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https://www.selleckchem.com/products/hydroxychloroquine-sulfate.html GNAQ-knockdown showed down-regulation of tumour growth through mitogen-activated protein kinase (MAPK) signalling in lung cancer cells, but not increased apoptosis. We found that GNAQ-knockdown induced EMT and promoted invasiveness. GNAQ-knockdown cells injected into the bone marrow of murine tibia induced tumour growth and bone-to-lung metastasis, whereas it did not in control mice. Moreover, the knockdown of GNAQ enhanced cancer stem cell-like properties in lung cancer cells, which resulted in the development of resistance to chemotherapy. The present study reveals that the GNAQ-knockdown induced cancer stem cell-like properties. Cite this article 2021;10(5)310-320. The present study reveals that the GNAQ-knockdown induced cancer stem cell-like properties. Cite this article Bone Joint Res 2021;10(5)310-320. Structural remodeling of the right ventricle (RV) is widely documented in athletes. However, functional adaptation, including RV pressure generation and systolic free-wall longitudinal mechanics, remains equivocal. This meta-analysis compared RV pressure and function in athletes and controls. A systematic review of online databases was conducted up to June 4, 2020. Meta-analyses were performed on RV systolic pressures, at rest and during exercise, tricuspid annular plane systolic displacement, myocardial velocity (S'), and global and regional longitudinal strain. Bias was assessed using Egger regression for asymmetry. Data were analyzed using random-effects models with weighted mean difference and 95% CI. Fifty-three studies were eligible for inclusion. RV systolic pressure was obtained from 21 studies at rest ( =10431651; controlsathletes) and 8 studies during exercise ( =240495) and was significantly greater in athletes at rest (weighted mean difference, 2.9 mmHg [CI, 1.3-4.5 mmHg]; =0.0005) and dapex strain gradient, is a normal feature of the athlete's heart, together with a slightly eleva

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