Ferroelectric capacitive memories have not achieved the commercial success originally hoped for them in large volume because the area of the capacitors ("footprint") is too large to scale them up to gigabit density devices, [ 1 ] and a restoring pulse is required after a destructive readout. The non-destructive readout of the binary information is possible from the bipolar switching between high-and low-conductance of a ferroelectric diode under two opposite polarizations, as fi rst discovered by Blom et al. in PbTiO 3 perovskite thin fi lms [ 2 ] and later reported by Choi et al. in bulk BiFeO 3 single crystals and Pb(Zr,Ti)O 3 fi lms. [3][4][5] Important properties of such memory are the ultrafast operating speed depending on the polarization fl ipping time (1-2 ps in principle) [ 6 ] and the high ratio of resistance in the forward and reverse directions (3000:1). [ 7 ] However, most ferroelectrics are insulating wide bandgap semiconductors at room temperature, which limits the maximum diode current to the order of ≈ 20 mA cm − 2 . [ 2 , 3 ] Therefore, reaching a suffi cient ferroresistive diode current for the stable detection of memory status using the sense amplifi ers in modern memory circuitry with tiny cell size is a major challenge.In such strongly insulating ferroelectrics, suffi cient diode currents can, in fact, only be observed in ultrathin fi lms, where quantum mechanical tunneling current dominates [ 8 ] and is modulated by varying the tunneling barrier height along with the polarization reversal. Although this effect has been reproducibly demonstrated through local electron transport from an atomic force microscope (AFM) tip into ferroelectric thin fi lms, [9][10][11] the local-probe-based data storage is incompatible with current complementary metal-oxide semiconductor integration processes. Meanwhile, with macroscopic capacitor-type upper and lower electrodes capping the ultrathin ferroelectric layer, an overwhelming leakage current through existing defect-mediated leakage paths could swamp the tunneling current, thereby making the switching signal unreadable. In addition, large lattice-mismatch stresses in ultrathin epitaxial fi lms prevent their use as longtime retention memories due to preferred domain orientations. [ 12 ] One solution to these diffi culties has been to more broadly consider resistive switching effects in (non-ferroelectric) metal oxides. [13][14][15][16][17] However, most of these resistive switching effects are based on a certain type of defect (ionic or electronic) mediated phenomenon, suggesting the inherent diffi culty in precise control of the switching behavior. In contrast, ferroresistive switching behavior is based on the intrinsic switching of ferroelectric domains without invoking of charged defect migration and may, therefore, possess a fundamental merit over defectmediated mechanisms for achieving reliable performance requisite for commercial production once reliable fabrication parameters are established. A critical measure of such success using ferroelectric s...

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Acute and chronic inflammation cause many changes in total body iron metabolism including the sequestration of iron in phagocytic cells of the reticuloendothelial system. This change in iron metabolism contributes to the development of the anemia of inflammation. MTP1, the duodenal enterocyte basolateral iron exporter, is also expressed in the cells of the reticuloendothelial system (RES) and is likely to be involved in iron recycling of these cells. In this study, we use a lipopolysaccharide model of the acute inflammation in the mouse and demonstrate that MTP1 expression in RES cells of the spleen, liver, and bone marrow is down-regulated by inflammation. The down-regulation of splenic expression of MTP1 by inflammation was also observed in a Leishmania donovani model of chronic infection. The response of MTP1 to lipopolysaccharide (LPS) requires signaling through the LPS receptor, Toll-like receptor 4 (TLR4). In mice lacking TLR4, MTP1 expression is not altered in response to LPS. In addition, mice lacking tumor necrosis factor-receptor 1a respond appropriately to LPS with down-regulation of MTP1, despite hyporesponsiveness to tumor necrosis factor-␣ signaling, suggesting that this cytokine may not be required for the LPS effect. We hypothesize that the iron sequestration in the RES system that accompanies inflammation is because of down-regulation of MTP1.Iron is an essential nutrient for growth and development of eucaryotes and most prokaryote species. A normal individual will absorb ϳ1 mg of elemental iron a day through the duodenum, to match an equivalent daily physiologic loss. The plasma turnover of iron is ϳ10 -20 mg a day and one source of this pool is iron released from the reticuloendothelial system (RES).

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There were positive correlation among tumor recurrence, circulating Tregs and liver graft injury after human transplantation for HCC patients. The knockout of CXCL10 decreased hepatic recruitment of CXCR3 Tregs and late phase tumor recurrence after hepatic IR injury.

Aims: We aimed to investigate the clinical significance of GPx3 in hepatocellular carcinoma (HCC) and to characterize its tumor suppressive role.Methods: HCC patients (113) who underwent hepatectomy were recruited to examine the clinical relevance of GPx3. The tumor suppressive role of GPx3 was studied by administration of recombinant GPx3 (rGPx3) or over-expression of GPx3 in HCC cells in vitro and in vivo. The therapeutic value of GPx3 for HCC was further investigated using human induced pluripotent stem cell derived mesenchymal stem cells (hiPSC-MSCs) as its delivery vehicle.Results: Down-regulation of GPx3 significantly correlated with advanced tumor stage (P = 0.024), venous infiltration (P = 0.043) and poor overall survival (P = 0.007) after hepatectomy. Lower plasma GPx3 in HCC patients was significantly associated with larger tumor size (P = 0.011), more tumor nodules (P = 0.032) and higher recurrence (P = 0.016). Over-expression of GPx3 or administration of rGPx3 significantly inhibited proliferation and invasiveness of HCC cells in vitro and in vivo. Tumor suppressive activity of GPx3 was mediated through Erk-NFκB-SIP1 pathway. GPx3 could be delivered by hiPSC-MSCs into the tumor and exhibited tumor suppressive activity in vivo.Conclusions: GPx3 is a tumor suppressor gene in HCC and may possess prognostic and therapeutic value for HCC patients.