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Seroma formation and poor wound healing are common complications of many surgeries that create anatomical dead space (i.e., mastectomy), often causing tissue infection and even necrosis. Although negative pressure drainage and tissue adhesives are investigated to alleviate fluid accumulation post-surgery, however, their therapeutic efficacy remains unsatisfactory in most cases. Herein, the catechol-rich chemically crosslinked gelatin microspheres (ca-CGMSs) have been developed as biodegradable reconstructive implants for preventing seroma formation and concurrently promoting subcutaneous wound healing. Compared with the most representative hydrogel adhesive, i.e. commercial porcine fibrin sealant (PFS), the loosely packed ca-CGMSs with diameters range from 50 to 350 μm, provide numerous cell-adhesive interfaces and interconnected macro-pores for enhanced cell adhesion, proliferation and migration. Subcutaneous embedding trials show the in situ swelling aggregation and wet tissue adhesion of ca-CGMSs as well as their capacity in recruiting autologous cells in rat mastectomy models. The trials in rabbit mastectomy models demonstrate that, compared with PFS gluing, the implanted dried ca-CGMSs not only significantly inhibit seroma formation, but also achieve enhanced wound healing by inducing the formation of vascularized neo-tissue. The ca-CGMSs show a great potential to be the next-generation of restorative materials for both preventing seroma formation and healing subcutaneous wounds.

Apoptosis repressor with caspase recruitment domain (ARC) is a highly potent and multifunctional suppressor of various types of programmed cell death (PCD) (e.g. apoptosis, necroptosis, and pyroptosis) and plays a key role in determining cell fate. Under physiological conditions, ARC is predominantly expressed in terminally differentiated cells, such as cardiomyocytes and skeletal muscle cells. Its expression and activity are tightly controlled by a complicated system consisting of transcription factor (TF), non-coding RNA (ncRNA), and post-translational modification (PTM). ARC dysregulation has been shown to be closely associated with many chronic diseases, including cardiovascular disease, cancer, diabetes, and neurodegenerative disease. However, the detailed mechanisms of ARC involved in the progression of these diseases remain unclear to a large extent. In this review, we mainly focus on the regulatory mechanisms of ARC expression and activity and its role in PCD. We also discuss the underlying mechanisms of ARC in health and disease and highlight the potential implications of ARC in the clinical treatment of patients with chronic diseases. This information may assist in developing ARC-based therapeutic strategies for patients with chronic diseases and expand researchers’ understanding of ARC.

Ferroptosis plays a vital role in the progression of various retinal diseases. The analysis of the mechanism of retinal cell ferroptosis has brought new targeted strategies for treating retinal vascular diseases, retinal degeneration and retinal nerve diseases, and is also a major scientific issue in the field of ferroptosis. In this review, we summarized results from currently available in vivo and in vitro studies of multiple eye disease models, clarified the pathological role and molecular mechanism of ferroptosis in retinal diseases, summed up the existing pharmacological agents targeting ferroptosis in retinal diseases as well as highlighting where future research efforts should be directed for the application of ferroptosis targeting agents. This review indicates that ferroptosis of retinal cells is involved in the progression of age-related/inherited macular degeneration, blue light-induced retinal degeneration, glaucoma, diabetic retinopathy, and retinal damage caused by retinal ischemia-reperfusion via multiple molecular mechanisms. Nearly 20 agents or extracts, including iron chelators and transporters, antioxidants, pharmacodynamic elements from traditional Chinese medicine, ferroptosis-related protein inhibitors, and neuroprotective agents, have a remissioning effect on retinal disease in animal models via ferroptosis inhibition. However, just a limited number of agents have received approval or are undergoing clinical trials for conditions such as iron overload-related diseases. The application of most ferroptosis-targeting agents in retinal diseases is still in the preclinical stage, and there are no clinical trials yet. Future research should focus on the development of more potent ferroptosis inhibitors, improved drug properties, and ideally clinical testing related to retinal diseases.

Abstract Background The development of neuropathic pain (NP) is one of the reasons why the pain is difficult to treat, and microglial activation plays an important role in NP. Recently, platelet-rich plasma (PRP) has emerged as a novel therapeutic method for knee osteoarthritis (KOA). However, it’s unclarified whether PRP has analgesic effects on NP induced by KOA and the underlying mechanisms unknown. Purpose To observe the analgesic effects of PRP on NP induced by KOA and explore the potential mechanisms of PRP in alleviating NP. Methods KOA was induced in male rats with intra-articular injections of monosodium iodoacetate (MIA) on day 0. The rats received PRP or NS (normal saline) treatment at days 15, 17, and 19 after modeling. The Von Frey and Hargreaves tests were applied to assess the pain-related behaviors at different time points. After euthanizing the rats with deep anesthesia at days 28 and 42, the corresponding tissues were taken for subsequent experiments. The expression of activating transcription factor 3 (ATF3) in dorsal root ganglia (DRG) and ionized-calcium-binding adapter molecule-1(Iba-1) in the spinal dorsal horn (SDH) was detected by immunohistochemical staining. In addition, the knee histological assessment was performed by hematoxylin-eosin (HE) staining. Results The results indicated that injection of MIA induced mechanical allodynia and thermal hyperalgesia, which could be reversed by PRP treatment. PRP downregulated the expression of ATF3 within the DRG and Iba-1 within the SDH. Furthermore, an inhibitory effect on cartilage degeneration was observed in the MIA + PRP group only on day 28. Conclusion These results indicate that PRP intra-articular injection therapy may be a potential therapeutic agent for relieving NP induced by KOA. This effect could be attributed to downregulation of microglial activation and reduction in nerve injury.

Background: Atrial fibrillation (AF) is a major public health problem with high rates of morbidity, disability and mortality, especially in the elderly population. This study explored the diagnosis and treatment status of AF in adults aged ≥65 years in the community through wearable dynamic electrocardiogram (ECG) monitoring. Methods: We conducted a cross-sectional study in 4 random communities within the Qingpu district of Shanghai, China. Between January 1, 2020 and June 30, 2022, the ECGs of 3852 adults aged 65 years or older were examined through wearable dynamic ECG monitoring. Data from 3839 participants were ultimately analyzed. Multivariate logistic regression was used to determine the independent predictors of AF. Results: Wearable dynamic ECG monitoring detected AF in 360 elderly people, 78 of whom were diagnosed with AF for the first time. Multivariate logistic regression analysis revealed that snoring, renal dysfunction, coronary heart disease and high CHA2DS2-VASc score were independent risk factors for AF. Among patients with unknown AF, 68 (87.20 %) met the criteria for anticoagulant therapy based on the CHA2DS2-VASc score. Only 4 (5.88 %) patients were taking anticoagulants. Of the patients with a clear history of AF, 249 (84.98 %) needed an anticoagulant strategy, but only 18 (7.23 %) took oral anticoagulants. Conclusion: Many elderly people have silent AF, and wearable dynamic ECG monitoring can be used to screen for AF effectively.

Lung cancer (LC) is a heterogeneous disease with high malignant degree, rapid growth, and early metastasis. The clinical outcomes of LC patients are generally poor due to the insufficient elucidation of pathological mechanisms, low efficiency of detection and assessment methods, and lack of individualized therapeutic strategies. Non-coding RNAs (ncRNAs), including microRNA (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA), are endogenous regulators that are widely involved in the modulation of almost all aspects of life activities, from organogenesis and aging to immunity and cancer. They commonly play vital roles in various biological processes by regulating gene expression via their interactions with DNA, RNA, or protein. An increasing amount of studies have demonstrated that ncRNAs are closely correlated with the initiation and development of LC. Their dysregulation promotes the progression of LC via distinct mechanisms, such as influencing protein activity, activating oncogenic signaling pathways, or altering specific gene expression. Furthermore, some ncRNAs present certain clinical values as biomarker candidates and therapeutic targets for LC patients. A complete understanding of their mechanisms in LC progression may be highly beneficial to developing ncRNA-based therapeutics for LC patients. This review mainly focuses on the intricate mechanisms of miRNA, lncRNA, and circRNA involved in LC progression and discuss their underlying applications in LC treatment.

Background Heart failure is a public health issue worldwide. However, no comprehensive study on the global burden of heart failure and its contributing causes has been reported. The present study aimed to quantify the burden, trends, and inequalities of heart failure globally. Methods and Results Heart failure data were extracted from the Global Burden of Diseases 2019 study. The number of cases, age‐standardized prevalence, and years lived with disability in different locations from 1990 to 2019 were presented and compared. Joinpoint regression analysis was performed to assess trends in heart failure from 1990 to 2019. In 2019, the global age‐standardized prevalence and years lived with disability rates for heart failure were 711.90 (95% uncertainty interval [UI], 591.15–858.29) and 63.92 (95% UI, 41.49–91.95) per 100 000 population, respectively. In general, the age‐standardized rate decreased globally at an average annual percentage change of 0.3% (95% UI, 0.2–0.3). However, the rate increased at an average annual percentage change of 0.6% (95% UI, 0.4–0.8) from 2017 to 2019. Several nations and territories demonstrated an increased trend from 1990 to 2019, especially in less‐developed countries. Ischemic heart disease and hypertensive heart disease accounted for the highest proportion of heart failure in 2019. Conclusions Heart failure remains a major health problem, with increased trends possible in the future. Efforts for prevention and control of heart failure should focus more on less‐developed regions. It is essential to prevent and treat primary diseases such as ischemic heart disease and hypertensive heart disease for the control of heart failure.

The initiation of atherosclerotic plaque is characterized by endothelial cell inflammation. In light of gasdermin E’s (GSDME) role in pyroptosis and inflammation, this study elucidates its function in atherosclerosis onset. Employing Gsdme- and apolipoprotein E-deficient (Gsdme−/−/ApoE−/−) and ApoE−/− mice, an atherosclerosis model was created on a Western diet (WD). In vitro examinations with human umbilical vein endothelial cells (HUVECs) included oxidized low-density lipoprotein (ox-LDL) exposure. To explore the downstream mechanisms linked to GSDME, we utilized an agonist targeting the stimulator of the interferon genes (STING) pathway. The results showed significant GSDME activation in ApoE−/− mice arterial tissues, corresponding with atherogenesis. Gsdme−/−/ApoE−/− mice displayed fewer plaques and decreased vascular inflammation. Meanwhile, GSDME’s presence was confirmed in endothelial cells. GSDME inhibition reduced the endothelial inflammation induced by ox-LDL. GSDME was linked to mitochondrial damage in endothelial cells, leading to an increase in cytoplasmic double-stranded DNA (dsDNA). Notably, STING activation partially offset the effects of GSDME inhibition in both in vivo and in vitro settings. Our findings underscore the pivotal role of GSDME in endothelial cells during atherogenesis and vascular inflammation, highlighting its influence on mitochondrial damage and the STING pathway, suggesting a potential therapeutic target for vascular pathologies.

In view of the fact that the existing robotic mobile mechanisms on the market are driven more， the control is cumbersome， and the stability is poor， a synchronous movement steering mechanism for dodge robots with all-round rapid movement in the plane is studied. The driving motor and the steering motor cooperate to achieve all-round movement. In order to check the rationality of the establishment of the moving mechanism model， the Lagrangian equation is used to complete the dynamics analysis of the moving mechanism. The Adams software is used to complete the simulation of the virtual prototype of the mobile mechanism， and the relevant torque curves are obtained. Finally， the experimental test of the moving mechanism is completed. Through theoretical calculations， simulations， and experimental tests， the mutual verification between the three has further verified the accuracy of the establishment of the dodge robot mobile mechanism model.

Acute myocardial infarction (AMI), one of the most severe and fatal cardiovascular diseases, remains the main cause of mortality and morbidity worldwide. The objective of this study is to investigate the potential biomarkers for AMI based on bioinformatics analysis. A total of 2102 differentially expressed genes (DEGs) were screened out from the data obtained from the gene expression omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) explored the co-expression network of DEGs and determined the key module. The brown module was selected as the key one correlated with AMI. Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses demonstrated that genes in the brown module were mainly enriched in ‘ribosomal subunit’ and ‘Ribosome’. Gene Set Enrichment Analysis revealed that ‘TNFA_SIGNALING_VIA_NFKB’ was remarkably enriched in AMI. Based on the protein–protein interaction network, ribosomal protein L9 (RPL9) and ribosomal protein L26 (RPL26) were identified as the hub genes. Additionally, the polymerase chain reaction (PCR) results indicated that the expression levels of RPL9 and RPL26 were both downregulated in AMI patients compared with controls, in accordance with the bioinformatics analysis. In summary, the identified DEGs, modules, pathways, and hub genes provide clues and shed light on the potential molecular mechanisms of AMI.