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 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 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 evaluate the predictive value of mechanical power (MP) on the risk of in-hospital mortality in critical ill patients in emergency department.Methods:A total of 105 critical ill patients with invasive mechanical ventilation in the Department of Emergency of Second Affiliated Hospital of Guangzhou Medical University between December 1, 2017 and October 31, 2020 were retrospectively analyzed. Based on the clinical prognosis, the patients were divided into the in-hospital survival group (80 patients) and the in-hospital death group (25 patients). The clinical data and ventilator parameters were recorded, and the MP of the two groups was calculated in order to assess the predictive efficacy of MP on in-hospital death.Results:Compared to the in-hospital death group, the oxygenation index PaO 2/FiO 2 was significantly higher (271 mmHg vs. 217 mmHg, P=0.020) and blood lactate (1.59 mmol/L vs. 2.56 mmol/L, P<0.001) and procalcitonin (0.31 ng/mL vs. 3.55 ng/mL, P=0.028), minute ventilation (7.03 L/min vs.8.32 mmol/L, P=0.013), MP (14.37 J/min vs. 16.12 J/min, P=0.041), SOFA score (5 vs. 8, P=0.001) and APACHE II score (16 vs. 22, P=0.041) were significantly lower in the in-hospital survival group. Multivariate Logistic regression analysis showed that PaO 2/FiO 2( OR=1.015, P=0.044), MP ( OR=1.813, P=0.039) and SOFA score( OR=2.651, P=0.010) were independent risk factors for predicting hospital mortality in patients with mechanical ventilation. The areas under the ROC curves (AUC) were 0.62, 0.63 and 0.75, respectively. Moreover, the MP combined with SOFA score for predicting in-hospital death was significantly higher than that of MP alone (0.77 vs. 0.63, P<0.05). Conclusions:MP is associated with in-hospital death in patients with invasive mechanical ventilation in emergency department. MP combined with SOFA score can enhance its predictive efficacy

Objective: To investigate the effect of hypoxia inducible factor 2α (HIF-2α) on regulating CUB domain-containing protein 1 (CDCP1) and its role in hepatocellular carcinoma metastasis. Methods: HIF-2α-knocked down and HIF-2α-stably overexpressing cells (MHCC97H) were prepared by small interfering RNA (siRNA) and lentivirus transfection, respectively. The expression of CDCP1 protein and mRNA in the above cells was detected by western blot and real-time PCR. The effect of HIF-2α on cell invasion ability was determined by Transwell assay. Furthermore, immunohistochemical staining was performed to detect the expression of CDCP1 in human HCC tissue samples. Results: Both HIF-2α and CDCP1 were induced under hypoxic conditions. The activation of CDCP1 under hypoxic conditions was dependent on the expression of HIF-2α.When HIF-2α was overexpressed, the mRNA level of CDCP1 was greatly upregulated (5.92±0.28, P<0.05). When HIF-2α was knocked down by siRNA for 48 h and 72 h, the expression of CDCP1 was significantly downregulated (48 h: 0.25±0.04; 72 h: 0.18±0.02, all P<0.05). Moreover, analysis of human HCC samples showed that CDCP1 expression was correlated with tumor-free survival (P<0.05). Conclusions The results of this study indicate that the expression of CDCP1 is regulated by HIF-2α and is correlated with the progression of HCC. Inhibition of HIF-2α/CDCP1 may play certain inhibitory role in the metastasis of HCC.