对6个国外城市街道规划设计导则的解析——“如何规划步行友好的城市街道开放空间？”

本文将“如何通过街道规划设计,营建步行友好的城市开放空间环境,提高居民生活质量？”作为研究视角,抽取了6个国外城市街道规划设计导则中与“如何规划设计步行友好的城市开放空间？”密切相关的内容,根据相关导则编制的逻辑将内容进行提炼、归纳和重组。针对中国通过改善街道步行环境建设高品质城市的诉求以及相关导则中缺少对使用者需求关注的现状,提出了将需求调查纳入规划规定环节、从环境特征角度出发进行街道分类与定位、关注地域特征与集约性生态设施的环境营造方法以及提升步行道功能多样性和空间相容性的建议。     

HIV-1 TAT-mediated protein transduction and subcellular localization using novel expression vectors

Several novel prokaryotic and eukaryotic expression vectors were constructed for protein transduction and subcellular localization. These vectors employed an N-terminal stretch of 11 basic amino acid residues (47-57) from the human immunodeficiency virus type 1 (HIV-1) TAT protein transduction domain (PTD) for protein translocation and cellular localization. The vectors also contained a six-histidine (His(6)) tag at the N- or C-terminus for convenient purification and detection, and a multiple cloning site for easy insertion of foreign genes. Some heterologous genes including HSV-TK, Bcl-rambo, Smac/DIABLO and GFP were fused in-frame to TAT PTD and successfully overexpressed in Escherichia coli. The purified TAT-GFP fusion protein was able to transduce into the mammalian cells and was found to locate mainly in the cytosol when exogenously added to the cell culture medium. However, using a transfection system, mammalian-expressed TAT-GFP predominantly displayed a nuclear localization and nucleolar accumulation in mammalian cell lines. This discrepancy implies that the exact subcellular localization of transduced protein may depend on cell type, the nature of imported proteins and delivery approach. Taken together, our results demonstrate that a TAT PTD length of 11 amino acids was sufficient to confer protein internalization and its subsequent cellular localization. These novel properties allow these vectors to be useful for studying protein transduction and nuclear import.     

Removing environmental organic pollutants with bioremediation and phytoremediation

Hazardous organic pollutants represent a threat to human, animal, and environmental health. If left unmanaged, these pollutants could cause concern. Many researchers have stepped up efforts to find more sustainable and cost-effective alternatives to using hazardous chemicals and treatments to remove existing harmful pollutants. Environmental biotechnology, such as bioremediation and phytoremediation, is a promising field that utilizes natural resources including microbes and plants to eliminate toxic organic contaminants. This technology offers an attractive alternative to other conventional remediation processes because of its relatively low cost and environmentally-friendly method. This review discusses current biological technologies for the removal of organic contaminants, including chlorinated hydrocarbons, focusing on their limitation and recent efforts to correct the drawbacks.     

Chimeric contribution of human extended pluripotent stem cells to monkey embryos ex vivo

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冬小麦不同生育时期水分亏缺胁迫对叶片保护酶系统的影响

利用盆栽试验研究了施Ｎ（底肥）与不施Ｎ条件下冬小麦不同生育时期水分有限亏缺对叶片保护酶系统的影响,结果表明,在无底肥条件下,３个生育时期水分亏缺均使保护酶系统活性有所降低,而在有底肥时酶活性多数则升高,各保护酶活性与ＭＤＡ相关分析表明,苗期ＳＯＤ活性与ＭＤＡ呈极显著负相关;拔节却是ＰＯＤ活性与ＭＤＡ呈极显著负相关;在灌浆期ＳＯＤ、ＰＯＤ、ＣＡＴ与ＭＤＡ含量均无显著相关性,但ＭＤＡ在叶片中累积至较高水平。各生育期水分处理叶片绿素含量与ＭＤＡ含量达极显著负相关。这些说明在不同生育时期,受水分亏缺和供的,保护酶系统各酶的变化有明显差异。其生理作用也有差异。     

Cell-surface-associated tissue transglutaminase is a target of MMP-2 proteolysis

MT1-MMP, a prototypic member of a membrane-type metalloproteinase subfamily, is an invasion promoting protease and an activator of MMP-2. In addition, MT1-MMP proteolysis regulates the functionality of cell-surface adhesion/signaling receptors including tissue transglutaminase (tTG). tTG is known to serve as an adhesion coreceptor for beta1/beta3 integrins and as an enzyme that catalyzes the cross-linking of proteins and the conjugation of polyamines to proteins. Here, we report that MMP-2, functioning in concert with MT1-MMP, hydrolyzes cell-surface-associated tTG, thereby further promoting the effect initiated by the activator of MMP-2. tTG, in return, preferentially associates with the activation intermediate of MMP-2. This event decreases the rate of MMP-2 maturation and protects tTG against proteolysis by MMP-2. Our cell culture, in vitro experiments, and in silico modeling indicate that the catalytic domain of MMP-2 directly associates with the core enzymatic domain II of tTG (the K(d) = 380 nM). The follow-up cleavage of the domain II eliminates both the receptor and the enzymatic activity of tTG. Our data illuminate the coordinated interplay involving the MT1-MMP/MMP-2 protease tandem in the regulation of the cell receptors and explain the underlying biochemical mechanisms of the extensive tTG proteolysis that exists at the normal tissue/tumor boundary. Our findings also suggest that neoplasms, which express functionally active MT1-MMP and, therefore, activate soluble MMP-2, can contribute to the degradation of tTG expressed in neighboring host cells. The loss of adhesive and enzymatic activities of tTG at the interface between tumor and normal tissue will decrease cell-matrix interactions and inhibit matrix cross-linking, causing multiple pathological alterations in host cell adhesion and locomotion.     

小鼠血管内膜增生模型的建立

该文主要介绍一种可以在小鼠中有效地诱导血管内膜增生的方法。该方法使用硅胶管嵌套小鼠股动脉,造成股动脉血管内膜增生。病理切片观察表明,实验组小鼠股动脉与假手术组相比出现了内膜层和中膜层不规则增厚,管腔狭窄,细胞排列紊乱,内膜炎症细胞浸润等。免疫组织化学染色显示内膜增生部分是由于血管平滑肌细胞（VsMCs）增生和基质积聚所致。该模型的建立对动脉粥样硬化病理机制研究和治疗药物的研发具有重要意义。     

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.