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Room-temperature hydrogen storage via two-dimensional potential well in mesoporous graphene oxide
Kim, Tae Hyung,Bae, Jaehyun,Lee, Tae Hoon,Hwang, Jeongwoon,Jung, Jong Hyun,Kim, Do Kyoung,Lee, Jin Seo,Kim, Dong Ok,Lee, Young Hee,Ihm, Jisoon Elsevier 2016 Nano energy Vol.27 No.-
<P><B>Abstract</B></P> <P>Hydrogen is an excellent energy carrier free of carbon dioxide emission, but safe and efficient storage of hydrogen has been a bottleneck for the commercial use of hydrogen as a fuel. Here, we present a strategy based on simple thermodynamic principles that the density of a gas residing in a potential well increases exponentially relative to the ambient gas by the corresponding Boltzmann factor. This mechanism allows for enormously enhanced H<SUB>2</SUB> storage in the form of delocalized gas permeating throughout the void space of a material, in contrast to conventional storage localized to specific adsorption sites. We create mesoporous graphene oxide that provides a two-dimensional potential well and efficient hydrogen diffusion pathways. The gravimetric storage density measured with quartz-crystal microbalance reaches 4.65wt% reproducibly at a modest pressure of 40atm at room temperature. Our work demonstrates the attainability of the long-standing goal of room-temperature hydrogen storage.</P> <P><B>Highlights</B></P> <P> <UL> <LI> The new theoretical model is built for gas-phase storage in a 2D potential well. </LI> <LI> The mesoporous GO achieves high hydrogen storage at room-temperature. </LI> <LI> We developed the quartz crystal microbalance system for a moisture free environment. </LI> <LI> Samples still survive and maintain their storage capacity consistently over three years. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P> <B>Hydrogen storage</B>: KOH-dispersed and hydrothermally treated freeze-dried GO (called MESOGO) presents efficient hydrogen diffusion pathways at room temperature. Atomic configurations and the corresponding potential landscapes experienced by an H<SUB>2</SUB> molecule adsorption on the plane passing through the center of two MESOGO layers for relaxed atomic structures of stored hydrogen molecules.</P> <P>[DISPLAY OMISSION]</P>
JEONGWOON HWANG,CHANGWON PARK,최근수,MOON-HYUN CHA,라제브아후자,DONG WOOK KIM,DONG OK KIM,KIL SAGONG,UI GAB JOUNG,HOGYUN JEONG,임지순 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2012 NANO Vol.7 No.6
We investigate the hydrogen storage capacity of the light transition metal (TM)-decorated metal organic frameworks (MOFs) by performing ab initio density functional theory calculations. We ¯nd that among all the light TM elements, divalent Ti and Fe are suitable for decorating MOFs to enhance the hydrogen uptake, considering the H2 binding energy on the TM atom and the reversibly usable number of H2 molecules attached to the metal site. In general, the magnetization of metal atoms undergoes a high-spin to low-spin state transition when H2molecules are adsorbed, which helps to stabilize the system energetically. By analyzing the projected density of states on each TM atom, it is shown that the d-level shift induced by the ligand ¯eld of the adsorbed H2 molecules contributes substantially to the H2 binding strength. We also study the stability of selected TM-decorated nanostructures against the attack of foreign molecules by examining the energetics of those contaminating molecules around the metal sites.
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.
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.