ObjectiveTo investigate the expression of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metallopropteinase-1 (TIMP-1) in the renal allografts of patients with chronic active antibody-mediated rejection (AMR), and to explore their role in the pathogenesis of AMR.MethodsImmunohistochemistry assay and computer-assisted image analysis were used to detect the expression of MMP-2 and TIMP-1 in the renal allografts with interstitial fibrosis and tubular atrophy (IF/TA) in 46 transplant recipients and 15 normal renal tissue specimens as the controls. The association of the expression level of either MMP-2 or TIMP-1 with the pathological grade of IF/TA in AMR was analyzed.ResultsThe expression of either MMP-2 or TIMP-1 was significantly increased in the renal allografts of the recipients as compared with the normal renal tissue (P < 0.05). MMP-2 expression tended to decrease, while TIMP-1 and serum creatinine increased along with the increase of pathological grade of IF/TA (P < 0.05). In IF/TA groups, the expression of TIMP-1 was positively correlated to serum creatinine level (r = 0.718, P < 0.05).ConclusionsIt is suggested by the results that abnormal expressions of MMP-2 and TIMP-1 might play roles in the development of renal fibrosis in chronic AMR.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1128474926172838
ObjectiveTo explore the expression of Glycogen synthase kinase 3 beta (GSK-3β) in renal allograft tissue and its significance in the pathogenesis of chronic allograft dysfunction.MethodsRenal allograft biopsy was performed in all of the renal allograft recipients with proteinuria or increased serum creatinine level who came into our hospital from January 2007 to December 2009. Among them 28 cases was diagnosed as chronic allograft dysfunction based on pahtological observation, including 21 males with a mean age of 45 ± 10 years old and 7 females with a mean age of 42 ± 9 years old. The time from kidney transplantation to biopsy were 1-9 (3.5) years. Their serum creatinine level were 206 ± 122 umol/L. Immunohistochemical assay and computer-assisted genuine color image analysis system (imagepro-plus 6.0) were used to detect the expression of GSK-3β in the renal allografts of 28 cases of recipients with chronic allograft dysfunction. Mean area and mean integrated optical density of GSK-3β expression were calculated. The relationship between expression level of GSK-3β and either the grade of inflammatory cell infiltration or interstitial fibrosis/tubular atrophy in renal allograft was analyzed. Five specimens of healthy renal tissue were used as controls.ResultsThe expression level of the GSK-3β was significantly increased in the renal allograft tissue of recipients with chronic allograft dysfunction, compared to normal renal tissues, and GSK-3β expression became stronger along with the increasing of the grade of either inflammatory cell infiltration or interstitial fibrosis/tubular atrophy in renal allograft tissue.ConclusionThere might be a positive correlation between either inflammatory cell infiltration or interstitial fibrosis/tubular atrophy and high GSK-3β expression in renal allograft tissue.Virtual slidesThe virtual slide(s) for this article can be found here:http://www.diagnosticpathology.diagnomx.eu/vs/9924478946162998.
Chronic antibody-mediated rejection (ABMR) is a major cause of the transplant renal interstitial fibrosis and transplanted kidney epithelial cell transdifferentiation is one of the main mechanisms. The transforming growth factor (TGF)-β1/integrin-linked kinase (ILK) signaling pathway has a significant role in the epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells; however, the molecular mechanisms of this process have remained elusive. The present study confirmed that Akt and glycogen synthase kinase (GSK)-3β, as TGF-β1 downstream signaling factors, are involved in fibrotic processes caused by kidney disease, which, however, has been rarely reported in the kidney transplant field. Based on the Banff 2009 standard, transplanted kidney specimens were classified according to the fibrosis level. The results showed that with the reduction of the interstitial fibrosis level, E-cadherin expression was gradually reduced, while α-smooth muscle actin expression progressively increased. The expression of Akt and GSK-3β in normal human kidney tissue was not obvious but showed a marked increase with the aggravation of the interstitial fibrosis level, which confirmed the occurrence of EMT during the fibrosis process, and that phosphorylated (p)-Akt and GSK-3β have an important role in the EMT process in the transplanted kidney. A correlation analysis of p-Akt, GSK-3β, TGF-β1 and ILK suggested that overexpression of p-Akt and GSK-3β may induce and mediate the transdifferentiation of renal tubular epithelial cells to myofibroblasts and that this proceeds via TGFβ1/ILK signaling pathways.
The smart grid is a key piece of infrastructure and its security has attracted widespread attention. The false data injection (FDI) attack is one of the important research issues in the field of smart grid security. Because this kind of attack has a great impact on the safe and stable operation of the smart grid, many effective detection methods have been proposed, such as an FDI detector based on the support vector machine (SVM). In this paper, we first analyze the problem existing in the detector based on SVM. Then, we propose a new attack method to reduce the detection effect of the FDI detector based on SVM and give a proof. The core of the method is that the FDI detector based on SVM cannot detect the attack vectors which are specially constructed and can replace the attack vectors into the training set when it is updated. Therefore, the training set is changed and then the next training result will be affected. With the increase of the number of the attack vectors which are injected into the positive space, the hyperplane moves to the side of the negative space, and the detection effect of the FDI detector based on SVM is reduced. Finally, we analyze the impact of different data injection modes for training results. Simulation experiments show that this attack method can impact the effectiveness of the FDI detector based on SVM.
Previous studies have demonstrated that false commands can cause severe damage to large-scale cyber-physical systems (CPSs). We focus on a kind of threat called false sequential command attack, with which attackers can generate false sequential commands, resulting in the illegal control of the physical process. We present a feasible attack model. Attackers delay the disaggregation of former commands by manipulating maliciously sub-controllers. Simultaneously, bad feedback data is injected to defeat the controller to issue latter commands. Thus, false command sequence is executed and the disruption of physical process can be obtained. It is also difficult for the detector to identify such attacks as injecting bad data. We also discuss other possible attack paths and analyze the corresponding disadvantages. Compared with other paths, the proposed model is more feasible and has more difficulties to be detected. A case study is given to validate the feasibility and effectiveness of proposed false sequential command attack model. Finally, we discuss the possible countermeasure.
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