ObjectiveTo study effect of brusatol （BR） on proliferation of human gastric cancer HGC-27 cells and its mechanism. MethodCell counting kit-8 （CCK-8） was used to detect the survival rate of HGC-27 cells at different concentrations of BR. HGC-27 cells were treated with BR （7.5， 15， 30 μmol·L^-1） for 24 h， and then the cell clone formation was analyzed. 2，7-Dichlorodihydrofluorescein diacetate （DCFH-DA） fluorescent probe and lipid peroxidation sensor （C11-BODIPY） were employed to detect the levels of intracellular reactive oxygen species （ROS） and lipid peroxidation， respectively. Real-time polymerase chain reaction （Real-time PCR） and Western blot were performed to detect the messenger ribonucleic acid （mRNA） and protein expressions of solute carrier family 7 member 11 （SLC7A11）， glutathione peroxidase 4 （GPX4）， solute carrier family 40 member 1 （SLC40A1）， transferrin， nuclear factor E₂-related factor 2 （Nrf2） and heme oxygenase-1 （HO-1）， respectively. ResultThe survival rate of HGC-27 cells was decreased with the increase of BR concentration， and the IC₅₀ was 15.34 μmol·L^-1. Compared with the conditions in blank group， the cell clone formation of BR （7.5， 15， 30 μmol·L^-1） groups was inhibited in a dose-dependent manner （P<0.05，P<0.01）， while the levels of intracellular ROS and lipid peroxidation， iron concentration， and lactic dehydrogenase （LDH） leakage were increased in a dose-dependent manner （P<0.05，P<0.01）. Compared with the blank group， the BR （15， 30 μmol·L^-1） groups lowered the mRNA and protein expressions of SLC7A11， GPX4， SLC40A1， Nrf2 and HO-1， while elevated the mRNA and protein expression of TRF in a dose-dependent manner （P<0.05，P<0.01）. ConclusionBR suppressed the proliferation of HGC-27 cells through inducing ferroptosis via inhibiting Nrf2/HO-1 pathway.

Objective:To investigate the expression level of small nucleolar RNA SNORD15A in bone marrow of patients with acute leukemia (AL) and its relationship with clinical characteristics and prognosis of patients.Methods:Bone marrow blood samples of 53 newly treated AL patients and 29 healthy subjects without clinical diagnosis of hematologic diseases or other malignant diseases (control group) at the Affiliated Hospital of Guangdong Medical University from March 2018 to December 2021 were collected. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the relative expression of SNORD15A in bone marrow blood mononuclear cells of the two groups. The median relative expression of SNORD15A (0.148) was used as the boundary, and AL patients were divided into low expression group (<0.148) and high expression group (≥0.148). The relationship between the expression level of SNORD15A and the clinical characteristics, clinical indicators and overall survival (OS) of AL patients was analyzed. Kaplan-Meier method was used for survival analysis and log-rank test was performed; Cox proportional hazards model was used for univariate and multivariate analyses of OS of patients.Results:The relative expression of SNORD15A was 0.148 (0.012-1.376) in newly treated AL patients and 0.921 (0.513-2.288) in the control group, and the difference was statistically significant ( Z = -6.85, P < 0.01). The differences in SNORD15A relative expression between patients with different prognostic stratification, efficacy and with or without fever and bleeding were statistically significant (all P < 0.05). The differences in platelet count, plateletcrit and albumin levels between SNORD15A low expression group and high expression group were statistically significant (all P < 0.05), and the differences in molecular biology and cytogenetic characteristics were not statistically significant (all P > 0.05). The patients in SNORD15A high expression group had better OS than the low expression group ( P < 0.05). The results of univariate Cox regression analysis showed that SNORD15A was an influencing factor for patients' OS ( HR = 0.063, 95% CI 0.005-0.766, P < 0.05); the results of multivariate Cox regression analysis showed that fatigue ( HR = 4.754, 95% CI 1.014-22.290), fever ( HR = 0.147, 95% CI 0.029-0.746) and hemoglobin ( HR = 0.970, 95% CI 0.944 -0.998) were independent influencing factors for OS (all P < 0.05). Conclusions:SNORD15A is lowly expressed in AL and may be an indicator for disease monitoring and prognostic assessment in AL patients.

Objective: To retrospectively analyze the efficacy and prognostic factors of postoperative intensity modulated radiotherapy for grade Ⅱ gliomas. Methods: Retrospective analysis was conducted on patients with postoperative grade Ⅱ glioma in our hospital from Jan. 2010 to Dec. 2018. The primary endpoint was progression-free survival, and the secondary endpoint was overall survival. Correlative analyses of prognosis by age, gender, initial resection status, the maximum diameter of the lesions, bi-hemisphere, astrocytoma, chemoradiation, adjuvant chemotherapy were conducted. Results: A total of 109 cases with grade Ⅱ glioma were enrolled. The follow-up rate was 91.75%, including 10 cases dead and 27 relapsed. There were 24 cases (88.9%) of in-field failure, and 3 cases (11.1%) of out-field failure. 14 cases of recurrence occurred in 81 cases of total resection group, accounting for 17.3%, and 13 in 28 cases of subtotal resection group, accounting for 46.4%. The recurrence rate in the subtotal resection group was significantly higher than that in the total resection group (χ ²=9.484, P<0.05). The 1-, 2-, 3-, 4- and 5-year progression-free survival rates were 92.5%, 86.0%, 80.6%, 77.5% and 66.8%, respectively. The 2-, 3-, 4- and 5-year overall survival rates were 97.2%, 90.8%, 87.7% and 84.5%, respectively. Multivariate analysis showed that patients with subtotal resection(HR=3.608, P<0.05) and bi-hemisphere(HR=3.183, P<0.05)were significantly correlated with the progression free survival. Conclusions Postoperative intensity modulated radiotherapy for grade Ⅱ gliomas can achieve a better PFS. Recurrence in the radiation field is the main failure mode. Initial resection status and bi-hemisphere of tumor are important influential factors for PFS of grade Ⅱ gliomas patients.