The carbon dioxide reduction reaction (CO 2 RR) presents the opportunity to consume CO 2 and produce desirable products. However, the alkaline conditions required for productive CO 2 RR result in the bulk of input CO 2 being lost to bicarbonate and carbonate. This loss imposes a 25% limit on the conversion of CO 2 to multicarbon (C 2+ ) products for systems that use anions as the charge carrierand overcoming this limit is a challenge of singular importance to the field. Here, we find that cation exchange membranes (CEMs) do not provide the required locally alkaline conditions, and bipolar membranes (BPMs) are unstable, delaminating at the membrane−membrane interface. We develop a permeable CO 2 regeneration layer (PCRL) that provides an alkaline environment at the CO 2 RR catalyst surface and enables local CO 2 regeneration. With the PCRL strategy, CO 2 crossover is limited to 15% of the amount of CO 2 converted into products, in all cases. Low crossover and low flow rate combine to enable a single pass CO 2 conversion of 85% (at 100 mA/cm 2 ), with a C 2+ faradaic efficiency and full cell voltage comparable to the anion-conducting membrane electrode assembly.

Ru/C catalyst was used in hydrogenation of levulinic acid to produce γ-valerolactone. The conversion rate and the selectivity of levulinic acid to γ-valerolactone with Ru/C as catalyst were higher than those with Pd/C, Raney nickel, and Urushibara nickel. The optimum preparation conditions of γ-valerolactone by hydrogenation of levulinic acid catalyzed by Ru/C were as follows: temperature at 130 °C, hydrogen pressure at 1.2 MPa, dosage of catalyst at 5.0% (based on the mass fraction of levulinic acid), the solvent being methanol, and a reaction time of 160 min. The conversion rate of levulinic acid to γ-valerolactone was found to be 92%, and the selectivity of γ-valerolactone was 99%. The surface structure variations of the fresh and used catalysts were characterized by XRD and XPS. Furthermore, the reaction pathway for the hydrogenation of levulinic acid was proposed.

The Hippo-YAP (Yes-associated protein) pathway is an evolutionarily and functionally conserved regulator of organ size and growth with crucial roles in cell proliferation, apoptosis, and differentiation. This pathway has great potential for therapeutic manipulation in different disease states and to promote organ regeneration. In this Review, we summarize findings from the past decade revealing the function and regulation of the Hippo-YAP pathway in cardiac development, growth, homeostasis, disease, and regeneration. In particular, we highlight the roles of the Hippo-YAP pathway in endogenous heart muscle renewal, including the pivotal role of the Hippo-YAP pathway in regulating cardiomyocyte proliferation and differentiation, stress response, and mechanical signalling. The human heart lacks the capacity to self-repair; therefore, the loss of cardiomyocytes after injury such as myocardial infarction can result in heart failure and death. Despite substantial advances in the treatment of heart failure, an enormous unmet clinical need exists for alternative treatment options. Targeting the Hippo-YAP pathway has tremendous potential for developing therapeutic strategies for cardiac repair and regeneration for currently intractable cardiovascular diseases such as heart failure. The lessons learned from cardiac repair and regeneration studies will also bring new insights into the regeneration of other tissues with limited regenerative capacity.

These observations suggest that LOX-1 and PCSK9 positively influence each other's expression, especially during an inflammatory reaction. mtROS appear to be important initiators of PCSK9/LOX-1 expression.