References of "Habyarimana, Jean"
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See detailLes nouveaux outils de diagnostic et de pronostic de la myopathie atypique
Habyarimana, Jean ULg; BOEMER, François ULg; Amory, Hélène ULg et al

in Proceeding de la 41ème Journée de la Recherche équine (2015)

In equines, ingestion of hypoglycin A, a toxin produced in the seeds (samaras) of sycamore maple (Acer pseudoplatanus) tree alters the energetic metabolism of muscle cells and results in atypical myopathy ... [more ▼]

In equines, ingestion of hypoglycin A, a toxin produced in the seeds (samaras) of sycamore maple (Acer pseudoplatanus) tree alters the energetic metabolism of muscle cells and results in atypical myopathy (AM). This alterations leads to a characteristic biochemical profile of acylcarnitines (AC) that enables to confirm the diagnosis of AM. This study aims at validating a methodology for the dosage of hypoglycin A in vegetal extracts but also in blood. In addition, the biochemical profile in AC has been determined in AM cases (5 survivors and 13 deceased) and in 5 horses suffering from exercise-induced myopathy. The AC profiles of these horses have been compared to the one of healthy horses (n = 35). This study showed that hypoglycin A was present in seeds and spring seedlings of sycamore and also in blood of AM cases horses. In addition, the establishment of AC profile contributes to the diagnostic and helps to assess the prognosis of AM cases. [less ▲]

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See detailInfluenza A strain-dependent pathogenesis in fatal H1N1 and H5N1 infections of mice
Garigliany, Mutien-Marie ULg; Habyarimana, Jean ULg; Lambrecht, Bénédicte et al

in Emerging Infectious Diseases (2010), 16(4), 595-603

Two different influenza A viruses showing no pathogenicity towards the laboratory mouse were forced to evolve by serial passaging. Although both adapted viruses evoked diffuse alveolar damage and showed a ... [more ▼]

Two different influenza A viruses showing no pathogenicity towards the laboratory mouse were forced to evolve by serial passaging. Although both adapted viruses evoked diffuse alveolar damage and showed a similar 50% mouse lethal dose and the same peak lung concentration, they elicited dramatically different pathological signatures and ARDS courses. In the absence of any virus labeling, a histologist unaware of which infection he was looking at could readily distinguish infections caused by these two viruses. This suggests that fatal infections caused by different highly virulent influenza A viruses do not necessarily share the same pathogenesis. The different histological pictures shown here refute the hypothesis of a single, universal “cytokine storm” underlying all fatal influenzal diseases. Research is thus crucially needed to identify underlying sets of virulence markers and to examine whether it might be advantageous to tailor treatment to the influenza virus pathotype. [less ▲]

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