Traumatic brain injury (TBI) leads to major membrane lipid breakdown. We investigated plasma lipids over 3 days post-TBI, to identify a signature of acute human TBI and assess its correlation with neuronal injury and inflammation. Plasma from patients with TBI (Abbreviated Injury Scale (AIS)3 - serious injury, n = 5; AIS4 - severe injury, n = 8), and controls (n = 13) was analysed for lipidomic profile, neurofilament light (NFL) and cytokines, and the omega-3 index was measured in red blood cells. A lipid signature separated TBI from controls, at 24 and 72 h. Major species driving the separation were: lysophosphatidylcholine (LPC), phosphatidylcholine (PC) and hexosylceramide (HexCer). Docosahexaenoic acid (DHA, 22:6) and LPC (0:0/22:6) decreased post-injury. NFL levels were increased at 24 and 72 h post-injury in AIS4 TBI vs. controls. Interleukin (IL-)6, IL-2 and IL-13 were elevated at 24 h in AIS4 patients vs. controls. NFL and IL-6 were negatively correlated with several lipids. The omega-3 index at admission was low in all patients (controls: 4.3 ± 1.1% and TBI: 4.0 ± 1.1%) and did not change significantly over 3 days post-injury. We have identified specific lipid changes, correlated with markers of injury and inflammation in acute TBI. These observations could inform future lipid-based therapeutic approaches.
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http://dx.doi.org/10.1177/0271678X241276951 | DOI Listing |
Tissue Cell
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Department of Human and Animal Physiology, Yerevan State University, Yerevan, 1 Alek Manukyan St, Yerevan 0025, Armenia; Research Institute of Biology, Yerevan State University, Yerevan, 1 Alek Manukyan St, Yerevan 0025, Armenia. Electronic address:
High altitude characterized by the low partial pressure of the oxygen is a life-threatening condition that contributes to the development of acute pulmonary edema and hypoxic lung injury. In this study, we aimed to investigate the contribution of some inflammatory and oxidative stress markers along with antioxidant system enzymes in the pathogenesis of HAPE (high-altitude pulmonary edema) formation. We incorporated the study on 42 male rats to unravel the role of mast cells (MCs) and TNF-α in the lung after the effect of acute hypobaric hypoxia.
View Article and Find Full Text PDFBraz J Biol
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Universitas Airlangga, Faculty of Science and Technology, Department of Biology, Mulyorejo, Surabaya, Indonesia.
Inflammation-proliferation transition plays a key role in the successful healing of a common burn type, second-degree burn. Gynura procumbens in vitro adventitious root nanohydrogel is currently being studied for its immunomodulatory to improve reparative environment. Root production and nanohydrogel preparation was done respectively by in vitro propagation and emulsion/ solvent diffusion with carbomer as a polymer.
View Article and Find Full Text PDFSci Transl Med
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Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
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View Article and Find Full Text PDFJ Trauma Acute Care Surg
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From the Department of Surgery and Sepsis and Critical Illness Research Center (J.A.M., L.S.K., E.E.P., C.G.A., K.B.K., L.E.B., P.A.E., A.M.M.), University of Florida College of Medicine, Gainesville; and The Gut Biome Lab, Department of Health, Nutrition, and Food Sciences (G.P., R.N.), Florida State University College of Education, Health, and Human Sciences, Tallahassee, Florida.
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View Article and Find Full Text PDFJ Am Chem Soc
January 2025
State Key Laboratory of High Performance Ceramics and Superfine Microstructure, Shanghai Institute of Ceramics, Chinese Academy of Sciences; Research Unit of Nanocatalytic Medicine in Specific Therapy for Serious Disease, Chinese Academy of Medical Sciences (2021RU012), Shanghai 200050, P. R. China.
Diabetic cardiomyopathy (DCM) is one of the most lethal complications of diabetes and is induced by the overproduction of reactive oxygen species (ROS) in cardiomyocytes due to sustained high glucose levels, leading to cardiac oxidative damage and final sudden death. Drugs and antioxidants currently applied to the clinical therapy of DCM fail to scavenge ROS efficiently, resulting in compromised therapeutic efficacy. Herein, a nanocatalytic antioxidative therapeutic strategy is proposed for DCM treatment.
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