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Background: Cardiac remodeling in heart failure involves macrophage-mediated immune responses. Recent studies have shown that a PRR (pattern recognition receptor) called dectin-1, expressed on macrophages, mediates proinflammatory responses. Whether dectin-1 plays a role in pathological cardiac remodeling is unknown. Here, we identified a potential role of dectin-1 in this disease. Methods: To model aberrant cardiac remodeling, we utilized mouse models of chronic Ang II (angiotensin II) infusion. In this model, we assessed the potential role of dectin-1 through using D1KO (dectin-1 knockout) mice and bone marrow transplantation chimeric mice. We then used cellular and molecular assays to discover the underlying mechanisms of dectin-1 function. Results: We found that macrophage dectin-1 is elevated in mouse heart tissues following chronic Ang II administration. D1KO mice were significantly protected against Ang II–induced cardiac dysfunction, hypertrophy, fibrosis, inflammatory responses, and macrophage infiltration. Further bone marrow transplantation studies showed that dectin-1 deficiency in bone marrow–derived cells prevented Ang II–induced cardiac inflammation and dysfunction. Through detailed molecular studies, we show that Ang II binds directly to dectin-1, causing dectin-1 homodimerization and activating the downstream Syk (spleen tyrosine kinase)/NF-κB (nuclear factor kappa B) signaling pathway to induce expression of inflammatory and chemoattractant factors. Mutagenesis studies identified R184 in the C-type lectin domain to interact with Ang II. Blocking dectin-1 in macrophages suppresses Ang II–induced inflammatory mediators and subsequent intercellular cross talk with cardiomyocytes and fibroblasts. Conclusions: Our study has discovered dectin-1 as a new nonclassical receptor of Ang II and a key player in cardiac remolding and dysfunction. These studies suggest that dectin-1 may be a new target for treating hypertension-related heart failure.

Fetal cystic hygroma (CH) is associated with poor prognosis and chromosomal anomalies. Recent studies have suggested that the genetic background of affected fetuses is essential for predicting pregnancy outcomes. However, the detection performance of different genetic approaches for the etiological diagnosis of fetal CH remains unclear. In this study, we aimed to compare the diagnostic efficiency of karyotyping and chromosomal microarray analysis (CMA) in a local fetal CH cohort, and tried to propose an optimized testing strategy that may help improve the cost-effectiveness of disease management. We reviewed all pregnancies that underwent invasive prenatal diagnosis between January 2017 and September 2021 at one of the largest prenatal diagnostic centers in Southeast China. We collected cases identified by the presence of fetal CH. Prenatal phenotypes and laboratory records of these patients were audited, collated, and analyzed. The detection rates of karyotyping and CMA were compared, and the concordance rate of these two methods was calculated. A total of 157 fetal CH cases were screened from 6,059 patients who underwent prenatal diagnosis. Diagnostic genetic variants were identified in 44.6% (70/157) of the cases. Karyotyping, CMA, and whole-exome sequencing (WES) identified pathogenic genetic variants in 63, 68, and 1 case, respectively. The Cohen’s κ coefficient between karyotyping and CMA was 0.96, with a concordance of 98.0%. Of the 18 cases in which cryptic copy number variants PIGN gene in a case undiagnosed by CMA and karyotyping. Our study demonstrated that chromosomal aneuploidy abnormalities are the main genetic cause of fetal CH. Based on this, we recommend karyotyping combined with rapid aneuploidy detection as a first-tier approach for the genetic diagnosis of fetal CH. WES and CMA could improve the diagnostic yield when routine genetic tests fail to determine the cause of fetal CH.

An in situ artificial LiF/Li–Sn solid electrolyte interface film possesses high Li+ conductivity and good electrical insulation, endowing the Li//LiFePO4 battery with 86.3% capacity after 1000 cycles.

A bidirectional relationship between insomnia and depression has been observed. However, few studies have used network analysis to explore the interaction patterns in that association at the symptom level. This study aimed to estimate network structures of insomnia and depressive symptoms among shift workers, as well as to compare the differences in network properties between individuals without and with insomnia symptoms and/or at risk of depression. A total of 1883 shift workers were included in our study. Insomnia symptoms were evaluated by three items based on the criteria of the Diagnostic and Statistical Manual of Mental Disorders, and depressive symptoms were assessed by the Center for Epidemiologic Studies Depression Scale. Network analyses were used for the statistical analysis. "Difficulty initiating sleep", "Hard to get started", and "Depressed mood" with higher expected influence (EI) values were identified as the most central symptoms within the insomnia-depressive networks among shift workers. The significant differences between individuals without and with insomnia symptoms and/or at risk of depression were observed in symptoms of "Difficulty initiating sleep" and "Hard to get started". "Depressed mood", "Difficulty initiating sleep", or "Hard to get started" were the most key symptoms that trigger and sustain the structure of insomnia and depressive symptom among shift workers. Hence, timely intervention for the above three symptoms in future research or clinical practice (e.g., cognitive behavioral therapy for insomnia) may be crucial in alleviating insomnia and depressive symptoms among shift workers.

The lithium (Li) ion and electron diffusion behaviors across the actual solid electrolyte interphase (SEI) play a critical role in regulating the Li nucleation and growth and improving the performance of lithium-sulfur (Li-S) batteries. To date, a number of researchers have pursued an SEI with high Li-ion conductivity while ignoring the Li dendrite growth caused by electron tunneling in the SEI. Herein, an artificial anti-electron tunneling layer with enriched lithium fluoride (LiF) and sodium fluoride (NaF) nanocrystals is constructed using a facile solution-soaking method. As evidenced theoretically and experimentally, the LiF/NaF artificial SEI exhibits an outstanding electron-blocking capability that can reduce electron tunneling, resulting in dendrite-free and dense Li deposition beneath the SEI, even with an ultrahigh areal capacity. In addition, the artificial anti-electron tunneling layer exhibits improved ionic conductivity and mechanical strength, compared to those of routine SEI. The symmetric cells with protected Li electrodes achieve a stable cycling of 1500 h. The LiF/NaF artificial SEI endows the Li-S full cells with long-term cyclability under conditions of high sulfur loading, lean electrolyte, and limited Li excess. This study provides a perspective on the design of the SEI for highly safe and practical Li-S batteries.

Early life stress (ELS) can cause long-term changes in gene expression, affect cognition, mood, and behavior, and increase susceptibility to post-traumatic stress disorder (PTSD) in adulthood, in which the histone acetylation plays a crucial role. Studies have found that environmental enrichment (EE) mitigated the unfavorable outcomes of ELS. However, the underlying mechanism of the histone acetylation is not yet completely clear. The purpose of this study was to explore the effect of EE on the histone acetylation after ELS. In this study, using single prolonged stress (SPS) paradigm in early adolescent rats explored the long-term effects of ELS on behavior, the activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs), as well as the acetylation levels of the lysine 9 site of histone H3 (H3K9) and lysine 12 site of histone H4 (H4K12) in the hippocampus and amygdala. Meanwhile, the protective effects of EE intervention were examined. We found that adult male rats exposed to ELS showed behavioral changes, including reduced locomotor activity, increased anxiety-like behaviors, impaired spatial learning and memory, enhanced contextual and cued fear memory, and the HATs/HDACs ratio and acetyl H3K9 (Ac-H3K9) and acetyl H4K12 (Ac-H4K12) were increased in the hippocampus and decreased in the amygdala. Furthermore, EE attenuated the behavioral abnormalities from ELS, possibly through down-regulating the activity of HATs in the hippocampus and up-regulating HDACs activities in the amygdala. These finding suggested that EE could ameliorate ELS-induced PTSD-like behaviors by regulating histone acetylation in the hippocampus and amygdala, reducing the susceptibility to PTSD in adulthood.

Lithium-sulfur (Li-S) batteries are widely considered to be next-generation storage technologies due to their high energy density, low cost and non-toxicity. However, the soluble lithium polysulfides (LiPS) migrating to the anode side inevitably causes side reactions with the Li anode, resulting in severe corrosion of the Li anode, loss of active materials, and rapid battery failure. Therefore, it is necessary to develop effective strategies to avoid LiPS exposure to Li anodes. Herein, a stable UiO-66-ClO

Objectives: An increasing number of young children spend time and eat at least one meal per day in childcare programs, highlighting the significance of early care and education (ECE) settings in promoting children's healthy dietary behaviors. The purpose of this review was to summarize quantitative studies on the relationship between the dietary environment in ECE settings and the eating behaviors of children aged 0-6 years. Methods: We consulted Web of Science, PsycInfo, ProQuest, and Emerald electronic databases, searching for empirical studies from 2000 to 2022. Results: Ultimately, we included 38 studies. Measures of the dietary environment varied considerably across studies. Following healthy diet regulations and nutrition-related activities were positively correlated with children's intake of healthy foods. Strategies such as serving fruits and vegetables in advance, serving small portion sizes, and providing children a variety of vegetables increased children's intake of healthy foods. Results on caregivers' feeding practices remained mixed. Conclusions: These findings reveal the necessity and importance of paying attention to different aspects of the dietary environment and to take a comprehensive approach to understanding the role that environment plays in cultivating children's dietary behaviors.

Diabetic nephropathy (DN) is one microvascular complication of diabetes. About 30% of diabetic patients can develop DN, which is closely related to the high incidence and mortality of heart diseases, and then develop end-stage renal diseases. Therefore, early detection and screening of high-risk patients with DN is important. Herein, we explored the differences of serum transcriptomics between DN and non-DN in type II diabetes mellitus (T2DM) patients. We obtained 110 target genes using weighted correlation network analysis. Gene Ontology enrichment analysis indicates these target genes are mainly related to membrane adhesion, alpha-amino acid biosynthesis, metabolism, and binding, terminus, inhibitory synapse, clathrinid-sculpted vesicle, kinase activity, hormone binding, receptor activity, and transporter activity. Kyoto Encyclopedia of Genes and Genomes analysis indicates the process of DN in diabetic patients can involve synaptic vesicle cycle, cysteine and methionine metabolism, N-Glycan biosynthesis, osteoclast differentiation, and cAMP signaling pathway. Next, we detected the expression levels of hub genes in a retrospective cohort. Then, we developed a risk score tool included in the prediction model for early DN in T2DM patients. The prediction model was well applied into clinical practice, as confirmed by internal validation and several other methods. A novel DN risk model with relatively high prediction accuracy was established based on clinical characteristics and hub genes of serum detection. The estimated risk score can help clinicians develop individualized intervention programs for DN in T2DM. External validation data are required before individualized intervention measures.

Nanoparticles can promote the accumulation of drugs in tumors. However, they find limited clinical applications because they cannot easily penetrate the stroma of cancer tissues, and it is difficult to control drug release. We developed a multiresponse multistage drug-delivery nanogel with improved tumor permeability and responsiveness to the tumor microenvironment for the controlled delivery of anticancer agents. For this purpose, ∼100 nm multistage drug delivery nanogels with pH, redox, near-infrared stimulation, and enzyme responsiveness were grown in situ using 20 nm gold nanoparticles (AuNPs) via an emulsion-aiding crosslinking technique with cysteine crosslinker. An alginate cysteine AuNP (ACA) nanocarrier can efficiently load the cationic drug doxorubicin (DOX) to produce a multistage drug delivery nanocarrier (DOX@ACA). DOX@ACA can maintain the slow release of DOX and reduce its toxicity. In cancer tissues, the high pH and reductase microenvironment combined with the in vitro delivery of alginate and near-infrared light drove drug release. The developed nanoparticles effectively inhibited cancer cells, and in vivo evaluations showed that they effectively enhanced antitumor activity while having negligible in vivo toxicity to major organs.

The Cultural Revolution, the full name of which was “the Great Proletarian Cultural Revolution,” was a political movement launched by Mao Zedong, the supreme leader of the Chinese Communist Party (CCP). Its goal was to rectify the CCP, which Mao considered to have become over-bureaucratized since it took power in 1949. Mao also wanted to revive the revolutionary spirit of the war period in order to maintain his personal charisma and domination within the CCP. The movement, however, took on a momentum of its own as a large number of the Chinese masses participated in it and became entangled in factional fights. Keywords: ideology

Globally, drug-resistant bacteria are a potential threat to human society owing to the overuse of antibiotics and thus, non-antibiotic bactericides are urgently needed. Herein, an innovative antibacterial nanoplatform based on quaternized chitosan (QCS)/ silver (Ag)/ cobalt phosphide (CoP) nanocomposites is envisaged for achieving near-infrared (NIR) laser-inducible rapid sterilisation. In the core-shell hybrids, Ag nanoparticles (NPs) with a size of ∼ 25 nm were uniformly deposited on CoP nanoneedles, upon which a layer of QCS (approximately 10 wt%), is coated. Numerical calculations revealed that under NIR irradiation, high-energy hot electrons arising from the surface plasmon resonance effect of Ag migrate into the interface between Ag and CoP, and amplify the photothermal effect of CoP. Meanwhile, photo-excited electrons from CoP are transported onto Ag NPs because the Schottky heterostructure facilitates the production of reactive oxygen species. Ag loading simultaneously enhances the photocatalytic and photothermal effects of CoP, achieving rapid antibacterial activity synergistically. The QCS coating improves the dispersibility of power in an aqueous system and provides contact between the antiseptics and bacteria. The ternary QCS/Ag/CoP nanocomposites achieved greater than 99.6% inactivation against S. aureus and E. coli within 10 min. In addition, the nanocomposites were confirmed to be noncytotoxic to mammals. Consequently, the QCS/Ag/CoP nanoplatforms possess great potential for rapid and effective antibacterial applications.

Background Clear cell renal cell carcinoma (ccRCC) is a fatal urological malignancy, and surgery remains the primary treatment. Members of the never in mitosis gene A (NIMA)-related kinase (NEK) family have been found to participate in the progression of several cancers and could be used as target genes to treat corresponding diseases. Nonetheless, the prognostic value and immune infiltration levels of NEK family genes in ccRCC remain unknown. Methods Gene Set Cancer Analysis (GSCA), Tumor Immune Estimation Resource (TIMER), and Gene Expression Profiling Interactive Analysis (GEPIA) databases were utilized to examine the differential expression of NEK family genes in ccRCC, and the Kaplan-Meier plotter was utilized to analyze the prognosis. The Search Tool for Retrieval of Interacting Genes(STRING) database was used to construct a protein-protein interaction network. Analysis of function was performed by the Sangerbox tool. Finally, the relationship between NEK family genes and immune cell infiltration was explored using the TIMER database. Results Transcriptional levels of NEK2, NEK3, NEK5, NEK6, and NEK11 significantly differed between ccRCC and normal tissues. Moreover, there was a significant correlation between NEK1, NEK2, NEK4, NEK8, NEK9, and NEK10 and their clinicopathological stages in patients with ccRCC. Based on survival analysis, ccRCC patients with high transcriptional levels of NEK2, NEK3, NEK8, and NEK10 and low transcriptional levels of NEK1, NEK4, NEK5, NEK6, NEK7, NEK9, NEK11 had shorter survival times. Additionally, a significant relationship was observed between immune cell infiltration and NEK family members. Conclusions These results indicate that NEK family members are significantly differentially expressed in ccRCC, and a significant correlation exists between the NEK family and prognosis and immune infiltration. NEK family members may act as therapeutic targets and prognostic indicators in ccRCC.

Background Accumulating evidence indicates that infertile individuals are often associated with poor mental health. However, there are few studies focus on the trauma exposure of infertile individuals. Meanwhile, adverse childhood experiences (ACE) are often associated with poor mental health, especially the development of post-traumatic stress symptoms (PTSS). Therefore, the present study aimed to investigate the condition of traumatic exposure and the prevalence of PTSS in people with infertile in Shanghai, and then explore the effect of ACE among infertile people of childbearing age who reported experiencing trauma exposure. Methods The cross-sectional study was conducted from October 2021 to September 2022. A total of 213 infertile patients in Shanghai Changzheng Hospital were selected by random sampling. After screening, a total of 194 experimental data were obtained. The participants filled out the demographic questionnaires, self-developed trauma exposure questionnaire. Childhood trauma questionnaire (CTQ) and the primary care PTSD screen for DSM-5 (PC-PTSD-5) were used to investigate ACE and PTSS, respectively. Results Traumatic events were experienced in 41.8% of infertility patients. Only 4.10% of infertile patients had PTSS. Maternal education level (p = 0.019) had significant influence on whether PTSS occurred in patients. Logistic regression analysis indicated age, emotional abuse (EA) and physical neglect (PN) increased the probability of patients reporting trauma exposure, while emotional neglect (EN) reduced the possibility of reporting trauma. Conclusions Undesirable the high incidence of traumatic experience of infertility population, especially ACE, has an important impact on their treatment and recovery at the moment, as well as the future development of mental health. More evidence between PTSS and trauma exposure are needed in the future to strengthen this conclusion.

Background: Heart failure (HF) is a common comorbidity in maintenance hemodialysis (MHD) patients, of which ejection fraction preserved heart failure (HFpEF) is the main cause, resulting in substantial mortality and morbidity. However, there are still no effective therapeutic agents available for HFpEF. Sacubitril/valsartan (SV) has been shown to significantly improve clinical symptoms and reverse ventricular remodeling in patients with reduced ejection fraction of heart failure (HFrEF). The effect of SV in MHD patients with HFpEF remains unclear. Our study aimed to evaluate the efficacy and safety of SV in MHD patients with HFpEF. Methods: A total of 90 MHD patients with HFpEF admitted to the Department of Nephrology of Hefei Second People's Hospital from January 2021 to January 2022 were collected, and they were divided into control group and observation group according to random number method. Both groups received consistent basic treatment based on the results of the test, and at this baseline, one group received ACEI/ARB drugs as the control group, and the other group received SV as the observation group. The starting dose of SV was 50mg bid, and the dose was gradually increased according to blood pressure and blood potassium level until the target dose of 100mg bid was reached for 3 months.After 3 months of treatment, relevant indicators before and after treatment, such as NYHA grade, echocardiography related indicators, NT-proBNP, 6 minute walking distance (6 MWD), blood pressure level, serum potassium and incidence of adverse reactions, were collected and compared. Results: 1. A total of 90 patients with MHD and HFpEF, no patients stopped during the follow-up. There were no significant differences in general clinical data (age, number of months of dialysis, sex, primary disease), NYHA grade, serum NT-proBNP, serum potassium, blood creatinine, hemoglobin, LVEF, 6 MWD, SBP and DBP between the two groups (all P> 0.05).2. After 3 months of treatment, in terms of treatment effect, 41 people were significantly effective, 35 were effective and 14 were ineffective. The efficacy of the observation group was significantly higher than that of the control group, and the difference was statistically significant (P 0.05). 4.After 3 months of treatment, the 6MWD of patients in both groups increased compared with the previous group, and the NT-proBNP decreased compared with the previous group, and the difference before and after treatment in the observation group was higher than that in the control group, and the difference before and after treatment in both groups was statistically significant (both P0.05). 6. During the treatment follow-up process, the incidence of adverse reactions in the observation group was lower than that in the control group, and the difference was statistically significant (P Conclusion: Our study shows that SV is effective and safe in the treatment of MHD patients with HFpEF.

Drosophila Down syndrome cell adhesion molecule 1 (Dscam1) encodes tens of thousands of cell recognition molecules via alternative splicing, which are required for neural function. A canonical self-avoidance model seems to provide a central mechanistic basis for Dscam1 functions in neuronal wiring. Here, we reveal extensive noncanonical functions of Dscam1 isoforms in neuronal wiring. We generated a series of allelic cis mutations in Dscam1, encoding a normal number of isoforms, but with an altered isoform composition. Despite normal dendritic self-avoidance and self-/nonself-discrimination in dendritic arborization (da) neurons, which is consistent with the canonical self-avoidance model, these mutants exhibited strikingly distinct spectra of phenotypic defects in the three types of neurons: up to ∼60% defects in mushroom bodies, a significant increase in branching and growth in da neurons, and mild axonal branching defects in mechanosensory neurons. Remarkably, the altered isoform composition resulted in increased dendrite growth yet inhibited axon growth. Moreover, reducing Dscam1 dosage exacerbated axonal defects in mushroom bodies and mechanosensory neurons but reverted dendritic branching and growth defects in da neurons. This splicing-tuned regulation strategy suggests that axon and dendrite growth in diverse neurons cell-autonomously require Dscam1 isoform composition. These findings provide important insights into the functions of Dscam1 isoforms in neuronal wiring.

Tumor suppressor p53 is inactivated by thousands of heterogeneous mutations in cancer, but their individual druggability remains largely elusive. Here, we evaluated 800 common p53 mutants for their rescue potencies by the representative generic rescue compound arsenic trioxide (ATO) in terms of transactivation activity, cell growth inhibition, and mouse tumor–suppressive activities. The rescue potencies were mainly determined by the solvent accessibility of the mutated residue, a key factor determining whether a mutation is a structural one, and the temperature sensitivity, the ability to reassemble the wild-type DNA binding surface at a low temperature, of the mutant protein. A total of 390 p53 mutants were rescued to varying degrees and thus were termed as type 1, type 2a, and type 2b mutations, depending on the degree to which they were rescued. The 33 type 1 mutations were rescued to amounts comparable to the wild type. In PDX mouse trials, ATO preferentially inhibited growth of tumors harboring type 1 and type 2a mutants. In an ATO clinical trial, we report the first-in-human mutant p53 reactivation in a patient harboring the type 1 V272M mutant. In 47 cell lines derived from 10 cancer types, ATO preferentially and effectively rescued type 1 and type 2a mutants, supporting the broad applicability of ATO in rescuing mutant p53. Our study provides the scientific and clinical communities with a resource of the druggabilities of numerous p53 mutations ( www.rescuep53.net ) and proposes a conceptual p53-targeting strategy based on individual mutant alleles rather than mutation type.

The ammunition body drive structural parts are typical components in the weaponry industry, with large size and wall thickness, the parts need to bear large loads when working, so their internal filling quality and mechanical properties have quite strict acceptance criteria. In this paper, we take an elastomeric transmission structure part made of ZL205A alloy as the research object, and use the metal type gravity casting technology for casting trial production, analyze the quality and mechanical properties of the molded parts of ZL205A alloy parts under different process parameters, optimize the casting process parameters, get the optimal combination of process parameters, and obtain large ZL205A castings with less internal quality defects and high mechanical properties. To solve the current problem of immaturity of domestic casting process technology for this ZL205A alloy large parts and promote the development of China's weapon and equipment manufacturing industry in the direction of light weight.

Melanoma is the most lethal type of skin cancer, originating from the malignant transformation of melanocyte. While the development of targeted therapy and immunotherapy has gained revolutionary advances in potentiating the therapeutic effect, the prognosis of patients with melanoma is still suboptimal. During tumor progression, melanoma frequently encounters stress from both endogenous and exogenous sources in tumor microenvironment. SIRT7 is a nuclear-localized deacetylase of which the activity is highly dependent on intracellular nicotinamide adenine dinucleotide (NAD+), with versatile biological functions in maintaining cell homeostasis. Nevertheless, whether SIRT7 regulates tumor cell biology and tumor immunology in melanoma under stressful tumor microenvironment remains elusive. Herein, we reported that SIRT7 orchestrates melanoma progression by simultaneously promoting tumor cell survival and immune evasion via the activation of unfolded protein response. We first identified that SIRT7 expression was the most significantly increased one in sirtuins family upon stress. Then, we proved that the deficiency of SIRT7 potentiated tumor cell death under stress in vitro and suppressed melanoma growth in vivo. Mechanistically, SIRT7 selectively activated the IRE1α-XBP1 axis to potentiate the pro-survival ERK signal pathway and the secretion of tumor-promoting cytokines. SIRT7 directly de-acetylated SMAD4 to antagonize the TGF-β-SMAD4 signal, which relieved the transcriptional repression on IRE1α and induced the activation of the IRE1α-XBP1 axis. Moreover, SIRT7 up-regulation eradicated anti-tumor immunity by promoting PD-L1 expression via the IRE1α-XBP1 axis. Additionally, the synergized therapeutic effect of SIRT7 suppression and anti-PD-1 immune checkpoint blockade was also investigated. Taken together, SIRT7 can be employed as a promising target to restrain tumor growth and increase the effect of melanoma immunotherapy.

Dendritic cells (DCs) are antigen-presenting cells that bridge innate and adaptive immune responses. Multiple cell types, including DCs, rely on cellular metabolism to determine their fate. DCs substantially alter cellular metabolic pathways during activation, such as oxidative phosphorylation, glycolysis, fatty acid and amino acid metabolism, which have crucial implications for their functionality. In this review, we summarize and discuss recent progress in DC metabolic studies, focusing on how metabolic reprogramming influences DC activation and functionality and the potential metabolic differences among DC subsets. Improving the understanding of the relationship between DC biology and metabolic regulation may provide promising therapeutic targets for immune-mediated inflammatory diseases.

Xiaoman Chen,1,2,&ast; Jing Zhou,3,&ast; Lili Wu,1 Xiang Zhu,1 Hong Deng1 1Department of Infectious Diseases, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, People’s Republic of China; 2Infectious Disease Center, Guangzhou Eighth People’s Hospital, Guangzhou Medical University, Guangzhou, People’s Republic of China; 3Department of Pathology, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Hong Deng; Xiang Zhu, Department of Infectious Diseases, Third Affiliated Hospital of Sun Yat-sen University, No. 600 Tianhe Road, Tianhe District, Guangzhou, People’s Republic of China, Tel +86-2085252506, Fax +86-2085252063, Email dhong@mail.sysu.edu.cn; zhuxiang@mail.sysu.edu.cnPurpose: Chronic hepatitis B (CHB) and metabolic associated fatty liver disease (MAFLD) are both important public health problems. The effect of concomitant MAFLD on patients with CHB is still unclear. This study aimed to explore the influence of MAFLD on liver fibrosis and inflammation in CHB patients with different hepatitis B e antigen (HBeAg) status.Patients and Methods: We retrospectively collected the clinical data of 399 treatment-naïve CHB patients who underwent liver biopsy. All patients were divided into two groups (HBeAg± group). Logistic regression analysis was used to identify factors associated with liver inflammatory activity and significant fibrosis in patients with CHB. Multivariable logistic regressions were repeated in subgroups stratified by HBeAg status.Results: In patients with CHB, MAFLD was independently associated with a risk of moderate-to-severe liver activity and significant fibrosis (P < 0.05). In the HBeAg-negative group, patients with MAFLD had significantly higher levels of alanine aminotransferase (ALT) (P < 0.05) and more severe liver inflammatory activity and fibrosis (P < 0.05) compared to those without MAFLD. MAFLD was independently associated with a risk of moderate-to-severe liver activity (A ≥ 3: OR 3.97, 95% CI 1.71– 9.22, P =0.001) and significant fibrosis (F ≥ 2: OR 2.02, 95% CI 1.09– 3.73, P =0.026). In the HBeAg-positive group, MAFLD was found to be independently associated with moderate-to-severe liver activity (OR 2.44, 95% CI 1.03– 5.79, P =0.044) but not fibrosis (P =0.618).Conclusion: MAFLD is associated with the risk of liver fibrosis and inflammatory activity in HBeAg-negative CHB patients. Sufficient attention should be paid to the prevention and treatment of MAFLD in patients with CHB, especially in HBeAg-negative patients.Keywords: chronic hepatitis B, metabolic associated fatty liver disease, nonalcoholic fatty liver disease, hepatitis B e antigen