Platelets are small, anucleated cells generated by cytoplasmic fragmentation and shedding from mature megakaryocytes. Upon vascular stimulation or injury, platelets become activated and adhere to exposed vascular endothelial cells, ultimately forming thrombi to promote blood coagulation and wound healing. In recent years, increasing evidence from in-depth studies on platelet function has revealed that autophagy plays a crucial role in platelet production and functional performance. Autophagy is an intracellular process of material recycling and reuse, involving autophagosome formation, cargo degradation, and nutrient recycling, which facilitates the maintenance of homeostasis and defense against pathogen infection. Numerous studies have demonstrated that autophagy participates in the regulation of platelet production, activation, and aggregation, and is closely implicated in the pathogenesis of platelet dysfunction-related diseases such as immune thrombocytopenia. Additionally, platelet-rich plasma therapy, by modulating the autophagic process, has shown great potential in treating osteoarthritis and promoting diabetic foot wound healing. This review thoroughly explores the potential roles of autophagy in regulating platelet production and function, as well as in platelet-related diseases. Future research should focus on the molecular mechanisms of platelet autophagy, investigate its dynamic changes under different disease conditions, and explore how autophagy modulation can improve platelet function and treat related diseases. This will provide a theoretical foundation for developing novel therapeutic strategies and is expected to bring breakthroughs in the treatment of platelet-related diseases.

Chronic heart failure （CHF） is a major global public health problem， and myocardial infarction is one of its main causes. The mouse model of heart failure induced by coronary artery ligation is widely used in the study of CHF， while the TCM syndrome attributes of this model have not yet been clarified. According to the theory of correspondence between prescriptions and syndromes， the method of syndrome identification by prescription efficacy is an important means of current syndrome research of animal models. This method deduces the syndrome characteristics of animal models through prescription efficacy. Taking the four basic syndrome elements of Qi， blood， Yin and Yang as the classification reference， this study used coronary artery ligation to construct a mouse model of CHF and treated the model with four representative TCM injections with the effects of replenishing Qi， warming Yang， nourishing Yin， and activating blood and enalapril. Echocardiography， tongue color parameters， histopathology， serum N-terminal pro-brain natriuretic peptide （NT-proBNP） and cardiac troponin Ⅰ （cTnⅠ） levels， and systematically explored the TCM syndrome attributes of this model. The results showed that the coronary ligation model presented an obvious cardiac function decline， myocardial fibrosis， infarct size expansion， and purple dark tongue， which were consistent with the basic syndrome characteristics of blood stasis in CHF. Danhong injection had significant effects of improving the cardiac function， alleviating myocardial fibrosis， and reducing serum NT-proBNP and cTnⅠ levels. Huangqi Injection and Shenfu injection can improve the cardiac function and tongue color parameters， with limited effects. The effect of Shenmai injection group was not obvious. This study verifies that the established model conforms to blood stasis syndrome through the method of syndrome identification by prescription efficacy， which provides an experimental basis for the study of TCM syndrome mechanism of CHF.

ObjectiveTo examine the influences of Shenfu injection on the endogenous metabolic byproducts in the myocardium of the rat model exhibiting chronic heart failure， thus deciphering the therapeutic mechanism of the Qi-reinforcing and Yang-warming method. MethodsSD rats were randomly allocated into a control group and a modeling group. Chronic heart failure with heart-Yang deficiency syndrome in rats was modeled by multi-point subcutaneous injection of isoproterenol， and the rats were fed for 14 days after modeling. The successfully modeled rats were randomized into model， Shenfu injection （6.0 mL·kg^-1）， and trimetazidine （10 mg·kg^-1） groups and treated with corresponding agents for 15 days. The control group and the model group were injected with equal doses of normal saline， and the samples were collected after the intervention was completed. Cardiac color ultrasound was performed. Hematoxylin-eosin （HE） staining was used to observe histopathological morphology， and the serum level of N-terminal pro-brain natriuretic peptide （NT-proBNP） was assessed by enzyme-linked immunosorbent assay （ELISA）. The mitochondrial morphological and structural changes of cardiomyocytes were observed by transmission electron microscopy， and the metabolic profiling was carried out by ultra high performance liquid chromatography-quantitative exactive-mass spectrometry （UHPLC-QE-MS）. Differential metabolites were screened and identified by orthogonal partial least squares-discriminant analysis （OPLS-DA） and other methods， and then the MetaboAnalyst database was used for further screening. The relevant biological pathways were obtained through pathway enrichment analysis. The receiver operating characteristic （ROC） curve was established to evaluate the diagnostic value of each potential biomarker for myocardial injury and the evaluation value for drug efficacy. ResultsThe results of color ultrasound showed that Shenfu Injection improved the cardiac function indexes of model rats （P<0.05）. The results of HE staining showed that Shenfu injection effectively alleviated the pathological phenomena such as myocardial tissue structure disorder and inflammatory cell infiltration in model rats. The results of ELISA showed that Shenfu injection effectively regulated the serum NT-proBNP level in the model rats. Transmission electron microscopy （TEM） showed that Shenfu injection effectively restored the mitochondrial morphological structure. The results of metabolomics showed that the metabolic phenotypes of myocardial samples presented markedly differences between groups. Nine differential metabolites could be significantly reversed in the Shenfu injection group， involving three metabolic pathways： pyruvate metabolism， histidine metabolism， and citric acid cycle （TCA cycle）. The results of ROC analysis showed that the area under the curve （AUC） values of all metabolites were between 0.75 and 1.0， indicating that the differential metabolites had high diagnostic accuracy for myocardial injury， and the changes in their expression levels could be used as potential markers for efficacy evaluation. ConclusionShenfu injection significantly alleviated the damage of cardiac function， myocardium， and mitochondrial structure in the rat model of chronic heart failure with heart-Yang deficiency syndrome by ameliorating energy metabolism remodeling. Reinforcing Qi and warming Yang is a key method for treating chronic heart failure with heart-Yang deficiency syndrome.

To explore the advantages of traditional Chinese medicine （TCM） and integrative TCM-Western medicine approaches in the treatment of diabetic microvascular complications （DMC）， refine key pathophysiological insights and treatment principles， and promote academic innovation and strategic research planning in the prevention and treatment of DMC. The 38th session of the Expert Salon on Diseases Responding Specifically to Traditional Chinese Medicine， hosted by the China Association of Chinese Medicine， was held in Beijing， 2024. Experts in TCM， Western medicine， and interdisciplinary fields convened to conduct a systematic discussion on the pathogenesis， diagnostic and treatment challenges， and mechanism research related to DMC， ultimately forming a consensus on key directions. Four major research recommendations were proposed. The first is addressing clinical bottlenecks in the prevention and control of DMC by optimizing TCM-based evidence evaluation systems. The second is refining TCM core pathogenesis across DMC stages and establishing corresponding "disease-pattern-time" framework. The third is innovating mechanism research strategies to facilitate a shift from holistic regulation to targeted intervention in TCM. The fourth is advancing interdisciplinary collaboration to enhance the role of TCM in new drug development， research prioritization， and guideline formulation. TCM and integrative approaches offer distinct advantages in managing DMC. With a focus on the diseases responding specifically to TCM， strengthening evidence-based support and mechanism interpretation and promoting the integration of clinical care and research innovation will provide strong momentum for the modernization of TCM and the advancement of national health strategies.

Background Pneumoconiosis remains a critical occupational disease in China. As a major industrial province, Hebei historically faced severe challenges regarding this condition. The 1986 national epidemiological survey ranked Hebei sixth in reported pneumoconiosis cases nationwide. Objective To analyze 76 years of pneumoconiosis data (1949–2024) in Hebei Province to provide evidence-based support for prevention and control strategies. Methods Occupational pneumoconiosis cases diagnosed in Hebei from 1949 to 2024 were included. Five-year intervals were used to analyze incidence composition, dust exposure duration, age at first diagnosis, and age at death. A hybrid model, integrating autoregressive integrated moving average (ARIMA) with generalized regression neural network (GRNN), was employed to predict case numbers for the 2025−2030 period. Results A total of 36107 cases of pneumoconiosis were recorded (2.10% female) in Hebei from 1949 to 2024. Stages I, II, and III accounted for 77.35%, 16.45%, and 6.20%, respectively. Silicosis (55.60%), coal workers’ pneumoconiosis (27.24%), and pottery workers’ pneumoconiosis (8.88%) were the predominant types. Observed trends included a shortened dust exposure duration [silicosis: (12.78±7.063) years in 2020–2024] and an increasing age at first diagnosis [(54.01±7.499) years in 2020–2024]. The case-fatality rate was 14.84%, with a rising age at death [(82.26±9.632) years in 2015–2019]. Three incidence peaks (1963, 1984, and 2014) correlated with national policies and industrialization phases. The number of pneumoconiosis cases showed a decreasing trend from 2015 to 2024. Chengde and Tangshan were identified as current high-risk areas. The ARIMA-GRNN model projected annual cases between 416 and 429 during 2025–2030. Conclusion In the past decade，the number of pneumoconiosis cases in Hebei Province had shown a decreasing trend, it is projected to plateau with no significant decline over the next five years. Furthermore, challenges such as the proportion of silicosis remaining high and shortened dust exposure duration remain severe. It is recommended to focus on key regions like Chengde (ore mining) and Tangshan (ceramics industry). A comprehensive strategy integrating stricter regulation, technological controls, model innovation, and targeted interventions should be implemented to achieve a further substantial reduction in pneumoconiosis incidence.

Background Pneumoconiosis remains a critical occupational disease in China. As a major industrial province, Hebei historically faced severe challenges regarding this condition. The 1986 national epidemiological survey ranked Hebei sixth in reported pneumoconiosis cases nationwide. Objective To analyze 76 years of pneumoconiosis data (1949–2024) in Hebei Province to provide evidence-based support for prevention and control strategies. Methods Occupational pneumoconiosis cases diagnosed in Hebei from 1949 to 2024 were included. Five-year intervals were used to analyze incidence composition, dust exposure duration, age at first diagnosis, and age at death. A hybrid model, integrating autoregressive integrated moving average (ARIMA) with generalized regression neural network (GRNN), was employed to predict case numbers for the 2025−2030 period. Results A total of 36107 cases of pneumoconiosis were recorded (2.10% female) in Hebei from 1949 to 2024. Stages I, II, and III accounted for 77.35%, 16.45%, and 6.20%, respectively. Silicosis (55.60%), coal workers’ pneumoconiosis (27.24%), and pottery workers’ pneumoconiosis (8.88%) were the predominant types. Observed trends included a shortened dust exposure duration [silicosis: (12.78±7.063) years in 2020–2024] and an increasing age at first diagnosis [(54.01±7.499) years in 2020–2024]. The case-fatality rate was 14.84%, with a rising age at death [(82.26±9.632) years in 2015–2019]. Three incidence peaks (1963, 1984, and 2014) correlated with national policies and industrialization phases. The number of pneumoconiosis cases showed a decreasing trend from 2015 to 2024. Chengde and Tangshan were identified as current high-risk areas. The ARIMA-GRNN model projected annual cases between 416 and 429 during 2025–2030. Conclusion In the past decade，the number of pneumoconiosis cases in Hebei Province had shown a decreasing trend, it is projected to plateau with no significant decline over the next five years. Furthermore, challenges such as the proportion of silicosis remaining high and shortened dust exposure duration remain severe. It is recommended to focus on key regions like Chengde (ore mining) and Tangshan (ceramics industry). A comprehensive strategy integrating stricter regulation, technological controls, model innovation, and targeted interventions should be implemented to achieve a further substantial reduction in pneumoconiosis incidence.

OBJECTIVE To explore the antidepressant mechanism of Wenyang jieyu granules （WYJYG） via the NOD-like receptor thermal protein domain associated protein 3 （NLRP3）/apoptosis-associated speck-like protein containing a CARD （ASC）/Caspase-1 pathway. METHODS A rat model of depression was established by chronic unpredictable mild stress combined with single-housing for 42 consecutive days.The experiment set up blank group， model group， MCC950 （NLRP3 inflammasome inhibitor） group （10 mg/kg）， fluoxetine group （positive control，2.08 mg/kg），low-dose WYJYG（3.78 g/kg） and high-dose WYJYG group （7.56 g/kg），with 10 rats in each group. From the 22nd day of the experiment， rats in the fluoxetine group， low-dose and high-dose WYJYG groups were intragastrically administered with the corresponding drugs and intraperitoneally injected with an equal volume of normal saline. Rats in the MCC950 group were intraperitoneally injected with MCC950 at the corresponding concentration and intragastrically administered with an equal volume of distilled water. Rats in the blank group and model group were given an equal volume of distilled water by gavage and an equal volume of normal saline by intraperitoneal injection. All interventions were performed once a day for 21 consecutive days. Behavioral tests were conducted once a week. After the last administration， the contents of ASC， ionized calcium binding adaptor molecule 1 （Iba1）， interleukin-1β （IL-1β）， and IL-18 in hippocampal tissues were detected. The protein expressions of NLRP3， cluster of differentiation 68 （CD68）， Caspase-1， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein were determined， and neuronal apoptosis was observed. RESULTS After the last administration， compared with the model group， the open-field activity time was significantly prolonged （ P ＜0.05）， and the latency to feed in a novel environment was significantly shortened （ P ＜0.05） in rats of the high-dose WYJYG group. In hippocampal tissue， the contents of ASC， Iba1， IL-1β， and IL-18， as well as the protein expression levels of NLRP3， Caspase-1， and CD68， and the positive rate of neuronal apoptosis were all significantly decreased/downregulated （ P ＜0.05）. Bcl-2 protein expression was significantly upregulated （ P ＜0.05）， and the density of neuronal apoptosis-positive cells was significantly reduced （ P ＜0.05）. CONCLUSIONS WYJYG play on antidepressant role by inhibiting the NLRP3/ASC/Caspase-1 pathway， reducing microglia-mediated neuroinflammation， and inhibiting hippocampal neurons apoptosis.

Ferroptosis, a regulated cell death process distinct from apoptosis, is characterized by iron dysregulation and reactive oxygen species (ROS) accumulation. After intracerebral hemorrhage (ICH), decreased cerebral blood flow and iron released from erythrocytes trigger lipid peroxidation-particularly of polyunsaturated fatty acids (PUFAs)-through a cascade of reactions in local brain tissues, promoting ferroptosis. Mitochondrial dysfunction and neuroinflammation further elevate ROS, exacerbating lipid peroxidation and accelerating neuronal ferroptosis. Thus, PUFA peroxidation and associated metabolic pathways play a critical role in ICH-related neuronal damage. This review summarizes current understanding of how PUFA peroxidation contributes to ferro-ptosis after ICH, discusses key regulatory mechanisms involving lipid and iron metabolism, and highlights potential therapeutic strategies targeting ferroptosis to improve neurological outcomes.
Ferroptosis/physiology* ; Humans ; Cerebral Hemorrhage/pathology* ; Lipid Peroxidation ; Fatty Acids, Unsaturated/metabolism* ; Reactive Oxygen Species/metabolism* ; Iron/metabolism* ; Animals ; Mitochondria/metabolism*

N⁶-methyladenosine (m⁶A) modification plays a critical role in cell cycle regulation, while the mechanism of m⁶A in regulating mitosis remains underexplored. Here, we found that the total m⁶A modification level in cells increased during mitosis by the liquid chromatography-mass spectrometry/mass spectrometry and m⁶A dot blot assays. Silencing methyltransferase-like 3 (METTL3) or METTL14 results in delayed mitosis, abnormal spindle assembly, and chromosome segregation defects by the immunofluorescence. By analyzing transcriptome-wide m⁶A targets in HeLa cells, we identified polo-like kinase 1 (PLK1) as a key gene modified by m⁶A in regulating mitosis. Specifically, through immunoblotting and RNA pulldown, m⁶A modification inhibits PLK1 translation via YTH N⁶-methyladenosine RNA binding protein 1, thus mediating cell cycle homeostasis. Demethylation of PLK1 mRNA leads to significant mitotic abnormalities. These findings highlight the critical role of m⁶A in regulating mitosis and the potential of m⁶A as a therapeutic target in proliferative diseases such as cancer.
Humans ; Polo-Like Kinase 1 ; Cell Cycle Proteins/metabolism* ; Proto-Oncogene Proteins/metabolism* ; Protein Serine-Threonine Kinases/metabolism* ; Mitosis/physiology* ; HeLa Cells ; Adenosine/genetics* ; Methyltransferases/metabolism* ; RNA, Messenger/metabolism* ; RNA-Binding Proteins/metabolism*

Objective: To evaluate the intervention efficacy of integrated group social skills training on social ability in school age patients with high functioning ASD, so as to provide a reference for improving social skills in children with high functioning ASD. Methods: From January 2021 to December 2023, 62 children aged 7-12 with high functioning ASD who visited the Children s Psychiatry Outpatient Department of the Affiliated Kangning Hospital of Ningbo University were recruited, and were randomly divided into a training ( n =31) and a control group ( n =31) by a random number table method. The training group received a 20 week structured group social training program (mental interpretation courses and social courses), while the control group received only conventional treatment. Chinese version of Griffith Empathy Measure Parent Ratings (GEM-PR) and Social Response Scale (SRS) were used to assess the symptoms of social deficits before and after treatment. Emotional face recognition tasks and eye movement trajectories were used to test the characteristics of social visual attention in children with ASD. Group comparison was conducted using t-test and Mann-Whitney U test. Results: At baseline, there were no significant differences in GEM-PR score ( t = -1.20 to -0.81), SRS score ( t =-0.36-1.75), emotional face recognition accuracy and reaction time ( t =-0.58-1.85), and eye movement trajectory ( U/t =-1.63-0.29) between the two group ( P >0.05). After intervention, the total GEM-PR score and empathic cognitive factor score of training group [18.00(10.00，24.00)，9.00(8.00，13.00)] were significantly higher than those of the control group [12.00(-1.00，18.00)，2.00(-2.00，7.00)], and the total SRS score and social cognition, social perception, social communication, social motivation (73.23±14.20, 16.16±2.72, 6.58±2.50, 24.29±5.61, 9.52±3.73) were significantly lower than those of the control group (95.26±15.29, 19.90±2.84, 12.58±2.49,31.94±6.38, 13.74±4.81) ( U/t =-2.38, -4.59; -5.88, -5.29, -9.47, -5.01, -3.87, P <0.05). The overall correct rate of emotional face recognition and the correct rate of angry, fearful and neutral faces recognition in the training group [(81.55±6.62)%，(76.86±12.06)%，(79.61±12.42)%，(94.27±6.26)%] were significantly higher than the control group [(70.55±13.82)%，(62.82±18.77)%，(67.18±18.85)%，(79.60±20.05)%], and the average reaction time [(2 226.70±274.43)ms] was lower than the control group [(2 417.27±324.10)ms] (t=4.00, 3.50, 3.07, 3.89, -2.42, P<0.05). The time to first eye gaze [764.74 (748.64, 793.73) ms] in the training group was significantly lower than that in the control group [810.92 (782.86, 877.42) ms], and the proportion of moderatetohigh intensity attention area in the face [(37.37±1.27)%] was significantly higher than that in the control group [(30.34±1.23)%] (U/t=3.44, 8.89, P<0.05). Conclusion Integrated group social training can significantly improve the social communication and empathy ability of high functioning ASD children, increase active attention and recognition ability of faces, and improve mental development of children with ASD.