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| 1 | Role of autophagy in liver physiology and pathophysiology显示文摘Autophagy is a highly conserved intracellular degradation pathway by which bulk cytoplasm and superfluous or damaged organelles are enveloped by double membrane structures termed autophagosomes. The autophago-somes then fuse with lysosomes for degradation of their contents, and the resulting amino acids can then recycle back to the cytosol. Autophagy is normally activated in response to nutrient deprivation and other stressors and occurs in all eukaryotes. In addition to maintaining energy and nutrient balance in the liver, it is now clear that autophagy plays a role in liver protein aggregates related diseases, hepatocyte cell death, steatohepatitis, hepatitis virus infection and hepatocellular carcinoma. In this review, I discuss the recent findings of autophagy with a focus on its role in liver pathophysiology. | Wen-Xing Ding, Department of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, MS 1018, 3901 Rainbow Blvd, Kansas City, Kansas, KS 66160, United States | 2010 | World Journal of Biological Chemistry2010,1,1: | 9 |
| 2 | Developmental Lead Exposure Alters the Distribution of Protein Kinase C Activity in the Rat Hippocampus显示文摘Chronic low-level lead (Pb) exposure in children is known to cause a deficit in learning and memory. In vitro studies have demonstrated that Pb altered protein kinase C (PKC) activityt Especially, hippocampal PKC has been correlated with performance in several learning tasks. The effects of Pb exposure on hippocampal PKC were investigated during development at various postnatal ages: postnatal day (PN) 7, 14, 28, and 56. Two-tenth % Pb acetate was administered to pregnant and lactating dams and then administered to weanling rats in drinking water. PKC activity was measured in both membrane and cytosolic fractions from the hippocampi of the controls and Pb-exposed animals. Pb-induced increase in PKC activity in the cytosolic fraction was obsereved in the PN56 rats. In contrast, PKC activity was decreased by Pb at PN7 in the membrane fraction. Furthermore, a significant decrease in the ratio of membrane to cytosolic PKC activity which is representative of PKC distribution was observed in the PN28 and PN56 Pb-exposed rats relative to the same-age controls. This study indicates that chronic Pb exposure during development influences hippocampal PKC activity and distribution. These changes may be involved in the subclinical neurotoxicity of chronic Pb exposure in young children. | HWEI-HSIEN CHEN TANGENG MA ARTHUR S. HUME AND ING K. HO(Deportment of Pharmacology and Toxicology, University ofMississippi Medical Center, 2500 North State Street,Jackson, MS 39216, USA) | 1998 | Biomedical and Environmental Sciences1998,11,1: | 7 |
| 3 | MATHEMATICAL MODELS FOR LIQUID-SOLID TWO-PHASE FLOW显示文摘The governing equations, interphase actions, constitutive relations and turbulence closures of the twofluid model and diffusion model for the liquid-solid two-phase flow are studied in this paper. The pressure actions in and between two phases are analyzed, and the governing equations of the two-fluid model are conveniently closed by adding the interphase pressure-difference force into the pressure terms of momentum equations. The constitutive relations for the liquid-solid mixture in the diffusion model are given by the models of Newtonian fluid and Bingham fluid, and the Bingham relation of shear stress and deformation rate for the single-directional shear flow of the mixture is extended to a general form for the multi-directional shear flow. The equation for the interphase velocity difference, which is used to close the generalized diffusion model, is derived from the momentum equations of two-fluid model and then simplified to more useful forms. For the turbulent flow, the mean movement equations of the two-fluid model and diffusion model are derived by using Reynolds averaging method. The closure techniques for the mean movement equations on the levels of zero-order turbulence model and κ-ε turbulence model are suggested. This paper presents the general basis of the mathematical models, which is to be followed by their validations and applications in the near future. | Weiming Wu and Sam S.Y. Wang National Center for Computational Hydroscience and Engineering, The University of Mississippi, MS 38677, U.S.A. | 2000 | International Journal of Sediment Research2000,15,3: | 5 |
| 4 | The MRP gene associated with a non-P-glycoprotein multidrug resistance encodes a 190- kDa membrane bound glycoprotein显示文摘 | Krishnamachary N Center MS | 1993 | Cancer Res1993,53,16: | 1 |
| 5 | The MRP gene associated with a non-pglycoprotein multidrug resistance encodes a 190-KDa membrane bound glycoprotein 显示文摘 | Krishnamachary N Center MS | 1993 | Cancer Res1993,53,7: | 1 |
| 6 | Cloning and sequence analysis of the promoter region of the MRP gene of HL60 cells isolated for resistance to adriamycin显示文摘 | Zhu Q Center MS | 1994 | Cancer Res1994,54,16: | 1 |
| 7 | The MRP gene associated with a non-p-glycoprotein multidrug resistance encodes a 190-kDa membrane bound glycoprotein显示文摘 | Center MS | 1993 | Cancer Res1993,53,16: | 1 |
| 8 | Involvement of vacuolar H(+)-adenosine triphosphatase activity in multidrug resistance in HL60 cells显示文摘 | Center MS | 1991 | J Natl Cancer Inst1991,83,15: | 1 |
| 9 | Mrp1 multidrug resistance-associated protein and P-glycoprotein expression in rat brain microvessel endothelial cells显示文摘 | Regina A Koman A Piciotti M El Hafny B Center MS Bergmann R Couraud PO Roux F | 1998 | J of Neurochem1998,71,: | 1 |
| 10 | Involvement of vacuolar H (+)-adenosine triphosphatase activity in multidrug resistance in HL60 cells显示文摘 | Marquardt D Center MS | 1991 | Natl Cancer Inst1991,83,: | 1 |
| 11 | The MRP gene associated with a non-P-glycoprotein multidrug resistance encodes a190kDa membrane bound glycoprotein 显示文摘 | Krishnamachary N Center MS | 1993 | Cancer Res1993,53,7: | 1 |
| 12 | The MRP gene associated with a non-pglyeoprotein multidrug resistance encodes a 190kD membrance bound glycoprotein 显示文摘 | Krishnamachary N Center MS | 1993 | Cancer Res1993,53,16: | 1 |
| 13 | The MRP gene associated with a non-P-glycoprotein 显示文摘 | Krishnamachary N Center MS | 1993 | Cancer Res1993,53,: | 1 |
| 14 | Involvement of vacuolar H (+)-a-denosine triphosphatase activity in multidrug resistance in HL60 cells显示文摘 | Marquardt D Center MS | 1991 | J Natl Cancer Inst1991,83,: | 1 |
| 15 | The MRP gene associated with a non-p-glycoprotein multidrug resistance encodes a 190-kDa membrane bound glycoprotein 显示文摘 | Center MS | 1993 | Cancer Res1993,53,: | 1 |
| 16 | The MRP gene associated with a non-p-glycoproteinmultidrug resistance encodes a 190 kD membrane bound glycoprotein 显示文摘 | Krishnamachary N Center MS | 1993 | Cancer Res1993,53,: | 1 |
| 17 | The MRP gene associated with a non-p-glycoprotein multidrug resistance encodes a 190 kD membrane bound glycoprotein显示文摘 | Krishnamachary N Center MS | 1993 | Cancer Res1993,53,16: | 1 |
| 18 | The MRP gene associated with a non-P-proglyprotein 显示文摘 | Krishnamachary N Center MS | 1993 | Cancer Res1993,53,21: | 1 |
| 19 | Phosphorylation of multidrug resistance- associated protein gene encoded protein P190 显示文摘 | Ma L Krishnamachary N Center MS | 1995 | Biochemistry1995,34,: | 1 |
| 20 | The MRP gene associated with a nonP-glycoprotein multidrug resistance encodes a 190 kDa membrane bound glycoprotein显示文摘 | Krishnamachary N Center MS | 1993 | Cancer Res1993,53,16: | 1 |