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Abstract The meticulous design of active sites and light absorbers holds the key to the development of high-performance photothermal catalysts for CO2 hydrogenation. Here, we report a nonmetallic plasmonic catalyst of Mo2N/MoO2-x nanosheets by integrating a localized surface plasmon resonance effect with two distinct types of active sites for CO2 hydrogenation. Leveraging the synergism of dual active sites, H2 and CO2 molecules can be simultaneously adsorbed and activated on N atom and O vacancy, respectively. Meanwhile, the plasmonic effect of this noble-metal-free catalyst signifies its promising ability to convert photon energy into localized heat. Consequently, Mo2N/MoO2-x nanosheets exhibit remarkable photothermal catalytic performance in reverse water-gas shift reaction. Under continuous full-spectrum light irradiation (3 W·cm−2) for a duration of 168 h, the nanosheets achieve a CO yield rate of 355 mmol·gcat−1·h−1 in a flow reactor with a selectivity exceeding 99%. This work offers valuable insights into the precise design of noble-metal-free active sites and the development of plasmonic catalysts for reducing carbon footprints.

Abstract Formate dehydrogenase (FDH) is widely applied in regeneration of redox cofactors. There are continuing interests to engineer FDH for improved catalytic activity and cofactor preference. In the crystal structure of FDH from Pseudomonas sp. 101 (pseFDH), the C terminus with 9 amino acid residues cannot be resolved. However, our earlier work showed mutations at C terminus led pseFDH variants to favor a non-natural cofactor nicotinamide cytosine dinucleotide (NCD). Here, we investigated the role of C-terminal residues on cofactor preference by truncating their corresponding C terminus of pseFDH variants. Sequence comparison analysis showed that C-terminal residues were barely conservative among different FDHs. pseFDH and mutants with their C termini truncated were constructed, and the resulted variants showed improved preference to NCD mainly because NAD-dependent activity dropped more substantially. Further structure analysis showed that these pseFDH variants had their cofactor binding domains reconstructed to favor molecular interactions with NCD. Our work indicated that C-terminal residues of pseFDH affected enzyme activity and cofactor preference, which provides a new approach for ameliorating the performance of redox enzymes.

Abstract In recent years, lung adenocarcinoma (LUAD) has become a focus of attention due to its low response to treatment, poor prognosis, and lack of reliable indicators to predict the progression or therapeutic effect of LUAD. Different cell death patterns play a crucial role in tumor development and are promising for predicting LUAD prognosis. From the TCGA and GEO databases, we obtained bulk transcriptomes, single-cell transcriptomes, and clinical information. Genes in 15 types of cell death were analyzed for cell death index (CDI) signature establishment. The CDI signature using necroptosis + immunologic cell death-related genes was established in the TCGA cohort with the 1-, 2-, 3-, 4- and 5-year AUC values were 0.772, 0.736, 0.723, 0.795, and 0.743, respectively. The prognosis was significantly better in the low CDI group than in the high CDI group. We also investigated the relationship between the CDI signature and clinical variables, published prognosis biomarkers, immune cell infiltration, functional enrichment pathways, and immunity biomarkers. In vitro assay showed that HNRNPF and FGF2 promoted lung cancer cell proliferation and migration and were also involved in cell death. Therefore, as a robust prognosis biomarker, CDI signatures can screen for patients who might benefit from immunotherapy and improve diagnostic accuracy and LUAD patient outcomes.

Abstract Surface analysis by X-ray photoelectron spectroscopy and time-of-flight secondary ion mass spectrometry was applied to investigate the origin of the enhanced surface passivity and resistance to a chloride-induced breakdown provided by the protective ultrathin oxide films formed on Cr–Fe–Co–Ni–Mo single-phase fcc multi-principal element alloys. A bilayer structure of the oxide films is observed with the inner barrier layer mostly constituted of Cr(III) oxide and the outer layer enriched in Cr(III) hydroxides and Mo(IV,VI) oxides. The Mo(VI) and Mo(IV) species are mainly located in the outer and inner parts of the outer layer, respectively. Anodic passivation promotes mainly the growth of the inner layer on the alloy of higher Cr bulk content and the outer layer on the alloy of higher Mo bulk content. Passivation also promotes the enrichment of Cr(III) hydroxide and Mo(IV) and Mo(VI) oxides in the outer layer. Depth distribution analysis suggests that the ultra-thin protective inner barrier contains Cr(III)-depleted heterogeneities acting as weak sites for chloride attack, which are reinforced by the Mo(IV) oxide species concentrated close to the inner barrier layer. This elemental distribution provides an explanation for the reinforcement of the resistance to localized corrosion observed on these Cr–Fe–Co–Ni–Mo alloys.

Abstract Enzymes with dedicated cofactor preference are essential for advanced biocatalysis and biomanufacturing, especially when employing nonnatural nicotinamide cofactors in redox reactions. However, directed evolution of an enzyme to switch its cofactor preference is often hindered by the lack of efficient and affordable method for screening as the cofactor per se or the substrate can be prohibitively expensive. Here, we developed a growth-based selection platform to identify nonnatural cofactor-dependent oxidoreductase mutants. The growth of bacteria depended on the nicotinamide cytosine dinucleotide (NCD) mediated conversion of non-metabolizable phosphite into phosphate. The strain BW14329 lacking the ability to oxidize phosphite was suitable as host, and NCD-dependent phosphite dehydrogenase (Pdh*) is essential to the selection platform. Previously confirmed NCD synthetase with NCD synthesis capacity and NCD-dependent malic enzyme were successfully identified by using the platform. The feasibility of this strategy was successfully demonstrated using derived NCD-active malic enzyme as well as for the directed evolution of NCD synthetase in Escherichia coli. A phosphite-based screening platform was built for identification of enzymes favoring nonnatural cofactor NCD. In the future, once Pdh variants favoring other biomimetic or nonnatural cofactors are available this selection platform may be readily redesigned to attain new enzyme variants with anticipated cofactor preference, providing opportunities to further expand the chemical space of redox cofactors in chemical biology and synthetic biology.

Nicotinamide cytosine dinucleotide is an NAD mimic that can be used to mediate redox reactions. Here the authors design an NCD synthetase for the intracellular production of NCD.

Abstract Appropriate drainage duration is vital for the postoperative rehabilitation of patients with breast cancer (BC) undergoing modified radical mastectomy (MRM). To provide better and individualized postoperative management for these patients, this study explored independent predictors of postoperative drainage duration in patients with BC. This was a single-center retrospective cohort study. Patients diagnosed with BC and treated with MRM from May 2016 to April 2020 were randomly divided into training (n = 729) and validation (n = 243) cohorts. Univariate and multivariate Cox analyses revealed that the body mass index, serum albumin level, hypertension, number of total dissected axillary lymph nodes, and ratio of positive axillary lymph nodes were independent predictors of postoperative drainage duration in the training cohort. Based on independent predictors, a nomogram was constructed to predict the median postoperative drainage duration and the probability of retaining the suction drain during this period. This nomogram had good concordance and discrimination both in the training and validation cohorts and could effectively predict the probability of retaining the suction drain during drainage, thus assisting clinicians in predicting postoperative drainage duration and providing individualized postoperative management for patients with BC.

TAp73 is a structural homolog of the tumor suppressor p53. Here they show that TAp73 is critical for promoting glycolysis as it stimulates the transcriptional expression of liver type of phosphofructokinase-1 (PFKL), which catalyzes the committed step in glycolysis.