Acute pancreatitis(AP)is an autopeptic disease,which can be accompanied by systemic inflammation and multiple organ failure.Mesenchymal stem cells(MSCs)have been used in the treatment of AP and have shown good application potential.MSCs can act through multiple mechanisms to reduce pancreatic inflammation and enhance tissue repair.These mechanisms include homing to injury sites,anti-inflammatory and immunomodulatory effects,oxidative stress reduction,inhibition of apoptosis and suppression of autophagy.Additionally,MSCs can mitigate multi-organ damage associated with AP,impacting lungs,intestines,heart and other organs.Research on the application of MSCs in treating AP is predominantly at the preclinical animal study stage,with limited clinical investigations reported.This article reviews the mechanisms and research progress of MSCs in the treatment of AP,aiming to provide references for basic research and clinical applications.

miR-101-3p is an evolutionarily conserved non-coding RNA that has shown aberrant expression and regulatory functios in various cardiovascular diseases(CVDs)in recent years.It participates in key pathological processes including post-infarction myocardial remodeling,myocardial fibrosis in heart failure and the development of atherosclerosis by modulating pathways such as apoptosis,autophagy and metabolism.In addition,it exhibits immunoregulatory potential in myocardium injury related to systemic diseases.This review summarizes the recent advances in understanding the role of miR-101-3p in CVDs,focusing on its expression dynamics and regulatory mechanisms in different disease models.It further elaborates on the biological effects of miR-101-3p in cardiovascular pathology and explores its potential as a diagnostic biomarker and therapeutic target.miR-101-3p is expected to provide novel insights for early detection and targeted intervention of cardiovascular diseases.

Acute pancreatitis(AP)is an autopeptic disease,which can be accompanied by systemic inflammation and multiple organ failure.Mesenchymal stem cells(MSCs)have been used in the treatment of AP and have shown good application potential.MSCs can act through multiple mechanisms to reduce pancreatic inflammation and enhance tissue repair.These mechanisms include homing to injury sites,anti-inflammatory and immunomodulatory effects,oxidative stress reduction,inhibition of apoptosis and suppression of autophagy.Additionally,MSCs can mitigate multi-organ damage associated with AP,impacting lungs,intestines,heart and other organs.Research on the application of MSCs in treating AP is predominantly at the preclinical animal study stage,with limited clinical investigations reported.This article reviews the mechanisms and research progress of MSCs in the treatment of AP,aiming to provide references for basic research and clinical applications.

Submucosal angiomyolipoma(AML)of rectum is clinically rare.This article reports the endoscopic diagnosis and treatment process of a case of rectal AML.By reviewing the clinical data of this patient and combining with literature review,we aim to deepen the current understanding of AML in the digestive tract and avoid misdiagnosis and mistreatment in clinical practice.

Submucosal angiomyolipoma(AML)of rectum is clinically rare.This article reports the endoscopic diagnosis and treatment process of a case of rectal AML.By reviewing the clinical data of this patient and combining with literature review,we aim to deepen the current understanding of AML in the digestive tract and avoid misdiagnosis and mistreatment in clinical practice.

Objective To design melatonin(Mel)-based nanomedicines(Mel-NMs)and evaluate their therapeutic effects on myocardial ischemia-reperfusion injury in mice.Methods Melatonin self-assembled peptides(Mel-NMs)were synthesized and their structure was characterized by transmission electron microscopy.Mice were divided randomly into five groups:Sham,Model,Mel,NMs,and Mel-NMs,and a myocardial ischemia-reperfusion injury model was established.Mel(5 mg/kg),NMs,or Mel-NMs(containing Mel 5 mg/kg)were administered intraperitoneally 10 minutes prior to reperfusion,and the sham group was treated with an equal volume of solvent.Cardiac function,apoptosis,and oxidative stress markers were assessed 24 hours after reperfusion.Results Transmission electron microscopy revealed that Mel-NMs formed worm-like structures.Treatment with Mel and Mel-NMs significantly improved cardiac function,reduced lactate dehydrogenase and malondialdehyde levels,and enhanced glutathione peroxidase and superoxide dismutase activities(P＜0.05),while also decreasing cardiomyocyte apoptosis(P＜0.05),with greater effects in the Mel-NMs group(P＜0.05).Conclusions Mel-NMs can effectively mitigate myocardial oxidative stress and apoptosis,offering a more potent cardioprotective effect than Mel alone.

miR-101-3p is an evolutionarily conserved non-coding RNA that has shown aberrant expression and regulatory functios in various cardiovascular diseases(CVDs)in recent years.It participates in key pathological processes including post-infarction myocardial remodeling,myocardial fibrosis in heart failure and the development of atherosclerosis by modulating pathways such as apoptosis,autophagy and metabolism.In addition,it exhibits immunoregulatory potential in myocardium injury related to systemic diseases.This review summarizes the recent advances in understanding the role of miR-101-3p in CVDs,focusing on its expression dynamics and regulatory mechanisms in different disease models.It further elaborates on the biological effects of miR-101-3p in cardiovascular pathology and explores its potential as a diagnostic biomarker and therapeutic target.miR-101-3p is expected to provide novel insights for early detection and targeted intervention of cardiovascular diseases.

Objective To design melatonin(Mel)-based nanomedicines(Mel-NMs)and evaluate their therapeutic effects on myocardial ischemia-reperfusion injury in mice.Methods Melatonin self-assembled peptides(Mel-NMs)were synthesized and their structure was characterized by transmission electron microscopy.Mice were divided randomly into five groups:Sham,Model,Mel,NMs,and Mel-NMs,and a myocardial ischemia-reperfusion injury model was established.Mel(5 mg/kg),NMs,or Mel-NMs(containing Mel 5 mg/kg)were administered intraperitoneally 10 minutes prior to reperfusion,and the sham group was treated with an equal volume of solvent.Cardiac function,apoptosis,and oxidative stress markers were assessed 24 hours after reperfusion.Results Transmission electron microscopy revealed that Mel-NMs formed worm-like structures.Treatment with Mel and Mel-NMs significantly improved cardiac function,reduced lactate dehydrogenase and malondialdehyde levels,and enhanced glutathione peroxidase and superoxide dismutase activities(P＜0.05),while also decreasing cardiomyocyte apoptosis(P＜0.05),with greater effects in the Mel-NMs group(P＜0.05).Conclusions Mel-NMs can effectively mitigate myocardial oxidative stress and apoptosis,offering a more potent cardioprotective effect than Mel alone.

Objective:To explore the effect and correlation of long non-coding RNA (lncRNA) IDI2-AS1/microRNA-33b-5p (miR-33b-5p)/nuclear receptor-associated protein NR4A2 competitive endogenous RNA (ceRNA) regulatory network on acute myocardial infarction (AMI), and to verify whether IDI2-AS1 regulates NR4A2 through miR-33b-5p to affect the occurrence and development of myocardial infarction.Methods:The miRNA and mRNA expression chips related to myocardial infarction were obtained from gene expression omnibus (GEO), and the differential expression was analyzed. The upstream regulatory mechanism of NR4A2 was predicted using TargetScan database. Thirty-two male C57/BL6 mice were divided into Sham group, AMI model group, miR-33b-5p mimic group [miR-33b-5p mimic lentivirus (5×10 7 TU) was injected locally into the heart tissue during ligation] and miR-33b-5p inhibitor group [miR-33b-5p inhibitor lentivirus (5×10 7 TU) was injected locally into the heart tissue during ligation] according to random number table method, with 8 mice per group. Left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) were asseessed by echocardiography, left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF) were calculated. After the last weighing, the anesthetized mice were sacrificed and the heart tissues were taken. Masson staining of the heart tissues was observed under light microscope, myocardial collagen volume fraction (CVF) and infarct size were calculated. Cardiomyocytes of SPF grade SD rats were collected. They were divided into normal control group (control group), ischemia-hypoxia model group, miR-33b-5p mimic transfection group (miR-33b-5p mimic transfection group before ischemia and hypoxia treatment) and miR-33b-5p inhibitor transfection group (miR-33b-5p inhibitor transfection group before ischemia and hypoxia treatment). The activity of caspase-3/7 in cardiomyocytes was measured. The levels of interleukins (IL-1β, IL-6) and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA). The levels of malondialdehyde (MDA), superoxide dismutase (SOD), creatine kinase (CK), MB isoenzyme of creatine kinase (CK-MB) and lactate dehydrogenase (LDH) were detected by colorimetry. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of apoptosis-related proteins Bax and Bcl-2, cytochrome C (Cyt C) and IDI2-AS1/miR-33b-5p/NR4A2 regulatory axis genes. Results:The myocardial infarction microarray analysis showed that NR4A2 expression was significantly up-regulated in myocardial infarction, with predicted upstream regulatory mechanisms indicating its possible influence through the IDI2-AS1/miR-33b-5p/NR4A2 regulatory axis. Echocardiographic detection showed that compared with AMI model group and miR-33b-5p inhibitor group, LVEF and LVFS in the heart tissue of mice in miR-33b-5p mimic group were significantly increased, while the levels of LVEDD, LVESD, CK, CK-MB and LDH were significantly decreased, with statistical significance. Light microscope showed myocardial fibrosis and myocardial infarction in AMI model group and miR-33b-5p inhibitor group. In the miR-33b-5p mimic group, the degree of myocardial fibrosis was decreased and the myocardial infarction size was significantly reduced. Compared with AMI model group and miR-33b-5p inhibitor group, the levels of MDA, IL-1β, IL-6, TNF-α and the expressions of Bax and Cyt C in the heart tissue of mice in miR-33b-5p mimic group were significantly decreased, while the levels of SOD and Bcl-2 expression were significantly increased, and the differences were statistically significant. The expressions of IDI2-AS1 and NR4A2 in the heart tissue of mice in miR-33b-5p mimic group were significantly lower than those in AMI model group and miR-33b-5p inhibitor group [IDI2-AS1 (2 -ΔΔCt): 1.96±0.08 vs. 2.73±0.08, 3.10±0.05, NR4A2 (2 -ΔΔCt): 2.36±0.07 vs. 3.16±0.08, 3.80±0.08, all P < 0.01]. The expression of miR-33b-5p was significantly higher than that of AMI model group and miR-33b-5p inhibitor group (2 -ΔΔCt: 0.88±0.07 vs. 0.57±0.07, 0.23±0.01, both P < 0.01). The cell experiment results showed that the caspase-3/7 activity of rat neonatal cardiomyocytes in the miR-33b-5p mimic transfection group was significantly lower than that in the ischemia-hypoxia model group and the miR-33b-5p inhibitor transfection group, suggesting that miR-33b-5p can significantly reduce the apoptosis level of the ischemia-hypoxia model. The levels of peroxidation and inflammation indexes, important genes of apoptosis pathway and the expression of IDI2-AS1/miR-33b-5p/NR4A2 regulatory axis of rat neonatal cardiomyocytes in all groups were consistent with the above. Conclusion:IDI2-AS1 can regulate NR4A2 through miR-33b-5p, thus affecting the occurrence and development of AMI.

Objective To explore the correlation of red cell distribution width/albumin ratio(RAR)and fibrinogen/albumin ratio(FAR)with severity of coronary artery disease(CAD)in patients with coronary heart disease(CHD),and to further explore the relationship of RAR and FAR with CAD severity in different glucose metabolic states.Methods A total of 577 CHD patients undergoing coronary angiography(CAG)in Department of Cardiology of Tianjin People's Hospital from January 2021 to December 2022 were enrolled,and according to the results of CAG,412 patients were diagnosed with multi-vessel CAD and the other 165 patients with single-vessel CAD.Their baseline data and results of laboratory tests were collected,and RAR and FAR values were calculated.Univariate and multivariate logistic regression analyses were performed with RAR and FAR as independent variables,and ROC curve was plotted to evaluate the predic-tive values of the 2 indicators for the severity of CAD.Spearman correlation analysis was applied to analyze the occurrence of major adverse cardiovascular events(MACEs)in the patients.Results Logistic regression analysis showed that RAR and FAR were independent risk factors for CAD(OR=1.974,95％CI:1.348-2.593,P=0.000;OR=1.737,95％CI:1.486-2.377,P=0.000).Un-der different glucose metabolic states,RAR had the highest correlation with the risk of CAD in diabetic patients(OR=2.828,95％CI:1.157-7.145),while FAR was associated with a relatively low risk of CAD in diabetic patients(OR=2.217,95％CI:1.533-5.570).ROC curve analysis showed that RAR(AUC=0.776,95％CI:0.731-0.821,P=0.000)and FAR(AUC=0.725,95％CI:0.676-0.774,P=0.000)had predictive value for the severity of CAD in CHD patients.Spearman correlation analysis indicated that RAR and FAR were positively correlated with occur-rence of MACEs in CHD patients(P＜0.001).Conclusion RAR and FAR are independent pre-dictors for CHD patients.RAR has a stronger predictive value for lesion severity in CHD patients with concomitant abnormal glucose metabolism.