One Iron for Two Iron Sites in a Metal-Organic Framework Toward Simultaneous N2-H2 Activation under Mild Conditions.

Iron-based catalysts play an important role in the ammonia industry. As one of the most abundant iron minerals, Fe3O4 containing FeII and FeIII sites is widely distributed in the earth's crust and even on exoplanets, theoretically giving it both economic and catalytic potentials in ammonia synthesis. However, in the absence of specific active co-catalyst and harsh conditions, Fe3O4 is impossible to achieve ammonia synthesis alone. Here, we designed to activate the relatively inert FeII and FeIII sites in Fe3O4 with a third FeIII site inlayed in a coordination framework (MIL-101(Fe)) to achieve the unpresented multi-site collaborative catalysis. In-depth mechanism study confirmed the roles of three different Fe sites in N2 activation, H2 activation, and product transfer, respectively. Efficient N2-H2 activation to NH3 on the Fe3O4-based catalytic system has been achieved at extremely mild conditions. Our research provides a theoretical basis and a new strategy for designing efficient non-noble metal-based ammonia synthesis catalyst with minimized energy consumption.

Enterovirus D68 3C protease antagonizes type I interferon signaling by cleaving signal transducer and activator of transcription 1.

Following the successful control of poliovirus, the re-emergence of respiratory enterovirus D68 (EV-D68), a prominent non-polio enterovirus, has become a serious public health concern worldwide. Host innate immune responses are the primary defense against EV-D68 invasion; however, the mechanism underlying viral evasion of the antiviral activity of interferons (IFN) remains unclear. In this study, we found that EV-D68 inhibited type I IFN signaling by cleaving signal transducer and activator of transcription 1 (STAT1), a crucial factor in cellular responses to interferons and other cytokines. We observed that the prototype and circulating EV-D68 strains conserved their ability to induce STAT1 cleavage and attenuate IFN signal transduction. Further investigation revealed that EV-D68 3C protease cleaves STAT1 at the 131Q residue. Interestingly, not all enterovirus-encoded 3C proteases exhibited this ability. EV-D68 and poliovirus 3C proteases efficiently induced STAT1 cleavage; whereas, 3C proteases from EV-A71, coxsackievirus A16, and echoviruses did not. STAT1 cleavage also abolished the nuclear translocation capacity of STAT1 in response to IFN stimulation to activate downstream signaling elements. Overall, these results suggest that STAT1, targeted by viral protease 3C, is utilized by EV-D68 to subvert the host's innate immune response.IMPORTANCEEnterovirus D68 (EV-D68) has significantly transformed over the past decade, evolving from a rare pathogen to a potential pandemic pathogen. The interferon (IFN) signaling pathway is an important defense mechanism and therapeutic target for the host to resist viral invasion. Previous studies have reported that the EV-D68 virus blocks or weakens immune recognition and IFN production in host cells through diverse strategies; however, the mechanisms of EV-D68 resistance to IFN signaling have not been fully elucidated. Our study revealed that EV-D68 relies on its own encoded protease, 3C, to directly cleave signal transducer and activator of transcription 1 (STAT1), a pivotal transduction component in the IFN signaling pathway, disrupting the IFN-mediated antiviral response. Previous studies on human enteroviruses have not documented direct cleavage of the STAT1 protein to evade cellular immune defenses. However, not all enteroviral 3C proteins can cleave STAT1. These findings highlight the diverse evolutionary strategies different human enteroviruses employ to evade host immunity.

Driving factors and clustering analysis of expressway vehicular CO2 emissions in Guizhou Province, China.

Expressways are essential for intercounty trips of passenger travel and freight mobility, which are also an important source of vehicular CO2 emissions in transportation sector. This study takes the expressway system of Guizhou Province as the research objective, and establishes the multi-year expressway vehicular CO2 emission inventories at the county level from 2011 to 2019. We employ the extended STIRPAT model incorporating ridge regression to identify driving factors from six different aspects, and then utilize the affinity propagation cluster method to conduct the differentiation research by dividing Guizhou's counties into four clusters. Based upon clustering analysis, localized and targeted policies are formulated for each cluster to reduce expressway vehicular CO2 emissions. The results indicate that generally: (1) Guizhou's expressway vehicular CO2 emissions manifest a continuously upward trend during 2011-2019. Small-duty passenger vehicle (SDV), light-duty truck (LDT), and heavy-duty truck (HDT) contribute to the largest CO2 emissions in eight vehicle types. (2) GDP and population are the foremost two positive driving factors, followed by urbanization rate and expressway length. The proportion of secondary industry is also a positive driver, but that of tertiary industry exhibits an opposite effect. (3) Regional disparity exists in four county clusters of Guizhou Province. Efficient policies are proposed, such as improving the layout and infrastructure of transportation hubs, promoting multimodal integration, and implementing industrial upgrading as per regional advantages. Sustainable expressway vehicular CO2 emission reduction is realized from both the source of industry and low-carbon modes of transport.

Ultrastable Cu-Based Dual-Channel Heterowire for the Switchable Electro-/Photocatalytic Reduction of CO2.

Catalytic conversion of CO2 into high value-added chemicals using renewable energy is an attractive strategy for the management of CO2 . However, achieving both efficiency and product selectivity remains a great challenge. Herein, a brand-new family of 1D dual-channel heterowires, Cu NWs@MOFs are constructed by coating metal-organic frameworks (MOFs) on Cu nanowires (Cu NWs) for electro-/photocatalytic CO2 reductions, where Cu NWs act as an electron channel to directionally transmit electrons, and the MOF cover acts as a molecule/photon channel to control the products and/or undertake photoelectric conversion. Through changing the type of MOF cover, the 1D heterowire is switched between electrocatalyst and photocatalyst for the reduction of CO2 with excellent selectivity, adjustable products, and the highest stability among the Cu-based CO2 RR catalysts, which leads to heterometallic MOF covered 1D composite, and especially the first 1D/1D-type Mott-Schottky heterojunction. Considering the diversity of MOF materials, the ultrastable heterowires offer a highly promising and feasible solution for CO2 reduction.

Protective Mechanism of Leucine and Isoleucine against H2O2-Induced Oxidative Damage in Bovine Mammary Epithelial Cells.

Leucine and isoleucine possess antioxidative and anti-inflammatory properties. However, their underlying protective mechanisms against oxidative damage remain unknown. Therefore, in this study, the protective mechanism of leucine and isoleucine against H2O2-induced oxidative damage in a bovine mammary epithelial cell lines (MAC-T cells) were investigated. Briefly, MAC-T cells exposed or free to H2O2 were incubated with different combinations of leucine and isoleucine. The cellular relative proliferation rate and viability, oxidative stress indicators, and inflammatory factors were determined by specific commercial kits. The genes related to barrier functions was measured by real-time quantitative PCR. The protein expression differences were explored by 4D label-free quantitative proteomic analyses and validated by parallel reaction monitoring. The results revealed that leucine and isoleucine increased cell proliferation, total antioxidant status (TAS), and the relative mRNA expression of occludin, as well as decreased malondialdehyde (MDA), total oxidant status (TOS)/TAS, IL-6, IL-1ß, and TOS. When leucine and isoleucine were combined, MDA, TOS/TAS, and the relative mRNA expression levels of claudin-1, occludin, and zonula occludens-1 increased when compared to leucine or isoleucine alone. Proteomics analyses revealed that leucine significantly upregulated the propanoate metabolism; valine, leucine, and isoleucine degradation; and thermogenesis pathways, whereas isoleucine significantly upregulated the peroxisome and propanoate metabolism pathways. In conclusion, leucine protected MAC-T cells from H2O2-induced oxidative stress by generating more ATP to supplement energy demands, and isoleucine improved the deficit in peroxisome transport and promoted acetyl-CoA production. The findings of this study enhance our understanding of the protective mechanisms of leucine and isoleucine against oxidative damage.