Articles: sepsis.
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Leaving university I started working for the Belgian National Radio as a journalist. I used to travel a lot and produce radio features about life abroad and how people all over the world dealt with the different challenges in society. A privileged job that I enjoyed doing for many years. ⋯ The Head of the ICU informed my husband that there was less than 5% chance to survive and if so, he could not predict what kind of damage there would be: the amount of drugs that I had been given, including noradrenaline, was so extremely high, that it became very unclear how my body would respond to it. And if, as by miracle, I would survive: what kind of damage would there be? Physical? Mental? Physical and mental? No specialist could answer those questions. But both the health care professionals and my family fought to keep me alive.
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Sepsis is a lethal clinical syndrome, and acute lung injury (ALI) is the earliest and most serious complication. We aimed to explore the role of growth differentiation factor 11 (GDF11) in sepsis-induced dysfunction of lung microvascular endothelial barrier in vivo and in vitro to elucidate its potential mechanism related to sirtuin 1 (SIRT1)/NADPH oxidase 4 (NOX4) signaling. Cecal ligation and puncture (CLP)-induced sepsis mice and lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial cells (PMECs) were used in this study. ⋯ Additionally, EX527 treatment relieved the impacts of GDF11 overexpression on ferroptosis and destruction of integrity of human pulmonary microvascular endothelial cells exposed to LPS. Taken together, GDF11 overexpression could alleviate sepsis-induced lung microvascular endothelial barrier damage by activating SIRT1/NOX4 signaling to inhibit ferroptosis. Our findings potentially provide new molecular target for clinical therapy of ALI.