Gotowa bibliografia na temat „Colite aiguë grave”
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Artykuły w czasopismach na temat "Colite aiguë grave"
Brun, Marc. "Colite aiguë grave". Hegel N° 1, nr 1 (2016): 39. http://dx.doi.org/10.4267/2042/58966.
Pełny tekst źródłaRibiere, Sophie, Mahaut Leconte, Stanislas Chaussade i Vered Abitbol. "La colite aiguë grave". La Presse Médicale 47, nr 4 (kwiecień 2018): 312–19. http://dx.doi.org/10.1016/j.lpm.2018.02.020.
Pełny tekst źródłaSeksik, P. "Colite aiguë grave : observation". Gastroentérologie Clinique et Biologique 32, nr 12 (grudzień 2008): 1038–40. http://dx.doi.org/10.1016/j.gcb.2008.10.004.
Pełny tekst źródłaBretagnol, F., i Y. Panis. "Colite aiguë grave: traitement chirurgical". Côlon & Rectum 2, nr 1 (luty 2008): 22–25. http://dx.doi.org/10.1007/s11725-008-0073-0.
Pełny tekst źródłaRibiere, Sophie, Mahaut Leconte, Stanislas Chaussade i Vered Abitbol. "Republication de : La colite aiguë grave". Journal Européen des Urgences et de Réanimation 30, nr 4 (grudzień 2018): 146–54. http://dx.doi.org/10.1016/j.jeurea.2018.10.002.
Pełny tekst źródłaTreton, X., i D. Laharie. "Prise en charge d’une colite aiguë grave". Gastroentérologie Clinique et Biologique 32, nr 12 (grudzień 2008): 1030–37. http://dx.doi.org/10.1016/j.gcb.2008.10.005.
Pełny tekst źródłaPappalardo, E., K. Pautrat, H. Duval i P. Valleur. "Colectomie subtotale par laparoscopie pour colite aiguë grave". Journal de Chirurgie 144, nr 2 (marzec 2007): 139–42. http://dx.doi.org/10.1016/s0021-7697(07)89488-9.
Pełny tekst źródłaBigard, M. A. "Colite aiguë grave au cours des MICI: l’étape diagnostique". Côlon & Rectum 2, nr 1 (luty 2008): 5–9. http://dx.doi.org/10.1007/s11725-008-0070-3.
Pełny tekst źródłaThibault, C. "Devenir des anastomoses iléo-rectales de Crohn après colite aiguë grave". Journal de Chirurgie Viscérale 157, nr 3 (wrzesień 2020): S152—S153. http://dx.doi.org/10.1016/j.jchirv.2020.07.032.
Pełny tekst źródłaPartensky, C., i G. Azzarello. "Colite aiguë grave: Tactique opératoire selon ľétendue des lésions et ľétiologie". Acta Endoscopica 17, S3 (maj 1987): 31–35. http://dx.doi.org/10.1007/bf02969462.
Pełny tekst źródłaRozprawy doktorskie na temat "Colite aiguë grave"
Rivière, Pauline Mayalen. "FMIcroorganisms as Triggers in Acute severe ulcerative Colitis and their influence on medical therapy efficacy : a multi-omics approach, the ITAC project". Electronic Thesis or Diss., Bordeaux, 2023. http://www.theses.fr/2023BORD0474.
Pełny tekst źródłaAcute severe ulcerative colitis is a specific ulcerative colitis (UC) flare characterised by systemic inflammation on top of bloody diarrhoea, leading to a 20% risk of colectomy and 1% mortality risk. Little is known about acute severe ulcerative colitis pathophysiology. Microorganisms have been proposed as triggers for acute severe ulcerative colitis because of the similarity, most notably systemic inflammation, between this phenotype and infectious colitis. Moreover, gut microbiota are key players for protection against pathogens and in UC inflammation. We hypothesised that a dysfunctional gut microbiome, characterised by a lack of diversity and the loss of anti-inflammatory bacterial species, would allow the proliferation of a pathobiont in the colonic lumen eliciting a systemic inflammatory response in hosts with permissive gut mucosal immunity leading to an acute severe ulcerative colitis flare. The general objective of my study was to identify the microbiome component(s) and the host factors leading to acute severe ulcerative colitis. We had three specific aims: (i) to compare the gut microbiota of patients with acute severe ulcerative colitis compared to patients with a non-severe ulcerative colitis flare using 16S rRNA gene sequencing of stool samples and rectal biopsies. Patients with acute severeulcerative colitis displayed significant alterations in their gut microbiota, characterised by reduced alpha-diversity, an increased presence of Proteobacteria, particularly members of the Escherichia/Shigella genus, and a reduction in the abundance of Lachnospiraceae and Ruminococcaceae family members; (ii) to identify the cellular subtypes and pathways involved in gut mucosal inflammation in acute severe ulcerative colitis patients compared to non-severe ulcerative colitis patients by single-cell RNA-Seq of rectal biopsies. In severe cases, plasmablasts exhibited a distinct transcriptomic profile with increased IgG production, 2and a specific T cell population expressing IL26 was expanded compared to non-severe cases. Innate immune cells displayed a pro-inflammatory profile. Both T cells and innate immune cells indicated a pro-Th17 mucosal environment; (iii) to determine the host pathways mediating the systemic inflammatory outburst using whole blood RNA-Seq in acute severe ulcerative colitis patients compared to non-severe ulcerative colitis patients. We found no clear distinction between severe and non-severe cases and did not identify any pathways enriched with differentially expressed genes. This observation suggests that in acute severe ulcerative colitis, the systemic inflammation is less likely to be orchestrated by cytokines originating from circulating cells but rather from inflammatory cells located in the colonic mucosa. This multi-omics study contributes valuable insights into the pivotal cellular and bacterial components involved in the pathogenesis of acute severe ulcerative colitis. These findings have the potential to guide future clinical research, directing efforts toward microbiome modulation, targeted interventions on plasmablasts, or nuanced inhibition of the Th17/IL-23 axis
BELVALETTE, CORINNE. "A propos d'un cas de colite pseudo-membraneuse post-antibiotique aigue grave". Amiens, 1989. http://www.theses.fr/1989AMIEM099.
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