5 research outputs found
Magnetization models for particle-based simulations of magnetorheological fluids
In this study, three-dimensional particle-based simulations are used to model
magnetorheological fluids. The numerical model of the MRF is implemented in the framework
of the Discrete Element Method (DEM) and takes into account the coupling of the
magnetic dipoles, the hydrodynamic drag forces and steric forces between particles. To
accurately treat the magnetic interaction between particles, the magnetic field at the
particles’ position is computed and an appropriate magnetization model is implemented.
DEM simulations with different volume fractions of the MRF are carried out and the
resulting magnetization curves are put in comparison with experimental data
Magnetization models for particle-based simulations of magnetorheological fluids
In this study, three-dimensional particle-based simulations are used to model
magnetorheological fluids. The numerical model of the MRF is implemented in the framework
of the Discrete Element Method (DEM) and takes into account the coupling of the
magnetic dipoles, the hydrodynamic drag forces and steric forces between particles. To
accurately treat the magnetic interaction between particles, the magnetic field at the
particles’ position is computed and an appropriate magnetization model is implemented.
DEM simulations with different volume fractions of the MRF are carried out and the
resulting magnetization curves are put in comparison with experimental data
HDAC1 Inactivation Induces Mitotic Defect and Caspase-Independent Autophagic Cell Death in Liver Cancer
Histone deacetylases (HDACs) are known to play a central role in the regulation of several cellular properties interlinked with the development and progression of cancer. Recently, HDAC1 has been reported to be overexpressed in hepatocellular carcinoma (HCC), but its biological roles in hepatocarcinogenesis remain to be elucidated. In this study, we demonstrated overexpression of HDAC1 in a subset of human HCCs and liver cancer cell lines. HDAC1 inactivation resulted in regression of tumor cell growth and activation of caspase-independent autophagic cell death, via LC3B-II activation pathway in Hep3B cells. In cell cycle regulation, HDAC1 inactivation selectively induced both p21WAF1/Cip1 and p27Kip1 expressions, and simultaneously suppressed the expression of cyclin D1 and CDK2. Consequently, HDAC1 inactivation led to the hypophosphorylation of pRb in G1/S transition, and thereby inactivated E2F/DP1 transcription activity. In addition, we demonstrated that HDAC1 suppresses p21WAF1/Cip1 transcriptional activity through Sp1-binding sites in the p21WAF1/Cip1 promoter. Furthermore, sustained suppression of HDAC1 attenuated in vitro colony formation and in vivo tumor growth in a mouse xenograft model. Taken together, we suggest the aberrant regulation of HDAC1 in HCC and its epigenetic regulation of gene transcription of autophagy and cell cycle components. Overexpression of HDAC1 may play a pivotal role through the systemic regulation of mitotic effectors in the development of HCC, providing a particularly relevant potential target in cancer therapy