Structural Heredity in Catalysis: CO2 Self-Selective CeO2 Nanocrystals for Efficient Photothermal CO2 Hydrogenation to Methane.

The chemical inertness of CO2 molecules makes their adsorption and activation on a catalyst surface one of the key challenges in recycling CO2 into chemical fuels. However, the traditional template synthesis and chemical modification strategies used to tackle this problem face severe structural collapse and modifier deactivation issues during the often-needed post-processing procedure. Herein, a CO2 self-selective hydrothermal growth strategy is proposed for the synthesis of CeO2 octahedral nanocrystals that participate in strong physicochemical interactions with CO2 molecules. The intense affinity for CO2 molecules persists during successive high-temperature treatments required for Ni deposition. This demonstrates the excellent structural heredity of the CO2 self-selective CeO2 nanocrystals, which leads to an outstanding photothermal CH4 productivity exceeding 9 mmol h-1 mcat -2 and an impressive selectivity of >99%. The excellent performance is correlated with the abundant oxygen vacancies and hydroxyl species on the CeO2 surface, which create many frustrated Lewis-pair active sites, and the strong interaction between Ni and CeO2 that promotes the dissociation of H2 molecules and the spillover of H atoms, thereby greatly benefitting the photothermal CO2 methanation reaction. This self-selective hydrothermal growth strategy represents a new pathway for the development of effective catalysts for targeted chemical reactions.

Feasibility of the application of deep learning-reconstructed ultra-fast respiratory-triggered T2-weighted imaging at 3 T in liver imaging.

OBJECTIVE: The evaluate the feasibility of a novel deep learning-reconstructed ultra-fast respiratory-triggered T2WI sequence (DL-RT-T2WI) In liver imaging, compared with respiratory-triggered Arms-T2WI (Arms-RT-T2WI) and respiratory-triggered FSE-T2WI (FSE-RT-T2WI) sequences. METHODS: 71 patients with liver lesions underwent 3-T MRI and were prospectively enrolled. Two readers independently analyzed images acquired with DL-RT-T2WI, Arms-RT-T2WI, and FSE-RT-T2WI. The qualitative evaluation indicators, including overall image quality (OIQ), sharpness, noise, artifacts, lesion detectability (LC), lesion characterization (LD), cardiacmotion-related signal loss (CSL), and diagnostic confidence (DC), were evaluated in two readers, and further statistically compared using paired Wilcoxon rank-sum test among three sequences. RESULTS: 176 lesions were detected in DL-RT-T2W and Arms-RT-T2WI, and 175 were detected in FSE-RT-T2WI. The acquisition time of DL-RT-T2WI was improved by 4.8-7.9 folds compared to the other two sequences. The OIQ was scored highest for DL-RT-T2WI (R1, 4.61 ± 0.52 and R2, 4.62 ± 0.49), was significantly superior to Arms-RT-T2WI (R1, 4.30 ± 0.66 and R2, 4.34 ± 0.69) and FSE-RT-T2WI (R1, 3.65 ± 1.08 and R2, 3.75 ± 1.01). Artifacts and sharpness scored highest for DL-RT-T2WI, followed by Arms-RT-T2WI, and were lowest for FSE-RT-T2WI in both two readers. Noise and CSL for DL-RT-T2WI scored similar to Arms-RT-T2WI (P > 0.05) and were significantly superior to FSE-RT-T2WI (P < 0.001). Both LD and LC for DL-RT-T2WI were significantly superior to Arms-RT-T2WI and FSE-RT-T2WI in two readers (P < 0.001). DC for DL-RT-T2WI scored best, significantly superior to Arms-RT-T2WI (P < 0.010) and FSE-RT-T2WI (P < 0.001). CONCLUSIONS: The novel ultra-fast DL-RT-T2WI is feasible for liver imaging and lesion characterization and diagnosis, not only offers a significant improvement in acquisition time but also outperforms Arms-RT-T2WI and FSE-RT-T2WI concerning image quality and DC.

Sacubitril/valsartan ameliorates tubulointerstitial fibrosis by restoring mitochondrial homeostasis in diabetic kidney disease.

BACKGROUND: Tubulointerstitial fibrosis plays an important role in the progression of diabetic kidney disease (DKD). Sacubitril/valsartan (Sac/Val) exerts a robust beneficial effect in DKD. However, the potential functional effect of Sac/Val on tubulointerstitial fibrosis in DKD is still largely unclear. METHODS: Streptozotocin-induced diabetic mice were given Sac/Val or Val by intragastric administration once a day for 12 weeks. The renal function, the pathological changes of tubule injury and tubulointerstitial fibrosis, as well as mitochondrial morphology of renal tubules in mice, were evaluated. Genome-wide gene expression analysis was performed to identify the potential mechanisms. Meanwhile, human tubular epithelial cells (HK-2) were cultured in high glucose condition containing LBQ657/valsartan (LBQ/Val). Further, mitochondrial functions and Sirt1/PGC1α pathway of tubular epithelial cells were assessed by Western blot, Real-time-PCR, JC-1, MitoSOX or MitoTracker. Finally, the Sirt1 specific inhibitor, EX527, was used to explore the potential effects of Sirt1 signaling in vivo and in vitro. RESULTS: We found that Sac/Val significantly ameliorated the decline of renal function and tubulointerstitial fibrosis in DKD mice. The enrichment analysis of gene expression indicated metabolism as an important modulator in DKD mice with Sac/Val administration, in which mitochondrial homeostasis plays a pivotal role. Then, the decreased expression of Tfam and Cox IV;, as well as changes of mitochondrial function and morphology, demonstrated the disruption of mitochondrial homeostasis under DKD conditions. Interestingly, Sac/Val administration was found to restore mitochondrial homeostasis in DKD mice and in vitro model of HK-2 cells. Further, we demonstrated that Sirt1/PGC1α, a crucial pathway in mitochondrial homeostasis, was activated by Sac/Val both in vivo and in vitro. Finally, the beneficial effects of Sac/Val on mitochondrial homeostasis and tubulointerstitial fibrosis was partially abolished in the presence of Sirt1 specific inhibitor. CONCLUSIONS: Taken together, we demonstrate that Sac/Val ameliorates tubulointerstitial fibrosis by restoring Sirt1/PGC1α pathway-mediated mitochondrial homeostasis in DKD, providing a theoretical basis for delaying the progression of DKD in clinical practice.