147 research outputs found

    Health-related quality of life of relapsing or remitting multiple sclerosis patients: A case-control study

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    Background: Patients with multiple sclerosis (MS) report lower health-related quality of life (HRQoL) than other chronic disease populations. This study aims to identify risk factors of relapsing or remitting multiple sclerosis (RRMS) and assess its impact on HRQoL in Lebanese MS patients. Patients and methods: A thre-month case-control study was performed among 75 RRMS case patients recruited from two clinics in Beirut and 225 controls from the general population. Results: Heavy cigarette smoking, moderate and heavy waterpipe smoking, vitamin D deficiency, cardiovascular disease, and psychological disorders were significantly associated with RRMS. Linear regression showed that the multiple sclerosis international quality of life global index significantly decreased with the number of relapses, the incomplete recovery between relapses, and the psychological disorder. Higher-income and physical activity had a positive effect on QoL. Conclusions: Findings of this study highlighted the risk factors of RRMS, which can be used for informed decision-making and targeted awareness campaigns. Other factors affecting the HRQoL of MS patients should be considered to improve their experience throughout and after treatment

    RHOG Activates RAC1 through CDC42 Leading to Tube Formation in Vascular Endothelial Cells

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    Angiogenesis is a hallmark of cancer cell malignancy. The role of the RHO family GTPase RHOG in angiogenesis in vascular endothelial cells has recently been elucidated. However, the regulation of RHOG during this process, as well as its cross-talk with other RHO GTPases, have yet to be fully examined. In this study, we found that siRNA-mediated depletion of RHOG strongly inhibits tube formation in vascular endothelial cells (ECV cells), an effect reversed by transfecting dominant active constructs of CDC42 or RAC1 in the RHOG-depleted cells. We also found CDC42 to be upstream from RAC1 in these cells. Inhibiting either Phosphatidyl inositol (3) kinase (PI3K) with Wortmannin or the mitogen-activated protein kinase extracellular-regulated kinase (MAPK ERK) with U0126 leads to the inhibition of tube formation. While knocking down either RHO, GTPase did not affect p-AKT levels, and p-ERK decreased in response to the knocking down of RHOG, CDC42 or RAC1. Recovering active RHO GTPases in U0126-treated cells also did not reverse the inhibition of tube formation, placing ERK downstream from PI3K-RHOG-CDC42-RAC1 in vascular endothelial cells. Finally, RHOA and the Rho activated protein kinases ROCK1 and ROCK2 positively regulated tube formation independently of ERK, while RHOC seemed to inhibit the process. Collectively, our data confirmed the essential role of RHOG in angiogenesis, shedding light on a potential new therapeutic target for cancer malignancy and metastasis

    KIDNEY ALLOGRAFT OBSTRUCTION BY SURGICEL

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