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The key to optimizing energy-consuming catalytic conversions lies in acquiring a fundamental understanding of the nature of the active sites and the mechanisms of elementary steps at an atomically precise level, while it is challenging to capture the crucial step that determines the overall temperature of a real-life catalytic reaction. Herein, benefiting from a newly-developed high-temperature ion trap reactor, the reverse water-gas shift (CO2 + H2 → CO + H2O) reaction catalyzed by the Rhn− (n = 3–11) clusters was investigated under variable temperatures (298–783 K) and the critical temperature that each elementary step (Rhn− + CO2 and RhnO− + H2) requires to take place was identified. The Rh4− cluster strikingly surpasses other Rhn− clusters to drive the catalysis at a mild starting temperature (∼440 K). This finding represents the first example that a specifically sized cluster catalyst that works under an optimum condition can be accurately filtered by using state-of-the-art mass spectrometric experiments and rationalized by quantum-chemical calculations. [ABSTRACT FROM AUTHOR]

Noble metals dispersed on transition-metal carbides exhibit extraordinary activity in CO2 catalytic conversion and bimetallic carbides generated at the interface were proposed to contribute to the observed activity. Heteronuclear metal carbide clusters (HMCCs) that compositionally resemble the bimetallic carbides are suitable models to get a fundamental understanding of the reactivity of the related condensed-phase catalysts, while the reaction of HMCCs with CO2 has not been touched in the gas phase. Herein, benefiting from the newly designed double ion trap reactors, the reaction of laser-ablation generated and mass-selected RhTaC2− clusters with CO2 was studied. The experimental results identified that RhTaC2− can reduce four CO2 molecules consecutively and generate the product RhTaC2O4−. The pivotal roles of Rh–Ta synergy and the C2 ligand in driving CO2 reduction were rationalized by theoretical calculations. The presence of an attached CO unit on the product RhTaC2O4− was evidenced by the collision-induced dissociation experiment, providing a fundamental strategy to alleviate carbon deposition under a CO2 atmosphere at elevated temperatures. [ABSTRACT FROM AUTHOR]

Objective: We want to investigate the effect of aquaporin-4 (AQP4) on cerebral edema induced by ischemic stroke in rats and explore whether inhibiting the expression of AQP4 through acetazolamide (AZA) could attenuate brain edema and protect cerebral function. Methods: The Sprague Dawley (SD) rats were randomly divided into four groups: sham + saline group, sham + AZA group, AZA intervention group, and nonintervention group. Each group was divided into five subgroups according to the time of cerebral ischemia (6 h, 1 day, 3 days, 5 days, and 7 days). The model of cerebral infarction in rats was adopted by means of the bilateral carotid arteries ligation (2-VO) method. The rats in intervention group were given intraperitoneal injection of AZA (35 mg/kg/day). Hematoxylin–eosin staining was performed for pathological analysis of the infarcted area. The brain water content was calculated to evaluate the degree of brain edema. The messenger RNA (mRNA) and protein expressions of AQP4 in the brain were measured by quantitative real-time polymerase chain reaction and immunohistochemistry, respectively. Results: Significant cerebral pathological damages were found in ischemic stroke rats. The brain water content, protein, and mRNA expression of AQP4 of the intervention and nonintervention groups were markedly higher than those of the sham groups. By contrast, AZA administration reduced the brain water content, whereas improved cerebral dysfunction was induced by ischemic stroke. Moreover, AZA obviously reduced the protein and mRNA expression of AQP4 after ischemic stroke in rats' brains. Conclusions: The expression of AQP4 was closely related to cerebral edema induced by ischemic stroke. Decreasing the expression of AQP4 mRNA by AZA administration can effectively relieve cerebral edema and decrease cerebral pathological damage. [ABSTRACT FROM AUTHOR]

Idiopathic pulmonary fibrosis (IPF) is a fibrotic interstitial lung disease in which collagen progressively deposits in the supporting framework of the lungs. The pathological collagen creates a recalcitrant barrier in mesenchyme for drug penetration, thus greatly restricting the therapeutical efficacy. On the other hand, this overloaded collagen is gradually exposed to the bloodstream at fibrotic sites because of the vascular hyperpermeability, thus serving as a potential target. Herein, pathological collagen targeting and penetrating liposomes (DP-CC) were constructed to deliver anti-fibrotic dual drugs including pirfenidone (PFD) and dexamethasone (DEX) deep into injured alveoli. The liposomes were co-decorated with collagen binding peptide (CBP) and collagenase (COL). CBP could help vehicle recognize the pathological collagen and target the fibrotic lungs efficiently because of its high affinity to collagen, and COL assisted in breaking through the collagen barrier and delivering vehicle to the center of injured sites. Then, the released dual drugs developed a synergistic anti-fibrotic effect to repair the damaged epithelium and remodel the extracellular matrix (ECM), thus rebuilding the lung architecture. This study provides a promising strategy to deliver drugs deep into pathological collagen accumulated sites for the enhanced treatment of IPF. Pathological collagen targeting and penetrating liposomes (DP-CC) target the fibrotic lungs and break through the collagen barrier, thus delivering drugs deep into injured alveoli for enhanced IPF therapy. [Display omitted] [ABSTRACT FROM AUTHOR]