荧光原位杂交（ f1uorescence in situ hybridization，FISH）技术是通过荧光标记的DNA探针与待测样本的DNA进行原位杂交，该技术具有快速、安全及灵敏度高等特点［1］。目前已广泛应用于细胞遗传学、基因扩增、血液疾病检测、产前诊断...荧光原位杂交（ f1uorescence in situ hybridization，FISH）技术是通过荧光标记的DNA探针与待测样本的DNA进行原位杂交，该技术具有快速、安全及灵敏度高等特点［1］。目前已广泛应用于细胞遗传学、基因扩增、血液疾病检测、产前诊断等领域。尤其在血液疾病中，对疾病的发病机制、诊断及预后提供重要的诊断依据。但由于该操作过程复杂，影响荧光信号的因素较多，因此，准确把握溶液的pH值、各步骤的温度及时间，及时发现洗涤液是否浑浊可避免出现信号弱或无信号等情况的发生［2］。标本的前期处理是 FISH检测血液疾病成功的关键，若标本处理不当，结果不易判读，其中细胞交联是影响判读的主要因素，本文就针对骨髓/血液细胞标本制片中出现的细胞交联进行改进。为骨髓/血液标本FISH检测提供最佳的制片方法。展开更多
The study used a naturally occurring crosslinking reagent-genipin to chemically modify acellular bovine pericardium, prepare cardiac valve tissue engineering scaffold material,and evaluated genipin crosslinked acellul...The study used a naturally occurring crosslinking reagent-genipin to chemically modify acellular bovine pericardium, prepare cardiac valve tissue engineering scaffold material,and evaluated genipin crosslinked acellular matrix of bovine pericardium by investigating the physical and chemical properties of the tissues, such as the surface properties, crosslinking characteristics, mechanical properties, resistance to enzymatic capacity in vitro, and hemolysis tests. The results showed that acellular bovine pericardium matrix erosslinked with genipin was strong hydrophilicity, high crosslinking index, and stable structure, which can maintain good mechanical properties. As a kind of scaffold material for valve tissue engineering, it has wide application prospect.展开更多
DNA is constantly exposed to a wide array of genotoxic agents, generating a variety of forms of DNA damage. DNA-protein crosslinks(DPCs)—the covalent linkage of proteins with a DNA strand—are one of the most deleter...DNA is constantly exposed to a wide array of genotoxic agents, generating a variety of forms of DNA damage. DNA-protein crosslinks(DPCs)—the covalent linkage of proteins with a DNA strand—are one of the most deleterious and understudied forms of DNA damage, posing as steric blockades to transcription and replication. If not properly repaired, these lesions can lead to mutations, genomic instability, and cell death. DPCs can be induced endogenously or through environmental carcinogens and chemotherapeutic agents. Endogenously, DPCs are commonly derived through reactions with aldehydes, as well as through trapping of various enzymatic intermediates onto the DNA. Proteolytic cleavage of the protein moiety of a DPC is a general strategy for removing the lesion. This can be accomplished through a DPC-specific protease and and/or proteasome-mediated degradation.Nucleotide excision repair and homologous recombination are each involved in repairing DPCs, with their respective roles likely dependent on the nature and size of the adduct. The Fanconi anemia pathway may also have a role in processing DPC repair intermediates. In this review, we discuss how these lesions are formed, strategies and mechanisms for their removal, and diseases associated with defective DPC repair.展开更多
基金National High-tech Research and Development Program(836 Prgoram) of Chinagrant number:2007AA02Z444+1 种基金National BasicProgram of China (973 Program)grant number:2009CB930000
文摘The study used a naturally occurring crosslinking reagent-genipin to chemically modify acellular bovine pericardium, prepare cardiac valve tissue engineering scaffold material,and evaluated genipin crosslinked acellular matrix of bovine pericardium by investigating the physical and chemical properties of the tissues, such as the surface properties, crosslinking characteristics, mechanical properties, resistance to enzymatic capacity in vitro, and hemolysis tests. The results showed that acellular bovine pericardium matrix erosslinked with genipin was strong hydrophilicity, high crosslinking index, and stable structure, which can maintain good mechanical properties. As a kind of scaffold material for valve tissue engineering, it has wide application prospect.
基金supported by the National Institutes of Health (CA179441, CA193124-Project 3 to Lei Li)
文摘DNA is constantly exposed to a wide array of genotoxic agents, generating a variety of forms of DNA damage. DNA-protein crosslinks(DPCs)—the covalent linkage of proteins with a DNA strand—are one of the most deleterious and understudied forms of DNA damage, posing as steric blockades to transcription and replication. If not properly repaired, these lesions can lead to mutations, genomic instability, and cell death. DPCs can be induced endogenously or through environmental carcinogens and chemotherapeutic agents. Endogenously, DPCs are commonly derived through reactions with aldehydes, as well as through trapping of various enzymatic intermediates onto the DNA. Proteolytic cleavage of the protein moiety of a DPC is a general strategy for removing the lesion. This can be accomplished through a DPC-specific protease and and/or proteasome-mediated degradation.Nucleotide excision repair and homologous recombination are each involved in repairing DPCs, with their respective roles likely dependent on the nature and size of the adduct. The Fanconi anemia pathway may also have a role in processing DPC repair intermediates. In this review, we discuss how these lesions are formed, strategies and mechanisms for their removal, and diseases associated with defective DPC repair.
