Objective:To explore the effects of aloe vera extra (AVE) on lipopolysaccharide (LPS)-induced inflammatory response of human periodontal ligament cells(hPDLCs).Methods:hPDLCs were induced with LPS at 1 μg/ml for the simulation of periodontitis model(model group) and then treated by AVE at 0.05,0.1,0.2 mg/ml respectively(AVE group).Cell viability was examined by MTT assay.The level of interleukin-6(IL-6) from cell culture medium was measured by ELISA.The expression of Toll like receptor 4(TLR4) protein was detected by immunocytochemistry staining and the transfer of nuclear factor-kappa B p65 (NF-κB-p65) was observed by immunofluorescence staining.Results:There was no significant difference of the cell viabilities among the groups.IL-6 in culture medium,the expression of TLR4 protein and the transfer of NF-κB-p65 into the nucleus were increased in model group.AVE at 0.05-0.2 mg/ml inhibited the secretion of IL-6 in the cell culture supernatant down-regulated the TLR4 expression,attenuated the transfer of NF-κB-p65 into the nucleus in a concentration-dependent manner.Conclusion:Aloe vera extract can inhibit the inflammation response of hPDLCs induced by LPS through TLR4/ NF-κB-p65 signaling pathway.

Objective To investigate the expressions and clinical significance of Ki-67,p53,and survivin in esophageal cancer and precancerosis.Methods The expressions of Ki-67,p53,and survivin proteins were detected by immunohistochemical staining in 40 normal esophageal mucosa,136 precancerosis (42 mild atypical hyperplasia,43 moderate atypical hyperplasia,and 51 severe atypical hyperplasia),and 68 esophageal cancer tissues.The correlation of three proteins expressed in esophageal carcinoma tissues was analyzed.Results The positive expression rate of Ki-67 was 0 (0/40)for normal epithelium,35.7％ (15/42) for mild dysplasia,51.2％ (22/43) for moderate dysplasia,74.5％ (38/51) for severe dysplasia,92.6％ (63/68) for squamous carcinoma,respectively.The positive expression rate of p53 protein was 0 (0/40) for normal epithelium,28.6％ (12/42) for mild dysplasia,46.5％ (20/43) for moderate dysplasia,52.9％ (27/51) for severe dysplasia,67.6％ (46/68) for squamous carcinoma,respectively.The positive expression rate of survivin protein was 0 (0/40) for normal epithelium,38.1％ (16/42) for mild dysplasia,55.8％ (24/43) for moderate dysplasia,64.7％ (33/51) for severe dysplasia,89.7％ (61/68) for squamous carcinoma,respectively.Rank correlation analysis showed that abnormal expressions of Ki-67,p53,and survivin were correlated significantly with the pathological grading of the lesions (r =0.637,0.454,0.590,P ＜0.01).The expressions of Ki-67,p53,and survivin were positively correlated in esophageal carcinoma (r =0.407,0.646,P ＜ 0.01).Conclusions The abnormal expressions of Ki67,p53,and survivin were associated with the processes of the esophageal canceration,and the joint detection with three parameters has important clinical value.

Studies show that metformin inhibits the proliferation of several types of cancer cells.All evidences,therefore propose the anti-tumor effect of metformin.Metformin can repress the oxygen consumption of tumor cells,and suppress hypoxia-inducible factor-1α (HIF-1ct) accumulation through the translational and posttranslational mechanisms,and suppress the expression of HIF-1α by activating AMP-activated protein kinase (AMPK).

Objective To investigate the potential vascular stimulation of potassium chloride and sodium chloride injection.Methods Sixteen rabbits were divided equally into two groups:group one and group two,with six rabbits in each group.According to the highest dose and maximum infusion speed for routine potassium supplementation in clinic,potassium chloride and sodium chloride injection or 0.9％ sodium chloride injection was administrated,respectively,at the same infusion speed and the same infusion volume via the marginal ear veins of rabbits.The vascular stimulation and the pathological changes of marginal ear vein and its surrounding tissue of rabbits were observed by the blinding method.Results Vascular stimulation,including hyperaemia,tumidness,necrosis and pathological changes,such as inflammatory cell infiltration and cellular necrosis,were not found in two groups.Conclusions Potassium chloride and sodium chloride injection has no stimulation to the wall of blood vessels.

Hepatocellular carcinoma (HCC) is a highly prevalent tumor in China. It has an insidious onset, rapid progression, early recurrence and poor prognosis. Most patients are already in the middle and late stages when they are diagnosed and lose the best time for surgery. Therefore, early diagnosis and treatment of HCC is crucial for patients. In recent years, contrast-enhanced ultrasound (CEUS) technology has been widely used in the diagnosis of liver diseases, especially in the diagnosis and treatment of HCC, which has an irreplaceable role. Meanwhile, the image fusion technology developed on the basis of CEUS can highlight the value of CEUS in the diagnosis and treatment of HCC.

Objective To study the effects of different concentration of chrysophanol on the activity and glutamate metabolism of primarily cultured astrocytes in vitro. Methods Primarily cultured mice astro-cytes were treated with chrysophanol at concentration of 10 , 20 , 40 , 60 , 80 , 100 , 200 , and 250 mg/L ( chry 1~8 group) for 1 d, 2 d, and 3 d. The cell activities were measured by MTT method, mRNA ex-pressions of glutamate/aspartate transporter (GLAST) and glutamate acid transporter 1(GLT-1) were de-tected by using RT-PCR, and the activities of glutamine synthetase ( GS ) and glutathione peroxidase ( GSH-Px ) were also determined. Results Time-dependence and concentration-dependence of the effects of chrysophanol showed on the following: activity of astrocytes inhibited, mRNA expressions of GLAST and GLT-1 upregulated, and the activities of GSH-Px and GS increased. However, the effect of chrysophanol on extra-cellular concentration of glutamate didn’ t depend on the number or activity of the cells. Conclusion Chrysophanol inhibited the activity of astrocytes in mice, and its effect on glutamate metabolism was concentration-and time-dependent.

Objective:To explore the mediating effect of psychological resilience on the aggressive coping confidence and post-traumatic growth of psychiatric nurses.Methods:From July to September 2022, convenience sampling was used to select 1 200 psychiatric nurses from 5 psychiatric hospitals in Guangdong Province who had experienced workplace violence incidents as the research subject. The General Information Questionnaire, Confidence in Coping with Patient Aggression Instrument (CCPAI) , Connor-Davidson Resilience Scale (CD-RISC) , and Post-Traumatic Growth Inventory (PTGI) were used to investigate psychiatric nurses. Pearson correlation analysis was used to explore the association between nurses' aggressive coping confidence, psychological resilience and post-traumatic growth. Multiple linear regression was used to analyze the influencing factors of post-traumatic growth, and the Process plug-in was used to conduct non parametric repeated measurement to test the mediating effect. A total of 1 200 questionnaires were distributed, with 135 invalid questionnaires excluded and an effective recovery rate of 88.75%.Results:1 065 psychiatric nurses scored (35.41±7.56) on their aggressive coping confidence, (65.55±16.73) on their psychological resilience, and (65.32±16.60) on their post-traumatic growth. The total score of post-traumatic growth was positively correlated with the aggressive coping confidence ( r=0.371, P<0.01) , and positively correlated with psychological resilience ( r=0.663, P<0.01) . Multiple linear regression analysis showed that aggressive coping confidence, toughness dimension, self-improvement dimension, marital status, and positional title were the main influencing factors for the post-traumatic growth of psychiatric nurses ( P<0.05) . Psychological resilience played a part of the mediating effect (36.69% of the total effect) in aggressive coping confidence and post-traumatic growth. Conclusions:The post-traumatic growth, aggressive coping confidence and psychological resilience of psychiatric nurses are at a medium level. The post-traumatic growth, aggression coping confidence and psychological resilience of psychiatric nurses who have experienced workplace violence are closely related. Psychological resilience has a mediating effect between aggression coping confidence and post-traumatic growth. The post-traumatic growth of psychiatric nurses can be improved by intervening their aggressive coping confidence and psychological resilience.

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.