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Wu J.,Armed Police Corps Hospital of Guangdong Province
Medical Journal of Wuhan University | Year: 2013

Objective: To evaluate the changes of brachial-ankle pulse wave conduction velocity after treatment with different antihypertensive drugs in essential hypertension patients. Methods: A total of 120 patients of essential hypertension were equally and randomly divided into three groups according to the antihypertensive drugs of telmisartan (ARB group), amlodipine (CCB group), and perindopril (ACEI group) respectively. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and brachial-ankle pulse wave conduction velocity (baPWV) were measured after 1month and 3months respectively. Results: The SBP, DB P, PP, HR, and baPWV of the three groups had no significant difference before the treatment (P>0.05). After treatment for one month and three months respectively, the SBP, DBP, PP, and baPWV were significantly decreased as compared with pre-treatment (all P<0.01). After treatment, the changes of baPWV (δbaPWV) were different among the three groups, as ARB group CCB group ACEI group (P<0.05). Conclusion: All the three kinds of drugs of perindopril, amlodipine, and telmisartan can improve arterial elasticity of hypertension patients, and telmisartan has the best effect.

Tian Y.,Southern Medical University | Tian Y.,Sun Yat Sen University | Zhang W.,Southern Medical University | Zhang W.,Guangzhou University | And 9 more authors.
Carcinogenesis | Year: 2015

Junctional adhesion molecule-A (JAM-A) is preferentially concentrated at tight junctions and influences epithelial cell morphology and migration. Epithelial-to-mesenchymal transition (EMT) is the conversion process of epithelial cells into mesenchymal cells, and it plays an important role in the invasiveness and metastasis of various cancers. However, the role of JAM-A in regulating the invasive behaviours of human nasopharyngeal carcinoma (NPC) is unknown. In this study, we found that JAM-A upregulation induced EMT, whereas silencing of endogenous JAM-A expression reversed EMT. Furthermore, upregulation of JAM-A led to EMT via activation phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway. PI3K inhibitors blocked JAM-A-induced EMT, suggesting that the kinase acts downstream of JAM-A. Finally, results from 172 human patients with NPC showed that high expression levels of JAM-A correlated with metastasis and poor prognosis in NPC. Taken together, these results suggest that high JAM-A expression positively correlates with poor prognosis in patients with NPC, and induces EMT of NPC cells in vitro and in vivo via the PI3K/Akt pathway. These data indicate novel functions in the JAM-A repertoire, and have clinical implications for the treatment of patients with NPC. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Xie Q.,Armed Police Corps Hospital of Guangdong Province | Huang Z.,Armed Police Corps Hospital of Guangdong Province | Liu Y.,Armed Police Corps Hospital of Guangdong Province | Liu X.,Armed Police Corps Hospital of Guangdong Province | Huang L.,Armed Police Corps Hospital of Guangdong Province
Nan fang yi ke da xue xue bao = Journal of Southern Medical University | Year: 2015

OBJECTIVE: To explore the molecular mechanisms by which mitochondrial estrogen receptor β (ERβ) suppresses non-small cell lung cancer cell apoptosis induced by apoptotic stimulations.METHODS: The mitochondrial localization of ERβ in non-small cell lung cancer cell lines A549 and 201T was determined using immunofluorescence and Western blotting. The changes of apoptosis of the cells with mitochondrial ERβ overexpression or knockdown in response to cisplatin and STS treatments were assessed, and mitochondrial ERβ interaction with the pro-apoptotic protein Bad was detected using co-immunoprecipitation and Western blotting.RESULTS: ERβ was localized in the mitochondria in A549 and 201T cells. ERβ overexpression significantly reduced while ERβ knockdown increased Bax activation and cell apoptosis induced by cisplatin and STS. Mitochondrial ERβ interaction with pro-apoptotic protein Bad may suppress Bax activation and its translocation to the mitochondria.CONCLUSION: Mitochondrial ERβ can suppress apoptosis of non-small cell lung cancer cells induced by cisplatin or STS through interaction with Bad, suggesting the value of mitochondrial ERβ as a new therapeutic target for treatment of non-small cell lung cancer.

Tian Y.,Southern Medical University | Tian Y.,Guangzhou University | Xie Q.,Armed Police Corps Hospital of Guangdong Province | He J.,Southern Medical University | And 6 more authors.
BMC Cancer | Year: 2015

Background: Glioblastoma multiforme (GBM) is the most common primary central nervous system neoplasm in adults. Radioactive 125I seed implantation has been widely applied in the treatment of cancers. Moreover, previous clinical trials have confirmed that 125I seeds treatment was an effective therapy in GBM. We sought to investigate the effect of 125I seed on GBM cell growth and Epithelial-mesenchymal transition (EMT). Methods: Cells were exposed to irradiation at different doses. Colony-formation assay, EdU assay, cell cycle analysis, and TUNEL assay were preformed to investigate the radiation sensitivity. The effects of 125I seeds irradiation on EMT were measured by transwell, Boyden and wound-healing assays. The levels of reactive oxygen species (ROS) were measured by DCF-DA assay. Moreover, the radiation sensitivity and EMT were investigated with or without pretreatment with glutathione. Additionally, nude mice with tumors were measured after treated with radiation. Results: Radioactive 125I seeds are more effective than X-ray irradiation in inhibiting GBM cell growth. Moreover, EMT was effectively inhibited by 125I seed irradiation. A mechanism study indicated that GBM cell growth and EMT inhibition were induced by 125I seeds with the involvement of a ROS-mediated signaling pathway. Conclusions: Radioactive 125I seeds exhibit novel anticancer activity via a ROS-mediated signaling pathway. These findings have clinical implications for the treatment of patients with GBM by 125I seeds. © Tian et al.; licensee BioMed Central.

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