With the advancement of more high-quality research, significant progress has been made in the diagnosis and treatment of acute pulmonary embolism. Based on the latest evidence in evidence-based medicine, the Chinese Society of Cardiology released the Guidelines for the Diagnosis and Treatment of Acute Pulmonary Embolism 2025 in June 2025. These guidelines provide comprehensive updates and optimizations in areas such as epidemiology, diagnostic strategies, and treatment options for acute pulmonary embolism. This article interprets the key aspects of the guidelines to promote their widespread dissemination and facilitate the implementation of their recommendations in clinical practice.

Objective:To investigate the value of Sequential Organ Failure (SOFA) score and its dynamics (ΔSOFA) in predicting mortality in hematology care unit (HCU) .Methods:A retrospective clinical study was conducted on 79 critically ill hematologic patients admitted to the Center for Critical Care Medicine, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, between May and June 2024. SOFA scores and ΔSOFA were calculated within 2 days before and after HCU admission. The predictive value of SOFA and ΔSOFA in mortality was assessed using receiver operating characteristic (ROC) curve analysis.Results:Among the 79 patients, the HCU mortality rate was 54.4%. The SOFA scores on days 1–3 (D1, D2, and D3) and ΔSOFA on day 1 (ΔD_1) of all patients, leukemia patients and hematopoietic stem cell transplantation (HSCT) patients were significantly higher in the death group compared with the non-death group (all P<0.05). ROC curve analysis revealed that the D_1, D_2, D_3 scores, and ΔD_1 significantly predicted mortality ( P<0.001), with areas under the curve (AUCs) of 0.786, 0.866, 0.901, and 0.843, respectively. The sensitivity values were 74.36%, 57.89%, 62.85%, and 86.84%, while specificity values were 70%, 100%, 100%, and 67.65%, respectively. In the HSCT group, the D_-1, D_1, D_2, D_ 3, scores and ΔD_1 were predictive of HCU mortality, with AUCs of 0.833, 0.794, 0.871, 0.846, and 0.795, respectively. Sensitivity values for these scores were 100%, 85.71%, 71.43%, 57.14%, and 57.14%, while specificity values were 73.33%, 70.59%, 91.33%, 100%, and 100%, respectively. In the leukemia group, the D_1, D_2, D_3 scores, and ΔD_1 were predictive of HCU mortality, with AUCs of 0.760, 0.829, 0.846, and 0.756, respectively. Sensitivity values were 71.43%, 78.57%, 53.85%, and 71.43%, while specificity values were 76.19%, 78.95%, 100%, and 63.16%, respectively. For all patients, the D_3 score exhibited the highest specificity, while the ΔD_1 demonstrated the highest sensitivity. For patients in both the HSCT and leukemia groups, the sensitivity and specificity values of the D_1 and D_3 scores exceeded those of the ΔD_1. Conclusion:For patients with hematologic critical illness, including leukemia and those undergoing HSCT hospitalized in the HCU, D_1, D_2, D_ 3 scores and ΔD_1 are significantly associated with HCU mortality.

Chronic thromboembolic pulmonary hypertension(CTEPH)is a form of pulmonary hypertension caused by unresolved thrombi and chronic embolization in the pulmonary arteries.In recent years,multi-omics technologies have provided multidimensional insights into CTEPH.Single-cell transcriptomics has identified key pathogenic cell subsets and related mechanisms;Genomics has revealed susceptibility genes associated with coagulation;Proteomics has uncovered differentially expressed proteins closely linked to vascular remodeling;And metabolomics has characterized metabolic reprogramming features and potential sub-typing biomarkers.This review summarizes re-cent advances in these omics fields and discusses their value and prospects in mechanistic exploration,biomarker discovery,and personalized therapeutic strategies.

Hypoxia inducible factors(HIFs)are core molecules that enable the body to adapt to hypoxia environments.By sensing changes in intracellular oxygen pressure,HIFs regulate gene expression related to hypoxia adaptation,thereby enhancing the body's hypoxia tolerance at cellular,tissue and organ levels.On the other hand,HIFs promote the generation of red blood cells,angiogenesis,and regulate the body's energy metabolism,thereby improving its hypoxia tolerance.The enhancement of hypoxia tolerance is of great significance for the prevention and treatment of hypoxia-related diseases,upgrading of athletes'performance,enhancement of workers'efficiency at high-altitudes,and the improvement of individu-als'quality of life.This article reviews the relationships between HIFs and hypoxia tolerance as well as related mechanisms in order to provide strategies for enhancing hypoxia tolerance in the body.

Angiopoietin-like proteins(ANGPTLs)are a family of proteins that are structurally similar to angio-poietin.So far,eight ANGPTLs have been discovered,namely ANGPTL1 to ANGPTL8.They are not only angiogenic fac-tors,but also play a pivotal role in various pathophysiological processes such as glucose and lipid metabolism,redox regu-lation,chronic inflammation and cancer,and having a close connection with the occurrence and development of metabolic diseases.This review focuses on the mechanism of action of ANGPTLs in metabolic associated fatty liver disease,in order to make a contribution to the prevention and treatment of MAFLD and concurrent diseases.

Angiopoietin-like proteins(ANGPTLs)are a family of proteins that are structurally similar to angio-poietin.So far,eight ANGPTLs have been discovered,namely ANGPTL1 to ANGPTL8.They are not only angiogenic fac-tors,but also play a pivotal role in various pathophysiological processes such as glucose and lipid metabolism,redox regu-lation,chronic inflammation and cancer,and having a close connection with the occurrence and development of metabolic diseases.This review focuses on the mechanism of action of ANGPTLs in metabolic associated fatty liver disease,in order to make a contribution to the prevention and treatment of MAFLD and concurrent diseases.

Objective:To investigate the value of Sequential Organ Failure (SOFA) score and its dynamics (ΔSOFA) in predicting mortality in hematology care unit (HCU) .Methods:A retrospective clinical study was conducted on 79 critically ill hematologic patients admitted to the Center for Critical Care Medicine, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, between May and June 2024. SOFA scores and ΔSOFA were calculated within 2 days before and after HCU admission. The predictive value of SOFA and ΔSOFA in mortality was assessed using receiver operating characteristic (ROC) curve analysis.Results:Among the 79 patients, the HCU mortality rate was 54.4%. The SOFA scores on days 1–3 (D1, D2, and D3) and ΔSOFA on day 1 (ΔD_1) of all patients, leukemia patients and hematopoietic stem cell transplantation (HSCT) patients were significantly higher in the death group compared with the non-death group (all P<0.05). ROC curve analysis revealed that the D_1, D_2, D_3 scores, and ΔD_1 significantly predicted mortality ( P<0.001), with areas under the curve (AUCs) of 0.786, 0.866, 0.901, and 0.843, respectively. The sensitivity values were 74.36%, 57.89%, 62.85%, and 86.84%, while specificity values were 70%, 100%, 100%, and 67.65%, respectively. In the HSCT group, the D_-1, D_1, D_2, D_ 3, scores and ΔD_1 were predictive of HCU mortality, with AUCs of 0.833, 0.794, 0.871, 0.846, and 0.795, respectively. Sensitivity values for these scores were 100%, 85.71%, 71.43%, 57.14%, and 57.14%, while specificity values were 73.33%, 70.59%, 91.33%, 100%, and 100%, respectively. In the leukemia group, the D_1, D_2, D_3 scores, and ΔD_1 were predictive of HCU mortality, with AUCs of 0.760, 0.829, 0.846, and 0.756, respectively. Sensitivity values were 71.43%, 78.57%, 53.85%, and 71.43%, while specificity values were 76.19%, 78.95%, 100%, and 63.16%, respectively. For all patients, the D_3 score exhibited the highest specificity, while the ΔD_1 demonstrated the highest sensitivity. For patients in both the HSCT and leukemia groups, the sensitivity and specificity values of the D_1 and D_3 scores exceeded those of the ΔD_1. Conclusion:For patients with hematologic critical illness, including leukemia and those undergoing HSCT hospitalized in the HCU, D_1, D_2, D_ 3 scores and ΔD_1 are significantly associated with HCU mortality.

Objective To explore the application and prospects of artificial intelligence (AI) in metabolic associated fatty liver disease (MAFLD) based on bibliometrics. Methods Relevant literature on the application of AI technology in MAFLD was retrieved from the Web of Science Core Collection (WoSCC) database. Bibliometric analysis was conducted using CiteSpace, VOSviewer, R package "bibliometrix", and online bibliometric analysis was platformed to identify hotspots and trends in this field. Results A total of 303 eligible articles were obtained. Since 2017, the number of papers in this field had experienced explosive growth. The United States was leading the research on the application of AI in MAFLD and was the most frequent participant in international cooperation. San Diego of University of California was the institution with the highest number of publications. Rohit Loomba was the author with the highest number of publications, having published 14 articles. The co-cited keyword clustering labels revealed 10 major clusters: digital image analysis, machine learning, computer-aided diagnosis, fibrosis stage, automated quantitative analysis, metaproteomics, non-invasive diagnosis, ultrasonography, electronic health records, and knowledge representation. Current research on the application of AI in MAFLD mainly focused on the diagnosis, differential diagnosis, and staging of MAFLD. Image recognition and analysis, intelligent assisted diagnosis, AI algorithms, and monitoring disease progression will be important research directions for AI in MAFLD. Conclusion Research on the application of AI in MAFLD is experiencing exponential growth. Given enormous potential and clinical application prospects of this field, the application of AI in MAFLD-related areas will remain a research hotspot in the future.

BACKGROUND:Clinical studies have found good analgesic effects of silver needle-thermal conduction therapy in patients with myofascial pain syndrome,but the exact mechanism remains unclear. OBJECTIVE:To observe the effect of silver needle-thermal conduction therapy on silent information regulator homolog 3(SIRT3)changes and mitochondrial ultrastructure in a rat model of myofascial pain syndrome. METHODS:Twenty rats were randomly selected from 26 Sprague-Dawley rats and were subjected to percussion combined with motor fatigue for replicating the rat model of myofascial pain syndrome.Sixteen rats that were successfully modeled were randomly divided into model group and silver needle-thermal conduction therapy group(treatment group),with eight rats in each group.The remaining rats were used as controls(normal group).The treatment group was treated with silver needle-thermal conduction therapy.Mechanical withdrawal threshold and thermal withdrawal latency of rats were measured at 1 day before modeling,1 day after modeling and 14 days after treatment.Electromyographic activities of the right medial femoral muscle were measured at 14 days after treatment.The right medial femoral muscle tissue was taken for hematoxylin-eosin staining to observe the local morphology and for transmission electron microscopy to observe the mitochondrial ultrastructure.Western blot assay was performed to detect SIRT3 expression. RESULTS AND CONCLUSION:Pain threshold:The mechanical withdrawal threshold and thermal withdrawal latency of the model and treatment groups were significantly decreased compared with those in the normal group and before modeling(P＜0.01).After treatment,the mechanical withdrawal threshold and thermal withdrawal latency of rats were significantly higher in the treatment group compared with the model group(P＜0.01).Electromyography:The rats in the model group showed spontaneous electrical activity in the right medial femur,while the rats in the treatment group showed reduced spontaneous electrical activity,longer time frame(P＜0.01)and lower wave amplitude(P＜0.05)compared with the model group.Hematoxylin-eosin staining:In the normal group,rat muscle fibers arranged closely and regularly.In the model group,the muscle fibers of rats were atrophied,degenerated,and disordered in arrangement.In the treatment group,rat muscle structure disorder improved.Mitochondrial microstructure:Under the transmission electron microscope,mitochondrial structure in the normal group was normal;mitochondrial swelling with broken or disappeared cristae appeared in the model group;mitochondrial swelling in the treatment group was obviously relieved or tended to be normal.SIRT3 expression:SIRT3 expression was significantly downregulated in the model group compared with the normal group,but was significantly upregulated in the treatment group compared with the model group(P＜0.05).To conclude,abnormalities in local muscle mitochondria and downregulation of SIRT3 expression suggest the presence of impaired energy metabolism in the rat model of myofascial pain syndrome.Mitochondrial changes recover and are close to normal after the silver needle-thermal conduction therapy,and the expression of SIRT3 is also upregulated close to the normal group,indicating the silver needle-thermal conduction therapy may play a therapeutic role by promoting mitochondrial repair and improving energy metabolism disorder.

Nonalcoholic fatty liver disease(NAFLD)has become the most common liver disease in the world and is an important risk factor for the progression to hepatocellular carcinoma.However,the pathogenesis of NAFLD remains unclear,and there is still a lack of specific treatment measures.Sterol regulatory element-binding proteins(SREBP)are an important nuclear transcription factor,which mainly maintains the balance of lipid metabolism inside the body by activating the genes associated with the synthesis and uptake of cholesterol,fatty acids,and triglycerides,and therefore,SREBP are a target for the treatment of metabolic diseases.This article reviews the latest advances in SREBP in the pathogenesis of NAFLD and the latest evidence of SREBP-targeted therapy for NAFLD.It is worth noting that recent studies have shown that SREBP inhibition can cause liver injury together with autophagy damage.Therefore,excessive inhibition of lipogenesis may exert a counterproductive effect on the treatment of NAFLD.In conclusion,SREBP is a promising therapeutic target for NAFLD;the molecular mechanism of SREBP in lipid metabolism is regulated by many factors,and these factors are being deeply explored and analyzed,which has an important clinical significance for the treatment of NAFLD.