Behavior of Longitudinal and Transverse Dispersion Coefficient in Three-Dimensional Open Channels

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchiv

Analysis of Transverse Mixing Using Natural Tracers Continuously Introduced from Tributaries

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchive

Copy Number Variation of Age-Related Macular Degeneration Relevant Genes in the Korean Population

PURPOSE: Studies that analyzed single nucleotide polymorphisms (SNP) in various genes have shown that genetic factors are strongly associated with age-related macular degeneration (AMD) susceptibility. Copy number variation (CNV) may be an additional type of genetic variation that contributes to AMD pathogenesis. This study investigated CNV in 4 AMD-relevant genes in Korean AMD patients and control subjects. METHODS: Four CNV candidate regions located in AMD-relevant genes (VEGFA, ARMS2/HTRA1, CFH and VLDLR), were selected based on the outcomes of our previous study which elucidated common CNVs in the Asian populations. Real-time PCR based TaqMan Copy Number Assays were performed on CNV candidates in 273 AMD patients and 257 control subjects. RESULTS: The predicted copy number (PCN, 0, 1, 2 or 3+) of each region was called using the CopyCaller program. All candidate genes except ARMS2/HTRA1 showed CNV in at least one individual, in which losses of VEGFA and VLDLR represent novel findings in the Asian population. When the frequencies of PCN were compared, only the gain in VLDLR showed significant differences between AMD patients and control subjects (p = 0.025). Comparisons of the raw copy values (RCV) revealed that 3 of 4 candidate genes showed significant differences (2.03 vs. 1.92 for VEGFA, p<0.01; 2.01 vs. 1.97 for CFH, p<0.01; 1.97 vs. 2.01, p<0.01 for ARMS2/HTRA1). CONCLUSION: CNVs located in AMD-relevant genes may be associated with AMD susceptibility. Further investigations encompassing larger patient cohorts are needed to elucidate the role of CNV in AMD pathogenesis

Stability Analysis of a Vector-Borne Disease with Variable Human Population

A mathematical model of a vector-borne disease involving variable human population is analyzed. The varying population size includes a term for disease-related deaths. Equilibria and stability are determined for the system of ordinary differential equations. If R0≤1, the disease-“free” equilibrium is globally asymptotically stable and the disease always dies out. If R0>1, a unique “endemic” equilibrium is globally asymptotically stable in the interior of feasible region and the disease persists at the “endemic” level. Our theoretical results are sustained by numerical simulations

Research on a Denial of Service (DoS) Detection System Based on Global Interdependent Behaviors in a Sensor Network Environment

This research suggests a Denial of Service (DoS) detection method based on the collection of interdependent behavior data in a sensor network environment. In order to collect the interdependent behavior data, we use a base station to analyze traffic and behaviors among nodes and introduce methods of detecting changes in the environment with precursor symptoms. The study presents a DoS Detection System based on Global Interdependent Behaviors and shows the result of detecting a sensor carrying out DoS attacks through the test-bed

Mathematical Analysis of a Malaria Model with Partial Immunity to Reinfection

A deterministic model with variable human population for the transmission dynamics of malaria disease, which allows transmission by the recovered humans, is first developed and rigorously analyzed. The model reveals the presence of the phenomenon of backward bifurcation, where a stable disease-free equilibrium coexists with one or more stable endemic equilibria when the associated reproduction number is less than unity. This phenomenon may arise due to the reinfection of host individuals who recovered from the disease. The model in an asymptotical constant population is also investigated. This results in a model with mass action incidence. A complete global analysis of the model with mass action incidence is given, which reveals that the global dynamics of malaria disease with reinfection is completely determined by the associated reproduction number. Moreover, it is shown that the phenomenon of backward bifurcation can be removed by replacing the standard incidence function with a mass action incidence. Graphical representations are provided to study the effect of reinfection rate and to qualitatively support the analytical results on the transmission dynamics of malaria

Inverse Problem for Color Doppler Ultrasound-Assisted Intracardiac Blood Flow Imaging

For the assessment of the left ventricle (LV), echocardiography has been widely used to visualize and quantify geometrical variations of LV. However, echocardiographic image itself is not sufficient to describe a swirling pattern which is a characteristic blood flow pattern inside LV without any treatment on the image. We propose a mathematical framework based on an inverse problem for three-dimensional (3D) LV blood flow reconstruction. The reconstruction model combines the incompressible Navier-Stokes equations with one-direction velocity component of the synthetic flow data (or color Doppler data) from the forward simulation (or measurement). Moreover, time-varying LV boundaries are extracted from the intensity data to determine boundary conditions of the reconstruction model. Forward simulations of intracardiac blood flow are performed using a fluid-structure interaction model in order to obtain synthetic flow data. The proposed model significantly reduces the local and global errors of the reconstructed flow fields. We demonstrate the feasibility and potential usefulness of the proposed reconstruction model in predicting dynamic swirling patterns inside the LV over a cardiac cycle

Cellular stress-induced up-regulation of FMRP promotes cell survival by modulating PI3K-Akt phosphorylation cascades

<p>Abstract</p> <p>Background</p> <p>Fragile X syndrome (FXS), the most commonly inherited mental retardation and single gene cause of autistic spectrum disorder, occurs when the Fmr1 gene is mutated. The product of Fmr1, fragile X linked mental retardation protein (FMRP) is widely expressed in HeLa cells, however the roles of FMRP within HeLa cells were not elucidated, yet. Interacting with a diverse range of mRNAs related to cellular survival regulatory signals, understanding the functions of FMRP in cellular context would provide better insights into the role of this interesting protein in FXS. Using HeLa cells treated with etoposide as a model, we tried to determine whether FMRP could play a role in cell survival.</p> <p>Methods</p> <p>Apoptotic cell death was induced by etoposide treatment on Hela cells. After we transiently modulated FMRP expression (silencing or enhancing) by using molecular biotechnological methods such as small hairpin RNA virus-induced knock down and overexpression using transfection with FMRP expression vectors, cellular viability was measured using propidium iodide staining, TUNEL staining, and FACS analysis along with the level of activation of PI3K-Akt pathway by Western blot. Expression level of FMRP and apoptotic regulator BcL-xL was analyzed by Western blot, RT-PCR and immunocytochemistry.</p> <p>Results</p> <p>An increased FMRP expression was measured in etoposide-treated HeLa cells, which was induced by PI3K-Akt activation. Without FMRP expression, cellular defence mechanism via PI3K-Akt-Bcl-xL was weakened and resulted in an augmented cell death by etoposide. In addition, FMRP over-expression lead to the activation of PI3K-Akt signalling pathway as well as increased FMRP and BcL-xL expression, which culminates with the increased cell survival in etoposide-treated HeLa cells.</p> <p>Conclusions</p> <p>Taken together, these results suggest that FMRP expression is an essential part of cellular survival mechanisms through the modulation of PI3K, Akt, and Bcl-xL signal pathways.</p