ObjectiveZheng’s San Qi San (ZSQS) power, a classic traditional Chinese medicine (TCM) formula, is used for treating soft tissue injuries involving muscles, tendons, and ligaments. However, its underlying therapeutic mechanisms remain unclear. This study aimed to screen and identify pharmaceutically active ingredients and their candidate biomolecule targets, and further elucidate the molecular mechanism of ZSQS in the treatment of skeletal muscle injury. MethodsNetwork pharmacology was employed to construct “ZSQS-component-target”, “protein-protein interaction (PPI)” and “active ingredient-core protein-pathway” networks to predict the key active ingredients and potential core targets of ZSQS for skeletal muscle injury. The predicted results were then validated via microarray data from the GEO database. Molecular docking was then performed to assess the binding ability between the screened active ingredients of ZSQS and the candidate core targets. Moreover, liquid chromatography-mass spectrometry (LC-MS) was used for qualitative and quantitative analysis to verify the active components of the drug and ZSQS serum. Finally, an animal model of eccentric exercise-induced skeletal muscle injury and a myotube cell model of oxidative stress-induced injury were established to validate the effects of ZSQS and its interventional effects on the biological functions of critical targets, thereby demonstrating the potential therapeutic mechanism of ZSQS. ResultsAmong the 111 active components identified in ZSQS and their corresponding 204 targets related to the skeletal muscle injury repair process, 14 core targets (including AKT1) and 4 core active components (quercetin, luteolin, kaempferol, and β‑sitosterol) were screened out, while the corresponding metabolites of quercetin, luteolin and kaempferol were detected in the ZSQS serum. Among these targets, 5 candidate genes (IL-6, CASP3, HIF1A, STAT3, and JUN) overlapped with the differential expression screening results with GEO data, and IL-6 was confirmed to be enriched in the PI3K/AKT pathway. Combined with the prediction results of the AKT expression levels, these findings suggest that the phosphorylation level of AKT1 plays a core role in the therapeutic mechanism of ZSQS. Molecular docking analysis further revealed that the PH domain of AKT1 had high binding energy with all 4 core active components, as verified by LC-MS. Finally, animal model studies have shown the promoting effect of ZSQS administration on skeletal muscle injury repair and its possible antioxidant damage mechanism. Cell model studies further demonstrated that ZSQS-containing serum, core active ingredient combination therapy, and quercetin monomer could increase the phosphorylation level of AKT, promote the nuclear translocation of Nrf2, upregulate the expression of downstream antioxidant enzymes (SOD, GPx, and GR), and inhibit the expression of inflammatory factors (IL-6 and TNF-α), thereby alleviating oxidative stress and the inflammatory response. ConclusionZSQS alleviates skeletal muscle injury mainly by activating the AKT/Nrf2 signaling pathway, enhancing cellular antioxidant and anti-inflammatory capabilities. The results of this study provide a scientific basis for the clinical application and modernized development of ZSQS.

BackgroundThe prevalence， disability rate and mortality rate of cerebral small vessel disease （CSVD） are relatively high among the elderly population， imposing a heavy burden on families and society. Among the various clinical manifestations of CSVD， cognitive impairment is the most common， and it is also the most closely related neuro-psychiatric syndrome to clinical practice in psychiatry. Previous studies on CSVD-related cognitive impairment （CSVD-CI） have mostly focused on the field of imaging， while studies on non-invasive electrophysiological and cerebral hemodynamic assessments are relatively scarce. ObjectiveTo analyze the characteristics of event-related potential （ERP） and functional near-infrared spectroscopy （fNIRS） in patients with CSVD-CI， and to explore their correlations with the severity of white matter lesions， in order to provide references for the objective assessment and early identification of CSVD-CI. MethodsA total of 40 patients with CSVD who met the diagnostic criteria of the Chinese Guideline for Diagnosis and Treatment of Cerebral Small Vessel Disease （2020） and had cognitive impairment， as well as were admitted to the Affiliated Hospital of North Sichuan Medical College from December 2024 to December 2025， were enrolled as the case group. Meanwhile， 40 healthy volunteers matched for gender， age and education level were recruited as the control group. Both groups underwent assessment using the Mini-Mental State Examination （MMSE）， ERP-P300 detection， and fNIRS examination. The ERP-P300 indicators， functional connectivity strength of the whole brain and cognitive-related regions of interest （ROI） in fNIRS of the two groups were compared. The severity of the patients' white matter lesions was classified as follows： the Fazekas grade I group （mild white matter lesions） and the Fazekas grades II to III group （moderate to severe white matter lesions）. Spearman correlation analysis was employed to investigate the correlation between the Fazekas grading of brain white matter lesions and the latency of ERP-P300， as well as the strength of functional connectivity measured by fNIRS. ResultsThe MMSE score of the CSVD-CI group was lower than that of the control group （Z=-6.250， P<0.01）， and ERP-P300 lantency was significantly longer than that of the control group （t=12.291， P<0.01）. The MMSE score of the sub-group with Fazekas grade I was higher than that of the sub-groups with grades II to III （Z=-2.420， P<0.05）， and showed a shorter P300 latency than that of the sub-groups with grades II to III （Z=-4.210， P<0.01）. All the differences were statistically significant. The resting-state whole-brain functional connectivity strength in the CSVD-CI group was lower than that in the control group， and the difference was statistically significant （t=10.243， P<0.05）. Compared with the control group， the differences in the functional connectivity strength within the left premotor cortex （PMC）， right PMC， left frontopolar cortex （FPC）， right FPC， left dorsolateral prefrontal cortex （DLPFC）， right DLPFC， left orbitofrontal cortex （OFC）， and right OFC regions in the CSVD-CI group were all statistically significant （P_{FDR correction}<0.01）. The differences in the functional connectivity strength between multiple prefrontal-related brain regions between the CSVD-CI group and the control group were all statistically significant （P_{FDR correction}<0.01）. The severity of white matter lesions in CSVD-CI patients was positively correlated with the P300 latency （r_s=0.891， P<0.05）， and negatively correlated with the fNIRS functional connectivity strength （r_s=-0.359， P<0.05）. ConclusionPatients with CSVD-CI exhibit prolonged P300 latency， as well as decreased functional connectivity strength in multiple brain regions including the whole brain and the prefrontal lobe during the resting state. Moreover， these indicators are correlated with the severity of white matter lesions.

OBJECTIVE To investigate the clinical characteristics of euglycemic diabetic ketoacidosis （euDKA） induced by empagliflozin， and provide references for safe medication. METHODS Case reports of euDKA induced by empagliflozin were retrieved and analyzed from PubMed， Web of Science， CNKI， and Wanfang Data. The Naranjo’s scale was adopted to assess the causal relationship between empagliflozin and euDKA. RESULTS A total of 29 patients were enrolled， including 16 males and 13 females，with a median age of 58 years. All patients were diagnosed with type 2 diabetes mellitus； 22 patients had at least one comorbidity. The median time to euDKA onset was 60 days after administration， and 7 cases occurred within 2 weeks of treatment. Perioperative periods，fasting，and low-carbohydrate or ketogenic diets were the main predisposing factors. Common presentations included nausea，vomiting， fatigue， tachypnea，and tachycardia. The causal relationship between empagliflozin and euDKA was assessed as “probable” in all cases. According to adverse reaction severity grading， 13 cases were grade 3 （severe） and 16 cases were grade 4 （life-threatening）. All patients discontinued empagliflozin and recovered after corresponding treatment. CONCLUSIONS euDKA is a serious adverse reaction to empagliflozin， which mostly occurs early in treatment. Perioperative periods， fasting， and ketogenic diets are prone to induce euDKA. Elderly patients and those with comorbidities are at higher risk. Risk assessment should be conducted before clinical administration； blood ketones and acid-base monitoring should be strengthened in the early medication period； withhold the drug before elective surgery， avoid prolonged fasting；upon diagnosis， discontinue empagliflozin and initiate intravenous insulin， provide fluid resuscitation promptly， and use other treatments to improve patient prognosis.

ObjectiveTo investigate the association between insulin resistance （IR） and cardiovascular metabolic indicators， including blood pressure， blood lipids， and serum uric acid， in a middle-aged population. MethodsBased on the baseline survey of the Hong Sifang cohort of China National Salt Industry Group， a total of 575 participants were included. According to the homeostasis model assessment of insulin resistance， the participants were divided into an IR group （n=116） and a non-IR group （n=459）. Differences between the two groups were compared using the t-test and chi-square test. Multivariate logistic regression analysis was performed to evaluate the associations between IR and abnormalities in metabolic indicators. ResultsA total of 575 participants were included， including 390 men and 185 women， with a mean age of （48.58 ± 5.14） years and a mean body mass index （BMI） of （24.16 ± 2.97） kg/m². Blood pressure， serum uric acid， and blood lipid levels were significantly higher in the IR group than in the non-IR group （P<0.001）. After adjusting for potential confounders including age， sex， and BMI， IR was independently associated with hypertension， dyslipidemia， and hyperuricemia， with odds ratios （OR） and 95% confidence intervals （CI） of 2.57 （1.61-4.09）， 3.81 （2.36-6.17）， and 2.68 （1.53-4.71）， respectively （all P<0.001）. ConclusionInsulin resistance is significantly associated with multiple cardiovascular metabolic risk factors in the middle-aged population. Monitoring IR may contribute to the early prevention and control of cardiovascular diseases.

ObjectiveTo construct and validate a risk assessment model for post-transplant diabetes mellitus （PTDM） using multiple machine learning algorithms， and to realize the early identification of PTDM. MethodsA retrospective analysis was performed for the clinical data of the patients who underwent allogeneic liver transplantation in The First Hospital of Shanxi Medical University from April 1， 2020 to December 31， 2024， and they were randomly divided into a training set and a validation set at a ratio of 7∶3. The LASSO regression analysis combined with 5-fold cross-validation was used for feature selection. Seven machine learning models were developed in the training set， i.e.， logistic regression （LR）， decision tree （DT）， Naive Bayes （NB）， random forest （RF）， K-nearest neighbor （KNN）， extreme gradient boosting （XGBoost）， and adaptive boosting （AdaBoost）. In the validation set， various methods were used to assess the predictive performance of each model， such as accuracy， precision， recall rate， specificity， F1 score， area under the receiver operating characteristic curve （AUROC）， and area under the precision-recall curve （AUPRC）. The Brier score and decision curve analysis were used to assess the calibration and clinical practicability of the models， and the SHAP method was used to analyze feature importance. The independent-samples t test or the Wilcoxon rank-sum test was used for comparison of continuous data between two groups， and the chi-square test or the Fisher’s exact test was used for comparison of categorical data between two groups. ResultsA total of 135 liver transplant recipients were enrolled， among whom 26 developed PTDM， and there were 94 patients in the training set and 41 in the validation set. Feature extraction and screening identified 7 key features of sex， overweight or obesity， anhepatic phase， time of operation， length of hospital stay， early postoperative hypomagnesemia， and impaired fasting glucose （IFG）. In the validation set， the XGBoost model showed the best predictive performance， with an AUROC of 0.907 （95% confidence interval ［CI］： 0.807 — 0.989）， an AUPRC of 0.649 （95%CI： 0.339 — 0.955）， an accuracy of 0.878， a precision of 0.667， a recall rate of 0.750， an F1-score of 0.706， a specificity of 0.909， and a Brier score of 0.104. The decision curve analysis showed that when the threshold probability was below 0.667， application of the XGBoost model in clinical decision-making provided relatively high net benefit. The SHAP analysis showed that the length of hospital stay ranked first in terms of feature importance， followed by time of operation， overweight or obesity， sex， IFG， anhepatic phase， and early postoperative hypomagnesemia. ConclusionThe risk assessment model for PTDM in liver transplant recipients based on XGBoost algorithm has excellent performance and can effectively identify high-risk individuals； however， multicenter large-sample data are needed for further validation.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveHepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. The main risk factors associated with HCC include viral hepatitis (B and/or C), alcohol abuse, and metabolic dysfunction-associated steatotic liver disease (MASLD), which progressively advance to liver fibrosis, cirrhosis, and ultimately evolve into HCC. Surgical resection represents the most effective treatment for HCC, while recent advances in immunotherapy, including immune checkpoint inhibitors and adoptive cell therapies, have provided improved treatment prospects for patients with unresectable HCC. However, the complex metabolic heterogeneity of HCC limits the therapeutic efficacy. Metabolic intermediates acyl-CoA not only provide energy and substrates for numerous biochemical reactions but also serve as donors for protein lysine acylation, a major class of post-translational modification (PTM). Therefore, a deeper understanding of the molecular mechanisms underlying protein lysine acylation and hepatocarcinogenesis is urgently needed. MethodsThe levels of protein lysine acylation and silence information regulator 5 (SIRT5) expression levels in clinical HCC samples were analyzed by Western blot. Quantitative malonylome and succinylome of HCC samples were analyzed by antibody-based affinity enrichment coupled with tandem mass spectrometry. The proliferation of HCC cells was analyzed with Cell Counting Kit-8 (CCK-8) assays, the apoptosis was quantified by Annexin V-FITC/propidium iodide (PI) staining coupled with flow cytometry, and the ability of cells to migrate was assayed by Transwell assays. The enzymatic activity of glutathione S-transferase Mu 1 (GSTM1) was quantified. Transgenic mice with hepatic overexpression of SIRT5 were constructed using CRISPR-Cas9, and primary hepatocarcinogenesis was induced by administration of diethylnitrosamine. ResultsWestern blot analysis indicated that the expression level of SIRT5 was elevated in clinical samples from HCC patients, and the levels of lysine malonylation, glutarylation, and succinylation were significantly reduced in HCC tissues. Knockout of SIRT5 in MHCC-97H and MHCC-97L hepatoma cells suppressed cell proliferation, and increased the percentage of apoptotic cells significantly. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the differentially malonylome and succinylome of HCC samples revealed significant enrichment in two major classes of biological processes: core energy metabolism (e.g., glycolysis/gluconeogenesis, tricarboxylic acid metabolic process, fatty acid beta oxidation) and detoxification and oxidative stress response (e.g., response to toxic substance, chemical carcinogenesis, reactive oxygen species (ROS)). SIRT5 removes malonylation from lysine residues in GSTM1 and restores its detoxification activity, which is crucial for the survival of hepatocytes under stressed conditions. More importantly, in vivo experiment indicated that hepatic-specific overexpression of SIRT5 in mice accelerated diethylnitrosamine-induced liver fibrosis and hepatocarcinogenesis, indicating the critical role of SIRT5 in HCC progression. ConclusionThis study highlights the previously unrecognized SIRT5-GSTM1 axis as a key regulator in hepatocarcinogenesis, and suggests a potential target for the treatment of patients with HCC.

Objective To compare imaging quality and detection capability of bone metastases between Insight NM/CT Pro SPECT/CT(Insight SPECT/CT)and Siemens Symbia T16 SPECT/CT(Symbia T16 SPECT/CT)scanners.Methods Totally 40 patients with diagnosed or suspected bone metastases were prospectively enrolled.Whole-body bone imaging and local tomographic fusion imaging were performed using Symbia T16 and Insight SPECT/CT scanners with same method and parameters,and imaging quality and detection capability were compared between 2 devices.Results Among whole-body bone imaging acquired with Symbia T 16 SPECT/CT,the imaging quality score was 5 in 35 cases and 4 in 5 cases,and detected 118 positive bone lesions,including 36 lesions involved chest,28 involved spinal cord,30 involved pelvic bones,20 involved limbs and 4 involved cranial bones.The imaging quality score of local tomographic fusion imaging obtained with Symbia T16 SPECT/CT was 5 in all 40 cases,and 59 positive lesions involved bone regions were detected,including 14 lesions presented as bone destruction,11 presented as increased bone density and 34 showed uneven bone density on CT.Meanwhile,the whole-body bone imaging quality score acquired with Insight SPECT/CT was 5 in 35 cases,4 in 4 cases and 3 in 1 case,and both the detected positive lesions and the involved bone regions were consistent with those of Symbia T 16 SPECT/CT.Furthermore,the imaging quality,detected positive lesions and their involved regions,as well as CT manifestations on local tomographic fusion imaging obtained with Insight SPECT/CT scanner were all consistent with those of Symbia T 16 scanner.Conclusion The imaging quality of whole-body bone imaging and local tomographic fusion imaging of bone metastases of domestic Insight SPECT/CT were comparable to those of Siemens Symbia T16 SPECT/CT.

Objective To investigate the role of additional platelet protein kinase C epsilon(PKCε)assay in risk stratification and additional diagnostic testing in elderly patients with acute chest pain and normal hypersensitive cardiac troponin I(hs-cTnI)level.Methods A prospective trial was conducted on 220 consecutive elderly patients with angina-like acute chest pain and normal hs-cTnI level in our hospital from April 2022 to April 2023.According to whether major adverse cardiovascular events(MACE)occurred during the 1-year follow-up period,they were assigned in-to MACE group(24 cases)and non-MACE group(196 cases).Their general clinical data and platelet PKCε expression were compared between the two groups.Kaplan-Meier survival curve was plotted to analyzed the event-free time between the platelet PKCε expression＜2.05％group and the≥2.05％group.Multivariate Cox regression analysis was used to investigate the impact of baseline data on the occurrence of MACE during the 1-year follow-up period.Decision tree model was employed to analyze the influencing factors for MACE.Results During 1-year follow-up,24 patients(10.91％)developed MACE.The platelet PKCε expression was significantly higher in the MACE group than the non-MACE group[9.25％(6.60％,15.25％)vs 1.70％(0.80％,3.25％),Z=-7.596,P＜0.01].Kaplan-Meier survival curve analysis showed that the patients in the PKCε＜2.05％group had no events within 360 d,while those in the ≥2.05％group had an average event-free time of 297.13±12.77 d,with a statistical difference(log rank Chi-square=27.051,P=0.000).Multivariate Cox regression analysis showed that highly suspicious angina,hs-cTnI and platelet PKCε were independent risk factors for MACE within 1 year of follow-up(HR=3.011,95％CI:1.049-8.641,P=0.040;HR=1.216,95％CI:1.044-1.418,P=0.012;HR=1.160,95％CI:1.104-1.218,P=0.000).In the decision tree model,the 1-year incidence of MACE was notably higher in the platelet PKCε≥2.05％group than the＜2.05％group(P=0.011).The probability of severe coronary artery stenosis or myocardial ischemia in the platelet PKCε≥2.05％group was remarkably higher than the＜2.05％group(P=0.006).Conclusion In elderly patients suffering from acute chest pain with normal hs-cTnI level,additional platelet PKCε detection appears to have a good prognostic gain.