Browsing by Author "Uysal, M."

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    Cooperative underwater acoustic communications
    (IEEE, 2013) Al-Dharrab, S.; Uysal, M.; Duman, T.
    This article presents a contemporary overview of underwater acoustic communication (UWAC) and investigates physical layer aspects on cooperative transmission techniques for future UWAC systems. Taking advantage of the broadcast nature of wireless transmission, cooperative communication realizes spatial diversity advantages in a distributed manner. The current literature on cooperative communication focuses on terrestrial wireless systems at radio frequencies with sporadic results on cooperative UWAC. In this article, we summarize initial results on cooperative UWAC and investigate the performance of a multicarrier cooperative UWAC considering the inherent unique characteristics of the underwater channel. Our simulation results demonstrate the superiority of cooperative UWAC systems over their point-to-point counterparts. © 1979-2012 IEEE.
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    Multi-resampling Doppler compensation in cooperative underwater OFDM systems
    (IEEE, 2013) Karakaya, B.; Hasna, M.O.; Duman, Tolga M.; Uysal, M.; Ghrayeb, A.
    We consider a multi-carrier cooperative underwater acoustic communication (UWAC) system and investigate the Doppler scaling problem arising due to the motion of different nodes. Specifically, we assume an orthogonal frequency division multiplexing (OFDM) system with amplify and forward (AF) relaying. Our channel model is built on large-scale path loss along with the short-term frequency-selective fading. For Doppler scaling compensation, we use multi-resampling (MR) receiver designs both at the relay and destination nodes. We present an extensive Monte Carlo simulation study to evaluate the error rate performance of the proposed UWAC system. In simulations, we use the publicly available VirTEX software in conjunction with the ray-tracing based BELLHOP software to precisely reflect the characteristics of an underwater geographical location and the movement of the nodes. © 2013 IEEE.
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    Systematic analysis of cytostatic TGF-Beta response in mesenchymal-like hepatocellular carcinoma cell lines
    (Springer, 2021-08-31) Güngör, M. Z.; Uysal, M.; Öztürk, Mehmet; Şentürk, Şerif
    Background Hepatocellular carcinoma (HCC) is one of the most challenging malignancies, with high morbidity and mortality rates. The transforming growth factor-β (TGF-β) pathway plays a dual role in HCC, acting as both tumor suppressor and promoter. A thorough understanding of the mechanisms underlying its opposing functions is important. The growth suppressive effects of TGF-β remain largely unknown for mesenchymal HCC cells. Using a systematic approach, here we assess the cytostatic TGF-β responses and intracellular transduction of the canonical TGF-β/Smad signaling cascade in mesenchymal-like HCC cell lines. Methods Nine mesenchymal-like HCC cell lines, including SNU182, SNU387, SNU398, SNU423, SNU449, SNU475, Mahlavu, Focus, and Sk-Hep1, were used in this study. The cytostatic effects of TGF-β were evaluated by cell cycle analysis, BrdU labeling, and SA-β-Gal assay. RT-PCR and western blot analysis were utilized to determine the mRNA and protein expression levels of TGF-β signaling components and cytostatic genes. Immunoperoxidase staining and luciferase reporter assays were performed to comprehend the transduction of the canonical TGF-β pathway. Results We report that mesenchymal-like HCC cell lines are resistant to TGF-β-induced growth suppression. The vast majority of cell lines have an active canonical signaling from the cell membrane to the nucleus. Three cell lines had lost the expression of cytostatic effector genes. Conclusion Our findings reveal that cytostatic TGF-β responses have been selectively lost in mesenchymal-like HCC cell lines. Notably, their lack of responsiveness was not associated with a widespread impairment of TGF-β signaling cascade. These cell lines may serve as valuable models for studying the molecular mechanisms underlying the loss of TGF-β-mediated cytostasis during hepatocarcinogenesis.