In recent years, the incidence of dry eye disease(DED)is increasing, positioning it as one of the most prevalent diseases affecting the ocular surface. Inflammatory response is the pathological basis of DED, involving various inflammatory mediators and inflammatory signaling pathways. Consequently, anti-inflammatory treatment emerges as a fundamental strategy for preventing and managing DED. This review summarizes the classic inflammatory factors involved in the development and progression of DED, including interleukins, tumor necrosis factor, matrix metalloproteinases, chemokines, and cell adhesion molecules. It also discusses the relevant inflammatory signaling pathways: the MAPKs pathway, NF-κB pathway, Wnt pathway and TLR pathway. Additionally, this review addresses the mechanisms of action and alterations in relevant biomarkers associated with current first-line recommended anti-inflammatory therapies, including corticosteroids, immunosuppressants, nonsteroidal anti-inflammatory drugs, and traditional Chinese medicine approaches to inflammation management. This comprehensive overview aims to enhance understanding of the inflammatory mechanisms underlying DED while exploring future therapeutic prospects.

In recent years, the incidence of dry eye disease(DED)is increasing, positioning it as one of the most prevalent diseases affecting the ocular surface. Inflammatory response is the pathological basis of DED, involving various inflammatory mediators and inflammatory signaling pathways. Consequently, anti-inflammatory treatment emerges as a fundamental strategy for preventing and managing DED. This review summarizes the classic inflammatory factors involved in the development and progression of DED, including interleukins, tumor necrosis factor, matrix metalloproteinases, chemokines, and cell adhesion molecules. It also discusses the relevant inflammatory signaling pathways: the MAPKs pathway, NF-κB pathway, Wnt pathway and TLR pathway. Additionally, this review addresses the mechanisms of action and alterations in relevant biomarkers associated with current first-line recommended anti-inflammatory therapies, including corticosteroids, immunosuppressants, nonsteroidal anti-inflammatory drugs, and traditional Chinese medicine approaches to inflammation management. This comprehensive overview aims to enhance understanding of the inflammatory mechanisms underlying DED while exploring future therapeutic prospects.

Cemental tear is a rare and indetectable condition unless obvious clinical signs present with the involvement of surrounding periodontal and periapical tissues. Due to its clinical manifestations similar to common dental issues, such as vertical root fracture, primary endodontic diseases, and periodontal diseases, as well as the low awareness of cemental tear for clinicians, misdiagnosis often occurs. The critical principle for cemental tear treatment is to remove torn fragments, and overlooking fragments leads to futile therapy, which could deteriorate the conditions of the affected teeth. Therefore, accurate diagnosis and subsequent appropriate interventions are vital for managing cemental tear. Novel diagnostic tools, including cone-beam computed tomography (CBCT), microscopes, and enamel matrix derivatives, have improved early detection and management, enhancing tooth retention. The implementation of standardized diagnostic criteria and treatment protocols, combined with improved clinical awareness among dental professionals, serves to mitigate risks of diagnostic errors and suboptimal therapeutic interventions. This expert consensus reviewed the epidemiology, pathogenesis, potential predisposing factors, clinical manifestations, diagnosis, differential diagnosis, treatment, and prognosis of cemental tear, aiming to provide a clinical guideline and facilitate clinicians to have a better understanding of cemental tear.
Humans ; Dental Cementum/injuries* ; Consensus ; Diagnosis, Differential ; Cone-Beam Computed Tomography ; Tooth Fractures/therapy*

Objective:To develop and validate a perioperative oral care protocol for patients undergoing oral vestibular approach endoscopic thyroid cancer radical surgery, providing practical guidance for clinical nursing.Methods:The protocol was constructed through literature analysis and Delphi expert consultation. A prospective non-randomized controlled study was conducted using convenience sampling, enrolling 60 patients who underwent oral vestibular approach endoscopic thyroid cancer radical surgery at the First Affiliated Hospital with Nanjing Medical University Thyroid Center between August 2023 and May 2024. Participants were divided into control group (from August to December, 2023) and experimental group (from January to May, 2024) based on admission dates with 30 cases in each group. The control group received routine care, while the experimental group received the developed oral care protocolin on the basis of the control group. Postoperative pain scores, mouth-opening difficulties, and oral cleanliness were compared on days 1, 3, and 7 after surgery.Results:The final protocol comprised 7 first-level indicators (team collaboration, health education, preoperative oral assessment, preoperative management, intraoperative management, postoperative management, and discharge follow-up), 17 second-level indicators, and 49 third-level indicators. The control group had 4 males and 26 females, with an age of (29.57 ± 5.34) years; the experimental group had 6 males and 24 females, with an age of (29.87 ± 6.25) years. On postoperative days 1, 3, and 7, the pain scores were 3.87 ± 1.01, 3.30 ± 0.92, and 2.53 ± 0.68 in the control group and 3.20 ± 0.87, 2.10 ± 0.76, and 1.50 ± 0.51 in the experimental group, respectively. The differences between the two groups were statistically significant ( t = 2.89, 5.12, 6.34, all P<0.05). For mouth-opening difficulties, the control group had 6, 13, and 15 patients with grade I on postoperativedays 1, 3, and 7, respectively, while the experimental group had 10, 20, and 25 patients with gradeⅠ. The control group had 20, 14, and 14 patients with gradeⅡonpostoperative days 1, 3, and 7, respectively, while the experimental group had 17, 10, and 5 patients with gradeⅡ. The control group had 4, 3, and 1 patients with grade Ⅲ on postoperative days 1, 3, and 7, respectively, while the experimental group had 3, 0, and 0 patients with grade Ⅲ. There were 0 cases in both groups with grade Ⅳ. The differences between the two groups on postoperative days 3, and 7 were statistically significant ( χ2 = 10.45, 18.67, both P<0.05). For oral cleanliness, the control group had 3, 4, and 5 patients with excellent cleanliness on postoperative days 1, 3, and 7, respectively, while the experimental group had 11, 16, and 19 patients with excellent cleanliness. The control group had 20, 22, and 23 patients with good cleanliness on postoperative days 1, 3, and 7, respectively, while the experimental group had 18, 13, and 10 patients with good cleanliness. The control group had 7 (23.33%), 4 (13.33%), and 2 (6.67%) patients with poor cleanliness on postoperative days 1, 3, and 7, respectively, while the experimental group had 1 (3.33%), 1 (3.33%), and 1 (3.33%) patients with poor cleanliness. The differences between the two groups were statistically significant ( χ2 = 9.19, 11.32, 16.68, all P<0.05). Conclusions:The developed perioperative oral care protocol is scientifically sound, feasible, and practical. Following the intervention, significant decreases in pain scores, alleviation of trismus symptoms, and marked improvements in oral cleanliness were observed in patients compared to pre-intervention assessments, and worth further clinical application.

Objective:To develop a Protection Motivation Questionnaire(PMQ)for frailty management in the elderly based on the Protection Motivation Theory(PMT), and test its reliability and validity.Methods:Guided by PMT, the initial questionnaire items were formulated through literature review, semi-structured interviews, and Delphi expert consultation.A total of 551 elderly patients with frailty from a tertiary hospital in Changsha were investigated.Item screening was conducted via critical ratio method, Cronbach's α coefficient, correlation analysis, and factor analysis.The reliability was assessed through internal consistency and test-retest reliability, while validity was evaluated via content validity and structural validity.Results:The final PMQ comprised 25 items across five dimensions: severity, susceptibility, response efficacy, response cost, and self-efficacy.The overall Cronbach's α coefficient was 0.818, with subscale coefficients ranging from 0.701 to 0.821.The split-half reliability was 0.811, test-retest reliability was 0.929, and content validity indexwas 0.86.Exploratory factor analysis extracted five factors, accounting for 52.0% of the cumulative variance.Confirmatory factor analysis demonstrated good model fit( χ2/df=1.626, RMSEA=0.05, CFI =0.914). Conclusions:The developed questionnaire exhibits strong reliability and validity, serving as an effective tool to assess protection motivation for frailty management in the elderly.

Background: Epimedii Folium, first recorded in the Shennong’s Classic of Materia Medica (Shen Nong Ben Cao Jing), is a traditional Chinese medicine (TCM) known for its effects of “benefiting Qi and strengthening the heart.” Icariside II (ICS II) is one of the main active components of Epimedii Folium, possessing cardiovascular protective and anti-inflammatory properties. However, the potential mechanisms of ICS II on myocardial ischemia (MI) remain unclear. Objective: The aim of the study was to investigate the effects and preliminary molecular mechanisms of ICS II in treating isoproterenolinduced MI in rats. Methods: A rat model of MI was established by subcutaneous injection of isoproterenol. Electrocardiography, echocardiography, myocardial enzymes analysis, heart weight index, triphenyltetrazolium chloride staining, histopathology, TUNEL staining, RT-qPCR, and Western blot were employed to evaluate the effects and preliminary molecular mechanisms of ICS II on MI rats. Results: Pharmacodynamic studies suggested that ICS II inhibited ST-segment elevation in electrocardiograms, improved cardiac function, reduced heart weight index and myocardial enzyme levels, decreased myocardial infarct size, alleviated cardiac histological damage, and inhibited apoptosis, thereby exerting cardioprotective effects in MI rats. Further studies revealed that ICS II may partially inhibit the expression of NLRP3/Caspase-1 axis-related targets at both protein and mRNA levels. Conclusions: Our findings indicate that ICS II exerts anti-MI effects, and its preliminary molecular mechanisms may be related to inhibiting the activation of the NLRP3/Caspase-1 axis to alleviate inflammatory responses.

Background: Epimedii Folium, first recorded in the Shennong’s Classic of Materia Medica (Shen Nong Ben Cao Jing), is a traditional Chinese medicine (TCM) known for its effects of “benefiting Qi and strengthening the heart.” Icariside II (ICS II) is one of the main active components of Epimedii Folium, possessing cardiovascular protective and anti-inflammatory properties. However, the potential mechanisms of ICS II on myocardial ischemia (MI) remain unclear. Objective: The aim of the study was to investigate the effects and preliminary molecular mechanisms of ICS II in treating isoproterenolinduced MI in rats. Methods: A rat model of MI was established by subcutaneous injection of isoproterenol. Electrocardiography, echocardiography, myocardial enzymes analysis, heart weight index, triphenyltetrazolium chloride staining, histopathology, TUNEL staining, RT-qPCR, and Western blot were employed to evaluate the effects and preliminary molecular mechanisms of ICS II on MI rats. Results: Pharmacodynamic studies suggested that ICS II inhibited ST-segment elevation in electrocardiograms, improved cardiac function, reduced heart weight index and myocardial enzyme levels, decreased myocardial infarct size, alleviated cardiac histological damage, and inhibited apoptosis, thereby exerting cardioprotective effects in MI rats. Further studies revealed that ICS II may partially inhibit the expression of NLRP3/Caspase-1 axis-related targets at both protein and mRNA levels. Conclusions: Our findings indicate that ICS II exerts anti-MI effects, and its preliminary molecular mechanisms may be related to inhibiting the activation of the NLRP3/Caspase-1 axis to alleviate inflammatory responses.

Background: Epimedii Folium, first recorded in the Shennong’s Classic of Materia Medica (Shen Nong Ben Cao Jing), is a traditional Chinese medicine (TCM) known for its effects of “benefiting Qi and strengthening the heart.” Icariside II (ICS II) is one of the main active components of Epimedii Folium, possessing cardiovascular protective and anti-inflammatory properties. However, the potential mechanisms of ICS II on myocardial ischemia (MI) remain unclear. Objective: The aim of the study was to investigate the effects and preliminary molecular mechanisms of ICS II in treating isoproterenolinduced MI in rats. Methods: A rat model of MI was established by subcutaneous injection of isoproterenol. Electrocardiography, echocardiography, myocardial enzymes analysis, heart weight index, triphenyltetrazolium chloride staining, histopathology, TUNEL staining, RT-qPCR, and Western blot were employed to evaluate the effects and preliminary molecular mechanisms of ICS II on MI rats. Results: Pharmacodynamic studies suggested that ICS II inhibited ST-segment elevation in electrocardiograms, improved cardiac function, reduced heart weight index and myocardial enzyme levels, decreased myocardial infarct size, alleviated cardiac histological damage, and inhibited apoptosis, thereby exerting cardioprotective effects in MI rats. Further studies revealed that ICS II may partially inhibit the expression of NLRP3/Caspase-1 axis-related targets at both protein and mRNA levels. Conclusions: Our findings indicate that ICS II exerts anti-MI effects, and its preliminary molecular mechanisms may be related to inhibiting the activation of the NLRP3/Caspase-1 axis to alleviate inflammatory responses.

AIM:To investigate the effects of emo-din on autophagy and apoptosis in rats with severe pneumonia(KP)caused by K.pneumoniae and its possible mechanism.METHODS:The KP rat model was established by infecting K pneumonia was treat-ed with Emodin.The rats were grouped into Sham surgery group,KP group,low concentration Emodin group,medium concentration Emodin group,high concentration Emodin group,and Emodin+sirtinol(SIRT1 activity inhibitor)group;Arterial partial pres-sure of carbon dioxide(PaCO2),arterial partial pres-sure of oxygen(PaO2)and arterial oxygen saturation(SaO2)were measured by blood gas analyzer;the white blood cells and neutrophils in bronchoalveo-lar lavage fluid(BALF)were measured by Wright-Gi-emsa staining;HE staining was applied to detect pathological changes in lung tissue in each group;ELISA was applied to detect the expression of IL-6,TNF-α,and IL-1β in lung tissues of each group;elec-tron microscopy scanning was applied to observe the autophagy of cells in lung tissues of each group;the expression of LC3B in lung tissues was observed by immunofluorescence staining;TUNEL method was applied to detect changes in cell apoptosis in lung tissue of rats in each group;Western blot was applied to detect the expression of silent informa-tion regulatory factor(SIRT1),adenosine monophos-phate activated protein kinase(AMPK),LC3-Ⅱ,LC3-Ⅰ,c-caspase-3,and caspase-3 proteins in lung tissue.RESULTS:K.pneumoniae caused severe lung tissue damage in rats with pneumonia,increased inflam-matory infiltration and cytokine release in the lungs,arterial blood PaO2 and SaO2 levels de-creased,PaCO2 levels increased,white blood cells and neutrophils count increased in BALF,increased cell apoptosis rate and c-caspase-3/caspase-3 level,and the cell autophagy and the levels of autophagy related proteins LC3-Ⅱ/LC3-Ⅰ were decreased(all P＜0.05),after Emodin treatment,SIRT1/AMPK signal-ing pathway was activated,PaO2 and SaO2 levels in arterial blood were increased,PaCO2 levels was de-creased,inflammatory reaction was inhibited,cell apoptosis in lung tissue was inhibited(all P＜0.05),and cell autophagy level was restored,sirtinol,a SIRT1 inhibitor,partially reversed the therapeutic ef-fect of Emodin on KP rats after inhibiting SIRT1/AMPK signaling pathway(P＜0.05).CONCLUSION:Emodin may enhance autophagy of lung tissue cells and inhibit apoptosis of rat lung tissue cells by acti-vating SIRT1/AMPK pathway,which may provide po-tential therapeutic options for KP.

Objective To investigate the expression of X-linked inhibitor of apoptosis associated factor 1(XAF1)and phosphoenolpyruvate carboxykinase 1(PCK1)in Luminal type B breast cancer and their relationship with the prognosis of patients.Methods From January 2016 to January 2018,95 patients with Luminal B breast cancer underwent surgical treatment.Cancer tissues and adjacent tissues＞5 cm from the cancer tissues were collected during the operation.The positive expressions of XAF1 and PCK1 proteins were detected by immunohistochemistry.The relationship between XAF1 and PCK1 protein expression and clinicopathological features of breast cancer was analyzed,and the survival curves of breast cancer patients with different XAF1 and PCK1 protein expression were plotted by Kaplan-Meier method,the survival rate was compared by Log-rank test.Multi-factor Cox-regression analysis was used to analyze the prognostic factors of breast cancer.Results GEPIA database analysis showed that the expression levels of XAF1 and PCK1 mRNA in breast cancer tissues were lower than those in normal tissues(P＜0.05).The positive expression rates of XAF1 and PCK1 proteins in cancer tissue were lower than adjacent tissues(P＜0.05).The positive expression of XAF1 in breast cancer tissue was related to clinical stage,lymph node metastasis and histological grade,Ki-67 expression status,while the positive expression of PCK1 was related to clinical stage,lymph node metastasis and Ki-67 expression status(P＜0.05).The 5-year overall survival rate of XAF1 positive expression patients was higher than that of negative expression patients(Log-rank x2=5.101,P=0.024),and the 5-year overall survival rate of PCK1 positive expression patients was higher than that of negative expression patients(Log-rank x2=6.515,P=0.011).Clinical stage Ⅲ,negative expression of XAF1,and negative expression of PCK1 were risk factors for poor prognosis(P＜0.05).Conclusion The positive expression rates of XAF1 and PCK1 in Luminal B type breast cancer tissue are reduced,which is related to some clinicopathological characteristics and 5-year survival rate after surgery.The 5-year survival rate was lower in patients with negative XAFI and PCKI expression.