BACKGROUND:The repair process of myocardial injury involves complex cellular and molecular mechanisms,especially mitochondrial calcium homeostasis,macrophage autophagy and pyroptosis pathways.Traditional Chinese medicine(TCM)has shown significant clinical efficacy in improving myocardial injury,but its mechanism of action needs to be thoroughly investigated. OBJECTIVE:To investigate the role of mitochondrial calcium homeostasis-mediated macrophage autophagy and pyroptosis pathways in myocardial injury,and to summarize the progress of TCM in this field. METHODS:A computerized search was performed for relevant literature from the database inception to March 2024 in the Web of Science,PubMed and CNKI.The search terms were"mitochondrial calcium homeostasis,macrophage autophagy,macrophage pyroptosis,traditional Chinese medicine,myocardial injury,myocardial injury reperfusion"in Chinese and English.Through literature review,we analyzed the relationship between mitochondrial calcium homeostasis and macrophage autophagy and pyroptosis,explored the mechanism of their roles in myocardial injury,and summarized the pathways of multi-targeted,multi-pathway effects of TCM. RESULTS AND CONCLUSION:The maintenance of mitochondrial calcium homeostasis has been found to be closely related to the normal function of cardiomyocytes.Macrophages can participate in the repair process of myocardial injury through autophagy and pyroptosis pathways.Autophagy contributes to cell clearance and regulation of inflammatory response,while pyroptosis affects myocardial repair by releasing inflammatory factors.TCM regulates mitochondrial calcium homeostasis and macrophage function through multiple mechanisms.For example,astragalosid regulates calcium homeostasis by lowering mitochondrial membrane potential and inhibiting cytochrome C,and epimedium glycoside plays a role in reducing β-amyloid deposition.In addition,herbal compounds and single drugs promote myocardial repair by activating or inhibiting specific signaling pathways,such as PI3K/AKT and nuclear factor-κB signaling pathways.Future studies should focus on the interactions between mitochondrial calcium homeostasis,autophagy and pyroptosis pathways,as well as how TCM can exert therapeutic effects through these pathways to provide new strategies and drugs for the treatment of myocardial injury.

Objective: To analyze respiratory syncytial virus(RSV) outbreaks surveillance results and the epidemiological characteristics in kindergarten and school in Shenzhen during 2017-2023 , so as to provide a scientific reference for control and prevention of RSV. Methods: Epidemiological data and surveillance results of RSV outbreaks in kindergarten and school from 2017 to 2023 were collected for descriptive analyses. Results: A total of 31 RSV outbreaks were identified in kindergarten and school in 2017-2023 in Shenzhen, 346 cases were reported, the average incidence rate was 22.02%. The most annual RSV outbreaks were reported in 2020 with 14 outbreaks, followed by 8 outbreaks in 2023. A total of 64.52% of RSV outbreaks were identified in kindergarten with rest occurring in primary school or middle school. The greatest monthly count of outbreak was 18 (58.06%) in September, followed by 3 outbreaks (9.68%) in March and October. A total of 244 swab samples were collected, 169 samples were positive for respiratory viruses, the positive rate was 69.26%, 121 samples were positive for RSV,from 31 respiratory syncytical virus outbreaks 57 and samples were positive for other respiratory viruses(9 samples were positive for two respiratory viruses). A toral of 14(45.16%) outbreaks are caused by RSV alone, 17 outbreaks (54.84%) were caused by RSV and other respiratory viruses. Conclusions Most RSV outbreaks in kindergarten and school are reported after 2020 in Shenzhen, most RSV outbreaks occur in kindergarten, peak seasons of RSV outbreaks are autumn and spring.

BackgroundMetabolic syndrome （MetS） is highly prevalent in patients with mental disorders， including elevated diastolic or systolic blood pressure， elevated fasting glucose， hypercholesterolemia， abdominal obesity and so on. As an important component of MetS， the relationship between hypercholesterolemia and mental disorder has been extensively reported， whereas few genome-wide association studies （GWAS） have been conducted to identify the causal role of mental disorders in hypercholesterolemia. ObjectiveTo explore the potential causal relationship between mental disorders and hypercholesterolemia by two-sample Mendelian randomization （MR） method. MethodsSummary data from GWAS were analyzed. Single nucleotide polymorphisms （SNPs） strongly associated with mental disorders were chosen as instrumental variables， and hypercholesterolemia was used as outcome variable. MR analysis utilized inverse-variance weighted （IVW）， MR-Egger regression and weighted median estimation （WME） as the primary analytical tool， and supplemented by simple mode （SM） and weighted mode （WM）. The causal relationship between mental disorders and the risk of hypercholesterolemia was illustrated in terms of odds ratio （OR）. ResultsA total of 36 SNPs associated with mental disorders were identified as instrumental variables. The primary findings from IVW revealed existence of a causal relationship between mental disorders and hypercholesterolemia （IVW： OR=1.067， 95% CI： 1.026~1.109， P=0.001）. Findings from the additional methods （MR-Egger regression， WME， SM， WM） were basically consistent with those reported in IVW method. Further verification indicated that the causal relationship between mental disorders and the risk of hypercholesterolemia was not affected by genetic polymorphism （P>0.05）. The absence of heterogeneity was confirmed through Cochran's Q test and MR-Egger regression （P>0.05）. Furthermore， no causal association in the reverse direction was found （P>0.05）. ConclusionThere is a causal relationship between mental disorders and hypercholesterolemia， and patients with mental disorders may have an increased probability of suffering from hypercholesterolemia.

The classic formula Fangji Fulingtang is from ZHANG Zhongjing's Synopsis of the Golden Chamber in the Eastern Han dynasty. It is composed of Stephaniae Tetrandrae Radix， Astragali Radix， Cinnamomi Ramulus， Poria， and Glycyrrhizae Radix et Rhizoma， with the effects of reinforcing Qi and invigorating spleen， warming Yang and promoting urination. By a review of ancient medical books， this paper summarizes the composition， original plants， processing， dosage， decocting methods， indications and other key information of Fangji Fulingtang， aiming to provide a literature basis for the research， development， and clinical application of preparations based on this formula. Synonyms of Fangji Fulingtang exist in ancient medical books， while the formula composition in the Synopsis of the Golden Chamber is more widespread and far-reaching. In this formula， Stephaniae Tetrandrae Radix， Astragali Radix， Cinnamomi Ramulus， Poria， and Glycyrrhizae Radix et Rhizoma are the dried root of Stephania tetrandra， the dried root of Astragalus embranaceus var. mongholicus， the dried shoot of Cinnamomum cassia， the dried sclerotium of Poria cocos， and the dried root and rhizome of Glycyrrhiza uralensis， respectively. Fangji Fulingtang is mainly produced into powder， with the dosage and decocting method used in the past dynasties basically following the original formula. Each bag is composed of Stephaniae Tetrandrae Radix 13.80 g， Astragali Radix 13.80 g， Cinnamomi Ramulus 13.80 g， Poria 27.60 g， and Glycyrrhizae Radix et Rhizoma 9.20 g. The raw materials are purified， decocted in water from 1 200 mL to 400 mL， and the decoction should be taken warm， 3 times a day. Fangji Fulingtang was originally designed for treating skin edema， and then it was used to treat impediment in the Qing dynasty. In modern times， it is mostly used to treat musculoskeletal and connective tissue diseases and circulatory system diseases， demonstrating definite effects on various types of edema and heart failure. This paper clarifies the inheritance of Fangji Fulingtang and reveals its key information （attached to the end of this paper）， aiming to provide a theoretical basis for the development of preparations based on this formula.

The classic formula Fangji Fulingtang is from ZHANG Zhongjing's Synopsis of the Golden Chamber in the Eastern Han dynasty. It is composed of Stephaniae Tetrandrae Radix， Astragali Radix， Cinnamomi Ramulus， Poria， and Glycyrrhizae Radix et Rhizoma， with the effects of reinforcing Qi and invigorating spleen， warming Yang and promoting urination. By a review of ancient medical books， this paper summarizes the composition， original plants， processing， dosage， decocting methods， indications and other key information of Fangji Fulingtang， aiming to provide a literature basis for the research， development， and clinical application of preparations based on this formula. Synonyms of Fangji Fulingtang exist in ancient medical books， while the formula composition in the Synopsis of the Golden Chamber is more widespread and far-reaching. In this formula， Stephaniae Tetrandrae Radix， Astragali Radix， Cinnamomi Ramulus， Poria， and Glycyrrhizae Radix et Rhizoma are the dried root of Stephania tetrandra， the dried root of Astragalus embranaceus var. mongholicus， the dried shoot of Cinnamomum cassia， the dried sclerotium of Poria cocos， and the dried root and rhizome of Glycyrrhiza uralensis， respectively. Fangji Fulingtang is mainly produced into powder， with the dosage and decocting method used in the past dynasties basically following the original formula. Each bag is composed of Stephaniae Tetrandrae Radix 13.80 g， Astragali Radix 13.80 g， Cinnamomi Ramulus 13.80 g， Poria 27.60 g， and Glycyrrhizae Radix et Rhizoma 9.20 g. The raw materials are purified， decocted in water from 1 200 mL to 400 mL， and the decoction should be taken warm， 3 times a day. Fangji Fulingtang was originally designed for treating skin edema， and then it was used to treat impediment in the Qing dynasty. In modern times， it is mostly used to treat musculoskeletal and connective tissue diseases and circulatory system diseases， demonstrating definite effects on various types of edema and heart failure. This paper clarifies the inheritance of Fangji Fulingtang and reveals its key information （attached to the end of this paper）， aiming to provide a theoretical basis for the development of preparations based on this formula.

OBJECTIVE To analyze the quantity transfer rule in the processing of Astragalus membranaceus before and after moistening-soaking and steaming-soaking followed by cutting. METHODS Three batches of A. membranaceus decoction pieces processed through moistening-soaking and steaming-soaking followed by cutting were prepared. The HPLC overlapping fingerprints of A. membranaceus and its decoction pieces were established through the Similarity Evaluation System of Chromatographic Fingerprints of TCM （2012 edition）. Combined with the previous qualitative analysis results， the common peaks were identified， the changes of common peak area were analyzed， and the principal component analysis was carried out. The contents of calycosin-7-glucoside， astragaloside Ⅰ and astragaloside Ⅳ in A. membranaceus and its decoction pieces were determined by HPLC， and the content differences of each component in different samples were compared. RESULTS The results of fingerprint analysis showed that 17 common peaks were identified. After steaming-soaking and moistening-soaking of A. membranaceus， the proportion of common peak area in the decoction pieces changed compared with the original medicine （for example， in A. membranaceus steaming-soaking decoction pieces， the proportion of peak area of malonyl calycosin-7-glucoside and malonyl astragaloside Ⅰ decreased， while the proportion of peak area of calycosin-7-glucoside increased）. The results of principal component analysis showed that A. membranaceus， and its decoction pieces after moistening-soaking and steaming-soaking followed by cutting were all clustered into one category respectively. The results of content determination showed that， compared with A. membranaceus， the average content of calycosin-7-glucoside in A. membranaceus moistening-soaking decoction pieces was significantly reduced （P＜0.05）； the average contents of calycosin-7-glucoside and astragaloside Ⅳ in A. membranaceus steaming- soaking decoction pieces were significantly increased （P＜0.05）； there was no significant difference in the average content of astragaloside Ⅳ in A. membranaceus moistening-soaking decoction pieces and astragaloside Ⅰ in the two decoction pieces （P＞ 0.05）. CONCLUSIONS There are differences in the quantity transfer rules of A. membranaceus before and after moistening-soaking and steaming-soaking followed by cutting. Steaming-soaking followed by cutting may make the transformation of unstable components （such as malonyl calycosin-7-glucoside and malonyl astragaloside Ⅰ） more complete.

OBJECTIVE To investigate the clinical efficacy of integrating pharmacists into family health teams （FHTs） for long-term medication therapeutical management （MTM） in stroke patients， and empirically evaluate the service model. METHODS A pharmacist team， jointly established by clinical and community pharmacists from the Affiliated Suzhou Hospital of Nanjing Medical University （hereinafter referred to as “our hospital”）， developed a pharmacist-supported MTM model integrated into FHTs. Using a prospective randomized controlled design， 170 stroke patients discharged from our hospital （July 2022-December 2023） and enrolled in FHTs at Suzhou Runda Community Hospital were randomly divided into trial group （88 cases） and control group （82 cases） according to random number table. The control group received routine FHTs care （without pharmacist involvement in the team collaboration）， while the trial group xhz8405@126.com received 12-month MTM services supported by pharmacists via an information platform. These services specifically included innovative interventions such as personalized medication regimen optimization based on the MTM framework， dynamic medication adherence management， medication safety monitoring， a home medication assessment system， and distinctive service offerings. Outcomes of the 2 grousp were compared before and after intervention， involving medication adherence （adherence rate， adherence score）， compliance rates for stroke recurrence risk factors [blood pressure， low-density lipoprotein cholesterol （LDL-C）]， and incidence of adverse drug reactions （ADR）. RESULTS After 12 months， the trial group exhibited significantly higher medication adherence rates， improved adherence scores， higher compliance rates for blood pressure and LDL-C targets compared to the control group （P＜0.05）. The incidence of ADR in the trial group （4.55%） was significantly lower than that in the control group （8.11%）， though the difference was not statistically significant （P＞ 0.05）. CONCLUSIONS Pharmacist involvement in FHTs to deliver MTM services significantly enhances medication adherence and optimizes risk factor for stroke recurrence， offering practical evidence for advancing pharmaceutical care in chronic disease management under the family doctor system.

Objective To investigate the effects and related mechanisms of mitochondrial-derived peptide MOTS-c on glycochenodeoxycholic acid (GCDCA)-induced injury in human hepatocytes (THLE-3 cells). Methods THLE-3 cells were cultured in vitro and treated with different concentrations of GCDCA and MOTS-c. The optimal concentrations of GCDCA and MOTS-c were determined by cell counting kit (CCK)-8 method. Subsequently, THLE-3 cells were treated or pre-treated with GCDCA (200 µmol/L), MOTS-c (15, 30, 60 µmol/L), the multidrug resistance protein 2 (MRP2) inhibitor Probenecid (500 µmol/L), and the nuclear factor erythroid 2-related factor 2 (Nrf2) inhibitor ML385 (10 µmol/L). Cell proliferation was assessed by CCK-8 method. Lactate dehydrogenase (LDH) levels in the culture medium were measured by biochemical method. Cell apoptosis rates were determined by flow cytometry. MRP2 messenger RNA (mRNA) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). MRP2 and Nrf2 protein expression levels were analyzed by Western blotting. Results As the concentration of GCDCA increased, the proliferation activity of THLE-3 cells gradually decreased, while LDH activity in the culture medium and apoptosis levels increased, and the expression levels of MRP2 in the cells decreased (all P<0.05). Treatment with 30 and 60 µmol/L MOTS-c significantly enhanced the proliferation activity of THLE-3 cells exposed to GCDCA, upregulated the expression of MRP2 and Nrf2, and reduced LDH activity and apoptosis levels (all P<0.05). Co-treatment with Probenecid partially reversed the protective effects of MOTS-c on GCDCA-induced THLE-3 cells injury, while co-treatment with ML385 partially inhibited the induction of MRP2 expression by MOTS-c in THLE-3 cells exposed to GCDCA. Conclusions MOTS-c may alleviate GCDCA-induced injury in human hepatocytes (THLE-3 cells), and its mechanism may be related to the upregulation of MRP2 expression mediated by Nrf2.

Objective: To investigate the potential of conventional cranial computed tomography (CT) in assessing the early neurological deterioration(END), long-term prognosis, and traditional Chinese medicine (TCM) syndrome elements during the acute phase in patients with acute ischemic stroke (AIS). Methods: This study included 101 patients with AIS onset within 24 h in the Emergency Department of Fangshan Hospital, Beijing University of Chinese Medicine, from November 2019 to May 2021. To investigate the correlation between the relevant characteristics of the first conventional cranial CT in patients with AIS onset within 24 h and END, 90 d prognosis, and initial syndrome elements, the presence or absence of END, the 90 d prognosis (non-disabling outcome or functionally independent outcome), and the establishment of syndrome elements (internal fire, phlegm-dampness, blood stasis, qi deficiency, yin deficiency) were used as dependent variables and grouping criteria. Results: This study included 61 males and 40 females, with an age of (64.43±10.56) years. The time from onset to conventional cranial CT examination was 3.50 (1.50, 9.75) h. Among the patients, there were 70 cases (69.3%) of mild AIS, 30 cases (29.7%) of moderate AIS, and one case (1.0%) of severe AIS. Fifteen patients (14.9%) received intravenous thrombolysis. Among the 101 patients, six syndrome elements were observed within 24 h of onset: internal wind in 101 cases (100.0%), internal fire in 58 cases (57.4%), phlegm-dampness in 60 cases (59.4%), blood stasis in 67 cases (66.3%), qi deficiency in 39 cases (38.6%), and yin deficiency in 23 cases (22.8%). The incidence of END was higher in patients with lesions in the contralateral cerebral hemisphere to the affected limb (32.9%) than in those without such lesions (10.7%), showing a strong positive correlation with END occurrence (OR=4.082, P = 0.026). The incidence of END was higher in patients with lesions in the basal ganglia region (33.3%) and the carotid system blood supply area (32.8%) than in those without lesions in the basal ganglia region (15.8%) and the carotid system territory (14.7%), showing moderate positive correlations with END occurrence (OR=2.667, P =0.047; OR=2.836, P=0.044). The proportion of non-disabling outcomes was lower among patients with white matter degeneration (30.8%) and lesions in the contralateral cerebral hemisphere to the affected limb (52.1%) than in those without white matter degeneration (63.6%) and without such lesions in the contralateral cerebral hemisphere to the affected limb (78.6%), both showing strong negative correlations with the occurrence of non-disabling outcomes (OR=0.254, P=0.034; OR=0.296, P=0.015). Similarly, the proportion of functionally independent outcomes was lower among individuals with white matter degeneration (30.8%) and lesions in the contralateral cerebral hemisphere to the affected limb (64.4%) than in those without white matter degeneration (77.3%) and without such lesions in the contralateral cerebral hemisphere to the affected limb (89.3%), both also showing strong negative correlations with the occurrence of functionally independent outcomes (OR=0.131, P=0.001; OR=0.217, P=0.014). The incidence rates of internal fire, blood stasis, and yin deficiency syndrome elements were 66.7%, 73.0%, and 30.2%, respectively, among patients with lesions in the basal ganglia region, compared to 42.1%, 55.3%, and 10.5% among those without lesions in this region. The presence of lesions in the basal ganglia region showed moderate to strong positive correlations with internal fire and yin deficiency syndrome elements (OR=2.750, P=0.016; OR=3.670, P=0.028). Patients with lesions in the centrum semiovale and corona radiata regions (66.7%) had a higher incidence of qi deficiency than those without lesions in this region (33.7%), showing a strong positive correlation with the occurrence of qi deficiency (OR=3.931, P=0.022). No CT characteristics were found to be correlated with phlegm-dampness syndrome elements. Conclusion The first cranial CT in patients with AIS has potential application value in predicting disease progression, assessing prognosis, and diagnosing syndromes, which can provide physicians with diagnostic and treatment decisions to improve the long-term prognosis of patients with AIS.

Autophagy, a highly conserved cellular degradation mechanism, maintains intracellular homeostasis by removing damaged organelles and abnormal proteins. Its dysregulation is closely associated with various diseases. Autophagy-related protein 12 (ATG12), a core member of the ubiquitin-like protein family, covalently binds to ATG5 through a ubiquitin-like conjugation system to form the ATG12-ATG5-ATG16L1 complex. This complex directly regulates the formation and maturation of autophagosomes, making ATG12 a key molecule in the initiation of autophagy. Recent studies have revealed that ATG12 functions extend far beyond the classical autophagy context. It promotes apoptosis by binding to anti-apoptotic proteins of the Bcl-2 family (e.g., Bcl-2 and Mcl-1) and enhances host antiviral immunity by regulating the NF-κB and interferon signaling pathways. Moreover, ATG12 deficiency can lead to mitochondrial biogenesis impairment, energy metabolism disorders, and substrate-dependent metabolic shifts, underscoring its pivotal role in cellular metabolic homeostasis. At the disease level, dysregulation of ATG12 expression is closely linked to tumorigenesis and cancer progression. By modulating the dynamic balance between autophagy and apoptosis, ATG12 influences cancer cell proliferation, metastasis, and chemoresistance. Notably, ATG12 is abnormally overexpressed in multiple cancers, including breast, liver, and gastric cancer, highlighting its potential as a therapeutic target. Furthermore, in neurodegenerative diseases such as Parkinson’s disease, ATG12 mitigates protein toxicity by enhancing mitochondrial autophagy. In cardiovascular diseases, it alleviates ischemia-reperfusion injury by regulating cardiomyocyte autophagy and apoptosis, demonstrating its broad regulatory role across various pathological conditions. Genetic studies further underscore the clinical significance of ATG12. Polymorphisms in the ATG12 gene (e.g., rs26537 and rs26538) have been significantly associated with the risk of head and neck squamous cell carcinoma, hepatocellular carcinoma, and atrophic gastritis. Notably, the risk allele of rs26537 enhances ATG12 promoter activity, leading to its overexpression and promoting tumorigenesis. These findings provide a molecular basis for individualized risk assessment and targeted interventions based on ATG12 genotype. Despite significant progress, many aspects of ATG12 biology remain unclear. The precise regulatory mechanisms of its post-translational modifications (e.g., ubiquitination and acetylation) are yet to be fully elucidated. Additionally, the molecular pathways underlying its non-canonical functions, such as metabolic regulation and immune modulation, require further investigation. Moreover, the functional heterogeneity of ATG12 in different tumor microenvironments and its role in drug resistance warrant in-depth exploration. Future research should integrate advanced technologies such as cryo-electron microscopy, single-cell sequencing, and organoid models to decipher the intricate regulatory network of ATG12. Additionally, developing small-molecule inhibitors or gene-editing tools targeting its protein interaction interfaces (e.g., the ATG12-ATG3 binding domain) may help overcome current therapeutic challenges. Through interdisciplinary collaboration and clinical translation, ATG12 holds promise as a next-generation molecular target for precision intervention in autophagy-related diseases. This review summarizes the structure and function of ATG12, its role in autophagy initiation, its physiological functions, and its involvement in disease pathogenesis. Furthermore, it discusses future research directions and potential challenges, emphasizing ATG12’s potential as a biomarker and therapeutic target in autophagy-related diseases.