10 results on '"Baptiste, Balança"'
Search Results
2. Intensive care-related loss of quality of life and autonomy at 6 months post-discharge: Does COVID-19 really make things worse?
- Author
-
Fabrice Thiolliere, Claire Falandry, Bernard Allaouchiche, Victor Geoffray, Laurent Bitker, Jean Reignier, Paul Abraham, Stephanie Malaquin, Baptiste Balança, Hélène Boyer, Philippe Seguin, Céline Guichon, Marie Simon, Arnaud Friggeri, Charles-Hervé Vacheron, and AZUREA Study Group
- Subjects
COVID-19 ,Autonomy ,Quality of life ,Medical emergencies. Critical care. Intensive care. First aid ,RC86-88.9 - Abstract
Abstract Objective To compare old patients hospitalized in ICU for respiratory distress due to COVID-19 with old patients hospitalized in ICU for a non-COVID-19-related reason in terms of autonomy and quality of life. Design Comparison of two prospective multi-centric studies. Setting This study was based on two prospective multi-centric studies, the Senior-COVID-Rea cohort (COVID-19-diagnosed ICU-admitted patients aged over 60) and the FRAGIREA cohort (ICU-admitted patients aged over 70). Patients We included herein the patients from both cohorts who had been evaluated at day 180 after admission (ADL score and quality of life). Interventions None. Measurements and main results A total of 93 COVID-19 patients and 185 control-ICU patients were included. Both groups were not balanced on age, body mass index, mechanical ventilation, length of ICU stay, and ADL and SAPS II scores. We modeled with ordered logistic regression the influence of COVID-19 on the quality of life and the ADL score. After adjustment on these factors, we observed COVID-19 patients were less likely to have a loss of usual activities (aOR [95% CI] 0.47 [0.23; 0.94]), a loss of mobility (aOR [95% CI] 0.30 [0.14; 0.63]), and a loss of ADL score (aOR [95% CI] 0.30 [0.14; 0.63]). On day 180, 52 (56%) COVID-19 patients presented signs of dyspnea, 37 (40%) still used analgesics, 17 (18%) used anxiolytics, and 14 (13%) used antidepressant. Conclusions COVID-19-related ICU stay was not associated with a lower quality of life or lower autonomy compared to non-COVID-19-related ICU stay.
- Published
- 2022
- Full Text
- View/download PDF
3. How to monitor thiopental administration in the intensive care unit for refectory status epilepticus or intracranial hypertension?
- Author
-
Erika Dabricot, Inès Seqat, Frédéric Dailler, Sylvain Rheims, Sebastien Boulogne, and Baptiste Balança
- Subjects
Medical emergencies. Critical care. Intensive care. First aid ,RC86-88.9 - Published
- 2021
- Full Text
- View/download PDF
4. Can prone positioning be a safe procedure in patients with acute brain injury and moderate-to-severe acute respiratory distress syndrome?
- Author
-
Pauline Bernon, Ségolène Mrozek, Guillaume Dupont, Frédéric Dailler, Anne-Claire Lukaszewicz, and Baptiste Balança
- Subjects
Medical emergencies. Critical care. Intensive care. First aid ,RC86-88.9 - Published
- 2021
- Full Text
- View/download PDF
5. Risk factors associated with day-30 mortality in patients over 60 years old admitted in ICU for severe COVID-19: the Senior-COVID-Rea Multicentre Survey protocol
- Author
-
Thomas Rimmele, Julien Berthiller, Anne-Claire Lukaszewicz, Laurent Jallades, Jean-Baptiste Pialat, Céline Monard, Christophe Leroy, Vincent Collange, Arnaud Friggeri, Mélanie Roche, Christine Ravot, Amélie Malapert, Max Haïne, David Dayde, Claire Falandry, Marie Simon, Céline Guichon, Paul Abraham, Camille Boin, Justine Dubreuil, Laurent Bitker, Baptiste Balança, Sylvie Goutte, Emilie Gadea, Alain Lepape, Fabrice Thiollière, Hodane Yonis, Antoine Garnier-Crussard, Loredana Baboi, Valérie Cerro, Carlos El Khoury, Emilie Gadéa-Deschamps, Marie-Catherine Fromont, Audrey Gelot, Anthéa Loïez, Maya Perrou, Laetitia Paradisi-Prieur, Marion Provent, Gulsum Sahin, Ghyslaine Thao, and Marine Thieux
- Subjects
Medicine - Abstract
Introduction With the spread of COVID-19 epidemic, health plans must be adapted continuously. There is an urgent need to define the best care courses of patients with COVID-19, especially in intensive care units (ICUs), according to their individualised benefit/risk ratio. Since older age is associated with poorer short-term and long-term outcomes, prediction models are needed, that may assist clinicians in their ICU admission decision. Senior-COVID-Rea was designed to evaluate, in patients over 60 years old admitted in ICU for severe COVID-19 disease, the impact of age and geriatric and paraclinical parameters on their mortality 30 days after ICU admission.Methods and analysis This is a multicentre survey protocol to be conducted in seven hospitals of the Auvergne-Rhône-Alpes region, France. All patients over 60 years old admitted in ICU for severe COVID-19 infection (or their legally acceptable representative) will be proposed to enter the study and to fill in a questionnaire regarding their functional and nutritional parameters 1 month before COVID-19 infection. Paraclinical parameters at ICU admission will be collected: lymphocytes and neutrophils counts, high-fluorescent lymphoid cells and immature granulocytes percentages (Sysmex data), D-dimers, C-reactive protein, lactate dehydrogenase (LDH), creatinine, CT scan for lung extension rate as well as clinical resuscitation scores, and the delay between the first signs of infection and ICU admission. The primary outcome will be the overall survival at day 30 post-ICU admission. The analysis of factors predicting mortality at day 30 will be carried out using univariate and multivariate logistic regressions. Multivariate logistic regression will consider up to 15 factors.The ambition of this trial, which takes into account the different approaches of geriatric vulnerability, is to define the respective abilities of different operational criteria of frailty to predict patients’ outcomes.Ethics and dissemination The study protocol was ethically approved. The results of the primary and secondary objectives will be published in peer-reviewed journals.Trial registration number NCT04422340.
- Published
- 2021
- Full Text
- View/download PDF
6. DAMPs and RAGE Pathophysiology at the Acute Phase of Brain Injury: An Overview
- Author
-
Baptiste Balança, Laurent Desmurs, Jérémy Grelier, Armand Perret-Liaudet, and Anne-Claire Lukaszewicz
- Subjects
acute brain injuries ,damage-associated molecular pattern molecules ,receptor for advanced glycation end-products ,biomarkers ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
Early or primary injury due to brain aggression, such as mechanical trauma, hemorrhage or is-chemia, triggers the release of damage-associated molecular patterns (DAMPs) in the extracellular space. Some DAMPs, such as S100B, participate in the regulation of cell growth and survival but may also trigger cellular damage as their concentration increases in the extracellular space. When DAMPs bind to pattern-recognition receptors, such as the receptor of advanced glycation end-products (RAGE), they lead to non-infectious inflammation that will contribute to necrotic cell clearance but may also worsen brain injury. In this narrative review, we describe the role and ki-netics of DAMPs and RAGE at the acute phase of brain injury. We searched the MEDLINE database for “DAMPs” or “RAGE” or “S100B” and “traumatic brain injury” or “subarachnoid hemorrhage” or “stroke”. We selected original articles reporting data on acute brain injury pathophysiology, from which we describe DAMPs release and clearance upon acute brain injury, and the implication of RAGE in the development of brain injury. We will also discuss the clinical strategies that emerge from this overview in terms of biomarkers and therapeutic perspectives
- Published
- 2021
- Full Text
- View/download PDF
7. DAMPs and RAGE Pathophysiology at the Acute Phase of Brain Injury: An Overview
- Author
-
Armand Perret-Liaudet, Jérémy Grelier, Laurent Desmurs, Anne-Claire Lukaszewicz, and Baptiste Balança
- Subjects
Glycation End Products, Advanced ,Subarachnoid hemorrhage ,Traumatic brain injury ,receptor for advanced glycation end-products ,Inflammation ,Review ,Catalysis ,RAGE (receptor) ,lcsh:Chemistry ,Inorganic Chemistry ,Extracellular ,medicine ,Alarmins ,Animals ,Humans ,Physical and Theoretical Chemistry ,Receptor ,lcsh:QH301-705.5 ,Molecular Biology ,Stroke ,Spectroscopy ,acute brain injuries ,business.industry ,Organic Chemistry ,biomarkers ,General Medicine ,damage-associated molecular pattern molecules ,medicine.disease ,Pathophysiology ,Computer Science Applications ,lcsh:Biology (General) ,lcsh:QD1-999 ,Brain Injuries ,Acute Disease ,medicine.symptom ,business ,Neuroscience - Abstract
Early or primary injury due to brain aggression, such as mechanical trauma, hemorrhage or is-chemia, triggers the release of damage-associated molecular patterns (DAMPs) in the extracellular space. Some DAMPs, such as S100B, participate in the regulation of cell growth and survival but may also trigger cellular damage as their concentration increases in the extracellular space. When DAMPs bind to pattern-recognition receptors, such as the receptor of advanced glycation end-products (RAGE), they lead to non-infectious inflammation that will contribute to necrotic cell clearance but may also worsen brain injury. In this narrative review, we describe the role and ki-netics of DAMPs and RAGE at the acute phase of brain injury. We searched the MEDLINE database for “DAMPs” or “RAGE” or “S100B” and “traumatic brain injury” or “subarachnoid hemorrhage” or “stroke”. We selected original articles reporting data on acute brain injury pathophysiology, from which we describe DAMPs release and clearance upon acute brain injury, and the implication of RAGE in the development of brain injury. We will also discuss the clinical strategies that emerge from this overview in terms of biomarkers and therapeutic perspectives
- Published
- 2021
8. Minimally invasive microelectrode biosensors reveal different neurochemical signature of spreading depolarization in rat cortex
- Author
-
Anne Meiller, Charles Chatard, Baptiste Balança, Andrei SABAC, Stéphane Marinesco, Translational and Integrative Group in Epilepsy Research (TIGER), Institut National de la Santé et de la Recherche Médicale (INSERM), Ampère, Département Bioingénierie (BioIng), Ampère (AMPERE), École Centrale de Lyon (ECL), Université de Lyon-Université de Lyon-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-École Centrale de Lyon (ECL), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Centre de recherche en neurosciences de Lyon (CRNL), Université Claude Bernard Lyon 1 (UCBL), and Université de Lyon-Université de Lyon-Université Jean Monnet [Saint-Étienne] (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)
- Subjects
[SDV]Life Sciences [q-bio] - Abstract
International audience; Monitoring the chemical composition of the brain interstitial fluid is an important challenge for both pre-clinical and clinical research on brain injury. Microelectrode biosensors are a promising technique with a temporal resolution in the order of seconds. Here, ultra-microelectrodes based on platinized carbon fibers were fabricated to obtain biosensors with less than 15 µm external diameter. Platinization was achieved by sputtering a 10 nm Cr adhesion layer followed by 100 nm of platinum. Platinized carbon fibers were then encased in a glass micropipette and covered with electropolymerized poly-phenylenediamine for selectivity, and covalently immobilized oxidase enzymes (glucose oxidase, lactate oxidase, D-amino acid oxidase or glutamate oxidase). After implantation in the rat parietal cortex, such biosensors detected a smaller basal lactate concentration and a slower diffusion of glucose and D-serine through the blood brain barrier compared to more conventional biosensors with 100 µm external diameter. Interestingly, spreading depolarization (SD) produced a smaller increase in lactate, a larger decrease in glucose, and a larger increase in D-serine at platinized carbon fibers microelectrode biosensors compared to larger sensors. Therefore, the neurochemical signature of SDs was significantly different when estimated with these new minimally invasive biosensors. Such small devices avoid major mechanical injury to blood vessels, preserve the blood brain barrier at the site of implantation, and therefore, provide more accurate measurements from the brain interstitial fluid. Developing smaller, less invasive probes for brain monitoring is therefore an important challenge in order to obtain meaningful information about the cellular mechanisms at work during brain injury.
- Published
- 2017
9. Recording, analysis, and interpretation of spreading depolarizations in neurointensive care: Review and recommendations of the COSBID research group
- Author
-
Erdem Güresir, Sergei A. Kirov, Egill Rostrup, Christoph Drenckhahn, Martyn G. Boutelle, Brian A. MacVicar, Michael Schöll, Andrew I R Maas, Michael Scheel, Daniel Kondziella, Clemens Reiffurth, Johannes Platz, Jason M. Hinzman, Juan Sahuquillo, M. Ross Bullock, Frank Richter, Tomas Watanabe, Ilan Shelef, Kazutaka Sugimoto, Martin Lauritzen, Bart Feyen, Julia S. Bretz, Brandon Foreman, David O. Okonkwo, Eun Jeung Kang, Hartmut Vatter, Markus Dahlem, Anthony J. Strong, Ana I Oliveira-Ferreira, Jens P. Dreier, Nils Hecht, Baptiste Balança, Otto W. Witte, Christina M. Kowoll, Yoash Chassidim, Sharon L. Jewell, Rudolf Graf, Nina Eriksen, Thomas Lieutaud, Gerrit Brinker, Johannes Woitzik, Alon Friedman, Andrew P. Carlson, Nora F. Dengler, Henning Piilgaard, Bente Pakkenberg, Svetlana Lublinsky, Lee S Chung, Maren K.L. Winkler, Gajanan S. Revankar, C. William Shuttleworth, Christian Dohmen, Jan Claassen, Janos Luckl, Delphine Feuerstein, André P. Schulte, Michiyasu Suzuki, Edgar Santos, Michael Reiner, Denny Milakara, Peter Vajkoczy, Jed A. Hartings, Lori Shutter, Sebastian Major, Stéphane Marinesco, Daniel N. Hertle, Martin Fabricius, Michel D. Ferrari, Paul Jahnke, Viktor Horst, Uwe Heinemann, Alois Josef Schiefecker, Oliver W. Sakowitz, Peter Martus, M. Brandon Westover, Cenk Ayata, Renán Sánchez-Porras, Rick M. Dijkhuizen, Kc Brennan, Christian K. Friberg, Norberto Andaluz, R. David Andrew, Karl Schoknecht, Eric Rosenthal, Oscar Herreras, Georg Bohner, Raimund Helbok, Anna Maslarova, Eszter Farkas, and Arn M. J. M. van den Maagdenberg
- Subjects
0301 basic medicine ,Spreading depolarization ,cerebral blood flow ,Review ,Epileptogenesis ,0302 clinical medicine ,anoxic depolarization ,asphyxial depolarization ,Gray Matter ,Electrocorticography ,Review Articles ,brain edema ,spreading depression ,medicine.diagnostic_test ,spreading ischemia ,Cortical Spreading Depression ,Depolarization ,Stroke ,peri-infarct depolarization ,neurocritical care ,Neurology ,Cerebral blood flow ,Cortical spreading depression ,Cerebrovascular Circulation ,Practice Guidelines as Topic ,brain trauma ,neuroprotection ,Cardiology and Cardiovascular Medicine ,Critical Care ,subarachnoid hemorrhage ,neurovascular coupling ,Ischemia ,Focal ischemia ,03 medical and health sciences ,Journal Article ,medicine ,Humans ,vasospasm ,business.industry ,Neurointensive care ,medicine.disease ,intracerebral hemorrhage ,Neurophysiological Monitoring ,global ischemia ,030104 developmental biology ,Brain Injuries ,focal ischemia ,epilepsy ,epileptogenesis ,Human medicine ,Neurology (clinical) ,business ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Spreading depolarizations (SD) are waves of abrupt, near-complete breakdown of neuronal transmembrane ion gradients, are the largest possible pathophysiologic disruption of viable cerebral gray matter, and are a crucial mechanism of lesion development. Spreading depolarizations are increasingly recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes. Further spreading depolarizations arise for hours to days due to energy supply-demand mismatch in viable tissue. Spreading depolarizations exacerbate neuronal injury through prolonged ionic breakdown and spreading depolarization-related hypoperfusion (spreading ischemia). Local duration of the depolarization indicates local tissue energy status and risk of injury. Regional electrocorticographic monitoring affords even remote detection of injury because spreading depolarizations propagate widely from ischemic or metabolically stressed zones; characteristic patterns, including temporal clusters of spreading depolarizations and persistent depression of spontaneous cortical activity, can be recognized and quantified. Here, we describe the experimental basis for interpreting these patterns and illustrate their translation to human disease. We further provide consensus recommendations for electrocorticographic methods to record, classify, and score spreading depolarizations and associated spreading depressions. These methods offer distinct advantages over other neuromonitoring modalities and allow for future refinement through less invasive and more automated approaches.
- Published
- 2016
10. Altered hypermetabolic response to cortical spreading depolarizations after traumatic brain injury in rats
- Author
-
Laurent Bezin, Baptiste Balança, Stéphane Marinesco, Anne Meiller, Thomas Lieutaud, and Jens P. Dreier
- Subjects
0301 basic medicine ,Male ,medicine.medical_specialty ,Traumatic brain injury ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,Brain Injuries, Traumatic ,medicine ,Animals ,In patient ,Lactic Acid ,Rats, Wistar ,Chemistry ,Penumbra ,Cortical Spreading Depression ,Brain ,Depolarization ,Original Articles ,medicine.disease ,Cerebrovascular Circulation ,Cortex (botany) ,Oxygen ,030104 developmental biology ,Endocrinology ,Glucose ,Neurology ,Cerebral blood flow ,Cortical spreading depression ,Anesthesia ,Neurology (clinical) ,Cardiology and Cardiovascular Medicine ,Energy Metabolism ,030217 neurology & neurosurgery - Abstract
Spreading depolarizations are waves of near-complete breakdown of neuronal transmembrane ion gradients, free energy starving, and mass depolarization. Spreading depolarizations in electrically inactive tissue are associated with poor outcome in patients with traumatic brain injury. Here, we studied changes in regional cerebral blood flow and brain oxygen (PbtO2), glucose ([Glc]b), and lactate ([Lac]b) concentrations in rats, using minimally invasive real-time sensors. Rats underwent either spreading depolarizations chemically triggered by KCl in naïve cortex in absence of traumatic brain injury or spontaneous spreading depolarizations in the traumatic penumbra after traumatic brain injury, or a cluster of spreading depolarizations triggered chemically by KCl in a remote window from which spreading depolarizations invaded penumbral tissue. Spreading depolarizations in noninjured cortex induced a hypermetabolic response characterized by a decline in [Glc]b and monophasic increases in regional cerebral blood flow, PbtO2, and [Lac]b, indicating transient hyperglycolysis. Following traumatic brain injury, spontaneous spreading depolarizations occurred, causing further decline in [Glc]b and reducing the increase in regional cerebral blood flow and biphasic responses of PbtO2 and [Lac]b, followed by prolonged decline. Recovery of PbtO2 and [Lac]b was significantly delayed in traumatized animals. Prespreading depolarization [Glc]b levels determined the metabolic response to clusters. The results suggest a compromised hypermetabolic response to spreading depolarizations and slower return to physiological conditions following traumatic brain injury-induced spreading depolarizations.
- Published
- 2016
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.