口服型HCV融合抗原DNA疫苗在小鼠诱导免疫应答

将编码一个外源信号肽、一个通用型辅助性T淋巴细胞抗原表位和HCV核心 包膜蛋白E2融合抗原基因的真核表达质粒pST CE2t(DNA疫苗 )转化到减毒鼠伤寒沙门菌SL72 0 7.将该重组菌口服接种BALB c小鼠 3次 .小鼠的抗HCV核心和E2抗体阳转率分别达 6 0 %和 70 % .体外以重组HCV核心或E2抗原刺激小鼠脾细胞 ,均使之发生明显的增殖反应 ,且小鼠脾细胞能有效杀伤表达HCV核心抗原的同系骨髓瘤细胞SP2 0 .这为研制高效免疫、成本低廉、接种方便的HCV疫苗提供了一个新的可行途径     

祁连山地区植被特征及其分布规律

分析和讨论了祁连山地区主要植被类型及其分布特征。祁连山地区随着青藏高原的强烈隆升表现为整体抬升,植被具有明显的生态地理边缘效应特征和高原地带性规律。该区植被虽然受到四周的较大影响,但各类高寒植被占有绝对优势,表现出与青藏高原植被整体明显的相似性和广泛的一致性。另一方面,本区植被也有其特殊性及与高原面存在一些差异。因此,建议把祁连山地区做为青藏高原植被区的次一级独立单元     

A Golgi-associated PDZ domain protein modulates cystic fibrosis transmembrane regulator plasma membrane expression.

We identified a novel cystic fibrosis transmembrane conductance regulator (CFTR)-associating, PDZ domain-containing protein, CAL (CFTR associated ligand) containing two predicted coiled-coiled domains and one PDZ domain. The PDZ domain of CAL binds to the C terminus of CFTR. Although CAL does not have any predicted transmembrane domains, CAL is associated with membranes mediated by a region containing the coiled-coil domains. CAL is located primarily at the Golgi apparatus, co-localizing with trans-Golgi markers and is sensitive to Brefeldin A treatment. Immunoprecipitation experiments suggest that CAL exists as a multimer. Overexpression of CAL reduces CFTR chloride currents in mammalian cells and decreases expression, rate of insertion and half-life of CFTR in the plasma membrane. The Na(+)/H(+) exchanger regulatory factor, NHE-RF, a subplasma membrane PDZ domain protein, restores cell surface expression of CFTR and chloride currents. In addition, NHE-RF inhibits the binding of CAL to CFTR. CAL modulates the surface expression of CFTR. CAL favors retention of CFTR within the cell, whereas NHE-RF favors surface expression by competing with CAL for the binding of CFTR. Thus, the regulation of CFTR in the plasma membrane involves the dynamic interaction between at least two PDZ domain proteins.     

军医大学学员坚毅性评价的内隐效应及脑电特征研究

目的:探寻军医大学学员内隐层面对自我和他人坚毅性评价的特点及脑电特征,为全面、客观的评估个体的坚毅性提供理论依据和客观指标。方法:使用E-Prime2.0参照经典内隐联想范式编制内隐联想-坚毅测验,对100名军医大学学员施测坚毅量表(Grit O),选取高、低坚毅水平被试(各20名)进行内隐联想-坚毅测验,并记录脑电,分析两组被试的内隐效应及主要脑电成分。结果:计算内隐效应D值,t检验显示高坚毅组(0.55±0.36)显著低于低坚毅组(0.87±0.49),t=-2.257,P0.05,Cohen'd=0.74。两组被试均诱发明显的N400和LPP,高坚毅组中N400在任务状态下主效应显著,F(1,17)=8.528,P0.05,η2=0.334,且在电极位置上主效应显著,F(10,170)=8.207,P0.001,η2=0.326。LPP在任务状态下主效应显著,F(1,17)=5.471,P0.05,η2=0.243,且在电极位置上主效应显著,F(10,170)=18.479,P0.001,η2=0.521;低坚毅组中N400在任务状态下主效应显著,F(1,17)=10.051,P0.05,η2=0.372,且在电极位置上主效应显著,F(10,170)=8.223,P0.001,η2=0.326,LPP在任务状态下主效应不显著。结论:1.军医大学学员坚毅性评价的内隐效应显著,即均倾向于认为自我的坚毅性高,他人的坚毅性低,通过问卷法评估坚毅性时应考虑坚毅评价的内隐效应。2.高、低坚毅性军医大学学员坚毅性内隐评价时的主要脑电成分N400、LPP存在差异,N400可作为坚毅性内隐评价符合程度的判断指标。3.内隐效应及N400可以作为对军医大学学员坚毅性评价时的客观指标。     

Downregulation of CENPF Remodels Prostate Cancer Cells and Alters Cellular Metabolism

Metabolic alterations in prostate cancer (PC) are associated with progression and aggressiveness. However, the underlying mechanisms behind PC metabolic functions are unknown. The authors’ group recently reported on the important role of centromere protein F (CENPF), a protein associated with the centromere–kinetochore complex and chromosomal segregation during mitosis, in PC MRI visibility. This study focuses on discerning the role of CENPF in metabolic perturbation in human PC3 cells. A series of bioinformatics analyses shows that CENPF is one gene that is strongly associated with aggressive PC and that its expression is positively correlated with metastasis. By identifying and reconstructing the CENPF network, additional associations with lipid regulation are found. Further untargeted metabolomics analysis using gas chromatography‐time‐of‐flight‐mass spectrometry reveals that silencing of CENPF alters the global metabolic profiles of PC cells and inhibits cell proliferation, which suggests that CENPF may be a critical regulator of PC metabolism. These findings provide useful scientific insights that can be applied in future studies investigating potential targets for PC treatment.     

Role of the sonchus yellow net virus N protein in formation of nuclear viroplasms

Sonchus yellow net virus is a plant nucleorhabdovirus whose nucleocapsid (N), phosphoprotein (P), and polymerase (L) proteins form large viroplasms in the nuclei of infected plants (C. R. F. Martins, J. A. Johnson, D. M. Lawrence, T. J. Choi, A. Pisi, S. L. Tobin, D. Lapidus, J. D. O. Wagner, S. Ruzin, K. McDonald, and A. O. Jackson, J. Virol. 72:5669-5679, 1998). When expressed alone, the N protein localizes to the nuclei of plant and yeast (Saccharomyces cerevisiae) cells and the P protein is distributed throughout the cells, but coexpression of N and P results in formation of subnuclear viroplasm-like foci (M. M. Goodin, J. Austin, R. Tobias, M. Fujita, C. Morales, and A. O. Jackson, J. Virol. 75:9393-9406, 2001; M. M. Goodin, R. G. Dietzgen, D. Schichnes, S. Ruzin, and A. O. Jackson, Plant J. 31:375-383, 2002). We now show that the N protein and various fluorescent derivatives form similar subnuclear foci in plant cells and that homologous interactions mediated by a helix-loop-helix region near the amino terminus are required for formation of the foci. Mutations within the helix-loop-helix region also interfere with N- and P-protein interactions that are required for N and P colocalization in the subnuclear foci. Affinity purification of N proteins harboring single mutations within the motif revealed that Tyr40 is critical for N-N and N-P interactions. Additional in vitro binding assays also indicated that the N protein binds to yeast and plant importin alpha homologues, whereas mutations in the carboxy-terminal nuclear localization signal abrogate importin alpha binding. The P protein did not bind to the importin alpha homologues, suggesting that the N and P proteins use different pathways for nuclear entry. Our results in toto support a model suggesting that during infection, the N and P proteins enter the nucleus independently, that viroplasm formation requires homologous N-protein interactions, and that P protein targeting to the viroplasm requires N-P protein interactions that occur after N and P protein import into the nucleus.     

扩散对破碎化景观上宿主-寄生种群动态的影响

景观破碎化和扩散是空间种群模型的重要因素,对生物入侵存在着深远的影响。本章将基于偶对近似模型,探讨由局部和全局宿主-寄生相互作用共同决定的扩散模式对破坏性景观上疾病入侵与传播的影响。其中,生境破坏由生境丧失量与生境破碎化程度来描述。模拟结果显示,宿主和病毒的全局扩散对疾病的入侵与种群密度产生不对称效应：病毒的全局扩散对系统产生的影响较宿主的全局扩散更为显著。不同扩散模式下,生境丧失越高或破碎化程度越低,均将越有害于寄生病毒的入侵;同时,生境的破坏程度也显著地影响了入侵阈值对扩散模式的响应机制。本文研究结果暗示,景观破碎化的空间分布格局以及病毒扩散的限制均可作为物种保护与管理中有效的疾病控制策略。该研究结果在一定意义上丰富和发展了寄生感染理论,为物种保护提供了生态学理论依据。     

DHP-Derivative and Low Oxygen Tension Effectively Induces Human Adipose Stromal Cell Reprogramming

Background and Methods

In this study, we utilized a combination of low oxygen tension and a novel anti-oxidant, 4-(3,4-dihydroxy-phenyl)-derivative (DHP-d) to directly induce adipose tissue stromal cells (ATSC) to de-differentiate into more primitive stem cells. De-differentiated ATSCs was overexpress stemness genes, Rex-1, Oct-4, Sox-2, and Nanog. Additionally, demethylation of the regulatory regions of Rex-1, stemnesses, and HIF1α and scavenging of reactive oxygen species were finally resulted in an improved stem cell behavior of de-differentiate ATSC (de-ATSC). Proliferation activity of ATSCs after dedifferentiation was induced by REX1, Oct4, and JAK/STAT3 directly or indirectly. De-ATSCs showed increased migration activity that mediated by P38/JUNK and ERK phosphorylation. Moreover, regenerative efficacy of de-ATSC engrafted spinal cord-injured rats and chemical-induced diabetes animals were significantly restored their functions.

Conclusions/Significance

Our stem cell remodeling system may provide a good model which would provide insight into the molecular mechanisms underlying ATSC proliferation and transdifferentiation. Also, these multipotent stem cells can be harvested may provide us with a valuable reservoir of primitive and autologous stem cells for use in a broad spectrum of regenerative cell-based disease therapy.