Search

Background & Objectives: LUC7L2 may be involved in the recognition of non-consensus splice donor sites in association with the U1 snRNP spliceosomal subunit. However, their detailed features and regulatory mechanisms of LUC7L2 in the development of human liver cancer have not been well characterized., Results: Herein, our results demonstrate that LUC7L2 promotes the proliferation of liver cancer cells in vitro and xenograft transplantation in vivo. The proliferation ability was significantly increased in the rLV-LUC7L2 group compared to rLV group (24th hour: P = 0.00043; 48th hour: P = 0.000017). The cellular colony formation ability was significantly increased in the rLV-LUC7L2 group compared to rLV group (25.18±6.94 % vs 67.63±9.57 %, P = 0.00009). The weight of transplanted tumors was significantly increased in the rLV-LUC7L2 group compared to rLV group (0.387±0.074 vs 0.958± 0.103 g, P = 0.00004) .Moreover, LUC7L2 effects on epigenetic regulation based on H3K4me3 in human liver cancer cells. e,g, RRAS. Furthermore, LUC7L2 affects transcriptome and proteome in liver cancer. In particular, LUC7L2 enhances the modification ability of H3K4me3and RNAPolII on the promoter region of RRAS and then enhances the expression of RRAS in liver cancer. Strikingly, LUC7L2 increases the increases the DNA damage repair ability dependent on RRAS. Although the DNA damage repair ability was significantly increased in the rLV-LUC7L2 group compared to rLV group(1.868±0.181 vs 0.17±0.034, P = 0.0000022), it was not significantly changed in rLV-LUC7L2+rLV-shRNA RRAS group compared with rLV group(1.868±0.181 vs 1.798±0.313, P = 0.317) . Importantly, LUC7L2 enhances the carcinogenic function dependent on RRAS. In particular, RRAS increased the DNA damage repair ability by enhancing the formation of DNA damage repair dependent on tri-methylation of histone H3 lysine 36 (H3K36me3)., Conclusions: It is implied that LUC7L2's role in liver cancer proliferation is largely dependent on RRAS. The first discovery provides a basis for the prevention and treatment of human liver cancer., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests., (Copyright © 2024. Published by Elsevier B.V.)

G protein-coupled receptor 39 (GPR39), a member of the growth hormone-releasing peptide family, exhibits widespread expression across various tissues and demonstrates high constitutive activity, primarily activated by zinc ions. It plays critical roles in cell proliferation, differentiation, survival, apoptosis, and ion transport through the recruitment of Gq/11, Gs, G12/13, and β-arrestin proteins. GPR39 is involved in anti-inflammatory and antioxidant responses, highlighting its diverse pathophysiological functions. Recent discoveries of endogenous ligands have enhanced our understanding of GPR39's physiological roles. Aberrant expression and reactivation of GPR39 have been implicated in a range of diseases, particularly central nervous system disorders, endocrine disruptions, cardiovascular diseases, cancers, and liver conditions. These findings position GPR39 as a promising therapeutic target, with the efficacy of synthetic ligands validated in various in vivo models. Nonetheless, their clinical applicability remains uncertain, necessitating further exploration of novel agonists-especially biased agonists-and antagonists. This review examines the unique residues contributing to the high constitutive activity of GPR39, its endogenous and synthetic ligands, and its pathophysiological implications, aiming to elucidate its pharmacological potential for clinical application in disease treatment., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Introduction: Niemann-Pick C1 (NPC1), a lysosomal cholesterol transport protein, is required for efficient efferocytosis. Patients with Npc1 mutation are frequently accompanied with hepatic symptoms, including hepatomegaly, elevated liver transaminases, or even acute liver failure, but the pathogenic mechanism remains unknown., Objectives: Our work aims to characterize the functional role of myeloid NPC1 in liver injury and elucidate its underlying mechanism., Methods: Analyses of injured livers from patients with liver diseases and mouse models were conducted to examine NPC1 expression. Myeloid cell-specific Npc1 knockout mice were constructed to determine the functional role of macrophage NPC1 in liver injury. Isolated macrophages were subjected to in vitro mechanistical assays., Results: We found that NPC1 is mainly expressed in hepatic macrophages. Its mRNA and protein expression are significantly elevated in injured livers from both patients and mouse models. Tissue-specific deletion of myeloid Npc1 increased liver inflammation, levels of serum liver function enzymes, and liver fibrosis in mouse models of liver injury induced by carbon tetrachloride (CCl 4 ) injection and methionine-and-choline-deficient (MCD) diets. Further analyses indicate that Npc1 deficiency in mouse models of liver injury resulted in increased levels of serum HMGB1 and mitochondrial DNA, promoted hepatic macrophage proinflammatory activation, M1 polarization, led to overproduction of hepatic inflammatory cytokines/chemokines, e.g. CCL2 and STING/NFκB pathway activation. In vitro mechanistical studies reveal that Npc1-deficient macrophages exhibited inefficient efferocytosis, partly due to impaired cargo degradation., Conclusions: These findings indicate that elevated expression of myeloid NPC1 in liver diseases protects liver from injury by promoting macrophage efferocytosis of damaged cells. Dysfunction of NPC1 aggravates liver injury, suggesting that NPC1 may be a potential therapeutic target for treating liver diseases., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Objectives: The objective of this study was to profile the transcriptional profiles of peripheral blood mononuclear cells (PBMCs) and their immune repertoires affected by anti-synthetase syndrome (ASS) at the single-cell level., Methods: We performed single-cell RNA sequencing (scRNA-seq) analysis of PBMCs and bulk RNA sequencing for patients with ASS (N=3) and patients with anti-melanoma differentiation-associated gene 5-positive dermatomyositis (MDA5 + DM, N=3) along with healthy controls (HCs, N=4). As ASS and MDA5 + DM have similar organ involvements, MDA5 + DM was used as a disease control. The immune repertoire was constructed by reusing the same scRNA-seq datasets. Importantly, flow cytometry was performed to verify the results from the scRNA-seq analysis., Results: After meticulous annotation of PBMCs, we noticed a significant decrease in the proportion of mucosal-associated invariant T (MAIT) cells in ASS patients compared to HCs, while there was a notable increase in the proportion of proliferative NKT cells. Compared with MDA5 + DM patients, in their PBMCs ASS patients presented substantial enrichment of interferon pathways, which were primarily mediated by IFN-II, and displayed a weak immune response. Furthermore, ASS patients exhibited more pronounced metabolic abnormalities, which may in turn affect oxidative phosphorylation pathways. Monocytes from ASS patients appear to play a crucial role as receptive signaling cells for the TNF pathway. Immunophenotyping analysis of PBMCs from ASS patients revealed an increasing trend for the clone type CQQSYSTPWTF., Conclusion: Using single-cell genomic datasets of ASS PBMCs, we revealed a distinctive profile in the immune system of individuals with ASS, compared to that with MDA5 + DM or healthy controls., Competing Interests: ZC is a scientific consultant to and GZ is an employee of Beijing SeekGene BioSciences Co. Ltd. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Ding, Li, Wang, Han, Chen, Du, Yang, Zhang, Wang, Xu, Wang, Xu, Wu, Hao, Liu, Zhang, Zhang, Sun, Cai and Wei.)

Rising environmental concerns associated with the domestic use of solid biofuels have driven the search for clean energy alternatives. This study investigated the in vitro toxicological characteristics of PM 2.5 emissions from residential biomass pellet burning using the A549 epithelial cell line. The potential of modern pellet applications to reduce PM 2.5 emissions was evaluated by considering both mass reduction and toxicity modification. PM 2.5 emissions from raw and pelletized biomass combustion reduced cell viability, indicative of acute toxicity, and also protein expression associated with epithelial barrier integrity, implying further systemic toxicity, potentially via an oxidative stress mechanism. Toxicity varied between PM 2.5 emissions from raw biomass and pellets, with pelletized straw and wood inducing cytotoxicity by factors of 0.54 and 1.30, and causing epithelial barrier damage by factors of 1.76 and 2.08, respectively, compared to their raw counterparts. Factoring in both mass reduction and toxicity modifications, PM 2.5 emissions from pelletized straw and wood dropped to 1.83 and 5.07 g/kg, respectively, from 30.1 to 9.32 g/kg for raw biomass combustion. This study underscores the effectiveness of pelletized biomass, particularly straw pellets, as a sustainable alternative to traditional biofuels and highlights the necessity of considering changes in toxicity when assessing the potential of clean fuels to mitigate emissions of the PM 2.5 complex.

Residential solid fuel combustion significantly impacts air quality and human health. Pelletized biomass fuels are promoted as a cleaner alternative, particularly for those who cannot afford the high costs of gas/electricity, but their emission characteristics and potential effects remain poorly understood. The present laboratory-based study evaluated pollution emissions from pelletized biomass burning, including CH 4 (methane), NMHC (nonmethane hydrocarbon compounds), CO, SO 2 , NO x , PM 2.5 (particulate matter with an aerodynamic diameter ≤2.5 μm), OC (organic carbon), EC (element carbon), PAHs (polycyclic aromatic hydrocarbons), EPFRs (environmentally persistent free radicals), and OP (oxidative potential) of PM 2.5 , and compared with those from raw biomass burning. For most targets, except for SO 2 and NO x , the mass-based emission factors for pelletized biomass were 62-96% lower than those for raw biomass. SO 2 and NO x levels were negatively correlated with other air pollutants ( p < 0.05). Based on real-world daily consumption data, this study estimated that households using pelletized biomass could achieve significant reductions (51-95%) in emissions of CH 4 , NMHC, CO, PM 2.5 , OC, EC, PAHs, and EPFRs compared to those using raw biomass, while the differences in emissions of NO x and SO 2 were statistically insignificant. The reduction rate of benzo(a)pyrene-equivalent emissions was only 16%, much lower than the reduction in the total PAH mass (78%). This is primarily attributed to the more PAHs with high toxic potentials, such as dibenz(a,h)anthracene, in the pelletized biomass emissions. Consequently, impacts on human health associated with PAHs might be overestimated if only the mass of total PAHs was counted. The OP of particles from the pellet burning was also significantly lower than that from raw biomass by 96%. The results suggested that pelletized biomass could be a transitional substitution option that can significantly improve air quality and mitigate human exposure.

Water contamination owing to anionic pollutants is a persisting and ubiquitous global threat. The current remediation technologies are mostly low in efficiency, expensive in materials and often associated with complicated processes. Herein, we report a characteristic zirconium-based nanocluster that can work as molecular robots for the efficient remediation of anions-contaminated water with great effectiveness and molecular-level accuracy. It exhibits a stimuli-responsive behavior to facilitate the water treatment process: dissolve in acidic aqueous solutions for molecular-level decontamination and quickly aggregate for post-remediation collection. It can precisely capture the representative anionic pollutants, whilst featuring satisfactory capacities (ca. 175 mg-arsenic/g, 60 mg-chromium/g, 45 mg-fluoride/g, 70 mg-phosphorus/g, respectively), super-fast kinetics (finishing uptake within seconds, which is two to four orders of magnitude faster than typical sorbents), as well as multi-cycle applications without appreciable loss of activity. The coexisting common ions show no effect on the target uptake. The responsible active site investigation shows that four active sites are responsible for the monovalent pollutant removal, and the active sites work in pairs to capture divalent chromate species. Cost analysis shows its economical applicability in practical applications. This work would lead to the development of effective water decontamination with higher effectiveness, more convenience, lower cost and more practical application value., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Metastasis is a crucial stage in tumour progression, and cancer-associated fibroblasts (CAFs) support metastasis through their participation in extracellular matrix (ECM) stiffness. CD248 is a possible biomarker for non-small cell lung cancer (NSCLC)-derived CAFs, but its role in mediating ECM stiffness to promote NSCLC metastasis is unknown. We investigated the significance of CD248 + CAFs in activating the Hippo axis and promoting connective tissue growth factor (CTGF) expression, which affects the stromal collagen I environment and improves ECM stiffness, thereby facilitating NSCLC metastasis. In this study, we found that higher levels of CD248 in CAFs induced the formation of collagen I, which in turn increased extracellular matrix stiffness, thereby enabling NSCLC cell infiltration and migration. Hippo axis activation by CD248 + CAFs induces CTGF expression, which facilitates the formation of the collagen I milieu in the stromal matrix. In a tumour lung metastasis model utilizing fibroblast-specific CD248 gene knockout mice, CD248 gene knockout mice showed a significantly reduced ability to develop tumour lung metastasis compared to that of WT mice. Our findings demonstrate that CD248 + CAFs activate the Hippo pathway, thereby inducing CTGF expression, which in turn facilitates the collagen I milieu of the stromal matrix, which promotes NSCLC metastasis., (© 2024 The Author(s). Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Irreversible electroporation (IRE) has emerged as a promising modality for tumor ablation, leveraging the controlled application of electrical pulses to induce cell death. However, the associated muscle contractions during the procedure pose challenges. This study introduces a novel approach, termed Synergistic Bipolar Irreversible Electroporation (SBIRE), aimed at achieving tumor ablation without the undesirable side effect of muscle contraction. SBIRE involves the simultaneous application of nanosecond bipolar electrical pulses (±1600 V per 0.2 cm or ±8000 V per 1 cm, ±500 ns, "+" to "-" delay 1 μs, "-" to "+" delay 200 μs, 5 cycles) and microsecond bipolar electrical pulses (±300 V per 0.2 cm or ±1500 V per 1 cm, ±2 μs, "+" to "-" delay 2 μs, "-" to "+" delay 1000 μs, 25 cycles), strategically designed to synergistically target tumor cells while minimizing the impact on adjacent muscle tissue. The experimental setup includes in vitro and in vivo studies utilizing tumor cells and animal models to assess the efficacy of SBIRE. Preliminary results demonstrate the effectiveness of SBIRE in inducing irreversible electroporation within the tumor, leading to cell death, and the ablation effect is better than other parameter forms (24.41±0.23 mm2 (SBIRE group) vs 12.93±0.31 mm2 (ns group), 6.55±0.23 mm2 (μs group), 19.54±0.25 mm2 (ns+μs group), p<0.0001). Notably, muscle contraction is significantly reduced compared to traditional IRE procedures, highlighting the potential of SBIRE to enhance patient comfort and procedural success. The development of SBIRE represents a significant advancement in the field of tumor ablation, addressing a fundamental limitation associated with muscle contraction during IRE. This technique not only offers a valuable and promising approach to tumor treatment but also holds promise for minimizing procedural side effects.

Efficiently generating 3D holograms is one of the most challenging research topics in the field of holography. This work introduces a method for generating multi-depth phase-only holograms using a fully convolutional neural network (FCN). The method primarily involves a forward-backward-diffraction framework to compute multi-depth diffraction fields, along with a layer-by-layer replacement method (L 2 RM) to handle occlusion relationships. The diffraction fields computed by the former are fed into the carefully designed FCN, which leverages its powerful non-linear fitting capability to generate multi-depth holograms of 3D scenes. The latter can smooth the boundaries of different layers in scene reconstruction by complementing information of occluded objects, thus enhancing the reconstruction quality of holograms. The proposed method can generate a multi-depth 3D hologram with a PSNR of 31.8 dB in just 90 ms for a resolution of 2160 × 3840 on the NVIDIA Tesla A100 40G tensor core GPU. Additionally, numerical and experimental results indicate that the generated holograms accurately reconstruct clear 3D scenes with correct occlusion relationships and provide excellent depth focusing., (© 2024 The Authors. Advanced Science published by Wiley‐VCH GmbH.)

Non-small cell lung cancer (NSCLC)-originating cancer-associated fibroblasts (CAFs) expressing CD248 regulate interaction with immune cells to accelerate cancer progression. Epithelial-mesenchymal transition (EMT) is a key feature of metastatic cells. In our pervious study, we found that CD248 + CAFs activated M2-polarized macrophages, enhancing the progression of NSCLC. However, it is yet unclear how CD248 + CAFs inducing M2-polarized macrophages induce EMT program in NSCLC cells. Herein, we examined CD248 expression from CAFs derived from NSCLC patient tumour tissues. Furthermore, we determined the influence of CD248 knock down CAFs on macrophages polarization. Next, we explored the influences of CD248-harboring CAFs-mediated M2 macrophage polarization to promote NSCLC cells EMT in vitro. We constructed fibroblasts specific CD248 gene knock out mice to examine the significance of CD248-harboring CAFs-induced M2-polarized macrophages to promote NSCLC cells EMT in vivo. Based on our analysis, CD248 is ubiquitously expressed within NSCLC-originating CAFs. CD248 + CAFs mediated macrophages polarized to M2 type macrophages. CD248 + CAFs induced M2 macrophage polarization to enhance NSCLC cells EMT both in vivo and in vitro. Our findings indicate that CD248-harboring CAFs promote NSCLC cells EMT by regulating M2-polarized macrophages., (© 2024. The Author(s).)

Drug-induced liver injury (DILI) occurs frequently and can be life-threatening. Increasing researches suggest that acetaminophen (APAP) overdose is a leading cause of drug-induced liver injury. Indole-3-carboxaldehyde (I3A) alleviates hepatic inflammation, fibrosis and atherosclerosis, suggesting a potential role in different disease development. However, the question of whether and how I3A protects against acetaminophen-induced liver injury remains unanswered. In this study, we demonstrated that I3A treatment effectively mitigates acetaminophen-induced liver injury. Serum alanine/aspartate aminotransferases (ALT/AST), liver malondialdehyde (MDA) activity, liver glutathione (GSH), and superoxide dismutase (SOD) levels confirmed the protective effect of I3A against APAP-induced liver injury. Liver histological examination provided further evidence of I3A-induced protection. Mechanistically, I3A reduced the expression of apoptosis-related factors and oxidative stress, alleviating disease symptoms. Finally, I3A treatment improved survival in mice receiving a lethal dose of APAP. In conclusion, our study demonstrates that I3A modulates hepatotoxicity and can be used as a potential therapeutic agent for DILI., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Polyacrylamide (PAM) hydrogels have garnered significant attention due to their unique swelling properties, biocompatibility, and stability, resulting in them being promising candidates for various applications, ranging from drug delivery to tissue engineering. However, traditional PAM hydrogels suffer from low strength and poor toughness, which limits their widespread use. In this study, based on the theory of filler-reinforced composites, we introduced ordered sulfonated polystyrene (SPS) particles into PAM hydrogels using electric field-assisted techniques. The effects of the geometric dimensions and filling concentration of SPS particles on thermal stability, swelling/deswelling behavior, and mechanical properties of composite hydrogels were investigated. When filled with ordered 100 nm SPS particles at a concentration of 2.0 g·L -1 , the resulting SPS/PAM composite exhibited improved water retention capacity, as well as a fracture elongation of 316 % and a tensile strength of 23 kPa. These findings in the paper provide valuable insights into the understanding of PAM hydrogels and open up new avenues for the development of advanced hydrogel-based systems with enhanced performance and functionality., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

As a highly economic berry fruit crop, blueberry is enjoyed by most people and has various potential health benefits, many of which are attributed to the relatively high concentrations of flavonoids. To obtain more accurate and comprehensive transcripts, the full-length transcriptome of half-highbush blueberry ( Vaccinium corymbosum/angustifolium cultivar Northland) obtained using single molecule real-time and next-generation sequencing technologies was reported for the first time. Overall, 147,569 consensus transcripts (average length, 2738 bp; N50, 3176 bp) were obtained. After quality control steps, 63,425 high-quality isoforms were obtained and 5030 novel genes, 3002 long non-coding RNAs, 3946 transcription factor genes (TFs), 30,540 alternative splicing events, and 2285 fusion gene pairs were identified. To better explore the molecular mechanism of flavonoid biosynthesis in mature blueberry fruit, an integrative analysis of the metabolome and transcriptome was performed on the exocarp, sarcocarp, and seed. A relatively complete biosynthesis pathway map of phenylpropanoids, flavonoids, and proanthocyanins in blueberry was constructed. The results of the joint analysis showed that the 228 functional genes and 42 TFs regulated 78 differentially expressed metabolites within the biosynthesis pathway of phenylpropanoids/flavonoids. O2PLS analysis results showed that the key metabolites differentially accumulated in blueberry fruit tissues were albireodelphin, delphinidin 3,5-diglucoside, delphinidin 3-O-rutinoside, and delphinidin 3-O-sophoroside, and 10 structural genes (4 Vc4CLs , 3 VcBZ1s , 1 VcUGT75C1 , 1 VcAT , and 1 VcUGAT ), 4 transporter genes (1 VcGSTF and 3 VcMATEs ), and 10 TFs (1 VcMYB , 2 VcbHLHs , 4 VcWD40s, and 3 VcNACs ) exhibited strong correlations with 4 delphinidin glycosides. These findings provide insights into the molecular mechanisms of flavonoid biosynthesis and accumulation in blueberry fruit.

Membrane-based separation has the merit of low carbon footprint. In this study, the pore size of metal-organic framework (MOF) membranes is rationally designed for discriminating various pairs of hydrocarbon isomers. Specifically, Zr-MOF UiO-66 (UiO stands for University of Oslo) membranes are developed for separating p/o-xylene due to their proper pore size. For n-hexane/2-methylpentane separation, the functional groups and proportion of the ligands in UiO-66 are gradually adjusted to effectively regulate the pore size, and UiO-66-33Br membranes are constructed. In addition, relying on the utilization of ligands with shorter length, MOF-801 membranes with smaller pore size are fabricated for n/i-butane separation., (© 2024 Wiley‐VCH GmbH.)

Membrane-based separation process for unconventional natural gas purification (mainly N 2 /CH 4 separation) has attracted more attention due to its considerable economic benefits. However, the majority of separation membranes at this stage, particularly N 2 -selective membranes, achieve the desired separation target by mainly relying on the diffusivity-selectivity mechanism. To overcome the limitation of a single mechanism, 2D lamellar MXene membranes with a double selectivity mechanism are prepared to enhance N 2 permeance and N 2 /CH 4 selectivity via introducing unsaturated metal sites into MXene, which can form specific interactions with N 2 molecules and enhance N 2 permeation. The resulting membranes exhibit an inspiring N 2 /CH 4 separation performance with an N 2 permeance of 344 GPU and N 2 /CH 4 selectivity of 13.76. The collaboration of the double selectivity mechanism provides a new idea for the development of a novel N 2 -selective membrane for N 2 removal and CH 4 purification, which further broadens the application prospects of membrane separation technology in the field of unconventional natural gas purification., (© 2023 Wiley‐VCH GmbH.)

Most scholars have suggested that dust emission mainly depends on the bombardment of saltation particles based on wind tunnel experiments, because the cohesive forces between finer particles. However, in recent years, researchers have found that dust can be entrained directly in field. To detect the dust emission mechanism in natural environments, two types of field observations were carried out. Long-term observations were implemented on the shore of the Zu Lake, and the results show that the sediments contain large fractions of particulate matter <10 μm (PM 10 ), which indicates that the entrainment of PM 10 in sediment cannot solely depend on saltation bombardment. Short-term observations were conducted across the Desert Steppe, the Mu Us Sandy Land, and the shore of the Zu Lake, and a total of 31 plots were observed, which revealed that in most of the plots, the threshold of the friction velocities (TFVs) for PM 10 entrainment was lower than for the entrainment of saltation particles, indicating that the PM 10 was easier to entrain than the saltation particles. Large fractions of emitted PM 10 were directly entrained, especially when the PM 10 emission was continuous regardless of whether the PM 10 contents of the soils were low or high, because the strong wind environment could renew the surface frequently and provided sufficient PM 10 to be emitted. Based on our observations, we concluded that in natural environments, direct dust entrainment is the dominant dust emission mechanism, especially in continuous emission processes. Herein, we developed a parameterization scheme for continuous dust emission in natural environments, and this scheme can accurately simulate dust emission on different surfaces. The results of this study provide robust validation for the fact that direct dust entrainment dominates the dust emission mechanism in natural environments. In addition, the results provide valuable observation data for parameterization of dust emission., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper that named “New insights into dust emission mechanism in natural environments based on a series of field observations”., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Lipophagy is a vital biological process that maintains the balance of intracellular lipid metabolism in nonalcoholic fatty liver disease (NAFLD). However, the precise regulatory mechanism of RNF186 in hepatic lipophagy is still unclear. This study investigates the roles and mechanisms of RNF186 in the regulation of lipophagy during the development of NAFLD., Methods: In this study, we employed RNF186 knockout mice as well as human liver cells and mouse primary hepatocytes (MPHs) to investigate the role and mechanisms of RNF186 in lipophagy during the progression of NAFLD. Additionally, liver specimens from individuals with NAFLD were examined to assess the expression of RNF186 and its associated factors., Results: Here, we provide evidence that depletion of RNF186 enhances lipophagy in hepatocytes of a NAFLD model. Mechanistically, RNF186 acts as an E3 ubiquitin ligase that targets cytoplasmic HMGB1 for lysine 48 (K48)- and K63-linked ubiquitination, leading to its subsequent proteasomal degradation. Importantly, the translocation of HMGB1 from the nucleus to the cytoplasm is responsible for inducing lipophagy in NAFLD samples. Knockdown of HMGB1 significantly reduces the activation of lipophagy and mediates the decrease in lipid accumulation caused by RNF186 depletion in hepatocytes. Furthermore, we find that maintaining the nuclear HMGB1 level and inhibiting its nuclear-cytoplasmic shuttling are critical for the proper function of RNF186 in NAFLD. Additionally, the expression of RNF186 and HMGB1 in human NAFLD samples, along with factors related to lipophagy, suggest that RNF186 may play a similar role in the pathogenesis of human fatty liver., Conclusion: RNF186 deficiency accelerates hepatic lipophagy in NAFLD through the inhibition of ubiquitination and degradation of cytoplasmic HMGB1. Consequently, targeting the RNF186-HMGB1 axis may offer a promising strategy for the prevention and treatment of NAFLD., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Inherited anemia continues to pose a significant public health concern on a global scale, owing to its extensive geographical prevalence, substantial patient population, and profound ramifications. Here, we investigated detailed information on inherited anemias (including thalassemias, thalassemias trait, sickle cell disease, sickle cell trait, G6PD deficiency, and G6PD trait) for the period 1990-2019 from the Global Burden of Disease study. Over the course of three decades, there has been a persistent rise in the incidence of inherited anemias worldwide, culminating in a total of 44,896,026 incident cases in 2019. However, the prevalence of inherited anemias has exhibited a consistent downward trend over successive years. Significantly, these inherited anemias primarily impact females, exhibiting a male-to-female ratio of 1:1.88. Among males, the most prevalent inherited anemia is G6PD deficiency, whereas G6PD trait prevails among females. The incidence rates of inherited anemias and their temporal trend exhibited significant variations across different regions, with Central Sub-Saharan Africa displaying the highest incidence rates and Central Latin America experiencing the most substantial decline. The findings of this study suggest a significant correlation between the Socio-Demographic index (SDI) and incidence rates of inherited anemias, particularly in regions with lower SDI levels such as Africa and South Asia. These results contribute valuable insights for the analysis of global trends in the burden of inherited anemias., (© 2023. The Author(s).)

Chemotherapy-resistant non-small cell lung cancer (NSCLC) presents a substantial barrier to effective care. It is still unclear how cancer-associated fibroblasts (CAFs) contribute to NSCLC resistance to chemotherapy. Here, we found that CD248 + CAFs released IL-8 in NSCLC, which, in turn, enhanced the cisplatin (CDDP) IC50 in A549 and NCI-H460 while decreasing the apoptotic percentage of A549 and NCI-H460 in vitro. The CD248 + CAFs-based IL-8 secretion induced NSCLC chemoresistance by stimulating nuclear factor kappa B (NF-κB) and elevating ATP-binding cassette transporter B1 (ABCB1). We also revealed that the CD248 + CAFs-based IL-8 release enhanced cisplatin chemoresistance in NSCLC mouse models in vivo. Relative to wild-type control mice, the CD248 conditional knockout mice exhibited significant reduction of IL-8 secretion, which, in turn, enhanced the therapeutic efficacy of cisplatin in vivo. In summary, our study identified CD248 activates the NF-κB axis, which, consecutively induces the CAFs-based secretion of IL-8, which promotes NSCLC chemoresistance. This report highlights a potential new approach to enhancing the chemotherapeutic potential of NSCLC-treating cisplatin., (© 2024 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Indole-3-carboxaldehyde (I3A), one of tryptophan metabolites derived from gut microbiota, extends the lifespan of mice after high-dose ionizing radiation exposure. Persistent myelosuppression is the most common and fatal complication for victims of nuclear accidents and patients undergoing radiotherapy, with few therapeutic options available. However, whether and how I3A protects ionizing radiation-induced hematopoietic toxicity remain unknown. In this study, we demonstrated that I3A treatment effectively ameliorated radiation-induced hematopoietic injury through accelerating peripheral blood cells recovery, promoting bone marrow cellularity restoration and enhancing functional HSPC regeneration. Additionally, I3A also suppressed intracellular reactive oxygen species production and inhibited apoptosis in irradiated HSPCs. Mechanistically, I3A treatment significantly increased HSPC quiescence, thus conferring HSPCs with resistance against radiation injury. Finally, I3A treatment could improve survival of lethally irradiated mice. Taken together, our data suggest that I3A acts as a gut microbiota-derived paracrine factor that regulates HSPC regeneration and may serve as a promising therapeutic agent for ionizing radiation-induced myelosuppression., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Polymeric membranes with high permeance and remarkable selectivity for simultaneous H 2 purification and CO 2 capture under industry-relevant conditions are absent. Herein, sub-micro pores with precise molecular sieving capability are created in ultra-thin (13-30 nm) polymer membranes via controllable transformation of amine-linked polymer (ALP) films into benzimidazole-and-amine-linked polymer (BIALP) layers. The BIALP membranes exhibit stable unprecedented H 2 /CO 2 selectivity of 120 with a H 2 permeance of 315 GPU. Furthermore, high pressure (up to 11 bar) and thermal (up to 300 °C) resistance is delivered. This work provides a concept on designing porous polymeric membranes for precise molecular discrimination., (© 2024. The Author(s).)

Objective: To explore a simple method for measuring the dynamic intrinsic positive end-expiratory pressure (PEEPi) during invasive mechanical ventilation., Methods: A 60-year-old male patient was admitted to the critical care medicine department of Dongying People's Hospital in September 2020. He underwent invasive mechanical ventilation treatment for respiratory failure due to head and chest trauma, and incomplete expiratory flow occurred during the treatment. The expiratory flow-time curve of this patient was served as the research object. The expiratory flow-time curve of the patient was observed, the start time of exhalation was taken as T0, the time before the initiation of inspiratory action (inspiratory force) was taken as T 1 , and the time when expiratory flow was reduced to zero by inspiratory drive (inspiratory force continued) was taken as T 2 . Taking T 1 as the starting point, the follow-up tracing line was drawn according to the evolution trending of the natural expiratory curve before the T 1 point, until the expiratory flow reached to 0, which was called T 3 point. According to the time phase, the intrapulmonary pressure at the time just from expiratory to inspiratory (T 1 point) was called PEEPi 1 . When the expiratory flow was reduced to 0 (T 2 point), the intrapulmonary pressure with the inhaling power being removed hypothetically was called PEEPi 2 . And it was equal to positive end-expiratory pressure (PEEP) set in the ventilator at T 3 point. The area under the expiratory flow-time curve (expiratory volume) between T 0 and T 1 was called S 1 . And it was S 2 between T 0 and T 2 , S 3 between T 0 and T 3 . After sedation, in the volume controlled ventilation mode, approximately one-third of the tidal volume was selected, and the static compliance of patient's respiratory system called "C" was measured using the inspiratory pause method. PEEPi 1 and PEEP 2 were calculated according to the formula "C = ΔV/ΔP". Here, ΔV was the change in alveolar volume during a certain period of time, and ΔP represented the change in intrapulmonary pressure during the same time period. This estimation method had obtained a National Invention Patent of China (ZL 2020 1 0391736.1)., Results: (1) PEEPi 1 : according to the formula "C = ΔV/ΔP", the expiratory volume span from T 1 to T 3 was "S 3 -S 1 ", and the intrapulmonary pressure decreased span was "PEEPi 1 -PEEP". So, C = (S 3 -S 1 )/(PEEPi 1 -PEEP), PEEPi 1 = PEEP+(S 3 -S 1 )/C. (2)PEEPi 2 : the expiratory volume span from T 2 to T 3 was "S 3 -S 2 ", and the intrapulmonary pressure decreased span was "PEEPi 2 -PEEP". So, C = (S 3 -S 2 )/(PEEPi 2 -PEEP), PEEPi 2 = PEEP+(S 3 -S 2 )/C., Conclusions: For patients with incomplete expiratory during invasive mechanical ventilation, the expiratory flow-time curve extension method can theoretically be used to estimate the dynamic PEEPi in real time.

Objective: To investigate the effect of flunarizine combined with ginkgo leaf extract and dipyridamole injection (GDI) on hemorheology of elderly patients with vertigo., Methods: Clinical data of 105 elderly patients with vertigo who were treated in The First People's Hospital of Lin'an District from June 2019 to December 2022 were retrospectively selected. Of them, 54 patients received flunarizine combined with GDI (Study group) while 51 patients received flunarizine treatment alone (Control group). The treatment effect and adverse reactions of the two groups, functional rehabilitation before and after treatment, including the Simplified Vertigo Symptom Score Scale (VSS-SF), Berg Balance Scale (BBS), and Dizziness Handicap Inventory (DHI) were measured. Hemodynamics including blood flow velocity (Vm) of basilar artery (BA), left vertebral artery (LVA), and right vertebral artery (RVA) before and after treatment were also assessed., Results: The total efficacy of the treatment in the study group was higher than that in the control group (94.4 % vs . 75.9%; P<0.05). After the treatment, the Vm of the BA, LVA, and RVA was increased in both groups compared to before treatment, and the increase was greater in the study group than in the control group (P<0.05). In addition, the BBS scores of the two groups after the treatment were higher than before the treatment, while the DHI and VSS-SF scores were lower than before the treatment. BBS scores of the study group were higher than those of the control group, while the DHI and VSS-SF scores were lower than those of the control group (P<0.05). There was no statistically significant difference in the incidence of adverse reactions between the study group (5.6%) and the control group (2.0%; P>0.05)., Conclusions: The combination of flunarizine and GDI in elderly patients with vertigo can effectively regulate hemodynamics of the patient, reduce the degree of vertigo, improve balance, and have a significant overall therapeutic effect without increasing the risk of adverse reactions., (Copyright: © Pakistan Journal of Medical Sciences.)

Competing Interests: The authors declare that they have no competing interests.

Household air pollution associated with solid fuel use is a long-standing public concern. The global population mainly using solid fuels for cooking remains large. Besides cooking, large amounts of coal and biomass fuels are burned for space heating during cold seasons in many regions. In this study, a wintertime multiple-region field campaign was carried out in north China to evaluate indoor PM 2.5 variations. With hourly resolved data from ∼1600 households, key influencing factors of indoor PM 2.5 were identified from a machine learning approach, and a random forest regression (RFR) model was further developed to quantitatively assess the impacts of household energy transition on indoor PM 2.5 . The indoor PM 2.5 concentration averaged at 120 μg/m 3 but ranged from 16 to ∼400 μg/m 3 . Indoor PM 2.5 was ∼60% lower in families using clean heating approaches compared to those burning traditional coal or biomass fuels. The RFR model had a good performance ( R 2 = 0.85), and the interpretation was consistent with the field observation. A transition to clean coals or biomass pellets can reduce indoor PM 2.5 by 20%, and further switching to clean modern energies would reduce it an additional 30%, suggesting many significant benefits in promoting clean transitions in household heating activities.

Countless individuals have fallen victim to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and have generated antibodies, reducing the risk of secondary infection in the short term. However, with the emergence of mutated strains, the probability of subsequent infections remains high. Consequently, the demand for simple and accessible methods for distinguishing between different variants is soaring. Although monitoring viral gene sequencing is an effective approach for differentiating between various types of SARS-CoV-2 variants, it may not be easily accessible to the general public. In this article, we provide an overview of the reported techniques that use combined approaches and adaptable testing methods that use editable recognition receptors for simultaneous detection and distinction of current and emerging SARS-CoV-2 variants. These techniques employ straightforward detection strategies, including tests capable of simultaneously identifying and differentiating between different variants. Furthermore, we recommend advancing the development of uncomplicated protocols for distinguishing between current and emerging variants. Additionally, we propose further development of facile protocols for the differentiation of existing and emerging variants., (© 2023. The Author(s), under exclusive licence to The Japan Society for Analytical Chemistry.)

Influenza pandemics have emerged as a significant global public health and security concern. PB2, a crucial subunit of the influenza RNA-dependent RNA polymerase (RdRP), has been identified as a promising target for influenza treatment. We herein report the discovery of a potent novel PB2 inhibitor, 7-51A, with a K D value of 1.64 nM as determined by ITC. The high activity of 7-51A was elucidated by the co-crystal structure of the PB2-7-51A complex, and comparative analysis revealed unique interactions that had never been observed before. The preliminary pharmacological evaluation indicated that 7-51A exhibited commendable cellular safety, hepatic microsomal metabolic safety and stability. Collectively, 7-51A was found to be an effective PB2 inhibitor and could be used as a lead compound for further studies., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Researches indicate miR-3200 is closely related to tumorigenesis, However, the role of miR-3200 in human hepatocarcinogenesis is still unclear. In this study, we clearly demonstrate that miR-3200 accelerates the growth of liver cancer cells in vivo and in vitro. Obviously, these findings are noteworthy that miR-3200 affects the transcriptional regulation for several genes, including DSP，BABAM2, Rab7A,SQSTM1,PRKAG2,CDK1,ABCE1,BECN1,PTEN,UPRT. And miR-3200 affects the transcriptional ability of several genes, such as, upregulating CADPS, DSP,FBXO32, PPCA,SGK1, PATXN7L1, PLK2,ITGB5,FZD3,HOXC8,HSPA1A,C-Myc,CyclnD1,CyclinE,PCNA and down -regulating SUV39H1, MYO1G, OLFML3, CBX5, PPDE2A, HOXA7, RAD54L, CDC45,SHMT7,MAD2L1,P27,IQGAP3,PTEN,P57,SCAMP3,etc...On the other hand, it is obvious that miR-3200 affects the translational ability of several genes, such as, upregulating GNS,UPRT,EIFAD,YOS1,SGK1,K-Ras,PKM2,C-myc,Pim1,CyclinD1,mTOR,erbB-2,CyclinE,PCNA,RRAS,ARAF,RAPH1,etc.. and down-regulating KDM2A, AATF, TMM17B, RAB8B, MYO1G,P21WAF1/Cip1,GADD45,PTEN,P27,P18,P57,SERBP1,RPL34,UFD1,Bax,ANXA6,GSK3β. Strikingly, miR-3200 affects some signaling pathway in liver cancer, including carbon metabolism signaling pathway, DNA replication pathway, FoxO signaling pathway, Hippo signaling pathway, serine and threonine metabolism signaling pathway, mTOR signaling pathway, Fatty acid biosynthesis signaling pathway, carcinogenesis-receptor activation signaling pathway, autophagy signaling pathway. Furthermore, our results suggest that miR-3200 enhances expression of RAB7A, and then Rab7A regulates the carcinogenic function of miR-3200 by increasing telomere remodeling in human liver cancer. These results are of great significance for the prevention and treatment of human liver cancer., Competing Interests: The authors declare that they have no competing interests., (© 2023 The Authors.)

miRNA is a noncoding RNA found in recent years and more than one third of human genes are the target of miRNAs. miR-624, located on human chromosome 14, is associated with tumorigenesis. However, the role of miR-624 in human hepatocarcinogenesis is still unclear. Herein, our results indicate that miR-624 accelerates the growth of liver cancer cells in vivo and in vitro. Moreover, the modification distribution of H3K9me1 on chromosomes is different between rLV group and rLV-miR-624 group. miR-624 affects epigenetic regulation of several genes in human liver cancer cells, such as RAB21, SMARCD3, MAPK6,PRRX1, ZFHX3, EMC3 (TMEM111). Furthermore, miR-624 affects transcriptome of some genes in liver cancer, including RAB21， UBE2N， PPP1CC，KPNA3， RAB7A，CPEB2,KLF4， MARK2， JUN， ARF6， TMEM39A. On the other hand, miR-624 affects proteome of several genes in liver cancer, such as, RBM5,PTK2, KDM2A,POLR2H, POLR2G,CDK6,KIF15,CUL2,FKBP2,ErbB-3,JUN, PKM2, CyclinE,PLK1, mTOR, PPAR γ , Rab7A,ARAF, UPF3B ，PTEN, SUZ12, GADD45, H3.3, CUL5, ARF6,EMC3,ATG4B,ATG14,CALR. Interestingly, miR-624 affects the RAB7A interaction network in liver cancer cells, involving in CLTC，ITGB1，HNRNPU， DARS1， RPS16， CTPS1，H3-3B，JUN,MYH10， CUL5， CPSF7. Strikingly, excessive MEC3 abrogates the carcinogenic functions of miR-624. Importantly, our findings indicate that miR-624 affects some signaling pathway in liver cancer, including Wnt signaling pathway，Hippo signaling pathway，mTOR signaling pathway, Ras signaling pathway，MAPK signaling pathway，PI3K-Akt signaling pathway, erbB signaling pathway. These results provide a basis for the treatment of human liver cancer., Competing Interests: The authors declare that they have no competing interests., (© 2023 The Authors.)

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by dysregulation of lipid metabolism, insulin resistance, and gut microbiota disorder. Compared to drug interventions, probiotic interventions may have a more enduring effect without producing any side effects. Thus, the potential of probiotics as a therapeutic approach for diabetes and other metabolic disorders has gained increasing attention in recent years. In this study, we evaluated the therapeutic efficacy of Lactobacillus gasseri CKCC1913, a potential probiotic strain, in high-fat diet-induced insulin-resistant diabetes using the C57BL/6J mouse animal model. From the results, L. gasseri CKCC1913 has been shown to increase glucose tolerance, reduce fasting blood glucose levels in diabetic mice, and reduce the expression of pro-inflammatory cytokines, such as TNF-α and IL-6. Besides, L. gasseri CKCC1913 intervention effectively alleviated oxidative stress damage by increasing SOD activity, decreasing MDA levels, reducing insulin resistance, and improving dyslipidemia caused by diabetes. The potential mechanism of L. gasseri CKCC1913 in improving metabolic health and alleviating diabetes involves an increased abundance of beneficial bacteria, such as Parabacteroides merdae , which directly produce short-chain fatty acids that help regulate immune cells and reduce inflammation. SCFAs also enter the bloodstream and promote antioxidant enzyme activity in the liver, protecting against oxidative damage. Additionally, L. gasseri CKCC1913 influences local bacterial metabolism pathways, such as the superpathway of unsaturated fatty acid biosynthesis, leading to an increase in unsaturated fatty acids, increasing high-density lipoprotein cholesterol (HDL-C) levels and improving lipid metabolism and glucose control in diabetic mice. In summary, in this study, L. gasseri CKCC1913 and its potential impact on metabolic health highlight the promising potential of probiotics as a therapeutic approach for diabetes. Future research should focus on identifying the optimal dose and duration, investigating the long-term effects and mechanisms of action, and exploring the potential use of probiotics as an adjunct to other therapies or in preventing metabolic disorders.

Background: Although CircHULC was overexpressed in several cancers, the role of CircHULC in malignancies has yet to be elucidated., Methods: Gene infection, tumorigenesis test in vitro and in vivo and the signaling pathway analysis were performed., Results: our results indicate that CircHULC promotes growth of human liver cancer stem cells and the malignant differentiation of hepatocyte-like cells. Mechanistically, CircHULC enhances the methylation modification of PKM2 via CARM1 and the deacetylase Sirt1. Moreover, CircHULC enhances the binding ability of TP53INP2/DOR with LC3 and LC3 with ATG4, ATG3, ATG5, ATG12. Therefore, CircHULC promotes the formation of autophagosomes. In particular, the binding ability of phosphorylated Beclin1 (Ser14) to Vps15, Vps34, ATG14L were significantly increased after CircHULC was overexpressed. Strikingly, CircHULC affects the expression of chromatin reprogramming factors and oncogenes through autophagy. Thereafter, Oct4, Sox2, KLF4, Nanog, and GADD45 were significantly decreased and C-myc was increased after CircHULC was overexpressed. Thus, CircHULC promotes the expression of H-Ras, SGK, P70S6K, 4E-BP1, Jun, and AKT. Interestingly, both CARM1 and Sirt1 determine the cancerous function of CircHULC dependent on autophagy., Conclusions: we shed light on the fact that the targeted attenuation of deregulated functioning of CircHULC could be a viable approach for cancer treatment, and CircHULC may acts as the potential biomarker and therapeutic target for liver cancer., Competing Interests: Declaration of Competing Interest “The authors declare that they have no competing interests”., (Copyright © 2023 Elsevier Inc. All rights reserved.)

A catalyst-free aza-Michael addition/C(sp 3 )-O bond formation tandem reaction of substituted amino ferrocenes with quinone esters was developed, which provided a green and efficient strategy for the construction of a C(sp 3 )-O bond from C(sp 3 )-H, and a series of N -ferrocene-substituted benzodihydrooxazoles were smoothly produced in moderate to excellent yields (up to >99% yield). The mechanism experiments showed that quinone esters performed as both substrate and oxidant. The salient features of this transformation include good functional group tolerance, broad substrate scope and mild conditions.

Background: Acute myeloid leukemia (AML) is a heterogeneous disease characterized by diverse genetic abnormalities. The NPM1 is the most commonly mutated gene in newly diagnosed patients. Optimizing risk stratification in this population could facilitate more rational clinical decision-making., Objectives: To identify biomarkers that optimize risk stratification in AML patients with NPM1 mutations., Material and Methods: Acute myeloid leukemia patients from multiple centers were included in this study. Univariate, multivariate and Kaplan-Meier survival analyses were used to assess risk factors and clinical outcomes. The gene set enrichment analysis (GSEA) was conducted to identify the related enrichment of biological function., Results: TG-interacting factor 1 (TGIF1) is a good prognostic indicator of disease progression in AML patients. It is closely related to NPM1 mutation, in which age and TGIF1 expression are independent prognostic factors. Multicenter data sources have shown that high expression of TGIF1 is beneficial for AML, regardless of whether patients received bone marrow transplantation. In the NPM1-mutated AML group, age, FLT3-ITD and TGIF1 were independent prognostic factors. Moreover, the NPM1-mutated subgroup could be well dichotomized into 2 groups with distinct prognoses through TGIF1 combined with European LeukemiaNet (ELN) 2017 risk stratification., Conclusions: The TGIF1 has an important value in the prognosis of AML. The NPM1-mutated patients were further subdivided into risk stratification groups based on TGIF1 expression, which could optimize the ELN 2017 to achieve individualized treatment.

Seed oil content is one of the most important quantitative traits in soybean ( Glycine max ) breeding. Here, we constructed a high-density single nucleotide polymorphism linkage map using two genetically similar parents, Heinong 84 and Kenfeng 17, that differ dramatically in their seed oil contents, and performed quantitative trait loci (QTL) mapping of seed oil content in a recombinant inbred line (RIL) population derived from their cross. We detected five QTL related to seed oil content distributed on five chromosomes. The QTL for seed oil content explained over 10% of the phenotypic variation over two years. This QTL was mapped to an interval containing 20 candidate genes, including a previously reported gene, soybean RING Finger 1a ( RNF1a ) encoding an E3 ubiquitin ligase. Notably, two short sequences were inserted in the GmRNF1a coding region of KF 17 compared to that of HN 84, resulting in a longer protein variant in KF 17. Our results thus provide information for uncovering the genetic mechanisms determining seed oil content in soybean, as well as identifying an additional QTL and highlighting GmRNF1a as candidate gene for modulating seed oil content in soybean., Supplementary Information: The online version contains supplementary material available at 10.1007/s11032-023-01384-2., Competing Interests: Competing interestsThe authors declare no competing interests., (© The Author(s), under exclusive licence to Springer Nature B.V. 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.)

Objectives: Interstitial lung disease (ILD) is common in anti-synthetase syndrome (ASS). Progressive fibrosing ILD (PF-ILD) may develop in ILD with autoimmune features. Data on PF-ILDs in ASS as a group are scarce. This study aimed to explore the characteristics and predictors of PF-ILD in ASS patients., Methods: This retrospective study enrolled 96 ASS-ILD patients. Baseline clinical data were collected. PF-ILD assessments were conducted at every hospital visit during windows of 24 months after initial diagnosis. Phenotypic, survival features and predictors of PF-ILD were estimated through SPSS 22.0., Results: The results revealed that 35.42% (34/96) were evaluated to be PF-ILD with a median interval time of 14.73 months. Nonspecific interstitial pneumonia was the most common radiological pattern of PF-ILD. Ground glass opacity (GGO), traction bronchiectasis and reticulation were representative high-resolution computed tomography findings of this group. Compared with the non-progressive group, PF-ILD patients had higher frequencies of anti-Ro-52 antibodies (91.18% vs 66.13%, P = 0.007) and GGO in the lower + middle and lower + middle + upper zones of the left lung, as well as lower + middle zones in the right lung (85.30% vs 54.84%, P = 0.003; 64.71% vs 38.71%, P = 0.015; 82.35% vs 58.06%, P = 0.016). Multivariate Cox analysis identified that anti-Ro-52 antibody (hazards ratio [HR] 3.55, 95% CI 1.06-11.90, P = 0.040) and GGO in left lower + middle lung zones (HR 22.11, 95% CI 1.95-250.90, P = 0.012) were independent risk factors for PF-ILD., Conclusions: PF-ILD was associated with poor prognosis. Over one-third of ASS-ILD patients may develop to PF-ILD. Anti-Ro-52 antibody positivity and GGO in left lower + middle lung zones were independent risk factors for PF-ILD in ASS patients., (© 2023 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd.)

Background: Inflammatory bowel disease (IBD) is a non-specific chronic inflammatory disease of the intestine. In addition to genetic susceptibility, environmental factors and dysregulated host immunity, the gut microbiota is implicated in the pathogenesis of Crohn's disease (CD) or ulcerative colitis (UC), the two primary types of IBD. The P2X4 receptor has been demonstrated to have a crucial role in preventing infection, inflammation, and organ damage. However, it remains unclear whether the P2X4 receptor affects IBD and the underlying mechanisms., Methods: Colitis was induced in mice administrated with dextran sodium sulphate (DSS). 16S rDNA sequencing was used to analyze the gut microbiota in knockout and wild-type mice. Clinical and histopathological parameters were monitored throughout the disease progression., Results: Gene Expression Omnibus analysis showed the downregulation of P2RX4 (P2rx4) expression in colonic tissues from patients or mice with IBD. However, its expression at the protein levels was upregulated on day 4 or 6 and then downregulated on day 7 in C57BL/6 mice treated with DSS. Gene ablation of P2rx4 aggravated DSS-induced colitis accompanying gut microbiota dysbiosis in mice. Moreover, P2X4 receptor-positive modulator ivermectin alleviated colitis and corrected dysregulated microbiota in wild-type C57BL/6 mice. Further antibiotic-treated gut microbiota depletion, cohousing experiment, and fecal microbiota transplantation proved that gut microbiota dysbiosis was associated with the aggravation of colitis in the mouse model initiated by P2rx4., Conclusions: Our findings elaborate on an unrevealed etiopathophysiological mechanism by which microbiota dysbiosis induced by the P2X4 receptor influences the development of colitis, indicating that the P2X4 receptor represents a promising target for treating patients with CD and UC., (© 2023 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.)

Key Message: IBD analysis clarified the dynamics of chromosomal recombination during the ZP pedigree breeding process and identified ten genomic regions resistant to SCN race3 combining association mapping. Soybean cyst nematode (SCN, Heterodera glycines Ichinohe) is one of the most devastating pathogens for soybean production worldwide. The cultivar Zhongpin03-5373 (ZP), derived from SCN-resistant progenitor parents, Peking, PI 437654 and Huipizhi Heidou, is an elite line with high resistance to SCN race3. In the current study, a pedigree variation map was generated for ZP and its ten progenitors using 3,025,264 high-quality SNPs identified from an average of 16.2 × re-sequencing for each genome. Through identity by decent (IBD) tracking, we showed the dynamic change of genome and detected important IBD fragments, which revealed the comprehensively artificial selection of important traits during ZP breeding process. A total of 2,353 IBD fragments related to SCN resistance including SCN-resistant genes rhg1, rhg4 and NSF RAN07 were identified based on the resistant-related genetic paths. Moreover, 23 genomic regions underlying resistance to SCN race3 were identified by genome-wide association study (GWAS) in 481 re-sequenced cultivated soybeans. Ten common loci were found by both IBD tracking and GWAS analysis. Haplotype analysis of 16 potential candidate genes suggested a causative SNP (C/T, - 1065) located in the promoter of Glyma.08G096500 and encoding a predicted TIFY5b-related protein on chr8 was highly correlated with SCN race3 resistance. Our results more thoroughly elucidated the dynamics of genomic fragments during ZP pedigree breeding and the genetic basis of SCN resistance, which will provide useful information for gene cloning and the development of resistant soybean cultivars using a marker-assisted selection approach., (© 2023. The Author(s).)

Indoor PM 2.5 , particulate matter no more than 2.5 μm in aerodynamic equivalent diameter, has very high spatiotemporal variabilities; and exploring the key factors influencing the variabilities is critical for purifying air and protecting human health. Here, we conducted a longer-term field monitoring campaign using low-cost sensors and evaluated inter- and intra-household PM 2.5 variations in rural areas where energy or stove stacking is common. Household PM 2.5 varied largely across different homes but also within households. Using generalized linear models and dominance analysis, we estimated that outdoor PM 2.5 explained 19% of the intrahousehold variation in indoor daily PM 2.5 , whereas factors like the outdoor temperature and indoor-outdoor temperature difference that was associated with energy use directly or indirectly, explained 26% of the temporal variation. Inter-household variation was lower than intrahousehold variation. The inter-household variation was strongly associated with distinct internal sources, with energy-use-associated factors explaining 35% of the variation. The statistical source apportionment model estimated that solid fuel burning for heating contributed an average of 31%-55% of PM 2.5 annually, whereas the contribution of sources originating from the outdoors was ≤10%. By replacing raw biomass or coal with biomass pellets in gasifier burners for heating, indoor PM 2.5 could be significantly reduced and indoor temperature substantially increased, providing thermal comforts in addition to improved air quality.

To improve household air quality, the Chinese government has launched a number of pilot stove renovation projects, but few studies have explored the impact of the project on people's perception of and willingness to participate in these renovations; moreover, factors affecting willingness to pay for the project in rural China are not yet clear. We conducted a field measurement and a corresponding door-to-door questionnaire survey using the renovated group and the unrenovated group. The results showed that (1) the stove renovation project could not only reduce PM 2.5 exposure and the excess mortality risk of rural residents, but also (2) improve residents' risk perception and self-protective willingness. (3) Specifically, the project had a deeper impact on female and low-income residents. (4) Meanwhile, the higher the income and the larger family size, the higher the risk perception and self-protective willingness. (5) Furthermore, willingness to pay for the project was related with residents' support for the project, benefit from renovation, income, and family size. Our results recommended that stove renovation policies should pay more attention to families with lower income and smaller size.

Mesenchymal stem cells (MSCs) have been demonstrated to protect against fatty liver diseases, but the mechanism is still not clear. Menstrual blood-derived endometrial stem cells (MenSCs) are a substantial population of MSCs that can be obtained in a noninvasive manner. In the present study, we investigated the therapeutic effects and underlying mechanisms of MenSC transplantation in mouse models of diet-induced nonalcoholic fatty liver disease (NAFLD). The results revealed that MenSCs markedly promoted hepatic glycogen storage and attenuated lipid accumulation after transplantation. We further identified Rnf186 as a novel regulator involved in MenSC-based therapy for NAFLD mice. Rnf186 deficiency substantially inhibited high-fat diet-induced insulin resistance and abnormal hepatic glucose and lipid metabolism in mice. Mechanistically, Rnf186 regulated glucose and lipid metabolism through the AMPK-mTOR pathway. More importantly, hepatocyte growth factor (HGF) is identified as the key functional cytokine secreted by MenSCs and decreases the expression of hepatic Rnf186. HGF deficient MenSCs cannot attenuate glucose and lipid accumulation after transplantation in NAFLD mice. Collectively, our results provide preliminary evidence for the protective roles of HGF secreted by MenSCs in fatty liver diseases through downregulation of hepatic Rnf186 and suggest that MenSCs or Rnf186 may be an alternative therapeutic approach/target for the treatment of NAFLD., (© The Author(s) 2022. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

In order to improve the response characteristics of the surface acoustic wave (SAW) sensor to trace gases, a SAW CO gas sensor based on a Pd-Pt/SnO 2 /Al 2 O 3 film with a high-frequency response performance is proposed in this paper. The gas sensitivity and humidity sensitivity of trace CO gas are tested and analyzed under normal temperatures and pressures. The research results show that, compared with the frequency response of the Pd-Pt/SnO 2 film, the CO gas sensor based on a Pd-Pt/SnO 2 /Al 2 O 3 film has a higher frequency response performance, and the sensor has high-frequency response characteristics to CO gas with a concentration in the range of 10-100 ppm. The average response recovery time of 90% ranges from 33.4 s to 37.2 s, respectively. When the CO gas with a concentration of 30 ppm is tested repeatedly, its frequency fluctuation is less than 5%, indicating that the sensor has good stability. In the range of relative humidity (RH) from 25% to 75%, it also has high-frequency response characteristics for CO gas with a 20 ppm concentration.

Surface Acoustic Wave (SAW) methane-sensing technology is a new way to detect methane at room temperature. However, the material and structure of the sensitive film are the important factors affecting the detection performance of the sensor. In this paper-with a SAW methane sensor using graphene-nickel cavitation-a composite film is proposed, which can work at room temperature. A delay linear dual-channel differential oscillator with center frequency of 204.3 MHz and insertion loss of -5.658 dB was designed; Cryptophane-A material was prepared by the "three-step method". The composite sensitive film was synthesized by a drop coating method, electrochemical deposition method and electroplating method. The composite film was characterized by SEM. The sensor performance test system and gas sensitivity test system were constructed to determine the response performance of the sensor at concentrations of 0~5% CH 4 . The results showed that the sensor had a good response recovery performance in the test concentration range, and the frequency offset was positively correlated with methane concentration. The 90% average response time and recovery times were 41.2 s and 57 s, respectively. The sensor sensitivity was 809.4 ± 6.93 Hz/(1% CH 4 ). This study provides a good theoretical basis for the development of surface acoustic-wave methane sensors.

Background: NDR1/HIN1-like ( NHL ) family genes are known to be involved in pathogen induced plant responses to biotic stress. Even though the NHL family genes have been identified and characterized in plant defense responses in some plants, the roles of these genes associated with the plant abiotic stress tolerance in wild soybean is not fully established yet, especially in response to alkaline stress., Methods: We identified the potential NHL family genes by using the Hidden Markov model and wild soybean genome. The maximum-likelihood phylogenetic tree and conserved motifs were generated by using the MEME online server and MEGA 7.0 software, respectively. Furthermore, the syntenic analysis was generated with Circos-0.69. Then we used the PlantCARE online software to predict and analyze the regulatory cis -acting elements in promoter regions. Hierarchical clustering trees was generated using TM4: MeV4.9 software. Additionally, the expression levels of NHL family genes under alkaline stress, ABA and MEJA treatment were identified by qRT-PCR., Results: In this study, we identified 59 potential NHL family genes in wild soybean. We identified that wild soybean NHL family genes could be mainly classified into five groups as well as exist with conserved motifs. Syntenic analysis of NHL family genes revealed genes location on 18 chromosomes and presence of 65 pairs of duplication genes. Moreover, NHL family genes consisted of a variety of putative hormone-related and abiotic stress responsive elements, where numbers of methyl jasmonate (MeJA) and abscisic acid (ABA) responsive elements were significantly larger than other elements. We confirmed the regulatory roles of NHL family genes in response to alkaline stress, ABA and MEJA treatment. In conclusion, we identified and provided valuable information on the wild soybean NHL family genes, and established a foundation to further explore the potential roles of NHL family genes in crosstalk with MeJA or ABA signal transduction mechanisms under alkaline stress., Competing Interests: The authors declare there are no competing interests., (©2022 Zhang et al.)

The society has high concerns on the inequality that people are disproportionately exposed to ambient air pollution, but with more time spent indoors, the disparity in the total exposure considering both indoor and outdoor exposure has not been explored; and with the socioeconomical development and efforts in fighting against air pollution, it is unknown how the exposure inequality changed over time. Based on the city-level panel data, this study revealed the Concentration Index (C) in ambient PM 2.5 exposure inequality was positive, indicating the low-income group exposed to lower ambient PM 2.5 ; however, the total PM 2.5 exposure was negatively correlated with the income, showing a negative C value. The low-income population exposed to high PM 2.5 associated with larger contributions of indoor exposure from the residential emissions. The total PM 2.5 exposure caused 1.13 (0.63-1.73) million premature deaths in 2019, with only 14 % were high-income population. The toughest-ever air pollution countermeasures have reduced ambient PM 2.5 exposures effectively that, however, benefited the rich population more than the others. The transition to clean household energy sources significantly affected on indoor air quality improvements, as well as alleviation of ambient air pollution, resulting in notable reductions of the total PM 2.5 exposure and especially benefiting the low-income groups. The negative C values decreased from 2000 to 2019, indicating a significantly reducing trend in the total PM 2.5 exposure inequality over time., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Rheumatoid arthritis (RA) is an autoinflammatory disease, its core treatment principle is to achieve remission as soon as possible. There is no good prediction model that can accurately predict the remission rate of patients to choose a good treatment scheme. Here, we aimed to verify the prognostic value of some inflammatory indicators in RA and establish a prediction model to predict the remission rate after treatment., Methods: A total of 223 patients were enrolled at Qilu Hospital from June 2014 to June 2020. Baseline clinical data were collected and plasma was obtained to detect the inflammatory indicators. All patients were treated with conventional synthetic disease-modifying antirheumatic drugs (csDMARDs). All patients were followed up and were recorded the time to reach the disease activity score-28 with erythrocyte sedimentation rate (DAS28-ESR) of <2.6. A total of 156 patients were randomly assigned to the development cohort, and 67 patients were assigned to the validation cohort. Inflammatory indicators in plasma were detected by enzyme-linked immunosorbent assay (ELISA). The predictive factors were screeded by using least absolute shrinkage and selection operator (LASSO) and Cox regression. The model was created and verified by using the standard method. A total of 6 independent risk factors were analyzed to construct a nomogram to predict the remission rate in 3, 6 and 12 months., Results: The remission rates after treatment in 3, 6 and 12 months were 38.76%, 58.91%, and 81.40%, respectively. Patient age, C-reactive protein (CRP), interleukin (IL)-6, galectin-9 (Gal-9), health assessment questionnaire (HAQ), and DAS28-ESR were included in the prognostic model to predict the remission rate. The resulting model had good discrimination ability in both the development cohort (C-index, 0.729) and the validation cohort (C-index, 0.710). Time-dependent receiver operating characteristic (ROC) curve, calibration analysis, and decision curve analysis (DCA) showed that the model has significant discriminant power and clinical practicability in predicting the remission rate., Conclusions: We established a new predictive model and validated it. The model can predict the remission rate in 3, 6 and 12 months after receiving csDMARDs treatment. By using this model, we can facilitate the identification of high-risk patients early and intervene with them as soon as possible., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-22-5791/coif). The authors have no conflicts of interest to declare., (2022 Annals of Translational Medicine. All rights reserved.)

Heinong 84 is one of the major soybean varieties growing in Northeast China, and is resistant to the infection of all strains of soybean mosaic virus (SMV) in the region including the most prevalent strain, N3. However, the resistance gene(s) in Heinong 84 and the resistant mechanism are still elusive. In this study, genetic and next-generation sequencing (NGS)-based bulk segregation analysis (BSA) were performed to map the resistance gene using a segregation population from the cross of Heinong 84 and a susceptible cultivar to strain N3, Zhonghuang 13. Results show that the resistance of Heinong 84 is controlled by a dominant gene on chromosome 13. Further analyses suggest that the resistance gene in Heinong 84 is probably an allele of Rsv1 . Finally, two pairs of single-nucleotide-polymorphism (SNP)-based primers that are tightly cosegregated with the resistance gene were designed for rapidly identifying resistant progenies in breeding via the cleaved amplified polymorphic sequence (CAPS) assay.

In this paper, the phase-only holograms with clear first diffraction orders have been generated based on the U-Net and the two-dimensional phase grating. Firstly, we proved the modulation effect of two-dimensional phase grating on diffraction field, and came to a conclusion that it could move the diffraction pattern of the hologram to the odd-numbered diffraction orders' center of that. Then we changed the generation process of phase-only holograms and the training strategy for U-Net according to this conclusion, which converted the optimization target of the U-Net from the zeroth diffraction order in the center of diffraction field to the first diffraction order in the edge of that. And we also used a method called "phase recombination" to improve the structure of U-Net for less memory footprint and faster generating speed. Finally, the holograms with the 4K resolution have been generated in 0.05s, and the average peak signal to noise ratio (PSNR) of the reconstructed images is about 37.2 dB in DIV2K-valid-HR dataset.

Nonsmall cell lung cancer (NSCLC) is among the most prevalent malignant tumours threatening human health. In the tumour microenvironment (TME), cancer-associated fibroblasts (CAFs) induce M2-polarized macrophages, which strongly regulate tumour progression. However, little is known about the association between CAFs and M2 macrophages. CD248 is a transmembrane glycoprotein found in several cancer cells, tumour stromal cells, and pericytes. Here, we isolated CAFs from tumour tissues of NSCLC patients to detect the relationship between CD248 expression and patient prognosis. We knocked down the expression of CD248 on CAFs to detect CXCL12 secretion and macrophage polarization. We then examined the effects of CD248-expressing CAF-induced M2 macrophage polarization to promote NSCLC progression in vitro and in vivo. We found that CD248 is expressed mainly in NSCLC-derived CAFs and that the expression of CD248 correlates with poor patient prognosis. Blocking CXCL12 receptor (CXCR4) drastically decreased M2 macrophage chemotaxis. CD248 promotes CAFs secreting CXCL12 to mediate M2-polarized macrophages to promote NSCLC progression both in vitro and in vivo. Collectively, our data suggest that CD248-positive CAFs induce NSCLC progression by mediating M2-polarized macrophages., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)