Flood Risk Management: An Illustrative Approach

Widespread flooding with significant damage in many countries, such as the Philippines in 2013, highlights the ongoing need for effective flood risk management (FRM). This hinges on comprehensive access to and dissemination of information about the elements and the people at risk. Simulations, real-time graphs, and maps illustrate the spatial distribution of flood risks, spatial allocation and dissemination of flood effects, if flood risk reduction measures are not implemented, as well as the benefits to be derived from the effective implementation and maintenance of flood risk management measures not realized. Using precipitation, river water, and tide levels, a real-time monitoring site was set up for the Shirakawa River, Kumamoto, Japan. The data gathered from the July 2012 flood event is used as a demonstrator, illustrating a flood event as well as how to utilize the information provided on this site to determine the future time and possibility of flooding. Additionally, an electronically generated flood hazard map making process is being developed for distribution across Japan. These illustrative approaches can be utilized in cities and communities around the globe

The change of plasma C-reactive protein and metabolite concentrations, and MPS sick degree score in Landrase selected for resistance to MPS, Large Yorkshire selected for immune performances and the crossbreed

Swine Mycoplasma Hyopneumoniea, hp, is known as a major factor to affect for the specific pneumonia (MPS). This damages is very serious because carrier rate of hp in piglets from 3 to 4 months of age is very high, the rate of piglets that the response of antibody to hp shows positive is 80 % over, and the rate that has very terrible tissue from MPS is 51% in Japanese pig farm. We bred a resistant strain to MPS by selection to decrease MPS pathogenic condition over 5 generations using Landrase (MPS strain), and a high immune performance strain by selection for peripheral phagocytosis, complement activity and antibody production against erysipelatous vaccine using Large Yorkshire (HI strain)

The effect of dexamethasone on defective nephrin transport caused by ER stress: A potential mechanism for the therapeutic action of glucocorticoids in the acquired glomerular diseases

The mechanism by which glucocorticoids govern antiproteinuric effect in nephrotic syndrome remains unknown. Present study examined the protective role of dexamethasone (DEX) in the intracellular trafficking of nephrin under endoplasmic reticulum (ER) stress. Human embryonic kidney-293 cell line expressing a full-length human nephrin was cultured in mediums containing 5.5 or 25 mM glucose with or without DEX. The result revealed that glucose starvation evoked a rapid ER stress leading to formation of underglycosylated nephrin that was remained in the ER as a complex with calreticulin/calnexin. DEX rescued this interfered trafficking through binding to its receptor and stimulating the mitochondrial transcripts and adenosine 5′ triphosphate (ATP) production, leading to synthesis of fully glycosylated nephrin. These results suggest that ER-stress in podocytes may cause alteration of nephrin N-glycosylation, which may be an underlying factor in the pathomechanism of the proteinuria in nephrotic syndrome. DEX may restore this imbalance by stimulating expression of mitochondrial genes, resulted in the production of ATP that is essential factor for proper folding machinery aided by the ER chaperones

A hybrid iterative method for common solutions of variational inequality problems and fixed point problems for single-valued and multi-valued mappings with applications

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Discovery of a Novel Activator of KCNQ1-KCNE1 K+ Channel Complexes

KCNQ1 voltage-gated K+ channels (Kv7.1) associate with the family of five KCNE peptides to form complexes with diverse gating properties and pharmacological sensitivities. The varied gating properties of the different KCNQ1-KCNE complexes enables the same K+ channel to function in both excitable and non excitable tissues. Small molecule activators would be valuable tools for dissecting the gating mechanisms of KCNQ1-KCNE complexes; however, there are very few known activators of KCNQ1 channels and most are ineffective on the physiologically relevant KCNQ1-KCNE complexes. Here we show that a simple boronic acid, phenylboronic acid (PBA), activates KCNQ1/KCNE1 complexes co-expressed in Xenopus oocytes at millimolar concentrations. PBA shifts the voltage sensitivity of KCNQ1 channel complexes to favor the open state at negative potentials. Analysis of different-sized charge carriers revealed that PBA also targets the permeation pathway of KCNQ1 channels. Activation by the boronic acid moiety has some specificity for the Kv7 family members (KCNQ1, KCNQ2/3, and KCNQ4) since PBA does not activate Shaker or hERG channels. Furthermore, the commercial availability of numerous PBA derivatives provides a large class of compounds to investigate the gating mechanisms of KCNQ1-KCNE complexes