Browsing by Author "Lin, P"
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Item Open Access An Energy Stable $C^0$ Finite Element Scheme for A Phase-Field Model of Vesicle Motion and Deformation(SIAM Journal on Scientific Computing, 2022-01) Shen, L; Xu, Z; Lin, P; Huang, H; Xu, SItem Open Access An energy stable C0 finite element scheme for a quasi-incompressible phase-field model of moving contact line with variable density(Journal of Computational Physics, 2020-03-15) Shen, L; Huang, H; Lin, P; Song, Z; Xu, SIn this paper, we focus on modeling and simulation of two-phase flow problems with moving contact lines and variable density. A thermodynamically consistent phase-field model with general Navier boundary condition is developed based on the concept of quasi-incompressibility and the energy variational method. A mass conserving C0 finite element scheme is proposed to solve the PDE system. Energy stability is achieved at the fully discrete level. Various numerical results confirm that the proposed scheme for both P1 element and P2 element are energy stable.Item Open Access Diffuse interface model for cell interaction and aggregation with Lennard-Jones type potential(Computer Methods in Applied Mechanics and Engineering, 2023-10-01) Shen, L; Lin, P; Xu, Z; Xu, SThis study introduces a phase-field model designed to simulate the interaction and aggregation of multicellular systems under flow conditions within a bounded spatial domain. The model incorporates a multi-dimensional Lennard-Jones potential to account for short-range repulsion and adhesive bonding between cells. To solve the governing equations while preserving energy law, a second-order accurate C0 finite element method is employed. The validity of the model is established through numerical tests, and experimental data from cell stretch tests is utilized for model calibration and validation. Additionally, the study investigates the impact of varying adhesion properties in red blood cells. Overall, this work presents a thermodynamically consistent and computationally efficient framework for simulating cell–cell and cell–wall interactions under flow conditions.Item Open Access Dysferlin, annexin A1, and mitsugumin 53 are upregulated in muscular dystrophy and localize to longitudinal tubules of the T-system with stretch.(Journal of neuropathology and experimental neurology, 2011-04) Waddell, LB; Lemckert, FA; Zheng, XF; Tran, J; Evesson, FJ; Hawkes, JM; Lek, A; Street, NE; Lin, P; Clarke, NF; Landstrom, AP; Ackerman, MJ; Weisleder, N; Ma, J; North, KN; Cooper, STMutations in dysferlin cause an inherited muscular dystrophy because of defective membrane repair. Three interacting partners of dysferlin are also implicated in membrane resealing: caveolin-3 (in limb girdle muscular dystrophy type 1C), annexin A1, and the newly identified protein mitsugumin 53 (MG53). Mitsugumin 53 accumulates at sites of membrane damage, and MG53-knockout mice display a progressive muscular dystrophy. This study explored the expression and localization of MG53 in human skeletal muscle, how membrane repair proteins are modulated in various forms of muscular dystrophy, and whether MG53 is a primary cause of human muscle disease. Mitsugumin 53 showed variable sarcolemmal and/or cytoplasmic immunolabeling in control human muscle and elevated levels in dystrophic patients. No pathogenic MG53 mutations were identified in 50 muscular dystrophy patients, suggesting that MG53 is unlikely to be a common cause of muscular dystrophy in Australia. Western blot analysis confirmed upregulation of MG53, as well as of dysferlin, annexin A1, and caveolin-3 to different degrees, in different muscular dystrophies. Importantly, MG53, annexin A1, and dysferlin localize to the t-tubule network and show enriched labeling at longitudinal tubules of the t-system in overstretch. Our results suggest that longitudinal tubules of the t-system may represent sites of physiological membrane damage targeted by this membrane repair complex.Item Open Access The genetic association between personality and major depression or bipolar disorder. A polygenic score analysis using genome-wide association data.(Translational psychiatry, 2011-10-18) Middeldorp, CM; de Moor, MHM; McGrath, LM; Gordon, SD; Blackwood, DH; Costa, PT; Terracciano, A; Krueger, RF; de Geus, EJC; Nyholt, DR; Tanaka, T; Esko, T; Madden, PAF; Derringer, J; Amin, N; Willemsen, G; Hottenga, J-J; Distel, MA; Uda, M; Sanna, S; Spinhoven, P; Hartman, CA; Ripke, S; Sullivan, PF; Realo, A; Allik, J; Heath, AC; Pergadia, ML; Agrawal, A; Lin, P; Grucza, RA; Widen, E; Cousminer, DL; Eriksson, JG; Palotie, A; Barnett, JH; Lee, PH; Luciano, M; Tenesa, A; Davies, G; Lopez, LM; Hansell, NK; Medland, SE; Ferrucci, L; Schlessinger, D; Montgomery, GW; Wright, MJ; Aulchenko, YS; Janssens, ACJW; Oostra, BA; Metspalu, A; Abecasis, GR; Deary, IJ; Räikkönen, K; Bierut, LJ; Martin, NG; Wray, NR; van Duijn, CM; Smoller, JW; Penninx, BWJH; Boomsma, DIThe relationship between major depressive disorder (MDD) and bipolar disorder (BD) remains controversial. Previous research has reported differences and similarities in risk factors for MDD and BD, such as predisposing personality traits. For example, high neuroticism is related to both disorders, whereas openness to experience is specific for BD. This study examined the genetic association between personality and MDD and BD by applying polygenic scores for neuroticism, extraversion, openness to experience, agreeableness and conscientiousness to both disorders. Polygenic scores reflect the weighted sum of multiple single-nucleotide polymorphism alleles associated with the trait for an individual and were based on a meta-analysis of genome-wide association studies for personality traits including 13,835 subjects. Polygenic scores were tested for MDD in the combined Genetic Association Information Network (GAIN-MDD) and MDD2000+ samples (N=8921) and for BD in the combined Systematic Treatment Enhancement Program for Bipolar Disorder and Wellcome Trust Case-Control Consortium samples (N=6329) using logistic regression analyses. At the phenotypic level, personality dimensions were associated with MDD and BD. Polygenic neuroticism scores were significantly positively associated with MDD, whereas polygenic extraversion scores were significantly positively associated with BD. The explained variance of MDD and BD, ∼0.1%, was highly comparable to the variance explained by the polygenic personality scores in the corresponding personality traits themselves (between 0.1 and 0.4%). This indicates that the proportions of variance explained in mood disorders are at the upper limit of what could have been expected. This study suggests shared genetic risk factors for neuroticism and MDD on the one hand and for extraversion and BD on the other.