Molecular engineering to tune the ligand environment of atomically dispersed nickel for efficient alcohol electrochemical oxidation

Altres ajuts: ICN2 is funded by the CERCA Programme /Generalitat de Catalunya. Part of the present work has been performed in the framework of Universitat Autònoma de Barcelona Materials Science Ph.D. program. J.L. is a Serra Húnter Fellow and is grateful to ICREA Academia program.Atomically dispersed metals maximize the number of catalytic sites and enhance their activity. However, their challenging synthesis and characterization strongly complicates their optimization. Here, the aim is to demonstrate that tuning the electronic environment of atomically dispersed metal catalysts through the modification of their edge coordination is an effective strategy to maximize their performance. This article focuses on optimizing nickel-based electrocatalysts toward alcohol electrooxidation in alkaline solution. A new organic framework with atomically dispersed nickel is first developed. The coordination environment of nickel within this framework is modified through the addition of carbonyl (CO) groups. The authors then demonstrate that such nickel-based organic frameworks, combined with carbon nanotubes, exhibit outstanding catalytic activity and durability toward the oxidation of methanol (CHOH), ethanol (CHCHOH), and benzyl alcohol (CHCHOH); the smaller molecule exhibits higher catalytic performance. These outstanding electrocatalytic activities for alcohol electrooxidation are attributed to the presence of the carbonyl group in the ligand chemical environment, which enhances the adsorption for alcohol, as revealed by density functional theory calculations. The work not only introduces a new atomically dispersed Ni-based catalyst, but also demonstrates a new strategy for designing and engineering high-performance catalysts through the tuning of their chemical environment

Nrf2−/− regulated lung DNA demethylation and CYP2E1 DNA methylation under PM2.5 exposure

Cytochrome P450 (CYP450) can mediate fine particulate matter (PM2.5) exposure leading to lung injury. Nuclear factor E2-related factor 2 (Nrf2) can regulate CYP450 expression; however, the mechanism by which Nrf2−/− (KO) regulates CYP450 expression via methylation of its promoter after PM2.5 exposure remains unclear. Here, Nrf2−/− (KO) mice and wild-type (WT) were placed in a PM2.5 exposure chamber (PM) or a filtered air chamber (FA) for 12 weeks using the real-ambient exposure system. The CYP2E1 expression trends were opposite between the WT and KO mice following PM2.5 exposure. After exposure to PM2.5,CYP2E1 mRNA and protein levels were increased in WT mice but decreased in KO mice, and CYP1A1 expression was increased after exposure to PM2.5 in both WT and KO mice. CYP2S1 expression decreased after exposure to PM2.5 in both the WT and KO groups. We studied the effect of PM2.5 exposure on CYP450 promoter methylation and global methylation levels in WT and KO mice. In WT and KO mice in the PM2.5 exposure chamber, among the methylation sites examined in the CYP2E1 promoter, the CpG2 methylation level showed an opposite trend with CYP2E1 mRNA expression. The same relationship was evident between CpG3 unit methylation in the CYP1A1 promoter and CYP1A1 mRNA expression, and between CpG1 unit methylation in the CYP2S1 promoter and CYP2S1 mRNA expression. This data suggests that methylation of these CpG units regulates the expression of the corresponding gene. After exposure to PM2.5, the expression of the DNA methylation markers ten-eleven translocation 3 (TET3) and 5-hydroxymethylcytosine (5hmC) was decreased in the WT group but significantly increased in the KO group. In summary, the changes in CYP2E1, CYP1A1, and CYP2S1 expression in the PM2.5 exposure chamber of WT and Nrf2−/− mice might be related to the specific methylation patterns in their promoter CpG units. After exposure to PM2.5, Nrf2 might regulate CYP2E1 expression by affecting CpG2 unit methylation and induce DNA demethylation via TET3 expression. Our study revealed the underlying mechanism for Nrf2 to regulate epigenetics after lung exposure to PM2.5

PSO Based Optimization of Testing and Maintenance Cost in NPPs

Testing and maintenance activities of safety equipment have drawn much attention in Nuclear Power Plant (NPP) to risk and cost control. The testing and maintenance activities are often implemented in compliance with the technical specification and maintenance requirements. Technical specification and maintenance-related parameters, that is, allowed outage time (AOT), maintenance period and duration, and so forth, in NPP are associated with controlling risk level and operating cost which need to be minimized. The above problems can be formulated by a constrained multiobjective optimization model, which is widely used in many other engineering problems. Particle swarm optimizations (PSOs) have proved their capability to solve these kinds of problems. In this paper, we adopt PSO as an optimizer to optimize the multiobjective optimization problem by iteratively trying to improve a candidate solution with regard to a given measure of quality. Numerical results have demonstrated the efficiency of our proposed algorithm

The Morphological Differentiation and Evolutionary Origins of <i>Artemia</i> in China

Artemia is a genus of halophilic zooplanktons comprising bisexual and parthenogenetic forms, which is an important model for investigating adaption to hypersaline ecosystems. The genus Artemia in China comprises four species: A. sinica, A. tibetiana, A. franciscana and A. parthenogenetica. To investigate the evolutionary relationship of bisexual and parthenogenetic Artemia in China, we analyzed the morphometrics and phylogenetics among twenty-two geographical populations in China. We found significant morphological differentiation across different species and strains of Artemia in China, which exhibited a high level of intra-population variation. We also found overlaps in morphological characteristics between populations, which may raise challenges for the classification of Artemia species using traditional morphological methods. A. franciscana, which originated from various regions in America, was generally distributed along the Chinese coastlines through multiple human introductions. Additionally, native Asian clades split into Western and Eastern Lineages during the late Miocene due to the Himalayan orogeny. Within the Western Lineage, A. tibetiana can be grouped into three taxon units: A. tibeitiana, A. sorgeloosi and A. urmiana. We also found that the distribution and genetic structure of A. sinica were influenced by climate oscillations during the Pleistocene, which might play a pivotal role in driving the formation of parthenogenetic strains in the Eastern Lineage. Overall, our study provides new insight into invertebrate evolution under geographical and climatic impacts in hypersaline environments

Cefotaxime Exposure-Caused Oxidative Stress, Intestinal Damage and Gut Microbial Disruption in <i>Artemia sinica</i>

Cefotaxime (CTX) is an easily detectable antibiotic pollutant in the water environment, but little is known about its toxic effects on aquatic invertebrates, especially on the intestine. Here, we determined the oxidative stress conditions of A. sinica under CTX exposure with five concentrations (0, 0.001, 0.01, 0.1 and 1 mg/L) for 14 days. After that, we focused on changes in intestinal tissue morphology and gut microbiota in A. sinica caused by CTX exposure at 0.01 mg/L. We found malondialdehyde (MDA) was elevated in CTX treatment groups, suggesting the obvious antibiotic-induced oxidative stress. We also found CTX exposure at 0.01 mg/L decreased the villus height and muscularis thickness in gut tissue. The 16S rRNA gene analysis indicated that CTX exposure reshaped the gut microbiota diversity and community composition. Proteobacteria, Actinobacteriota and Bacteroidota were the most widely represented phyla in A. sinica gut. The exposure to CTX led to the absence of Verrucomicrobia in dominant phyla and an increase in Bacteroidota abundance. At the genus level, eleven genera with an abundance greater than 0.1% exhibited statistically significant differences among groups. Furthermore, changes in gut microbiota composition were accompanied by modifications in gut microbiota functions, with an up-regulation in amino acid and drug metabolism functions and a down-regulation in xenobiotic biodegradation and lipid metabolism-related functions under CTX exposure. Overall, our study enhances our understanding of the intestinal damage and microbiota disorder caused by the cefotaxime pollutant in aquatic invertebrates, which would provide guidance for healthy aquaculture

Temporal Characteristics of Debris Flow Surges

Debris flow is one of the most destructive geomorphological events in mountainous watersheds, which usually appears in the form of successive surge waves as observed all over the world. In particular, debris flows in the Jiangjia Gully in southwest China have displayed a great variety of surge phenomena; each debris flow event contains tens or hundreds of separate surges originating from different sources. Therefore, the surge sequence of an event must encode the information of debris flow developing. The unmanned aerial vehicle photos provide an overview of debris flow sources, showing the different potentials of the debris flow and surge sequences present various patterns responding to the rainfall events. Then the variety of rainfalls and material sources determine the diversity of surge sequence. Using time series analysis to the surge discharge sequences, we calculate the Hurst exponent, the autocorrelation function, and the power spectrum exponent and find that all the sequences commonly share the property of long-term memory and these parameters are correlated in an exponential form, with values depending on rainfall patterns. Moreover, all events show a gross trend of discharge decay, despite the local rainfall process, which implies the intrinsic nature of the surge sequence as a systematic behavior of watershed. It is expected that these findings are heuristic for establishing mechanisms of debris flow initiation and evolution in a watershed

Inactivation of p15INK4b in chronic arsenic poisoning cases

Arsenic exposure from burning high arsenic-containing coal has been associated with human skin lesion and cancer. However, the mechanisms of arsenic-related carcinogenesis are not fully understood. Inactivation of critical tumor suppression genes by epigenetic regulation or genetic modification might contribute to arsenic-induced carcinogenicity. This study aims to clarify the correlation between arsenic pollution and functional defect of p15INK4b gene in arsenic exposure residents from a region of Guizhou Province, China. To this end, 103 arsenic exposure residents and 105 control subjects were recruited in this study. The results showed that the exposure group exhibited higher levels of urinary and hair arsenic compared with the control group (55.28 vs 28.87 μg/L, 5.16 vs 1.36 μg/g). Subjects with higher arsenic concentrations are more likely to have p15INK4b methylation and gene deletion (χ2 = 4.28, P = 0.04 and χ2 = 4.31, P = 0.04). We also found that the degree of p15INK4b hypermethylation and gene deletion occurred at higher incidence in the poisoning cases with skin cancer (3.7% and 14.81% in non-skin cancer group, 41.18% and 47.06 in skin cancer group), and were significantly associated with the stage of skin lesions (χ2 = 12.82, P < 0.01 and χ2 = 7.835, P = 0.005). These observations indicate that inactivation of p15INK4b through genetic alteration or epigenetic modification is a common event that is associated with arsenic exposure and the development of arsenicosis

Two birds with one stone: engineering polymeric carbon nitride with n-π∗ electronic transition for extending light absorption and reducing charge recombination

The weak visible light harvesting and high charge recombination are two main problems that lead to a low photocatalytic H2 generation of polymeric carbon nitride (p-CN). To date, the approaches that are extensively invoked to address this problem mainly rely on heteroatom-doping and heterostructures, and it remains a grand challenge in regulating dopant-free p-CN for increasing H2 generation. Here, we report utilizing the inherent n-π∗ electronic transition to simultaneously realize extended light absorption and reduced charge recombination on p-CN nanosheets. Such n-π∗ electronic transition yields a new absorption peak of 490 ​nm, which extends the light absorption edge of p-CN to approximately 590 ​nm. Meanwhile, as revealed by the photoluminescence (PL) spectra of p-CN at the single-particle level, the n-π∗ electronic transition gives rise to an almost quenched PL signal at room temperature, unravelling a dramatically reduced charge recombination. As a consequence, a remarkably improved photocatalytic performance is realized under visible light irradiation, with a H2 generation rate of 5553 ​μmol ​g−1∙h−1, ∼ 12 times higher than that of pristine p-CN (460 ​μmol∙g−1∙h−1) in the absence of the n-π∗ transition. This work illustrates the highlights of using the inherent n-π∗ electronic transition to improve the photocatalytic performance of dopant-free carbon nitrides.Published versionThis work was financially supported by the National Natural Science Foundation of China (52072001, 51872003, 22102002), Anhui Provincial Natural Science Foundation (1908085J21 and 2108085QE192), and Horizontal Cooperation Project of Fuyang Municipal Government – Fuyang Normal University (SXHZ202102)

Type 1 diabetes and diet-induced obesity predispose C57BL/6J mice to PM2.5-induced lung injury: a comparative study

Abstract Background Pre-existing metabolic diseases may predispose individuals to particulate matter (PM)-induced adverse health effects. However, the differences in susceptibility of various metabolic diseases to PM-induced lung injury and their underlying mechanisms have yet to be fully elucidated. Results Type 1 diabetes (T1D) murine models were constructed by streptozotocin injection, while diet-induced obesity (DIO) models were generated by feeding 45% high-fat diet 6 weeks prior to and throughout the experiment. Mice were subjected to real-ambient PM exposure in Shijiazhuang City, China for 4 weeks at a mean PM2.5 concentration of 95.77 µg/m3. Lung and systemic injury were assessed, and the underlying mechanisms were explored through transcriptomics analysis. Compared with normal diet (ND)-fed mice, T1D mice exhibited severe hyperglycemia with a blood glucose of 350 mg/dL, while DIO mice displayed moderate obesity and marked dyslipidemia with a slightly elevated blood glucose of 180 mg/dL. T1D and DIO mice were susceptible to PM-induced lung injury, manifested by inflammatory changes such as interstitial neutrophil infiltration and alveolar septal thickening. Notably, the acute lung injury scores of T1D and DIO mice were higher by 79.57% and 48.47%, respectively, than that of ND-fed mice. Lung transcriptome analysis revealed that increased susceptibility to PM exposure was associated with perturbations in multiple pathways including glucose and lipid metabolism, inflammatory responses, oxidative stress, cellular senescence, and tissue remodeling. Functional experiments confirmed that changes in biomarkers of macrophage (F4/80), lipid peroxidation (4-HNE), cellular senescence (SA-β-gal), and airway repair (CCSP) were most pronounced in the lungs of PM-exposed T1D mice. Furthermore, pathways associated with xenobiotic metabolism showed metabolic state- and tissue-specific perturbation patterns. Upon PM exposure, activation of nuclear receptor (NR) pathways and inhibition of the glutathione (GSH)-mediated detoxification pathway were evident in the lungs of T1D mice, and a significant upregulation of NR pathways was present in the livers of T1D mice. Conclusions These differences might contribute to differential susceptibility to PM exposure between T1D and DIO mice. These findings provide new insights into the health risk assessment of PM exposure in populations with metabolic diseases