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Band Structure Engineering of Layered WSe<sub>2</sub><i>via</i> One-Step Chemical Functionalization
Park, Jun Hong,Rai, Amritesh,Hwang, Jeongwoon,Zhang, Chenxi,Kwak, Iljo,Wolf, Steven F.,Vishwanath, Suresh,Liu, Xinyu,Dobrowolska, Malgorzata,Furdyna, Jacek,Xing, Huili Grace,Cho, Kyeongjae,Banerjee, S American Chemical Society 2019 ACS NANO Vol.13 No.7
<P>Chemical functionalization is demonstrated to enhance the p-type electrical performance of two-dimensional (2D) layered tungsten diselenide (WSe<SUB>2</SUB>) field-effect transistors (FETs) using a one-step dipping process in an aqueous solution of ammonium sulfide [(NH<SUB>4</SUB>)<SUB>2</SUB>S(aq)]. Molecularly resolved scanning tunneling microscopy and spectroscopy reveal that molecular adsorption on a monolayer WSe<SUB>2</SUB> surface induces a reduction of the electronic band gap from 2.1 to 1.1 eV and a Fermi level shift toward the WSe<SUB>2</SUB> valence band edge (VBE), consistent with an increase in the density of positive charge carriers. The mechanism of electronic transformation of WSe<SUB>2</SUB> by (NH<SUB>4</SUB>)<SUB>2</SUB>S(aq) chemical treatment is elucidated using density functional theory calculations which reveal that molecular “SH” adsorption on the WSe<SUB>2</SUB> surface introduces additional in-gap states near the VBE, thereby, inducing a Fermi level shift toward the VBE along with a reduction in the electronic band gap. As a result of the (NH<SUB>4</SUB>)<SUB>2</SUB>S(aq) chemical treatment, the p-branch ON-currents (<I>I</I><SUB>ON</SUB>) of back-gated few-layer ambipolar WSe<SUB>2</SUB> FETs are enhanced by about 2 orders of magnitude, and a ∼6× increase in the hole field-effect mobility is observed, the latter primarily resulting from the p-doping-induced narrowing of the Schottky barrier width leading to an enhanced hole injection at the WSe<SUB>2</SUB>/contact metal interface. This (NH<SUB>4</SUB>)<SUB>2</SUB>S(aq) chemical functionalization technique can serve as a model method to control the electronic band structure and enhance the performance of devices based on 2D layered transition-metal dichalcogenides.</P> [FIG OMISSION]</BR>
ACN9 Regulates the Inflammatory Responses in Human Bronchial Epithelial Cells
( Jae Hoon Jeong ),( Jeeyoung Kim ),( Jeongwoon Kim ),( Hye-ryeon Heo ),( Jin Seon Jeong ),( Young-joon Ryu ),( Yoonki Hong ),( Seon-sook Han ),( Seok-ho Hong ),( Seung-joon Lee ),( Woo Jin Kim ) 대한결핵 및 호흡기학회 2017 Tuberculosis and Respiratory Diseases Vol.80 No.3
Background: Airway epithelial cells are the first line of defense, against pathogens and environmental pollutants, in the lungs. Cellular stress by cadmium (Cd), resulting in airway inflammation, is assumed to be directly involved in tissue injury, linked to the development of lung cancer, and chronic obstructive pulmonary disease (COPD). We had earlier shown that ACN9 (chromosome 7q21), is a potential candidate gene for COPD, and identified significant interaction with smoking, based on genetic studies. However, the role of ACN9 in the inflammatory response, in the airway cells, has not yet been reported. Methods: We first checked the anatomical distribution of ACN9 in lung tissues, using mRNA in situ hybridization, and immunohistochemistry. Gene expression profiling in bronchial epithelial cells (BEAS-2B), was performed, after silencing ACN9 . We further tested the roles of ACN9, in the intracellular mechanism, leading to Cd-induced production, of proinflammatory cytokines in BEAS-2B. Results: ACN9 was localized in lymphoid, and epithelial cells, of human lung tissues. ACN9 silencing, led to differential expression of 216 genes. Pathways of sensory perception to chemical stimuli, and cell surface receptor-linked signal transduction, were significantly enriched. ACN9 silencing, further increased the expression of proinflammatory cytokines, in BEAS-2B after Cd exposure. Conclusion: Our findings suggest, that ACN9 may have a role, in the inflammatory response in the airway.
ACN9 Regulates the Inflammatory Responses in Human Bronchial Epithelial Cells
Jeong, Jae Hoon,Kim, Jeeyoung,Kim, Jeongwoon,Heo, Hye-Ryeon,Jeong, Jin Seon,Ryu, Young-Joon,Hong, Yoonki,Han, Seon-Sook,Hong, Seok-Ho,Lee, Seung-Joon,Kim, Woo Jin The Korean Academy of Tuberculosis and Respiratory 2017 Tuberculosis and Respiratory Diseases Vol.80 No.3
Background: Airway epithelial cells are the first line of defense, against pathogens and environmental pollutants, in the lungs. Cellular stress by cadmium (Cd), resulting in airway inflammation, is assumed to be directly involved in tissue injury, linked to the development of lung cancer, and chronic obstructive pulmonary disease (COPD). We had earlier shown that ACN9 (chromosome 7q21), is a potential candidate gene for COPD, and identified significant interaction with smoking, based on genetic studies. However, the role of ACN9 in the inflammatory response, in the airway cells, has not yet been reported. Methods: We first checked the anatomical distribution of ACN9 in lung tissues, using mRNA in situ hybridization, and immunohistochemistry. Gene expression profiling in bronchial epithelial cells (BEAS-2B), was performed, after silencing ACN9. We further tested the roles of ACN9, in the intracellular mechanism, leading to Cd-induced production, of proinflammatory cytokines in BEAS-2B. Results: ACN9 was localized in lymphoid, and epithelial cells, of human lung tissues. ACN9 silencing, led to differential expression of 216 genes. Pathways of sensory perception to chemical stimuli, and cell surface receptor-linked signal transduction, were significantly enriched. ACN9 silencing, further increased the expression of proinflammatory cytokines, in BEAS-2B after Cd exposure. Conclusion: Our findings suggest, that ACN9 may have a role, in the inflammatory response in the airway.