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Artykuły w czasopismach na temat "Paludisme – Complications (médecine) – Chez l'enfant"
Ag Iknane, Akory. "EDITORIAL". Mali Santé Publique, 31.10.2018, 05. http://dx.doi.org/10.53318/msp.v8i01.1460.
Pełny tekst źródłaSANOGO, Rokia, Daouda DEMBELE, Sékou DOUMBIA, Aichata B. A. MARIKO i Mohamed Yacine FOFANA. "De la recherche à la production industrielle des produits de santé (Présentations d'expériences réussies) Expérience n°1 : Médicaments Traditionnels Améliorés (MTA) sous forme de pommade au Mali." Journal Africain de Technologie Pharmaceutique et Biopharmacie (JATPB) 2, nr 3 (20.12.2023). http://dx.doi.org/10.57220/jatpb.v2i3.172.
Pełny tekst źródłaRozprawy doktorskie na temat "Paludisme – Complications (médecine) – Chez l'enfant"
Vianou, Koffi Bertin. "Analyse du système hôte-parasite chez le patient pour un traitement adapté du neuropaludisme". Electronic Thesis or Diss., Université de Toulouse (2023-....), 2024. http://www.theses.fr/2024TLSES008.
Pełny tekst źródłaAnalysis of host-parasite interaction in cerebral malaria patients for appropriate treatment. Cerebral malaria, a fatal neurological complication of Plasmodium falciparum infection, occurs mainly in children under the age of five in sub-Saharan Africa. Despite treatment with intravenous artesunate, mortality remains high. A better understanding of the pathophysiology of cerebral malaria will enable us to envisage new, more suitable types of treatment. A cohort of Beninese children presenting with either uncomplicated malaria (UM) or cerebral malaria (CM) was set up. Children with CM were followed up at three days and 1 month (D3, D30) after their inclusion in the study (D0). This thesis focused on three aspects of the host response through the following questions: 1) Is endothelial activation impacted by the type of parasite infecting the host? 2) Is the monocyte response affected during cerebral malaria? and 3) Can we identify specific biomarkers of death during cerebral malaria? Using a co-culture model (Hbec-5i and infected red blood cells -iRBCs- from patients), we showed́ by RT-qPCR that cytoadherence of infected red blood cells from children with CM to endothelial cells increased the expression level of the Nrf2 gene on the endothelial cells. Comparison between clinical groups (CM and UM) of endothelial activation biomarkers measured in co-culture supernatants (with or without contact between the two cell types) showed no significant difference. These results suggest that cytoadherence of iRBCs to ECs alone is not sufficient to induce the production of activation biomarkers by ECs. Concerning the impact of cerebral malaria on monocyte response, the results showed a decrease in the proportion of non-classical monocytes and an alteration in the phagocytosis capacity of total monocytes during acute cerebral malaria (D0), followed by a return to a normal distribution at D3 and then D30. Non-classical monocytes showed a better opsonic and non-opsonic phagocytosis capacity compared with the phagocytosis capacity of the classical and intermediate monocytes. Transcriptional profiling of monocytes revealed that malaria severity was associated with altered expression of CD16, CR1, CR3, TLR2, involved in opsonic phagocytosis, and Tim3, involved in modulating parasite clearance. These results suggest that non-classical monocytes play a key role in the immune response set up during cerebral malaria, and that monocyte function would be controlled at the transcriptomic level. Further studies are required to identify the origin of these control mechanisms. Finally, plasma and urinary biomarkers were measured in children suffering from cerebral malaria. Univariate analysis revealed associations between the occurrence of death from CM and elevated plasma levels of TNF, IL-1, IL-10, CXCL9, Granzyme B, angiopoietin-2 and low levels of urinary PGEM. After multivariate logistic regression analysis, IL-8 appeared to be strongly associated with the occurrence of death for a plasma concentration 57.5 pg/mL at D0 followed by a rapid decreasing at D3 and D30 in surviving children. Biomarkers kinetics (D0, D3, D30) enabled us to distinguish a marker profiles of disease aggravation and resolution. This work reveals that cerebral malaria generates an activation of the antioxidant response by the vascular endothelium, as well as an alteration of the monocyte response via the diminished capacity of non-classical monocytes to eliminate iRBCs by phagocytosis. Furthermore, IL-8 as a biomarker associated with death also underlines the importance of the neutrophil response during cerebral malaria
Martin, Ingrid. "La chimiothérapie anticancéreuse chez l'enfant : complications, prévention et traitement". Paris 5, 1994. http://www.theses.fr/1994PA05P051.
Pełny tekst źródłaMasson, Philippe. "Etude des facteurs de risque de calcification rénale chez l'enfant broncho-dysplasique". Bordeaux 2, 1992. http://www.theses.fr/1992BOR23016.
Pełny tekst źródłaDuval, Cécile. "Thrombophlébite septique du sinus caverneux chez l'enfant : à propos d'un cas". Bordeaux 2, 1999. http://www.theses.fr/1999BOR2M108.
Pełny tekst źródłaMoret, Valérie. "Le reflux gastro-oesophagien chez l'enfant". Paris 5, 1994. http://www.theses.fr/1994PA05P069.
Pełny tekst źródłaDuboze, Muriel. "Cécité acquise au cours de l'hémoglobinose SC : à propos d'un cas". Bordeaux 2, 1999. http://www.theses.fr/1999BOR2M096.
Pełny tekst źródłaEl, Moutassir Zineb. "Risques et complications thromboemboliques au cours des maladies inflammatoires chroniques de l'intestin chez l'enfant". Paris 5, 1996. http://www.theses.fr/1996PA05P181.
Pełny tekst źródłaTölg, Cécilia. "Cholécystectomie chez l'enfant drépanocytaire : étude rétrospective des huit dernières années en Martinique". Bordeaux 2, 2000. http://www.theses.fr/2000BOR23095.
Pełny tekst źródłaViaud, Brigitte. "Les granulomatoses hépatiques infectieuses chez l'enfant : à propos de 8 cas". Bordeaux 2, 1993. http://www.theses.fr/1993BOR23100.
Pełny tekst źródłaRichier, Marie-Anne. "Aspects des mastoi͏̈dites de l'enfant au centre hospitalier de Pau". Bordeaux 2, 1994. http://www.theses.fr/1994BOR2M053.
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