Adsorptive removal of CO2 from CO2-CH4 mixture using cation-exchanged zeolites

Raw natural gas and landfill gas contains methane as its major component, but it also contains considerable amounts of contaminants such as CO2 and H2S (i.e. acid gases) that can cause corrosion and fouling of the pipeline and equipment during transportation and liquefaction. Amine-based CO2 gas removal processes have been employed in the gas industry, but these processes have disadvantages including high regeneration energy requirements and inefficiencies; these issues have not been adequately solved to date. Currently, adsorptive acid gas removal technologies have received significant interest because of the simplicity of adsorbent regeneration by thermal or pressure variation1). Numerous micro- and mesoporous adsorbents including zeolites [2-3], titanosilicates[4], activated carbons[5-6], metal-organic-framework (MOF) [7], and silica-alumina materials[8-9] were studied for this type of application. However, the CO2/CH4 selectivity of the aforementioned adsorbents was not high enough for commercial applications.In this study, different cation-exchanged zeolites were synthesized, physicochemically characterized, and evaluated for adsorptive removal of CO2 from CO2-CH4 mixtures. The adsorption isotherms of CO2 and CH4 in the pressure and temperature ranges 0 − 3MPa and 10 – 40 oC, respectively, for different cation-exchanged zeolites were measured and compared. The ideal-adsorbed solution theory (IAST) was employed for the estimation of CO2/CH4 selectivity for the different cation-exchanged zeolites. References 1) D. Aaron, C. Tsouris, Separ. Sci. Technol. 2005, 40, 321–348 2) J. Collins, US Patent No. 3,751,878. 1973. 3) M. W. Seery, US Patent No. 5,938,819. 1999 4) W. B. Dolan, M.J. Mitariten, US Patent No. 6,610,124 B1. 2003 5) A. Kapoor, R.T. Yang, Chem. Eng. Sci. 1989, 44, 1723–1733 6) A. Jayaraman, Chiao, A. S.; Padin, J.; Yang, R. T.; Munson, C. L., Separ. Sci. Technol. 2002 37, 2505–2528 7) L. Hamon, E. Jolimaitre, G. Pringruber , Ind. Eng. Chem. Res. 2010, 49, 7497-7503 8) W.B. Dolan, M.J. Mitariten, US patent No. 2003/0047071, 2003 9) G. Bellussi, P. Broccia, A. Carati, R. Millini, P. Pollesel, C. Rizzo, M. Tagliabue, Micropor. Mesopor. Mat., 2011, 146, 134–14

Quantitative agreement of Dzyaloshinskii-Moriya interactions for domain-wall motion and spin-wave propagation

The magnetic exchange interaction is the one of the key factors governing the basic characteristics of magnetic systems. Unlike the symmetric nature of the Heisenberg exchange interaction, the interfacial Dzyaloshinskii-Moriya interaction (DMI) generates an antisymmetric exchange interaction which offers challenging opportunities in spintronics with intriguing antisymmetric phenomena. The role of the DMI, however, is still being debated, largely because distinct strengths of DMI have been measured for different magnetic objects, particularly chiral magnetic domain walls (DWs) and non-reciprocal spin waves (SWs). In this paper, we show that, after careful data analysis, both the DWs and SWs experience the same strength of DMI. This was confirmed by spin-torque efficiency measurement for the DWs, and Brillouin light scattering measurement for the SWs. This observation, therefore, indicates the unique role of the DMI on the magnetic DW and SW dynamics and also guarantees the compatibility of several DMI-measurement schemes recently proposed.Comment: 24 pages, 5 figure

An Electrophilic Deguelin Analogue Inhibits STAT3 Signaling in H-Ras-Transformed Human Mammary Epithelial Cells: The Cysteine 259 Residue as a Potential Target

Signal transducer and activator of transcription 3 (STAT3) is a point of convergence for numerous oncogenic signals that are often constitutively activated in many cancerous or transformed cells and some stromal cells in the tumor microenvironment. Persistent STAT3 activation in malignant cells stimulates proliferation, survival, angiogenesis, invasion, and tumor-promoting inflammation. STAT3 undergoes activation through phosphorylation on tyrosine 705, which facilitates its dimerization. Dimeric STAT3 translocates to the nucleus, where it regulates the transcription of genes involved in cell proliferation, survival, etc. In the present study, a synthetic deguelin analogue SH48, discovered by virtual screening, inhibited the phosphorylation, nuclear translocation, and transcriptional activity of STAT3 in H-ras transformed human mammary epithelial MCF-10A cells (MCF10A-ras). We speculated that SH48 bearing an alpha,beta-unsaturated carbonyl group could interact with a thiol residue of STAT3, thereby inactivating this transcription factor. Non-electrophilic analogues of SH48 failed to inhibit STAT3 activation, lending support to the above supposition. By utilizing a biotinylated SH48, we were able to demonstrate the complex formation between SH48 and STAT3. SH48 treatment to MCF10A-ras cells induced autophagy, which was verified by staining with a fluorescent acidotropic probe, LysoTracker Red, as well as upregulating the expression of LC3II and p62. In conclusion, the electrophilic analogue of deguelin interacts with STAT3 and inhibits its activation in MCF10A-ras cells, which may account for its induction of autophagic death.

Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification

The present study was aimed to investigate the effects of curcumin, a representative chemopreventive phytochemical with pronounced antioxidant and anti-inflammatory properties, on activation of Nrf2 and expression of its target protein heme oxygenase-1 (HO-1) in mouse skin in vivo and in cultured murine epidermal cells. Treatment of mouse epidermal JB6 cells with curcumin resulted in the induction of HO-1 expression, and this was abrogated in cells transiently transfected with Nrf2 siRNA. While curcumin treatment increased protein expression of Nrf2, it did not alter the steady-state level of the Nrf2 mRNA transcript. Treatment of cells with curcumin stabilized Nrf2 by inhibiting ubiquitination and subsequent 26S proteasomal degradation of this transcription factor. Tetrahydrocurcumin, a non-electrophilic analogue of curcumin that lacks the alpha,beta-unsaturated carbonyl group, failed to induce HO-1 expression as well as nuclear translocation of Nrf2 and its binding to the antioxidant/electrophile response elements. Cells transfected with a mutant Keap1 protein in which cysteine 151 (Cys151) is replaced by serine exhibited marked reduction in curcumin-induced Nrf2 transactivation. Mass spectrometric analysis revealed that curcumin binds to Keap1 Cys151, supporting that this amino acid is a critical target for curcumin modification of Keap1, which facilitates the liberation of Nrf2. Thus, it is likely that the alpha,beta-unsaturated carbonyl moiety of curcumin is essential for its binding to Keap1 and stabilization of Nrf2 by hampering ubiquitination and proteasomal degradation.

17-Oxo-docosahexaenoic acid induces Nrf2-mediated expression of heme oxygenase-1 in mouse skin in vivo and in cultured murine epidermal cells

Recently, growing attention has been given to new classes of bioactive lipid mediators derived from omega-3 polyunsaturated fatty acids, such as docosahexaenoic acid (DHA), especially in the context of their role as endogenous signal modulators. One such molecule is 17-oxo-DHA, generated from DHA by the action of COX2 and a dehydrogenase. The redox-sensitive transcription factor, Nrf2 plays a key role in cellular stress responses. In the present study, the effects of 17-oxo-DHA on Nrf2-mediated expression of cytoprotective enzymes were examined in mouse skin in vivo and cultured murine epidermal JB6 cells. Topical application of 17-oxo-DHA markedly elevated the nuclear localization of Nrf2 and expression of heme oxygenase-1 (HO-1) and NAD(P) H:quinone oxidoreductase-1 in hairless mouse skin. In contrast to 17-oxo-DHA, the non-electrophilic metabolic precursor 17-hydroxy-DHA was a much weaker inducer of Nrf2 activation and its target protein expression. Likewise, 17-oxo-DHA significantly enhanced nuclear translocation and transcriptional activity of Nrf2 with concomitant upregulation of HO-1 expression in cultured JB6 cells. 17-Oxo-DHA was a much stronger inducer of Nrf2-mediated antioxidant response than its parent molecule, DHA. HO-1 expression was abolished in Nrf2 knockdown JB6 cells or embryo fibroblasts from Nrf2 knock out mice. 17-Oxo-DHA also markedly reduced the level of Keap1 protein by inducing ubiquitination. Mutation of Cys151 and Cys273 in Keap1 abrogated 17-oxo-DHA-induced ubiquitination and proteasome-mediated degradation of Keap1 as well as HO-1 expression, suggesting that these cysteine residues are putative sites for 17-oxo-DHA binding. Further, Keap1 degradation stimulated by 17-oxo-DHA coincided with accumulation of the autophagy substrate, p62/SQSTM1.

Extensive Late-Acquired Incomplete Stent Apposition After Sirolimus-Eluting Stent Implantation

Late-acquired incomplete stent apposition (ISA) is frequently observed after drug-eluting stent (DES) implantation. Most incidences of late-acquired ISA induced by positive vascular remodeling were of the focal type and occurred in a single vessel. We present an unusual case of a 45-year-old male subject diagnosed with late-acquired ISA that occurred in multiple vessels

A Case of Hemolytic Uremic Syndrome Caused by Escherichia coli O104:H4

A 29-year-old woman presented with bloody diarrhea, abdominal pain, hemolytic anemia, thrombocytopenia, and acute renal failure. She was diagnosed with Escherichia coli O104:H4-associated hemolytic-uremic syndrome (HUS) and treated with plasmapheresis and hemodialysis for 3 weeks. She recovered without sequelae. To the best of our knowledge, this is the first report of Escherichia coli O104:H4-associated HUS in Korea. We recommend that Escherichia coli O104:H4, as well as the more common O157:H7, be considered in the diagnosis of bloody diarrhea-associated HUS