3D Modal Solution for Tidally Induced Lagrangian Residual Velocity with Variations in Eddy Viscosity and Bathymetry in a Narrow Model Bay

In this study, we examine the results obtained by the Finite-volume Coastal Ocean Circulation Model(FVCOM) regarding the effects of eddy viscosity and bathymetry on the three-dimensional(3 D) Lagrangian residual velocity(LRV) in a narrow bay. The results are cast in terms of two nondimensional numbers: the ratio of friction to local acceleration(δ) and the ratio of the minimum depth over shoals to the maximum depth in the channel(ε). The ratio δ depends on the eddy viscosity and mean depth. For a given eddy viscosity, when ε > 0.5, the along-estuary LRV tends to be vertically sheared and when ε < 0.5, the exchange is laterally sheared. When ε << 1, the structure of the 3 D, depth-integrated, and breadth-averaged LRV changes only slightly as δ increases. For ε values between 0.33 and 0.5, the structure of the 3 D LRV is mainly laterally sheared. In the same ε range, the 3 D and depth-integrated LRV exhibit reversed structures from high to low δ values. In addition, the breadth-averaged LRV weakens the typical twolayered circulation when δ decreases. When ε is 1, the two-layered vertical structure reverses direction, and a three-layered vertical structure develops in the outer bay as δ decreases.

抑制HDAC6可增强自噬减轻肾脏缺血再灌注损伤

目的探讨HDAC6在小鼠肾脏缺血再灌注损伤中对α-微管蛋白和自噬相关基因表达的影响。方法通过夹闭肾动脉建立小鼠肾缺血再灌注损伤模型,检测小鼠血清肌酐、尿素氮,用HE染色观测肾脏形态学,用Western blot法和qPCR法检测HDAC6在缺血再灌注损伤过程中蛋白和基因表达的变化。建立小鼠肾小管上皮缺氧复氧模型,用Western blot法检测α-微管蛋白和自噬相关蛋白表达,用CCK-8检测细胞活力,用凋亡试剂盒检测细胞凋亡。结果在小鼠肾脏缺血再灌注损伤后,小鼠肾脏组织中HDAC6含量增加(P<0.05)。在细胞缺氧复氧加HDAC6选择性抑制剂tubastatin A(TA)组,细胞活力增强,细胞凋亡减少(P<0.05)。肾小管细胞缺氧复氧后,α-微管蛋白乙酰化水平降低,肾小管细胞缺氧复氧加TA组,α-微管蛋白乙酰化水平升高。肾小管细胞缺氧复氧后,自噬相关基因LC3、ATG7、Beclin-1表达增加,自噬激活,加TA组LC-3、ATG7、Beclin-1表达较单纯缺氧复氧组增多,自噬增强(P<0.05)。结论HDAC6抑制剂可通过激活自噬减轻肾脏缺血再灌注损伤。