RESUMO
4H-silicon carbide (4H-SiC) possesses a high Baliga figure of merit, making it a promising material for power electronics. However, its applications are limited by low hole mobility. Herein, we found that the hole mobility of 4H-SiC is mainly limited by the strong interband electron-phonon scattering using mode-level first-principles calculations. Our research indicates that applying compressive strain can reverse the sign of crystal-field splitting and change the ordering of electron bands close to the valence band maximum. Therefore, the interband electron-phonon scattering is severely suppressed and the electron group velocity is significantly increased. The out-of-plane hole mobility of 4H-SiC can be greatly enhanced by â¼200% with 2% uniaxial compressive strain applied. This work provides new insights into the electron transport mechanisms in semiconductors and suggests a strategy to improve hole mobility that could be applied to other semiconductors with hexagonal crystalline geometries.
RESUMO
Diabetic nephropathy (DN) is a diabetic complication that threatens the health of patients with diabetes. In addition, podocyte injury can lead to the occurrence of DN. The protein 6phosphofructo2kinase/fructose2,6-biphosphatase 3 (PFKFB3) may be associated with diabetes; however, the effects of PFKFB3 knockdown by small interfering (si)RNA on the growth of podocytes remains unknown. To investigate the mechanism by which PFKFB3 mediates podocyte injury, MPC5 mouse podocyte cells were treated with highglucose (HG), and cell viability and apoptosis were examined by Cell Counting Kit8 assay and flow cytometry, respectively. In addition, the expression of autophagyrelated proteins were measured using western blot analysis and immunofluorescence staining. Cell migration was investigated using a Transwell assay and phalloidin staining was performed to observe the cytoskeleton. The results revealed that silencing of PFKFB3 significantly promoted MPC5 cell viability and inhibited apoptosis. In addition, the migration of the MPC5 cells was notably downregulated by siPFKFB3. Moreover, PFKFB3 silencing notably reversed the HGinduced decrease in oxygen consumption rate, and the HGinduced increase in extracellular acidification rate was rescued by PFKFB3 siRNA. Furthermore, silencing of PFKFB3 induced autophagy in HGtreated podocytes through inactivating phosphorylated (p)mTOR, pAMPKα, LC3 and sirtuin 1, and activating p62. In conclusion, silencing of PFKFB3 may protect podocytes from HGinduced injury by inducing autophagy. Therefore, PFKFB3 may serve as a potential target for treatment of DN.
Assuntos
Autofagia/efeitos dos fármacos , Nefropatias Diabéticas/metabolismo , Glucose/metabolismo , Fosfofrutoquinase-2/fisiologia , Podócitos/metabolismo , Animais , Linhagem Celular , Humanos , Camundongos , Podócitos/patologiaRESUMO
OBJECTIVE: To investigate the relationship between chronic pyelonephritis (CPN) and immune function, and the therapeutic mechanism of Yishenkang granule (YSKG). METHODS: One hundred and twenty patients of CPN were divided into 3 groups randomly, the YSKG group (treated with YSKG), the control A group (treated with Sanjin tablet) and the control B group (treated with western medicine). Serum levels of immunoglobulin (Ig), complement 3 (C3), interleukin-2 (IL-2), peripheral T-lymphocyte subsets, and urinary secretory immunoglobulin A (sIgA) were determined before and after treatment with monoclonal antibody assay, agar diffusion method, radioimmunoassay (RIA), and radioimmuno-equilibrium method, and compared with normal control. RESULTS: There were disorders of T-lymphocyte subsets in CPN, lowering of serum Ig, C3 and urinary sIgA, and increase of blood IL-2 (P < 0.05 or P < 0.01). These abnormalities could be normalized after YSKG treatment. CONCLUSION: Functional disorders of cellular and humoral immunity exist in CPN patients of chronic stage, YSKG could correct the immune functional disorder, control the recurrence of CPN effectively and alleviate the immunopathological damage.