腾冲嗜酸两性菌硫氧化还原酶分子结构中铁原子结合位点的新特征

前期研究表明, 铁原子对于嗜酸两性菌中硫氧化还原酶(SOR)的活性至关重要. 本研究表明, 2,2′-联吡啶、1,2-二羟基苯-3,5-二磺酸钠、8-羟基喹啉等特异性铁离子螯合剂强烈抑制腾冲嗜酸两性菌SOR酶活性, 进一步表明铁原子是SOR酶活必需. 对目前基因组数据库中的SOR基因或者SOR类似基因进行序列比对, 发现了一个潜在的铁原子结合模体(H⁸⁶-X₃- H⁹⁰-X_n-E¹¹⁴-X_n-E¹²⁹). 据此, 本研究采用定点突变技术, 将氨基酸残基H⁸⁶, H⁹⁰和E¹²⁹分别突变为苯丙氨酸或者丙氨酸, 圆二色光谱测定发现突变体(H⁸⁶F, H⁹⁰F和E¹²⁹A)的二级结构没有明显改变, 但是这3个突变体全部丧失了酶活性. 突变体蛋白中铁原子含量测定结果表明, 3个突变体全部或者部分丢失了铁原子, 而之前研究中获得的3个半胱氨酸突变体(完全丧失了酶活)铁原子含量没有变化. 根据本研究并结合前期实验结果可知, SOR分子中模体C³¹-X_n-C¹⁰¹-X₂-C¹⁰⁴是底物硫分子活化区域; 而模体H⁸⁶-X₃-H⁹⁰-X₂₃-E¹¹⁴-X_¹⁴-(E/D)¹²⁹是SOR分子中铁原子的结合区域, 与铁原子结合形成一个非卟啉铁中心, 是SOR的氧化还原中心; 这两个区域均是SOR酶活性的必需部分.     

乳腺癌血清多肽图研究

乳腺癌一直是全世界范围内威胁妇女健康的恶性疾病, 尽管人们已经进行了大量的研究以减少乳腺癌对人类的危害, 但是乳腺癌仍然是目前导致死亡的恶性肿瘤之一. 乳腺癌的早期发现对于患者的愈后与生存意义重大, 可以明显提高病人生存时间、降低病人的死亡率. 据统计, 在过去的5年里, 早期诊断每年可减少3.2%因乳腺癌死亡的患者. 然而研究表明, 目前常用的乳腺癌诊断技术, 如乳腺X射线摄影和乳房检查均无法诊断出40%的早期乳癌患者和大多数年轻女性的乳腺肿瘤. 因此在乳腺癌临床治疗中, 急需发展新型的高效诊断技术.     

GaInP/GaAs/Ge三结叠层光电池光谱响应的温度特性

利用金属有机物化学气相沉积法(MOCVD)制备了转化效率达27.1%的GaInP/GaAs/Ge三结叠层电池, 并对其光谱响应的温度特性进行了测量研究. 通过光谱响应曲线观察到各子电池的吸收边随温度升高发生红移, 这主要归因于电池材料禁带宽度的变窄效应. 根据光谱响应数据计算得到的GaInP/GaAs/Ge叠层电池各子电池在室温下的短路电流密度分别为12.9, 13.7和17 mA/cm², 且叠层电池的短路电流密度的温度系数为8.9 μA/(cm²·℃). 最后, 根据叠层电池的串联结构推导了其电压温度系数为-6.27 mV/℃.     

冷热交替治疗对肿瘤微循环的损伤及机理研究

肿瘤微循环对肿瘤生长和转移至关重要. 冷热交替治疗已被证实优于以往的单一冷疗或热疗, 其对于肿瘤微循环的损伤程度及机理是肿瘤成功治疗的关键, 但目前该方向的研究甚少. 利用裸鼠脊背皮翼肿瘤视窗模型结合激光共聚焦显微镜技术综合比较了单冷、单热及冷热交替对肿瘤微循环的损伤程度, 并建立了分析肿瘤血管在热物理作用下受力的理论模型, 通过数值计算获得了冷热交替治疗过程中肿瘤微循环血管壁的受力大小. 研究结果发现, 冷热交替造成了肿瘤微循环尤其是肿瘤中央成熟血管严重的结构性损伤. 冷热交替过程中, 血管壁先后受到迅速变化的方向相反的热应力, 有可能在血管壁形成微小裂纹. 随后加热造成的血流快速再灌注对血管壁的作用力存在应力集中现象, 推测血液流动对肿瘤血管壁的快速冲击力很可能是造成血管壁破裂的关键因素, 初步揭示了冷热交替治疗过程中肿瘤血管发生严重损伤的机理.     

大气降水中低分子有机酸的季节变化及对酸雨形成的贡献(以贵阳市和尚重镇为例)

低分子有机酸是大气中普遍存在的一种化学成分, 对酸雨的形成有重要的贡献. 西南地区是酸雨污染重灾区, 2006年4月到2007年4月用离子色谱法测定了贵阳市和尚重镇大气降水中的7种低分子有机酸. 实验结果表明: 两地大气降水中, 甲酸、乙酸和草酸是最主要的有机酸, 贵阳市其雨量加权平均值分别为14.24, 9.35和2.79 μmol/L, 而尚重镇则分别为4.95, 1.35和2.31 μmol/L. 尚重镇大气降水中低分子有机酸生长季节浓度高于非生长季节浓度, 说明植物或土壤的释放可能是尚重镇大气有机酸的主要来源; 与之相反, 贵阳市大气降水中有机酸非生长季节浓度高于生长季节浓度, 可能与该地区冬季降水次数少, 每次雨量小以及降水同时易伴随颗粒物沉降有关. 贵阳市有机酸对自由酸贡献分别为: 甲酸?7.9%, 乙酸?4.7%, 草酸?6.1%, 3种主要有机酸贡献了18.7%的自由酸; 尚重镇分别为: 甲酸?25.1%, 乙酸?7.5%, 草酸?25.5%, 有机酸对自由酸贡献为58.1%. 贵阳市降水中有机酸根占阴离子总和的1.7%~19.2%, 平均值为6.6%. 尚重镇降水中有机酸根对总阴离子的贡献为0.5%~92.2%, 平均贡献为13.2%. 由此可见, 低分子有机酸, 尤其是边远地区, 对大气降水酸化的影响不可忽视.     

建筑用铝合金的疲劳性能试验

作为一种建筑金属材料,铝合金对应力集中和裂纹比较敏感。经过固熔热处理、人工时效、挤压成型等处理后,铝合金构件的疲劳强度相对较低,抗疲劳能力差。为研究6061-T 6和6005-T 5两种典型的铝合金材料的疲劳性能,通过常规试验方法分别对这两组铝合金光滑板试件进行了轴向拉伸疲劳试验。在循环次数为104~2×106时测定了两种材料的S-N曲线。试验结果发现:铝合金的疲劳强度大致与抗拉强度成正比,抗拉强度高的疲劳强度也高。     

On-chip natural assembly of silicon photonic bandgap crystals.

Photonic bandgap crystals can reflect light for any direction of propagation in specific wavelength ranges. This property, which can be used to confine, manipulate and guide photons, should allow the creation of all-optical integrated circuits. To achieve this goal, conventional semiconductor nanofabrication techniques have been adapted to make photonic crystals. A potentially simpler and cheaper approach for creating three-dimensional periodic structures is the natural assembly of colloidal microspheres. However, this approach yields irregular, polycrystalline photonic crystals that are difficult to incorporate into a device. More importantly, it leads to many structural defects that can destroy the photonic bandgap. Here we show that by assembling a thin layer of colloidal spheres on a silicon substrate, we can obtain planar, single-crystalline silicon photonic crystals that have defect densities sufficiently low that the bandgap survives. As expected from theory, we observe unity reflectance in two crystalline directions of our photonic crystals around a wavelength of 1.3 micrometres. We also show that additional fabrication steps, intentional doping and patterning, can be performed, so demonstrating the potential for specific device applications.     

Programmable and autonomous computing machine made of biomolecules.

Devices that convert information from one form into another according to a definite procedure are known as automata. One such hypothetical device is the universal Turing machine, which stimulated work leading to the development of modern computers. The Turing machine and its special cases, including finite automata, operate by scanning a data tape, whose striking analogy to information-encoding biopolymers inspired several designs for molecular DNA computers. Laboratory-scale computing using DNA and human-assisted protocols has been demonstrated, but the realization of computing devices operating autonomously on the molecular scale remains rare. Here we describe a programmable finite automaton comprising DNA and DNA-manipulating enzymes that solves computational problems autonomously. The automaton's hardware consists of a restriction nuclease and ligase, the software and input are encoded by double-stranded DNA, and programming amounts to choosing appropriate software molecules. Upon mixing solutions containing these components, the automaton processes the input molecule via a cascade of restriction, hybridization and ligation cycles, producing a detectable output molecule that encodes the automaton's final state, and thus the computational result. In our implementation 1012 automata sharing the same software run independently and in parallel on inputs (which could, in principle, be distinct) in 120 microl solution at room temperature at a combined rate of 109 transitions per second with a transition fidelity greater than 99.8%, consuming less than 10-10 W.     

Seborrhea-like dermatitis with psoriasiform elements caused by a mutation in ZNF750, encoding a putative C2H2 zinc finger protein

We describe an Israeli Jewish Moroccan family presenting with autosomal dominant seborrhea-like dermatosis with psoriasiform elements, including enhanced keratinocyte proliferation, parakeratosis, follicular plugging, Pityrosporum ovale overgrowth and dermal CD4 lymphocyte infiltrate. We mapped the disease gene to a 0.5-cM region overlapping the PSORS2 locus (17q25) and identified a frameshift mutation in ZNF750, which encodes a putative C2H2 zinc finger protein. ZNF750 is normally expressed in keratinocytes but not in fibroblasts and is barely detectable in CD4 lymphocytes.     

Heritable germline epimutation of MSH2 in a family with hereditary nonpolyposis colorectal cancer

Epimutations in the germline, such as methylation of the MLH1 gene, may contribute to hereditary cancer syndrome in human, but their transmission to offspring has never been documented. Here we report a family with inheritance, in three successive generations, of germline allele-specific and mosaic hypermethylation of the MSH2 gene, without evidence of DNA mismatch repair gene mutation. Three siblings carrying the germline methylation developed early-onset colorectal or endometrial cancers, all with microsatellite instability and MSH2 protein loss. Clonal bisulfite sequencing and pyrosequencing showed different methylation levels in different somatic tissues, with the highest level recorded in rectal mucosa and colon cancer tissue, and the lowest in blood leukocytes. This mosaic state of germline methylation with different tissue distribution could act as the first hit and provide a mechanism for genetic disease inheritance that may deviate from the mendelian pattern and be overlooked in conventional leukocyte-based genetic diagnosis strategy.