Traumatisme (médecine)

Un traumatisme (du grec τραῦμα (trauma) = « blessure ») est un dommage, ou choc, provoqué par une blessure physique grave et soudaine. Il peut être décrit en tant que « blessure ou dommage physique, tel qu'une fracture ». Le traumatisme majeur (défini par un degré de sévérité plus élevé que 15) peut conduire à des complications secondaires comme un collapsus, une insuffisance respiratoire et la mort. Ramener à la vie un patient souffrant d'un traumatisme implique souvent de multiples procédures médicales. Le traumatisme est la sixième cause de mort dans le monde, comptant 10 % de mortalité, et un très grave problème de santé avec des coûts sociaux significatifs. Classification Le traumatisme peut être classifié selon la zone affectée du corps.

Polytraumatisme (environ 40 %)
Traumatisme crânien (environ 30 %)
Traumatisme thoracique (20 %)
Traumatisme abdominal (10 %)
Traumatisme des extrémités (2 %)

Causes et facteurs de risque Les co

Electrical spinal cord stimulation protocols to regulate neurological functions after spinal cord injury

Salif Axel Komi

Spinal cord injury (SCI) is a life-changing event. People who suffer from it lose their abilityto move normally and are subject to life-threatening symptoms. When the insult is not toosevere, partial recovery is possible. Otherwise, for severely affected people, the perspectives toever retrieve normal functions is almost non-existent. A critically important window to promoteplasticity is in the acute phase after the trauma (weeks to months). However, at this stage,people cannot take active part in rehabilitation programs due to their incapacity to activate theirlimbs and to the apparition of severe autonomic symptoms such as orthostatic hypotension.Hence, current activity-based treatments are of little help for this population. Consequently, SCIdramatically affects their autonomy and quality of life on the life-long term.Continuous Epidural Electrical Stimulation (EES) of the spinal cord has been proposed as amethod to reactivate dormant neural networks innervated below the site of injury. It enablesrobust control over locomotion and autonomic functions. In animal models of severe lesion,continuous EES promoted long lasting recovery of motor abilities when coupled with an intensivetraining. In human, its recent application indeed supported overground walking in chronicallyand severely injured people, but only showed limited plastic effects when compared to animals.Why? Recent advances support that continuous EES abolishes proprioceptive feedback thatis essential to promote recovery. Moreover, late treatment of severe injuries consistently fail apromoting recuperation of functions. Alternatively, over the last decade, our laboratory developeda spatio-temporally patterned approach to EES. In addition to restore fine control over motorfunctions, this technique avoids the caveats of continuous EES, and hypothetically opens a windowof opportunity for plasticity to happen. In this thesis, we propose a translation of this concept tohumans. We first demonstrate that spatio-temporal EES restores robust and versatile locomotorcontrol in people with chronic incomplete, though severe, SCI. Furthermore, the results supportan aptitude of this approach to promote long lasting recovery of functions without stimulationafter 5 months of intensive training. We then report on a patient-tailored technology, thatincludes personalized computational models enabling precise pre-operative planning strategies, anew electrode-lead and control softwares. This technology enables restoration of various motorfunctions in people with chronic and motor-complete injuries within few hours after beginningof therapy. Finally, we transfer this targeted approach to the control of blood pressure. Wedemonstrate that closed-loop stimulation protocols support a precise control over arterial bloodpressure in rodents, non-humane primates and humans with severe SCI submitted to challengingcardiovascular conditions. Combined, the results presented in this manuscript open a clinicallyrealistic perspective for the application of EES acutely after injury and to potentially promoterobust recovery in severe SCI.

EPFL2021

Ablation of the Tumor Suppressor Histidine Triad Nucleotide Binding Protein 1 is Protective Against Hepatic Ischemia/Reperfusion Injury

Gisèle Ferrand

The identification of cellular pathways capable of limiting ischemia/reperfusion (I/R) injury remains a frontier in medicine, and its clinical relevance is urgent. Histidine triad nucleotide binding protein 1 (HINT1) is a tumor suppressor that influences apoptosis. Because apoptotic pathways are a feature of I/R injury, we asked whether Hint1 influences hepatic I/R injury. Hint1(-/-) and C57BL/6 mice were subjected to 70% liver ischemia followed by reperfusion for 3 or 24 hours or to a sham operation. The serum aminotransferase levels, histological lesions, apoptosis, reactive oxygen species, and expression of B cell lymphoma 2-associated X protein (Bax), heme oxygenase 1 (HO-1), interleukin-6 (IL-6), IL-10, tumor necrosis factor-a, Src, nuclear factor kappa B (p65/RelA), and c-Jun were quantified. The responses to toll-like receptor ligands and nicotinamide adenine dinucleotide phosphate oxidase activity in Kupffer cells were compared in Hint1(-/-) mice and C57BL/6 mice. After I/R, the levels of serum aminotransferases, parenchymal necrosis, and hepatocellular apoptosis were significantly lower in Hint1(-/-) mice versus control mice. Furthermore, Bax expression decreased more than 2-fold in Hint1(-/-) mice, and the increases in reactive oxygen species and HO-1 expression that were evident in wild-type mice after I/R were absent in Hint1(-/-) mice. The phosphorylation of Src and the nuclear translocation of p65 were increased in Hint1(-/-) mice, whereas the nuclear expression of phosphorylated c-Jun was decreased. The levels of the protective cytokines IL-6 and IL-10 were increased in Hint1(-/-) mice. These effects increased survival after I/R in mice lacking Hint1. Hint1(-/-) Kupffer cells were less activated than control cells after stimulation with lipopolysaccharides. Conclusion: The Hint1 protein influences the course of I/R injury, and its ablation in Kupffer cells may limit the extent of the injury. (HEPATOLOGY 2011;53:243-252)

2011

Ablation of the Tumor Suppressor Histidine Triad Nucleotide Binding Protein 1 is Protective Against Hepatic Ischemia/Reperfusion Injury

Gisèle Ferrand

2011

Electrical spinal cord stimulation protocols to regulate neurological functions after spinal cord injury

Salif Axel Komi

EPFL2021

Electrical spinal cord stimulation protocols to regulate neurological functions after spinal cord injury

Ablation of the Tumor Suppressor Histidine Triad Nucleotide Binding Protein 1 is Protective Against Hepatic Ischemia/Reperfusion Injury

Estimating uncertainty of alcohol-attributable fractions for infectious and chronic diseases

Estimating uncertainty of alcohol-attributable fractions for infectious and chronic diseases

Ablation of the Tumor Suppressor Histidine Triad Nucleotide Binding Protein 1 is Protective Against Hepatic Ischemia/Reperfusion Injury

Electrical spinal cord stimulation protocols to regulate neurological functions after spinal cord injury