三点弯曲试件塑性转动因子的试验研究

通过试验及理论分析，讨论了屈服强度对三点弯曲试件塑性转动因子的影响．试验结果表明：随着屈服强度的增加，塑性转动因子增大．

低碳钢裂纹转动因子r的研究

自英国制定了DD19以来,COD这一断裂判据已得到了广泛的应用.虽然有关计算COD的公式曾有所变化,但公式中始终存在着转动因子r这个关键参量.锅炉、压力容器等是最广泛运用断裂力学规范进行工程设计和安全评定的设备,由于制造工艺、技术以及使用等方面的原因(如水压实验),这些设备的有关部位(如接管处)会发生不同程度的塑性变形.目前,在产品设计和对缺陷进行安全评定时所使用的各种断裂力学参数通常是取用未发生塑性变形的材料的.而实际上许多裂纹等缺陷是在材料发生塑性变形后产生的,因此,本文结合实验及有限元计算分析两方面来研究预应变对20g钢转动因子r的影响,这对工程实际具有一定的参考价值.

硬化指数对塑性转动因子的影响

探讨了材料的主要机械性能硬化指数对三点弯曲试作ＣＯＤ值、Ｊ积分值及塑性转动因子的影响。

CT型试样在应变疲劳中的转动因子研究

一引言 W.D.DOVER在研究应变疲劳条件下的裂纹扩展速率工作中提出了用△σ来描述da/dN规律的可能性与优点。为了实现循环变形中的全反复,他采用了TPB试样进行四点弯曲的方法。即在每半个周期后,就将试样翻转一次。所以虽然da/dN-△σ_i的定性关系被发现了,但要测定一个具体材料的定量数据,这种方法是十分不便的。如果采用CT型试样,试验将会方便得多,问题是COD方法自提出以来,由于直接地测量裂纹顶端张开位移很困难,一直都是利用三点弯曲试样的变形特征,以测量裂纹咀的张开来间接测定裂尖的张开位移。

深浅裂纹转动因子的研究

对具有贯穿深裂纹和浅裂纹的直三点弯曲试样的转动因子ｒ进行了实验研究及理论分析．结果表明，深裂纹试件转动因子ｒ值随ａｗ旦的变化不大，并与试件尺寸无关；而浅裂纹试件的转动因子ｒ值随ａｗ的增大而增加，并与材料的硬化特性有关．在三点弯曲试样加载过程中，从材料的弹性到塑性阶段，其转动因子ｒ也存在着一定的变４也规律，这对于裂纹张开位移ＣＯＤ的进一步研究，提供了参考依据①．

转动阻力因子试验在新加坡电力蓄电池双能源工程车上的应用

EN 14363定义的转动因子X是转向架安全通过曲线的一个重要性能指标,对转向架悬挂参数设计具有重要指导意义。南车株机公司在实施"走出去"的战略中,首次将转动因子试验在出口新加坡电力蓄电池双能源工程车上进行了应用,并逐步推广,对国内轨道交通技术的发展起到了很好的推动作用。

Gitelman综合征的诊断

由于Gitelman综合征(GS)与Bartter综合征(BS)的临床表现有些近似,容易将GS误诊为BS,临床对此亦引起重视.1995年Gladziwa报道成人慢性低钾血症患者27例,其中滥用利尿剂、催吐剂与泻剂的有15例,余12例均诊为BS.但经过详查后均改正诊断为GS[1].

基于LabVIEW的轨道车辆曲线模拟测控试验台

文章介绍了轨道车辆曲线模拟测控试验台的基本组成,从硬件平台、软件设计等方面较详细分析了基于LabVIEW的轨道车辆曲线模拟测控系统的开发应用。

Isolation of a Genomic DNA for Gastrodia Antifungal Protein and Analyses of Its Promoter in Transgenic Tobacco

A genomic DNA containing 5'-upstream region and complete open reading frame of a Gastrodia antifungal protein was isolated by screening of a genomic library from Gastrodia elata B1. To investigate the promoter activity, the 5'-flanking region - 1 157 lip upstream from the putative transcription start site was fused to the coding sequence of beta-glucuronidase (GUS) gene and transformed into Nicotiana tabacum. The strongest GUS activity was detected in the roots of transgenic tobacco, followed by stems. The leaves only showed a low GUS activity. Furthermore, the promoter established inducible expression pattern in transgenic tobacco upon fungus Trichoderma viride inoculation and jasmonic acid and salicylic acid treatments.

Mammalian Models Based on RCAS-TVA Technique

The retroviral vector （RCAS） has been widely used in avian system to study development and diseases, but is not suitable for mammals which do not produce the retrovirus receptor TVA. In this review, we trace the current uses of RCAS-TVA approach in mammalian system with improved strategies, including generation of tv-a transgenic mice, use of soluble TVA receptor and retroviral receptor-ligand fusion proteins, improvement of RCAS vectors, and compare a series of mammalian models in variant studies of gene function, development, oncogenesis and gene therapy. All those studies demonstrate that the RCAS-TVA based mammalian models are powerful tools for understanding the mechanisms and target treating of human diseases.

Study of Transcription Activity of X-Box Binding Protein 1 Gene in Human Different Cell Lines

Human X-box binding protein 1 （XBP1）, an important transcription factor, participates in many signal transduction processes. To further investigate the biological function of XBP1, sequences of XBP1 promoter and its two deletion mutants were first determined using bioinformatic analysis. The report vectors containing XBP1 promoter and its deletion mutants were then constructed, namely, p1-XBPlp, p2-XBPlp, and p3-XBPlp. Each reporter vector was separately transfected into HepG2, L02, K562, SMMC-7721, HSF, and Lipocyte lto Cell line using FuGENE 6 transfection reagents. The activity of chloramphenicol acetyltransferase （CAT） in each group of transfected cells was detected by ELISA assay, which in turn reflects the transcription activity of the XBP1 gene promoter. The activity involving p3-XBPlp was the highest in HepG2, which was 12.4-fold of that of pCAT3-Basic. The activities of p3-XBPlp in K562 and SMMC-7721 were the second and the third highest, which were 10.9-fold and 10.0-fold of that of the pCAT3-Basic, respectively. The CAT activity in L02 was lower than that in the above-mentioned abnormal cell, and no reporter activity was detected in HSF and Ito Cell. The XBP1 transcription and expression in K562, HepG2 and SMMC-7721 were found to be higher than that in L02, HSF and Ito cells, based on the results of real-time RT-PCR and Western blot. The XBP1 transcription and expression in L02, HSF was lower, whereas that in Ito cells was totally lacking. The result was similar to that of CAT-ELISA. Therefore, the XBP1 gene promoter can drive its downstream gene expression and its activity is cell line-dependent. The core sequence of XBP1 promoter was found between -227bp and 66bp sequence. This sequence was closely associated with the transcriptional activity of XBP1 promoter.

浅裂纹滑移线场的分析与计算

本文通过简化的三点弯曲试件滑移线场的理论分析建立了塑性转动因子γ_P、静水应力σ_H、加载处ω角、裂尖处β角四个参数的函数关系式,并讨论了浅裂纹中ω、β对σ_H和γ_P的影响。最后应用三维弹塑性有限元计算了裂尖处的σ_0,β以及加载处ω角等与塑性区的关系。

Andrographolide inhibits NF-KB activation and attenuates neointimal hyperplasia in arterial restenosis

The NF-kB transcription factors modulate the expression of tissue factor （TF）, E-selectin （CD62E） and vascular cell adhesion molecule-1 （VCAM-1）, which are essential for thrombosis and inflammation. We have previously shown that andrographolide （Andro） covalently modifies the reduced cysteine^62 of p50-a major subunit of NF-kB transcription factors, thus blocking the binding of NF-kB transcription factors to the promoters of their target genes, preventing NF-kB activation and inhibiting inflammation in vitro and in vivo. Here we report that Andro, but not its inactive structural analog 4H-Andro, significantly suppressed the proliferation of arterial neointima （-60% reduction） in a murine model of arterial restenosis. Consistently, p50^-/- mice manifested attenuated neointimal hyperplasia upon arterial ligation. Notably, the same dosage of Andro did not further reduce neointimal formation in p50^-/- mice, which implicates the specificity of Andro on p50 for treating experimental arterial restenosis. The upregulation of NF-kB target genes, including TF, E-selectin and VCAM-1, and the increased deposition of leukocytes （mainly CD68^＋ macrophages） were clearly detected within the injured arterial walls, all of which were significantly abolished by treatment with Andro or genetic deletion of p50. The expression ofTF, E-selectin and VCAM-I was also markedly upregulated in the patient sample of thrombotic vasculitis, indicating the clinical relevance of NF-kB activation in the pathogeneses of occlusive arterial diseases. Our data thus indicate that, by the downregulation of the NF-kB target genes that are critical in thrombosis and inflammation, specific inhibitors of p50, such as Andro, may be therapeutically valuable for preventing and treating thrombotic arterial diseases, including neointimal hyperplasia in arterial restenosis.

Visualization of bHLH transcription factor interactions in living mammalian cell nuclei and developing chicken neural tube by FRET

Members of the basic helix-loop-helix （bHLH） gene family play important roles in vertebrate neurogenesis. In this study, confocal microscopy-based fluorescence resonance energy transfer （FRET） is used to monitor bHLH protein-protein interactions under various physiological conditions. Tissue-specific bHLH activators, NeuroD 1, Mash 1, Neurogenin 1 （Ngn 1）, Neurogenin2 （Ngn2）, and ubiquitous expressed E47 protein are tagged with enhanced yellow fluorescence protein （EYFP） and enhanced cyan fluorescence protein （ECFP）, respectively. The subcellular localization and mobility ofbHLH fusion proteins are examined in HEK293 cells. By transient transfection and in ovo electroporation, four pairs of tissue-specific bHLH activators and E47 protein are over-expressed in HEK293 cells and developing chick embryo neural tube. With the acceptor photobleaching method, FRET could be detected between these bHLH protein pairs in the nuclei of transfected cells and developing neural tubes. Mashl/E47 and Ngn2/E47 FRET pairs show higher FRET efficiencies in the medial and the lateral half of chick embryo neural tube, respectively. It suggests that these bHLH protein pairs formed functional DNA-protein complexes with regulatory elements of their downstream target genes in the specific regions. This work will help one understand the behaviours of bHLH factors in vivo.

EXPRESSION AND LOCALIZATION OF SMAD4 PROTEIN IN RAT TESTIS DURING THE POSTNATAL DEVELOPMENT

Objective.To study expression and localiza tion of Smad4protein,the common-mediator Smad,which is one of intracellular signaling molecules of transforming growth factor-afamily,in rat t estis during postnatal development.Methods.In this study,whole testes were co llected from S.D rats aged3days,7days,14days and28days,and adult respe ctively.We examined the cellular localization and developmental change of Smad 4in rat testis by immunohistochemical ABC method with glucose oxidase-DAB-nic kel enhancement technique;the quantitative analysis of the immunostaining by t he image analysis system;the Smads pro-teins coexistence in the adult rat test is by the double immune staining for CD14-Smad4and Smad2-Smad4;the prote in expression of Smad during rat testicular development by means of Western blo ts.Results.The protein of Smad4was present in rats from3days of age to adul thood,and the im-munolocalization was exclusively localized to the cytoplasm o f Leydig cells with negative nuclei in the in-terstitial tissue at any time po int.No expression was detected in germ cells.The result of image and sta-tis tical analysis showed that generally,there was a tendency that the expression o f Smad4in the testes increased gradually with the rats developing maturation.C onclusion.Our data provide direct evidence for the molecular mechanism of TGF-aaction in rat testes during postnatal development and spermatogenesis of ra ts.

Insights into restrictive cardiomyopathy from clinical and animal studies

Cardiomyopathies are diseases that primarily affect the myocardium, leading to serious cardiac dysfunction and heart failure. Out of the three major categories of cardiomyopathies （hypertrophic, dilated and restrictive）, restrictive cardiomyopathy （RCM） is less common and also the least studied. However, the prognosis for RCM is poor as some patients dying in their childhood. The molecular mechanisms behind the disease development and progression are not very clear and the treatment of RCM is very difficult and often ineffective. In this article, we reviewed the recent progress in RCM research from the clinical studies and the translational studies done on diseased transgenic animal models. This will help for a better understanding of the mechanisms underlying the etiology and development of RCM and for the design of better treatments for the disease.

Making a tooth:growth factors,transcription factors,and stem cells

Mammalian tooth development is largely dependent on sequential and reciprocal epithelial-mesenchymal interactions. These processes involve a series of inductive and permissive interactions that result in the determination, differentiation, and organization of odontogenic tissues. Multiple signaling molecules, including BMPs, FGFs, Shh, and Wnt proteins, have been implicated in mediating these tissue interactions. Transcription factors participate in epithelial-mesenchymal interactions via linking the signaling loops between tissue layers by responding to inductive signals and regulating the expression of other signaling molecules. Adult stem cells are highly plastic and multipotent. These cells including dental pulp stem cells and bone marrow stromal cells could be reprogrammed into odontogenic fate and participated in tooth formation. Recent progress in the studies of molecular basis of tooth development, adult stem cell biology, and regene- ration will provide fundamental knowledge for the realization of human tooth regeneration in the near future.

TRANSFORMING GROWTH FACTOR-β1 AND SMAD4 SIGNALING PATHWAY DOWN-REGULATES RENAL EXTRACELLULAR MATRIX DEGRADATION IN DIABETIC RATS

Objective To investigate the role of transforming growth factor-131 （TGF-β1）/Smad4 pathway in development of renal fibrosis in streptozotocin （STZ）-induced diabetic nephropathy （DN） rats and explore its possible mechanism. Methods Male Wistar rats weighing 180-220 g were divided into 5 groups： group A （ normal control）, group B [ diabetes mellitus （DM） 2 weeks ], group C （ DM 4 weeks）, group D （ DM 8 weeks）, and group E （ DM 16 weeks）. Except for the normal control group, other groups were induced DM by single injection of STZ （55 mg/kg） respectively. Blood glucose level, serum creatinine, and 24-hour urine protein were examined. Expressions of TGF-β1 and Smad4 protein and mRNA in kidney were detected using immunohistochemical technique, Western blot, and real-time PCR. mRNA expressions of stromelysin-1 （ MMP-3 ）, tissue inhibitor of metalloproteinase-1 （ TIMP-1 ）, and collagen Ⅲ in kidney were also detected by real-time PCR. Results The levels of blood glucose, serum creatinine, and 24-hour urine protein in rats of group B, C, D, and E were higher than those of the control group. With the progression of renal fibrosis, the expressions of TGF-β1 and Smad4 protein and mRNA in kidney of diabetic rats elevated. In addition, the renal MMP-3 mRNA expression diminished in diabetic rats, while TIMP-1 and collagen Ⅲ mRNA increased. Conclusions In STZ-induced diabetic rats, the TGF-β1/Smad4 appears to play an important role in renal fibrosis of DN. The increased expression of TGF-β1 and Smad4 might result in the transcriptional regulation of downstream target genes of TGF-β1/Smad4 pathway, which contributes to the progression of renal fibrosis in diabetic rats.

Effects of interferon-alpha on expression of hepatic stellate cell and transforming growth factor-pi and a-smooth muscle actin in rats with hepatic fibrosis

AIM:To investigate the effect of interferon-a (IFN-α) on preventing or reversing hepatic fibrosis in rat experimental model induced by CCI4. METHODS: One hundred and ten Sprague-Dawley rats were divided into five groups: group A (normal controls, n = 18), group B (fibrotic model controls, n = 22), group C (IFN-α prevention, n = 22) initially treated with intramuscular injection of IFN-a in saline daily at the doses of 1× 105 U for 6 wk, group D (IFN-a treatment, n = 24) treated with intra-muscular injection of IFN-a in saline daily at the doses of 1×105 U for 6 wk after the first 6 wk, group E (0.9% sodium chloride treatment control, n = 24) treated with intra-muscular injection of 0.01 mL/kg daily for 6 wk after the first 6 wk. At the end of the experiment, all rats of each group were killed. Samples of the liver obtained by biopsy were subjected to histological, immunohistochemical and electron microscopic studies for the expressions of transforming growth factor-pi (TGF- μ41) and α-smooth muscle actin (α-SMA). RESULTS: The expressions of TGF-pl, the number of activated hepatic stellate cells and a-SMA in hepatic tissue of group C were significantly less than those of group B (P<0.01). The degree of fibrosis score in group B was also significantly less than that of group C under light microscope (P<0.01). CONCLUSION: IFN-a can inhibit the production of TGF-pl, decrease HSC activation and stimulate its apoptosis.

Negative regulation of TGF-β signaling in development

The TGF-β superfamily members have important roles in controlling patterning and tissue formation in both invertebrates and vertebrates. Two types of signal transducers, receptors and Smads, mediate the signaling to regulate expression of their target genes. Despite of the relatively simple signal transduction pathway, many modulators have been found to contribute to a tight regulation of this pathway in a variety of mechanisms. This article reviews the negative regulation of TGF-β signaling with focus on its roles in vertebrate development.