337 research outputs found
Mobile Supplicant for SIM Authentication
No full textThis Master’s thesis proposes a solution for utilizing the GSM SIM to authenticate users to distributed services accessed through the mobile terminal. By combining the GSM SIM authentication mechanisms with the EAP-SIM framework we achieve mutual authentication between the parties. By combining the fact that the GSM SIM is a tamper resistant Smart Card, and that users have to present a valid PIN to activate the system, we have also achieved strong two-factor authentication that fulfils the highest security level defined by NIST. The proposed system is secure, easy to use and inexpensive, because most of the components needed already exist in the GSM network today. Existing strong user authentication systems for mobile handsets require several devices to be able to offer secure services. The proposed system only requires one device, namely the mobile handset which the user is carrying anyway. The only user interaction required is typing the PIN. The authors’ major contribution to the proposed system is the Supplicant, residing on the mobile handset and communicating with the SIM through the SATSA-APDU interface. By running the Supplicant as a local proxy on the mobile handset, it is able to communicate with all kinds of client applications supporting HTTP, e.g. mobile browsers, J2ME MIDlets and native applications. A prototype implementing several of the components in the proposed system has been developed. Unfortunately, due to several reasons, the prototype cannot be deployed on a real mobile handset today’s date. We are missing the necessarily certificate required to get access to the SIM and neither of today’s mobile handsets support all the functionality needed. However, the prototype has been implemented successfully on a PC running the Wireless Toolkit from Sun, which simulates the SIM environment. Based on results from this thesis, the author has written the paper "A Unified Authentication Solution for Mobile Services". The paper was accepted and published on the ERCIM workshop on eMobility in Coimbra, Portugal, on May 2007
Mobile Supplicant for SIM Authentication
No full textThis Master’s thesis proposes a solution for utilizing the GSM SIM to authenticate users to distributed services accessed through the mobile terminal. By combining the GSM SIM authentication mechanisms with the EAP-SIM framework we achieve mutual authentication between the parties. By combining the fact that the GSM SIM is a tamper resistant Smart Card, and that users have to present a valid PIN to activate the system, we have also achieved strong two-factor authentication that fulfils the highest security level defined by NIST. The proposed system is secure, easy to use and inexpensive, because most of the components needed already exist in the GSM network today. Existing strong user authentication systems for mobile handsets require several devices to be able to offer secure services. The proposed system only requires one device, namely the mobile handset which the user is carrying anyway. The only user interaction required is typing the PIN. The authors’ major contribution to the proposed system is the Supplicant, residing on the mobile handset and communicating with the SIM through the SATSA-APDU interface. By running the Supplicant as a local proxy on the mobile handset, it is able to communicate with all kinds of client applications supporting HTTP, e.g. mobile browsers, J2ME MIDlets and native applications. A prototype implementing several of the components in the proposed system has been developed. Unfortunately, due to several reasons, the prototype cannot be deployed on a real mobile handset today’s date. We are missing the necessarily certificate required to get access to the SIM and neither of today’s mobile handsets support all the functionality needed. However, the prototype has been implemented successfully on a PC running the Wireless Toolkit from Sun, which simulates the SIM environment. Based on results from this thesis, the author has written the paper "A Unified Authentication Solution for Mobile Services". The paper was accepted and published on the ERCIM workshop on eMobility in Coimbra, Portugal, on May 2007
CLINICAL BENEFIT OF PERCUTANEOUS CORONARY INTERVENTION IN EARLY LATECOMERS WITH ACUTE ST-ELEVATION MYOCARDIAL INFARCTION
No full textBENEFIT OF NEW ANGIOTENSIN RECEPTOR BLOCKER, FIMASARTAN, IN A PORCINE MODEL OF ACUTE MYOCARDIAL INFARCTION
No full textCLINICAL BENEFIT OF GLYCOPROTEIN IIB/IIIA RECEPTOR INHIBITOR IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION COMPLICATED BY CARDIOGENIC SHOCK
No full textTCTAP A-049 Cardio Protective Effect of Substance P in a Porcine Model of Acute Myocardial Infarction
No full text
Differences in the Korea Acute Myocardial Infarction Registry Compared with Western Registries
No full text
Simvastatin Attenuates TGF-β1-Induced Epithelial-Mesenchymal Transition in Human Alveolar Epithelial Cells
No full textBackground: Transforming growth factor-β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) of alveolar epithelial cells (AEC) may contribute to idiopathic pulmonary fibrosis (IPF). TGF-β1-induced EMT in A549 cells (a human AEC cell line) resulted in the adoption of mesenchymal responses that were predominantly mediated via the TGF-β1-Smad2/3 signaling pathway. Simvastatin (Sim), a 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase inhibitor, has been previously reported to inhibit EMT in human proximal tubular epithelial cells and porcine lens epithelial cells and to suppress Smad2/3 phosphorylation in animal models. However, whether Sim can attenuate TGF-β1-induced EMT in A549 cells and its underlying mechanisms remains unknown. Methods: Cells were incubated with TGF-β1 in the presence or absence of Sim. The epithelial marker E-cadherin (E-Cad) and the mesenchymal markers, α-smooth muscle actin (α-SMA), vimentin (Vi) and fibronectin (FN), were detected using western blotting analyses and immunofluorescence. Phosphorylated Smad2 and Smad3 levels and connective tissue growth factor (CTGF) were analyzed using western blotting. In addition, a cell migration assay was performed. Moreover, the levels of matrix metalloproteinase (MMP)-2 and -9 in the culture medium were examined using ELISA. Results: Sim significantly attenuated the TGF-β1-induced decrease in E-Cad levels and elevated the levels of α-SMA, Vi and FN via the suppression of Smad2 and Smad3 phosphorylation. Furthermore, Sim inhibited the mesenchymal-like responses in A549 cells, including cell migration, CTGF expression and secretion of MMP-2 and -9. However, Sim failed to reverse the cell morphologial changes induced by TGF-β1 in A549 cells. Conclusion: Sim attenuated TGF-β1-induced EMT in A549 cells and might be a promising therapeutic agent for treating IPF
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