References of "SCHUMACHER, Katharina"
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See detailEvaluation de l’efficacité de la simulation haute fidélité dans la prise en charge des troubles du rythme cardiaque chez l’enfant: étude pilote
SCHUMACHER, Katharina ULg; Seghaye, Marie-Christine ULg; Baugnon, Thomas et al

in Tijdschrift van de Belgische Kinderarts = Journal du Pédiatre Belge (2015, March), 17(1),

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See detailImplémentation d’un cours avec simulation haute fidélité pour la préparation des internes débutant leur formation en pédiatrie et en médecine d’urgence
SCHUMACHER, Katharina ULg; Seghaye, Marie-Christine ULg; Solowianiuk, Marie et al

in Tijdschrift van de Belgische Kinderarts = Journal du Pédiatre Belge (2015), 17(1),

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See detailMyocardial expression of cytokines influences postoperative outcome after cardiac surgery for congenital cardiac defects
Sprute, Johanna; Heying, Ruth; Buding, Brigitte et al

Conference (2014, January)

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See detailCardiac malformations in neonates born from mothers with gestational diabetes
Antole, Nathalie; Jacquemart, Caroline; GKIOUGKI, Evangelia ULg et al

Conference (2014, January)

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See detailMyocardial cardiotrophin-1 is differentially induced in congenital cardiac defects depending on hypoxemia.
Heying, Ruth; Qing, Ma; SCHUMACHER, Katharina ULg et al

in Future cardiology (2014), 10(1), 53-62

Aim: Cardiotrophin-1 (CT-1) is upregulated by hypoxemia and hemodynamic overload and is characterized by potent hypertrophic and protective properties on cardiac cells. This study aimed to investigate ... [more ▼]

Aim: Cardiotrophin-1 (CT-1) is upregulated by hypoxemia and hemodynamic overload and is characterized by potent hypertrophic and protective properties on cardiac cells. This study aimed to investigate whether CT-1 is differentially induced in the myocardium of infants with congenital cardiac defects depending on hypoxemia. Methods & results: Infants with Tetralogy of Fallot (n = 8) or with large nonrestrictive ventricular septal defect (n = 8) undergoing corrective surgery were investigated. Expression of CT-1 was assessed at mRNA and protein levels in the right atrial and ventricular myocardium. The activation of the STAT-3 and VEGF were measured. Degradation of cardiac troponin-I served as a marker of myocardial damage. CT-1 was detected in all patients with levels negatively correlating to the arterial oxygen saturation. Higher CT-1 expression in Tetralogy of Fallot patients was associated with activation of the JAK/STAT pathway and higher cardiac troponin-I degradation. Conclusion: CT-1 may mediate myocardial hypertrophy and dysfunction in infants with congenital cardiac defects, particularly in those with hypoxemia. [less ▲]

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See detailInterleukin-6 as a marker of inflammatory related post-operative myocardial dysfunction
von der Stück, H.; SCHUMACHER, Katharina ULg; Buding, B. et al

Conference (2013, May)

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See detailDelayed diagnosis of cardiomyopathy in a girl treated for asthma bronchiale
MASTOURI, M.; FUDVOYE, Julie ULg; ANTOLE, N. et al

Conference (2013, March)

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See detailCardiac malformations in neonates born from mothers with gestational diabetes
ANTOLE, N.; JACQUEMART, C.; GKIOUGKI, Evangelia ULg et al

Conference (2013, March)

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See detailDexamethasone pretreatment provides antiinflammatory and myocardial protection in neonatal arterial switch operation.
Heying, Ruth; Wehage, Edith; SCHUMACHER, Katharina ULg et al

in Annals of Thoracic Surgery (2012), 93(3), 869-76

BACKGROUND: This prospective double-blinded randomized study tested the hypothesis that preoperative treatment with dexamethasone would attenuate inflammatory priming of the myocardium, reduce the ... [more ▼]

BACKGROUND: This prospective double-blinded randomized study tested the hypothesis that preoperative treatment with dexamethasone would attenuate inflammatory priming of the myocardium, reduce the systemic inflammatory reaction upon cardiac operation, and provide organ protection in neonates. METHODS: Twenty neonates (age, 8 to 21 days) with transposition of the great arteries scheduled for arterial switch operation were included. Nine received dexamethasone (1 mg/kg body weight) 4 hours before cardiopulmonary bypass, and 11 received natrium chloride. We studied intramyocardial messenger RNA expression of interleukin (IL)-6, IL-8, IL-1beta, and tumor necrosis factor-alpha (TNF-alpha), as well as IL-10 and expression of TNF-alpha on protein level in right atrial tissue taken before institution of CPB. We measured plasma levels of IL-6, IL-10, lipopolysaccharide binding protein, and cardiac troponin T. Cytokine expression was related to postoperative outcome. RESULTS: Pretreatment with dexamethasone led to a significant decrease in myocardial expression of IL-6, IL-8, IL-1beta, and TNF-alpha messenger RNA and to a decrease in protein synthesis of TNF-alpha. Plasma concentrations of IL-6 were significantly lower and those of IL-10 significantly higher in pretreated patients. This was associated with lower cardiac troponin T values and lower dobutamine requirement. Levels of lipopolysaccharide binding protein were significantly higher postoperatively in pretreated neonates. CONCLUSIONS: Dexamethasone administration before arterial switch operation leads to a shift in the myocardial and systemic cytokine expression profile in neonates with transposition of the great arteries, with downregulation of proinflammatory and upregulation of antiinflammatory cytokines. Lower myocardial cell damage and lower catecholamine requirement suggest myocardial protection in treated patients. [less ▲]

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See detailThe hypoxia-inducible factor HIF-1 promotes intramyocardial expression of VEGF in infants with congenital cardiac defects.
Qing, Ma; Gorlach, Agnes; SCHUMACHER, Katharina ULg et al

in Basic Research in Cardiology (2007), 102(3), 224-232

OBJECTIVES: The response to hypoxia is primarily mediated by the transcription factor hypoxia-inducible factor-1 (HIF-1) which leads to the induction of a variety of adaptive gene products including ... [more ▼]

OBJECTIVES: The response to hypoxia is primarily mediated by the transcription factor hypoxia-inducible factor-1 (HIF-1) which leads to the induction of a variety of adaptive gene products including vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS). This study was designed to test the hypothesis that HIF-1 and its target genes would be upregulated in the ventricular myocardium of infants with cyanotic congenital cardiac defects. METHODS: 14 infants with cyanotic (n = 7) or acyanotic cardiac defects (n = 7) were investigated. Samples from the right ventricular myocardium taken immediately after aortic clamping were studied for protein expression and DNA-binding activity. RESULTS: Protein levels of HIF-1alpha were significantly elevated in patients with cyanotic compared to acyanotic congenital heart disease and inversely correlated with the degree of hypoxemia. This response was accompanied by significantly enhanced HIF-1 DNA binding activity. Furthermore, protein levels of VEGF and eNOS were significantly higher in the myocardium of cyanotic than of acyanotic infants. To test the potential involvement of upstream regulatory pathways, activation of MAP kinases was determined. Intramyocardial levels of phosphorylated p38 MAP kinase, but not of ERK1/2 were significantly higher in infants with cyanotic compared to those with acyanotic congenital heart disease and inversely correlated to hypoxemia. CONCLUSIONS: These findings show that chronic hypoxemia is associated with the induction and stabilization of the transcription factor HIF-1 as well as its target genes VEGF and eNOS in the myocardium of infants with cyanotic cardiac defects. Thus, stabilization of HIF-1 and induction of the adaptive hypoxia response could particularly participate in myocardial remodeling in children with congenital cardiac defects and chronic hypoxemia. [less ▲]

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