The incidence rate of hepatic fibrosis remains at a high level， and there is still a lack of specific therapeutic drugs， posing a serious threat to human health. As a type of natural active components widely present in plants， flavonoids have multiple physiological functions such as antioxidant， anti-inflammatory， and anti-fibrotic activities， and a large number of studies have confirmed the anti-hepatic fibrosis effect of flavonoids. As for the mechanism of action， flavonoids can target the functions of hepatic stellate cells by inhibiting their proliferation and differentiation， promoting their apoptosis， regulating the level of autophagy， reducing the formation of extracellular matrix， and regulating iron metabolism in hepatic stellate cells， and meanwhile， they can inhibit chronic liver inflammatory response， improve oxidative stress status， regulate intestinal flora balance， and block epithelial-mesenchymal transition， thereby blocking the progression of fibrosis through multiple dimensions. At the level of signaling pathways， flavonoids mainly exert an anti-fibrotic effect by regulating the abnormal activation of the signaling pathways such as transforming growth factor-β1/Smad， Janus kinase/signal transducer and activator of transcription， nuclear factor erythroid 2-related factor 2， nuclear factor-kappa B， phosphatidylinositol 3-kinase/protein kinase B， mitogen-activated protein kinase， Wnt/β-catenin， and adenosine 5'-monophosphate-activated protein kinase. This article summarizes the research advances in the anti-fibrotic effect of flavonoids， in order to provide a theoretical basis for further exploring their medicinal potential.

Objective:To investigate the application value of nasolabial flaps in addressing tissue defects after resection of benign and malignant nasal vestibular lesions. Methods:The clinical data of patients with benign and malignant nasal vestibular lesions were analyzed retrospectively. There were 4 cases of squamous cell carcinoma, 2 cases of black hairy nevus and 1 case of chronic proliferative inflammatory lesions, all of which were repaired by adjacent nasolabial flap. Results:After 6 months of follow-up, none of the patients developed nasal vestibular contracture or nostril stenosis, and postoperative nasal ventilation function was good. Conclusion:The preoperative design of individual nasolabial flaps is very important for maintaining maxillofacial aesthetics, protectingthe nasolabial framework, and preserving postoperative nasal ventilation function.
Humans ; Retrospective Studies ; Middle Aged ; Nose Neoplasms/surgery* ; Surgical Flaps ; Male ; Female ; Adult ; Nose/surgery* ; Plastic Surgery Procedures/methods* ; Carcinoma, Squamous Cell/surgery* ; Aged ; Skin Transplantation

Objective To investigate the potential factors influencing the occurrence of major adverse cardiovascular events (MACE) in patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI) and develop an efficient and accurate predictive model. Methods Clinical data of AMI patients treated in the emergency department of Jining Medical University Affiliated Hospital between January and December 2020 were retrospectively collected. Patients were divided into two groups based on the occurrence of in-hospital MACE,the MACE group and the non-MACE group. Clinical indicators of the two groups were compared,and statistically significant variables were selected for inclusion in a multivariate logistic regression analysis. Based on this analysis,a nomogram model was constructed to predict the risk of in-hospital MACE in AMI patients after PCI. The model's predictive accuracy was evaluated using the receiver operating characteristic (ROC) curve,and the goodness of fit was assessed using the Hosmer-Lemeshow test. Results A total of 583 patients were included after screening based on inclusion and exclusion criteria,of whom 85 (14.58％) experienced in-hospital MACE. Univariate analysis showed that compared to the non-MACE group,the MACE group had higher values for age,Killip classification,myoglobin (MYO),brain natriuretic peptide (BNP),white blood cell count (WBC),prothrombin time (PT),T-wave changes on electrocardiogram (ECG),abnormal wall motion on echocardiography,ischemia duration greater than 6 hours,the number of MACE before PCI,and left anterior descending artery stenosis. In contrast,the number of patients with a history of oral antiplatelet medication use,coronary artery disease (CAD),family history of CAD,admission systolic blood pressure,and left ventricular ejection fraction (LVEF) were lower in the MACE group. Multivariate analysis indicated that Killip classification,BNP,ischemia duration greater than 6 hours,and MACE before PCI were independent risk factors for in-hospital MACE in AMI patients after PCI,while pre-onset use of antiplatelet medications and LVEF were independent protective factors. The nomogram model constructed based on independent risk factors demonstrated good predictive ability,with an area under the ROC curve (AUC) of 0.817,a sensitivity of 81.48％,and a specificity of 67.66％. The Hosmer-Lemeshow test confirmed the model's good fit (x2=1.937,P=0.983). Conclusion The nomogram model developed in this study effectively assesses the risk of in-hospital MACE in AMI patients after PCI,providing a valuable tool for predicting patient outcomes post-PCI.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Objective:To investigate the prognostic value of N-terminal B-type brain natriuretic peptide precursor (NT-proBNP), cardiac troponin I (cTnI) and aVL lead T-wave changes in acute coronary syndrome (ACS).Methods:Clinical data of 162 patients with ACS admitted to the Emergency Chest Pain Center of the Affiliated Hospital of Jining Medical University from January 2020 to December 2021 were retrospectively collected, including 84 patients with unstable angina pectoris (UAP) and 46 patients with ST-segment elevation myocardial infarction (STEMI). 32 patients with non-ST elevation myocardial infarction (NSTEMI); There were 66 patients with single-vessel disease, 70 patients with double-vessel disease, 26 patients with multi-vessel disease, and 51 patients with major cardiovascular adverse events (MACE). The levels of NT-proBNP, cTnI and T-wave change ratio of aVL lead were compared in different patients.Results:The NT-proBNP and cTnI of UAP patients were 510.42(365.56, 630.54)pg/ml and 8.20(6.50, 10.50)ng/ml, respectively, which were significantly lower than those of STEMI and NSTEMI patients (all P<0.05). There was no significant difference in NT-proBNP and cTnI between STEMI and NSTEMI patients (all P>0.05). The T-wave change proportions of NT-proBNP, cTnI and aVL leads in patients with multi-vessel lesions were 804.90(680.87, 980.05)pg/ml, 13.90(10.12, 15.65)ng/ml and 88.46%(23/26), respectively. It was significantly higher than that in patients with single and double vessel lesions (all P<0.05). The T-wave change ratio of NT-proBNP, cTnI and aVL leads in patients with double-vessel disease was 680.84(525.50, 810.62)pg/ml, 10.40(8.92, 13.60)ng/ml and 67.14%(47/70), respectively, which was significantly higher than that in patients with single-vessel disease (all P<0.05). The proportions of T-wave changes of NT-proBNP, cTnI and aVL leads in MACE patients were 744.54(621.17, 905.54)pg/ml, 12.21(8.65, 15.54)ng/ml and 86.27%(44/51), respectively. It was significantly higher than those without MACE (all P<0.05). The area under receiver operating characteristic (ROC) curve of NT-proBNP, cTnI and aVL lead T-wave changes independently and jointly predicted the occurrence of MACE were 0.937, 0.677, 0.706 and 0.799, respectively, among which NT-proBNP had a higher value in predicting the occurrence of MACE. Conclusions:The T-wave changes of NT-proBNP, cTnI and aVL leads are related to the type of lesions, the number of lesions and the occurrence of MACE in ACS patients, and NT-proBNP has a high value in predicting prognosis.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Polysaccharides, predominantly extracted from traditional Chinese medicinal herbs such as Lycium barbarum, Angelica sinensis, Astragalus membranaceus, Dendrobium officinale, Ganoderma lucidum, and Poria cocos, represent principal bioactive constituents extensively utilized in Chinese medicine. These compounds have demonstrated significant anti-inflammatory capabilities, especially anti-liver injury activities, while exhibiting minimal adverse effects. This review summarized recent studies to elucidate the hepatoprotective efficacy and underlying molecular mechanisms of these herbal polysaccharides. It underscored the role of these polysaccharides in regulating hepatic function, enhancing immunological responses, and improving antioxidant capacities, thus contributing to the attenuation of hepatocyte apoptosis and liver protection. Analyses of molecular pathways in these studies revealed the intricate and indispensable functions of traditional Chinese herbal polysaccharides in liver injury management. Therefore, this review provides a thorough examination of the hepatoprotective attributes and molecular mechanisms of these medicinal polysaccharides, thereby offering valuable insights for the advancement of polysaccharide-based therapeutic research and their potential clinical applications in liver disease treatment.
Humans ; Drugs, Chinese Herbal/pharmacology* ; Liver Diseases/drug therapy* ; Antioxidants ; Polysaccharides/therapeutic use* ; Medicine, Chinese Traditional

Objective To investigate the potential factors influencing the occurrence of major adverse cardiovascular events (MACE) in patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI) and develop an efficient and accurate predictive model. Methods Clinical data of AMI patients treated in the emergency department of Jining Medical University Affiliated Hospital between January and December 2020 were retrospectively collected. Patients were divided into two groups based on the occurrence of in-hospital MACE,the MACE group and the non-MACE group. Clinical indicators of the two groups were compared,and statistically significant variables were selected for inclusion in a multivariate logistic regression analysis. Based on this analysis,a nomogram model was constructed to predict the risk of in-hospital MACE in AMI patients after PCI. The model's predictive accuracy was evaluated using the receiver operating characteristic (ROC) curve,and the goodness of fit was assessed using the Hosmer-Lemeshow test. Results A total of 583 patients were included after screening based on inclusion and exclusion criteria,of whom 85 (14.58％) experienced in-hospital MACE. Univariate analysis showed that compared to the non-MACE group,the MACE group had higher values for age,Killip classification,myoglobin (MYO),brain natriuretic peptide (BNP),white blood cell count (WBC),prothrombin time (PT),T-wave changes on electrocardiogram (ECG),abnormal wall motion on echocardiography,ischemia duration greater than 6 hours,the number of MACE before PCI,and left anterior descending artery stenosis. In contrast,the number of patients with a history of oral antiplatelet medication use,coronary artery disease (CAD),family history of CAD,admission systolic blood pressure,and left ventricular ejection fraction (LVEF) were lower in the MACE group. Multivariate analysis indicated that Killip classification,BNP,ischemia duration greater than 6 hours,and MACE before PCI were independent risk factors for in-hospital MACE in AMI patients after PCI,while pre-onset use of antiplatelet medications and LVEF were independent protective factors. The nomogram model constructed based on independent risk factors demonstrated good predictive ability,with an area under the ROC curve (AUC) of 0.817,a sensitivity of 81.48％,and a specificity of 67.66％. The Hosmer-Lemeshow test confirmed the model's good fit (x2=1.937,P=0.983). Conclusion The nomogram model developed in this study effectively assesses the risk of in-hospital MACE in AMI patients after PCI,providing a valuable tool for predicting patient outcomes post-PCI.