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Urea electrosyntehsis from CO2 and NOx is a challenging reaction that is becoming increasingly important. This work uses ab initio molecular dynamics simulations to reveal the origin of C-N coupling mechanisms and reaction networks in urea synthesis.

Abstract A comparative study about riblets-controlled turbulent boundary layers has been performed to investigate the turbulence characteristics associated with drag reduction in a compressive flat-plate flow (where the free-stream Mach number is 0.7) by means of direct numerical simulations (DNSs). With a setting of the triangular riblets (s + ≈ 30.82, h + ≈ 15.41) settled on the Re τ ≈ 500 turbulent boundary layer, an effective global drag reduction was achieved. By comparing velocity and its fluctuation distribution, vorticity fluctuation and streaks structures between the smooth and riblets flat-plate cases, two roles of lifting and rectification in terms of riblets drag control are revealed that the micro-scale riblets can lift up logarithmic-law region of the boundary layer, which leads to a smaller wall friction velocity and thus a drag reduction. The streamwise vortices and its fluctuation structures are shifted upward, thus the interactions between them and the wall surface are weakened, which causes the suppressed intensity of Reynolds normal stresses, streamwise vorticity and turbulent kinetic energy production inside the riblets. Moreover, the streaks associated with streamwise velocity or 3D vortices are ruled from the distorted to long and straight structures as they pass through the riblets, indicating an ability of riblets to turn turbulence into a more ordered state.

Alkali attack of aluminosilicate refractories has been a long-term problem in the industry. In this paper, XRD, SEM, and CT scanning methods were used to analyze the phase and structure characteristics of postmortem corundum-mullite refractory used in hot stoves for more than 10 years, and the anti-corrosion mechanism of the refractory was explored. Results show that the corundum-mullite refractory after long-term corrosion by hot stove gas maintains excellent physical properties, and its cold compressive strength can still reach 92.7 MPa. The mullite network formed by the interpenetration of short columnar mullite endows the corundum-mullite refractory with excellent resistance to gas corrosion: Under the working conditions of the hot stoves, mullite network plays a role in dispersing impurities in refractory, so that the CaO entrained in hot stove gas can be transformed into high melting point CAS2 instead of low melting point phase with high Ca content in the working layer of refractory; CAS2 has good resistance to alkaline gases such as K2O(g) and Na2O(g), and the blocking of pores in the working layer of refractory by CAS2 finally makes the refractory free from the corrosion of hot stove gas.

It is of high interest to convert CO2 into valuable ethanol product. Here the authors demonstrate the asymmetric C-C coupling triggered on Ag-modified oxide-derived Cu sites can accelerate and steer the reaction pathway for ethanol production with high faradaic efficiency and current density.

Abstract Background Although gemcitabine has been considered as the first-line drug for advanced pancreatic cancer (PC), development of resistance to gemcitabine severely limits the effectiveness of this chemotherapy, and the underlying mechanism of gemcitabine resistance remains unclear. Various factors, such as ATP binding cassette (ABC) transporters, microRNAs and their downstream signaling pathways are included in chemoresistance to gemcitabine. This study investigated the potential mechanisms of microRNAs and ABC transporters related signaling pathways for PC resistance to gemcitabine both in vivo and in vitro. Methods Immunohistochemistry and Western blotting were applied to detect the expression of ABC transporters. Molecular docking analysis was performed to explore whether gemcitabine interacted with ABC transporters. Gain-of-function and loss-of-function analyses were performed to investigate the functions of hsa-miR-3178 in vitro and in vivo. Bioinformatics analysis, Western blotting and dual-luciferase reporter assay were used to confirm the downstream regulatory mechanisms of hsa-miR-3178. Results We found that P-gp, BCRP and MRP1 were highly expressed in gemcitabine-resistant PC tissues and cells. Molecular docking analysis revealed that gemcitabine can bind to the ABC transporters. Hsa-miR-3178 was upregulated in gemcitabine resistance PANC-1 cells as compared to its parental PANC-1 cells. Moreover, we found that hsa-miR-3178 promoted gemcitabine resistance in PC cells. These results were also verified by animal experiments. RhoB was down-regulated in gemcitabine-resistant PC cells and it was a downstream target of hsa-miR-3178. Kaplan–Meier survival curve showed that lower RhoB expression was significantly associated with poor overall survival in PC patients. Rescue assays demonstrated that RhoB could reverse hsa-miR-3178-mediated gemcitabine resistance. Interestingly, hsa-miR-3178 promoted gemcitabine resistance in PC by activating the PI3K/Akt pathway-mediated upregulation of ABC transporters. Conclusions Our results indicate that hsa-miR-3178 promotes gemcitabine resistance via RhoB/PI3K/Akt signaling pathway-mediated upregulation of ABC transporters. These findings suggest that hsa-miR-3178 could be a novel therapeutic target for overcoming gemcitabine resistance in PC.

In this paper, we investigate the existence of insensitizing controls for the micropolar fluids in a bounded domain with homogeneous Dirichlet boundary conditions and arbitrarily located internal controller. The study of insensitizing controls is essential to solve a stability problem, which means that we look for controls such that some functionals of the velocity fields (the so‐called sentinels) are insensitive to the small perturbations of initial data. The problem of insensitizing controls is transformed into a suitable controllability problem for a cascade system. Our proof relies on a new global Carleman inequality and the inverse mapping theorem. [ABSTRACT FROM AUTHOR]

Most reported members of Microascaceae that have been reported originate from the terrestrial environment, where they act as saprobes or plant pathogens. However, our understanding of their species diversity and distribution in the marine environment remains vastly limited, with only 22 species in nine genera having been reported so far. A survey of the fungal diversity in intertidal areas of China’s mainland has revealed the discovery of several Microascaceae strains from 14 marine algae and 15 sediment samples. Based on morphological characteristics and LSU-ITS-tef1-tub2 multilocus phylogeny using Bayesian inference and maximum likelihood methods, 48 strains were identified as 18 species belonging to six genera. Among these, six new species were discovered: Gamsia sedimenticola, Microascus algicola, M. gennadii, Scedosporium ellipsosporium, S. shenzhenensis, and S. sphaerospermum. Additionally, the worldwide distribution of the species within this family across various marine habitats was briefly reviewed and discussed. Our study expands the knowledge of species diversity and distribution of Microascaceae in the marine environment.

Recent studies have revealed a significant presence of microplastics (MPs) in freshwater ecosystems, raising concerns about their potential negative impacts on the growth and development of freshwater organisms. The present study was conducted to examine the effects of chronic sub-lethal doses of polystyrene microsphere MPs on the oxidative status (ROS, SOD) and the immune response (IL-1ß, TNF-α) of genetically improved farmed tilapia (a kind of tilapia hereafter referred to as GIFT). GIFT juveniles (5.1 ± 0.2 g) were exposed to different concentrations of substances. The experimental groups were as follows: group A (control, no exposure), group B (exposed to a concentration of 75 nm), group C (exposed to a concentration of 7.5 μm), group D (exposed to a concentration of 750 μm), group E (exposed to a combination of 75 nm, 7.5 μm, and 750 μm), and group F (exposed to a combination of 75 nm and Chlorella). The ROS contents in the brain and gills were significantly decreased in group F, while a significant increase was observed in group D following a 14-day exposure. SOD activities in the intestine showed an elevation in group F, as did those in the brain and gills in group D, while the SOD levels in the gills generally decreased over time in groups B and F. Notably, the highest ROS and SOD were observed in the brain of group D, whereas the lowest were in the intestines at the same concentration. The activity of IL-1β in the liver was significantly up-regulated in all of the exposure groups. IL-1β was significantly up-regulated in the brain of group B and in the gills of group D. Similarly, TNF-α was significantly up-regulated in the brain of groups B/D/E, in the liver of groups B/C/D, in the intestine of group B, and in the gills of group D. Notably, the highest levels of IL-1β and TNF-α activities were recorded in the brain, while the lowest were recorded in the intestine of group D. Overall, this study revealed that GIFT’s immune response and antioxidant system can be affected by MPs.

Abstract Converting CO2 into high‐value fuels and chemicals by renewable‐electricity‐powered electrochemical CO2 reduction reaction (CRR) is a viable approach toward carbon‐emissions‐neutral processes. Unlike the thermocatalytic hydrogenation of CO2 at the solid‐gas interface, the CRR takes place at the three‐phase gas/solid/liquid interface near the electrode surface in aqueous solution, which leads to major challenges including the limited mass diffusion of CO2 reactant, competitive hydrogen evolution reaction, and poor product selectivity. Here we critically examine the various methods of surface and interface engineering of the electrocatalysts to optimize the microenvironment for CRR, which can address the above issues. The effective modification strategies for the gas transport, electrolyte composition, controlling intermediate states, and catalyst engineering are discussed. The key emphasis is made on the diverse atomic‐precision modifications to increase the local CO2 concentration, lower the energy barriers for CO2 activation, decrease the H2O coverage, and stabilize intermediates to effectively control the catalytic activity and selectivity. The perspectives on the challenges and outlook for the future applications of three‐phase interface engineering for CRR and other gas‐involving electrocatalytic reactions conclude the article.

Abstract Background Previous studies on the relationship between ACE I/D, ACE2 G8790A and CYP11B2-344T/C gene polymorphisms and essential hypertension (EH) were inconsistent. Moreover, few studies have reported the combined effect of these gene polymorphisms and noise exposure on EH. The purpose of this study was to explore the combined and separate effects of ACE I/D, ACE2 G8790A and CYP11B2-344T/C gene polymorphisms and noise on EH among steelworkers. Methods A case–control study was conducted on 725 male workers between March 2014 and July 2014 in the Tangsteel Company, China. The noise exposure of the workers were measured. Logistic regression and crossover analysis were used to analyse the effects of the interactions on the EH among steelworkers. GMDR was used to determine the best combination model of gene–noise interactions. Results Multivariate logistic regression showed that noise exposure increased the odds of EH, and the OR is 1.52 (95% CI 1.04–2.22). The risk of having EH for ACE I/D DD genotype carriers was 1.99 times that for II genotype carriers (95% CI 1.14–3.51). There was a negative additive interaction between ACE2 G8790A and CYP11B2-344T/C on EH (U3 = − 2.221, P = 0.026, and S = 0.128) and a positive multiplicative interaction between ACE I/D and CYP11B2-344T/C on essential hypertension (P = 0.041). In addition, there was no significant gene–noise interaction model through the GMDR method after adjusting the confounders. Conclusions The ACE DD genotype may make men susceptible to EH. Simultaneously carrying the DD genotype of ACE I/D and the TC genotype of CYP11B2-344T/C increased the risk of EH.

We explore individual differences in tiger personality. We first asked—is there evidence of personality dimensions (analogous to the Big Five in human personality research) in the Amur tiger? We then asked, are any discoverable personality dimensions associated with measured outcomes, including group status, health and mating frequency? 152 of our participating tigers live in the world's largest semi-wild tiger sanctuary in North Eastern China. Our second sample of 96 tigers also lives in a sanctuary. Having two samples allowed us to assess the replicability of the personality dimensions or factors reported in our first sample. We found that two factors (explaining 21% and 17% of the variance among items) which we call, for descriptive ease, Majesty and Steadiness, provide the best fit to the data. Tigers that score higher on Majesty are healthier, eat more live prey, have higher group status (among other tigers as assessed by human raters) and mate more often. We provide some ethological context to put flesh on the quantitative bones of our findings concerning these magnificent and charismatic animals.

BackgroundMany studies have reported that N6-methyladenosine (m6A) modification plays a critical role in the epigenetic regulation of organisms and especially in the pathogenesis of malignant diseases. However, m6A research has mainly focused on methyltransferase activity mediated by METTL3, and few studies have focused on METTL16. The aim of this study was to investigate the mechanism of METTL16, which mediates m6A modification, and its role in pancreatic adenocarcinoma (PDAC) cell proliferation.MethodsClinicopathologic and survival data were retrospectively collected from 175 PDAC patients from multiple clinical centers to detect the expression of METTL16. CCK-8, cell cycle, EdU and xenograft mouse model experiments were used to evaluate the proliferation effect of METTL16. Potential downstream pathways and mechanisms were explored via RNA sequencing, m6A sequencing, and bioinformatic analyses. Regulatory mechanisms were studied through methyltransferase inhibition, RIP, MeRIP‒qPCR assays.ResultsWe found that METTL16 expression was markedly downregulated in PDAC, and multivariate Cox regression analyses revealed that METTL16 was a protective factor for PDAC patients. We also demonstrated that METTL16 overexpression inhibited PDAC cell proliferation. Furthermore, we identified a METTL16-p21 signaling axis, with downregulation of METTL16 resulting in inhibition of CDKN1A (p21). Additionally, METTL16 silencing and overexpression experiments highlighted m6A modification alterations in PDAC.ConclusionsMETTL16 plays a tumor-suppressive role and suppresses PDAC cell proliferation through the p21 pathway by mediating m6A modification. METTL16 may be a novel marker of PDAC carcinogenesis and target for the treatment of PDAC.

Paneth cells are a group of unique intestinal epithelial cells, and they play an important role in host-microbiota interactions. At the origin of Paneth cell life, several pathways such as Wnt, Notch, and BMP signaling, affect the differentiation of Paneth cells. After lineage commitment, Paneth cells migrate downward and reside in the base of crypts, and they possess abundant granules in their apical cytoplasm. These granules contain some important substances such as antimicrobial peptides and growth factors. Antimicrobial peptides can regulate the composition of microbiota and defend against mucosal penetration by commensal and pathogenic bacteria to protect the intestinal epithelia. The growth factors derived from Paneth cells contribute to the maintenance of the normal functions of intestinal stem cells. The presence of Paneth cells ensures the sterile environment and clearance of apoptotic cells from crypts to maintain the intestinal homeostasis. At the end of their lives, Paneth cells experience different types of programmed cell death such as apoptosis and necroptosis. During intestinal injury, Paneth cells can acquire stem cell features to restore the intestinal epithelial integrity. In view of the crucial roles of Paneth cells in the intestinal homeostasis, research on Paneth cells has rapidly developed in recent years, and the existing reviews on Paneth cells have mainly focused on their functions of antimicrobial peptide secretion and intestinal stem cell support. This review aims to summarize the approaches to studying Paneth cells and introduce the whole life experience of Paneth cells from birth to death.