蝗的细胞遗传学和细胞分类学提供了染色体及其显带方面的资料.     

祁连圆柏生长特性研究

[目的]为祁连圆柏的抚育改造和管理提供理论依据.[方法]对祁连山寺大隆林区的祁连圆柏林分进行调查,选择标准木进行树干解析,分析祁连圆柏林分的生长过程.[结果]树高、胸径和材积连年生长量达到峰值的时间分别是80、120和 200年.其生长遵循一定规律,自变量树高总生长量与因变量年龄的曲线模型为y=e<'(2 459 8-61.206/χ)>(R<'2>=0.982).胸径总生长量随年龄变化曲线模型为y=e<'(3.329-124.00/χ)>R<'2>=0.946),材积总生长量与年龄的回归方程为y=2.2×10<'-8>χ<'2.770 7>(R<'2>=0.994).[结论]祁连圆柏的生长遵循一定的规律.>     

Ph阴性伴Y染色体缺失的不典型慢性粒细胞白血病一例并文献复习

目的 对一例Ph阴性、bcr-abl融合基因阴性伴Y染色体缺失的不典型慢性粒细胞白血病(CML)患者进行荧光原位杂交(FISH)分析,以检测其是否存在隐蔽的bcr-abl基因重排,排除bcr-abl融合基因假阴性可能,验证其Y染色体缺失的异常核型.方法 采用位点特异性探针GLPbcr-abl(绿/红)额外信号(ES)探针检测bcr-abl基因重排;采用着丝粒探针CSP 18/CSP X/CSP Y(蓝/绿/红)检测Y染色体缺失.结果 GLP bcr-abl ES探针计数200个间期细胞,100%为两红、两绿信号,Ph染色体为阴性;着丝粒CSP 18/CSPX/CSP Y探针计数200个间期细胞,67%细胞为两蓝一绿信号,色信号丢失,存在Y染色体缺失.结合其病情特点,Y染色体缺失为后天获得性.该例Ph阴性、bcr-abl融合基因阴性伴Y染色体缺失的不典型CML患者预后差.结论 Ph阴性、bcr-abl融合基因阴性伴Y染色体缺失的不典型CML患者病情进展凶险,预后差;FISH技术检测染色体异常特异、可靠,有助于对不典型CML患者确诊,关于不典型CML患者的分子生物学本质有待进一步病例积累及研究揭示.     

紫外分光光度法测定垃圾渗滤液中的DEHP含量

[目的]建立紫外分光光度法测定垃圾渗滤液中DEHP含量的方法.[方法]以三氯甲烷为溶剂萃取50 ml垃圾渗滤液样品中的DEHP,然后利用紫外分光光度法进行测定.[结果]DEHP浓度的线性范围为30～100 mg/L,其标准曲线方程Y=0.003x+0.015 1,相关系数R<'2>=0.998 8,加标回收率为92.02%～102.93%.对标准DEHP溶液进行6次平行测定,RSD为0.045%～0.164%.[结论]该测定方法操作简便,有较高的准确度,能够满足垃圾渗滤液中DEHP含量的测定,具有一定的应用价值.     

伴3'RARα亚显微缺失的急性早幼粒细胞白血病一例

目的 报道1例伴RARα 3'-末端(3'RARα)亚显微缺失的M3r亚型急性早幼粒细胞白血病(APL)病例及其形态学、细胞遗传学、分子遗传学和分子生物学的研究结果.方法 骨髓细胞直接法和短期培养法制备染色体,应用反带技术进行核型分析;分别用CEPX/Yα-卫星DNA探针、LSI PML-RARα双色双融合探针和LSI RAR α双色断裂点分离探针进行荧光原位杂交(FISH)分析;实时定量反转录聚合酶链反应(RT-PCR)方法检测PML-RARα融合基因转录本;多重巢式RT-PCR技术检测急性白血病29种染色体畸变所形成的融合基因,包括PML-RARα,PLZF-RARα和NPM-RARα融合基因转录本.结果 反带分析显示核型为45,X,-Y[6]/46,XY[8],CEPX/Y探针FISH进一步证实了Y染色体丢失;RARα双色断裂点分离探针FISH分析显示1个RARα等位基因的整个3'-末端缺失;通过细胞遗传学、FISH以及RT-PCR等方法检测,排除PML-RARα、PLZF-RARα、NPM-RARα、NuMA-RARα和STAT5b-RARα重排.结论 识别APL中一种新的RARα基因重排类型(3'RARα亚显微缺失而无X-RARα融合),RARα双色断裂点分离探针FISH分析是明确该异常的有效手段,其分子学结果有待进一步阐明.     

哈巴河县打瓜产量与气象因子的关系及产量预测

利用哈巴河县2000～2008年5～9月打瓜生育期间的气象资料,采用线性回归方法,得到打瓜气象产量和温度、降水、湿度、地湿4个因子呈显著相关特性.逐步回归后建立打瓜产量预测的数学模型:Y = 2 262.677-42.639X1-12.309X2+68.710X3+3.795X4,经检验其平均偏差为0.69%,可知预测模型较准确,能满足业务要求.     

Screening for chromosomal abnormality

PURPOSE: To investigate if stents with hooks and barbs will improve stent-graft fixation in the abdominal aorta. METHODS: Sixteen- to 24-mm-diameter Dacron grafts were deployed inside cadaveric aortas. The grafts were anchored by stents as in endovascular abdominal aortic aneurysm repair. One hundred thirty-seven stent-graft deployments were carried out with modified self-expanding Z-stents with (A) no hooks and barbs (n = 75), (B) 4 5-mm-long hooks and barbs (n = 39), (C) 8 10-mm-long, strengthened hooks and barbs (n = 19), or (D) hooks only (n = 4). Increasing longitudinal traction was applied to determine the displacement force needed to extract the stent-grafts. The radial force of the stents was measured and correlated to the displacement force. RESULTS: The median (interquartile range) displacement force needed to extract grafts anchored by stent A was 2.5 N (2.0 to 3.4), stent B 7.8 N (7.4 to 10.8), and stent C 22.5 N (17.1 to 27.9), p < 0.001. Both hooks and barbs added anchoring strength. During traction, the weaker barbs were distorted or caused intimal tears. The stronger barbs engaged the entire aortic wall. The radial force of the stents had no impact on fixation, while aortic calcification and graft oversizing had marginal effects. CONCLUSIONS: Stent barbs and hooks increased the fixation of stent-grafts tenfold, while the radial force of stents had no impact. These data may prove important in future endograft development to prevent stent-graft migration after aneurysm exclusion.     

Revised estimates of enterococcal chromosomal sizes

We previously reported that the chromosomal sizes of four strains of enterococci ranged from 2,045 to 2,761 kb. Extensive analysis and mapping subsequently confirmed the size of Enterococcus faecalis strain OG1 as 2,825 kb (prior size estimate range, 2,750-2,761 kb) (Murray et al., J. Bacteriol. 175, 5216, 1993). However, using variable conditions of electrophoresis and additional digestions, revised size estimates for the other strains are 2,852-3,093 kb for E. faecalis strain JH2-2 (prior range, 2,008-2,135 kb), 2,910-3,065 kb for E. faecalis strain HH67 (prior range, 2,170-2,288 kb), and 2,334-2,558 for E. faecium strain GE-1 (prior range, 2,045-2,155 kb). The earlier underestimations of the chromosomal sizes were due to the inconsistent presence of a large fragment, likely caused by shearing of the DNA during handling, causing it to be considered a partial digestion product, and failure to resolve multiple fragments of the same approximate size.     

Mechanisms of the origin of chromosomal aberrations

The most probable factor connecting premature infant problems such as retinopathy, intraventricular hemorrhage and chronic lung disease appears to be the excessive production of oxygen free radicals which can occur as a consequence of oxygen therapy. The aim of our investigation was to elucidate the possible correlations between lipid peroxidation, in this study measured as hydroperoxides production, and antioxidant concentrations in erythrocyte membranes of both full term and preterm infants. Hydroperoxide concentrations were found to be high, especially in premature infants, in erythrocyte membranes at birth and in the initial days of life. The erythrocyte membranes were also found to contain low levels and/or low activities of antioxidant defense mechanisms which was more evident in premature newborns where alpha-tochopherol levels were significantly lower in comparison to full term infant levels. Furthermore, when premature infants undergo oxygen therapy these effects were exacerbated. These results demonstrate that at birth, particularly in the premature newborn, the degree of oxidative stress outweighs the antioxidant defense mechanisms.     

Involvement of telomeric sequences in chromosomal aberrations

The genomes of higher eukaryotes are not homogeneous in terms of structure or function. Many examples of chromosomal regions particularly prone to involvement in aberrations have been reported. The molecular structures of some of these regions have now been determined, most notably the folate-sensitive fragile sites and FRA16B-a distamycin A-sensitive fragile site. In addition, a number of cytological studies suggest that telomeric sequences can in some circumstances be involved in chromosomal aberrations more frequently than expected. Here, the roles of telomeric DNA sequences, both terminal and interstitial, and telomerase in chromosomal aberration formation are reviewed.     

A chromosomal deletion map of human malformations

Malformations are common causes of pediatric morbidity and mortality, and genetic factors are a significant component of their etiology. Autosomal deletions, in almost all cases, cause a nonspecific embryopathy that presents after birth as growth failure, mental retardation, and multiple malformations. We have constructed a chromosome map of autosomal deletions associated with 47 different congenital malformations, using detailed clinical and cytogenetic information on 1,753 patients with nonmosaic single contiguous autosomal deletions. The 1,753 deletions involved 258 (89%) of 289 possible autosomal bands (by the use of ISCN 400-band nomenclature), giving a total of 4,190 deleted autosomal bands for analysis. We compared the band distributions of deletions associated with common major malformations with the distribution of all 1,753 deletions. We noted 283 positive associations between deleted bands and specific malformations, of which 199 were significant (P<.05, P>.001) and 84 were highly significant (P<.001). These "malformation-associated bands" (MABs) were distributed among 137 malformation-associated chromosome regions (MACRs). An average of 6 MABs in 2.9 MACRs were detected per malformation studied; 18 (6%) of 283 MABs contain a locus known to be associated with the particular malformation. A further 18 (6%) of 283 are in seven recognized specific malformation-associated aneuploid regions. Therefore, 36 (26%) of 137 of the MACRs contain an MAB coinciding with a previously recognized locus or malformation-associated aneuploid region. This map should facilitate identification of genes important in human development.     

Mitotic chromosomal anomalies among 1210 infertile men

Detailed medical and clinical examinations were carried out on 1608 men attending an infertility clinic to determine if any of those exhibiting abnormal semenograms also had any other readily identifiable clinical condition. In all, 1210 men showed abnormal semenograms according to World Health Organization criteria. Karyotyping of the white blood cells in these 1210 men revealed 44 (3.6%) individuals with either autosomal or sex chromosomal aberrations. However, no single characteristic feature of their semenogram or clinical condition was of any diagnostic value to predict the existence of a chromosomal anomaly.     

Radiation induced chromosomal instability in human T-lymphocytes

Rats transgenic for HLA-B27 and human beta 2-microglobulin develop a spontaneous, multisystem, inflammatory disease that resembles human B27-associated disease and that involves the gut mucosa. This model predominantly affects the colon and is characterized by an extensive infiltration of the mucosa by inflammatory cells, largely composed of mononuclear cells. In addition, an increased plasma level of nitric oxide (NO)-derived metabolites was described in this model. Deficiency in the anti-inflammatory cytokine, interleukin-10 (IL-10), leads to the development of colitis in IL-10 knockout mice, suggesting that IL-10 plays a major role in the control of gut inflammation. The objectives of this work were to study the mechanisms of the inflammatory bowel disease (IBD) in HLA-B27 rats and to determine the effects of treatment with IL-10. The 33-3 line of HLA-B27 recombinant rats with established disease was treated in two consecutive experiments with murine recombinant IL-10 for five weeks. Assessment of the effect of this treatment was performed, based on clinical, histological and biological (myeloperoxidase and inducible NO synthase activities; tumor necrosis factor-alpha, interferon-delta, CD3, iNOS and beta-actin mRNA expression. In 33-3 rats with established disease, mesenteric lymph nodes were hyperplastic, and colonic cellularity and MPO and iNOS activities in the colonic mucosa were increased without any detectable effects of IL-10 administration. IFN-gamma and iNOS mRNA were only detected in the colon of transgenic rats. Despite a lack of effect on disease expression, IL-10 strikingly reduced the level of IFN-gamma mRNA in gut mucosa. Up-regulation of IFN-gamma mRNA suggests that the IBD of HLA-B27 rats is mediated by T-helper 1 lymphocytes. Sustained administration of IL-10, in HLA-B27 rats with established disease, efficiently inhibited IFN-gamma mRNA expression but did not influence disease expression: these results indicate that IFN-gamma may exert a critical role at an earlier stage of the disease rather in the maintenance of the lesions.     

Amino-terminal arginylation of chromosomal proteins by arginyl-tRNA

Arginine was transferred from arginyl-tRNA to the amino-terminal end of chromatin proteins by L-arginyl-transferase. The reaction was dependent on the presence of potassium ion and beta-mercaptoethanol and was sensitive to RNase and trypsin. Treatment with DNase partially inhibited the transfer of arginine from arginyl-tRNA suggesting that intact chromatin structure is necessary for modification of chromatin. The radioactivity incorporated into chromatin was sensitive to trypsin but not to DNase or RNase. Most of the incorporated radioactivity was recovered in the phenol fraction, supporting the notion that modification of chromatin takes place in proteins but not in nucleic acids of chromatin. Modification of the proteins by transfer of arginine from arginyl-tRNA takes place mainly in the nonhistone fraction of chromatin. Major portions of chromosomal proteins modified in this manner appear to be released from chromatin. Incubation of incorporated radioactive product with [12C]arginyl-tRNA did not alter the product, showing that incorporated arginine is stable and does not exchange with added arginine or arginyl-tRNA. These observations suggest that aminoacyl-transferase may function in the modification of chromosomal proteins and that modification of chromatin may alter the regulatory mechanisms of cellular functions.     

Diagnosis of genetic defects by chromosomal analysis

Of 901 karyotypes performed over a period of 4 years, genetic anomalies were detected in 162 cases. Down's syndrome (trisomy 21) was the most common (168.8%) genetic disorder followed by Turner's syndrome, Philadelphia chromosome, Klinefelter's syndrome, Edward's syndrome (trisomy 18) and Patau's syndrome (trisomy 13). All the three trisomies were detected very early in life. Mean age at the time of diagnosis for Turner's syndrome was 13.3 years, allowing a timely hormone replacement therapy to improve secondary sexual characters. Patients with Klinefelter's syndrome were diagnosed late (mean age 23.6 years), which greatly reduced their chances of an effective therapy to improve the clinical and social outcome.