Chronic heart failure (CHF) is a pathological state in which the cardiac ejection fraction is insufficient to meet an individual's metabolic needs owing to changes in the cardiac structure or function. Various etiologies such as myocardial infarction and inflammation are implicated, and the main symptoms are dyspnea, lower limb edema, fatigue, and discomfort during rest or exercise. CHF is the primary outcome of cardiovascular disease, and the increasing morbidity and mortality rates highlight the significant risks of this condition. According to traditional Chinese medicine, the pathogenesis of CHF is deficiency of heart qi and heart yang, which predominantly affects the heart, but may also impede the function of other zang-organs such as the spleen and kidney, and aggravate the symptoms of heart failure. With technological advancements and enhanced awareness of health conditions and disease prevention, China has promoted traditional medicine practices such as medicine and food homology (MFH), which has received increasing attention in recent years. This concept stipulates that certain medicines and foods have the same origin; ergo, these foods have medicinal properties, with many being used in the prevention and treatment of CHF. However, the efficacy and safety of MHF substances have yet to be determined, and there is no consensus regarding the development of disease prevention and treatment strategies. This article therefore reviews the current evidence for MFH in the prevention and treatment of CHF by summarizing the therapeutic potential of this practice and discussing treatment strategies and aims to improve the understanding of Chinese medicine and food homologous substances in the treatment of this condition, as well as highlight the current literature and avenues for future research.

Objective: To explore the network structure of dietary intake and physical fitness subtypes among junior and senior high school students, so as to provide precise and efficient intervention guidance for improving abnormal physical health issues in adolescents. Methods: Based on the 2020-2021 Database of Youth Health (DYH), a total of 9 730 junior and senior high school students in Shandong Province were included for analysis. Dietary intake was assessed using a modified Chinese Dietary Quality Questionnaire, and physical fitness was evaluated according to the "2014 National Student Physical Fitness Standard". The Kmeans clustering algorithm was employed to identify potential subtypes of physical fitness in junior and high school students. Network analysis was used to construct a network linking dietary intake and physical fitness symptoms and to identify clusters of dietary behaviors and physical fitness symptoms among adolescents of different genders. Results: The physical fitness among junior and senior high school students of different genders were categorized into two subtypes: the baseline steady type (3 427 male students, 4 039 female students) and the morphological deviation type (1 294 male students, 970 female students). Statistically significant differences were observed in network strength and network connectivity strength among different genders and physical fitness subtypes (all P<0.05). Connections between food intake and physical health symptom clusters across different genders and physical health types among junior and senior high school students were primarily achieved through instant noodle intake and physical fitness (males of morphological deviation type, weight=0.06), fruit intake and physical fitness (males of baseline steady type, weight=-0.07), potato intake and vital capacity (females of morphological deviation type, weight=0.09), and processed meat intake and vital capacity (females of baseline steady type, weight=0.05). Conclusions Dietary intake serves as a significant modifiable risk factor for the physical fitness of junior and high school students. Interventions should focus on promoting healthy eating habits.

In recent years,significant progress has been made in diabetes research both domestically and internationally,new diagno-sis and treatment techniques and methods have been constantly emerging,and clinical research evidence has been continuously accu-mulated and updated.To keep pace with these important developments,the Diabetes Branch of the Chinese Medical Association has ac-tively organized experts to update the China Guidelines for the Prevention and Treatment of Diabetes.This update aims to provide a more comprehensive and scientific guide for diabetes prevention and treatment,greatly promote the standardized and integrated man-agement of diabetes by clinicians,and ensure that patients receive standardized and personalized treatment plans to improve therapeu-tic outcomes and quality of life.

Over the years,the American Diabetes Association(ADA)has been actively committed to the development and promotion of standards for the diagnosis,treatment,and daily care of diabetes.Since 1989,it has updated the diabetes diagnosis and treatment standards every year,which have become one of the most authoritative guidelines in diabetes and have been recognized and adopted by various countries.On December 10,2024,the 2025 Standards of Care in Diabetes were released,incorporating the latest evidence-based medicine content related to diabetes and its complications and comorbidities.It aims to provide guidance on the diagnosis,treat-ment,and management of the condition for clinicians,patients and their families,and researchers.This article interprets the major up-dates from the Standards.

With the acceleration of population aging in China,the management of elderly patients with diabetes has become a critical issue in the field of public health.By integrating international evidence-based medical research data with the specific conditions of China,the 2024 edition of Guideline for the management of diabetes mellitus in the elderly in China proposes individualized diagnosis and treatment strategies for elderly patients with diabetes.This article gives a systematic interpretation of the guideline from a nursing perspective,with a focus on the core contents closely associated with nursing practice,and it also elaborates on the implications for nursing work,summarizes and analyzes the challenges in the management of elderly patients with diabetes,and proposes corresponding strategies,in order to provide a theoretical basis and practical guidance for implementing nursing management of elderly patients with diabetes among clinical nurses.

The Guideline for the prevention and treatment of diabetes mellitus in China(2024 edition),released by the Chinese Dia-betes Society on January 20,2025,has updated evidence on diabetes mellitus from various aspects including its epidemiological status in China,diagnosis and treatment progress,and complication management,aiming to guide and facilitate standardized comprehensive management of diabetes mellitus in clinical practice.This paper interprets the guideline from the perspective of nursing practice,focus-ing on nursing care for special diabetic conditions,lifestyle and behavioral interventions,and the procedures of relevant nursing tech-niques.We hope to provide nursing professionals with standardized guidance on diabetes prevention and treatment,thereby further standardizing and refining specialized nursing care for diabetes mellitus,enhancing the quality of patient care,and improving patient prognosis.

Objective To predict and preliminarily validate potential shared key genes involved in cardiac complications caused by influenza A virus(IAV)and severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infections.Methods Differentially expressed genes(DEGs)associated with cardiac complications were obtained from the Gene Expression Omnibus(GEO)database.A hierarchical intersection strategy was applied.First,cardiac complication related DEGs were overlapped with 2 independent virus related gene sets:3 454 human genes linked to IAV infection in GeneCards and 333 human protein-coding genes interacting with SARS-CoV-2 in the Human Protein Atlas.The 2 overlap results were then intersected to yield 22 hub genes.Lasso regression,random forest(RF)and support vector machine algorithms(SVM)were employed to refine this list.Predicted genes were validated in vitro in H1N1-infected human cardiomyocyte AC16 cells and in vivo in IFITM3 knockout mice challenged with H1N1,assessing transcriptional changes.Results A total of 22 hub genes were identified through integrative bioinformatics analysis.Application of the 3 machine learning algorithms resulted in 5 common key genes:ACE2,TBK1,NUP210,PUSL1,and MEPCE.In vitro infection of AC16 cells with H1N1 revealed dynamic transcriptional changes in all 5 genes post-infection(P<0.05).In vivo experiments using H1N1-infected IFITM3 knockout mice confirmed the dynamic mRNA expression changes of these 5 genes,consistent with the in vitro results(P<0.05).Conclusion By combining multilayered bioinformatics analysis with 3 machine learning approaches,5 common key genes are identified:ACE2,TBK1,NUP210,PUSL1 and MEPCE.Validation in H1N1 infection models confirms their relevance to IAV-induced cardiac complications.

Background: Acetaminophen (APAP)-induced hepatotoxicity has attracted considerable attention in clinical settings due to the limited treatment options available. Liensinine stands out as a key alkaloid known for its pharmaceutical activities. However, the role of liensinine in mitigating APAP-induced liver injury remains unclear. Objective: The aim of the study was to explore the protective effects of liensinine against APAP-induced liver injury. Methods: C57BL/6 male mice were treated with a dose of 200 mg/kg N-acetylcysteine or varying doses of liensinine (10 or 20 mg/kg) for seven consecutive days. APAP (400 mg/kg, i.g.) was then administered to induce liver damage for 12 hours. Blood samples and hepatic tissues were collected for further analysis. Liver enzyme levels and histopathological analysis were employed to assess liver injury. RNA-seq was conducted to evaluate the dynamic changes in gene expression. Biochemical assays were used to measure oxidative stress and inflammation, while the TUNEL assay was performed to assess hepatocyte apoptosis. Results: The results demonstrated that the administration of liensinine mitigated serum liver enzyme levels and tissue damage resulting from APAP overdose. Transcriptome analysis revealed significant and coordinated changes in genes related to the peroxisome proliferator-activated receptor signaling pathway, mitogen-activated protein kinase signaling pathway, and apoptosis pathway in response to APAP-induced hepatotoxicity. The expression alterations of key genes within these three pathways, associated with inflammation, oxidative stress, and cell apoptosis, were reversed by liensinine, indicating its potential in alleviating APAP-induced liver damage through multiple signaling pathways. This suggests the diverse therapeutic effects of liensinine, including inflammation suppression, oxidative stress reduction, and cell apoptosis inhibition. Indeed, pretreatment with liensinine effectively reduced inflammatory cytokines, oxidative stress indicators, and apoptotic cells induced by APAP. Conclusions: Liensinine mitigates APAP-induced hepatotoxicity in mice through multifaceted pathways, providing anti-inflammatory, antioxidant, and anti-apoptotic benefits.

Background: Acetaminophen (APAP)-induced hepatotoxicity has attracted considerable attention in clinical settings due to the limited treatment options available. Liensinine stands out as a key alkaloid known for its pharmaceutical activities. However, the role of liensinine in mitigating APAP-induced liver injury remains unclear. Objective: The aim of the study was to explore the protective effects of liensinine against APAP-induced liver injury. Methods: C57BL/6 male mice were treated with a dose of 200 mg/kg N-acetylcysteine or varying doses of liensinine (10 or 20 mg/kg) for seven consecutive days. APAP (400 mg/kg, i.g.) was then administered to induce liver damage for 12 hours. Blood samples and hepatic tissues were collected for further analysis. Liver enzyme levels and histopathological analysis were employed to assess liver injury. RNA-seq was conducted to evaluate the dynamic changes in gene expression. Biochemical assays were used to measure oxidative stress and inflammation, while the TUNEL assay was performed to assess hepatocyte apoptosis. Results: The results demonstrated that the administration of liensinine mitigated serum liver enzyme levels and tissue damage resulting from APAP overdose. Transcriptome analysis revealed significant and coordinated changes in genes related to the peroxisome proliferator-activated receptor signaling pathway, mitogen-activated protein kinase signaling pathway, and apoptosis pathway in response to APAP-induced hepatotoxicity. The expression alterations of key genes within these three pathways, associated with inflammation, oxidative stress, and cell apoptosis, were reversed by liensinine, indicating its potential in alleviating APAP-induced liver damage through multiple signaling pathways. This suggests the diverse therapeutic effects of liensinine, including inflammation suppression, oxidative stress reduction, and cell apoptosis inhibition. Indeed, pretreatment with liensinine effectively reduced inflammatory cytokines, oxidative stress indicators, and apoptotic cells induced by APAP. Conclusions: Liensinine mitigates APAP-induced hepatotoxicity in mice through multifaceted pathways, providing anti-inflammatory, antioxidant, and anti-apoptotic benefits.

Background: Acetaminophen (APAP)-induced hepatotoxicity has attracted considerable attention in clinical settings due to the limited treatment options available. Liensinine stands out as a key alkaloid known for its pharmaceutical activities. However, the role of liensinine in mitigating APAP-induced liver injury remains unclear. Objective: The aim of the study was to explore the protective effects of liensinine against APAP-induced liver injury. Methods: C57BL/6 male mice were treated with a dose of 200 mg/kg N-acetylcysteine or varying doses of liensinine (10 or 20 mg/kg) for seven consecutive days. APAP (400 mg/kg, i.g.) was then administered to induce liver damage for 12 hours. Blood samples and hepatic tissues were collected for further analysis. Liver enzyme levels and histopathological analysis were employed to assess liver injury. RNA-seq was conducted to evaluate the dynamic changes in gene expression. Biochemical assays were used to measure oxidative stress and inflammation, while the TUNEL assay was performed to assess hepatocyte apoptosis. Results: The results demonstrated that the administration of liensinine mitigated serum liver enzyme levels and tissue damage resulting from APAP overdose. Transcriptome analysis revealed significant and coordinated changes in genes related to the peroxisome proliferator-activated receptor signaling pathway, mitogen-activated protein kinase signaling pathway, and apoptosis pathway in response to APAP-induced hepatotoxicity. The expression alterations of key genes within these three pathways, associated with inflammation, oxidative stress, and cell apoptosis, were reversed by liensinine, indicating its potential in alleviating APAP-induced liver damage through multiple signaling pathways. This suggests the diverse therapeutic effects of liensinine, including inflammation suppression, oxidative stress reduction, and cell apoptosis inhibition. Indeed, pretreatment with liensinine effectively reduced inflammatory cytokines, oxidative stress indicators, and apoptotic cells induced by APAP. Conclusions: Liensinine mitigates APAP-induced hepatotoxicity in mice through multifaceted pathways, providing anti-inflammatory, antioxidant, and anti-apoptotic benefits.