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Gradient-structured ternary Fe-Co-Ni alloy coatings electrodeposited on steel substrates at various current densities from chloride baths were numerically and experimentally investigated. The electrodeposition process, considering hydrogen evolution and hydrolysis reaction, was modelled using the finite element method (FEM) and was based on the tertiary current distribution. The experimentally tested coating thickness and elemental contents were used to verify the simulation model. Although there was a deviation between the simulation and experiments, the numerical model was still able to predict the variation trend of the coating thickness and elemental contents. The influence of the current density on the coating characterization was experimentally studied. Due to hydrogen evolution, the coating surface exhibited microcracks. The crack density on the coating surface appeared smaller with increasing applied current density. The XRD patterns showed that the deposited coatings consisted of solid-solution phases α-Fe and γ (Fe, Ni) and the metallic compound Co3Fe7; the current density in the present studied range had a small influence on the phase composition. The grain sizes on the coating surface varied from 15 nm to 20 nm. The microhardness of the deposited coatings ranged from 625 HV to 655 HV. Meanwhile, the average microhardness increased slightly as the current density increased from 5 A/dm2 to 10 A/dm2 and then decreased as the current density further increased. Finally, the degree of anomaly along with the metal ion and hydrogen atom concentrations in the vicinity of the cathodic surface were calculated to investigate the anomalous codeposition behaviour.

Rotator cuff tear (RCT) is the primary cause of shoulder pain and disability and frequently trigger muscle degeneration characterised by muscle atrophy, fatty infiltration and fibrosis. Single‐nucleus RNA sequencing (snRNA‐seq) was used to reveal the transcriptional changes in the supraspinatus muscle after RCT. Supraspinatus muscles were obtained from patients with habitual shoulder dislocation (n = 3) and RCT (n = 3). In response to the RCT, trajectory analysis showed progression from normal myonuclei to ANKRD1+ myonuclei, which captured atrophy‐and fatty infiltration‐related regulons (KLF5, KLF10, FOSL1 and BHLHE40). Transcriptomic alterations in fibro/adipogenic progenitors (FAPs) and muscle satellite cells (MuSCs) have also been studied. By predicting cell–cell interactions, we observed communication alterations between myofibers and muscle‐resident cells following RCT. Our findings reveal the plasticity of muscle cells in response to RCT and offer valuable insights into the molecular mechanisms and potential therapeutic targets of RCT. We performed single‐nucleus RNA‐seq to reveal the transcriptional heterogeneity in myofibers after rotator cuff tear (RCT). Gene signatures of all muscle tissue populations were identified after RCT to reveal the potential transitions of myofibers and other resident cells. Our findings offered a valuable insight for exploring the molecular mechanisms and potential therapeutic targets for RCT.

Proteins exhibit remarkable molecular recognition by dynamically adjusting their conformations to selectively interact with ligands at specialized binding sites. To bind hydrated ligands, proteins leverage amino acid residues with similar water affinities as the substrate, minimizing the energy required to strip water molecules from the hydrophilic substrates. In synthetic receptor design, replicating this sophisticated adaptability remains a challenge, as most artificial receptors are optimized to bind desolvated substances. Here, we show that proline-based synthetic receptors can mimic the conformational dynamics of proteins to achieve selective binding of hydrophilic and amphiphilic fluoride substances in aqueous environments. This finding highlights the critical role of receptor flexibility and strategic hydrophilicity in enhancing ligand recognition and affinity in water. Moreover, it establishes a new framework for designing versatile synthetic receptors with tunable hydrophobicity and hydrophilicity profiles. Proteins dynamically adjust their conformations to interact with their ligands through binding sites that accommodate either amphiphilic or hydrophilic substrates, but most synthetic receptors are designed to bind desolvated substances. Here, the authors design proline-based receptors capable of binding hydrated and amphiphilic substances.

This paper proposes a dynamic evolutionary model to quantify the domino effect of ship engine room fires. Based on the spatial and temporal characteristics of fire accidents, the dynamic probability of the domino effect of multiple accident units is calculated using matrix calculation and Monte Carlo simulation. The uncertainties of shipboard personnel, automatic detection systems, sprinkler systems, and the synergistic effects of multiple escalation vectors from different units are addressed. The dynamic probability of the domino effect of multiple accident units is calculated, and a risk assessment of complex fire scenarios in ship engine rooms is implemented. This study also presents the model feasibility in terms of fire risk assessment in cabins with numerous pieces of equipment. The results indicate that 2 min and 4 min are vital time nodes for the development and spread of fires. The extinguishing work on key equipment in the path of the fire's spread can effectively restrain its further expansion. The results can provide critical references for ship fire prevention, fire suppression, and fire protection design.

Acute pancreatitis (AP) is a common acute inflammatory abdominal condition. Severe acute pancreatitis (SAP) can provoke a systemic inflammatory response and lead to multiple organ failure. The S100A9 protein, recognized as a major inflammatory biomarker, plays a significant role in both infection and inflammatory responses. Despite its known role in inflammation, the precise role of S100A9 in AP remains poorly understood. This study aimed to elucidate the potential role of S100A9 in AP and investigate the underlying mechanism. We employed a mouse model of AP and the AR42J cell line to investigate the functional role of S100A9. The effect of S100A9 on pancreatic injury and the expression of inflammatory factors (IL-6, IL-1β, and TNF-α) was assessed through targeted inhibition of S100A9 expression in the mouse model of AP. Furthermore, the modulatory effect of cerulein-induced inflammatory responses on AR42J cells was assessed after adding the S100A9 recombinant protein. In the mouse model of AP, targeted inhibition of S100A9 markedly ameliorated pancreatic injury and significantly decreased the expression levels of IL-6, IL-1β, and TNF-α. Moreover, increased levels of S100A9 were positively correlated with elevated expression of receptor for advanced glycation endproducts (RAGE) in pancreatic acinar cells. In AR42J cells, the introduction of S100A9 recombinant protein enhanced RAGE expression and exacerbated cerulein-induced inflammatory response. S100A9 inhibition significantly alleviated the pancreatic inflammatory response by downregulating RAGE expression, thereby improving AP.

The purpose of this study is to use a material library to investigate the effect of raw material properties on ribbon tensile strength (TS) and solid fraction (SF) in the roll compaction (RC) process. A total of 81 pharmaceutical materials, including 53 excipients and 28 natural product powders (NPPs), were characterized by 22 material descriptors and were compacted under five different hydraulic pressures. The transversal and longitudinal splitting behaviors of the ribbons were summarized. The TS-porosity and TS-pressure relationships were used to explain the roll compaction behavior of powdered materials. Through defining the target ribbon quality (i.e., 0.6 ≤ SF ≤ 0.8 and TS ≥ 1 MPa), the roll compaction behavior classification system (RCBCS) was built and 81 materials were classified into three categories. A total of 24 excipients and five NPPs were classified as Category I materials, which fulfilled the target ribbon quality and had less occurrence of transversal splitting. Moreover, the multivariate relationships between raw material descriptors, the hydraulic pressure and ribbon quality attributes were obtained by PLS regression. Four density-related material descriptors and the cohesion index were identified as critical material attributes (CMAs). The multi-objective design space summarizing the feasible material properties and operational region for the RC process were visualized. The RCBCS presented in this paper enables a formulator to perform the initial risk assessment of any new materials, and the data modeling method helps to predict the impact of formulation ingredients on strength and porosity of compacts.

Background DnaJA proteins, a prominent subfamily of the DnaJ family, function as molecular chaperones that respond to various external stresses. Extensive studies on the DnaJ family have been conducted in plants. However, research on this subfamily in tobacco remains relatively scarce. Results In this study, we identified 24 DnaJA genes in tobacco, and classified them into three individual groups. A comprehensive analysis based on gene structure, motif composition, and evolutionary pattern revealed the divergence of tobacco DnaJA genes. For the evolution of the NtDnaJA genes, purification selection was the major factor. In addition, the potential regulatory network unveiled that NtDnaJA s could be regulated by miRNAs and various transcription factors associated with diverse stress responses. Through expression pattern analysis of public RNA-seq datasets and qRT-PCR experiments, it was observed that many NtDnaJAs displayed tissue-specific expression and might play significant roles in different biotic and abiotic stresses. Additionally, the pivotal role of NtDnaJA3 in boosting plant drought resistance was confirmed. Conclusions This study provides important perspectives on the evolution of NtDnaJA genes and their involvement in stress responses, laying the groundwork for future research into the roles of DnaJA regulatory genes in tobacco. Graphical Abstract

Environmental contaminants (ECs) are increasingly recognized as crucial drivers of dyslipidemia and cardiovascular disease (CVD), but the comprehensive impact spectrum and interlinking mechanisms remain uncertain. We aimed to systematically evaluate the association between exposure to 80 ECs across seven divergent categories and markers of dyslipidemia and investigate their underpinning biomolecular mechanisms via an unbiased integrative approach of internal chemical exposome and multi-omics. A longitudinal study involving 76 healthy older adults was conducted in Jinan, China, and participants were followed five times from 10 September 2018 to 19 January 2019 in 1-month intervals. A broad spectrum of seven chemical categories covering the prototypes and metabolites of 102 ECs in serum or urine as well as six serum dyslipidemia markers [total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, apolipoprotein (Apo)A1, ApoB, and ApoE4] were measured. Multi-omics, including the blood transcriptome, serum/urine metabolome, and serum lipidome, were profiled concurrently. Exposome-wide association study and the deletion/substitution/addition algorithms were applied to explore the associations between 80 EC exposures detection frequency and dyslipidemia markers. Weighted quantile sum regression was used to assess the mixture effects and relative contributions. Multi-omics profiling, causal inference model, and pathway analysis were conducted to interpret the mediating biomolecules and underlying mechanisms. Examination of cytokines and electrocardiograms was further conducted to validate the observed associations and biomolecular pathways. Eight main ECs [1-naphthalene, 1-pyrene, 2-fluorene, dibutyl phosphate, tri-phenyl phosphate, mono-(2-ethyl-5-hydroxyhexyl) phthalate, chromium, and vanadium] were significantly associated with most dyslipidemia markers. Multi-omics indicated that the associations were mediated by endogenous biomolecules and pathways, primarily pertinent to CVD, inflammation, and metabolism. Clinical measures of cytokines and electrocardiograms further cross-validated the association of these exogenous ECs with systemic inflammation and cardiac function, demonstrating their potential mechanisms in driving dyslipidemia pathogenesis. It is imperative to prioritize mitigating exposure to these ECs in the primary prevention and control of the dyslipidemia epidemic. https://doi.org/10.1289/EHP13864.