• KSCE Journal of Civil and Environmental Engineering Research
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• v.29 no.5A
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• pp.457-465
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• 2009

This study presents a moving least squares (MLS) finite difference method for solving elastic crack problems with stress singularity at the crack tip. Near-tip functions are intrinsically employed in the MLS approximation to model near-tip field inducing singularity in stress field. employment of the functions does not lose the merit of the MLS Taylor polynomial approximation which approximates the derivatives of a function without actual differentiating process. In the formulation of crack problem, computational efficiency is considerably improved by taking the strong formulation instead of weak formulation involving time consuming numerical quadrature Difference equations are constructed on the nodes distributed in computational domain. Numerical experiments for crack problems show that the intrinsically enriched MLS finite difference method can sharply capture the singular behavior of near-tip stress and accurately evaluate stress intensity factors.

• Molecules and Cells
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• v.44 no.11
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• pp.805-829
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• 2021

CCCTC-binding factor (CTCF) critically contributes to 3D chromatin organization by determining topologically associated domain (TAD) borders. Although CTCF primarily binds at TAD borders, there also exist putative CTCF-binding sites within TADs, which are spread throughout the genome by retrotransposition. However, the detailed mechanism responsible for masking the putative CTCF-binding sites remains largely elusive. Here, we show that the ATP-dependent chromatin remodeler, chromodomain helicase DNA-binding 4 (CHD4), regulates chromatin accessibility to conceal aberrant CTCF-binding sites embedded in H3K9me3-enriched heterochromatic B2 short interspersed nuclear elements (SINEs) in mouse embryonic stem cells (mESCs). Upon CHD4 depletion, these aberrant CTCF-binding sites become accessible and aberrant CTCF recruitment occurs within TADs, resulting in disorganization of local TADs. RNA-binding intrinsically disordered domains (IDRs) of CHD4 are required to prevent this aberrant CTCF binding, and CHD4 is critical for the repression of B2 SINE transcripts. These results collectively reveal that a CHD4-mediated mechanism ensures appropriate CTCF binding and associated TAD organization in mESCs.