Two-dimensional (2D) transition-metal dichalcogenides have attracted significant attention as gas-sensing materials owing to their superior responsivity at room temperature and their possible application as flexible electronic devices. Especially, reliable responsivity and selectivity for various environmentally harmful gases are the main requirements for the future chemiresistive-type gas sensor applications. In this study, we demonstrate improved sensitivity of a 2D MoS 2 -based gas sensor by controlling the Schottky barrier height. Chemical vapor deposition process was performed at low temperature to obtain layer-controlled 2D MoS 2 , and the NO 2 gas responsivity was confirmed by the fabricated gas sensor. Then, the number of MoS 2 layers was fixed and the types of electrode materials were varied for controlling the Schottky barrier height. As the Schottky barrier height increased, the NO 2 responsivity increased, and it was found to be effective for CO and CO 2 gases, which had little reactivity in 2D MoS 2 -based gas sensors.

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We investigated an October 2014 outbreak of illness caused by Shigella sonnei in a daycare center in the Republic of Korea (South Korea). The outbreak strain was resistant to extended-spectrum cephalosporins and fluoroquinolones and was traced to a child who had traveled to Vietnam. Improved hygiene and infection control practices are needed for prevention of shigellosis.

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Some non-antiarrhythmic drugs have the undesirable property of delaying cardiac repolarization, an effect that can be measured empirically as a prolongation of the QT interval by surface electrocardiogram (ECG). The QT prolongation and proarrhythmia potential of famotidine are largely unknown, particularly in individuals that have cardiovascular risk factors such as abnormal electrolyte levels. Based on an analysis of QT/QTc intervals from a database of ECG recordings from a large Korean population (ECG-ViEW, 710,369 ECG recordings from 371,401 individuals), we observed that famotidine administration induced a prolonged QTc interval (above 480 ms, p < 0.05 compared to before-treatment, based on a McNemar test). Furthermore, famotidine induced QT prolongations in 10 out of 14 patients with hypocalcemia and 11 out of 13 patients with hypomagnesemia [difference of mean between before and after famotidine administration; 38.00 ms (95% confidence interval 2.72-73.28) and 67.08 ms (95% confidence interval 24.94-109.21), p < 0.05 and p < 0.01 by paired t test, respectively]. In vitro, the IC50 of famotidine for human-ether-a-go-go gene (hERG) channel inhibition was higher than 100 μM as determined by automated patch clamp hERG current assay, implying that hERG channel inhibition is not the underlying mechanism for QT prolongation. These results suggest that famotidine administration increases a proarrhythmic potential, especially in subjects with electrolytes imbalance.

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