Summary： Abnormal cholesterol metabolism is associated with an elevated risk of developing athero- sclerosis, hypertension, and diabetes etc. Na＋/K＋-ATPase was found to regulate cholesterol synthesis, distribution ...Summary： Abnormal cholesterol metabolism is associated with an elevated risk of developing athero- sclerosis, hypertension, and diabetes etc. Na＋/K＋-ATPase was found to regulate cholesterol synthesis, distribution and trafficking. This study aimed to examine the effect of high-fat diet on cholesterol me- tabolism in rats and the role of Na＋/K＋-ATPase/Src/ERK signaling pathway in the process. Forty male SD rats were evenly divided into high-fat diet group and control group at random. Animals in the former group were fed on high-fat diet for 12 weeks, and those fed on basic diet served as control. Blood lipids, including total cholesterol （TC）, triglyceride （TG）, high density lipoprotein-cholesterol （HDL-C）, and low density lipoprotein-cholesteral （LDL-C） levels, were detected at 3, 6 and 12 weeks. The ratio of cholesterol content in cytoplasm to that in cell membrane was detected in liver tissues. RT-PCR and Western blotting were used to measure the expression of lipid metabolism-associated genes （HMG-CoA reductase and SREBP-2） after 12-week high-fat diet. Na＋/K＋-ATPase/Src/ERK signaling path- way-related components （Na＋/K＋-ATPase ctl, Src-PY418 and pERK1/2） were also measured by West- ern blotting. The results showed that the serum TC, TG, and LDL-C levels were significantly higher in high-fat diet group than those in control group, while the HDL-C level was significantly lower in high-fat diet group at 6 weeks （P〈0.01）. High-fat diet led to an increase in the cholesterol content in the cytoplasm and cell membrane. The ratio of cholesterol content in cytoplasm to that in cell membrane was elevated over time. The expression of HMG-CoA reductase and SREBP-2 was significantly sup- pressed at mRNA and protein levels after 12-week high-fat diet （P〈0.05）. Moreover, high-fat diet pro- moted the expression of Na＋/K＋-ATPase α1 but suppressed the phosphorylation of Src-PY418 and ERK1/2 at 12 weeks （P〈0.05）. It was concluded that high-fat diet regulates cholesterol metabolism, and Na＋/K＋-ATPase signaling pathway is involved in the process possibly by regulating the expression of lipid metabolism-associated proteins HMG-CoA reductase and SREBP-2.展开更多
二硫化钨(WS_(2))属于过渡金属硫族化合物(TMDs)材料,具有较宽的可调带隙(1.3~2.1 e V),缺陷密度相对较低,且有超高的表面积比,可通过外界掺杂或相变处理来改善载流子传输性能,在低功耗场效应晶体管和超灵敏光电探测器等领域有广阔的应...二硫化钨(WS_(2))属于过渡金属硫族化合物(TMDs)材料,具有较宽的可调带隙(1.3~2.1 e V),缺陷密度相对较低,且有超高的表面积比,可通过外界掺杂或相变处理来改善载流子传输性能,在低功耗场效应晶体管和超灵敏光电探测器等领域有广阔的应用前景。采用微机械剥离的方法将多层WS_(2)薄膜转移到氧化铪(HfO2)介质层上,制备出具有高栅控、低功耗的WS_(2)背栅场效应晶体管,通过注入三乙胺(TEA)实现WS_(2)薄膜的表面电子掺杂。实验结果表明,修饰后的多层WS_(2)薄膜的面内振动模式有轻微位移,拉曼特征峰强度变弱,证明三乙胺溶液能有效增加WS_(2)薄膜内的电子浓度;薄膜与金属电极之间的欧姆接触良好,器件的电子迁移率由10.87 cm^(2)·V^(-1)·s^(-1)提升到24.89 cm^(2)·V^(-1)·s^(-1),室温下的电流开关比保持在106,亚阈值摆幅为190.11 m V/dec。结合理论分析TEA对WS_(2)原子薄层的掺杂机理,TEA通过表面电荷转移的方式来增加WS_(2)半导体内的电子浓度,完成WS_(2)背栅场效应晶体管的n型掺杂。器件较高的电流开关比及电子迁移率的提升证明了TEA的表面修饰能有效调控多层WS_(2)晶体管器件的电子传输特性。展开更多
基金supported by a grant from the National Natural Science Foundation of China(No.81200637)
文摘Summary： Abnormal cholesterol metabolism is associated with an elevated risk of developing athero- sclerosis, hypertension, and diabetes etc. Na＋/K＋-ATPase was found to regulate cholesterol synthesis, distribution and trafficking. This study aimed to examine the effect of high-fat diet on cholesterol me- tabolism in rats and the role of Na＋/K＋-ATPase/Src/ERK signaling pathway in the process. Forty male SD rats were evenly divided into high-fat diet group and control group at random. Animals in the former group were fed on high-fat diet for 12 weeks, and those fed on basic diet served as control. Blood lipids, including total cholesterol （TC）, triglyceride （TG）, high density lipoprotein-cholesterol （HDL-C）, and low density lipoprotein-cholesteral （LDL-C） levels, were detected at 3, 6 and 12 weeks. The ratio of cholesterol content in cytoplasm to that in cell membrane was detected in liver tissues. RT-PCR and Western blotting were used to measure the expression of lipid metabolism-associated genes （HMG-CoA reductase and SREBP-2） after 12-week high-fat diet. Na＋/K＋-ATPase/Src/ERK signaling path- way-related components （Na＋/K＋-ATPase ctl, Src-PY418 and pERK1/2） were also measured by West- ern blotting. The results showed that the serum TC, TG, and LDL-C levels were significantly higher in high-fat diet group than those in control group, while the HDL-C level was significantly lower in high-fat diet group at 6 weeks （P〈0.01）. High-fat diet led to an increase in the cholesterol content in the cytoplasm and cell membrane. The ratio of cholesterol content in cytoplasm to that in cell membrane was elevated over time. The expression of HMG-CoA reductase and SREBP-2 was significantly sup- pressed at mRNA and protein levels after 12-week high-fat diet （P〈0.05）. Moreover, high-fat diet pro- moted the expression of Na＋/K＋-ATPase α1 but suppressed the phosphorylation of Src-PY418 and ERK1/2 at 12 weeks （P〈0.05）. It was concluded that high-fat diet regulates cholesterol metabolism, and Na＋/K＋-ATPase signaling pathway is involved in the process possibly by regulating the expression of lipid metabolism-associated proteins HMG-CoA reductase and SREBP-2.
文摘二硫化钨(WS_(2))属于过渡金属硫族化合物(TMDs)材料,具有较宽的可调带隙(1.3~2.1 e V),缺陷密度相对较低,且有超高的表面积比,可通过外界掺杂或相变处理来改善载流子传输性能,在低功耗场效应晶体管和超灵敏光电探测器等领域有广阔的应用前景。采用微机械剥离的方法将多层WS_(2)薄膜转移到氧化铪(HfO2)介质层上,制备出具有高栅控、低功耗的WS_(2)背栅场效应晶体管,通过注入三乙胺(TEA)实现WS_(2)薄膜的表面电子掺杂。实验结果表明,修饰后的多层WS_(2)薄膜的面内振动模式有轻微位移,拉曼特征峰强度变弱,证明三乙胺溶液能有效增加WS_(2)薄膜内的电子浓度;薄膜与金属电极之间的欧姆接触良好,器件的电子迁移率由10.87 cm^(2)·V^(-1)·s^(-1)提升到24.89 cm^(2)·V^(-1)·s^(-1),室温下的电流开关比保持在106,亚阈值摆幅为190.11 m V/dec。结合理论分析TEA对WS_(2)原子薄层的掺杂机理,TEA通过表面电荷转移的方式来增加WS_(2)半导体内的电子浓度,完成WS_(2)背栅场效应晶体管的n型掺杂。器件较高的电流开关比及电子迁移率的提升证明了TEA的表面修饰能有效调控多层WS_(2)晶体管器件的电子传输特性。
