昆虫精子获能与顶体反应的研究

综述了近年来国内外在昆虫精子获能与顶体反应方面的研究概况,并系统地简述了昆虫精子顶体复合体基本结构,以及目前用于动物精子获能与顶体反应方面先进的方法和技术,同时对昆虫受精机理的研究进行了展望     

中祁连地块东段元古宙基底湟源群沉积构造环境

通过对中祁连地块东段元古宙基底湟源群原岩建造及其地球化学特征的研究,认为：湟源群主要由各种千枚岩、片岩、变粒岩、大理岩、石英岩和斜长角闪岩等组成的中浅变质的表壳岩组合;其原岩为一套由陆源碎屑岩、不纯碳酸盐岩、中基性大山岩等组成的火山岩沉积岩组合;湟源群中变质沉积岩系中沉积韵律、沉积条带构造的广泛发育以及浊积层的存在等,指示了其原岩建造具有复理石或类复理石建造的特征;其中变质杂砂岩的地球化学特征类似于大陆岛弧或安底斯岛弧型杂砂岩的特征;湟源群变质中基性火山岩的地球化学特征类似于岛弧或活动大陆边缘的钙碱性火山岩的特征。经综合分析得出,湟源群沉积构造环境可能为陆缘弧后盆地且靠近大陆一侧。     

极性小分子助剂对六甲基二硅氮烷改性纳米SiO2的作用机理

选择水、乙醇作为助剂,利用六甲基二硅氮烷(HMDS)在气固流化床中对纳米SiO2进行表面改性处理,采用FT—IR、TEM等多种手段表征了HMDS对纳米SiO2的改性效果。水和乙醇的引入能有效提高HMDS对纳米SiO2的改性效果及纳米SiO2的疏水程度,改善其在有机相中的分散性。极性小分子助剂在HMDS改性纳米SiO2中的作用机理分析表明：水可以促进HMDS水解。又可以补充纳米SiO2的表面羟基;乙醇一方面与纳米SiO2发生酯化反应,另一部分作为分散HMDS的溶剂。     

Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse.

Amyloid-beta peptide (Abeta) seems to have a central role in the neuropathology of Alzheimer's disease (AD). Familial forms of the disease have been linked to mutations in the amyloid precursor protein (APP) and the presenilin genes. Disease-linked mutations in these genes result in increased production of the 42-amino-acid form of the peptide (Abeta42), which is the predominant form found in the amyloid plaques of Alzheimer's disease. The PDAPP transgenic mouse, which overexpresses mutant human APP (in which the amino acid at position 717 is phenylalanine instead of the normal valine), progressively develops many of the neuropathological hallmarks of Alzheimer's disease in an age- and brain-region-dependent manner. In the present study, transgenic animals were immunized with Abeta42, either before the onset of AD-type neuropathologies (at 6 weeks of age) or at an older age (11 months), when amyloid-beta deposition and several of the subsequent neuropathological changes were well established. We report that immunization of the young animals essentially prevented the development of beta-amyloid-plaque formation, neuritic dystrophy and astrogliosis. Treatment of the older animals also markedly reduced the extent and progression of these AD-like neuropathologies. Our results raise the possibility that immunization with amyloid-beta may be effective in preventing and treating Alzheimer's disease.     

Genetic variation in the gene encoding calpain-10 is associated with type 2 diabetes mellitus

Type 2 or non-insulin-dependent diabetes mellitus (NIDDM) is the most common form of diabetes worldwide, affecting approximately 4% of the world's adult population. It is multifactorial in origin with both genetic and environmental factors contributing to its development. A genome-wide screen for type 2 diabetes genes carried out in Mexican Americans localized a susceptibility gene, designated NIDDM1, to chromosome 2. Here we describe the positional cloning of a gene located in the NIDDM1 region that shows association with type 2 diabetes in Mexican Americans and a Northern European population from the Botnia region of Finland. This putative diabetes-susceptibility gene encodes a ubiquitously expressed member of the calpain-like cysteine protease family, calpain-10 (CAPN10). This finding suggests a novel pathway that may contribute to the development of type 2 diabetes.     

The biological indication of SO2

Conclusion The biological indication approach is necessary in environmental management, and should go hand in hand with conventional analytical-chemical techniques. It is essential that the characterization of environmental quality should also include the observations of skilled biologists. If not, we are likely in the future to face many unforeseen environmental problems at a very late stage of their development. The use of biological indicators represents one aspect of the biologist's characterization of environmental quality.     

Recognition of haemagglutinins on virus-infected cells by NKp46 activates lysis by human NK cells

Natural killer (NK) cells destroy virus-infected and tumour cells, apparently without the need for previous antigen stimulation. In part, target cells are recognized by their diminished expression of major histocompatibility complex (MHC) class I molecules, which normally interact with inhibitory receptors on the NK cell surface. NK cells also express triggering receptors that are specific for non-MHC ligands; but the nature of the ligands recognized on target cells is undefined. NKp46 is thought to be the main activating receptor for human NK cells. Here we show that a soluble NKp46-immunoglobulin fusion protein binds to both the haemagglutinin of influenza virus and the haemagglutinin-neuraminidase of parainfluenza virus. In a substantial subset of NK cells, recognition by NKp46 is required to lyse cells expressing the corresponding viral glycoproteins. The binding requires the sialylation of NKp46 oligosaccharides, which is consistent with the known sialic binding capacity of the viral glycoproteins. These findings indicate how NKp46-expressing NK cells may recognize target cells infected by influenza or parainfluenza without the decreased expression of target-cell MHC class I protein.