This study is to identify the risk factors for postoperative delirium (PODE) in patients undergoing microvascular decompression (MVD) for the treatment of primary cranial nerve disorders. We retrospectively reviewed the data of 912 patients (354 men, 558 women) with primary cranial nerve disorders (trigeminal neuralgia, 602 patients; hemifacial spasm, 296 patients; glossopharyngeal neuralgia, 14 patients) who underwent MVD in the Neurosurgery Department of Lanzhou University Second Hospital between July 2007 and June 2018. Potential risk factors for PODE were identified using univariate and multivariate stepwise logistic regression analysis.Of the 912 patients, 221 (24.2%) patients developed PODE. Patients with PODE were significantly older and significantly more likely to be male than patients without PODE. A history of hypertension, preoperative carbamazepine therapy, and postoperative sleep disturbance and tension pneumocephalus were independently associated with PODE. Variables such as body-mass index, smoking and drinking habits, cardiac disease, diabetes mellitus, cerebrovascular disease, mean operative time, affected vessel, mean blood loss, postoperative intensive care unit stay, postoperative fever (>38°C), and routine laboratory results were not associated with PODE in our patients.PODE is a common complication after MVD, and is associated with multiple risk factors, including old age, male sex, hypertension, preoperative carbamazepine use, postoperative sleep disturbance, and tension pneumocephalus.
Abstract. Athough it is well known that apoptosis contributes to cancer cell death, the role of autophagy in cancer cell death has remained in dispute. Atorvastatin has been suggested to exhibit anti-cancer effects. The present study aimed to examine atorvastatin-induced autophagy-associated cell death and the autophagy-associated gene expression profile in the PC3 prostate carcinoma cell line. The atorvastatin-induced process of autophagy in PC3 cells was determined via evaluation of the cellular expression levels of autophagosomal marker light-chain-3 (LC3)-II, using immunoblotting and counting of green fluorescent protein (GFP)-LC3-transfected autophagic cells. Apoptosis was examined by terminal deoxynucleotidyl transferase dUTP nick end labeling assay and an MTT assay was used to evaluate cell viability. Total RNA of PC3 cells was isolated for characterization of the gene expression profile following atorvastatin treatment. Atorvastatin treatment of PC3 cells for 24 h increased the expression of green fluorescent protein-LC3-II by >25%, and expression continued for >72 h, while apoptosis was not significantly induced within this time period. Four genes associated with the autophagy machinery were also significantly upregulated. In the presence of atorvastatin, autophagy may be unable to abrogate cell damage and may therefore contribute to cellular dysfunction, leading to autophagic/type II programmed cell death. In response to atorvastatin treatment, the expression of genes involved in autophagic mediating pathways may have a role in tumor suppression. IntroductionProstate cancer is the most frequently diagnosed non-cutaneous malignancy and the second leading cause of death due to cancer amongst males worldwide (1). Treatment options for localized disease include watchful waiting, surgery and radiotherapy (2). However, in terms of a definitive treatment, despite developments in systemic chemotherapy strategies, minimal improvements in the quality of life and overall survival have been achieved amongst patients with prostate cancer (3). The development of novel treatment strategies for patients with advanced metastatic prostate cancers remains a challenge.The PC3 human prostate cancer cell line [p53-and phosphatase and tensin homolog (PTEN)-] was established from a prostatic adenocarcinoma, which was metastatic to bone. It has been extensively used as a cell model for the study of prostate cancer and is generally assumed to model an advanced stage of prostate cancer (4). PC3 cells are resistant to numerous chemotherapy drugs and apoptosis inducers (5,6).At o r va s t a t i n, a 3 -hyd r ox y-3 -m e t hylg lu t a r yl (HMG)-coenzyme A reductase inhibitor, is among the widely prescribed drugs used to lower cholesterol and prevent cardiovascular diseases (7). In addition to its cholesterol-lowering effect, atorvastatin has pro-apoptotic and anti-metastatic effects on prostate cancer cells (8,9). Parikh et al (10) hypothesized that atorvastatin may induce autophagy-associated cell death in PC3 cells. However, the...
Background Prostate cancer (PCa) is considered to be the 4 th most common cancer in males in the world. This study aimed to explore effects of atorvastatin on colony formation of PCa cells and radio-resistance of xenograft tumor models. Material/Methods PCa cell lines, including PC3, DU145, and Lncap, were treated with irradiation (4 Gy) and/or atorvastatin (6 μg/mL). Cells were divided into tumor cell group, irradiation treatment group (IR group) and irradiation+atorvastatin treatment group (IR-AS group). Xenograft tumor mouse model was established. Plate clone formation assay (multi-target/single-hit model) was conducted to evaluate colony formation. Flow cytometry analysis was employed to detect apoptosis. Interaction between Bcl-2 and MSH2 was evaluated with immuno-fluorescence assay. Results According to the plate colony formation assay and multi-target/single-hit model, IR-treatment significantly suppressed colony formation in PCa cells (including PC3, DU145, and Lncap cells) compared to no-IR treated cells ( P <0.05). Atorvastatin remarkably enhanced inhibitive effects of irradiation on colony formation of PCa cells ( P <0.05), however, the IR+AS group demonstrated no effects on apoptosis, comparing to IR group ( P >0.05). Atorvastatin administration (IR+AS group) significantly reduced tumor size of IR-treated PCa cells-induced xenograft tumor mice ( P <0.05). Bcl-2 interacted with MSH2 both in tumor tissues of xenograft tumor mice. Conclusions Atorvastatin administration inhibited colony formation in PCa cells and enhanced effects of radiotherapy on tumor growth of xenograft tumor mice, which might be associated with interaction between Bcl-2 and MSH2 molecule.
Background: Prostate cancer (PCa) is the fourth most common tumor in males. Objective: To investigate effects of atorvastatin (AS) on PCa cells proliferation and clarify the associated mechanisms. Methods: PCa cell lines were cultured and treated with irradiation (IR) (4 Gy), AS (6 μg/ml), transfected with Bcl-2 siRNA, and then divided into different groups. Xenograft tumor mouse model was established. Bcl-2 and MSH2 gene transcription and protein expression were evaluated using RT-PCR assay and western blot assay. Plate clone formation assay was employed to examine colony formation. MTT assay was used to detect cell viabilities. Flow cytometry analysis was utilized to verify apoptosis. Co-immunoprecipitation and immuno-fluorescence assay were used to identify interaction between Bcl-2 and MSH2. Results: IR significantly reduced colony formation, enhanced Bcl-2 and reduced MSH2 gene transcription in PCa cells compared to un-treated cells (p<0.05). AS significantly strengthened radio-therapeutic effects of IR on colony formation, decreased cell apoptosis and increased Bcl-2 gene transcription/protein expression in PCa cells compared to single IR treatment cells (p<0.05). AS combining IR down-regulated MSH2 gene transcription/protein expression in PCa cells compared to single IR treatment cells (p<0.05). Bcl-2 interacted with MSH2 both in PCa cells and tumor tissues administrating with AS. AS enhanced reductive effects of IR on tumor size of Xenograft tumor mice. Conclusion: Atorvastatin administration enhanced inhibitory effects of IR either on PCa cells or on tumor size of Xenograft tumor mice. The inhibitory effects of atorvastatin were mediated by reducing MSH2 expression and triggering interaction between Bcl-2 and MSH2, both in vitro and in vivo levels.
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