CO2 Hydrogenation on Metal-Organic Frameworks-Based Catalysts: A Mini Review

Conversion of carbon dioxide (CO2) into value-added fuels and chemicals can not only reduce the emission amount of CO2 in the atmosphere and alleviate the greenhouse effect but also realize carbon recycling. Through hydrogenation with renewable hydrogen (H2), CO2 can be transformed into various hydrocarbons and oxygenates, including methanol, ethanol, methane and light olefins, etc. Recently, metal-organic frameworks (MOFs) have attracted extensive attention in the fields of adsorption, gas separation, and catalysis due to their high surface area, abundant metal sites, and tunable metal-support interface interaction. In CO2 hydrogenation, MOFs are regarded as important supports or sacrificed precursors for the preparation of high-efficient catalysts, which can uniformly disperse metal nanoparticles (NPs) and enhance the interaction between metal and support to prevent sintering and aggregation of active metal species. This work summarizes the recent process on hydrogenation of CO2 to methanol, methane and other C2+ products over various MOFs-based catalysts, and it will provide some dues for the design of MOFs materials in energy-efficient conversion and utilization

Hyperglycemia in apolipoprotein E-deficient mouse strains with different atherosclerosis susceptibility

<p>Abstract</p> <p>Background</p> <p>Type 2 diabetes mellitus (T2DM) is associated with an increased risk of atherosclerotic vascular disease, but it is unknown whether the other way around is true too. C57BL/6 (B6) and BALB/cJ (BALB) are two mouse strains that differ markedly in their susceptibility to atherosclerosis. In this study we investigated the development of diet-induced T2DM in these two strains.</p> <p>Methods and Results</p> <p>When deficient in apolipoprotein E (apoE^-/-) and fed a Western diet for 12 weeks, atherosclerosis-susceptible B6 mice developed significant hyperglycemia. In contrast, atherosclerosis-resistant BALB apoE^-/-mice had much lower plasma glucose levels than B6.apoE^-/-mice on either chow or Western diet and during an intraperitoneal glucose tolerance test. In response to glucose BALB.apoE^-/-mice displayed both the first and second phases of insulin secretion but the second phase of insulin secretion was absent in B6.apoE^-/-mice. In response to insulin B6.apoE^-/-mice showed a deeper and longer-lasting fall in blood glucose levels while BALB.apoE^-/-mice showed little reduction in glucose levels. Pancreatic islet area of BALB.apoE^-/-mice on light microscopy nearly doubled the area of B6.apoE^-/-mice. Most circulating proinflammatory cytokines were lower in BALB.apoE^-/-than in B6.apoE^-/-mice on the Western diet, as determined by protein arrays. Increased macrophage infiltration in islets was observed in B6.apoE^-/-mice by immunostaining for Mac2 and also by flow cytometry.</p> <p>Conclusion</p> <p>This study demonstrates that defects in insulin secretion rather than defects in insulin resistance explain the marketed difference in susceptibility to T2DM in the B6.apoE^-/-and BALB.apoE^-/-mouse model. A smaller islet mass and more prominent islet inflammation may explain the vulnerability of B6.apoE^-/-mice to diet-induced diabetes.</p

Identification of Soat1 as a Quantitative Trait Locus Gene on Mouse Chromosome 1 Contributing to Hyperlipidemia

We previously identified two closely linked quantitative trait loci (QTL) on distal chromosome 1 contributing to major variations in plasma cholesterol and triglyceride levels in an intercross derived from C57BL/6 (B6) and C3H/HeJ (C3H) apolipoprotein E-deficient (apoE−/−) mice. Soat1, encoding sterol o-acyltransferase 1, is a functional candidate gene located underneath the proximal linkage peak. We sequenced the coding region of Soat1 and identified four single nucleotide polymorphisms (SNPs) between B6 and C3H mice. Two of the SNPs resulted in amino-acid substitutions (Ile147Val and His205Tyr). Functional assay revealed an increased enzyme activity of Soat1 in peritoneal macrophages of C3H mice relative to those of B6 mice despite comparable protein expression levels. Allelic variants of Soat1 were associated with variations in plasma cholesterol and triglyceride levels in an intercross between B6.apoE−/− and C3H.apoE−/− mice. Inheritance of the C3H allele resulted in significantly higher plasma lipid levels than inheritance of the B6 allele. Soat1 variants were also significantly linked to major variations in plasma esterified cholesterol levels but not with free cholesterol levels. Trangenic expression of C3H Soat1 in B6.apoE−/− mice resulted in elevations of plasma cholesterol and triglyceride levels. These results indicate that Soat1 is a QTL gene contributing to hyperlipidemia

Establishment of a Novel In Situ Rat Model for Direct Measuring of Intestinal Drug Absorption: Confirmation of Inhibitory Effects of Daijokito on the Absorption of Ranitidine

【Background】 Daijokito (DJKT), a classical traditional Kampo and Chinese medicine, has been used to treat acute pancreatitis in China. In our previous study, DJKT was found to reduce the area under the plasma concentration-time curve (AUC) of ranitidine in humans. Therefore, we established a novel rat model to examine the direct absorption of ranitidine after daijokito administration. 【Methods】 An in situ intestinal injection with portal vein sampling (IIPS) model was created to determine the rate of intestinal drug absorption. Rats were divided into two groups: the ranitidine group (R, n = 6) or the ranitidine and daijokito group (RD, n = 6). Blood was collected after intestinal injection of drugs. After the experiment, the concentrations of ranitidine were measured by LC/MS/MS analysis. 【Results】 The concentrations of ranitidine increased linearly with time in both groups. Compared with the R group, the concentrations of ranitidine in RD group significantly decreased throughout the experiment. 【Conclusion】 Co-administration of ranitidine with DJKT resulted in significant decreases in intestinal absorption in rats. The reduction of the systemic ranitidine concentration by co-administration of DJKT may be due, at least in part, to the inhibition of intestinal absorption of ranitidine

Accelerating relaxation through Liouvillian exceptional point

We investigate speeding up of relaxation of Markovian open quantum systems with the Liouvillian exceptional point (LEP), where the slowest decay mode degenerate with a faster decay mode. The degeneracy significantly increases the gap of the Liouvillian operator, which determines the timescale of such systems in converging to stationarity, and hence accelerates the relaxation process. We explore an experimentally relevant three level atomic system, whose eigenmatrices and eigenspectra are obtained completely analytically. This allows us to gain insights in the LEP and examine respective dynamics with details. We illustrate that the gap can be further widened through Floquet engineering, which further accelerates the relaxation process. Finally, we extend this approach to analyze laser cooling of trapped ions, where vibrations (phonons) couple to the electronic states. An optimal cooling condition is obtained analytically, which agrees with both existing experiments and numerical simulations. Our study provides analytical insights in understanding LEP, as well as in controlling and optimizing dissipative dynamics of atoms and trapped ions