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Islam, Siraj-Ul,Haq, Fazal-I,Tirmizi, Ikram A. The Korean Society for Computational and Applied M 2010 Journal of applied mathematics & informatics Vol.28 No.3
A Numerical scheme based on collocation method using quartic B-spline functions is designed for the numerical solution of one-dimensional modified equal width wave (MEW) wave equation. Using Von-Neumann approach the scheme is shown to be unconditionally stable. Performance of the method is validated through test problems including single wave, interaction of two waves and use of Maxwellian initial condition. Using error norms $L_2$ and $L_{\infty}$ and conservative properties of mass, momentum and energy, accuracy and efficiency of the suggested method is established through comparison with the existing numerical techniques.
Islam, Salman Ul,Ahmed, Muhammad Bilal,Lee, Su Jin,Shehzad, Adeeb,Sonn, Jong Kyung,Kwon, Oh-Shin,Lee, Young Sup Elsevier 2018 Experimental cell research Vol.369 No.1
<P><B>Abstract</B></P> <P>Cell actin cytoskeleton is primarily modulated by Rho family proteins. RhoA regulates several downstream targets, including Rho-associated protein kinase (ROCK), LIM-Kinase (LIMK), and cofilin. Pre-mRNA processing factor 4B (PRP4) modulates the actin cytoskeleton of cancer cells via RhoA activity inhibition. In this study, we discovered that PRP4 over-expression in HCT116 colon cancer cells induces cofilin dephosphorylation by inhibiting the Rho-ROCK-LIMK-cofilin pathway. Two-dimensional gel electrophoresis, and matrix-assisted laser desorption/ionization time-of-flight mass-spectrometry (MALDI-TOF MS) analysis indicated increased expression of protein phosphatase 1A (PP1A) in PRP4-transfected HCT116 cells. The presence of PRP4 increased the expression of PP1A both at the mRNA and protein levels, which possibly activated cofilin through dephosphorylation and subsequently modulated the cell actin cytoskeleton. Furthermore, we found that PRP4 over-expression did not induce cofilin dephosphorylation in the presence of okadaic acid, a potent phosphatase inhibitor. Moreover, we discovered that PRP4 over-expression in HCT116 cells induced dephosphorylation of migration and invasion inhibitory protein (MIIP), and down-regulation of E-cadherin protein levels, which were further restored by the presence of okadaic acid. These findings indicate a possible molecular mechanism of PRP4-induced actin cytoskeleton remodeling and epithelial-mesenchymal transition, and make PRP4 an important target in colon cancer.</P> <P><B>Highlights</B></P> <P> <UL> <LI> PRP4 is involved in pre-mRNA splicing and cell signalling. </LI> <LI> PRP4 modulates the actin cytoskeleton of cancer cells via RhoA activity inhibition. </LI> <LI> PRP4 induces cofilin dephosphorylation by inhibiting the Rho-ROCK-LIMK-cofilin pathway in HCT116 cells. </LI> <LI> Dephosphorylation of cofilin results in F-actin stabilization, re-distribution of cytoplasmic actin, formation of actin stress fibers, and inhibition of cell motility. </LI> <LI> PRP4 over-expression induces the expressions of PP1A, which directly or indirectly dephosphorylates cofilin, resulting in actin cytoskeleton rearrangement, downregulation of E-cadherin, and EMT induction. Cofilin activation may be associated with EMT properties, and promotes the progression of human colon cancer. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P> <B>Proposed model for PRP4-induced cofilin and MIIP dephosphorylation and epithelial-mesenchymal transition (EMT) induction</B>. PRP4 over-expression results in cofilin and MIIP dephosphorylation, causing actin dynamics to increase, which may lead to EMT. Another proposed pathway for EMT induction by dephosphorylated MIIP is illustrated in the black-dotted panel. MIIP may inhibit the Rac1 signaling pathway through PAK1 (Rac1 downstream target) binding competition, which results in reduced lamellipodia formation and, finally, EMT.</P> <P>[DISPLAY OMISSION]</P>
Antimicrobial and Biocompatible Properties of Nanomaterials
Ul-Islam, M.,Shehzad, A.,Khan, S.,Khattak, W.A.,Ullah, M.W.,Park, J.K. American Scientific Publishers 2014 Journal of Nanoscience and Nanotechnology Vol.14 No.1
The rapid development of drug-resistant characteristics in pathogenic viral, bacterial, and fungal species and the consequent spread of infectious diseases are currently receiving serious attention. Indeed, there is a pressing demand to explore novel materials and develop new strategies that can address these issues of serious concern. Nanomaterials are currently proving to be the most capable therapeutic agents to cope with such hazards. The exceptional physiochemical properties and impressive antimicrobial capabilities of nanoparticles have provoked their utilization in biomedical fields. Nanomaterials of both organic and inorganic nature have shown the capabilities of disrupting microbial cells through different mechanisms. Along with the direct influence on the microbial cell membrane, DNA and proteins, these nanomaterials produce reactive oxygen species (ROS) that damage cell components and viruses. Currently, a serious hazard associated with these antimicrobial nanomaterials is their toxicity to human and animal cells. Extensive studies have reported the dose, time, and cell-dependent toxicology of various nanomaterials, and some have shown excellent biocompatible properties. Nevertheless, there is still debate regarding the use of nanomaterials for medical applications. Therefore, in this review, the antimicrobial activities of various nanomaterials with details of their acting mechanisms were compiled. The relative toxic and biocompatible behavior of nanomaterials emphasized in this study provides information pertaining to their practical applicability in medical fields.