Objective To analyze the factors influencing the deterioration of nutritional status after radiotherapy/radiochemotherapy for esophageal cancer,so as to provide reference for nutritional management during antitumor therapy.Methods A total of 106 patients with esophageal cancer who received radiotherapy or radiochemotherapy at Anqing First People's Hospital of Anhui Medical University from Dec.2017 to Dec.2023 were enrolled.Patients'gender,age,surgical history,timing of radiotherapy intervention,synchronous chemoradiotherapy,radiotherapy dose,clinical stage,initial nutritional status,and performance status score were collected.The patient generated subjective global assessment scale(PG-SGA)scores were monitored before and after antitumor treatment.According to the nutritional status at the beginning of enrollment and at the end of radiotherapy,the patients were assigned to deterioration group or non-deterioration(stable or improved)group.The clinical characteristics of the 2 groups were compared.The factors influencing the deterioration of nutritional status were screened by logistic regression analysis.The correlation between nutritional status deterioration and adverse reactions(radiation esophagitis,pulmonary infection,neutropenia,thrombocytopenia,and elevated aminotransferase)was analyzed by Spearman correlation analysis.Results There were no significant differences in gender,radiotherapy dose,initial nutritional status,or performance status score between the 2 groups for the deterioration of nutritional status after radiotherapy(all P＞0.05).The proportions of patients with previous surgical history of esophageal cancer,synchronous chemoradiotherapy,initiation of radiotherapy at less than 90%of target calorie requirement,and clinical stage Ⅳ were significantly higher in the deterioration group than those in the non-deterioration group(all P＜0.05).Logistic regression analysis showed that clinical stage Ⅳ(odds ratio[OR]=4.684,95%confidence interval[CI]1.252-17.519,P=0.022)and previous surgical history of esophageal cancer(OR=7.338,95%CI 1.878-28.666,P=0.004)were the independent adverse risk factors for the deterioration of nutritional status after radiotherapy/radiochemotherapy.The timing of radiotherapy intervention was also an independent risk factor for the deterioration of nutritional status,and taking the tolerance of 70%-90%target energy as the reference level,starting radiotherapy when the tolerance of 90%-100%target energy had the optimal protection of nutritional status(OR=0.166,95%CI 0.050-0.551,P=0.003).Spearman correlation analysis showed that the deterioration of nutritional status was positively correlated with elevated transaminases after radiotherapy(rs=0.283,P=0.003),while it was not correlated with the other adverse reactions(all P＞0.05).Conclusion Under the standard nutritional intervention model,patients with previous surgery and recurrent metastatic esophageal cancer who receive radiotherapy/chemoradiotherapy are still at risk of nutritional status deterioration.Tolerance to 90%-100%target energy requirement may be a more appropriate timing for radiotherapy intervention.When the nutritional status deteriorates during treatment,it is necessary to be alert to the elevated transaminases.

Due to the limitations of current anti-HBV therapies, the HBV core (HBc or HBcAg) protein assembly modulators (CpAMs) are believed to be potential anti-HBV agents. Therefore, discovering safe and efficient CpAMs is of great value. In this study, we established a HiBiT-based high-throughput screening system targeting HBc and screened novel CpAMs from an in-house marine chemicals library. A novel lead compound 8a, a derivative of the marine natural product naamidine J, has been successfully screened for potential anti-HBV activity. Bioactivity-driven synthesis was then conducted, and the structure‒activity relationship was analyzed, resulting in the discovery of the most effective compound 11a (IC₅₀ = 0.24 μmol/L). Furthermore, 11a was found to significantly inhibit HBV replication in multiple cell models and exhibit a synergistic effect with tenofovir disoproxil fumarate (TDF) and IFNa2 in vitro for anti-HBV activity. Treatment with 11a in a hydrodynamic-injection mouse model demonstrated significant anti-HBV activity without apparent hepatotoxicity. These findings suggest that the naamidine J derivative 11a could be used as the HBV core protein assembly modulator to develop safe and effective anti-HBV therapies.

Objective:To investigate the expression of annexin A2 pseudogene 1 (ANXA2P1) in glioblastoma (GBM) tissues and its biological function in U87 cells.Methods:The expression level of ANXA2P1 in GBM tissues was analyzed by Cancer Genome Atlas (TCGA). Cell transfection was used to up-regulate or down-regulate the expression of ANXA2P1 in GBM tissues or U87 cells. Cell Counting Kit-8 (CCK-8) was used to detect the proliferation ability of U87 cells. Western blotting was used to detect the changes of protein expression in signaling pathway of U87 cells.Results:The TCGA analysis showed that the expression level of ANXA2P1 in high-level GBM tissues was significantly higher than that in low-level GBM tissues ( P<0.01). In GBM tissues, the expression level of ANXA2 was positively correlated with that of ANXA2P1 ( r=0.752, P<0.01). The proliferation capacity of U87 cells with ANXA2P1 overexpression was higher than that of the control group, while the proliferation capacity of U87 cells transfected by Si-ANXA2P1 was lower than that of the control group. At 72 h after transfection, the expression level of p-S6K protein in the ANXA2PI-overexpressed cells was higher than that in the control group ( P<0.05), while the expression level of p-S6K protein in the Si-ANXA2P1 cells was lower than that in the control group ( P<0.05). Conclusion:ANXA2P1 may promote the proliferation of U87 cells through mTOR signaling pathway.

Objective:To investigate the expression of annexin A2 pseudogene 1 (ANXA2P1) in glioblastoma (GBM) tissues and its biological function in U87 cells.Methods:The expression level of ANXA2P1 in GBM tissues was analyzed by Cancer Genome Atlas (TCGA). Cell transfection was used to up-regulate or down-regulate the expression of ANXA2P1 in GBM tissues or U87 cells. Cell Counting Kit-8 (CCK-8) was used to detect the proliferation ability of U87 cells. Western blotting was used to detect the changes of protein expression in signaling pathway of U87 cells.Results:The TCGA analysis showed that the expression level of ANXA2P1 in high-level GBM tissues was significantly higher than that in low-level GBM tissues ( P<0.01). In GBM tissues, the expression level of ANXA2 was positively correlated with that of ANXA2P1 ( r=0.752, P<0.01). The proliferation capacity of U87 cells with ANXA2P1 overexpression was higher than that of the control group, while the proliferation capacity of U87 cells transfected by Si-ANXA2P1 was lower than that of the control group. At 72 h after transfection, the expression level of p-S6K protein in the ANXA2PI-overexpressed cells was higher than that in the control group ( P<0.05), while the expression level of p-S6K protein in the Si-ANXA2P1 cells was lower than that in the control group ( P<0.05). Conclusion:ANXA2P1 may promote the proliferation of U87 cells through mTOR signaling pathway.