Browsing by Author "Ozcan, A."

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Open Access
Low power zinc-oxide based charge trapping memory with embedded silicon nanoparticles via poole-frenkel hole emission
(2014) El-Atab, N.; Ozcan, A.; Alkis, S.; Okyay, Ali Kemal; Nayfeh, A.
A low power zinc-oxide (ZnO) charge trapping memory with embedded silicon (Si) nanoparticles is demonstrated. The charge trapping layer is formed by spin coating 2 nm silicon nanoparticles between Atomic Layer Deposited ZnO steps. The threshold voltage shift (ΔVt) vs. programming voltage is studied with and without the silicon nanoparticles. Applying -1 V for 5 s at the gate of the memory with nanoparticles results in a ΔVt of 3.4 V, and the memory window can be up to 8 V with an excellent retention characteristic (>10 yr). Without nanoparticles, at -1 V programming voltage, the ΔVt is negligible. In order to get ΔVt of 3.4 V without nanoparticles, programming voltage in excess of 10 V is required. The negative voltage on the gate programs the memory indicating that holes are being trapped in the charge trapping layer. In addition, at 1 V the electric field across the 3.6 nm tunnel oxide is calculated to be 0.36 MV/cm, which is too small for significant tunneling. Moreover, the ΔVt vs. electric field across the tunnel oxide shows square root dependence at low fields (E 1 MV/cm) and a square dependence at higher fields (E > 2.7 MV/cm). This indicates that Poole-Frenkel Effect is the main mechanism for holes emission at low fields and Phonon Assisted Tunneling at higher fields. © 2014 AIP Publishing LLC.
Open Access
Novel monoclonal antibodies detect Smad-interacting protein 1 (SIP1) in the cytoplasm of human cells from multiple tumor tissue arrays
(Elsevier, 2010) Oztas, E.; Avci, M. E.; Ozcan, A.; Sayan, A. E.; Tulchinsky, E.; Yagci, T.
Smad-interacting protein 1 (SIP1, also known as ZEB2) represses the transcription of E-cadherin and mediates epithelial-mesenchymal transition in development and tumor metastasis. Due to the lack of human SIP1-specific antibodies, its expression in human tumor tissues has not been studied in detail by immunohistochemistry. Hence, we generated two anti-SIP1 monoclonal antibodies, clones 1C6 and 6E5, with IgG1 and IgG2a isotypes, respectively. The specificity of these antibodies was shown by Western blotting studies using siRNA mediated downregulation of SIP1 and ZEB1 in a human osteosarcoma cell line. In the same context, we also compared them with 5 commercially available SIP1 antibodies. Antibody specificity was further verified in an inducible cell line system by immunofluorescence. By using both antibodies, we evaluated the tissue expression of SIP1 in paraffin-embedded tissue microarrays consisting of 22 normal and 101 tumoral tissues of kidney, colon, stomach, lung, esophagus, uterus, rectum, breast and liver. Interestingly, SIP1 predominantly displayed a cytoplasmic expression, while the nuclear localization of SIP1 was observed in only 6 cases. Strong expression of SIP1 was found in distal tubules of kidney, glandular epithelial cells of stomach and hepatocytes, implicating a co-expression of SIP1 and E-cadherin. Squamous epithelium of the esophagus and surface epithelium of colon and rectum were stained with moderate to weak intensity. Normal uterus, breast and lung tissues remained completely negative. By comparison with their normal tissues, we observed SIP1 overexpression in cancers of the kidney, breast, lung and uterus. However, SIP1 expression was found to be downregulated in tumors from colon, rectum, esophagus, liver and stomach tissues. Finally we did nuclear/cytoplasmic fractionation in 3 carcinoma cell lines and detected SIP1 in both fractions, nucleus being the dominant one. To our best knowledge, this is the first comprehensive immunohistochemical study of the expression of SIP1 in a series of human cancers. Our finding that SIP1 is not exclusively localized to nucleus suggests that the subcellular localization of SIP1 is regulated in normal and tumor tissues. These novel monoclonal antibodies may help elucidate the role of SIP1 in tumor development. © 2010 Elsevier Inc.
Open Access
Resistive Switching based electro-optical modulation
(Wiley, 2014-09-08) Battal, E.; Ozcan, A.; Okyay, Ali Kemal
Resistive switching enables optical modulation via atomic scale modifications that induce change in the refractive index of active device materials. The formation of filaments and migration of atoms around these filaments between high resistance and low resistance states results in the modulation of the free carrier concentration and, hence, the optical constants of the material.
Open Access
Silicon nanoparticle charge trapping memory cell
(Wiley-VCH Verlag, 2014) El-Atab, N.; Ozcan, A.; Alkis, S.; Okyay, Ali Kemal; Nayfeh, A.
A charge trapping memory with 2 nm silicon nanoparticles (Si NPs) is demonstrated. A zinc oxide (ZnO) active layer is deposited by atomic layer deposition (ALD), preceded by Al2O3 which acts as the gate, blocking and tunneling oxide. Spin coating technique is used to deposit Si NPs across the sample between Al2O3 steps. The Si nanoparticle memory exhibits a threshold voltage (Vt) shift of 2.9 V at a negative programming voltage of -10 V indicating that holes are emitted from channel to charge trapping layer. The negligible measured Vt shift without the nanoparticles and the good re- tention of charges (>10 years) with Si NPs confirm that the Si NPs act as deep energy states within the bandgap of the Al2O3 layer. In order to determine the mechanism for hole emission, we study the effect of the electric field across the tunnel oxide on the magnitude and trend of the Vt shift. The Vt shift is only achieved at electric fields above 1 MV/cm. This high field indicates that tunneling is the main mechanism. More specifically, phonon-assisted tunneling (PAT) dominates at electric fields between 1.2 MV/cm < E < 2.1 MV/cm, while Fowler-Nordheim tunneling leads at higher fields (E > 2.1 MV/cm). © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.