A scalable metal-organic framework as a durable physisorbent for carbon dioxide capture.

Metal-organic frameworks (MOFs) as solid sorbents for carbon dioxide (CO2) capture face the challenge of merging efficient capture with economical regeneration in a durable, scalable material. Zinc-based Calgary Framework 20 (CALF-20) physisorbs CO2 with high capacity but is also selective over water. Competitive separations on structured CALF-20 show not just preferential CO2 physisorption below 40% relative humidity but also suppression of water sorption by CO2, which was corroborated by computational modeling. CALF-20 has a low enthalpic regeneration penalty and shows durability to steam (>450,000 cycles) and wet acid gases. It can be prepared in one step, formed as composite materials, and its synthesis can be scaled to multikilogram batches.

CREG improves cardiac function by regulating cardiomyocytes' autophagy in diabetic myocardial infarction rats.

OBJECTIVE: We aimed to observe the changes of cardiac function, cell morphology, cellular repressor of E1A-stimulated genes (CREG) and LC3-II after myocardial infarction (MI) in non-diabetic and diabetic rats, and to explore the relationship between myocardial damage and CREG and autophagy in diabetic rats. MATERIALS AND METHODS: Diabetic rat models were prepared by intraperitoneal injection of low concentration (50 mg/kg) streptozotocin (STZ). MI models were established in normal rats and diabetic rats. The cardiac function of each group was detected by echocardiography. The pathological results of myocardial tissue in the infarcted area were observed under light microscope. The expression of CREG was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Myocardial protein CREG LC3-II expression was measured by Western blot. Autophagy levels were also detected at the cellular level. Construction of CREG overexpressing adenovirus transfected H9c2 cells, and injection of rats with AAV-CREG to achieve the purpose of overexpressing CREG. In vitro and in vivo experiments were conducted to explore the effects of CREG on autophagy and cardiac function in a diabetic MI model. RESULTS: Compared with the non-diabetic sham (NS) group, there were no marked differences in cardiac function and CREG levels in the diabetic sham (DS) group. Compared with the NS group, the cardiac function of the non-diabetic myocardial infarction (NI) group and the diabetic infarction myocardial (DI) group were reduced, and the levels of autophagy were increased. However, the cardiac function of the DI group was worse than that of the NI group, and the autophagy level of the DI group was lower than the NI group. The results at the cellular level were similar to the experiments in vivo. The overexpression of CREG in vivo or in vitro can increase autophagy levels and improve cardiac function. CONCLUSIONS: The exacerbation of myocardial injury after MI in diabetic rats may be related to the inhibition of CREG in myocardial cells of infarcted area by diabetes.

Mechanisms of Myocardial Ischemia Inducing Sudden Cardiac Death in Athletes with Anomalous Coronary Origin from the Opposite Sinus: Insights from a computational fluid dynamic study.

AIMS: The left coronary anomalous origin from the opposite sinus (L- ACAOS) constitutes the most clinically relevant arterial abnormality among the wide spectrum of coronary artery anomalies. We investigated the physiology of L-ACAOS with and without intramural course (IM) in athletes, using the computational fluid dynamic (CFD) analysis. METHODS AND RESULTS: The coronary artery circulation with L-ACAOS with and without IM has been segmented and then reconstructed, after reviewing both the angiographic and computed tomography findings of 13 consecutive athletes (10 males, mean age 45.1 ±â€¯8.2 years) with L-ACAOS collected in our institution between 1st January 2003 and 1st January 2018. Vorticity magnitude, static pressure and wall shear stress (WSS) have been analysed in a model of L-ACAOS with no IM course and in L-ACAOS-IM at rest and during exercise. The mean vorticity magnitude and WSS significantly increased from rest to exercise in both models, in right coronary artery, left anterior descending and left circumflex coronary arteries. The mean static pressure significantly increased with exercise in IM (1.118e + 004 vs 1.164e + 004 Pa, p < 0.001) as well as the mean vorticity magnitude and the mean WSS (7012.78 1/s vs 9019.56 1/s, p < 0.001, Δ = 2006.78 1/s and 3.02 Pa vs 2.11 Pa, p < 0.001, Δ = 0.91 Pa). This net increment was transmitted to the entire left coronary system in L-ACAOS-IM but not in L-ACAOS with no IM. CONCLUSIONS: In L-ACAOS, different hemodynamic parameters observed in the intramural segment seem to confirm that IM is compressed during exercise. These rheological properties might propagated along the left coronary system, potentially predisposing, if confirmed in vivo, distal coronary segments to a higher risk of spasm and thrombosis in athletes.