Development of Eco-VE Function for Construction

AbstractRecently accepted “Paris Agreement” has restricted the Earth temperature increase to be below 1.5 degrees Celsius contrast to previous industrialization. To follow this agreement, there should be efforts such as carbon emission reduction and eco design etc. One of these efforts is development of eco-VE function that applied eco-friendly concept on VE which is commonly used at design phase. Concept of this model includes carbon productivity concept and potential environment pollution index that reflects eco-VE function on original VE. The carbon productivity concept is a cause of production increase that offset production decrease factor depending on green-house gas reduction. The potential environment pollution index presents the possibility of environment pollution through construction phase. The carbon productivity is ‘Construction cost/Carbon emission’. The construction costs are consisted of material, equipment, labour cost and indirect expenses. Carbon emissions are calculated by emission for material production and equipment fuel consumption. The potential environment pollution index is composed of environmental pollution and conservation cost. The environmental pollution cost includes environmental damage and destruction cost. The environmental conservation cost includes environmental pollution prevention cost, waste treatment cost, environmental pollution compensation, environmental pollution test research funds and law cost

Recombinant mussel proximal thread matrix protein promotes osteoblast cell adhesion and proliferation

BACKGROUND: von Willebrand factor (VWF) is a key load bearing domain for mamalian cell adhesion by binding various macromolecular ligands in extracellular matrix such as, collagens, elastin, and glycosaminoglycans. Interestingly, vWF like domains are also commonly found in load bearing systems of marine organisms such as in underwater adhesive of mussel and sea star, and nacre of marine abalone, and play a critical load bearing function. Recently, Proximal Thread Matrix Protein1 (PTMP1) in mussel composed of two vWF type A like domains has characterized and it is known to bind both mussel collagens and mammalian collagens. RESULTS: Here, we cloned and mass produced a recombinant PTMP1 from E. coli system after switching all the minor codons to the major codons of E. coli. Recombinant PTMP1 has an ability to enhance mouse osteoblast cell adhesion, spreading, and cell proliferation. In addition, PTMP1 showed vWF-like properties as promoting collagen expression as well as binding to collagen type I, subsequently enhanced cell viability. Consequently, we found that recombinant PTMP1 acts as a vWF domain by mediating cell adhesion, spreading, proliferation, and formation of actin cytoskeleton. CONCLUSIONS: This study suggests that both mammalian cell adhesion and marine underwater adhesion exploits a strong vWF-collagen interaction for successful wet adhesion. In addition, vWF like domains containing proteins including PTMP1 have a great potential for tissue engineering and the development of biomedical adhesives as a component for extra-cellular matrix

Electrochemical performance of NixCo1-xMoO4 (0 ≤ x ≤ 1) nanowire anodes for lithium-ion batteries

NixCo1-xMoO4 (0 ≤ x ≤ 1) nanowire electrodes for lithium-ion rechargeable batteries have been synthesized via a hydrothermal method, followed by thermal post-annealing at 500°C for 2 h. The chemical composition of the nanowires was varied, and their morphological features and crystalline structures were characterized using field-emission scanning electron microscopy and X-ray powder diffraction. The reversible capacity of NiMoO4 and Ni0.75Co0.25MoO4 nanowire electrodes was larger (≈520 mA h/g after 20 cycles at a rate of 196 mA/g) than that of the other nanowires. This enhanced electrochemical performance of NixCo1-xMoO4 nanowires with high Ni content was ascribed to their larger surface area and efficient electron transport path facilitated by their one-dimensional nanostructure

Chiral magnetoresistance in Pt/Co/Pt zigzag wires

The Rashba effect leads to a chiral precession of the spins of moving electrons while the Dzyaloshinskii-Moriya interaction (DMI) generates preference towards a chiral profile of local spins. We predict that the exchange interaction between these two spin systems results in a 'chiral' magnetoresistance depending on the chirality of the local spin texture. We observe this magnetoresistance by measuring the domain wall (DW) resistance in a uniquely designed Pt/Co/Pt zigzag wire, and by changing the chirality of the DW with applying an in-plane magnetic field. A chirality-dependent DW resistance is found, and a quantitative analysis shows a good agreement with a theory based on the Rashba model. Moreover, the DW resistance measurement allows us to independently determine the strength of the Rashba effect and the DMI simultaneously, and the result implies a possible correlation between the Rashba effect, the DMI, and the symmetric Heisenberg exchange

pH-responsive aqueous/LC interfaces using SGLCP-b-polyacrylic acid block copolymers

Block copolymers that combine a side-group liquid crystalline polymer (SGLCP) block and a pH-responsivehydrophilic block, poly(acrylic acid) (PAA), are shown to confer pH-dependent anchoring of the director orientation at the aqueous/LC interface. The SGLCP block, poly(4-cyanobiphenyl-4-oxyundecylacrylate), was chosen based on its ability to influence the director field of the 5CB (4-cyano-4'-pentylbiphenyl). At low pH the PAA block collapses and the inherent, planar alignment tendency of 5CB at a water interface prevails. As pH increases, the polyelectrolyte block becomes increasingly charged and expands, producing a change to homeotropic anchoring. The change in anchoring occurs as quickly as the buffer can be changed (within ~2 s) and is reversible, with a response that is repeatable over as many cycles as were tested (approximately 20 cycles). The polymer-mediated anchoring persists for 6 days, indicating that the SGLCP block secures the self-assembled layer on the 5CB, even under conditions that cause repulsive interactions among the PAA blocks. Thus, SGLCP blocks can translate conformational changes of a responsive hydrophilic block into rapid, reversible changes in the director fiel

A Novel Pinkish-White Flower Color Variant Is Caused by a New Allele of Flower Color Gene W1 in Wild Soybean (Glycine soja)

The enzyme flavonoid 3',5'-hydroxylase (F3'5'H) plays an important role in producing anthocyanin pigments in soybean. Loss of function of the W1 locus encoding F3'5'H always produces white flowers. However, few color variations have been reported in wild soybean. In the present study, we isolated a new color variant of wild soybean accession (IT261811) with pinkish-white flowers. We found that the flower's pinkish-white color is caused by w1-s3, a single recessive allele of W1. The SNP detected in the mutant caused amino acid substitution (A(304)S) in a highly conserved SRS4 domain of F3'5'H proteins. On the basis of the results of the protein variation effect analyzer (PROVEAN) tool, we suggest that this mutation may lead to hypofunctional F3'5'H activity rather than non-functional activity, which thereby results in its pinkish-white color

Matrix Metalloproteinase-3 Causes Dopaminergic Neuronal Death through Nox1-Regenerated Oxidative Stress

In the present study we investigated the interplay between matrix metalloproteinase 3 (MMP3) and NADPH oxidase 1 (Nox1) in the process of dopamine (DA) neuronal death. We found that MMP3 activation causes the induction of Nox1 via mitochondrial reactive oxygen species (ROS) production and subsequently Rac1 activation, eventually leading to Nox1-derived superoxide generation in a rat DA neuronal N27 cells exposed to 6-OHDA. While a MMP3 inhibitor, NNGH, largely attenuated mitochondrial ROS and subsequent Nox1 induction, both apocynin, a putative Nox inhibitor and GKT137831, a Nox1 selective inhibitor failed to reduce 6-OHDA-induced mitochondrial ROS. However, both inhibitors for MMP3 and Nox1 similarly attenuated 6-OHDA-induced N27 cell death. RNAi-mediated selective inhibition of MMP3 or Nox1 showed that knockdown of either MMP3 or Nox1 significantly reduced 6-OHDA-induced ROS generation in N27 cells. While 6-OHDA-induced Nox1 was abolished by MMP3 knockdown, Nox1 knockdown did not alter MMP3 expression. Direct overexpression of autoactivated MMP3 (actMMP3) in N27 cells or in rat substantia nigra (SN) increased expression of Nox1. Selective knockdown of Nox1 in the SN achieved by adeno-associated virus-mediated overexpression of Nox1-specific shRNA largely attenuated the actMMP3-mediated dopaminergic neuronal loss. Furthermore, Nox1 expression was significantly attenuated in Mmp3 null mice treated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Together we established novel molecular mechanisms underlying oxidative stress-mediated dopaminergic neuronal death in which MMP3 activation is a key upstream event that leads to mitochondrial ROS, Nox1 induction and eventual dopaminergic neuronal death. Our findings may lead to the development of novel therapeutic approach

Matrix Metalloproteinase-3 Causes Dopaminergic Neuronal Death through Nox1-Regenerated Oxidative Stress

In the present study we investigated the interplay between matrix metalloproteinase 3 (MMP3) and NADPH oxidase 1 (Nox1) in the process of dopamine (DA) neuronal death. We found that MMP3 activation causes the induction of Nox1 via mitochondrial reactive oxygen species (ROS) production and subsequently Rac1 activation, eventually leading to Nox1-derived superoxide generation in a rat DA neuronal N27 cells exposed to 6-OHDA. While a MMP3 inhibitor, NNGH, largely attenuated mitochondrial ROS and subsequent Nox1 induction, both apocynin, a putative Nox inhibitor and GKT137831, a Nox1 selective inhibitor failed to reduce 6-OHDA-induced mitochondrial ROS. However, both inhibitors for MMP3 and Nox1 similarly attenuated 6-OHDA-induced N27 cell death. RNAi-mediated selective inhibition of MMP3 or Nox1 showed that knockdown of either MMP3 or Nox1 significantly reduced 6-OHDA-induced ROS generation in N27 cells. While 6-OHDA-induced Nox1 was abolished by MMP3 knockdown, Nox1 knockdown did not alter MMP3 expression. Direct overexpression of autoactivated MMP3 (actMMP3) in N27 cells or in rat substantia nigra (SN) increased expression of Nox1. Selective knockdown of Nox1 in the SN achieved by adeno-associated virus-mediated overexpression of Nox1-specific shRNA largely attenuated the actMMP3-mediated dopaminergic neuronal loss. Furthermore, Nox1 expression was significantly attenuated in Mmp3 null mice treated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Together we established novel molecular mechanisms underlying oxidative stress-mediated dopaminergic neuronal death in which MMP3 activation is a key upstream event that leads to mitochondrial ROS, Nox1 induction and eventual dopaminergic neuronal death. Our findings may lead to the development of novel therapeutic approach

Gene expression profiling of cancer stem cell in human lung adenocarcinoma A549 cells

<p>Abstract</p> <p>Background</p> <p>The studies on cancer-stem-cells (CSCs) have attracted so much attention in recent years as possible therapeutic implications. This study was carried out to investigate the gene expression profile of CSCs in human lung adenocarcinoma A549 cells.</p> <p>Results</p> <p>We isolated CSCs from A549 cell line of which side population (SP) phenotype revealed several stem cell properties. After staining the cell line with Hoechst 33342 dye, the SP and non-side population (non-SP) cells were sorted using flow cytometric analysis. The mRNA expression profiles were measured using an Affymetrix GeneChip^®oligonucleotide array. Among the sixty one differentially expressed genes, the twelve genes inclusive three poor prognostic genes; Aldo-keto reductase family 1, member C1/C2 (AKR1C1/C2), Transmembrane 4 L six family member 1 nuclear receptor (TM4SF1), and Nuclear receptor subfamily 0, group B, member 1 (NR0B1) were significantly up-regulated in SP compared to non-SP cells.</p> <p>Conclusion</p> <p>This is the first report indicating the differences of gene expression pattern between SP and non-SP cells in A549 cells. We suggest that the up-regulations of the genes AKR1C1/C2, TM4SF1 and NR0B1 in SP of human adenocarcinoma A549 cells could be a target of poor prognosis in anti-cancer therapy.</p