ObjectiveTo investigate the role and mechanism of action of paeoniflorin （PF） in protecting HepG2 cells induced by palmitic acid （PA）. MethodsHepG2 cells were stimulated with PA at a concentration of 250 μmol/L to establish a NAFLD model. Compound C at a concentration of 10 μmol/L was used as an inhibitor， and PF at a concentration of 25 μmol/L was used for intervention. The experiment was divided into normal group （CON group） treated with complete culture medium， model group （MOD group） treated with PA， PF treatment group （MOD+PF group） treated with PA and PF， model+inhibitor group （MOD+COM group） treated with PA and Compound C， and model+inhibitor+PF group （MOD+COM+PF group） treated with PA， Compound C， and PF. Kits were used to measure lipid deposition indicators， liver function parameters， oxidative stress indicators， and inflammation indicators； oil red O staining was used to observe lipid deposition； Western Blot was used to measure the protein expression levels of AMPK， SIRT1， PGC-1α， mTOR， Beclin-1， LC3， and P62 in cells. The one-way analysis of variance was used for comparison of quantitative data between groups， while the Tukey’s test was used for comparison between two groups. ResultsCompared with the MOD group， PF improved the levels of TC and TG （P<0.05）， reduced the levels of ALT， AST， CRP， TNF-α， IL-1β， and IL-6 （P<0.05）， increased the activity of SOD and CAT and the level of GSH， and reduced the level of MDA in cells （all P<0.05）. Oil red O staining showed that PF alleviated lipid deposition in cells. Western blot results showed that compared with the MOD group， PF increased the protein expression levels of p-AMPK， SIRT1， PGC-1α， LC3Ⅱ/LC3Ⅰ， and Beclin-1 and reduced the protein expression levels of p-mTOR and P62 （all P<0.05）. ConclusionPF can inhibit PA-induced oxidative stress and inflammatory response in HepG2 cells， improve lipid deposition， and promote autophagy via the AMPK/SIRT1/PGC-1α/mTOR signaling pathway.

ObjectiveTo develop a scale for evaluating the syndrome of internal retention of dampness and turbidity in nonalcoholic fatty liver disease （NAFLD） that combines disease and syndrome and has the characteristics of traditional Chinese medicine （TCM）. MethodsAn item pool was established for evaluating the syndrome of internal retention of dampness and turbidity in nonalcoholic fatty liver disease （NAFLD） with reference to the guideline for developing international scales. A clinical survey was conducted among the outpatients and inpatients who were diagnosed with NAFLD and had the syndrome of internal retention of dampness and turbidity in Department of Hepatology and Spleen-Stomach， The First Affiliated Hospital of Henan University of Chinese Medicine， from June to August， 2023， and the items were screened based on the classical test theory and the item response theory. An expert questionnaire was developed， and expert discussions were conducted using the Delphi method to identify the items for evaluating the syndrome of internal retention of dampness and turbidity in NAFLD. Finally， the scale was given scientific scores. ResultsA preliminary item pool was established， with 16 primary items and 22 secondary items， and it was divided into the two dimensions of disease and syndrome type. Clinical pre-survey suggested to retain 9 primary items and 14 secondary items， while the Delphi expert questionnaire recommended to retain 11 primary items and 15 secondary items， and tongue manifestation and pulse manifestation were no longer used for assessing the severity of syndrome. After hierarchical analysis and scientific assignment of scores， the scale for evaluating the syndrome of internal retention of dampness and turbidity in NAFLD had a total score of 123 points and 9 important items， i.e.， discomfort in the hypochondrium， abdominal fullness and distension， obesity， heaviness of the head and body， loose stool， anorexia， coughing up phlegm， nausea with a tendency to vomit， and lethargy. ConclusionA preliminary scale is established for evaluating the syndrome of internal retention of dampness and turbidity in NAFLD， which fills the gap in this research field and provides a basis for further clinical application.

[This corrects the article DOI: 10.1016/j.apsb.2021.07.004.].

Apical microsurgery is accurate and minimally invasive, produces few complications, and has a success rate of more than 90%. However, due to the lack of awareness and understanding of apical microsurgery by dental general practitioners and even endodontists, many clinical problems remain to be overcome. The consensus has gathered well-known domestic experts to hold a series of special discussions and reached the consensus. This document specifies the indications, contraindications, preoperative preparations, operational procedures, complication prevention measures, and efficacy evaluation of apical microsurgery and is applicable to dentists who perform apical microsurgery after systematic training.
Microsurgery/standards* ; Humans ; Apicoectomy ; Contraindications, Procedure ; Tooth Apex/diagnostic imaging* ; Postoperative Complications/prevention & control* ; Consensus ; Treatment Outcome

Pulpotomy, which belongs to vital pulp therapy, has become a strategy for managing pulpitis in recent decades. This minimally invasive treatment reflects the recognition of preserving healthy dental pulp and optimizing long-term patient-centered outcomes. Pulpotomy is categorized into partial pulpotomy (PP), the removal of a partial segment of the coronal pulp tissue, and full pulpotomy (FP), the removal of whole coronal pulp, which is followed by applying the biomaterials onto the remaining pulp tissue and ultimately restoring the tooth. Procedural decisions for the amount of pulp tissue removal or retention depend on the diagnostic of pulp vitality, the overall treatment plan, the patient's general health status, and pulp inflammation reassessment during operation. This statement represents the consensus of an expert committee convened by the Society of Cariology and Endodontics, Chinese Stomatological Association. It addresses the current evidence to support the application of pulpotomy as a potential alternative to root canal treatment (RCT) on mature permanent teeth with pulpitis from a biological basis, the development of capping biomaterial, and the diagnostic considerations to evidence-based medicine. This expert statement intends to provide a clinical protocol of pulpotomy, which facilitates practitioners in choosing the optimal procedure and increasing their confidence in this rapidly evolving field.
Humans ; Calcium Compounds/therapeutic use* ; Consensus ; Dental Pulp ; Dentition, Permanent ; Oxides/therapeutic use* ; Pulpitis/therapy* ; Pulpotomy/standards*

Intentional tooth replantation (ITR) is an advanced treatment modality and the procedure of last resort for preserving teeth with inaccessible endodontic or resorptive lesions. ITR is defined as the deliberate extraction of a tooth; evaluation of the root surface, endodontic manipulation, and repair; and placement of the tooth back into its original socket. Case reports, case series, cohort studies, and randomized controlled trials have demonstrated the efficacy of ITR in the retention of natural teeth that are untreatable or difficult to manage with root canal treatment or endodontic microsurgery. However, variations in clinical protocols for ITR exist due to the empirical nature of the original protocols and rapid advancements in the field of oral biology and dental materials. This heterogeneity in protocols may cause confusion among dental practitioners; therefore, guidelines and considerations for ITR should be explicated. This expert consensus discusses the biological foundation of ITR, the available clinical protocols and current status of ITR in treating teeth with refractory apical periodontitis or anatomical aberration, and the main complications of this treatment, aiming to refine the clinical management of ITR in accordance with the progress of basic research and clinical studies; the findings suggest that ITR may become a more consistent evidence-based option in dental treatment.
Humans ; Tooth Replantation/methods* ; Consensus ; Periapical Periodontitis/surgery*

Instrument separation is a critical complication during root canal therapy, impacting treatment success and long-term tooth preservation. The etiology of instrument separation is multifactorial, involving the intricate anatomy of the root canal system, instrument-related factors, and instrumentation techniques. Instrument separation can hinder thorough cleaning, shaping, and obturation of the root canal, posing challenges to successful treatment outcomes. Although retrieval of separated instrument is often feasible, it carries risks including perforation, excessive removal of tooth structure and root fractures. Effective management of separated instruments requires a comprehensive understanding of the contributing factors, meticulous preoperative assessment, and precise evaluation of the retrieval difficulty. The application of appropriate retrieval techniques is essential to minimize complications and optimize clinical outcomes. The current manuscript provides a framework for understanding the causes, risk factors, and clinical management principles of instrument separation. By integrating effective strategies, endodontists can enhance decision-making, improve endodontic treatment success and ensure the preservation of natural dentition.
Humans ; Root Canal Therapy/adverse effects* ; Consensus ; Root Canal Preparation/adverse effects*

OBJECTIVE To investigate the inhibitory effect and mechanism of 5,6-dimethylxanthe-none-4-acetic acid(DMXAA)on metastasis of Lewis lung cancer(LLC)in mice.METHODS The inhibi-tory effect of DMXAA on tumor metastasis was analyzed via an LLC xenograft tumor model and LLC metastatic tumor model.The mice of LLC xenograft tumor model were randomly divided into three groups:model group(physiological saline containing 1%DMSO,ip,once every two days),model+suni-tinib group(30 mg·kg-1,ip,once every two days),and model+DMXAA group(25 mg·kg-1,ip,once).Tumor volume and body mass were measured once every two days after administration.Two and five days after administration,tumor mass was measured by sacrificing the mice,followed by immunofluores-cence staining of tumor tissues.Platelet/endothelial cell adhesion molecule-1(CD31)and α-smooth muscle actin(α-SMA)were used to analyze the vascular structure of tumor tissues.The tumor hypoxia level was detected using the hypoxia probe pimonidazole staining.The mice of LLC metastatic tumor model were randomly divided into three groups:model group(physiological saline containing 1%DMSO,ip,twice a week),model+sunitinib group(60 mg·kg-1,ip,twice a week),and model+DMXAA group(25 mg·kg-1,ip,once).At the Two and five weeks after administration,the in vivo tumor growth and metastasis were observed and quantified using a small animal live imaging system.RESULTS Compared with the model group,the tumor volume and mass of the model+sunitinib group and model+ DMXAA group were significantly reduced(P<0.05,P<0.01),and DMXAA took effect faster and more significantly than sunitinib.At the same time,compared with the model group,the body mass in the model+sunitinib group decreased significantly(P<0.05),but there was no significant difference in body mass the model+DMXAA group.Compared with the model group,model+sunitinib had no effect on tumor metastasis,but model+DMXAA significantly reduced tumor metastasis two weeks after administration(P<0.01).Compared with the model group,the coverage rate of α-SMA/CD31 in the model+sunitinib group and model+DMXAA group increased significantly(P<0.05).Compared with the model group,there was no significant change in the tumor hypoxia area in the model+sunitinib group,but this in the model+DMXAA group decreased significantly(P<0.01).CONCLUSION DMXAA significantly inhibits the growth and metastasis of LLC in mice,and its mechanism may be related to its improvement of tumor vascular normalization and hyposic microenvironments.

Objective To investigate the risk factors for the development of advanced liver fibrosis by analyzing the clinical features of patients with in nonalcoholic fatty liver disease(NAFLD)and advanced liver fibrosis,and to establish a nomogram model for predicting the risk of advanced liver fibrosis.Methods A retrospective analysis was performed for the clinical data of 406 NAFLD patients who attended The First Affiliated Hospital of Henan University of Chinese Medicine from January 2022 to October 2023,and according to whether liver stiffness measurement(LSM)measured by FibroScan was≥11.0 kPa,the patients were divided into advanced liver fibrosis group with 65 patients and non-advanced liver fibrosis group with 341 patients.Related data were collected,including general information,laboratory markers,and medical history.The independent-samples t test was used for comparison of normally distributed continuous data between two groups,and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups;the chi-square test was used for comparison of categorical data between two groups.A multivariate Logistic regression analysis was used to identify independent risk factors,and a nomogram model was established based on these factors.The receiver operating characteristic(ROC)curve was used to evaluate the discriminatory ability of the nomogram model,and the calibration curve was used to evaluate its effectiveness.Results The univariate analysis showed that there were significant differences between the advanced liver fibrosis group and the non-advanced liver fibrosis group in age,controlled attenuation parameter(CAP),total bilirubin,direct bilirubin(DBil),indirect bilirubin,globin,alanine aminotransferase,aspartate aminotransferase,alkaline phosphatase(ALP),gamma-glutamyl transpeptidase(GGT),glucose,body mass index(BMI),and history of diabetes(all P<0.05).The multivariate Logistic regression analysis showed that CAP(odds ratio[OR]=1.015,95%confidence interval[CI]:1.006-1.024,P=0.010),DBil(OR=1.345,95%CI:1.139-1.590,P=0.001),ALP(OR=1.019,95%CI:1.008-1.029,P=0.001),GGT(OR=1.004,95%CI:1.000-1.008,P=0.035)and BMI(OR=1.240,95%CI:1.137-1.353,P=0.001)were independent risk factors for the development of advanced liver fibrosis in NAFLD.A nomogram model was established based on the results of the multivariate Logistic regression analysis.The ROC curve analysis showed that this nomogram model had an area under the ROC curve of 0.841(95%CI:0.791-0.891)in predicting the development of advanced liver fibrosis in the NAFLD population,and the calibration curve showed a good degree of fitting between the observed and predicted values for the development of advanced liver fibrosis.Conclusion Elevated levels of CAP,BMI,DBil,ALP,and GGT are independent risk factors for advanced liver fibrosis in NAFLD.The nomogram model established based on these factors has good predictive performance and a certain value in predicting advanced liver fibrosis.

OBJECTIVE To investigate the damage effect and potential toxic mechanism of SARS-CoV-2 spike protein(S protein)on human neuroblastomacells(SH-SY5Y).METHODS SH-SY5Y were treated with S protein at concentrations of 25,50,75,and 100 mg·L-1 for 24 h.Cell viability of SH-SY5Y was detected using the CCK-8 assay.The cytotoxic lactate dehydrogenase(LDH)detection kit was used to measure the release rate of LDH,and the 5-ethynyl-2′-deoxyuridine(EdU)-488 cell prolifera-tion kit was used to assess cell proliferation.The ATP detection kit was used to measure intracellular ATP content.The JC-1 fluorescent probe method was employed to detect the mitochondrial membrane potential(MMP)of cells.Seahorse XF was used to measure mitochondrial respiratory and glycolytic capacity.RESULTS Compared with the cell control group,cell viability was significantly reduced in S protein 25,50,75 and 100 mg·L-1 groups(P<0.01),and the half-inhibition concentration(IC50)was 65.05 mg·L-1.The LDH release rate wassignificantly increased(P<0.01)and the proportion of EdU positive cellswas significantly reduced(P<0.01)in S protein 25,50,75 and 100 mg·L-1 groups.S protein signifi-cantly reduced intracellular ATP content(P<0.01)at the concentrations of 75 and 100 mg·L-1,while significantly reduced intracellular MMP(P<0.05,P<0.01)at the concentrations of 50 and 75 mg·L-1.S protein 50 mg·L-1 increased the maximum value of basal glycolysis levels and glycolytic capacity(P<0.05,P<0.01),and S protein 25 and 50 mg·L-1 increased the maximum value of respiration capacity(P<0.05,P<0.01).SH-SY5Y cell viability was positively correlated with the intracellular ATP content and the MMP level(r2=0.9209,P=0.001;r2=0.6170,P=0.0025),and negatively correlated with the maximum level of basal glycolysis and glycolytic capacity(r2=0.5194,P=0.0285;r2=0.6664,P=0.0073),and nega-tively correlated with ATP production capacity(r2=0.8204,P=0.0008).CONCLUSIONS protein decreases the viability of SH-SY5Y cells and inhibited cell proliferation.The mechanism may be closely related to the disorder of energy metabolism.