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Abstract Background Existing researches have predominantly focused on the implications of dynamic alterations in the triglyceride-glucose (TyG) index and traditional obesity measures for cardiovascular disease (CVD) risk. However, the application of the weight-adjusted waist index (WWI), which incorporates the dynamically changing body composition factors of weight and waist circumference, alongside the TyG index for predicting CVD risk, remains unexplored. This study explores the relationships between baseline TyG-WWI index and its dynamic changes with CVD risk. Methods Subjects were drawn from the China Health and Retirement Longitudinal Study. Logistic regression analyses were conducted to determine the relationships between baseline and longitudinal changes in the TyG-WWI index and CVD risk, quantified through odds ratios (ORs) and 95% confidence intervals (CIs). The robustness of results was confirmed via subgroup analyses and E-values. Additionally, restricted cubic spline and quartile-based methods evaluated the relationships between baseline and cumulative TyG-WWI indices and CVD risk. Results Over two survey waves, 613 CVD events were recorded. Analysis using adjusted multivariable models demonstrated a significant relationship between the cumulative TyG-WWI index and increased CVD risk, with an adjusted OR (95% CI) of 1.005 (1.000, 1.009). Class 2 of the TyG-WWI index change showed greater risk of CVD compared to Class 1, with ORs of 1.270 (1.008, 1.605). However, no significant connection was observed between the baseline TyG-WWI index and CVD risk (OR = 1.007, 95% CI: 0.996, 1.019). These findings were corroborated through extensive sensitivity analyses. Graphical Abstract

Abstract Background Renal Denervation (RDN) is a novel non-pharmacological technique to treat hypertension. This technique lowers blood pressure by blocking the sympathetic nerve fibers around the renal artery, then causing a decrease in system sympathetic nerve excitability. This study aimed to visualize and analyze research hotspots and development trends in the field of RDN for hypertension through bibliometric analysis. Methods In total, 1479 studies were retrieved on the Web of Science Core Collection (WoSCC) database from 2004 to 2023. Using CiteSpace (6.2.R4) and VOSviewer (1.6.18), visualization maps were generated by relevant literature in the field of RDN for hypertension to demonstrate the research status and frontiers. Results The number of publications was found to be generally increasing. Europe and the United States were the first countries to carry out research on different techniques and related RDN clinical trials. The efficacy and safety of RDN have been repeatedly verified and gained increasing attention. The study involves multiple disciplines, including the cardiovascular system, peripheral vascular disease, and physiological pathology, among others. Research hotspots focus on elucidating the mechanism of RDN in the treatment of hypertension and the advantages of RDN in appliance therapy. Additionally, the research frontiers include improvement of RDN instruments and techniques, as well as exploration of the therapeutic effects of RDN in diseases with increased sympathetic nerve activity. Conclusion The research hotspots and frontiers reflect the status and development trend of RDN in hypertension. In the future, it is necessary to strengthen international collaboration and cooperation, conduct long-term clinical studies with a large sample size, and continuously improve RDN technology and devices. These measures will provide new options for more patients with hypertension, thereby improving their quality of life.

A growing body of research indicates the promising potential of vaccines in both preventing and treating atherosclerosis (AS). To gain a comprehensive understanding of the current research landscape and emerging trends in this field, this study conducted a bibliometric analysis of publications on AS vaccines using the Web of Science Core Collection (WoSCC) database, based on the “bibliometric” R package and VOSviewer software. From 1991 to 2024, a total of 462 publications were identified in the WoSCC. The United States appeared as the leading contributor in terms of both total publications and citations. The Vaccine journal exhibited the highest publications output. Nilsson J from the Lund University in Sweden was the author with the most published articles, total citations and Hirsch index (H-index). Keywords analysis and thematic maps analysis revealed the passive immunotherapy (AS protective antibodies vaccines) was a hot mature theme, the active immunotherapy (AS antigens vaccines) was an emerging and booming theme, while the efficacy and safety of AS vaccines was a niche and well-developed theme. These findings offered valuable insights into the AS vaccination and provided guidance for future research in this domain.

Cardiac remodeling is a shared pathological change in most cardiovascular diseases. Encompassing both adaptive physiological responses and decompensated pathological changes. Anatomically, atrial remodeling is primarily caused by atrial fibrillation, whereas ventricular remodeling is typically induced by myocardial infarction, hypertension, or cardiomyopathy. Mitochondria, the powerhouse of cardiomyocytes, collaborate with other organelles such as the endoplasmic reticulum to control a variety of pathophysiological processes such as calcium signaling, lipid transfer, mitochondrial dynamics, biogenesis, and mitophagy. This mechanism is proven to be essential for cardiac remodeling. Post-translational modifications can regulate intracellular signaling pathways, gene expression, and cellular stress responses in cardiac cells by modulating protein function, stability, and interactions, consequently shaping the myocardial response to injury and stress. These modifications, in particular phosphorylation, acetylation, and ubiquitination, are essential for the regulation of the complex molecular pathways that underlie cardiac remodeling. This review provides a comprehensive overview of the crosstalk between the endoplasmic reticulum and mitochondria during cardiac remodeling, focusing on the regulatory effects of various post-translational modifications on these interactions.

BackgroundVaried intake of dietary minerals critically affects cardiovascular health. This study examines the associations of nine dietary minerals intake with all-cause mortality in atherosclerotic cardiovascular diseases (ASCVDs).MethodsThis study analyzed 4,125 individuals with ASCVD from the National Health and Nutrition Examination Survey, employing Kaplan–Meier survival analyses, weighted Cox models, and restricted cubic splines to assess linear and nonlinear relationships between dietary minerals intake and all-cause mortality. Associations across different body mass index (BMI) categories were also evaluated separately.ResultsOver 6.25 years of median follow-up, 1,582 deaths were documented. Adjusted for potential covariates, results show a negative linear correlation between dietary magnesium intake and all-cause mortality (p for trend

Background: In the study of atrial fibrillation (AF), a prevalent cardiac arrhythmia, the utilization of artificial intelligence (AI) in diagnostic and therapeutic strategies holds the potential to address existing limitations. This research employs bibliometrics to objectively investigate research hotspots, development trends, and existing issues in the application of AI within the AF field, aiming to provide targeted recommendations for relevant researchers. Methods: Relevant publications on the application of AI in AF field were retrieved from the Web of Science Core Collection (WoSCC) database from 2013 to 2023. The bibliometric analysis was conducted by the R (4.2.2) “bibliometrix” package and VOSviewer(1.6.19). Results: Analysis of 912 publications reveals that the field of AI in AF is currently experiencing rapid development. The United States, China, and the United Kingdom have made outstanding contributions to this field. Acharya UR is a notable contributor and pioneer in the area. The following topics have been elucidated: AI's application in managing the risk of AF complications is a hot mature topic; AI-electrocardiograph for AF diagnosis and AI-assisted catheter ablation surgery are the emerging and booming topics; smart wearables for real-time AF monitoring and AI for individualized AF medication are niche and well-developed topics. Conclusion: This study offers comprehensive analysis of the origin, current status, and future trends of AI applications in AF, aiming to advance the development of the field.

Summary: Premature ovarian failure (POF) is a complex and heterogeneous disease that causes infertility and subfertility. However, the molecular mechanism of POF has not been fully elucidated. Here, we show that the loss of adenylyl cyclase III (Adcy3) in female mice leads to POF and a shortened reproductive lifespan. We found that Adcy3 is abundantly expressed in mouse oocytes. Adcy3 knockout mice exhibited the excessive activation of primordial follicles, progressive follicle loss, follicular atresia, and ultimately POF. Mechanistically, we found that mitochondrial oxidative stress in oocytes significantly increased with age in Adcy3-deficient mice and was accompanied by oocyte apoptosis and defective folliculogenesis. In contrast, compared with wild-type female mice, humanized ADCY3 knock-in female mice exhibited improved fertility with age. Collectively, these results reveal that the previously unrecognized Adcy3 signaling pathway is tightly linked to female ovarian aging, providing potential pharmaceutical targets for preventing and treating POF.

BackgroundPrevious studies have indicated a strong link between blood metabolites and hypertension, however the causality of metabolites and hypertension is unknown.MethodsTwo-sample Mendelian randomization (MR) analysis was performed to assess the causal relationship between 486 blood metabolites and essential hypertension (EHT). Blood metabolite GWAS data was utilized as the exposure, with EHT GWAS data as the outcome. To further verify the results, another different source of EHT GWAS data was repeatedly analyzed. The major MR analytic approach used to determine causality was inverse variance weighted (IVW), with MR-Egger, Weighted Median, and MR-PRESSO models serving as supplements. We used the Cochran Q test to examine heterogeneity. Horizontal pleiotropy was examined using MR-Egger intercept and MR-PRESSO global test. The MR Steiger test confirmed the causal relationship between blood metabolites and EHT.ResultsIn this study, nine blood metabolites associated with EHT were preliminarily identified by MR analysis, including four known metabolites (N-acetylornithine, X-12510–2-aminooctanoic acid, creatine, hexadecanedioate) and five unknown metabolites. Then another source of EHT GWAS data was repeatedly analyzed for further verification, and two overlapped metabolites (N-acetylornithine, X-12510-2-aminooctanoic acid) were found. There was a negative correlation between N-acetylornithine and EHT (OR = 0.987, 95% CI = 0.980–0.993, P = 1.01 × 10−4), Cochran's Q test suggested there was no heterogeneity (Q = 31.7586, P = 0.1331), MR-Egger intercept and MR-PRESSO global test suggested there was no horizontal pleiotropy (P > 0.05), Leave-one-out analysis indicated that no single single-nucleotide polymorphism (SNP) had a significant effect on the results, and MR Steiger test confirmed that the direction of causality was correct (P

Abstract Background Atrial fibrillation (AF) is a very common arrhythmia with significant incidence rate and mortality. Several studies have shown a notable correlation between non-alcoholic fatty liver disease (NAFLD) and AF. It has been observed that serum cholinesterase (SChE) levels are elevated in individuals with fatty liver. However, the relationship between the SChE index and AF is still unclear. Therefore, the purpose of this study is to explore the association between the SChE index and the prevalence of AF in patients with hypertension. Method We collected cross-sectional data from January 2018 to April 2021 based on a retrospective study of cardiovascular disease. A total of 748 patients with hypertension were included, of whom 165 had AF. We used logistic regression models to test the relationship between SChE and the prevalence of AF in hypertensive patients. Result In hypertensive patients, the SChE index was significantly associated with AF (OR = 0.723, P

This study aimed to dynamically track the priorities and potential research hotspots in the field of heart failure with sarcopenia. Using CiteSpace, we analyzed the literature on heart failure with sarcopenia from the Web of Science database from 1995 to 2022. The analysis encompassed 507 records, revealing an overall upward trend in annual publication volume. Europe and the United States emerged as the primary regions for publishing, particularly driven by contributions from developed countries such as the United States, Germany, and Italy. Productive institutions included the Charite Universitatsmedizin Berlin, University Medical Center Gottingen, the German Center for Cardiovascular Research (DZHK), Universita Cattolica del Sacro Cuore, and the National Institute on Aging (NIA). Noteworthy academic groups have formed around these institutions; von Haehling S, Anker Stefan D, Springer J, and Doehner W frequently collaborated. The core journals that frequently published articles in this area included Circulation, European Heart Journal, and The Journals of Gerontology Series A-Biological Sciences and Medical Sciences.Based on the keyword analysis, we identified three key research areas. First, the diagnosis and definition of sarcopenia emerged as significant themes. Second, researchers have focused on exploring the mechanisms underlying heart failure with sarcopenia, including inflammation, insulin resistance, and oxidative stress. Finally, treatment strategies, such as physical activity and nutritional support, constitute another critical research theme. Furthermore, potential research hotspots within this field include clinical randomized controlled trials, investigations into inflammatory mechanisms, cardiac rehabilitation, studies on physical activity, androgen receptor modulators, and investigations into clinical outcomes such as cognitive impairment.

Abstract Background One of the most prominent features of living organisms is their circadian rhythm, which governs a wide range of physiological processes and plays a critical role in maintaining optimal health and function in response to daily environmental changes. This work applied bibliometric analysis to explore quantitative and qualitative trends in circadian rhythm in cardiovascular diseases (CVD). It also aims to identify research hotspots and provide fresh suggestions for future research. Methods The Web of Science Core Collection was used to search the data on circadian rhythm in CVD. HistCite, CiteSpace, and VOSviewer were used for bibliometric analysis and visualization. The analysis included the overall distribution of yearly outputs, top nations, active institutions and authors, core journals, co-cited references, and keywords. To assess the quality and efficacy of publications, the total global citation score (TGCS) and total local citation score (TLCS) were calculated. Results There were 2102 papers found to be associated with the circadian rhythm in CVD, with the overall number of publications increasing year after year. The United States had the most research citations and was the most prolific country. Hermida RC, Young ME, and Ayala DE were the top three writers. The three most notable journals on the subject were Chronobiology International, Hypertension Research, and Hypertension. In the early years, the major emphasis of circadian rhythm in CVD was hormones. Inflammation, atherosclerosis, and myocardial infarction were the top developing research hotspots. Conclusion Circadian rhythm in CVD has recently received a lot of interest from the medical field. These topics, namely inflammation, atherosclerosis, and myocardial infarction, are critical areas of investigation for understanding the role of circadian rhythm in CVD. Although they may not be future research priorities, they remain of significant importance. In addition, how to implement these chronotherapy theories in clinical practice will depend on additional clinical trials to get sufficient trustworthy clinical evidence.

ABSTRACTAtherosclerosis (AS) is the main underlying cause of cardiovascular disease, and B cells are considered a key immune cell type to regulate AS. So far, there is no bibliometric study on B cell and AS. This study aims to comprehensively analyze the scientific output about B cell and AS, summarize the literature characteristics, explore research hotspots, and point out emerging trends. We searched the literature from 2003 to 2022 from the Web of Science Core Collection (WoSCC) database. CiteSpace, VOSviewer, and the R package “Bibliometrix” were used for literature analysis and visualization. A total of 1,062 articles and reviews were identified. The number of annual publications generally showed an upward trend. The United States and China were the most productive countries. Medical University of Vienna was the most productive research institution, and Binder Christoph J. was the most productive author, who was also from Medical University of Vienna. “Arteriosclerosis Thrombosis and Vascular Biology” was the most published journal and the most frequently cited journal. The most cited reference was written by Caligiuri G (2002) in “Journal of Clinical Investigation.” The most frequent keywords were “inflammation,” “macrophages,” “cardiovascular disease,” “T cells,” “apoptosis,” “immunity,” “cytokines,” “lymphocytes,” etc. The trend topics were mainly focused on “immune infiltration,” “immunoglobulins,” and “biomarkers.” The complex role of B cell subtypes and a variety of B cell mediators is the main research direction at present. In-depth analysis of B cell-specific targets can provide new ideas and methods for the prevention and treatment of AS.

Background: Tanshinone IIA, derived from Radix Salviae Miltiorrhizae (Salvia miltiorrhiza Bunge), constitutes a significant component of this traditional Chinese medicine. Numerous studies have reported positive outcomes regarding its influence on cardiac function. However, a comprehensive comprehension of the intricate mechanisms responsible for its cardioprotective effects is still lacking.Methods: A rat model of heart failure (HF) induced by acute myocardial infarction (AMI) was established via ligation of the left anterior descending coronary artery. Rats received oral administration of tanshinone IIA (1.5 mg/kg) and captopril (10 mg/kg) for 8 weeks. Cardiac function was assessed through various evaluations. Histological changes in myocardial tissue were observed using staining techniques, including Hematoxylin and Eosin (HE), Masson, and transmission electron microscopy. Tunel staining was used to detect cell apoptosis. Serum levels of NT-pro-BNP, IL-1β, and IL-18 were quantified using enzyme-linked immunosorbent assay (ELISA). Expression levels of TLR4, NF-κB p65, and pyroptosis-related proteins were determined via western blotting (WB). H9C2 cardiomyocytes underwent hypoxia-reoxygenation (H/R) to simulate ischemia-reperfusion (I/R) injury, and cell viability and apoptosis were assessed post treatment with different tanshinone IIA concentrations (0.05 μg/ml, 0.1 μg/ml). ELISA measured IL-1β, IL-18, and LDH expression in the cell supernatant, while WB analysis evaluated TLR4, NF-κB p65, and pyroptosis-related protein levels. NF-κB p65 protein nuclear translocation was observed using laser confocal microscopy.Results: Tanshinone IIA treatment exhibited enhanced cardiac function, mitigated histological cardiac tissue damage, lowered serum levels of NT-pro-BNP, IL-1β, and IL-18, and suppressed myocardial cell apoptosis. Moreover, tanshinone IIA downregulated the expression of TLR4, NF-κB p65, IL-1β, pro-IL-1β, NLRP3, Caspase-1, and GSDMD-N pyroptosis-related proteins in myocardial tissue. Additionally, it bolstered H/R H9C2 cardiomyocyte viability, curbed cardiomyocyte apoptosis, and reduced the levels of TLR4, NF-κB p65, IL-1β, pro-IL-1β, NLRP3, Caspase-1, and GSDMD-N pyroptosis-related proteins in H/R H9C2 cells. Furthermore, it hindered NF-κB p65 protein nuclear translocation.Conclusion: These findings indicate that tanshinone IIA enhances cardiac function and alleviates myocardial injury in HF rats following AMI. Moreover, tanshinone IIA demonstrates potential suppression of cardiomyocyte pyroptosis. These effects likely arise from the inhibition of the TLR4/NF-κB p65 signaling pathway, presenting a promising therapeutic target.

Abstract Background Analyzing disease–disease relationships plays an important role for understanding etiology, disease classification, and drug repositioning. However, as cardiovascular diseases with causative links, the molecular relationship among stable angina pectoris (SAP), ischemic cardiomyopathy (ICM) and chronic heart failure (CHF) is not clear. Methods In this study, by integrating the multi-database data, we constructed paired disease progression modules (PDPMs) to identified relationship among SAP, ICM and CHF based on module reconstruction pairs (MRPs) of K-value calculation (a Euclidean distance optimization by integrating module topology parameters and their weights) methods. Finally, enrichment analysis, literature validation and structural variation (SV) were performed to verify the relationship between the three diseases in PDPMs. Results Total 16 PDPMs were found with K > 0.3777 among SAP, ICM and CHF, in which 6 pairs in SAP–ICM, 5 pairs for both ICM–CHF and SAP–CHF. SAP–ICM was the most closely related by having the smallest average K-value (K = 0.3899) while the maximum is SAP–CHF (K = 0.4006). According to the function of the validation gene, inflammatory response were through each stage of SAP–ICM–CHF, while SAP–ICM was uniquely involved in fibrosis, and genes were related in affecting the upstream of PI3K–Akt signaling pathway. 4 of the 11 genes (FLT1, KDR, ANGPT2 and PGF) in SAP–ICM–CHF related to angiogenesis in HIF-1 signaling pathway. Furthermore, we identified 62.96% SVs were protein deletion in SAP–ICM–CHF, and 53.85% SVs were defined as protein replication in SAP–ICM, while ICM–CHF genes were mainly affected by protein deletion. Conclusion The PDPMs analysis approach combined with genomic structural variation provides a new avenue for determining target associations contributing to disease progression and reveals that inflammation and angiogenesis may be important links among SAP, ICM and CHF progression.

Background Sepsis is an infection-caused systemic inflammatory response syndrome, with relatively high morbidity and fatality rate. Early diagnosis and treatment are vital for prevention and treatment of sepsis. However, there are no simple clinical biomarkers that could rapidly and effectively detecting sepsis. Objective To assess the combined predictive value of toll-like receptor 4 (TLR4) in peripheral blood mononuclear cells and serum procalcitonin (PCT) for sepsis. Methods One hundred and ten sepsis patients (sepsis group) , 113 patients with infection but without sepsis (non-sepsis group) , and 95 healthy individuals (control group) were recruited from Renmin Hospital of Wuhan University from October 2020 to November 2021. Sepsis patients were divided into non-shock subgroup and shock subgroup according to the shock situation. Laboratory indicators, TLR4 in peripheral blood mononuclear cells and serum PCT of three groups were collected and analyzed. The quick Sepsis-related Organ Failure Assessment (qSOFA) score, infectious pathogens, and sites of infection of sepsis and non-sepsis groups were comparatively analyzed. The receiver operating characteristic curve (ROC) and area under the curve (AUC) were used to analyze the diagnostic value of TLR4 mRNA and PCT, alone and in combination, for sepsis. Results The levels of red blood cell (RBC) count, white blood cell (WBC) count, neutrophil count, hemoglobin (Hb) , hematocrit (HCT) , platelet count, alanine aminotransferase (ALT) , aspartate aminotransferase (AST) and direct bilirubin (DBiL) differed significantly across the three groups (P

BackgroundBlood metabolites have been found related to atrial fibrillation (AF), but the causal role is still unclear. Mendel randomization (MR) can give information about the causality between blood metabolites and AF.MethodsTwo-sample MR analysis was used to evaluate the causality between 486 blood metabolites and AF. Firstly, the genome-wide association study (GWAS) data for AF (from Nielsen et al.) was analyzed and some metabolites were identified. Then another GWAS data for AF (from Roselli et al.) was repeatedly analyzed to verify the results. Inverse variance weighted method was mainly used to determine the causality, and MR-egger, Weighted Median, and MR-PRESSO models were used as supplements of MR. Cochran's Q test was used to assess heterogeneity. And MR-Egger intercept and MR-PRESSO global test were performed to measure pleiotropy.ResultsThe study used Bonferroni's corrected P value (P

Abstract Background Heart failure (HF) is the most common potential cause of death, causing a huge health and economic burden all over the world. So far, some impressive progress has been made in the study of pathogenesis. However, the underlying molecular mechanisms leading to this disease remain to be fully elucidated. Methods The microarray data sets of GSE76701, GSE21610 and GSE8331 were retrieved from the gene expression comprehensive database (GEO). After merging all microarray data and adjusting batch effects, differentially expressed genes (DEG) were determined. Functional enrichment analysis was performed based on Gene Ontology (GO) resources, Kyoto Encyclopedia of Genes and Genomes (KEGG) resources, gene set enrichment analysis (GSEA), response pathway database and Disease Ontology (DO). Protein protein interaction (PPI) network was constructed using string database. Combined with the above important bioinformatics information, the potential key genes were selected. The comparative toxicological genomics database (CTD) is used to explore the interaction between potential key genes and HF. Results We identified 38 patients with heart failure and 16 normal controls. There were 315 DEGs among HF samples, including 278 up-regulated genes and 37 down-regulated genes. Pathway enrichment analysis showed that most DEGs were significantly enriched in BMP signal pathway, transmembrane receptor protein serine/threonine kinase signal pathway, extracellular matrix, basement membrane, glycosaminoglycan binding, sulfur compound binding and so on. Similarly, GSEA enrichment analysis showed that DEGs were mainly enriched in extracellular matrix and extracellular matrix related proteins. BBS9, CHRD, BMP4, MYH6, NPPA and CCL5 are central genes in PPI networks and modules. Conclusions The enrichment pathway of DEGs and GO may reveal the molecular mechanism of HF. Among them, target genes EIF1AY, RPS4Y1, USP9Y, KDM5D, DDX3Y, NPPA, HBB, TSIX, LOC28556 and XIST are expected to become new targets for heart failure. Our findings provide potential biomarkers or therapeutic targets for the further study of heart failure and contribute to the development of advanced prediction, diagnosis and treatment strategies.

The mitochondrial unfolded protein response (UPRmt) is a stress response pathway that regulates the expression of mitochondrial chaperones, proteases, and other proteins involved in protein folding and degradation, thereby ensuring proper mitochondrial function. In addition to this critical function, the UPRmt also plays a role in other cellular processes such as mitochondrial biogenesis, energy metabolism, and cellular signaling. Moreover, the UPRmt is strongly associated with various diseases. From 2004 to 2022, there has been a lot of interest in UPRmt. The present study aims to utilized bibliometric tools to assess the genesis, current areas of focus, and research trends pertaining to UPRmt, thereby highlighting avenues for future research. There were 442 papers discovered to be related to UPRmt, with the overall number of publications rising yearly. International Journal of Molecular Sciences was the most prominent journal in this field. 2421 authors from 1,402 institutions in 184 nations published studies on UPRmt. The United States was the most productive country (197 documents). The top three authors were Johan Auwerx, Cole M Haynes, and Dongryeol Ryu. The early focus of UPRmt is “protein.” And then the UPRmt research shifted from Caenorhabditis elegans back to mammals, and its close link to aging and various diseases. The top emerging research hotspots are neurodegenerative diseases and metabolic diseases. These findings provide the trends and frontiers in the field of UPRmt, and valuable information for clinicians and scientists to identify new perspectives with potential collaborators and cooperative countries.

It is a new advertising marketing method for commodity companies to use vloggers to endorse their products, and to influence consumers' attitudes and decisions. In view of this phenomenon, there are few studies on the relationship between vloggers and consumers, and this study aims to explore how the persuasive strategies used by vloggers to promote products influence consumers' purchase intentions. Based on the concepts of Aristotle's persuasion theory, this study extracts two specific persuasive approaches, “two-sided messages” and “emotional appeal,” to explore consumers' perceptions of them and the effectiveness of these two strategies. At the same time, para-social interaction and perceived value as intermediary factors are also included in the study for further discussion. The study empirically analyzed a sample of 511 questionnaires from participants who had purchased products recommended by vloggers and came to the following conclusions: (1) vloggers can enhance consumers' purchase intention by adopting two-sided messages persuasion when promoting products; (2) vloggers' emotional persuasion can enhance consumers' purchase intention; (3) as an intermediary variable, para-social interaction plays a more obvious role in vloggers' persuasion by appealing to emotions. The audience can have common feelings with vloggers, and they are more connected with each other, thus increasing their willingness to buy; (4) Perceived value, as an intermediary variable, plays a more obvious role in vloggers' persuasion with the two-sided messages. The two-sided messages can show vloggers' credibility and more abundant information about products, so that consumers have a positive perception of product value, and the direct persuasion effect of the two-sided messages is greater. Based on the results of the study, this paper helps vloggers to adopt different persuasive approaches for different types of audiences, choose the proper marketing methods, attract the potential customers, and achieve such purposes as enriching product marketing forms and increasing market share.

BackgroundThe global community has been affected by the coronavirus disease 2019 (COVID-19), which emerged in December 2019. Since then, many studies have been conducted on cardiovascular diseases (CVDs) and COVID-19. The aim of this study was to perform a bibliometric and visual analysis of the published relationship between CVDs and COVID-19.Methods1,890 publications were retrieved from the Web of Science Core Collection database on January 5, 2022. Microsoft Office Excel and CiteSpace were then used to carry out scientometric analysis on the relevant literature according to seven aspects: document type, countries/regions, institutions, authors, journals, references, and keywords.ResultsThe research on CVDs and COVID-19 is currently in a period of rapid development, with China, USA, England, and Italy leading the field. There is active cooperation between most countries and institutions. Harvard Medical School stands out among the many institutions not only for the largest number of publications, but also for their high quality. Banerjee A, Solomon SD and Narula J are three representative authors in this field. Frontiers in Cardiovascular Medicine was the journal with the highest number of published studies, and The Lancet was the most cited journal. Two documents with a high degree of significance in this field were identified. Popular research topics in this field are specific diseases, such as acute coronary syndrome and heart failure; pathogenesis related to ACE2, insulin resistance and pericyte; the specific therapeutic drug chloroquine; and clinical characteristics, physical activity, and mental health. ACE2 and NF-κB will be the focus of future research.ConclusionsThis study provides useful information for the research of CVDs and COVID-19, including potential collaborators, popular research topics, and a reference for more extensive and in-depth research in the future.

In complex citrus orchard environments, light changes, branch shading, and fruit overlapping impact citrus detection accuracy. This paper proposes the citrus detection model YOLO-DCA in complex environments based on the YOLOv7-tiny model. We used depth-separable convolution (DWConv) to replace the ordinary convolution in ELAN, which reduces the number of parameters of the model; we embedded coordinate attention (CA) into the convolution to make it a coordinate attention convolution (CAConv) to replace the ordinary convolution of the neck network convolution; and we used a dynamic detection head to replace the original detection head. We trained and evaluated the test model using a homemade citrus dataset. The model size is 4.5 MB, the number of parameters is 2.1 M, mAP is 96.98%, and the detection time of a single image is 5.9 ms, which is higher than in similar models. In the application test, it has a better detection effect on citrus in occlusion, light transformation, and motion change scenes. The model has the advantages of high detection accuracy, small model space occupation, easy application deployment, and strong robustness, which can help citrus-picking robots and improve their intelligence level.

Deep-learning-based methods for plant disease recognition pose challenges due to their high number of network parameters, extensive computational requirements, and overall complexity. To address this issue, we propose an improved residual-network-based multi-plant disease recognition method that combines the characteristics of plant diseases. Our approach introduces a lightweight technique called maximum grouping convolution to the ResNet18 model. We made three enhancements to adapt this method to the characteristics of plant diseases and ultimately reduced the convolution kernel requirements, resulting in the final model, Model_Lite. The experimental dataset comprises 20 types of plant diseases, including 13 selected from the publicly available Plant Village dataset and seven self-constructed images of apple leaves with complex backgrounds containing disease symptoms. The experimental results demonstrated that our improved network model, Model_Lite, contains only about 1/344th of the parameters and requires 1/35th of the computational effort compared to the original ResNet18 model, with a marginal decrease in the average accuracy of only 0.34%. Comparing Model_Lite with MobileNet, ShuffleNet, SqueezeNet, and GhostNet, our proposed Model_Lite model achieved a superior average recognition accuracy while maintaining a much smaller number of parameters and computational requirements than the above models. Thus, the Model_Lite model holds significant potential for widespread application in plant disease recognition and can serve as a valuable reference for future research on lightweight network model design.

BackgroundThere is growing evidence that interleukin 35 (IL-35) represents a potential diagnostic biomarker for sepsis. The purpose of this meta-analysis was to evaluate the overall diagnostic accuracy of IL-35 in sepsis.Materials and methodsFrom October 1998 to May 2022, set retrieval standards were used to search literature Databases. Each included study was assessed diagnostic accuracy study quality assessment tool. Two researchers independently extracted the data and research features. If there are differences, the issue will be resolved by mutual agreement. Meta-disc and Stata software were utilized to calculate combined sensitivity, specificity, and summary diagnostic odds ratio (SDOR), I2, or Cochrane Q in order to detection for heterogeneity, and meta-regression was performed to figure out the cause of heterogeneity. Utilizing funnel plots, we tested for publication bias.ResultsIn this meta-analysis, eight publications were included. The combined sensitivity, specificity, and DOR were 0.87 (95% CI, 0.77–0.93), 0.73 (95% CI, 0.60–0.83), and 18.26 (95% CI, 9.70–34.37), respectively. In addition, 0.88 (95% CI, 0.84–0.90) was the area under the summary receiver operating characteristic curve. In the heterogeneity analysis, the sensitivity of comprehensive I2 statistic was 84.38, and the specificity was 87.82. Deeks’ funnel plot showed no publication bias in this meta-analysis (P = 0.17). A meta-analysis revealed that IL-35 has a modest sensitivity (AUC = 0.88) for diagnosing sepsis. We also compared the diagnostic accuracy of IL-35 and procalcitonin (PCT), and our results showed that the diagnostic accuracy parameters for IL-35 were significantly higher than those for PCT.ConclusionInterleukin 35 is a valuable biomarker for the early detection of sepsis. However, the data should be combined with clinical symptoms, signs, and laboratory and microbiological findings.

ObjectiveEmpagliflozin (EMPA), a sodium-glucose cotransporter 2 inhibitor (SGLT2i), is recommended for all patients with Heart failure (HF) to reduce the risk of Cardiovascular death, hospitalization, and HF exacerbation. Qualitative and quantitative evaluation was conducted by searching relevant literatures of EMPA for Heart Failure from 2013 to 2022, and visual analysis in this field was conducted.MethodsThe data were from the Web of Science Core Collection database (WOSCC). The bibliometric tools, CiteSpace and VOSviewer, were used for econometric analysis to probe the evolvement of disciplines and research hotspots in the field of EMPA for Heart Failure.ResultsA total of 1461 literatures with 43861 references about EMPA for Heart Failure in the decade were extracted from WOSCC, and the number of manuscripts were on a rise. In the terms of co-authorship, USA leads the field in research maturity and exerts a crucial role in the field of EMPA for Heart Failure. Multidisciplinary research is conducive to future development. With regards to literatures, we obtained 9 hot paper, 93 highly cited literatures, and 10 co-cited references. The current research focuses on the following three aspects: EMPA improves left ventricular remodeling, exert renal protection, and increases heart rate variability.ConclusionBased on methods such as bibliometrics, citation analysis and knowledge graph, this study analyzed the current situation and trend of EMPA for Heart Failure, sorted out the knowledge context in this field, and provided reference for current and future prevention and scientific research.

Atherosclerosis (AS) is widespread and develops into circulatory system problems. T cells play an essential regulatory role in AS occurrence and development. So far, there is no bibliometric research on T cells and AS. To learn more about T cell and AS development, 4,381 records were retrieved from Web of Science™ Core Collection. Then, these records were scientometrically analyzed using CiteSpace and VOSviewer in terms of spatiotemporal distribution, author distribution, subject categories, topic distribution, references, and keywords. Our analysis provides basic information on research in the field, demonstrates that the field has stabilized over the past decade, and identifies potential partners for interested researchers. Current research hotspots in this field mainly include the inflammatory mechanism, immune mechanism, related diseases, and related cytokines of AS. B cell, mortality, inhibition, and monocyte represent the frontiers of research in this field, undergoing an explosive phase. We hope that this work will provide new ideas for advancing the scientific research and clinical application of T cell and AS.

Cardiovascular disease is a group of diseases with high mortality in clinic, including hypertension, coronary heart disease, cardiomyopathy, heart valve disease, heart failure, to name a few. In the development of cardiovascular diseases, pathological cardiac remodeling is the most common cardiac pathological change, which often becomes a domino to accelerate the deterioration of the disease. Therefore, inhibiting pathological cardiac remodeling may delay the occurrence and development of cardiovascular diseases and provide patients with greater long-term benefits. Resveratrol is a non-flavonoid polyphenol compound. It mainly exists in grapes, berries, peanuts and red wine, and has cardiovascular protective effects, such as anti-oxidation, inhibiting inflammatory reaction, antithrombotic, dilating blood vessels, inhibiting apoptosis and delaying atherosclerosis. At present, the research of resveratrol has made rich progress. This review aims to summarize the possible mechanism of resveratrol against pathological cardiac remodeling, in order to provide some help for the in-depth exploration of the mechanism of inhibiting pathological cardiac remodeling and the development and research of drug targets.

Background: The underlying pathogenesis of patients with salt-sensitive hypertension expressing higher blood pressure and severer renal damage remains uncertain. Methods: We recruited 329 subjects, 131 in salt-sensitive (SS) group, 148 in nonsalt-sensitive (NSS) group, and 50 healthy people in normal group and tested their renal function, 24-h ambulatory blood pressure, and growth factor series. Results: The SS group showed worse renal function with lower estimated glomerular filtration rate and higher urinary microalbumin, α-microglobulin, urinary protein Cr ratio, and urinary immunoglobulin. Most indicators in 24-h ambulatory blood pressure of the SS group were significantly enhanced than the NSS group, indicating their higher blood pressure. The significantly elevated growth factors in the SS group were AR, BMP-5, EG-VEGF, GH, HGF, IGFBP-2, IGFBP-3, IGFBP-6, MCSFR, NT-4, PDGF-AA, SCF, SCFR, VEGFR2, VEGFR3, and VEGF-D, compared to other 2 groups or one of them. PI3K-AKT pathway was activated in the SS group. Conclusions: Differences in growth factors and pathways may account for the manifestations of the SS group. Activated PI3K-AKT pathway with higher IGFBP-3 and GH can lead to renal damage. Higher MCSFR in the SS group indicates that high blood pressure and severe kidney damage may be associated with the activation of the immune system. EG-VEGF, VEGFR2, VEGFR3, and VEGF-D can also explain the elevated blood pressure due to the dilated lymphatic system which drains excess sodium and water back into circulation. The SS group presented higher AR and HGF which may worsen renal function by regulating cell proliferation and tumor formation. However, due to the potential low awareness rate of hypertension at the very beginning, we cannot ensure the exact occurrence order of blood pressure, renal damage, and salt sensitivity. Therefore, further studies which can track data from the onset of hypertension are needed.

N6-methyladenosine (m6A) RNA methylation is one of the most common epigenetic modifications in RNA nucleotides. It is known that m6A methylation is involved in regulation, including gene expression, homeostasis, mRNA stability and other biological processes, affecting metabolism and a variety of biochemical regulation processes, and affecting the occurrence and development of a variety of diseases. Cardiovascular disease has high morbidity, disability rate and mortality in the world, of which heart failure is the final stage. Deeper understanding of the potential molecular mechanism of heart failure and exploring more effective treatment strategies will bring good news to the sick population. At present, m6A methylation is the latest research direction, which reveals some potential links between epigenetics and pathogenesis of heart failure. And m6A methylation will bring new directions and ideas for the prevention, diagnosis and treatment of heart failure. The purpose of this paper is to review the physiological and pathological mechanisms of m6A methylation that may be involved in cardiac remodeling in heart failure, so as to explain the possible role of m6A methylation in the occurrence and development of heart failure. And we hope to help m6A methylation obtain more in-depth research in the occurrence and development of heart failure.

The aim of this study was to gain insight into the progress and dynamics of psycho-cardiological disease research and track its hot spots. We have analyzed psycho-cardiological disease-related literature extracted from the Web of Science (WOS) Core Collection from 2001 to 2021 with the help of Cite Space. As a result, we have included 5,032 records. Then, we have analyzed connected networks for the country, author, subject category, keywords, and cited reference. We have summarized the findings in four aspects. First, the annual quantitative distribution of publications is on the rise, although there is a slight drop. Second, in terms of country analysis, the United States, England, Australia, Germany, and Italy are the main research forces in psycho-cardiological diseases. At the same time, several academic entities represented by Andrew Steptoe and Roland von Känel, MD, have been formed based on the early consciousness of physical and mental health in these countries. Besides, China is also more concerned about it due to the rapid population aging process and the largest population. Third, the psycho-cardiological disease is multidisciplinary, including psychology, psychiatry, clinical medicine, such as cardiovascular system and neurology, public environmental and occupational health, and pharmacology. Finally, the results of keyword analysis and co-cited references indicate the hot spots and frontiers in psycho-cardiological disease. The hot spots in psycho-cardiological disease include three aspects. The first aspect includes psychosocial factors, such as depression, lack of social support, and low economic and social status; the second aspect includes priority populations, such as Alzheimer’s disease dementia caregivers, elderly, and patients with cancer, and the third aspect includes interventions, such as exercise therapy and diet. In addition, there are three future research frontiers. The first is a psycho-cardiological disease in patients with COVID-19; the second is cardiac rehabilitation, especially exercise therapy and health behavior evaluation; and the final is evidence-based medical evaluation, such as systematic reviews and meta-analyses.

Pyroptosis is a kind of programmed cell death closely related to inflammation. The pathways that mediate pyroptosis can be divided into the Caspase-1-dependent canonical pathway and the Caspase4/5/11-dependent non-canonical pathway. The most significant difference from other cell death is that pyroptosis rapidly causes rupture of the plasma membrane, cell expansion, dissolution and rupture of the cell membrane, the release of cell contents and a large number of inflammatory factors, and send pro-inflammatory signals to adjacent cells, recruit inflammatory cells and induce inflammatory responses. Cardiac remodeling is the basic mechanism of heart failure (HF) and the core of pathophysiological research on the underlying mechanism. A large number of studies have shown that pyroptosis can cause cardiac fibrosis, cardiac hypertrophy, cardiomyocytes death, myocardial dysfunction, excessive inflammation, and cardiac remodeling. Therefore, targeting pyroptosis has a good prospect in improving cardiac remodeling in HF. In this review, the basic molecular mechanism of pyroptosis is summarized, the relationship between pyroptosis and cardiac remodeling in HF is analyzed in-depth, and the potential therapy of targeting pyroptosis to improve adverse cardiac remodeling in HF is discussed, providing some ideas for improving the study of adverse cardiac remodeling in HF.

Ulcerative colitis (UC) is a disease with complex pathological mechanisms. We explored the potential molecular mechanisms behind the therapeutic functions of Qingzi Zhitong decoction (QZZTD) in the treatment of UC by network pharmacology and molecular docking. QZZTD is a formula of Chinese traditional medicine consisting of 10 herbs. The potential active ingredients of QZZTD and their target genes were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform database, and UC-related target genes were obtained from GeneCards and OMIM databases. A total of 138 co-identified target genes were obtained by plotting the intersection target Venn diagram, and then the STRING database and Cytoscape software were used to establish protein–protein interaction networks and herb–ingredient–target networks. Four key active compounds and nine key proteins were identified. Then, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses showed that the biological functions of potential target genes were associated with DNA transcription, signaling receptor and ligand activity, cytokine activity, cellular autophagy, and antioxidant pathways, with related pathways involving the phosphatidylinositol 3-kinase (PI3K)–Akt signaling pathway, advanced glycosylation end product (AGE)–RAGE signaling pathway, tumor necrosis factor (TNF) signaling pathway, and IL-17 signaling pathway. Moreover, the binding activities of key target genes and essential active compounds of Chinese herbal medicines in QZZTD were further validated by molecular docking. This demonstrated that quercetin, luteolin, hyndarin, and beta-sitosterol had good binding to eight key proteins, and Akt1 was the target protein with the best binding activity, suggesting that Akt1 could be the essential mediator responsible for signaling transduction after QZZTD administration. The rat experiment verified that QZZTD inhibited PI3K-Akt pathway activation and reduced inflammation in UC. In conclusion, our study suggested four potential key active components, including quercetin, were identified in QZZTD, which could interact with Akt1 and modulate the activation of the PI3K-Akt pathway. The other three pathways may also be involved in the signaling transduction induced by QZZTD in the treatment of UC.

The crosstalk between the heart and kidney is carried out through various bidirectional pathways. Cardiorenal syndrome (CRS) is a pathological condition in which acute or chronic dysfunction in the heart or kidneys induces acute or chronic dysfunction of the other organ. Complex hemodynamic factors and biochemical and hormonal pathways contribute to the development of CRS. In addition to playing a critical role in generating metabolic energy in eukaryotic cells and serving as signaling hubs during several vital processes, mitochondria rapidly sense and respond to a wide range of stress stimuli in the external environment. Impaired adaptive responses ultimately lead to mitochondrial dysfunction, inducing cell death and tissue damage. Subsequently, these changes result in organ failure and trigger a vicious cycle. In vitro and animal studies have identified an important role of mitochondrial dysfunction in heart failure (HF) and chronic kidney disease (CKD). Maintaining mitochondrial homeostasis may be a promising therapeutic strategy to interrupt the vicious cycle between HF and acute kidney injury (AKI)/CKD. In this review, we hypothesize that mitochondrial dysfunction may also play a central role in the development and progression of CRS. We first focus on the role of mitochondrial dysfunction in the pathophysiology of HF and AKI/CKD, then discuss the current research evidence supporting that mitochondrial dysfunction is involved in various types of CRS.

Background: Traditional observational studies have demonstrated an association between heart failure and Alzheimer’s disease. The strengths of observational studies lie in their speed of implementation, cost, and applicability to rare diseases. However, observational studies have several limitations, such as uncontrollable confounders. Therefore, we employed Mendelian randomization of genetic variants to evaluate the causal relationships existing between AD and HF, which can avoid these limitations.Materials and Methods: A two-sample bidirectional MR analysis was employed. All datasets were results from the UK’s Medical Research Council Integrative Epidemiology Unit genome-wide association study database, and we conducted a series of control steps to select the most suitable single-nucleotide polymorphisms for MR analysis, for which five primary methods are offered. We reversed the functions of exposure and outcomes to explore the causal direction of HF and AD. Sensitivity analysis was used to conduct several tests to avoid heterogeneity and pleiotropic bias in the MR results.Results: Our MR studies did not support a meaningful causal relationship between AD on HF (MR-Egger, p = 0.634 > 0.05; weighted median (WM), p = 0.337 > 0.05; inverse variance weighted (IVW), p = 0.471 > 0.05; simple mode, p = 0.454 > 0.05; weighted mode, p = 0.401 > 0.05). At the same time, we did not find a significant causal relationship between HF and AD with four of the methods (MR-Egger, p = 0.195 > 0.05; IVW, p = 0.0879 > 0.05; simple mode, p = 0.170 > 0.05; weighted mode, p = 0.110 > 0.05), but the WM method indicated a significant effect of HF on AD (p = 0.025 < 0.05). Because the statistical powers of IVW and MR-Egger are more than that of WM, we think that there is no causal effect of HF on AD. Sensitivity analysis and horizontal pleiotropy were not detected in the MR analysis.Conclusion: Our results did not provide significant evidence indicating any causal relationships between HF and AD in the European population. Therefore, more large-scale datasets or datasets related to similar factors are expected for further MR analysis.

Growth differentiation factor 15 (GDF15) is involved in the occurrence and development of many diseases, and there are few studies on its relationship with sepsis. This article aims to explore the clinical value of GDF15 in sepsis and to preliminarily explore its prospective regulatory effect on macrophage inflammation and its functions. We recruited 320 subjects (132 cases in sepsis group, 93 cases in nonsepsis group, and 95 cases in control group), then detected the serum GDF15 levels and laboratory indicators, and further investigated the correlation between GDF15 and laboratory indicators, and also analyzed the clinical value of GDF15 in sepsis diagnosis, severity assessment, and prognosis. In vitro, we used LPS to stimulate THP-1 and RAW264.7 cells to establish the inflammatory model, and detected the expression of GDF15 in the culture medium and cells under the inflammatory state. After that, we added GDF15 recombinant protein (rGDF15) pretreatment to explore its prospective regulatory effect on macrophage inflammation and its functions. The results showed that the serum GDF15 levels were significantly increased in the sepsis group, which was correlated with laboratory indexes of organ damage, coagulation indexes, inflammatory factors, and SOFA score. GDF15 also has a high AUC in the diagnosis of sepsis, which can be further improved by combining with other indicators. The dynamic monitoring of GDF15 levels can play an important role in the judgment and prognosis of sepsis. In the inflammatory state, the expression of intracellular and extracellular GDF15 increased. GDF15 can reduce the levels of cytokines, inhibit M1 polarization induced by LPS, and promote M2 polarization. Moreover, GDF15 also enhances the phagocytosis and bactericidal function of macrophages. Finally, we observed a decreased level of the phosphorylation of JAK1/STAT3 signaling pathway and the nuclear translocation of NF-κB p65 with the pretreatment of rGDF15. In summary, our study found that GDF15 has good clinical application value in sepsis and plays a protective role in the development of sepsis by regulating the functions of macrophages and inhibiting the activation of JAK1/STAT3 pathway and nuclear translocation of NF-κB p65.

The vascular endothelial growth factor (VEGF) family, the regulator of blood and lymphatic vessels, is mostly investigated in the tumor and ophthalmic field. However, the functions it enjoys can also interfere with the development of atherosclerosis (AS) and further diseases like coronary heart disease (CHD). The source, regulating mechanisms including upregulation and downregulation, target cells/tissues, and known functions about VEGF-A, VEGF-B, VEGF-C, and VEGF-D are covered in the review. VEGF-A can regulate angiogenesis, vascular permeability, and inflammation by binding with VEGFR-1 and VEGFR-2. VEGF-B can regulate angiogenesis, redox, and apoptosis by binding with VEGFR-1. VEGF-C can regulate inflammation, lymphangiogenesis, angiogenesis, apoptosis, and fibrogenesis by binding with VEGFR-2 and VEGFR-3. VEGF-D can regulate lymphangiogenesis, angiogenesis, fibrogenesis, and apoptosis by binding with VEGFR-2 and VEGFR-3. These functions present great potential of applying the VEGF family for treating CHD. For instance, angiogenesis can compensate for hypoxia and ischemia by growing novel blood vessels. Lymphangiogenesis can degrade inflammation by providing exits for accumulated inflammatory cytokines. Anti-apoptosis can protect myocardium from impairment after myocardial infarction (MI). Fibrogenesis can promote myocardial fibrosis after MI to benefit cardiac recovery. In addition, all these factors have been confirmed to keep a link with lipid metabolism, the research about which is still in the early stage and exact mechanisms are relatively obscure. Because few reviews have been published about the summarized role of the VEGF family for treating CHD, the aim of this review article is to present an overview of the available evidence supporting it and give hints for further research.

Cardiovascular disease (CVD) is a serious threat to global public health due to its high prevalence and disability rate. Meanwhile, cardiac rehabilitation (CR) has attracted increasing attention for its positive effects on the cardiovascular system. There is overwhelming evidence that CR for patients with CVD is effective in reducing cardiovascular morbidity and mortality. To learn more about the development of CR, 5,567 papers about CR and related research were retrieved in the Web of Science Core Collection from 2001 to 2020. Then, these publications were scientometrically analyzed based on CiteSpace in terms of spatiotemporal distribution, author distribution, subject categories, topic distribution, and references. The results can be elaborated from three aspects. Firstly, the number of annual publications related to CR has increased year by year in general over the past two decades. Secondly, a co-occurrence analysis of the output countries and authors shows that a few developed countries such as the United States, Canada, and the UK are the most active in carrying out CR and where regional academic communities represented by Sherry Grace and Ross Arena were formed. Thirdly, an analysis of the subject categories and topic distribution of the papers reveals that CR is a typical interdiscipline with a wide range of disciplines involved, including clinical medicine, basic medicine, public health management, and sports science. The research topics cover the participants and implementers, components, and the objectives and requirements of CR. The current research hotspots are the three core modalities of CR, namely patient education, exercise training and mental support, as well as mobile health (mHealth) dependent on computer science. In conclusion, this work has provided some useful information for acquiring knowledge about CR, including identifying potential collaborators for researchers interested in CR, and discovering research trends and hot topics in CR, which can offer some guidance for more extensive and in-depth CR-related studies in the future.

Objective: To analyze the serum complement C1q levels in children with sepsis, and explore the suggestive effect of serum C1q levels on the condition of children with sepsis.Methods: The clinical and laboratory data of children with sepsis (n = 95) and healthy children (n = 71) in Renmin Hospital of Wuhan University from January 2019 to October 2019 were collected, and each index of the two groups was compared. Then we divided children with sepsis into three subgroups based on the Pediatric Critical Illness Score (PCIS): non-critical group, critical group, and extremely critical group. The serum C1q and PCT levels of the three subgroups were analyzed, and the correlation analysis was carried out between the levels of serum C1q and PCT levels as well as PCIS among children with sepsis. Finally, we analyzed the serum C1q levels of septic children infected by different pathogens.Results: The serum C1q levels of children with sepsis were significantly higher than those of healthy children (median 198.4 vs. 186.2 mg/L, P < 0.001). In the analysis of subgroups, the serum C1q levels of non-critical group, critical group, and extremely critical group septic children were 182.80 (166.75, 195.85) mg/L, 219.90 (209.10, 246.40) mg/L and 249.95 (239.10, 272.25) mg/L, respectively, which were correlated with the severity of the disease. At the same time, we also found that serum C1q in children with sepsis was positively correlated with PCT levels (r = 0.5982, P < 0.001), and negatively correlated with PCIS score (r = −0.6607, P < 0.001). The serum C1q levels of septic children with bacterial infections, mycoplasma infections, viral infections, and co-infection were higher than those of the control group (P < 0.05).Conclusion: The serum levels of C1q in children with sepsis were increased and related to the severity of sepsis, suggesting that C1q may be involved in the occurrence and development of sepsis, which had reference value for the preliminary diagnosis and severity classification of sepsis.

Objective: Physical exercise is recommended to help prevent lifestyle diseases. The present study was designed to quantify the efficacy of physical exercise on the quality of life (QoL), exercise ability and cardiopulmonary fitness of patients with atrial fibrillation (AF).Method: A comprehensive systematic literature search was performed in Medline, Embase, Cochrane Library, Web of Science and PubMed databases (from 1970 to December 1st, 2019) for randomized controlled trials (RCTs) comparing physical exercise combined with AF routine treatments to routine treatments alone. The meta-analysis was conducted following PRISMA guidelines. Our main outcomes were QoL (measured by the Short-Form 36 scale, SF-36), exercise ability (measured by the 6-min walk test, 6MWT) and cardiopulmonary fitness (measured by peak oxygen uptake and resting heart rate). Quality assessments were conducted using the Cochrane Collaboration tool.Results: Twelve trials involving 819 patients met the criteria for analysis. The results showed that physical exercise improved the QoL by enhancing physical functioning [standardized mean difference (SMD) = 0.63, 95%CI: 0.18–1.09; p = 0.006], general health perceptions (SMD = 0.64, 95%CI: 0.35–0.93; p < 0.001) and vitality (SMD = 0.51, 95%CI: 0.31–0.71; p < 0.001); increased exercise ability by improving the 6MWT performance (SMD = 0.69, 95%CI: 0.19–1.119; p = 0.007); and enhanced peak VO2 (SMD = 0.37, 95%CI: 0.16–0.57; p < 0.001) while reducing resting heart rate (SMD = −0.39, 95%CI: −0.65 to −0.13; p = 0.004). In addition, meta-regression analysis showed that training mode (pphysicalfunctioning = 0.012, pgeneralhealthperceptions = 0.035) and training duration (p = 0.047) were the main factors of an intervention that influenced the effect size. Following sub-group analysis, we found that aerobics, Yoga and longer training durations (≥60 min) showed larger improvements.Conclusion: In summary, our meta-analysis shows that physical exercise has a positive effect on the QoL, exercise ability and cardiopulmonary fitness in AF patients. When physicians offer exercise recommendations to AF patients, they should consider both the training mode and training duration to achieve maximum results.

Background: Homozygous familial hypercholesterolaemia (HoFH) patients have little or no low-density lipoprotein receptor (LDLR) function. HMG-CoA (3-hydroxy-3-methyl glutaryl coenzyme A) reductase inhibitors (statins) and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have limited lipid-lowering effects, therefore, there is an urgent need to develop new HoFH treatments. In 2012, the US Food and Drug Administration (FDA) approved the administration of lomitapide for lowering low-density lipoprotein cholesterol (LDL-C) levels. However, lomitapide is associated with various gastrointestinal disorders, elevated hepatic alanine aminotransferase (ALT) levels and other adverse reactions, thus, its long-term efficacy and safety in pediatrics and adults should be evaluated. A systematic review conducted in 2017 reported the efficacy and safety of lomitapide in Family hypercholesterolaemia (FH) patients. In this systematic review, we elucidate on the efficacy and safety of lomitapide in HoFH patients. Methods: A search was conducted in PubMed, Embase, Web of Science and Cochrane library databases to identify valid studies involving lomitapide-treated HoFH patients published before 11th August 2021. Results: A total of 18 clinical studies involving 120 lomitapide-treated HoFH patients were identified. Lomitapide significantly suppressed LDL-C levels in HoFH patients. Clinical manifestations for lomitapide in children were comparable to those in adults. The most common adverse events were gastrointestinal disturbances and elevated ALT levels. However, most patients tolerated the treatment-associated adverse reactions. Low-fat diets and drug dose adjustments were appropriate measures for controlling the treatment-associated adverse reactions. Conclusions: In pediatric and adult HoFH patients, lomitapide significantly suppresses LDL-C levels, therefore, it is an important option for HoFH treatment. The most common adverse events of lomitapide treatment include gastrointestinal disorders and elevated hepatic ALT levels. Despite the limitations, lomitapide is feasible for long-term treatment of HoFH patients, with dietary and safety monitoring. Registration Number in PROSPERO: CRD42021284425.

At present, the treatment of heart failure has entered the plateau phase, and it is necessary to thoroughly study the pathogenesis of heart failure and find out the corresponding treatment methods. Myocardial mitochondria is the main site of cardiac energy metabolism, whose dysfunction is an important factor leading to cardiac dysfunction and heart failure. Mitochondria are highly dynamic organelles. Continuous biogenesis, fusion, fission and mitophagy, contribute to the balance of mitochondria's morphology, quantity, and quality, which is called mitochondrial quality control. Mitochondrial quality control is the cornerstone of normal mitochondrial function and is found to play an important role in the pathological process of heart failure. Here, we provide an overview of the mechanisms of mitochondrial quality control and recent studies on mitochondrial quality control in heart failure, hoping to provide new ideas for drug development in heart failure.

Abstract Background The CD2-associated protein (CD2AP) was initially identified in peripheral immune cells and regulates cytoskeleton and protein trafficking. Single nucleotide polymorphisms (SNPs) in the CD2AP gene have been associated with Alzheimer’s disease (AD). However, the functional role of CD2AP, especially its role in microglia during AD onset, remains elusive. Methods CD2AP protein levels in cultured primary cells and in 5xFAD mice was studied. Microglial CD2AP-deficient mice were crossed with 5xFAD mice and the offspring were subjected to neuropathological assessment, behavioral tests, electrophysiology, RNA-seq, Golgi staining, and biochemistry analysis. Primary microglia were also isolated for assessing their uptake and morphology changes. Results We find that CD2AP is abundantly expressed in microglia and its levels are elevated in the brain of AD patients and the 5xFAD model mice at pathological stages. We demonstrate that CD2AP haploinsufficiency in microglia significantly attenuates cognitive and synaptic deficits, weakens the response of microglia to Aβ and the formation of disease-associated microglia (DAM), and alleviates synapse loss in 5xFAD mice. We show that CD2AP-deficient microglia exhibit compromised uptake ability. In addition, we find that CD2AP expression is positively correlated with the expression of the complement C1q that is important for synapse phagocytosis and the formation of DAM in response to Aβ deposition. Moreover, we reveal that CD2AP interacts with colony stimulating factor 1 receptor (CSF1R) and regulates CSF1R cell surface levels, which may further affect C1q expression. Conclusions Our results demonstrate that CD2AP regulates microgliosis and identify a protective function of microglial CD2AP deficiency against Aβ deposition, suggesting the importance of detailed investigation of AD-associated genes in different brain cells for thoroughly understanding their exact contribution to AD.