ABSTRACT
Objective: To elucidate the expression levels of key immune biomarkers, phosphate and tension homology deleted on chromosome ten (PTEN) and programmed cell death protein1(PD-1),of different immune tolerance pathway in classic Hodgkin's lymphoma (CHL) to further determine their clinical role and prognostic significance. Methods: The clinical features and prognostic factors of 56 CHL patients, who were admitted to the TianJin Medical University Cancer Institute from February 2003 to August 2013, were retrospectively analyzed. PTEN and PD-1 protein expression levels were analyzed by immunohistochemistry, Epstein-Barr virus encoded RNA (EBER) was performed by in situ hybridization assay. Correlations between the expression of biomarkers and clinicopathologic parameters were examined and survival analyses were performed. Results: This cohort of 56 CHL patients included 34 males and 22 females with a median age of 25 years (ranged from 7 to 71 years). In a univariate analysis, age≥45, IPS score >2, EBER positive, high expression of PTEN protein conferred inferior 5-year OS and 5-year PFS; In a multivariate model, age≥45, IPS score >2, EBER positive, high expression of PTEN protein were identified as the independent adverse prognostic factors for CHL. Conclusions: This study suggested for the first time that PTEN was independent prognostic immune biomarkers in CHL, which provided the novel therapeutic strategy of immune therapy for CHL.
Subject(s)
Adolescent , Adult , Aged , Child , Female , Humans , Male , Middle Aged , Young Adult , Hodgkin Disease , PTEN Phosphohydrolase/analysis , Prognosis , Programmed Cell Death 1 Receptor/analysis , Retrospective StudiesABSTRACT
Objective The aim of this work was to study whether PM2. 5 induces oxidative stress and histopatholog-ical changes in uterine tissue of rats. Methods Thirty 4-week-old female Sprague-Dawley rats were randomly divided into the control group (normal saline), the low dose of PM2.5 group (1. 5 mg/kg) and the high dose of PM2.5 group (37. 5 mg/kg) . After exposed to PM2. 5 for 10 days, the rats were sacrificed to examine the histopathological changes in uterine tissues using H&E staining. The contents of SOD, GSH, MDA and LDH were also determined in the uterine tissues. Results Compared with the control group, PM2. 5 caused changes in the uterine structure, showing a thinner endometrial epithelium and reduction of stromal cells and blood vessels. The assessment of oxidative stress parameters showed that the levels of MDA and LDH in the high dose group were (6. 53 ± 1. 24) nmol/mg prot and (265. 62 ± 24. 65) U/g prot, significantly higher than those in the control group ( P<0. 05 ) . Compared with the control group, the levels of SOD and GSH in the high dose and low dose groups were significantly decreased (P<0. 05). Conclusions PM2.5 exposure can cause damages in the rat uterus by inducing oxidative stress.
ABSTRACT
Objective The aim of this work was to study whether PM2. 5 induces oxidative stress and histopatholog-ical changes in uterine tissue of rats. Methods Thirty 4-week-old female Sprague-Dawley rats were randomly divided into the control group (normal saline), the low dose of PM2.5 group (1. 5 mg/kg) and the high dose of PM2.5 group (37. 5 mg/kg) . After exposed to PM2. 5 for 10 days, the rats were sacrificed to examine the histopathological changes in uterine tissues using H&E staining. The contents of SOD, GSH, MDA and LDH were also determined in the uterine tissues. Results Compared with the control group, PM2. 5 caused changes in the uterine structure, showing a thinner endometrial epithelium and reduction of stromal cells and blood vessels. The assessment of oxidative stress parameters showed that the levels of MDA and LDH in the high dose group were (6. 53 ± 1. 24) nmol/mg prot and (265. 62 ± 24. 65) U/g prot, significantly higher than those in the control group ( P<0. 05 ) . Compared with the control group, the levels of SOD and GSH in the high dose and low dose groups were significantly decreased (P<0. 05). Conclusions PM2.5 exposure can cause damages in the rat uterus by inducing oxidative stress.