Anti-EGI (C-terminal) polyclonal antibody

This paper presents a new motion sensing algorithm for airborne synthetic aperture radar (SAR). Image processing in SAR requires highly accurate and precise motion information which is used for matched filter in range and azimuth compression of the range Doppler algorithm (RDA). If an embedded global positioning system and inertial navigation system (EGI) is used for motion sensing, it can sense the motion more accurately than using INS or GPS alone. However, the discontinuity in the position error occurs because GPS updates the measurement periodically, and this discontinuity significantly degrades the SAR image quality. To resolve this problem, a parametric error modeling (PEM) is proposed to mitigate the discontinuity errors. The PEM is a method that estimates polynomial parameters of INS error compared to EGI which can be assumed by a polynomial in short term. Then, when the error estimated by PEM is subtracted from the INS position, the discontinuity error of EGI can be eliminated. Numerical simulation shows that applying PEM perfectly eliminates discontinuity of EGI output; then, point target simulation using RDA shows improvement for impulse response function quality. Experimental result verifies the above result and demonstrates that the image quality is improved in SAR imagery.

Clinical treatment options for human cholangiocarcinoma (CC) are limited. c-MET, a high-affinity receptor for hepatocyte growth factor (HGF), is deregulated in many cancers. Its role in cholangiocarcinogenesis remains unclear. In current study, 23 corresponding tumor-and non-tumor tissues, taken from patients with intrahepatic (iCC) and perihilar cholangiocarcinoma (pCC), who underwent liver resection, were analyzed. The relationship of clinicopathological features and c-MET, as well as c-jun N-terminal kinase (JNK) was evaluated. The anti-tumor effects of Tivantinib, a small-molecule inhibitor with potent activity against the c-MET kinase, was investigated in three human CC cell lines, namely HUCC-T1, TFK-1, and EGI-1. In comparison with the results obtained in non-tumor tissue samples, c-MET was overexpressed in 91.3 % of tumor tissues (p < 0.01). The JNK expression was higher in tumor tissue compared with the corresponding non-tumor tissue sample in 17.4% patients (p < 0.01). The inhibition of aberrant c-MET expression in human CC cell lines was achieved by blocking the phosphorylation of c-MET with Tivantinib. Notable losses in cell viability and colony-forming capability were detected (p < 0.01). Synergistic activation of the JNK/c-jun pathway was demonstrated after Tivantinib treatment. Knockdown of the JNK by siRNA or competitive binding of c-MET receptor by stimulation with HGF-antagonized anti-tumor effects of Tivantinib was observed. Our data suggest that inhibition of c-MET could be a possible alternative approach for the treatment of human CC, for which Tivantinib may an effective inhibitor. The synergistic activation of the JNK/c-jun pathway contributed to the elevated apoptosis in CC cells via treatment with Tivantinib.