ROBUST ADAPTIVE BEAMFORMING WITH BROAD NULLS

ITC/USA 2007 Conference Proceedings / The Forty-Third Annual International Telemetering Conference and Technical Exhibition / October 22-25, 2007 / Riviera Hotel & Convention Center, Las Vegas, NevadaRobust adaptive beamforming using worst-case performance optimization is developed in recent years. It had good performance against array response errors, but it cannot reject strong interferences. In this paper, we propose a scheme for robust adaptive beamforming with broad nulls to reject strong interferences. We add a quadratic constraint to suppress the power of the array response over a spatial region of the interferences. The optimal weighting vector is then obtained by minimizing the power of the array output subject to quadratic constrains on the desired signal and interferences, respectively. We derive the formulations for the optimization problem and solve it efficiently using Newton recursive algorithm. Numerical examples are presented to compare the performances of the robust adaptive beamforming with no null constrains, sharp nulls and broad nulls. The results show its powerful ability to reject strong interferences.International Foundation for TelemeteringProceedings from the International Telemetering Conference are made available by the International Foundation for Telemetering and the University of Arizona Libraries. Visit http://www.telemetry.org/index.php/contact-us if you have questions about items in this collection

Solid Pseudopapillary Neoplasm of the Pancreas: Clinicopathologic Feature, Risk Factors of Malignancy, and Survival Analysis of 53 Cases from a Single Center

Introduction. Solid pseudopapillary neoplasm (SPN) of the pancreas is a rare tumor of low malignant potential. The aim of this study was designed to evaluate the clinicopathologic feature, predictive factors of malignancy, and survival from experience of a single center. Methods. 53 consecutive patients who underwent surgery for a pathologically definitive SPN were retrospectively reviewed. Results. A total of 53 cases included 7 male cases and 46 female cases with the median age of 35.4 years (14–67). Abdominal pain and mass were the most common clinical presentations. The radiological presentations were consistent with solid and cystic pattern in 18 cases, solid pattern in 25 cases, and cystic pattern in 10 cases. The predominant location of tumor was pancreatic body and tail. The mean size of the tumors was 6.4 cm. Aggressive en bloc resection combined with organ-preserving should be indicated whenever feasible. Follow-up information was available for 48 patients with a median follow-up time of 48 months. The 5-year disease-specific survival was 95.7%. Incomplete capsule was not only the predictive factor of malignancy but also the significant predictor of disease-specific survival. Conclusion. Incomplete capsule may suggest a malignant SPN and a prognostic indicator of disease-specific survival. We recommend that surgeons consider a more radical resection with an incomplete capsule of tumor

Suppression of Non-Small Cell Lung Cancer Growth and Metastasis by a Novel Small Molecular Activator of RECK

Background/Aims: Reversion-inducing cysteine-rich protein with kazal motifs (RECK) is a novel tumor suppressor gene that is critical for regulating tumor cell invasion and metastasis. The expression of RECK is dramatically down-regulated in human cancers. Harmine, a tricyclic compound from Peganum harmala, has been shown to have potential anti-cancer activity. Methods: Cell proliferation assay (CCK-8 cell viability assay), cell cycle analysis (detection by flow cytometry), apoptosis staining assay (TUNEL staining), cell migration assay and invasion assay (transwell assay) were carried out to investigate the Harmine’s efficacy on non-small cell lung cancer (NSCLC) cells in vitro. A549-luciferase cell orthotropic transplantation xenograft mouse model was used to determine the effect of Harmine treatment on NSCLC in vivo. Western blotting analysis of cell growth and metastasis related signal pathways was conducted to investigate the molecular mechanism of Harmine’s inhibitory effect on NSCLC. Results: Harmine treatment effectively inhibited cell proliferation and induced the G1/S cell cycle arrest of NSCLC cells. Further study proved that Harmine treatment led to apoptosis induction. Furthermore, treatment with NSCLC cells with Hamine resulted in decreased cell migration and cell invasion in vitro. More importantly, Harmine treatment significantly suppressed the NSCLC tumor growth and metastasis in mouse xenograft model in vivo. Mechanistically, in Harmine-treated NSCLC cells, RECK expression and its downstream signaling cascade were dramatically activated. As a consequence, the expression level of MMP-9 and E-cadherin were significantly decreased. Conclusion: These findings identify Harmine as a promising activator of RECK signaling for metastatic NSCLC treatment