Scoping review of obesity interventions: Research frontiers and publication status.

Obesity and overweight are significant global health issues, and numerous obesity intervention studies have been conducted. Summarizing current knowledge of interventions aims to inform researchers and policymakers to keep up-to-date with the latest scientific advancements and trends. In this review, we comprehensively retrieved and screened 4,541 studies on obesity intervention published between 2018 and 2022 in the Web of Science Core Collection, and objectively presented research frontiers using bibliometric analysis. The research frontiers of intervention are mainly focused on dietary, exercise, pharmacological interventions, bariatric surgery, environmental, and cognitive interventions. Time-restricted eating is the hottest research topic, followed by probiotics and Roux-en-Y gastric bypass. Gut microbiota is located in the "Basic and transversal themes" quadrant with a high centrality and low density, which has great development potentiality. Obesity intervention is becoming increasingly common,and we advocate for researchers to undertake more focused research endeavors that consider the specific characteristics of diverse populations or patients.

LncRNA MEG3 Reduces the Ratio of M2/M1 Macrophages Through the HuR/CCL5 Axis in Hepatocellular Carcinoma.

Objective: Tumor-associated macrophages play a crucial role in the development of hepatocellular carcinoma (HCC). Our study aimed to investigate the relationship between long coding RNA (lncRNA) maternally expressed gene 3 (MEG3), RNA-binding protein human antigen R (HuR), and messenger RNA C-C motif chemokine 5 (CCL5) in the modulation of M1 and M2 macrophage polarization in HCC. Methods: To induce M1 or M2 polarization, LPS/IFNγ- or IL4/IL13 were used to treat bone marrow derived macrophages (BMDMs). The localization of MEG3 in M1 and M2 macrophages was assessed using fluorescence in situ hybridization assay. Expression levels of MEG3, HuR, CCL5, M1, and M2 markers were measured by RT-qPCR or immunofluorescence staining. Flow cytometry was performed to determine the proportion of F4/80+CD206+ and F4/80+CD68+ cells. RNA pulldown assay was performed to detect the binding of lncRNA MEG3 and HuR. The impacts of HuR on CCL5 stability and activity of CCL5 promoter were evaluated using actinomycin D treatment and luciferase reporter assay. Cell migration, invasiveness, and angiogenesis were assessed using transwell migration and invasion assays and a tube formation assay. A mixture of Huh-7 cells and macrophages were injected into nude mice to explore the effect of MEG3 on tumorigenesis. Results: MEG3 promoted M1-like polarization while dampening M2-like polarization of BMDMs. MEG3 bound to HuR in M1 and M2 macrophages. HuR downregulated CCL5 by inhibiting CCL5 transcription in macrophages. In addition, overexpression of MEG3 suppressed cell metastasis, invasion, and angiogenesis by obstructing macrophage M2 polarization. MEG3 inhibited tumorigenesis in HCC via promotion of M1-like polarization and inhibition of M2-like polarization. Rescue experiments showed that depletion of CCL5 in M2 macrophages reversed MEG3-induced suppressive effect on cell migration, invasion, and tube formation. Conclusion: MEG3 suppresses HCC progression by promoting M1-like while inhibiting M2-like macrophage polarization via binding to HuR and thus upregulating CCL5.

New and emerging mechanisms of insecticide resistance.

The continuous use of insecticides over the last eight decades has led to the development of resistance to these insecticides. Research in the last few decades showed that the mechanisms underlying resistance are diverse but can generally be classified under several modes of resistance such as target-site resistance, metabolic resistance, and penetration resistance. In this review, we highlight new discoveries in insecticide resistance research made over the past few years, including an emerging new mode of resistance, sequestration resistance, where the overexpression of olfactory proteins binds and sequesters insecticides in resistant strains, as well as recent research on how posttranscriptional regulation can impact resistance. Future research will determine the generality of these emerging mechanisms across insect species.

METTL3 and METTL14-mediated N6-methyladenosine modification of SREBF2-AS1 facilitates hepatocellular carcinoma progression and sorafenib resistance through DNA demethylation of SREBF2.

As the most prevalent epitranscriptomic modification, N6-methyladenosine (m6A) shows important roles in a variety of diseases through regulating the processing, stability and translation of target RNAs. However, the potential contributions of m6A to RNA functions are unclear. Here, we identified a functional and prognosis-related m6A-modified RNA SREBF2-AS1 in hepatocellular carcinoma (HCC). The expression of SREBF2-AS1 and SREBF2 in HCC tissues and cells was measured by RT-qPCR. m6A modification level of SREBF2-AS1 was measured by methylated RNA immunoprecipitation assay. The roles of SREBF2-AS1 in HCC progression and sorafenib resistance were investigated by proliferation, apoptosis, migration, and cell viability assays. The regulatory mechanisms of SREBF2-AS1 on SREBF2 were investigated by Chromatin isolation by RNA purification, RNA immunoprecipitation, CUT&RUN, and bisulfite DNA sequencing assays. Our findings showed that the expression of SREBF2-AS1 was increased in HCC tissues and cells, and positively correlated with poor survival of HCC patients. m6A modification level of SREBF2-AS1 was also increased in HCC and positively correlated with poor prognosis of HCC patients. METTL3 and METTL14-induced m6A modification upregulated SREBF2-AS1 expression through increasing SREBF2-AS1 transcript stability. Functional assays showed that only m6A-modified, but not non-modified SREBF2-AS1 promoted HCC progression and sorafenib resistance. Mechanistic investigations revealed that m6A-modified SREBF2-AS1 bound and recruited m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1 to SREBF2 promoter, leading to DNA demethylation at SREBF2 promoter and the upregulation of SREBF2 transcription. Functional rescue assays showed that SREBF2 was the critical mediator of the oncogenic roles of SREBF2-AS1 in HCC. Together, this study showed that m6A-modified SREBF2-AS1 exerted oncogenic roles in HCC through inducing DNA demethylation and transcriptional activation of SREBF2, and suggested m6A-modified SREBF2-AS1 as a prognostic biomarker and therapeutic target for HCC.

[Characterization of otorhinolaryngologic manifestations in children with mucopolysaccharide storage disease typeâ and type â ¡].

Objective:To analyze the characteristics of otorhinolaryngological clinical manifestations in children with Mucopolysaccharide（MPS） type Ⅰ and type II in order to improve the knowledge of otorhinolaryngologists about this disease. Methods:Clinical data related to 55 children with MPS type Ⅰ and type II were retrospectively analyzed to investigate the clinical manifestations of MPS in ENT. Results:All 40 patients（72.72%） with MPS had at least one ENT symptom during the course of the disease, with 95% of them having an ENT symptom prior to the diagnosis of MPS; upper airway obstruction was the most common ENT symptom（34, 85.00%）, followed by recurrent upper respiratory tract infections（23, 57.50%）, and lastly, hearing loss（11, 27.50%）; all 26 patients had undergone at least one surgical procedure, of which 15（57.69%） had undergone ENT surgery, and all of these patients underwent ENT surgery before diagnosis. The most common ENT surgery was adenoidectomy. Conclusion:Early clinical manifestations of MPS patients are atypical, but the early and prevalent appearance of otolaryngologic symptoms and increased awareness of the disease among otolaryngologists has a positive impact on the prognosis of MPS.

METTL3/16-mediated m6A modification of ZNNT1 promotes hepatocellular carcinoma progression by activating ZNNT1/osteopontin/S100A9 positive feedback loop-mediated crosstalk between macrophages and tumour cells.

Macrophages are the major components of tumour microenvironment, which play critical roles in tumour development. N6-methyladenosine (m6A) also contributes to tumour progression. However, the potential roles of m6A in modulating macrophages in hepatocellular carcinoma (HCC) are poorly understood. Here, we identified ZNNT1 as an HCC-related m6A modification target, which was upregulated and associated with poor prognosis of HCC. METTL3 and METTL16-mediated m6A modification contributed to ZNNT1 upregulation through stabilizing ZNNT1 transcript. ZNNT1 exerted oncogenic roles in HCC. Furthermore, ZNNT1 recruited and induced M2 polarization of macrophages via up-regulating osteopontin (OPN) expression and secretion. M2 Macrophages-recruited by ZNNT1-overexpressed HCC cells secreted S100A9, which further upregulated ZNNT1 expression in HCC cells via AGER/NF-κB signaling. Thus, this study demonstrates that m6A modification activated the ZNNT1/OPN/S100A9 positive feedback loop, which promoted macrophages recruitment and M2 polarization, and enhanced malignant features of HCC cells. m6A modification-triggered ZNNT1/OPN/S100A9 feedback loop represents potential therapeutic target for HCC.

New insights into the concentration-dependent regulation of membrane biofouling formation via continuous nanoplastics stimulation.

The release of nanoplastics (NPs) into the environment is growing due to the extensive use of plastic products. Numerous studies have confirmed the negative effects of NPs on microorganisms, which poses uncertainties concerning their impact on nanofiltration (NF) membrane biofouling. This study investigated the initial cell adhesion process, NF membrane biofouling kinetic processes and bacterial responses of Pseudomonas aeruginosa (P. aeruginosa) exposed to varied NPs concentrations (0-50 mg·L-1). Transcriptome analysis demonstrated that low concentration of NPs (0.1 mg·L-1) promoted bacterial quorum sensing, energy metabolism, exopolysaccharide biosynthesis and bacterial secretion systems. Correspondingly, the polysaccharide content increased remarkably to 2.77 times the unexposed control, which served as a protective barrier for bacteria to avoid the impact of NPs-induced stress. Suppressed homologous recombination, microbial metabolic potentials and flagellar assembly were detected in bacteria exposed to a high concentration (50 mg·L-1) of NPs, mainly due to the triggered reactive oxygen species (ROS) generation, genomic DNA damage, and decreased energy production. Overall, enhanced formation of the extracellular polymeric substances (EPS) and aggravated membrane flux decline were observed when NPs interacted with the membrane surface by cell secretions (low NPs levels) or cell lysis (high NPs levels). These findings shed light on understanding the microbial metabolism mechanism and membrane biofouling propensity with NPs stress at both the molecular and gene levels.

Enhancement of tolerance against flonicamid in Solenopsis invicta (Hymenoptera: Formicidae) through overexpression of CYP6A14.

Solenopsis invicta is a main issue in southern China and is causing significant damage to the local ecological environment. The extensive use of insecticides has resulted in the development of tolerance in S. invicta. In our study, ten S. invicta colonies from Sichuan Province exhibited varying degrees of tolerance against flonicamid, with LC50 values from 0.49 mg/L to 8.54 mg/L. The sensitivity of S. invicta to flonicamid significantly increased after treatment with the P450 enzyme inhibitor piperonyl butoxide (PBO). Additionally, the activity of P450 in S. invicta was significantly enhanced after being treated with flonicamid. Flonicamid induced the expression levels of CYP4aa1, CYP9e2, CYP4C1, and CYP6A14. The expression levels of these P450 genes were significantly higher in the tolerant colonies compared to the sensitive colonies, and the relative copy numbers of CYP6A14 in the tolerant colonies were 2.01-2.15 fold. RNAi feeding treatment effectively inhibited the expression of P450 genes, thereby reducing the tolerance of S. invicta against flonicamid. In addition, the overexpression of CYP6A14 in D. melanogaster resulted in reduced sensitivity to flonicamid. Our investigations revealed hydrophobic interactions between flonicamid and seven amino acid residues of CYP6A14, along with the formation of a hydrogen bond between Glu306 and flonicamid. Our findings suggest that flonicamid can effectively control S. invicta and P450 plays a pivotal role in the tolerance of S. invicta against flonicamid. The overexpression of CYP6A14 also increased tolerance to flonicamid.

m6A modification of AC026356.1 facilitates hepatocellular carcinoma progression by regulating the IGF2BP1-IL11 axis.

N6-methyladenosine (m6A) is the most common RNA modification in eukaryotic RNAs. Although the important roles of m6A in RNA fate have been revealed, the potential contribution of m6A to RNA function in various diseases, including hepatocellular carcinoma (HCC), is still unclear. In this study, we identified a novel m6A-modified RNA AC026356.1. We found that AC026356.1 was increased in HCC tissues and cell lines. High expression of AC026356.1 was correlated with poor survival of HCC patients. m6A modification level of AC026356.1 was also increased in HCC and more significantly correlated with poor survival of HCC patients. Functional assays showed that m6A-modified AC026356.1 promoted HCC cellular proliferation, migration, and liver metastasis. Gene set enrichment analysis showed that AC026356.1 activated IL11/STAT3 signaling. Mechanistic investigation showed that m6A-modified AC026356.1 bound to IGF2BP1. The interaction between m6A-modified AC026356.1 and IGF2BP1 promoted the binding of IL11 mRNA to IGF2BP1, leading to increased IL11 mRNA stability and IL11 secretion. Functional rescue assays showed that depletion of IL11 reversed the oncogenic roles of AC026356.1. These findings revealed the potential influences of m6A modification on RNA biological functions and suggested that targeting m6A modification may be a novel strategy for HCC treatment.

N6-Methyladenosine-Modified LEAWBIH Drives Hepatocellular Carcinoma Progression through Epigenetically Activating Wnt/ß-Catenin Signaling.

Purpose: N6-methyladenosine (m6A) modification plays an important role in regulating RNA maturation, stability, and translation. Thus, m6A modification is involved in various pathophysiological processes including hepatocellular carcinoma (HCC). However, the direct contribution of m6A modifications to RNA function in HCC remains unclear. Here, we identified LEAWBIH (long non-coding RNA epigenetically activating Wnt/ß-catenin signalling in HCC) as an m6A-modified long non-coding RNA (lncRNA) and investigated the effects of m6A on the function of LEAWBIH in HCC. Methods: Quantitative polymerase chain reaction was performed to measure the gene expression in tissues and cells. The level of m6A modification was detected using a methylated RNA immunoprecipitation assay and single-base elongation- and ligation-based qPCR amplification method. Cell proliferation was evaluated using the Glo cell viability and CCK-8 assays. Cell migration and invasion were evaluated using Transwell migration and invasion assays. The mechanisms of m6A modified LEAWBIH were investigated using chromatin isolation by RNA purification, chromatin immunoprecipitation, and dual-luciferase reporter assays. Results: LEAWBIH was highly expressed and correlated with poor survival in HCC patients. LEAWBIH was identified as a m6A-modified transcript. m6A modification increased LEAWBIH transcript stability. The m6A modification level of LEAWBIH was increased in HCC, and a high m6A modification level of LEAWBIH predicted poor survival. LEAWBIH promotes HCC cell proliferation, migration, and invasion in an m6A modification-dependent manner. Mechanistic investigations revealed that m6A-modified LEAWBIH activated Wnt/ß-catenin signaling. m6A-modified LEAWBIH binds to the m6A reader YTHDC1, which further interacts with and recruits H3K9me2 demethylase KDM3B to CTNNB1 promoter, leading to H3K9me2 demethylation and CTNNB1 transcription activation. Functional rescue assays showed that blocking Wnt/ß-catenin signaling abolished the role of LEAWBIH in HCC. Conclusion: m6A-modified LEAWBIH exerts oncogenic effects in HCC by epigenetically activating Wnt/ß-catenin signaling, highlighting m6A-modified LEAWBIH as a promising therapeutic target for HCC.

Boosting the Electrocatalytic Activity of Pr0.5Ba0.5FeO3-δ via Ni Doping in Symmetric Solid Oxide Electrolysis Cells.

Symmetric solid oxide electrolysis cells (SSOECs) have garnered significant scientific interest due to their simplified cell architecture, robust operational reliability, and cost-effectiveness, for which a highly electrocatalytically active electrode is the decisive main factor. This work evaluates the electrochemical performance of Ni-doped Pr0.5Ba0.5FeO3-δ (PBF) perovskite materials, with a focus on Pr0.5Ba0.5Fe0.8Ni0.2O3-δ (PBFN). The experimental findings herein prove the exceptional electrocatalytic ability of PBFN in facilitating the oxygen evolution and carbon dioxide reduction reaction, surpassing the electrochemical performance of PBF. In addition, the PBFN symmetric cell has excellent performance for CO2 electrolysis, and the cell has a low polarization resistance value of 0.1 Ω·cm2. Moreover, it achieves an impressive current density value of 1.118 A·cm-2 under operating conditions of 2.0 V and 800 °C, which is superior to those of the PBF symmetric cell and the PBFN asymmetric cell. It also has a good structural and performance stability. These results imply a bright development prospect of PBFN as electrodes for SSOECs.

Recent Progress and Future Prospects of Anions O-site Doped Perovskite Oxides in Electrocatalysis for Various Electrochemical Systems.

With the rapid development of novel energy conversion and storage technologies, there is a growing demand for enhanced performance in a wide range of electrocatalysts. Perovskite oxides (ABO3 ) have caused widespread concerns due to their excellent electrocatalytic properties, low cost, stable and reliable performance. In recent years, the research on anion O-site doping of perovskite oxides has been a cynosure, which is considered as a promising route for enhancing performance. However, a systematic review summarizing the research progress of anion-doped perovskite oxides is still lacking. Therefore, this review mainly introduces the elements and strategies of various common anions doped at O-site of perovskite oxides, analyzes their influence on the physical and chemical properties of perovskites, and separately concludes their applications in electrocatalysis. This review will provide ideas and prospects for the development of subsequent anion doping strategies for high performance perovskite oxides.

Prediagnosis ultra-processed food consumption and prognosis of patients with colorectal, lung, prostate, or breast cancer: a large prospective multicenter study.

Background and aims: Whether ultra-processed food consumption is associated with cancer prognosis remains unknown. We aimed to test whether prediagnosis ultra-processed food consumption is positively associated with all-cause and cancer-specific mortality in patients with colorectal, lung, prostate, or breast cancer. Methods: This study included 1,100 colorectal cancer patients, 1750 lung cancer patients, 4,336 prostate cancer patients, and 2,443 breast cancer patients. Ultra-processed foods were assessed using the NOVA classification before the diagnosis of the first cancer. Multivariable Cox regression was used to calculate hazard ratio (HR) and 95% confidence interval (CI) for all-cause and cancer-specific mortality. Results: High ultra-processed food consumption before cancer diagnosis was significantly associated with an increased risk of all-cause mortality in lung (HRquartile 4 vs. 1: 1.18; 95% CI: 0.98, 1.40; Ptrend = 0.021) and prostate (HRquartile 4 vs. 1: 1.18; 95% CI: 1.00, 1.39; Ptrend = 0.017) cancer patients in a nonlinear dose-response manner (all Pnonlinearity < 0.05), whereas no significant results were found for other associations of interest. Subgroup analyses additionally revealed a significantly positive association with colorectal cancer-specific mortality among colorectal cancer patients in stages I and II but not among those in stages III and IV (Pinteraction = 0.006), and with prostate cancer-specific mortality among prostate cancer patients with body mass index <25 but not among those with body mass index ≥25 (Pinteraction = 0.001). Conclusion: Our study suggests that reducing ultra-processed food consumption before cancer diagnosis may improve the overall survival of patients with lung or prostate cancer, and the cancer-specific survival of certain subgroups of patients with colorectal or prostate cancer.

HIF­1α and RACGAP1 promote the progression of hepatocellular carcinoma in a mutually regulatory way.

Hypoxia, a condition characterized by low oxygen levels, serves an important role in the progression of hepatocellular carcinoma (HCC). However, the precise molecular mechanisms underlying hypoxia­induced HCC progression are yet to be fully elucidated. The present study assessed the involvement of two key factors, hypoxia­inducible factor­1α (HIF­1α) and Rac GTPase activating protein 1 (RACGAP1), in HCC development under hypoxic conditions. HIF­1α and RACGAP1 genes were overexpressed and knocked down in Hep3B and Huh7 cells using lentiviral transduction and the levels of HIF­1α and RACGAP1 in the cells were assessed using quantitative PCR, western blotting and immunofluorescence. Co­immunoprecipitation experiments were performed to evaluate the interaction between HIF­1α and RACGAP1. Subsequently, the proliferation, apoptosis, migration and invasion of Hep3B and Huh7 cells were assessed using the Cell Counting Kit­8 assay, flow cytometry, Transwell assay and migration experiments. The expression levels of HIF­1α and RACGAP1 in normal and HCC tumor samples were analyzed utilizing the Gene Expression Profiling Interactive Analysis database. Furthermore, correlations between HIF­1α/RACGAP1 gene expression levels and patient survival outcomes were evaluated using the Kaplan­Meier plotter. Knockdown of HIF­1α resulted in a significant decrease in RACGAP1 expression, whilst overexpression of HIF­1α resulted in a significant increase in RACGAP1 expression. Moreover, overexpression and knockdown of RACGAP1 had the same effect on HIF­1α expression. Additionally, it was demonstrated that HIF­1α and RACGAP1 interacted directly within a complex. Overexpression of HIF­1α or RACGAP1 significantly increased proliferation, invasion and migration, and significantly decreased the proportion of apoptotic Hep3B and Huh7 cells. Conversely, knockdown of HIF­1α or RACGAP1 significantly decreased proliferation, invasion and migration, and significantly increased the proportion of apoptotic Hep3B and Huh7 cells. In addition, the combined knockdown or overexpression of HIF­1α and RACGAP1 had a more pronounced effect on HCC cell migration compared with knockdown of HIF­1α alone. Furthermore, there was a significant positive correlation between the expression levels of HIF­1α and RACGAP1 in HCC tissues and patients with HCC and upregulation of both HIF­1α and RACGAP1 demonstrated a lower overall survival probability. In conclusion, HIF­1α and RACGAP1 may synergistically contribute to the development of HCC, highlighting their potential as valuable targets for HCC therapy.

Metabolic Resistance of Sogatella furcifera (Hemiptera: Delphacidae) toward Pymetrozine Involves the Overexpression of CYP6FJ3.

Sogatella furcifera (Horváth), which mainly threatens rice, shows various levels of pesticide resistance due to long-term overuse of pesticides. Our resistance monitoring of 20 field populations in Sichuan, China, revealed that they were susceptible to highly resistant toward pymetrozine (0.4-142.2 RR), and JL21 reached the highest level of resistance. The JL21 population exhibited cross-resistance to triflumezopyrim and dinotefuran but sensitivity to sulfoxaflor, acetamiprid, clothianidin, and nitenpyram. The increased P450 activity were support to involve in pymetrozine resistance by detoxification enzyme activities and synergist determination. Among 16 candidate P450 genes, CYP6FJ3 (5.25-fold) was the most up-regulated in JL21, while no significant change was found after LC25 pymetrozine treatment. Furthermore, the knockdown by RNAi and heterologous overexpression by the GAL4/UAS system confirmed that the CYP6FJ3 overexpression was involved in the pymetrozine resistance, and recombination in vitro confirmed that CYP6FJ3 could hydroxylate pymetrozine. Therefore, the overexpression of CYP6FJ3 promotes pymetrozine metabolic resistance in S. furcifera.

N6-Methyladenosine-Modified ATP8B1-AS1 Exerts Oncogenic Roles in Hepatocellular Carcinoma via Epigenetically Activating MYC.

Purpose: N6-methyladenosine (m6A) modification has shown critical roles in regulating mRNA fate. Non-coding RNAs also have important roles in various diseases, including hepatocellular carcinoma (HCC). However, the potential influences of m6A modification on non-coding RNAs are still unclear. In this study, we identified a novel m6A-modified ATP8B1-AS1 and aimed to investigate the effects of m6A on the expression and role of ATP8B1-AS1 in HCC. Methods: qPCR was performed to measure the expression of related genes. The correlation between gene expression and prognosis was analyzed using public database. m6A modification level was measured using MeRIP and single-base elongation- and ligation-based qPCR amplification method. The roles of ATP8B1-AS1 in HCC were investigated using in vitro and in vivo functional assays. The mechanisms underlying the roles of ATP8B1-AS1 were investigated by ChIRP and ChIP assays. Results: ATP8B1-AS1 is highly expressed in HCC tissues and cell lines. High expression of ATP8B1-AS1 is correlated with poor overall survival of HCC patients. ATP8B1-AS1 is m6A modified and the 792 site of ATP8B1-AS1 is identified as an m6A modification site. m6A modification increases the stability of ATP8B1-AS1 transcript. m6A modification level of ATP8B1-AS1 is increased in HCC tissues and cell lines, and correlated with poor overall survival of HCC patients. ATP8B1-AS1 promotes HCC cell proliferation, migration, and invasion, which were abolished by the mutation of m6A-modified 792 site. Mechanistic investigation revealed that m6A-modified ATP8B1-AS1 interacts with and recruits m6A reader YTHDC1 and histone demethylase KDM3B to MYC promoter region, leading to the reduction of H3K9me2 level at MYC promoter region and activation of MYC transcription. Functional rescue assays showed that depletion of MYC largely abolished the oncogenic roles of ATP8B1-AS1. Conclusion: m6A modification level of ATP8B1-AS1 is increased and correlated with poor prognosis in HCC. m6A-modified ATP8B1-AS1 exerts oncogenic roles in HCC via epigenetically activating MYC expression.

Revealing the composite fretting-corrosion mechanisms of Ti6Al4V alloy against zirconia-toughened alumina ceramic in simulated body fluid.

The composite fretting-corrosion damage due to combinations of radial, tangential, rotational, and other fretting causes local adverse tissue reactions and failure of artificial joints. Previous studies have mainly focused on the single fretting mode, while ignoring the coupled effects of multimode fretting. The fretting-corrosion mechanisms between the components are not yet fully understood. In this study, the tangential-radial composite fretting was realized by applying a normal alternating load to the tangential fretting. The composite fretting corrosion behavior of zirconia toughened alumina ceramic/Ti6Al4V alloy used for the head-neck interface of an artificial hip joint under simulated body fluid was investigated. The effects of displacement and alternating load amplitude were considered. The alternating load amplitude was given by the maximum normal load and minimum normal load ratio R. The results showed that the composite fretting damage mechanisms of this pair were mainly abrasion and tribocorrosion. Cracking also existed under large displacement. The effect of alternating load on fretting corrosion was found to be mainly caused by changes in the contact area and instantaneous contact state. In addition, the alternating load during the composite fretting promoted the formation of the three-body layer in the contact area. A decrease in load ratio caused fretting to change from gross to partial slip. In the case of small displacement, the load ratio had little effect on the friction work or wear scar profile. The corrosion rate of materials and the concentration of metal ions released into the solution increased as load ratio decreased. In cases of large and medium displacement, load ratio reduction increased the friction work and expanded the wear scar. The reduction in load ratio also caused the corrosion rate of the material to increase and then decrease, and the metal ion concentration decreased.

Evolution of a fatty acyl-CoA elongase underlies desert adaptation in Drosophila.

Traits that allow species to survive in extreme environments such as hot-arid deserts have independently evolved in multiple taxa. However, the genetic and evolutionary mechanisms underlying these traits have thus far not been elucidated. Here, we show that Drosophila mojavensis, a desert-adapted fruit fly species, has evolved high desiccation resistance by producing long-chain methyl-branched cuticular hydrocarbons (mbCHCs) that contribute to a cuticular lipid layer reducing water loss. We show that the ability to synthesize these longer mbCHCs is due to evolutionary changes in a fatty acyl-CoA elongase (mElo). mElo knockout in D. mojavensis led to loss of longer mbCHCs and reduction of desiccation resistance at high temperatures but did not affect mortality at either high temperatures or desiccating conditions individually. Phylogenetic analysis showed that mElo is a Drosophila-specific gene, suggesting that while the physiological mechanisms underlying desert adaptation may be similar between species, the genes involved in these mechanisms may be species or lineage specific.

Combined pollution effects of Cu and benzotriazole in rice (Oryza sativa L.) verified by split-root experiment.

Although the combined effect of organic ligands and heavy metals in the environment on plants have been frequently reported, their complexed interaction in plants and the physiological effects remain to be revealed. Metal complexing agent benzotriazole (BTR) has extensive environmental pollution. In this study, root-splitting experiments were designed to identify the in vivo and in vitro effects of BTR on the accumulation and translocation of Cu in rice (Oryza sativa L.), and the concentrations and translocation factor (TF) of Cu and BTR in different parts of rice were measured. In the in vitro interaction treatments, low BTR concentrations enhanced Cu uptake and lateral transport in rice, while higher levels of BTR's exposure (i.e., ≥ 100 µM) resulted in opposite effects. Differently, significant increase in the lateral transport of Cu and vertical translocation of BTR in rice presented in the in vivo interaction treatments. TF of Cu from root A to root B (TFRA-RB) increased from 0.05 to 0.272 with the BTR concentration increasing from 0 to 100 µM, and higher TF of BTR from root to shoot (TFR-S), ranging from 1.00 to 1.75, compared with single BTR exposure treatments was observed. The phytotoxicity of BTR expressed by the catalase activity was significantly alleviated by the in vivo accumulated Cu in rice.