We present a theoretical study of electron mobility in cylindrical gated silicon nanowires at 300 K based on the Kubo-Greenwood formula and the self-consistent solution of the Schrödinger and Poisson equations. A rigorous surface roughness scattering model is derived, which takes into account the roughness-induced fluctuation of the subband wave function, of the electron charge, and of the interface polarization charge. Dielectric screening of the scattering potential is modeled within the random phase approximation, wherein a generalized dielectric function for a multi-subband quasi-one-dimensional electron gas system is derived accounting for the presence of the gate electrode and the mismatch of the dielectric constant between the semiconductor and gate insulator. A nonparabolic correction method is also presented, which is applied to the calculation of the density of states, the matrix element of the scattering potential, and the generalized Lindhard function. The Coulomb scattering due to the fixed interface charge and the intra- and intervalley phonon scattering are included in the mobility calculation in addition to the surface roughness scattering. Using these models, we study the low-field electron mobility and its dependence on the silicon body diameter, effective field, dielectric constant, and gate insulator thickness.

No abstract

No abstract

Based on the nonequilibrium Green’s function formalism, we have developed a three-dimensional (3D) simulation framework capable of handling electronic transport in nanoscale silicon devices within the effective mass and Hartree approximations. Using the deformation potential theory and the self-consistent Born approximation, we obtain the spatially local self-energy functions for the intravalley and intervalley phonon scattering mechanisms. To make the 3D simulation practicable, we reduce the computational complexity by using the mode space approach suitable for the device whose cross section is relatively uniform along the transport direction. We also obtain the expression for the phonon-limited low field mobility in the long channel limit from the linear response theory. As an application, we study the quantum transport of the silicon nanowire transistor whose channel length is 15nm in the ballistic limit and in the presence of the electron-phonon interactions. We can observe various effects of the electron-phonon interactions such as the reduction of the drain current, broadening of the local density of states, and the energy relaxation of the electrons injected from the source.

Generating kidney models of T1N0M0 tumors with 3D printing are feasible with refinements to be performed. Face and content validity was obtained when those models were presented to experienced urologists for making practical planning and training. Understandings of the disease and procedure from patients were well appreciated with this novel technology.

No abstract

No abstract

Aims Proprotein convertase subtilisin/kexin type-9 (PCSK9), a molecular determinant of low-density lipoprotein (LDL) receptor (LDLR) fate, has emerged as a promising therapeutic target for atherosclerotic cardiovascular diseases. However, the precise mechanism by which PCSK9 regulates the internalization and lysosomal degradation of LDLR is unknown. Recently, we identified adenylyl cyclase-associated protein 1 (CAP1) as a receptor for human resistin whose globular C-terminus is structurally similar to the C-terminal cysteine-rich domain (CRD) of PCSK9. Herein, we investigated the role of CAP1 in PCSK9-mediated lysosomal degradation of LDLR and plasma LDL cholesterol (LDL-C) levels. Methods and results The direct binding between PCSK9 and CAP1 was confirmed by immunoprecipitation assay, far-western blot, biomolecular fluorescence complementation, and surface plasmon resonance assay. Fine mapping revealed that the CRD of PCSK9 binds with the Src homology 3 binding domain (SH3BD) of CAP1. Two loss-of-function polymorphisms found in human PCSK9 (S668R and G670E in CRD) were attributed to a defective interaction with CAP1. siRNA against CAP1 reduced the PCSK9-mediated degradation of LDLR in vitro. We generated CAP1 knock-out mice and found that the viable heterozygous CAP1 knock-out mice had higher protein levels of LDLR and lower LDL-C levels in the liver and plasma, respectively, than the control mice. Mechanistic analysis revealed that PCSK9-induced endocytosis and lysosomal degradation of LDLR were mediated by caveolin but not by clathrin, and they were dependent on binding between CAP1 and caveolin-1. Conclusion We identified CAP1 as a new binding partner of PCSK9 and a key mediator of caveolae-dependent endocytosis and lysosomal degradation of LDLR.