Myocardial infarction is a cardiovascular disease (CVD) with high morbidity and mortality, which can trigger a cascade of cardiac pathophysiological changes, including fibrosis, inflammation, ischemia-reperfusion injury (IRI), and ventricular remodeling, ultimately leading to heart failure (HF). While conventional pharmacological treatments and clinical reperfusion therapy may enhance short-term prognoses and emergency survival rates, both approaches have limitations and adverse effects. Natural products (NPs) are extensively utilized as therapeutics globally, with some demonstrating potentially favorable therapeutic effects in preclinical and clinical pharmacological studies, positioning them as potential alternatives to modern drugs. This review comprehensively elucidates the pathophysiological mechanisms during myocardial infarction and summarizes the mechanisms by which NPs exert cardiac beneficial effects. These include classical mechanisms such as inhibition of inflammation and oxidative stress, alleviation of cardiomyocyte death, attenuation of cardiac fibrosis, improvement of angiogenesis, and emerging mechanisms such as cardiac metabolic regulation and histone modification. Furthermore, the review emphasizes the modulation by NPs of novel targets or signaling pathways in classical mechanisms, including other forms of regulated cell death (RCD), endothelial-mesenchymal transition, non-coding ribonucleic acids (ncRNAs) cascade, and endothelial progenitor cell (EPC) function. Additionally, NPs influencing a particular mechanism are categorized based on their chemical structure, and their relevance is discussed. Finally, the current limitations and prospects of NPs therapy are considered, highlighting their potential for use in myocardial infarction management and identifying issues that require urgent attention.
Humans ; Myocardial Infarction/genetics* ; Biological Products/therapeutic use* ; Animals ; Oxidative Stress/drug effects* ; Signal Transduction/drug effects*

Objective To develop an intelligent model for differential diagnosis of atrioventricular nodal re-entrant tachycardia(AVNRT)and atrioventricular re-entrant tachycardia(AVRT)using 12-lead wearable electrocardiogram devices.Methods A total of 356 samples of 12-lead supraventricular tachycardia(SVT)electrocardiograms recorded by wearable devices were randomly divided into training and validation sets using 5-fold cross validation to establish the intelligent classification model,and 101 patients with the diagnosis of SVT undergoing electrophysiological studies and radiofrequency ablation from October,2021 to March,2023 were selected as the testing set.The changes in electrocardiogram parameters before and during induced tachycardia were compared.Based on multiscale deep neural network,an intelligent diagnosis model for classifying SVT mechanisms was constructed and validated.The 3-lead electrocardiogram signals from Ⅱ,Ⅲ,and V1 were extracted to build new classification models,whose diagnostic efficacy was compared with that of the 12-lead model.Results Of the 101 patients with SVT in the testing set,68 were diagnosed with AVNRT and 33 were diagnosed with AVRT by electrophysiological study.The pre-trained model achieved a high area under the precision-recall curve(0.9492)and F1 score(0.8195)for identifying AVNRT in the validation set.The total F1 scores of the lead Ⅱ,Ⅲ,V1,3-lead and 12-lead intelligent diagnostic models in the testing set were 0.5597,0.6061,0.3419,0.6003 and 0.6136,respectively.Compared with the 12-lead classification model,the lead-Ⅲ model had a net reclassification index improvement of-0.029(P=0.878)and an integrated discrimination index improvement of-0.005(P=0.965).Conclusion The intelligent diagnostic model based on multiscale deep neural network using wearable electrocardiogram devices has an acceptable accuracy for classifying SVT mechanisms.

Objective To develop an intelligent model for differential diagnosis of atrioventricular nodal re-entrant tachycardia(AVNRT)and atrioventricular re-entrant tachycardia(AVRT)using 12-lead wearable electrocardiogram devices.Methods A total of 356 samples of 12-lead supraventricular tachycardia(SVT)electrocardiograms recorded by wearable devices were randomly divided into training and validation sets using 5-fold cross validation to establish the intelligent classification model,and 101 patients with the diagnosis of SVT undergoing electrophysiological studies and radiofrequency ablation from October,2021 to March,2023 were selected as the testing set.The changes in electrocardiogram parameters before and during induced tachycardia were compared.Based on multiscale deep neural network,an intelligent diagnosis model for classifying SVT mechanisms was constructed and validated.The 3-lead electrocardiogram signals from Ⅱ,Ⅲ,and V1 were extracted to build new classification models,whose diagnostic efficacy was compared with that of the 12-lead model.Results Of the 101 patients with SVT in the testing set,68 were diagnosed with AVNRT and 33 were diagnosed with AVRT by electrophysiological study.The pre-trained model achieved a high area under the precision-recall curve(0.9492)and F1 score(0.8195)for identifying AVNRT in the validation set.The total F1 scores of the lead Ⅱ,Ⅲ,V1,3-lead and 12-lead intelligent diagnostic models in the testing set were 0.5597,0.6061,0.3419,0.6003 and 0.6136,respectively.Compared with the 12-lead classification model,the lead-Ⅲ model had a net reclassification index improvement of-0.029(P=0.878)and an integrated discrimination index improvement of-0.005(P=0.965).Conclusion The intelligent diagnostic model based on multiscale deep neural network using wearable electrocardiogram devices has an acceptable accuracy for classifying SVT mechanisms.

Objective To establish a gene sequencing method for ABO blood group,to analyze the mu-tation sites at the DNA level in order to accurately identify ABO blood group.Methods Twenty blood sam-ples were selected,in which 18 samples were ABO normal blood group and 2 samples were the ABO subtype. Exons 6 and 7 of ABO blood group gene were amplified by sequence-specific primer PCR (PCR-SSP),and then the gene sequence was directly sequenced and analyzed by PCR,and the ABO blood group was identified by comparing with the ABO reference sequence.Results The gene sequencing results of 20 blood samples were consistent with the serological results.In 2 subtype samples,the genotype in 1 sample was BA.02/O.01 and its phenotype was B(A) subtype.C>G mutation occurred at position 700 of the 7th exon,which resulted in proline changing to alanine at position 234 during amino acid translation.The genotype of the other sample was AW.37/B.01 and the phenotype was AxB subtype.The position 940 of the 7th exon mutates from ade-nine to guanine,resulting in the mutation of lysine changing to glutamic acid at position 314 during protein translation.Conclusion A method of ABO blood group gene sequencing suitable for laboratory is estab-lished,which could accurately identify ABO blood group.

Objective To investigate the effects of lycium barbarum polysaccharide(LBP)on the proliferation and metastasis of gallbladder cancer cells(NOZ and SGC-996)by regulating cellular ferroptosis.Methods NOZ and SGC-996 cells were cul-tured in vitro by treatment with different doses of LBP.The cells were divided into control group,20 μmol/L LBP group,40μmol/L LBP group,60 μmol/L LBP group,80 μmol/L LBP group,and LBP+Fe-1 groups.Cell activity was detected by MTT assay.Cell proliferation was detected by EdU assay.Cell invasion ability was detected by Transwell assay.Fe2+level was detec-ted by colorimetric assay,reactive oxygen species(ROS)and malondialdehyde(MDA)levels were determined by BODIPYT 581/591 C11 molecular probe.Western blot was used to detect glutathione peroxidase 4(GPX4),acyl-CoA Synthetase long-chain family member 4(ACSL4),β-catenin,and Wnt3A protein expression.Results Compared with the control group,cell viability,proliferation,and invasion were significantly decreased in the 40 μmol/L LBP,and 60 μmol/L LBP groups(all P＜0.05),and Fe2+level,ROS,and MDA activities were significantly increased(all P＜0.05),and GPX4,β-catenin,and Wnt3A protein ex-pressions were significantly reduced,and ACSL4 protein expression was significantly increased(all P＜0.05).Compared with the LBP group,cell viability,proliferation,and invasion ability were significantly increased in the LBP+Fer-1 group(all P＜0.05).Conclusion LBP inhibits the proliferation and metastasis of gallbladder cancer cells by inducing ferroptosis.

Purpose: Erectile dysfunction (ED) is a common postoperative complication of pelvic surgery for which there is currently no effective treatment. This study investigated the therapeutic effects and potential mechanisms of adipose derived mesenchymal stem cells-derived mitochondria (ADSCs-mito) transplantation in a rat model of bilateral cavernous nerve injury (CNI) ED. Materials and Methods: We isolated mitochondria from ADSCs and tested their quality. In vivo, twenty male Sprague Dawley rats were randomly divided into four groups: sham operation group and CNI groups that received intracavernous injection of either phosphate buffer solution, ADSCs-mito or ADSCs. Two weeks after therapy, the erectile function of the rats was evaluated and the penile tissues were harvested for histologic analysis and western blotting. In vitro, the apoptosis rate, reactive oxygen species (ROS), mitochondria derived active oxygen (mtROS) and adenosine triphosphate (ATP) levels were detected in corpus cavernosum smooth muscle cells (CCSMCs) after the incubation with ADSCs-mito. In addition, intercellular mitochondrial transfer was visualized by co-culture of ADSCs and CCSMCs. Results: The ADSCs, ADSCs-mito and CCSMCs were isolated and identified successfully. ADSCs-mito transplantation notably restored the erectile function and smooth muscle content of CNI ED rats. Moreover, the levels of ROS, mtROS and cleaved-caspase 3 were reduced and the levels of superoxide dismutase and ATP were increased after ADSCs-mito transplantation. In CNI ED rats, the mitochondrial structure of cells in penile tissues was destroyed. ADSCs could transfer its own mitochondria to CCSMCs. Pre-treatment with ADSCs-mito could significantly decrease apoptosis rate, ROS levels and mtROS levels as well as restore the ATP level in CCSMCs. Conclusions ADSCs-mito transplantation significantly ameliorated ED induced by CNI, with similar potency to ADSCs treatment. The ADSCs-mito might exert their effects via anti-oxidative stress, anti-apoptosis and modulating energy metabolism of CCSMCs. Mitochondrial transplantation should be a promising therapeutic method for treating CNI ED in the future.

Bone defects caused by different causes such as trauma, severe bone infection and other factors are common in clinic and difficult to treat. Usually, bone substitutes are required for repair. Current bone grafting materials used clinically include autologous bones, allogeneic bones, xenografts, and synthetic materials, etc. Other than autologous bones, the major hurdles of rest bone grafts have various degrees of poor biological activity and lack of active ingredients to provide osteogenic impetus. Bone marrow contains various components such as stem cells and bioactive factors, which are contributive to osteogenesis. In response, the technique of bone marrow enrichment, based on the efficient utilization of components within bone marrow, has been risen, aiming to extract osteogenic cells and factors from bone marrow of patients and incorporate them into 3D scaffolds for fabricating bone grafts with high osteoinductivity. However, the scientific guidance and application specification are lacked with regard to the clinical scope, approach, safety and effectiveness. In this context, under the organization of Chinese Orthopedic Association, the Expert consensus for the clinical application of autologous bone marrow enrichment technique for bone repair ( version 2023) is formulated based on the evidence-based medicine. The consensus covers the topics of the characteristics, range of application, safety and application notes of the technique of autologous bone marrow enrichment and proposes corresponding recommendations, hoping to provide better guidance for clinical practice of the technique.

Methcathinone (MCAT) belongs to the designer drugs called synthetic cathinones, which are abused worldwide for recreational purposes. It has strong stimulant effects, including enhanced euphoria, sensation, alertness, and empathy. However, little is known about how MCAT modulates neuronal activity in vivo. Here, we evaluated the effect of MCAT on neuronal activity with a series of functional approaches. C-Fos immunostaining showed that MCAT increased the number of activated neurons by 6-fold, especially in sensory and motor cortices, striatum, and midbrain motor nuclei. In vivo single-unit recording and two-photon Ca²⁺ imaging revealed that a large proportion of neurons increased spiking activity upon MCAT administration. Notably, MCAT induced a strong de-correlation of population activity and increased trial-to-trial reliability, specifically during a natural movie stimulus. It improved the information-processing efficiency by enhancing the single-neuron coding capacity, suggesting a cortical network mechanism of the enhanced perception produced by psychoactive stimulants.
Mice ; Animals ; Reproducibility of Results ; Neurons ; Sensation ; Perception

Background Furniture manufacturing is one of the typical labor-intensive industries, and workers in this industry face a high risk of work-related musculoskeletal disorders (WMSDs), which seriously affect the physical and mental health of workers. Objective To explore the prevalence and potential risk factors of WMSDs among workers in a large-scale furniture manufacturing factory. Methods A cross-sectional study of 3431 workers in a furniture factory in Guangdong Province was conducted from September to December 2019. Information including reported WMSDs in various body parts in the past year, demographic characteristics, work organization factors, job characteristics, and work postures was collected by an electronic version of Musculoskeletal Disorders Questionnaire. Pearson χ² test and binary logistic regression were used to analyze the risk factors leading to WMSDs. Results The overall prevalence rate of WMSDs was 32.12% (1102/3431). The most common WMSDs symptoms occurred in the neck (16.85%), followed by the feet (15.27%), shoulders (14.81%), and hands (14.25%). The prevalence rates of WMSDs in the neck, shoulders, elbows, hands, legs, and feet were significantly different among different types of work (P<0.05). The results of multiple logistic regression analysis showed that individual factors, work organization factors, job characteristics, and awkward work postures were associated with the frequency of reporting WMSDs in specific parts of workers. Comparatively poor physical health (including moderate, poor, and very poor) was positively correlated with neck, shoulder, hand, and foot WMSDs (OR=1.479-4.077); working with an uncomfortable posture (OR=1.983) and doing the same task almost every day (OR=1.783) were positively correlated with neck pain; doing the same task almost every day (OR=2.408) and neck twisting for a long time (OR=1.830) were positively correlated with shoulder pain; bending wrists up and down frequently (OR=1.948) and bending wrists for a long time (OR=2.081) were positively correlated with hand pain; prolonged standing (OR=1.953) and often working overtime (OR=1.627) were positively correlated with feet pain; sufficient rest time was negatively correlated with WMSDs in the neck, shoulders, hands, and foot (OR=0.544-0.717). Conclusion The prevalence rate of WMSDs in furniture manufacturing workers is relatively high, and neck, feet, shoulders, and hands are the most involved body parts. The frequency of reporting WMSDs is related to individual factors, work organization factors, job characteristics, and awkward work postures.

Objective·To investigate the causal relationship between atrial fibrillation(AF)and cognitive impairment.Methods·A two-sample Mendelian randomization(TSMR)analysis was used to assess the potential causality of AF on cognitive dysfunction.Single nucleotide polymorphisms(SNPs)strongly associated with AF were extracted as instrumental variables by using a dataset of a large-scale genome-wide association study(GWAS)on AF.The associations of SNPs with Alzheimer's disease dementia,Parkinson's disease dementia,vascular dementia,Lewy body dementia,frontotemporal dementia,undefined dementia,and overall cognitive function assessment were extracted separately from publicly available GWAS data on cognitive dysfunction.The inverse variance-weighted(IVW)method was used for the main analysis,and sensitivity analyses were conducted by using Cochran's Q test,MR-Egger regression,and leave-one-out method.To verify the robustness of the results,replicate analyses and meta-analyses were performed by using different GWAS data.Results·In the initial analysis,101 SNPs were extracted as instrumental variables from a meta-analysis of a genome-wide association study involving up to 1 030 836 individuals.The IVW analysis showed no evidence for causal associations between AF and dementia[dementia(OR=1.032;95％CI 0.973-1.094;P=0.290),Parkinson's disease dementia(OR=1.004;95％CI 0.780-1.291;P=0.977),vascular dementia(OR=1.123;95％CI 0.969-1.301;P=0.125),or unspecified dementia(OR=1.013;95％CI 0.910-1.129;P=0.807)].In the replication analysis,27 SNPs were extracted as instrumental variables from the FinnGen AF GWAS data,and the 1VW analysis were consistent with the initial analysis[cognitive function(OR=0.999;95％CI 0.982-1.016;P=0.874),Alzheimer's disease dementia(OR=0.977;95％CI 0.943-1.012;P=0.193),Lewy body dementia(OR=1.014;95％CI 0.898-1.145;P=0.826),or frontotemporal dementia(OR=0.996;95％CI 0.745-1.333;P=0.980)].Both Mendelian randomization analyses and meta-analyses showed no evidence of an association between genetically predicted AF and different types of dementia or overall cognitive function assessment.MR-Egger regression suggested no horizontal pleiotropy and leave-one-out analysis showed stable results after individually removing each SNP.Conclusion·No evidence of a causal relationship between AF and cognitive impairment was found.The associations observed in observational studies can be partially attributed to confounding factors such as shared biology or co-morbidities.