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A temperature sensor embedded in an In-Ga-Zn oxide (IGZO) TFT was evaluated after fabrication to facilitate monitoring of the temperature distribution on a thin-film transistor (TFT) array. Because the proposed temperature sensor uses the same material as the TFT, no additional process or material is required. Moreover, it can be used as a light shield layer because the temperature sensor is located on a TFT. The temperature sensor used in this study was serially connected to indium tin oxide and a metal. As the temperature increased to 120 °C, the output voltage of the temperature sensor increased to 176.6 mV. The sensitivity, hysteresis, and repeatability were 0.85 mV/°C, 3.56 %, and 0.04 %, respectively. The temperature sensor was integrated into an amorphous IGZO bottom-gate TFT. The TFT exhibited a field-effect mobility of 8.2 cm2V−1·s−1 and threshold voltage of 5.2 V. As the drain current increased from 300 µA to 1.1 mA, the temperature increased from 26 to 32.9 °C, and the output voltages of the temperature sensor augmented from 66 to 76 mV. The integrated temperature sensors enable us to measure the temperature distribution in a display panel and compensate for image deterioration due to increased temperature.

Potential risk of high-dose vitamin C consumption is often ignored. Recently, gram-dose vitamin C is being intravenously injected for the treatment of cancer, which can expose circulating blood cells to extremely high concentrations of vitamin C. As well as platelets, red blood cells (RBCs) can actively participate in thrombosis through procoagulant activation. Here, we examined the procoagulant and prothrombotic risks associated with the intravenous injection of gram-dose vitamin C. Vitamin C (0.5-5mM) increased procoagulant activity of freshly isolated human RBCs via the externalization of phosphatidylserine (PS) to outer cellular membrane and the formation of PS-bearing microvesicles. PS exposure was induced by the dysregulation of key enzymes for the maintenance of membrane phospholipid asymmetry, which was from vitamin C-induced oxidative stress, and resultant disruption of calcium and thiol homeostasis. Indeed, the intravenous injection of vitamin C (0.5-1.0 g/kg) in rats in vivo significantly increased thrombosis. Notably, the prothrombotic effects of vitamin C were more prominent in RBCs isolated from cancer patients, who are at increased risks of thrombotic events. Vitamin C-induced procoagulant and prothrombotic activation of RBCs, and increased thrombosis in vivo. RBCs from cancer patients exhibited increased sensitivity to the prothrombotic effects of vitamin C, reflecting that intravenous gram-dose vitamin C therapy needs to be carefully revisited. [ABSTRACT FROM AUTHOR]

Background: Nephrotoxicity associated with lead poisoning has been frequently reported in epidemiological studies, but the underlying mechanisms have not been fully described. Objectives: We examined the role of erythrocytes, one of the major lead reservoirs, in lead-associated nephrotoxicity. Methods and results: Co-incubation of lead-exposed human erythrocytes with HK-2 human renal proximal tubular cells resulted in renal tubular cytotoxicity, suggesting a role of erythrocytes in lead-induced nephrotoxicity. Morphological and flow cytometric analyses revealed that HK-2 cells actively phagocytized lead-exposed erythrocytes, which was associated with phosphatidylserine (PS) externalization on the erythrocyte membrane and generation of PS-bearing microvesicles. Increased oxidative stress and up-regulation of nephrotoxic biomarkers, such as NGAL, were observed in HK-2 cells undergoing erythrophagocytosis. Moreover, TGF-β, a marker of fibrosis, was also significantly up-regulated. We examined the significance of erythrophagocytosis in lead-induced nephrotoxicity in rats exposed to lead via drinking water for 12 weeks. We observed iron deposition and generation of oxidative stress in renal tissues of lead-exposed rats, as well as the histopathological alterations such as tubulointerstitial lesions, fibrosis, and up-regulation of KIM-1, NGAL, and TGF-β. Conclusions: Our data strongly suggest that erythrophagocytosis and subsequent iron deposition in renal tubular cells could significantly enhance nephrotoxicity following lead exposure, providing insight on lead-associated kidney damages. [ABSTRACT FROM AUTHOR]