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Geosynthetic-Reinforced Soil Structures to Mitigate Natural Disasters
F. Tatsuoka,M. Tateyama,J. Koseki 한국토목섬유학회 2011 한국토목섬유학회 학술발표회 Vol.2011 No.11
The total length of permanent geosynthetic-reinforced soil (GRS) retaining walls (RWs) with staged-constructed full-height rigid (FHR) facing for railways, including high-speed train lines, highways and so on is now more than 125 km in Japan. Many were also constructed replacing conventional type RWs and embankments that collapsed during recent earthquakes, heavy rains, floodings and storms. It is proposed to construct GRS coastal dikes with FHR facing connected to geosynthetic reinforcement layers as a tsunami barrier. Based on the GRS RW technology, a number of bridge abutments with geosynthetic-reinforced backfill were constructed. The latest version, called the GRS integrated bridge, comprises a continuous girder integrated to a pair of RC facing, not using bearings, and the \backfill reinforced with geosynthetic reinforcement layers firmly connected to the facing. The advantageous features of this new bridge system are summarized. It is proposed to apply this new bridge system to replace conventional type bridges that collapsed by earthquakes, flooding and tsunami and also to newly construct those having high resistance against these natural disasters.
Choi, D.,Na, W.,Kabir, M.,Yi, E.,Kwon, S.,Yeom, J.,Ahn, J.W.,Choi, H.H.,Lee, Y.,Seo, K.,Shin, M.,Park, S.H.,Yoo, H.,Isono, K.i.,Koseki, H.,Kim, S.T.,Lee, C.,Kwon, Y.,Choi, C. Cell Press 2013 Molecular cell Vol.51 No.3
WIP1 (wild-type p53-induced phosphatase 1) functions as a homeostatic regulator of the ataxia telangiectasia mutated (ATM)-mediated signaling pathway in response to ionizing radiation (IR). Here we identify homeodomain-interacting protein kinase 2 (HIPK2) as a protein kinase that targets WIP1 for phosphorylation and proteasomal degradation. In unstressed cells, WIP1 is constitutively phosphorylated by HIPK2 and maintained at a low level by proteasomal degradation. In response to IR, ATM-dependent AMPKα2-mediated HIPK2 phosphorylation promotes inhibition of WIP1 phosphorylation through dissociation of WIP1 from HIPK2, followed by stabilization of WIP1 for termination of the ATM-mediated double-strand break (DSB) signaling cascade. Notably, HIPK2 depletion impairs IR-induced γ-H2AX foci formation, cell-cycle checkpoint activation, and DNA repair signaling, and the survival rate of hipk2<SUP>+/-</SUP> mice upon γ-irradiation is markedly reduced compared to wild-type mice. Taken together, HIPK2 plays a critical role in the initiation of DSB repair signaling by controlling WIP1 levels in response to IR.
Biological, clinical and population relevance of 95 loci for blood lipids
Teslovich, Tanya M.,Musunuru, Kiran,Smith, Albert V.,Edmondson, Andrew C.,Stylianou, Ioannis M.,Koseki, Masahiro,Pirruccello, James P.,Ripatti, Samuli,Chasman, Daniel I.,Willer, Cristen J.,Johansen, C Nature Publishing Group, a division of Macmillan P 2010 Nature Vol.466 No.7307
Plasma concentrations of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides are among the most important risk factors for coronary artery disease (CAD) and are targets for therapeutic intervention. We screened the genome for common variants associated with plasma lipids in >100,000 individuals of European ancestry. Here we report 95 significantly associated loci (P??<??5?????10<SUP>??8</SUP>), with 59 showing genome-wide significant association with lipid traits for the first time. The newly reported associations include single nucleotide polymorphisms (SNPs) near known lipid regulators (for example, CYP7A1, NPC1L1 and SCARB1) as well as in scores of loci not previously implicated in lipoprotein metabolism. The 95 loci contribute not only to normal variation in lipid traits but also to extreme lipid phenotypes and have an impact on lipid traits in three non-European populations (East Asians, South Asians and African Americans). Our results identify several novel loci associated with plasma lipids that are also associated with CAD. Finally, we validated three of the novel genes??GALNT2, PPP1R3B and TTC39B??with experiments in mouse models. Taken together, our findings provide the foundation to develop a broader biological understanding of lipoprotein metabolism and to identify new therapeutic opportunities for the prevention of CAD.