ObjectiveTo explore the mechanism by which Sini San （SNS） inhibits ferroptosis， alleviates inflammation and myocardial injury， and improves myocardial infarction （MI）. MethodsThe active ingredients of SNS were obtained by searching the Traditional Chinese Medicine System Pharmacology Platform （TCMSP） database， its target sites were predicted using the SwissTargetPrediction Database， and the core components were screened out using the CytoNCA plug-in. The targets of MI and ferroptosis were obtained by using GeneCards， Online Mendelian Inheritance in Man （OMIM） database， DrugBank， Therapeutic Target Database （TTD）， FerrDb database and literature review， respectively. The intersection of these targets of SNS-MI-ferroptosis was plotted as a Venn diagram. The protein-protein interaction （PPI） network was constructed using the STRING database， and the visualization graph was prepared using Cytoscape. The core targets were screened out using the CytoNCA plug-in， and the biological functions were clustered by the MCODE plug-in. Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis were performed using the David database. Molecular docking was performed using AutoDock and visualized with PyMOL2.5.2. The Kunming mice were randomly divided into the control group， the model group， the SNS group， and the trimetazidine （TMZ） group. The mice were subcutaneously injected with isoprenaline （ISO， 5 mg·kg^-1·d^-1） to establish an MI model. The drug was continuously intervened for 7 days. The ST-segment changes were recorded by electrocardiogram （ECG）， and the tissue morphology changes were observed by hematoxylin-eosin （HE） staining. Cardiomyocyte ferroptosis was investigated by transmission electron microscopy. Serum creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， reduced glutathione （GSH）， and malondialdehyde （MDA） levels were detected by biochemical assay. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of interleukin （IL）-6 and 4-hydroxynonenal （4-HNE）. Immunohistochemical staining was employed to detect IL-6 and phosphorylated signal transducer and transcription activator 3 （p-STAT3） in cardiac tissues. Western blot was used to detect STAT3 and p-STAT3 in cardiac tissues. Real-time PCR was used to detect the levels of IL-6， IL-18， solute carrier family 7 member 11 （SLC7A11）， arachidonic acid 15-lipoxygenase （ALOX15）， and glutathione peroxidase 4 （GPx4） in cardiac tissues. ResultsA total of 121 active ingredients of SNS were obtained， and 58 potential targets of SNS in the treatment of MI by regulating ferroptosis were screened. The three protein modules with a score5 were mainly related to the inflammatory response. The GO function was mainly related to inflammation， and KEGG enrichment analysis showed that SNS mainly regulated ferroptosis- and inflammation- related signaling pathways. Molecular docking indicated that the core component had a higher binding force to the target site. Animal experiments confirmed that SNS reduced the level of p-STAT3 （P0.01）， down-regulated the expression of ALOX15 mRNA （P0.01）， up-regulated the level of serum GSH， and the expressions of SLC7A11 and GPx4 mRNA， reduced MDA and 4-HNE levels （P0.05， P0.01）. Additionally， SNS improved the mitochondrial injury induced by cardiomyocyte ferroptosis， reduced the area of MI， alleviated inflammation and myocardial injury， lowered the levels of serum CK， CK-MB， LDH， IL-6， and the mRNA expression levels of IL-16 and IL-18 （P0.05）， and improved ST segment elevation. ConclusionSNS can reduce ISO-induced STAT3 phosphorylation levels， inhibit ferroptosis in cardiomyocytes， alleviate inflammation and myocardial injury， thereby improving MI.

ObjectiveTo explore the mechanism by which Sini San （SNS） inhibits ferroptosis， alleviates inflammation and myocardial injury， and improves myocardial infarction （MI）. MethodsThe active ingredients of SNS were obtained by searching the Traditional Chinese Medicine System Pharmacology Platform （TCMSP） database， its target sites were predicted using the SwissTargetPrediction Database， and the core components were screened out using the CytoNCA plug-in. The targets of MI and ferroptosis were obtained by using GeneCards， Online Mendelian Inheritance in Man （OMIM） database， DrugBank， Therapeutic Target Database （TTD）， FerrDb database and literature review， respectively. The intersection of these targets of SNS-MI-ferroptosis was plotted as a Venn diagram. The protein-protein interaction （PPI） network was constructed using the STRING database， and the visualization graph was prepared using Cytoscape. The core targets were screened out using the CytoNCA plug-in， and the biological functions were clustered by the MCODE plug-in. Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis were performed using the David database. Molecular docking was performed using AutoDock and visualized with PyMOL2.5.2. The Kunming mice were randomly divided into the control group， the model group， the SNS group， and the trimetazidine （TMZ） group. The mice were subcutaneously injected with isoprenaline （ISO， 5 mg·kg^-1·d^-1） to establish an MI model. The drug was continuously intervened for 7 days. The ST-segment changes were recorded by electrocardiogram （ECG）， and the tissue morphology changes were observed by hematoxylin-eosin （HE） staining. Cardiomyocyte ferroptosis was investigated by transmission electron microscopy. Serum creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， reduced glutathione （GSH）， and malondialdehyde （MDA） levels were detected by biochemical assay. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of interleukin （IL）-6 and 4-hydroxynonenal （4-HNE）. Immunohistochemical staining was employed to detect IL-6 and phosphorylated signal transducer and transcription activator 3 （p-STAT3） in cardiac tissues. Western blot was used to detect STAT3 and p-STAT3 in cardiac tissues. Real-time PCR was used to detect the levels of IL-6， IL-18， solute carrier family 7 member 11 （SLC7A11）， arachidonic acid 15-lipoxygenase （ALOX15）， and glutathione peroxidase 4 （GPx4） in cardiac tissues. ResultsA total of 121 active ingredients of SNS were obtained， and 58 potential targets of SNS in the treatment of MI by regulating ferroptosis were screened. The three protein modules with a score5 were mainly related to the inflammatory response. The GO function was mainly related to inflammation， and KEGG enrichment analysis showed that SNS mainly regulated ferroptosis- and inflammation- related signaling pathways. Molecular docking indicated that the core component had a higher binding force to the target site. Animal experiments confirmed that SNS reduced the level of p-STAT3 （P0.01）， down-regulated the expression of ALOX15 mRNA （P0.01）， up-regulated the level of serum GSH， and the expressions of SLC7A11 and GPx4 mRNA， reduced MDA and 4-HNE levels （P0.05， P0.01）. Additionally， SNS improved the mitochondrial injury induced by cardiomyocyte ferroptosis， reduced the area of MI， alleviated inflammation and myocardial injury， lowered the levels of serum CK， CK-MB， LDH， IL-6， and the mRNA expression levels of IL-16 and IL-18 （P0.05）， and improved ST segment elevation. ConclusionSNS can reduce ISO-induced STAT3 phosphorylation levels， inhibit ferroptosis in cardiomyocytes， alleviate inflammation and myocardial injury， thereby improving MI.

Objective:To observe and evaluate the clinical efficacy and safety of albumin-bound paclitaxel as first-line treatment for patients with advanced pancreatic cancer in China, and to explore the prognosis-related molecules in pancreatic cancer based on next-generation sequencing (NGS) of tumor tissues.Methods:From December 2018 to December 2020, patients with locally advanced or metastatic pancreatic cancer were recruited to accept albumin-bound paclitaxel as first-line treatment in the oncology departments of 24 hospitals in East China. The primary endpoints were overall survival (OS) and treatment related adverse events, and the secondary endpoint was progression-free survival (PFS). Adverse effects were graded using Common Terminology Criteria for Adverse Events 5.0 (CTCAE 5.0). NGS sequencing on the primary or metastatic tissue samples of pancreatic cancer obtained through surgical resection or biopsy was performed.Results:This study recruited 229 patients, including 70 patients with locally advanced pancreatic cancer (LAPC) and 159 patients with metastatic pancreatic cancer (mPC). The disease control rate was 79.9% and the objective response rate is 36.3%.The common adverse effects during treatment were anaemia (159 cases), leucopenia (170 cases), neutropenia (169 cases), increased aminotransferases (110 cases), and thrombocytopenia (95 cases), and the incidence of grade 3-4 neutropenia is 12.2% (28/229). The median follow-up time was 21.2 months (95% CI: 18.5-23.1 months). The median PFS (mPFS) was 5.3 months (95% CI: 4.37-4.07 months) and the median OS (mOS) was 11.2 months (95% CI: 9.5-12.9 months). The mPFS of patients with LAPC was 7.4 months (95% CI: 6.6-11.2 months), and their mOS was 15.5 months (95% CI: 12.6-NA months). The mPFS of patients with mPC was 3.9 months (95% CI: 3.4-5.1 months), and their mOS was 9.3 months (95% CI: 8.0-10.8 months). Multivariate Cox regression analysis showed that clinical stage ( HR=1.47, 95% CI: 1.06-2.04), primary tumor site ( HR=0.64, 95% CI: 0.48-0.86), Eastern Cooperative Oncology Group Performance Status (ECOG PS) score ( HR=2.66, 95% CI: 1.53-4.65), and whether to combine radiotherapy ( HR=0.65, 95% CI: 0.42-1.00) were independent influencing factors for the PFS of these patients. The primary tumor site ( HR=0.68, 95% CI: 0.48-0.95), ECOG score ( HR=5.82, 95% CI: 3.14-10.82), and whether to combine radiotherapy ( HR=0.58, 95% CI: 0.35-0.96) were independent influencing factors of the OS of these patients. The most frequent gene mutations in these advanced stage pancreatic patients were KRAS (89.66%), TP53 (77.01%), CDKN2A (32.18%), and SMAD4 (21.84%) by NGS of tumor tissues from 87 pancreatic cancer patients with sufficient specimens. Further analysis revealed that mutations in CDKN2B, PTEN, FGF6, and RBBP8 genes were significantly associated with an increased risk of death ( P＜0.05). Conclusion:Albumin-bound paclitaxel as first-line treatment demonstrated feasible anti-tumor efficacy and manageable safety for patients with advanced pancreatic cancer in China.

Objective:To explore the relationship between serum C-X-C motif chemokine ligand 16 (CXCL16) and thioredoxin 80 (Trx80) in patients with Alzheimer′s disease (AD) and cognitive function and prognosis.Methods:A total of 189 AD patients admitted to the Zhangjiakou First Hospital from January 2020 to August 2021 were selected as the AD group, and 110 healthy volunteers who underwent physical examinations in our hospital during the same period were selected as the control group. The serum levels of CXCL16 and Trx80 were detected using enzyme-linked immunosorbent assay (ELISA), and cognitive function was evaluated using the Mini Mental State Examination (MMSE) score. The Spearman correlation method was used to analyze the correlation between serum CXCL16, Trx80 levels and MMSE scores in AD patients. 189 AD patients were divided into poor prognosis group and good prognosis group based on their prognosis. Univariate and multivariate logistic regression methods were used to analyze the influencing factors of poor prognosis in AD patients. Receiver operating characteristic (ROC) curves were used to analyze the predictive value of serum CXCL16 and Trx80 levels for poor prognosis in AD patients.Results:Compared with the control group, the AD group had higher serum levels of CXCL16 and Trx80, and lower MMSE scores (all P<0.05). Spearman correlation analysis showed that the serum levels of CXCL16 and Trx80 in AD patients were negatively correlated with MMSE scores (all P<0.05). After a one-year follow-up, the poor prognosis rate of 189 AD patients was 32.80%(62/189). Univariate analysis showed that age, disease duration, β-amyloid protein (Aβ) 1-40, Aβ 1-42, MMSE score, CXCL16, and Trx80 are associated with poor prognosis in AD patients (all P<0.05). Multivariate logistic regression analysis showed that age, prolonged disease course, and elevated levels of CXCL16 and Trx80 were risk factors for poor prognosis in AD patients (all P<0.05), while an increase in MMSE score was a protective factor ( P<0.05). ROC curve analysis showed that the area under the curve (AUC) of MMSE score, CXCL16, Trx80, CXCL16+ Trx80 combination, and MMSE score+ CXCL16+ Trx80 combination predicting poor prognosis in AD patients were 0.750, 0.763, 0.771, 0.851, and 0.896, respectively. The AUC of the three combination predicting poor prognosis in AD patients was the highest. Conclusions:Elevated serum levels of CXCL16 and Trx80 in AD patients are associated with decreased cognitive function and poor prognosis, and may become auxiliary predictive indicators for poor prognosis in AD patients.

ObjectiveTo explore the effect of Tanreqing injection combined with Ceftazide on the clinical efficacy， lung function， and laboratory inflammatory index of patients suffering from phlegm heat obstructing lung syndrome in acute exacerbation of chronic obstructive pulmonary disease （AECOPD）. MethodFrom June 2021 to June 2023， 76 patients diagnosed with phlegm heat obstructing lung syndrome in AECOPD were enrolled in the respiratory and critical medical department of Jieshou Hospital of Traditional Chinese Medicine. They were randomly divided into a control group and an observation group with 38 cases each. The control group used Ceftazidime intravenous drip and other conventional oxygen inhalation and antispasmodic treatment measures of western medicine. The observation group received Tanreqing injection intravenous drip based on the treatment of the control group， with a course of 10 days. The changes of laboratory indicators such as hs-CRP， calcitonin （PCT）， and interleukin-6 （IL-6） before and after treatment were analyzed， and the improvement of forced expiratory volume in the first second （FEV₁）， forced vital capacity （FVC）， one second rate （FEV₁/FVC）， assessment and improvement of the British Medical Research Society’s dyspnea index （mMRC）， self-evaluation test of chronic obstructive pulmonary disease patients （CAT）， and traditional Chinese medicine syndrome score was compared. In addition， the total effective rate between the two groups after treatment was compared. ResultAfter treatment， the hs-CRP， PCT， IL-6， FEV₁， FVC， FEV₁/FVC， mMRC， CAT scores， and traditional Chinese medicine syndrome evaluation of both groups improved （P<0.01）. After treatment， compared with the control group， the observation group showed more significant improvements in hs-CRP， PCT， IL-6， FEV₁， FVC， FEV₁/FVC， mMRC， CAT scores， and traditional Chinese medicine syndrome evaluation， and the difference was statistically significant （P<0.05，P<0.01）. The total clinical effective rate of the control group was 86.84% （33/38）， while that of the observation group was 94.74% （36/38）. The therapeutic effect of the observation group was better than that of the control group （χ²=8.471， P<0.05）. ConclusionTanreqing injection combined with Ceftazidime has obvious efficacy in the treatment of phlegm heat obstructing lung syndrome in AECOPD， which is better than the treatment of Ceftazidime antibiotics alone. It can reduce the risk of acute exacerbation， alleviate clinical symptoms， and delay the decline of lung function.

Objective:To observe and evaluate the clinical efficacy and safety of albumin-bound paclitaxel as first-line treatment for patients with advanced pancreatic cancer in China, and to explore the prognosis-related molecules in pancreatic cancer based on next-generation sequencing (NGS) of tumor tissues.Methods:From December 2018 to December 2020, patients with locally advanced or metastatic pancreatic cancer were recruited to accept albumin-bound paclitaxel as first-line treatment in the oncology departments of 24 hospitals in East China. The primary endpoints were overall survival (OS) and treatment related adverse events, and the secondary endpoint was progression-free survival (PFS). Adverse effects were graded using Common Terminology Criteria for Adverse Events 5.0 (CTCAE 5.0). NGS sequencing on the primary or metastatic tissue samples of pancreatic cancer obtained through surgical resection or biopsy was performed.Results:This study recruited 229 patients, including 70 patients with locally advanced pancreatic cancer (LAPC) and 159 patients with metastatic pancreatic cancer (mPC). The disease control rate was 79.9% and the objective response rate is 36.3%.The common adverse effects during treatment were anaemia (159 cases), leucopenia (170 cases), neutropenia (169 cases), increased aminotransferases (110 cases), and thrombocytopenia (95 cases), and the incidence of grade 3-4 neutropenia is 12.2% (28/229). The median follow-up time was 21.2 months (95% CI: 18.5-23.1 months). The median PFS (mPFS) was 5.3 months (95% CI: 4.37-4.07 months) and the median OS (mOS) was 11.2 months (95% CI: 9.5-12.9 months). The mPFS of patients with LAPC was 7.4 months (95% CI: 6.6-11.2 months), and their mOS was 15.5 months (95% CI: 12.6-NA months). The mPFS of patients with mPC was 3.9 months (95% CI: 3.4-5.1 months), and their mOS was 9.3 months (95% CI: 8.0-10.8 months). Multivariate Cox regression analysis showed that clinical stage ( HR=1.47, 95% CI: 1.06-2.04), primary tumor site ( HR=0.64, 95% CI: 0.48-0.86), Eastern Cooperative Oncology Group Performance Status (ECOG PS) score ( HR=2.66, 95% CI: 1.53-4.65), and whether to combine radiotherapy ( HR=0.65, 95% CI: 0.42-1.00) were independent influencing factors for the PFS of these patients. The primary tumor site ( HR=0.68, 95% CI: 0.48-0.95), ECOG score ( HR=5.82, 95% CI: 3.14-10.82), and whether to combine radiotherapy ( HR=0.58, 95% CI: 0.35-0.96) were independent influencing factors of the OS of these patients. The most frequent gene mutations in these advanced stage pancreatic patients were KRAS (89.66%), TP53 (77.01%), CDKN2A (32.18%), and SMAD4 (21.84%) by NGS of tumor tissues from 87 pancreatic cancer patients with sufficient specimens. Further analysis revealed that mutations in CDKN2B, PTEN, FGF6, and RBBP8 genes were significantly associated with an increased risk of death ( P＜0.05). Conclusion:Albumin-bound paclitaxel as first-line treatment demonstrated feasible anti-tumor efficacy and manageable safety for patients with advanced pancreatic cancer in China.

In recent years,radiation therapy has become a cornerstone in the treatment of head and neck tumors,significantly improving patient survival rates.However,the issue of radiation-induced carotid artery stenosis has garnered increasing attention.Characterized by multiple,long-segment,and unstable lesions,radiation-induced carotid stenosis presents unique challenges that traditional therapeutic approaches struggle to address.This review systematically summarized the pathological features and underlying mechanisms of radiation-induced carotid stenosis,with a focus on the roles of endothelial cells,smooth muscle cells,and vasa vasorum damage.Future research directions and preventive strategies are also discussed.

Cognitive dysfunction refers to dysfunction of individual perception,memory,understanding,learning,creation and other dysfunctions caused by abnormal brain function and structure.Based on the fact that the spleen can't regulate transportation and transformation,govern blood and send up essential substance,combined with the microbiota-gut-brain axis,this article discussed the etiology and pathogenesis of intestinal flora imbalance affecting cognitive dysfunction in TCM.It was proposed that the spleen in TCM and intestinal flora are connected in physiology and pathology:the spleen regulates spirit and governs cognition,when the spleen fails to function normally that it can't dominate transportation and transformation,govern blood and send up essential substance will cause that the brain spirit can not be nourished;intestinal flora is closely related to the spleen in TCM,and affects brain function through the nervous system,endocrine,immune and metabolic mechanisms.This article can provide explore new ideas for the clinical research and treatment of cognitive dysfunction of traditional Chinese and Western medicine.

Acute lung injury (ALI), as a common clinical emergency, is pulmonary edema and diffuse lung infiltration caused by inflammation. The lack of non-invasive alert strategy, resulting in failure to carry out preventive treatment, means high mortality and poor prognosis. Stimulator of interferon genes (STING) is a key molecular biomarker of innate immunity in response to inflammation, but there is still a lack of STING-targeted strategy. In this study, a novel STING-targeted PET tracer, [¹⁸F]FBTA, was labeled with high radiochemical yield (79.7 ± 4.3%) and molar activity (32.5 ± 2.9 GBq/μmol). We confirmed that [¹⁸F]FBTA has a strong STING binding affinity (K_d = 26.86 ± 6.79 nmol/L) and can be used for PET imaging in ALI mice to alert early lung inflammation and to assess the efficacy of drug therapy. Our STING-targeted strategy also reveals that [¹⁸F]FBTA can trace ALI before reaching the computed tomography (CT) diagnostic criteria, and demonstrates its better specificity and distribution than [¹⁸F]fluorodeoxyglucose ([¹⁸F]FDG).

Objective:To explore the expression and predictive value of serum CD36 level in cardio-vascular risk in patients with rheumatoid arthritis (RA) and to provide a new theoretical basis for clinical iden-tification and prediction of patients at moderate and high cardiovascular risk in RA patients.Methods:Eighty-four RA patients hospitalized to the Department of Rheumatology and Immunology of the second hospital of Lanzhou University in Gansu Province were selected as the study subjects, and 34 healthy people were selected as the controls. All RA patients were divided into low cardiovascular risk groups and medium and high cardiovascular risk groups according to prediction for ASCVD risk in China (China-PAR) cardiovascular risk assessment. At the same time, they were tested for serological indicators at admission. Statistical Product and Service Solutions (SPSS)) 26.0 software was used for the statistical data analysis. T-test and nonparametric test were used for comparison of the measurement data. The Chi-square test and Fisher's exact test were used for the comparison of classified data. Variables with P<0.05 in univariate analysis were included into the Logistic regression model. Results:Compared with the healthy control group, the number of patients with medium and high cardiovascular risk in RA[8 cases (23.5)% and 38 cases (45.2)%, χ2=4.80, P=0.029] was significantly higher and was negatively correlated with serum CD36 ( r=-0.27, P<0.05). Logistic regression analysis showed that age [ OR(95% CI)=1.654(1.157, 2.365), P=0.006] and diastolic blood pressure [ OR(95% CI)=1.225(1.040, 1.442) , P=0.015] were independent risk factors for medium and high cardiovascular risk in RA patients, and serum CD36 level [ OR(95% CI)=0.569(0.352, 0.922) , P=0.022] was the protective factor of medium and high cardiovascular risk in RA patients according to the results of Logistic regression analysis. The area under the receiver operating characteristic (ROC) area under the curve (AUC) was 0.691, the cut-off value was 4.27 pg/ml, and the sensitivity and specificity were 89.7% and 41.0% respectively. Conclusion:The serum CD36 level decreases with the increase of cardiovascular risk in RA patients. A higher serum CD36 level is a protective factor of cardiovascular risk in RA patients, and CD36 has a certain predictive value for cardiovascular risk in RA patients and is a potential predictor.