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Due to the wide application of relaxed static stability in the field of advanced fighter design and the value of further research on the related active control technology,it is necessary to conduct a more comprehensive analysis on the influence of relaxed static stability on the longitudinal flight performance of aircraft. In this paper,the center of gravity is taken backward as the way to relax the static stability,the relationship between the relaxed static stability and the pitching moment coefficient of a certain fighter jet is analyzed to build the nonlinear model of fighter jets and analyze the open-loop characteristics. On this basis,the influence mechanism of the relaxed static stability on the operational equilibrium of the aircraft is analyzed to linearize the nonlinear model of the fighter aircraft,and the influence of the relaxed static stability on the step response characteristics and the long and short period modal characteristics of the longitudinal linear model of the aircraft is analyzed. The simulation results show that the relaxed static stability can increase the pitching moment coefficient and improve the aircraft performance,but it may cause the modal characteristics of the aircraft body to deteriorate,which needs to be considered in the design of control rate.

Background: Deltamethrin, as a highly effective and broad-spectrum insecticide, has been widely used for agricultural pest control such as Aphis gossypii worldwide. Increasing evidence has shown that despite great economic benefits brought by it, deltamethrin has also non-negligible side effects. However, the potential risks and related molecular mechanisms remain largely unclear., Results: Herein, the life table parameters and transcriptome sequencing analyses of the four successive aphid generations were performed to investigate the hormesis and transgenerational effects of deltamethrin on A. gossypii. The life table analysis showed that although the exposure of G0 aphid to 30% lethal concentration (LC 30 ) deltamethrin significantly reduced the net reproduction rate (R 0 ), intrinsic rate of increase (r), and fecundity of G0, but it significantly enhanced the R 0 and fecundity of subsequent two generations (G1 and G2) of A. gossypii. Moreover, transcriptomic analyses showed that the signaling pathways related to posttranscriptional regulation (spliceosome), protein processing, longevity regulating, and cell proliferation (DNA replication, homologous recombination and non-homologous end-joining) were significantly up-regulated in G1 or G2 under LC 30 deltamethrin treatment. Additionally, we also found that the deltamethrin-sulfoxaflor rotation of G0 and G1 still induced reproductive stimulation, but the reproductive stimulation induced by insecticides rotation treatment was significantly lower than that in the deltamethrin exposure alone., Conclusion: Our study demonstrates that sublethal concentrations of deltamethrin significantly enhanced the offspring fecundity of cotton aphid. In addition, our study also reveals the transcriptional response mechanism of hormesis-induced fecundity increase, providing valuable reference for optimizing the application of deltamethrin in integrated pest management. © 2024 Society of Chemical Industry., (© 2024 Society of Chemical Industry.)

Cardiovascular diseases (CVDs) are a major global health concern, highlighting the need for effective diagnostic tools. Zinc ions (Zn 2+ ) play a role in CVDs, but their detection is challenging. This study presents a multifunctional optical sensor, HD-Zn , designed to detect Zn 2+ in relation to CVDs. We developed a novel fluorescence probe, HD-Zn , by conjugating N,N -di(2-picolyl)ethylenediamine (DPEN) to HD via an amide bond, which results in fluorescence quenching due to photoinduced electron transfer (PeT). Adding Zn 2+ significantly increased fluorescence intensity in the near-infrared region (NIR-I). The probe showed a linear response to varying Zn 2+ concentrations, with a detection limit of 9.8 nM, appropriate for physiological conditions. Fluorescence imaging in RAW264.7 macrophages indicated lower intracellular Zn 2+ levels in foam cells compared to healthy cells, linked to CVDsprogression. In vivo imaging in mouse models showed decreased fluorescence intensity in the aorta with disease progression. Our findings confirm that HD-Zn is a reliable tool for measuring Zn 2+ levels in plaques and demonstrate its biosafety for detecting Zn 2+ in serum and urine, offering potential for clinical applications in CVDs diagnosis and monitoring.

Background: Observational studies suggest that hypertension affects brain cortical structure. However, the potential causal association has yet to be entirely determined. Thus, we aim to assess the causality between hypertension and abnormal cortical structure., Methods: We conducted a bidirectional Mendelian randomization (MR) study to estimate their relationship. Genome-wide association study summary statistics of hypertension (n = 484,598) and brain cortical (surface area and thickness) (n = 51,665) were derived from publicly available databases. Sensitivity analyses were applied to ensure the robustness of the results., Results: The study showed that hypertension was associated with a decline in total brain cortical thickness [β, -0.0308 mm; 95 % confidence interval (CI), -0.0610 to -0.0007; p  = 0.045] and the insula thickness [β, -0.0415 mm; 95 % CI, -0.0772 to -0.0057; p  = 0.023]. A null association was observed between hypertension and other brain regions. In the reverse MR analysis, the total cortical surface area (per 1 SD increase) significantly decreased the incidence of hypertension [odds ratio (OR), 0.976; 95 % CI, 0.963 to 0.990; p  = 5.15E-04]. The caudal anterior cingulate cortex thickness (per 1 SD increase) was significantly associated with an increased risk of hypertension [OR, 1.057; 95 % CI, 1.034 to 1.082; p  = 1.08E-06]. Moreover, we found several nominally associated gyri, including cuneus, isthmus cingulate, middle temporal, para hippocampal, posterior cingulate, superior temporal, and medial orbitofrontal, influence the incidence of hypertension., Conclusion: Our study showed causal relationships between hypertension and changes in specific brain cortical, providing new evidence for the heart-brain axis theory., (© 2024 The Authors.)

Species of the genus Cyaforma Wang are reviewed. One new species, C. chayuica Chen from Xizang, China is described and illustrated. C. tonkinensis (Zia) is newly recorded from China. The males of C. macula (Wang) and C. tonkinensis are described for the first time. A key to the known species of this genus is provided. Additionally, biological notes on the genus are reported.

Introduction: Symbiotic bacteria play key roles in a variety of important life processes of insects such as development, reproduction and environmental adaptation, and the elucidation of symbiont population structure and dynamics is crucial for revealing the underlying regulatory mechanisms. The marmalade hoverfly ( Episyrphus balteatus ) is not only a remarkable aphid predator, but also a worldwide pollinator second to honeybees. However, its symbiont composition and dynamics remain unclear., Methods: Herein, we investigate the symbiotic bacterial dynamics in marmalade hoverfly throughout whole life cycle, across two sexes, and in its prey Megoura crassicauda by 16S rRNA sequencing., Results: In general, the dominant phyla were Proteobacteria and Firmicutes, and the dominant genera were Serratia and Wolbachia . Serratia mainly existed in the larval stage of hoverfly with the highest relative abundance of 86.24% in the 1st instar larvae. Wolbachia was found in adults and eggs with the highest relative abundance of 62.80% in eggs. Significant difference in species diversity was observed between the adults feeding on pollen and larvae feeding on M. crassicauda , in which the dominant symbiotic bacteria were Asaia and Serratia , respectively. However, between two sexes, the symbionts exhibited high similarity in species composition. In addition, our results suggested that E. balteatus obtainded Serratia mainly through horizontal transmission by feeding on prey aphids, whereas it acquired Wolbachia mainly through intergeneration vertical transmission. Taken together, our study revealed the effects of development stages, diet types and genders of E. balteatus on symbionts, and explored transmission modes of dominant bacteria Serratia and Wolbachia ., Discussion: Our findings lay a foundation for further studying the roles of symbiotic bacteria in E. balteatus life cycle, which will benefit for revealing the co-adaptation mechanisms of insects and symbiotic bacteria., Competing Interests: LC was employed the Xinjiang Tianyu Agricultural Science Modern Agricultural Industrialization Development 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 Wang, Huangfu, Chen, Zhang, Li, Gao, Li, Wang, Zhu, Ji, Luo and Cui.)

Background: Inflammation and hyperlipidemia can cause atherosclerosis. Prebiotic inulin has been proven to effectively reduce inflammation and blood lipid levels. Utilizing a mouse model induced by a high-fat diet, this study aimed to explore whether the characteristic intestinal flora and its metabolites mediate the effects of inulin intervention on atherosclerosis and to clarify the specific mechanism., Methods: Thirty apolipoprotein E-deficient (ApoE-/-) mice were randomly divided into three groups. They were fed with a normal diet, a high-fat diet or an inulin+high-fat diet for 16 weeks. The total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) in the three groups were compared. The gross aorta and aortic sinus of mice were stained with oil red O, and the area of atherosclerotic plaque was observed and compared. The diversity and structure of the mouse fecal flora were detected by sequencing the V3-V4 region of the 16S rRNA gene, and the levels of metabolites in mouse feces were assessed by gas chromatography-mass spectrometry. The plasma lipopolysaccharide (LPS) levels and aortic inflammatory factors were measured by multi-index flow cytometry (CBA)., Results: ApoE-/- mice fed with the high-fat diet exhibited an increase of approximately 46% in the area of atherosclerotic lesions, and the levels of TC, TG and LDL-C were significantly increased ( P < 0.05) compared with levels in the normal diet group. After inulin was added to the high-fat group, the area of atherosclerotic lesions, the level of serum LPS and aortic inflammation were reduced, and the levels of TC, TG and LDL-C were decreased ( P  < 0.05). Based on 16S rRNA gene detection, we found that the composition of the intestinal microbiota, such as Prevotella, and metabolites, such as L-arginine, changed significantly due to hyperlipidemia, and the dietary inulin intervention partially reversed the relevant changes., Conclusion: Inulin can inhibit the formation of atherosclerotic plaques, which may be related to the changes in lipid metabolism, the composition of the intestinal microbial community and its metabolites, and the inhibition of the expression of related inflammatory factors. Our study identified the relationships among the characteristic intestinal microbiota, metabolites and atherosclerosis, aiming to provide a new direction for future research to delay or treat atherosclerosis by changing the composition and function of the host intestinal microbiota and metabolites., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)

Aphis gossypii Glover is one of the most agriculturally important phloem-feeding economic pests, causing tremendous loss in crop yield annually. The hormesis is an important cause of A. gossypii resistance formation, population resurgence, and re-outbreak. However, whether the hormesises induced by different insecticides interact mutually remain largely unclear. In the study, four-generation A. gossypii experiment found that the 24-h sublethal-dose (LC 20 ) sulfoxaflor treatment on G0 significantly increased the net reproductive rate (R0) and fecundity of G1 and G2 generation A. gossypii, but it did not significantly affect the fecundity of G3 and G4 individuals. Transcriptomic analyses revealed that the insecticide-induced significant up-regulation of pathways ribosome, energy metabolism, and the DNA replication and reparation might be responsible for the enhancement of fecundity in G1 and G2 A. gossypii. Notably, G0 exposure to LC 20 sulfoxaflor followed by G1 exposure to LC 30 deltamethrin resulted in a stronger reproductive stimulation than sulfoxaflor or deltamethrin exposure alone. Our findings provide valuable reference for optimizing sulfoxaflor application in integrated pest management strategies., Competing Interests: Declaration of competing interest The authors declare no competing interests., (Copyright © 2024. Published by Elsevier Inc.)

Episyrphus balteatus can provide dual ecosystem services including pest control and pollination, which the larvae are excellent predators of aphid pest whereas adults are efficient pollinator. In this study, we assembled a high-quality genome of E. balteatus from northern China geographical population at the chromosome level by using Illumina, PacBio long reads, and Hi-C technologies. The 467.42 Mb genome was obtained from 723 contigs, with a contig N50 of 9.16 Mb and Scaffold N50 of 118.85 Mb, and 90.25% (431.75 Mb) of the assembly was anchored to 4 pseudo-autosomes and one pseudo-heterosome. In total, 14,848 protein-coding genes were annotated, and 95.14% of genes were fully represented in NR, GO, KEGG databases. Besides, we also obtained the mitochondrial genome of E. balteatus of 16, 837 bp in length with 37 typical mitochondrial genes. Overall, this high-quality genome is valuable for evolutionary and genetic studies of E. balteatus and other Syrphidae hoverfly species., (© 2024. The Author(s).)

(1) Background: Mitochondrial genomes are important markers for the study of phylogenetics and systematics. Triozidae includes some primary pests of Populus euphratica . The phylogenetic relationships of this group remain controversial due to the lack of molecular data. (2) Methods: Mitochondria of Egeirotrioza Boselli were sequenced and assembled. We analyzed the sequence length, nucleotide composition, and evolutionary rate of Triozidae, combined with the 13 published mitochondrial genomes. (3) Results: The evolutionary rate of protein-coding genes was as follows: ATP8 > ND6 > ND5 > ND2 > ND4 > ND4L > ND1 > ND3 > APT6 > CYTB > COX3 > COX2 > COX1 . We reconstructed the phylogenetic relationships of Triozidae based on 16 triozid mitochondrial genomes (thirteen ingroups and three outgroups) using the maximum likelihood (ML) and Bayesian inference (BI) approaches. The phylogenetic analysis of the 16 Triozidae mitochondrial genomes showed that Egeirotrioza was closely related to Leptynoptera . (4) Conclusions: We have identified 13 PCGs, 22 tRNAs, 2 rRNAs, and 1 control region (CR) of all newly sequenced mitochondrial genomes, which were the mitochondrial gene type in animals. The results of this study provide valuable genomic information for the study of psyllid species.

Cardiovascular diseases (CVDs) still maintain high morbidity and mortality globally. Helicases, a unique class of enzymes, are extensively implicated in the processes of nucleic acid (NA) metabolism across various organisms. They play a pivotal role in gene expression, inflammatory response, lipid metabolism, and so forth. However, abnormal helicase expression has been associated with immune response, cancer, and intellectual disability in humans. Superfamily II (SFII) is one of the largest and most diverse of the helicase superfamilies. Increasing evidence has implicated SFⅡ helicases in the pathogenesis of multiple CVDs. In this review, we comprehensively review the regulation mechanism of SFⅡ helicases in CVDs including atherosclerosis, myocardial infarction, cardiomyopathies, and heart failure, which will contribute to the investigation of ideal therapeutic targets for CVDs., Competing Interests: The 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., (© 2023 Fang, Wang and Huangfu.)

Aims: Epidemiological evidence for the link of interleukin 1 (IL-1) and its inhibition with cardiovascular diseases (CVDs) remains controversial. We aim to investigate the cardiovascular effects of IL-1 receptor antagonist (IL-1Ra) and underlying mechanisms., Methods: Genetic variants identified from a genome-wide association study involving 30,931 individuals were used as instrumental variables for the serum IL-1Ra concentrations. Genetic associations with CVDs and cardiometabolic risk factors were obtained from international genetic consortia. Inverse-variance weighted method was utilized to derive effect estimates, while supplementary analyses employing various statistical approaches., Results: Genetically determined IL-1Ra level was associated with increased risk of coronary heart disease (CHD; OR, 1.07; 95% CI: 1.03-1.17) and myocardial infarction (OR, 1.13; 95% CI: 1.04-1.21). The main results remained consistent in supplementary analyses. Besides, IL-1Ra was associated with circulating levels of various lipoprotein lipids, apolipoproteins and fasting glucose. Interestingly, observed association pattern with CHD was reversed when adjusting for apolipoprotein B (OR, 0.84; 95%CI: 0.71-0.99) and slightly attenuated on accounting for other cardiometabolic risk factors. Appropriate lifestyle intervention was found to lower IL-1Ra concentration and mitigate the heightened CHD risk it posed., Conclusion: Apolipoprotein B represents the key driver, and a potential target for reversal of the causal link between serum IL-1Ra and increased risk of CHD/MI. The combined therapy involving IL-1 inhibition and lipid-modifying treatment aimed at apolipoprotein B merit further exploration., Competing Interests: The 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 © 2023 Yang, Huangfu, Shen, Su, Zhu, Cui and Yuan.)

Atherosclerosis (AS) is the main cause of cerebrovascular diseases, and macrophages play important roles in atherosclerosis. DExH-Box helicase 9 (DHX9), as a member of DExD/H-box RNA helicase superfamily II, is identified as an autoantigen in the sera of systemic lupus erythematosus patients to trigger inflammation. The aim of this study was to investigate whether DHX9 is involved in AS development, especially in macrophages-mediated-inflammatory responses. We find that DHX9 expression is significantly increased in oxLDL or interferon-γ-treated macrophages and peripheral blood mononuclear cells (PBMCs) from patients with coronary artery disease (CAD). Knockdown of DHX9 inhibits lipid uptake and pro-inflammatory factors expression in macrophages, and ameliorates TNF-α-mediated monocyte adhesion capacity. Furthermore, we find that oxLDL stimulation promotes DHX9 interaction with p65 in macrophages, and further enhances the transcriptional activity of DHX9-p65-RNA Polymerase II complex to produce inflammatory factors. Moreover, using ApoE -/- mice fed with western diet to establish AS model, we find that knockdown of DHX9 mediated by adeno-associated virus-Sh-DHX9 through tail vein injection evidently alleviates AS progression in vivo. Finally, we also find that knockdown of DHX9 inhibits p65 activation, inflammatory factors expression, and the transcriptional activity of p65-RNA Polymerase II complex in PBMCs from patients with CAD. Overall, these results indicate that DHX9 promotes AS progression by enhancing inflammation in macrophages, and suggest DHX9 as a potential target for developing therapeutic drug., (© 2023. The Author(s).)

The oriental armyworm, Mythimna separata, is an extremely destructive polyphagous pest with a broad host range that seriously threatens the safety of agricultural production. Here, a high-quality chromosome-level genome was assembled using Illumina, PacBio HiFi long sequencing, and Hi-C scaffolding technologies. The genome size was 706.30 Mb with a contig N50 of 22.08 Mb, and 99.2% of the assembled sequences were anchored to 31 chromosomes. In addition, 20,375 protein-coding genes and 258.68 Mb transposable elements were identified. The chromosome-level genome assembly of M. separata provides a significant genetic resource for future studies of this insect and contributes to the development of management strategies., (© 2023. Springer Nature Limited.)

Background: Observational studies have reported inconsistent associations between micronutrient levels and the risk of coronary artery disease (CAD) in diabetic patients. We aim to explore the causal association between genetically predicted concentrations of micronutrients (phosphorus, magnesium, selenium, iron, zinc, and copper) and CAD in patients with diabetes., Methods: Single nucleotide polymorphisms (SNPs) connected to serum micronutrient levels were extracted from the corresponding published genome-wide association studies (GWASs). Summary-level statistics for CAD in diabetic patients were obtained from a GWAS of 15,666 patients with diabetes. The primary analysis was carried out with the inverse variance weighted approach, and sensitivity analyses using other statistical methods were further employed to assess the robustness of the results., Results: Genetically predicted selenium level was causally associated with a higher risk of CAD in diabetic patients (odds ratio [OR]: 1.25; 95% confidence interval [CI]: 1.10-1.42; p  = 5.01 × 10 -4 ). While, genetically predicted iron concentrations in patients with diabetes were inversely associated with the risk of CAD (OR: 0.82; 95% CI: 0.75-0.90; p  = 2.16 × 10 -5 ). The association pattern kept robust in most sensitivity analyses. Nominally significant associations were observed for magnesium and copper with the risk of CAD in patients with diabetes. No consistent evidence was found for the causal associations between phosphorus and zinc levels, and the risk of CAD in patients with diabetes., Conclusion: We provide consistent evidence for the causal effect of increased selenium and decreased iron levels on CAD in patients with diabetes, highlighting the necessity of micronutrient monitoring and application in these patients., Competing Interests: The 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 © 2023 Tian, Hu, Ying, Cui and Huangfu.)

Background: Left bundle branch pacemakers (LBBPs) can better maintain ventricular electrical synchronization than traditional right ventricular pacing (RVP). Temporary cardiac pacing (TCP) is needed to ensure the safety of the operation in patients undergoing LBBP. Currently, there are two methods of installing TCP in conventional permanent pacemaker implantation., Hypothesis: To evaluate the safety and efficiency of replacing femoral vein pacing with atrial spiral pacing in the right ventricle for temporary cardiac pacing (TCP) during left bundle branch pacemaker (LBBP) implantation., Method: A total of 179 patients who underwent TCP during LBBP were selected for retrospective analysis from April 2019 to 2021 and divided into two groups: the atrial spiral electrode group (n = 76) and the femoral vein electrode group (n = 103). The following were observed: operation time; radiation dose; radiation time; operation expenses; hospitalization time; pacemaker parameters immediately after the operation and at 1 week, 1 month, 3 months, and 6 months after the operation; operation complications and femoral vein puncture point complications were observed in the two groups., Results: Compared to the femoral vein electrode group, the atrial electrode group had significantly lower operation times ([116.86 ± 24.63] versus [128.94 ± 25.27] min, p < 0.05), radiation doses ([805.07 ± 132.94] versus [846.42 ± 87.37] mgy, p < 0.05), and decreased risk of a displaced or dislodged temporary pacing electrode during the operation ([0.00%] versus [4.85%], p < 0.05). The atrial electrode group did not have significant operation costs or material costs associated with femoral vein temporary pacing electrode implantation. In addition, the atrial electrode group did not have an increased risk of pacemaker-related infections, and the parameters of the pacemaker were unaffected. However, some puncture point complications appeared in the femoral vein electrode group (8 cases of local subcutaneous hematoma, 3 cases of pseudoaneurysms, 3 cases of arteriovenous fistula)., Conclusion: The replacement of the femoral vein pacing electrode with an atrial spiral pacing electrode in the right ventricle for TCP during LBBP implantation was safe and effective., (© 2023 The Authors. Clinical Cardiology published by Wiley Periodicals, LLC.)

Background and Aims: The association between sleep traits and coronary artery disease (CAD) in patients with diabetes has been reported in previous observational studies. However, whether these potential relationships are causal remains unclear. We aim to assess the causal relationship between sleep traits and CAD in diabetic., Methods: Genetic instrumental variables associated with five sleep-related traits (insomnia, sleep duration, ease of getting up, morningness and snoring) were extracted from corresponding genome-wide association studies (GWAS). The associations of genetic variants with CAD were based on 15,666 individuals with diabetes (3,968 CAD cases and 11,696 controls). The primary analysis was derived using the inverse variance weighting method. Further sensitivity analysis was conducted to confirm the robustness and consistency of the main results., Results: Genetic liability to insomnia was significantly related to the increased risk of CAD in individuals with diabetes [odds ratio (OR): 1.163; 95% CI: 1.072-1.254; p  = 0.001]. Suggestive evidence was found for the borderline associations between both sleep duration (OR: 0.629; 95% CI: 0.380-1.042, p  = 0.072) and snoring (OR: 1.010, 95% CI: 1.000-1.020, p  = 0.050) with CAD risk. However, no consistent evidence was found for the association between ease of getting up and morningness with the risk of CAD in diabetic. Similar results can be verified in most sensitivity analyses., Conclusions: We provide consistent evidence for the causal effect of insomnia on the increased risk of CAD in individuals with diabetes. The management of sleep health should be emphasized to prevent CAD in diabetic patients., Competing Interests: The 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., (© 2023 Tian, Ma, Shen, Hu, Cui and Huangfu.)

Background: Observational studies have indicated that psychosocial factors contribute to hypertension; however, the causality of these associations remains unclear due to reverse causality and confounders. We aim to assess the causal associations of mental health disorders with hypertension., Methods: Instrumental variables of anxiety disorder, attention deficit/hyperactivity disorder, autism spectrum disorder, depression, obsessive-compulsive disorder, post-traumatic stress disorder, schizophrenia, and subjective well-being measure were obtained from the corresponding largest genome-wide association studies. Summary statistics for the association of essential hypertension were obtained from the FinnGen Study (42,857 cases and 162,837 controls) and UK Biobank cohort (54,358 cases and 408,652 controls). The multiplicative random-effects inverse-variance weighted method was utilized as the primary analysis and three other statistical methods were conducted in the supplementary analyses. The results were combined using the fixed-effects method., Results: In the pooled analyses, genetic liability to depression was associated with higher risk of hypertension (odds ratio [OR], 1.25; 95% confidence interval [CI], 1.17-1.35; p  < 0.001). Besides, a suggestive association was found between genetically predicted higher weighted neuroticism sum-score and increased risk of hypertension (OR, 1.16; 95% CI, 1.02-1.33; p  < 0.05). No associations were found for other mental health disorders. Sensitivity analyses revealed consistent evidence as the main results., Conclusion: We provide consistent evidence for the causal effect of genetic liability to depression on hypertension, which highlights the importance of blood pressure measurement and monitoring in patients with depression., Competing Interests: The 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 © 2023 Huangfu, Lu, Ma, Hu, Cui and Yang.)

Introduction: Reproductive polymorphism and symbiotic bacteria are commonly observed in aphids, but their interaction remains largely unclear. In polymorphic aphid species ( Aphis gossypii ), offspring of parthenogenetic females (PFs) develops into sexuparae which produces gynoparae and males successively. Gynoparae further produces sexual females (SFs), and these sexual females mate with males to produce offspring., Methods: In this study, we investigated the dynamic changes of symbiotic bacteria during the above-mentioned five reproductive morph switch in A. gossypii via 16S rRNA sequencing technology., Results: The results showed that species richness and community diversity of symbiotic bacteria in males were the highest. Proteobacteria was absolutely dominant bacterial phylum (with relative abundance of more than 90%) in the five reproductive morphs of A. gossypii , and Buchnera was absolutely dominant genus (with relative abundance of >90%), followed by Rhodococcus, Pseudomonas, and Pantoea . Male-killing symbiont Arsenophonus presented the highest relative abundance in gynoparae, a specific morph whose offsprings were exclusively sexual females. Both principal component analysis (PCA) and clustering analysis showed trans-generation similarity in microbial community structure between sexuparae and sexual females, between PFs and gynoparae. PICRUSt 2 analysis showed that symbiotic bacteria in the five reproductive morphs were mainly enriched in metabolic pathways., Discussion: Reproductive morph switch induced by environmental changes might be associated with bacterial community variation and sexual polymorphism of aphids. This study provides a new perspective for further deciphering the interactions between microbes and reproductive polymorphism in host aphids., Competing Interests: The 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 © 2023 Chen, Luo, Zhu, Wang, Zhang, Li, Gao, Niu, Huangfu, Ma, Ji and Cui.)

The insulin receptor substrate (IRS), as the core cytoplasmic adapter protein in the insulin/insulin-like signaling (IIS) pathway, is an important mediator of cellular signaling. However, it is still unknown how IRS crosstalk with hormone signaling regulates insect growth, development, and reproduction. In this study, we demonstrated that knockdown of IRS1 significantly inhibited oogenesis, vitellogenesis, and the development of nurse cells and follicular epithelial cells. In addition, qRT-PCR results showed that FOXO transcription factors significantly responded to silencing of the IRS1 gene. However, IRS1 silencing had no significant effect on the expression of juvenile hormone/20-hydroxyecdysone (JH/20E)-signaling genes, JH synthesis, and degradation enzyme-related genes and the JH/20E titers. Our results suggested that the IIS pathway regulated ovarian development and Vg production through FOXO , independent of JH and 20E signaling pathways. This study revealed the reproductive regulation mechanism in Propylea japonica , which provides a theoretical basis for large-scale expansion of P. japonica as an environment-friendly biological control strategy.

Background and Aims: Observational studies have indicated that sedentary behavior is associated with myocardial infarction (MI), heart failure (HF), and atrial fibrillation (AF). Nevertheless, whether these associations are causal remain controversial, due to confounding factors (e.g., physical activity) and reverse causality., Methods and Results: Instrumental variables were obtained from the largest genome-wide association studies of sedentary behavior (408,815 individuals) to date. We obtained summary statistics of MI from the CARDIoGRAMplusC4D consortium (171,875 individuals), HF from the HERMES Consortium (977,323 individuals), and AF from the Atrial Fibrillation Consortium (588,190 individuals). The inverse-variance weighted method was applied to obtain Mendelian randomization (MR) estimates, and other statistical methods were conducted in the sensitivity analyses. The main analyses were repeated using data from the FinnGen study. Multivariable MR analysis and mediation analysis were performed to evaluate the role of physical activity and other confounders. Genetically determined television watching was associated with MI (odds ratio [OR], 1.38; 95% CI, 1.19-1.59; p = 1.9 × 10 -5 ) and HF (OR, 1.23; 95%CI, 1.09-1.38; p = 7.0 × 10 -4 ) but not AF. The main results kept robust in most sensitivity analyses. The effect of sedentary behavior on MI and HF was partly mediated by body mass index (BMI). No consistent evidence was found for the causal effect of computer use and driving on MI, HF, or AF., Conclusions: Genetic liability to prolonged television watching is associated with higher risks of MI and HF. Interventions for reducing television watching time, such as public education and awareness campaigns, should be further investigated., Competing Interests: Declaration of competing interest The 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 © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.)

Background: Abdominal aortic aneurysm (AAA) is a fatal disease characterized by high morbidity and mortality in old population. Globally, effective drugs for AAA are still limited. Si-Miao-Yong-An decoction (SMYAD), a traditional Chinese medicine (TCM) formula with a high medical value, was reported to be successfully used in an old AAA patient. Thus, we reason that SMYAD may serve as a potential anti-AAA regime., Objective: The exact effects and detailed mechanisms of SMYAD on AAA were explored by using the experimental study and bioinformatics analysis., Methods: Firstly, C57BL/6N mice induced by Bap and Ang II were utilized to reproduce the AAA model, and the effects of SMYAD were systematically assessed according to histology, immunohistochemistry, and enzyme-linked immunosorbent assay (ELISA). Then, network pharmacology was applied to identify the biological processes, pathways, and hub targets of SMYAD against AAA; moreover, molecular docking was utilized to identify the binding ability and action targets., Results: In an animal experiment, SMYAD was found to effectively alleviate the degree of pathological expansion of abdominal aorta and reduce the incidence of Bap/Ang II-induced AAA, along with reducing the damage to elastic lamella, attenuating infiltration of macrophage, and lowering the circulating IL-6 level corresponding to the animal study, and network pharmacology revealed the detailed mechanisms of SMYAD on AAA that were related to pathways of inflammatory response, defense response, apoptotic, cell migration and adhesion, and reactive oxygen species metabolic process. Then, seven targets, IL-6, TNF, HSP90AA1, RELA, PTGS2, ESR1, and MMP9, were identified as hub targets of SMYAD against AAA. Furthermore, molecular docking verification revealed that the active compounds of SMYAD had good binding ability and clear binding site with core targets related to AAA formation., Conclusion: SMYAD can suppress AAA development through multicompound, multitarget, and multipathway, which provides a research direction for further study., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2022 Zhenyu Xu et al.)

Fruit flies in the family Tephritidae are well known as economically important pests of edible fruits and can often cause serious damage and losses to both agriculture and the economy. One of the common parasitoids of fruit flies, Aceratoneuromyia indica (Silvestri), has been used in biological programs. However, the biocontrol utilities of parasitoids are impeded by the difficulties of proper identification. Species of the genus Aceratoneuromyia Girault (Hymenoptera: Eulophidae), usually developed as parasitoids of fruit flies, are studied here. Trjapitzinichus Kostjukov and Kosheleva is proposed as a new synonym under Aceratoneuromyia. Three new species of Aceratoneuromyia, A. bilinis Huangfu and Cao sp. nov., A. carinata Cao and Zhu sp. nov., and A. trilinus Cao and Zhu sp. nov., are described and illustrated from China. Aceratoneuromyia indica is also treated here with diagnosis and illustrations. DNA barcodes of A. bilinis and A. indica and a key to the world species of Aceratoneuromyia are provided. This study provided important identification information of parasitoids with morphology and molecular evidence, which is useful for imperative needs regarding the identity of parasitoids attacking fruit flies.

Background: Atherosclerosis (AS) is the main cause of cerebrovascular diseases, and macrophages act important roles during the AS pathological process through regulating inflammation. Modification of the novel N(6)-methyladenine (m6A) RNA is reported to be associated with AS, but its role in AS is largely unknown. The aim of this study was to investigate the role and mechanism of m6A modification in inflammation triggered by oxidized low-density lipoprotein (oxLDL) in macrophages during AS., Methods: RAW264.7 macrophage cells were stimulated with 40 μg/ml ox-LDL, Dot blot, Immunoprecipitation, western blot, Rip and chip experiments were used in our study., Results: We found oxLDL stimulation significantly promoted m6A modification level of mRNA in macrophages and knockdown of Methyltransferase-Like Protein 3 (Mettl3) inhibited oxLDL-induced m6A modification and inflammatory response. Mettl3 promoted oxLDL-induced inflammatory response in macrophages through regulating m6A modification of Signal transducer and activator of transcription 1 (STAT1) mRNA, thereby affecting STAT1 expression and activation. Moreover, oxLDL stimulation enhanced the interaction between Mettl3 and STAT1 protein, promoting STAT1 transcriptional regulation of inflammatory factor expression in macrophages eventually., Conclusions: These results indicate that Mettl3 promotes oxLDL-triggered inflammation through interacting with STAT1 protein and mRNA in RAW264.7 macrophages, suggesting that Mettl3 may be as a potential target for the clinical treatment of AS., (© 2021 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC.)

Objective: Atherosclerosis (AS), characterized by cholesterol overloaded-macrophages accumulation and plaque formation in blood vessels, is the major cause of cardiovascular disease. Transactive response DNA-binding protein∼43 kDa (TDP43) has recently been identified as an independent driver of neurodegenerative diseases through triggering inflammatory response. This study investigated whether TDP43 is involved in AS development, especially in macrophages-mediated-foam cell formation and inflammatory responses., Methods: Transactive response DNA-binding protein∼43 kDa expressions in oxidized low-density lipoprotein (oxLDL)-treated macrophages and peripheral blood mononuclear cells (PBMCs) from patients with coronary artery disease (CAD) were detected by real time-polymerase chain reaction (RT-PCR), Western blot, and immunofluorescence. Gene gain or loss of function was used to investigate the effects of TDP43 on macrophages-mediated lipid untake and inflammation with ELISA, protein immunoprecipitation, RT-PCR, Western blot, and immunofluorescence. Macrophage TDP43 specific knockout mice with ApoE -/- background were fed with western diet for 12 weeks to establish AS model, and used to explore the role of TDP43 on AS progression., Results: Transactive response DNA-binding protein∼43 kDa expression increases in oxLDL-treated macrophages and PBMCs from patients with CAD. Furthermore, we find that TDP43 promotes activation of NF-κB to increase inflammatory factor expression in macrophages through triggering mitochondrial DNA release to activate cGAS-STING signaling. Moreover, TDP43 strengthens lipid uptake of macrophages through regulating β-catenin and PPAR-γ complex to promote scavenger receptor gene CD36 transcription. Finally, using macrophage TDP43 specific knockout mice with ApoE -/- background fed with western diet for 12 weeks to establish AS model, we find that specific knockout of TDP43 in macrophages obviously alleviates western diet-induced AS progression in mice., Conclusions: Transactive response DNA-binding protein∼43 kDa exacerbates atherosclerosis progression by promoting inflammation and lipid uptake of macrophages, suggesting TDP43 as a potential target for developing atherosclerotic drug., Competing Interests: The 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 © 2021 Huangfu, Wang, Xu, Zheng, Tao, Li, Hu and Chen.)

Propylea japonica has been regarded as one of the most remarkable natural enemies against aphid in China. However, the mechanism of juvenile hormone (JH) regulation of reproduction in P. japonica is still unclear. In this study, we investigated the JH titers of P. japonica and the development of the ovaries. We selected the six different developmental stages of ladybeetle females for transcriptome sequencing. We identified 583 genes involved in insect reproduction regulation, including 107 insect hormone synthesis signaling pathway-related genes and 476 nutrition-sensing signaling pathway-related genes. Transcriptome analysis indicated that a large number JH synthesis- and metabolism-related enzyme genes and some potential nutrient signal sensing- and transduction-related genes were significantly differentially expressed during P. japonica development. We investigated the effects of Met gene silencing on the reproduction of female adults and found that the ovarian maturation, vitellogenesis, and follicular epithelium development in the dsMet treatment group were significantly inhibited., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Myocardium functions as an immune organ, and myocardial ischemia-reperfusion (I/R) is known to initiate myocardial innate immune response to induce myocardial injury. However, the mechanisms underlying interferon-β (IFN-β)-mediated myocardial injury during I/R and whether long non-coding RNAs (lncRNAs) are involved in IFN-β-mediated myocardial injury remain unknown. This study identified that I/R significantly induced IFN-β expression in induced pluripotent stem cell-derived cardiomyocytes, and IFN-β further enhanced I/R-induced myocardial apoptosis. Furthermore, it was demonstrated that the lncRNA BRAF-activated non-coding RNA (BANCR) was highly expressed in cardiomyocytes, and BANCR-knockdown suppressed signal transducer and activator of transcription 1 (STAT1) phosphorylation and IFN-β-induced cardiomyocyte apoptosis. Furthermore, it was identified that BANCR specifically interacted with STAT1 to promote IFN-β-STAT1 signaling and enhanced the expression of pro-apoptotic interferon stimulated genes. Overall, the present study reports that lncRNA BANCR promotes IFN-β-mediated cardiomyocyte apoptosis following I/R injury by interacting with STAT1, suggesting lncRNA BANCR is involved in IFN-β-induced cardiomyocyte apoptosis., Competing Interests: None., (IJCEP Copyright © 2020.)

M1/M2 macrophages polarization play important roles in regulating tissue homeostasis. Recently, RNA-binding motif 4 (RBM4) has been reported to modulate the proliferation and expression of inflammatory factors in HeLa cells. However, whether RBM4 is involved in regulating macrophage polarization and inflammatory factor expression are still unknown. In this study, RAW264.7, a mouse macrophage cell line, were stimulated with interferon γ (IFN-γ) or interleukin-4 (IL-4) to induce M1/M2 macrophages polarization. We found that IFN-γ, but not IL-4, stimulation decreased RBM4 expression in macrophages, and RBM4 overexpression inhibits IFN-γ-induced M1 macrophage polarization. Furthermore, RNA-Sequencing, protein immunoprecipitation accompanied with mass spectrometry, and extracellular acidification rate analysis showed that RBM4 suppresses IFN-γ-induced M1 macrophage polarization though inhibiting glycolysis. Moreover, RBM4 knockdown promoted IFN-γ-induced signal transducer and activator of transcription 1 (STAT1) activation via increasing STAT1 mRNA stability, leading to the increase of glycolysis-related gene transcripts regulated by STAT1. Finally, we find that RBM4 interacts with YTH N6-methyladenosine RNA binding protein 2 (YTHDF2) to degrade m6A modified STAT1 mRNA, thereby regulating glycolysis and M1 macrophage polarization. Collectively, the current study firstly reports that RBM4 regulates M1 macrophages polarization through targeting STAT1-mediated glycolysis and shows that RBM4 is a possible candidate for regulating macrophage M1 polarization and inflammatory responses., Competing Interests: Declaration of Competing Interest There are no conflicts of interest to disclose for all authors., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

Backgrounds: Clopidogrel resistance (CR), which was manifested as the failure of platelet inhibition in clopidogrel treatment, was likely to lead to cardiovascular events. Our study was aimed to explore the contribution of DNA methylation in glucokinase (GCK) to the CR risk., Methods: Among 36 CR and 36 non-CR acute coronary syndrome (ACS) patients, the platelet functions were evaluated by VerifyNow P2Y12 assay (turbidimetric-based optical detection) and DNA methylation levels on two fragments of the CGI from the GCK were investigated through bisulfite pyrosequencing methods. In addition, the GCK mRNA expression was analyzed via quantitative real-time PCR. Lastly, the logistic regression was employed to test the interaction between GCK methylation and nongenetic variables in CR patients., Results: Subunit analysis showed that in male patients without DM but suffering from dyslipidemia, the increased methylation of cg18492943 indicated a risk of poor clopidogrel response (male, NCR vs CR(%): 84.86 ± 6.29 vs 88.16 ± 4.32, P = .032; without DM, NCR vs CR (%): 84.66 ± 6.18 vs 88.16 ± 4.17, P = .029; and dyslipidemia, NCR vs CR (%): 83.81 ± 6.96 vs 88.39 ± 4.74, P = .042).In addition, GCK mRNA expression was reduced in CR patients without DM. Moreover, regression analysis indicated that the values of platelet distribution width (PDW), total cholesterol (TC), and uric acid (UA) were correlated with the incidence of CR, and hypertension lowered the CR risk., Conclusions: A higher methylation of cg18492943 in GCK gene would lower the expression of GCK mRNA, which might contribute to CR in patients without DM. Meanwhile, PDW and TC might be risk factors in CR., (© 2019 The Authors. Journal of Clinical Laboratory Analysis Published by Wiley Periodicals, Inc.)

Oxidative stress serves important roles in cardiac injury during the process of ischemia/reperfusion (I/R). Y‑box protein 1 (YB1), a member of the highly conserved Y‑box protein family, is closely associated with inflammation and stress responses by regulating gene transcription, RNA splicing and mRNA translation. However, the roles of YB1 in oxidative stress‑induced myocardial‑I/R (M‑I/R) injury are unknown. The aim of the present study was to examine the effects of YB1 on H2O2‑induced cardiomyocyte injury and its underlying mechanism. The results demonstrated that YB1 expression was upregulated during H2O2‑induced myocardial injury. YB1 knockdown through transfection of small interfering RNA significantly aggravated cardiac cell apoptosis. Furthermore, YB1 knockdown significantly reversed the H2O2‑mediated increase in phosphorylated signal transducer and activator of transcription (STAT)3, but did not affect the phosphorylation of P38, extracellular signal‑regulated kinases 1/2, c‑Jun N‑terminal kinases, P65, Janus kinase 1 and 2 or STAT1. Moreover, protein co‑immunoprecipitation and RNA‑binding protein immunoprecipitation assays revealed that YB1 interacted with protein inhibitor of activated STAT 3 (PIAS3) mRNA but not its translated protein. YB1 overexpression may have promoted PIAS3 mRNA decay, decreasing PIAS3 protein levels, and therefore increased the levels of phosphorylated STAT3. Finally, YB1 knockdown, mediated by a lentivirus carrying YB1 targeted short hairpin RNA, significantly decreased left ventricle percentage fractional shortening and ejection fraction values, while increasing the infarct sizes in a rat model of M‑I/R injury. These results demonstrated for the first time (to the best of our knowledge) that YB1 may protect cardiac myocytes against H2O2 or M‑I/R‑induced injury by binding to PIAS3 mRNA and resulting in the phosphorylation of STAT3.

Purine metabolism in the circulatory system yields uric acid as its final oxidation product, which is believed to be linked to the development of gout and kidney stones. Hyperuricemia is closely correlated with cardiovascular disease, metabolic syndrome, and chronic kidney disease, as attested by the epidemiological and empirical research. In this review, we summarize the recent knowledge about hyperuricemia, with a special focus on its physiology, epidemiology, and correlation with cardiovascular disease. This review also discusses the possible positive effects of treatment to reduce urate levels in patients with cardiovascular disease and hyperuricemia, which may lead to an improved clinical treatment plan., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Oxidized low density lipoprotein (ox-LDL)-induced macrophage apoptosis contributes to the formation of atherosclerosis. Metformin, an antidiabetic drug, has been reported to attenuate lipid accumulation in macrophages. In this study, the effects of metformin on ox-LDL-induced macrophage apoptosis were investigated and the mechanisms involved in this process were examined. By performing flow cytometry analysis, it was demonstrated that metformin inhibited ox-LDL-induced macrophage apoptosis. Increased expression of endoplasmic reticulum (ER) stress marker proteins, including C/EBP-homologous protein, eukaryotic translation initiation factor 2A, and glucose-regulated protein 78 kDa, induced by ox-LDL was also reversed by metformin. Furthermore, ox-LDL-induced cytochrome c (cyto-c) release and mitochondrial membrane potential loss were inhibited by metformin. As lipid uptake in macrophages contributed to ER stress, cyto-c release and mitochondrial membrane potential loss, the mechanisms involved in metformin-inhibited macrophage lipid uptake were investigated. Expression of scavenger receptors, including scavenger receptor A, cluster of differentiation 36 and lectin-type oxidized LDL receptor 1 was examined in the presence or absence of metformin with ox-LDL treatment. Additionally, the upstream regulatory mechanism of scavenger receptors by metformin was also analyzed. In conclusion, metformin protects against ox-LDL-induced macrophage apoptosis and inhibits macrophage lipid uptake.

The expression of scavenger receptors in macrophages regulating lipid uptake plays an important role in foam cell formation and the subsequent atherosclerotic plaque formation. Long non-coding RNA MALAT1 is abundantly expressed in THP-1-derived macrophages, and oxidized low-density lipoprotein promotes its transcription by qRT-PCR and RNA FISH detection. Through chemical inhibitor treatments and by performing a dual luciferase reporter analysis, we found that oxLDL induces MALAT1 transcription through the NF-κB pathway. The knockdown of MALAT1 using siRNA transfection affects lipid uptake in macrophages. To understand the details, we checked the scavenger receptors, which mainly control lipid uptake, and found that MALAT1 knockdown decreased CD36 expression. Additionally, we also incubated macrophages with actinomycin D, combined with a dual luciferase reporter analysis, and we found that MALAT1 influenced CD36 expression at the transcription level. We aim to investigate the detailed mechanism by which MALAT1 promotes CD36 transcription, and thus, we designed and synthesized biotin-TEG labeled oligonucleotides to precipitate the MALAT1 RNA-DNA-protein complex in vivo. Combined with SDS-PAGE electrophoresis and a subsequent mass spectra analysis, β-catenin, a transcription factor that promotes CD36 transcription, was found in the complex. By performing R-IPs, we validated that β-catenin was bound to MALAT1 under the oxLDL treatment. In addition, using VAX939, a chemical inhibitor of β-catenin, MALAT1 was demonstrated to promote CD36 transcription partly via β-catenin. We also performed chips to detect whether MALAT1 affects β-catenin accumulation in the binding sites of the CD36 promoter and found that MALAT1 knockdown decreases β-catenin binding to the CD36 promoter and vice versa. In conclusion, oxLDL induced MALAT1 transcription and MALAT1 recruits β-catenin to binding sites on the CD36 promoter to induce CD36 expression, which enhances lipid uptake in macrophages., (Copyright © 2017 Elsevier Inc. All rights reserved.)