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1. Ultrafine Grain 316L Stainless Steel Manufactured by Ball Milling and Spark Plasma Sintering: Consequences on the Corrosion Resistance in Chloride Media

Author

Eric Hug, Clément Keller, Cendrine Folton, Jade Papin, Kostiantyn Tabalaiev, and Gaël Marnier

Subjects
corrosion, passivity, pitting, grain size, 316L, SPS, Mining engineering. Metallurgy, TN1-997
Abstract

This paper reports experimental results concerning the corrosion of 316L austenitic stainless steels produced by ball milling and spark plasma sintering in NaCl electrolyte. Specimens with grain sizes ranging from 0.3 µm to 3 µm, without crystallographic texture, were obtained and compared with a cast that is 110 µm in grain size and an annealed reference. The potentiodynamic experiments showed that the reduction in grain size leads to a degradation of the electrochemical passivation behavior. This detrimental effect can be overcome by appropriate passivation in a HNO3 concentrated solution before consolidation. The Mott–Schottky measurements showed that the semiconducting properties of the passive layer do not vary significantly on the grain size, especially the donor density, which is responsible for the chemical passivation breakdown by chloride anions. The total electrical resistance of the layer, measured by impedance spectroscopy is always lower than the one of a cast and annealed 316L, but it slightly increases with a reduction in grain size in the ultrafine grain range. This is followed by a slight increase in the thickness of the oxide layer. The effect of chloride ions is very pronounced in terms of passivation breakdown if the powder is not passivated prior to sintering. This leads to the nucleation and growth of subsurface main pits and the formation of secondary satellite pits, especially for the smallest grain sizes. Passivation of the 316L powder before sintering has been found to be an effective way to prevent this phenomenon.

Published
2024
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2. Kinetics of monocyte subpopulations during experimental cerebral malaria and its resolution in a model of late chloroquine treatment

Author

Jade Royo, Aissata Camara, Benedicte Bertrand, Philippe Batigne, Agnes Coste, Bernard Pipy, Agnes Aubouy, the NeuroCM Group, Dissou Affolabi, Jules Alao, Daniel Ajzenberg, Linda Ayédadjou, Gwladys Bertin, Bibiane Biokou, Farid Boumédiène, Josselin Brisset, Michel Cot, Jean-Eudes Degbelo, Philippe Deloron, Ida Dossou-Dagba, Latifou Dramane, Jean François Faucher, Sandrine Houzé, Sayeh Jafari-Guemouri, Claire Kamaliddin, Elisée Kinkpé, Anaïs Labrunie, Yélé Ladipo, Thomas Lathiere, Achille Massougbodji, Audrey Mowendabeka, Jade Papin, Pierre-Marie Preux, Marie Raymondeau, Darius Sossou, Brigitte Techer, Bertin Vianou, and Laurence Watier

Subjects
cerebral malaria (CM), mice, monocyte, brain, spleen, blood, Microbiology, QR1-502
Abstract

Cerebral malaria (CM) is one of the most severe forms of malaria and is a neuropathology that can lead to death. Monocytes have been shown to accumulate in the brain microvasculature at the onset of neurological symptoms during CM. Monocytes have a remarkable ability to adapt their function to their microenvironment from pro-inflammatory to resolving activities. This study aimed to describe the behavior of monocyte subpopulations during infection and its resolution. C57BL/6 mice were infected with the Plasmodium berghei ANKA strain and treated or not with chloroquine (CQ) on the first day of the onset of neurological symptoms (day 6) for 4 days and followed until day 12 to mimic neuroinflammation and its resolution during experimental CM. Ly6C monocyte subpopulations were identified by flow cytometry of cells from the spleen, peripheral blood, and brain and then quantified and characterized at different time points. In the brain, the Ly6Cint and Ly6Clow monocytes were associated with neuroinflammation, while Ly6Chi and Ly6Cint were mobilized from the peripheral blood to the brain for resolution. During neuroinflammation, CD36 and CD163 were both involved via splenic monocytes, whereas our results suggest that the low CD36 expression in the brain during the neuroinflammation phase was due to degradation. The resolution phase was characterized by increased expressions of CD36 and CD163 in blood Ly6Clow monocytes, a higher expression of CD36 in the microglia, and restored high expression levels of CD163 in Ly6Chi monocytes localized in the brain. Thus, our results suggest that increasing the expressions of CD36 and CD163 specifically in the brain during the neuroinflammatory phase contributes to its resolution.

Published
2022
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6. Non-traumatic coma in young children in Benin: are viral and bacterial infections gaining ground on cerebral malaria?

Author

Josselin, Brisset, Karl, Angendu Baki, Laurence, Watier, Elisée, Kinkpé, Justine, Bailly, Linda, Ayédadjou, Maroufou Jules, Alao, Ida, Dossou-Dagba, Gwladys I, Bertin, Michel, Cot, Farid, Boumédiène, Daniel, Ajzenberg, Agnès, Aubouy, Sandrine, Houzé, Jean-François, Faucher, Bertin, Vianou, Service des Maladies infectieuses et tropicales [CHU Limoges], CHU Limoges, Epidémiologie des Maladies Chroniques en zone tropicale (EpiMaCT), CHU Limoges-Institut d'Epidémiologie Neurologique et de Neurologie Tropicale-Institut National de la Santé et de la Recherche Médicale (INSERM)-OmégaHealth (ΩHealth), Université de Limoges (UNILIM)-Université de Limoges (UNILIM), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Epidémiologie et modélisation de la résistance aux antimicrobiens - Epidemiology and modelling of bacterial escape to antimicrobials (EMAE), Institut Pasteur [Paris] (IP)-Université Paris Cité (UPCité), Centre Hospitalier Universitaire de Zone d'Abomey Calavi / Sô-Ava (CHUZ / AS), Mère et enfant en milieu tropical : pathogènes, système de santé et transition épidémiologique (MERIT - UMR_D 261), Institut de Recherche pour le Développement (IRD)-Université Paris Cité (UPCité), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre Hospitalier Universitaire de la Mère et de l'Enfant Lagune (CHU-MEL), Service de Parasitologie Mycologie [CHU Limoges], Institut de Recherche Clinique du Bénin [Abomey-Calavi, Bénin] (IRCB), Pharmacochimie et Biologie pour le Développement (PHARMA-DEV), Institut de Recherche pour le Développement (IRD)-Institut de Chimie de Toulouse (ICT), Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT), This work was funded by the French National Research Agency (ANR-17-CE17-0001)., NeuroCM group: Dissou Affolabi (Pediatric Department, Calavi Hospital, Calavi, Benin), Nicolas Argy (MERIT UMR 261, IRD, Université de Paris, Paris, France), Bibiane Biokou (Pediatric Department, Mother and Child University and Hospital Center (CHUMEL), Cotonou, Benin), Jean-Eudes Degbelo (Institut de Recherche Clinique du Bénin (IRCB), Calavi, Benin), Philippe Deloron (MERIT UMR 261, IRD, Université de Paris, Paris, France), Latifou Dramane (Institut de Recherche Clinique du Bénin (IRCB), Abomey Calavi, Benin), Jérémy Fraering (MERIT UMR 261, IRD, Université de Paris, Paris, France), Emilie Guillochon (MERIT UMR 261, IRD, Université de Paris, Paris, France), Sayeh Jafari-Guemouri (MERIT UMR 261, IRD, Université de Paris, Paris, France), Ludivine Houzé (MERIT UMR 261, IRD, Université de Paris, Paris, France), Valentin Joste (MERIT UMR 261, IRD, Université de Paris, Paris, France), Claire Kamaliddin (MERIT UMR 261, IRD, Université de Paris, Paris, France), Anaïs Labrunie (NET, INSERM, Université de Limoges, Limoges, France), Yélé Ladipo (Pediatric Department, Mother and Child University and Hospital Center (CHUMEL), Cotonou, Benin), Thomas Lathiere (Ophtalmology department, Limoges University Hospital, Limoges, France), Achille Massougbodji (Institut de Recherche Clinique du Bénin (IRCB), Abomey Calavi, Benin), Audrey Mowendabeka (Paediatric Department, Hopital de la Mère et de l'Enfant, Limoges, France), Jade Papin (MERIT UMR 261, IRD, Université de Paris, Paris, France), Bernard Pipy (PHARMADEV, Université de Toulouse, IRD, UPS, France), Pierre-Marie Preux (NET, INSERM, Université de Limoges, Limoges, France), Marie Raymondeau (NET, INSERM, Université de Limoges, Limoges, France), Jade Royo (PHARMADEV, Université de Toulouse, IRD, UPS, France), Darius Sossou (Institut de Recherche Clinique du Bénin (IRCB), Abomey Calavi, Benin), Brigitte Techer (MERIT UMR 261, IRD, Université de Paris, Paris, France), Bertin Vianou (Institut de Recherche Clinique du Bénin (IRCB), Abomey Calavi, Benin)., ANR-17-CE17-0001,NEUROCM,Identification des facteurs parasitaires et de l'hôte à l'origine de la neuroinflammation et de sa résolution dans un contexte de neuropaludisme(2017), Grelier, Elisabeth, Identification des facteurs parasitaires et de l'hôte à l'origine de la neuroinflammation et de sa résolution dans un contexte de neuropaludisme - - NEUROCM2017 - ANR-17-CE17-0001 - AAPG2017 - VALID, Mère et enfant en milieu tropical : pathogènes, système de santé et transition épidémiologique (MERIT - UMR_D 216), Institut de Recherche pour le Développement (IRD)-Institut de Chimie de Toulouse (ICT-FR 2599), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), and Université Fédérale Toulouse Midi-Pyrénées

Subjects
MESH: Bacterial Infections, Malaria, Cerebral, Non-traumatic coma, MESH: Malaria, Cerebral, [SDV.MHEP.PED] Life Sciences [q-bio]/Human health and pathology/Pediatrics, MESH: Benin, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, MESH: Child, West Africa, Odds Ratio, Benin, Humans, Prospective Studies, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Child, Cerebral malaria, [SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/Pediatrics, MESH: Humans, MESH: Child, Preschool, Public Health, Environmental and Occupational Health, Bacterial Infections, General Medicine, Central nervous system infection, MESH: Odds Ratio, MESH: Prospective Studies, Co-infection, Infectious Diseases, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, Child, Preschool, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie
Abstract

Background While malaria morbidity and mortality have declined since 2000, viral central nervous system infections appear to be an important, underestimated cause of coma in malaria-endemic Eastern Africa. We aimed to describe the etiology of non-traumatic comas in young children in Benin, as well as their management and early outcomes, and to identify factors associated with death. Methods From March to November 2018, we enrolled all HIV-negative children aged between 2 and 6 years, with a Blantyre Coma Score ≤ 2, in this prospective observational study. Children were screened for malaria severity signs and assessed using a systematic diagnostic protocol, including blood cultures, malaria diagnostics, and cerebrospinal fluid analysis using multiplex PCR. To determine factors associated with death, univariate and multivariate analyses were performed. Results From 3244 admissions, 84 children were included: malaria was diagnosed in 78, eight of whom had a viral or bacterial co-infection. Six children had a non-malarial infection or no identified cause. The mortality rate was 29.8% (25/84), with 20 children dying in the first 24 h. Co-infected children appeared to have a poorer prognosis. Of the 76 children who consulted a healthcare professional before admission, only 5 were prescribed adequate antimalarial oral therapy. Predictors of early death were jaundice or increased bilirubin [odd ratio (OR)= 8.6; 95% confidential interval (CI): 2.03–36.1] and lactate > 5 mmol/L (OR = 5.1; 95% CI: 1.49–17.30). Antibiotic use before admission (OR = 0.1; 95% CI: 0.02–0.85) and vaccination against yellow fever (OR = 0.2, 95% CI: 0.05–0.79) protected against mortality. Conclusions Infections were found in all children who died, and cerebral malaria was by far the most common cause of non-traumatic coma. Missed opportunities to receive early effective antimalarial treatment were common. Other central nervous system infections must be considered in their management. Some factors that proved to be protective against early death were unexpected.

Published
2022
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