The aim of this study was to determine whether overexpression of the RIP3 gene could sensitize human breast cancer cells to parthenolide in vitro. Methods: The expression of RIP3 mRNA in human breast cancer cell lines (MCF-7, MDA-MB-231, MDA-MB-435 and T47D) was detected using
RT-PCR. Both MDA-MB-231 and MCF-7 cells were transfected with RIP3 expression or blank vectors via lentivirus. Cell viability was measured with MTT assay; intracellular ROS level and cell apoptosis were analyzed using flow cytometry. Results: RIP3 mRNA expression was not detected in the four human breast cancer cell lines tested. However, the transfection induced higher levels of RIP3 protein in MCF-7 and MDA-MB-231 cells. Furthermore, overexpression of RIP3 decreased the IC50 values of parthenolide from 17.6 to 12.6 GSK2399872A cost mu mol/L in MCF-7 cells; and from 16.6 to 9.9 mu mol/L in MDA-MB-231 cells. Moreover, overexpression of RIP3 significantly increased parthenolide-induced apoptosis and ROS accumulation in MCF-7 and MDA-MB-231 cells. Pretreatment with N-acetyl-cysteine abrogated the increased sensitivity of RIP3-transfected MCF-7 and MDA-MB-231 cells to parthenolide. Conclusion: Overexpression of RIP3 sensitizes MCF-7 and MDA-MB-231 breast
cancer cells to parthenolide in vitro via intracellular ROS accumulation.”
“N-2-saturated 2-propanol solutions containing styrene and maleimide
were gelled by the addition of hydroxypropylcellulose and irradiated by proton, He and C-ion beams. The trend in the dose rate and LET effects on selleck screening library the yield and molecular weight distribution of the polymer produced in the gel was almost the same in the solution. On the contrary, the dose rate effect in the gel was higher than that in the solution. This effect was accelerated for irradiations Pexidartinib in vitro by proton as well as heavier ion with a higher LET value. (C) 2014 Elsevier B.V. All rights reserved.”
“The association of white-coat hypertension (WCH) with target organ damage is still debated; in particular, the relationship of this blood pressure phenotype with subclinical vascular damage remains controversial. Thus, we carried out a systematic review and meta-analysis to provide updated information on carotid structural changes in WCH. Studies were identified using the following search terms: ‘white coat hypertension’, ‘isolated clinic hypertension’, ‘carotid artery’, ‘carotid atherosclerosis’, ‘carotid intima-media thickness’, ‘carotid damage’, ‘carotid thickening’. Full articles published in the English language in the last two decades reporting studies on adults were considered. A total of 3478 untreated patients, 940 normotensive (48% men), 666 WCH (48% men), and 1872 hypertensive individuals (57% men) included in 10 studies, were analyzed.