Substructuring Method in Structural Health Monitoring

In sensitivity-based finite element model updating, the eigensolutions and eigensensitivities are calculated repeatedly, which is a time-consuming process for large-scale structures. In this chapter, a forward substructuring method and an inverse substructuring method are proposed to fulfill the model updating of large-scale structures. In the forward substructuring method, the analytical FE model of the global structure is divided into several independent substructures. The eigensolutions of each independent substructure are used to recover the eigensolutions and eigensensitivities of the global structure. Consequently, only some specific substructures are reanalyzed in model updating and assembled with other untouched substructures to recover the eigensolutions and eigensensitivities of the global structure. In the inverse substructuring method, the experimental modal data of the global structure are disassembled into substructural flexibility. Afterwards, each substructure is treated as an independent structure to reproduce its flexibility through a model-updating process. Employing the substructuring method, the model updating of a substructure can be conducted by measuring the local area of the concerned substructure solely. Finally, application of the proposed methods to a laboratory tested frame structure reveals that the forward and inverse substructuring methods are effective in model updating and damage identification

Study on the Road Network Connectivity Reliability of Valley City Based on Complex Network

Based on the research progress in related fields and the distribution characteristics of road networks in valley cities, the complex network model of a city road network is established to study its connectivity reliability. Taking Lanzhou as the example, several parameters of the complex network abstracted from the road network are calculated and the practical meanings of them are described, respectively. On this basis, through computing the global efficiency and the relative size of the largest connecting subgraph under intentional attacks and random attacks, respectively, the curves of the above two parameters varying with the attacking times are drawn. The detailed investigation of connectivity reliability of Lanzhou road network is done by analyzing the curves’ tendency. Finally, we find that the network of a valley city has a poor connection and has a lot of dead ends. Besides, the average length of the roads is very long and the holistic connectivity reliability is at a lower level; these are suitable to the group-type distribution of valley city’s road network, and the connectivity reliability of the road network is stronger under random attacks than that under intentional attacks

Activation of the Extracellular Signal-Regulated Kinase Signaling Is Critical for Human Umbilical Cord Mesenchymal Stem Cell Osteogenic Differentiation

Human umbilical cord mesenchymal stem cells (hUCMSCs) are recognized as candidate progenitor cells for bone regeneration. However, the mechanism of hUCMSC osteogenesis remains unclear. In this study, we revealed that mitogen-activated protein kinases (MAPKs) signaling is involved in hUCMSC osteogenic differentiation in vitro. Particularly, the activation of c-Jun N-terminal kinases (JNK) and p38 signaling pathways maintained a consistent level in hUCMSCs through the entire 21-day osteogenic differentiation period. At the same time, the activation of extracellular signal-regulated kinases (ERK) signaling significantly increased from day 5, peaked at day 9, and declined thereafter. Moreover, gene profiling of osteogenic markers, alkaline phosphatase (ALP) activity measurement, and alizarin red staining demonstrated that the application of U0126, a specific inhibitor for ERK activation, completely prohibited hUCMSC osteogenic differentiation. However, when U0126 was removed from the culture at day 9, ERK activation and osteogenic differentiation of hUCMSCs were partially recovered. Together, these findings demonstrate that the activation of ERK signaling is essential for hUCMSC osteogenic differentiation, which points out the significance of ERK signaling pathway to regulate the osteogenic differentiation of hUCMSCs as an alternative cell source for bone tissue engineering. Copyright © 2016 Chen-Shuang Li et al

Sphingosine kinase 2 activates autophagy and protects neurons against ischemic injury through interaction with Bcl-2 via its putative BH3 domain

Our previous findings suggest that sphingosine kinase 2 (SPK2) mediates ischemic tolerance and autophagy in cerebral preconditioning. The aim of this study was to determine by which mechanism SPK2 activates autophagy in neural cells. In both primary murine cortical neurons and HT22 hippocampal neuronal cells, overexpression of SPK2 increased LC3II and enhanced the autophagy flux. SPK2 overexpression protected cortical neurons against oxygen glucose deprivation (OGD) injury, as evidenced by improvement of neuronal morphology, increased cell viability and reduced lactate dehydrogenase release. The inhibition of autophagy effectively suppressed the neuroprotective effect of SPK2. SPK2 overexpression reduced the co-immunoprecipitation of Beclin-1 and Bcl-2, while Beclin-1 knockdown inhibited SPK2-induced autophagy. Both co-immunoprecipitation and GST pull-down analysis suggest that SPK2 directly interacts with Bcl-2. SPK2 might interact to Bcl-2 in the cytoplasm. Notably, an SPK2 mutant with L219A substitution in its putative BH3 domain was not able to activate autophagy. A Tat peptide fused to an 18-amino acid peptide encompassing the native, but not the L219A mutated BH3 domain of SPK2 activated autophagy in neural cells. The Tat-SPK2 peptide also protected neurons against OGD injury through autophagy activation. These results suggest that SPK2 interacts with Bcl-2 via its BH3 domain, thereby dissociating it from Beclin-1 and activating autophagy. The observation that Tat-SPK2 peptide designed from the BH3 domain of SPK2 activates autophagy and protects neural cells against OGD injury suggest that this structure may provide the basis for a novel class of therapeutic agents against ischemic stroke

Influence of Reducing Agents on Biosafety and Biocompatibility of Gold Nanoparticles

Extensive biomedical applications of nanoparticles are mainly determined by their safety and compatibility in biological systems. The aim of this study was to compare the biosafety and biocompatibility of gold nanoparticles (GNPs) prepared with HEPES buffer, which is popular for cell culture, and sodium citrate, a frequent reducing agent. From experimental results on the body weight and organ coefficients of acute oral toxicity tests, it could be observed that HEPES-prepared GNPs are biologically safer than citric-prepared GNPs at the same dose of 500 μg/kg. The in vitro cell viability was higher for HEPES-prepared GNPs than citric-prepared GNPs at 5.0- and 10.0-ug/mL concentrations. More reactive oxygen species (ROS) were generated in the cell suspension when supplemented with citric-prepared GNPs than HEPES-prepared GNPs when their concentrations were higher than 20 μg/mL. The results stated that HEPES-prepared GNPs had better biosafety and biocompatibility than citric-prepared GNPs. This study not only revealed the influence of reducing agent on biosafety and biocompatibility of nanomaterials but also provided accumulative evidence for nanomaterials in biomedical applications. [Figure: see text

{6,6′-Dimeth­oxy-2,2′-[4-bromo-o-phenyl­enebis(nitrilo­methyl­idyne)]diphenolato}nickel(II) methanol solvate

In the title compound, [Ni(C22H17BrN2O4)]·CH3OH, the NiII ion is in a slightly distorted square-planar geometry involving an N2O2 atom set of the tetra­dentate Schiff base ligand. The asymmetric unit contains one nickel complex and one methanol solvent mol­ecule. The dihedral angle between the aromatic ring planes of the central aromatic ring and other two aromatic rings are 10.8 (3) and 6.0 (2)°. The crystal structure is stabilized by inter­molecular C—H⋯O and C—H⋯Br and by intra­molecular O—H⋯O hydrogen bonds

Bioinformatic analysis of the human DHRS4 gene cluster and a proposed mechanism for its transcriptional regulation

<p>Abstract</p> <p>Background</p> <p>The human <it>DHRS4 </it>gene cluster consists of three genes, <it>DHRS4</it>, <it>DHRS4L2 </it>and <it>DHRS4L1</it>. Among them, <it>DHRS4 </it>encodes NADP(H)-dependent retinol dehydrogenase/reductase. In a previous study, we investigated the alternative splicing of <it>DHRS4 </it>and <it>DHRS4L2</it>. <it>DHRS4L1 </it>was added to the gene cluster recently, but little is known about its structure and expression. To reveal the regulatory mechanism of the <it>DHRS4 </it>gene cluster expression, we studied the structure and transcription of <it>DHRS4L1 </it>in the context of the transcriptional behaviors of the human <it>DHRS4 </it>gene cluster. Based on the results of bioinformatics analysis, we propose a possible mechanism for the transcriptional regulation of the human <it>DHRS4 </it>gene cluster.</p> <p>Results</p> <p>The homologous comparison analysis suggests that <it>DHRS4</it>, <it>DHRS4L2 </it>and <it>DHRS4L1 </it>are three homologous genes in human. <it>DHRS4L1 </it>and <it>DHRS4L2 </it>are paralogues of <it>DHRS4</it>, and <it>DHRS4L2 </it>is the most recent member of the <it>DHRS4 </it>gene cluster. In the minus strand of the human <it>DHRS4 </it>gene cluster, a gene transcribed in an antisense direction was found containing a 5' sequence overlapping the region of exon 1 and promoter of <it>DHRS4</it>. By cloning the full length of RNA variants through 5'RACE and 3'RACE, we identified two transcription start sites, within exon <it>a2 </it>and exon 1, of this newly named gene <it>DHRS4L1 </it>using neuroblastoma cell line BE(2)-M17. Analysis of exon composition in the transcripts of <it>DHRS4 </it>gene cluster revealed that exon 1 was absent in all the transcripts initiated from exon <it>a1 </it>of <it>DHRS4L2 </it>and exon <it>a2 </it>of <it>DHRS4L1</it>.</p> <p>Conclusions</p> <p>Alternatively spliced RNA variants are prevalent in the human <it>DHRS4 </it>gene cluster. Based on the analysis of gene transcripts and bioinformatic prediction, we propose here that antisense transcription may be involved in the transcriptional initiation regulation of <it>DHRS4 </it>and in the posttranscriptional splicing of <it>DHRS4L2 </it>and <it>DRHS4L1 </it>for the homologous identity of <it>DHRS4 </it>gene cluster. Beside the alternative transcriptional start sites, the antisense RNA is novel possible factor serving to remove exon 1 from the transcripts initiated from exon <it>a1 </it>and exon <it>a2</it>.</p

Mitigation of chronic unpredictable stress–induced cognitive deficits in mice by Lycium barbarum L (Solanaceae) polysaccharides

Purpose: To investigate the neuroprotective effects of Lycium barbarum polysaccharide (LBP) against concomitant cognitive dysfunction and changes in hippocampal CREB-BDNF signaling pathway in chronically unpredictable stressed mice.Methods: The mice were subjected to different unpredictable stressors for a period of 4 weeks. Behavioral tests, including open field (OFT) and Morris water maze (MWMT) tests were used to evaluate pharmacological effects. Serum corticosterone levels, protein expression level of BDNF and pCREB/CREB in hippocampus were assessed by ELISA, Western blot and immunohistochemistry methods, respectively. Morphological changes in pyramidal neurons in the hippocampus were studied by Nissl staining.Results: LBP improved mice performance in MWMT, indicating that it reversed chronic unpredictable stress (CUS)-induced cognitive deficits. LBP treatment reduced serum corticosterone levels and prevented neuron loss in the hippocampus. It maintained expression levels of BDNF and phosphorylation of CREB in hippocampus during CUS procedure.Conclusion: Lycium barbarum polysaccharide protects CREB-BDNF signaling pathway in hippocampus and relieves CUS-induced cognitive deficits. These results suggest that Lycium barbarum polysaccharides is potentially an alternative neuro-protective agent against stress-induced psychopathological dysfunction.Keywords: Lycium barbarum, Polysaccharide, Chronic unpredictable stress, Cognitive deficits, Brainderived neurotrophic factor, Calcium/cyclic-AMP responsive binding protei