Influence of gender and age on the Nasality Severity Index 2.0 in Dutch-speaking Flemish children and adults

This study aimed to explore the influence of gender and age on the Nasality Severity Index 2.0 (NSI 2.0), an instrumental multiparametric index to determine hypernasality. Additionally, reference values will be established for this new index. Influence of gender and age on the NSI 2.0 was explored in 80 Flemish-speaking children (4-12 years; 40 boys, 40 girls) and 60 Flemish-speaking adults (18-60 years, 30 men, 30 women) without resonance disorders by determining its incorporated acoustic parameters: nasalance of the vowel/u/and an oral text, determined by a Nasometer, and voice low tone to high tone ratio (VLHR) of the vowel/i/. The equation yields NSI 2.0=13.20-(0.0824 x nasalance/u/(%))-(0.26 x nasalance oral text (%))-(0.242 x VLHR/i/4.47*F0Hz (dB)). No effect of gender or age was found on the NSI 2.0 in children. However, significant differences were found for the NSI 2.0, nasalance of/u/and an oral text between adult men and women. Additionally, an interaction effect between gender and age was found for these parameters. Consequently, separate reference values for the NSI 2.0 in children, adult men and adult women were established. Based on these reference scores, deviation of the NSI 2.0 score in patients with resonance disorders can be defined, which can determine the need for (additional) intervention. Further research can explore the possible influence of language on the index

Gasdermin D independent canonical inflammasome responses cooperate with caspase-8 to establish host defense against gastrointestinal Citrobacter rodentium infection

Abstract Citrobacter rodentium is an enteropathogen that causes intestinal inflammatory responses in mice reminiscent of the pathology provoked by enteropathogenic and enterohemorrhagic Escherichia coli infections in humans. C. rodentium expresses various virulence factors that target specific signaling proteins involved in executing apoptotic, necroptotic and pyroptotic cell death, suggesting that each of these distinct cell death modes performs essential host defense functions that the pathogen aims to disturb. However, the relative contributions of apoptosis, necroptosis and pyroptosis in protecting the host against C. rodentium have not been elucidated. Here we used mice with single or combined deficiencies in essential signaling proteins controlling apoptotic, necroptotic or pyroptotic cell death to reveal the roles of these cell death modes in host defense against C. rodentium. Gastrointestinal C. rodentium infections in mice lacking GSDMD and/or MLKL showed that both pyroptosis and necroptosis were dispensable for pathogen clearance. In contrast, while RIPK3-deficient mice showed normal C. rodentium clearance, mice with combined caspase-8 and RIPK3 deficiencies failed to clear intestinal pathogen loads. Although this demonstrated a crucial role for caspase-8 signaling in establishing intestinal host defense, Casp8–/–Ripk3–/– mice remained capable of preventing systemic pathogen persistence. This systemic host defense relied on inflammasome signaling, as Casp8–/–Ripk3–/– mice with combined caspase-1 and -11 deletion succumbed to C. rodentium infection. Interestingly, although it is known that C. rodentium can activate the non-canonical caspase-11 inflammasome, selectively disabling canonical inflammasome signaling by single caspase-1 deletion sufficed to render Casp8–/–Ripk3–/– mice vulnerable to C. rodentium-induced lethality. Moreover, Casp8–/–Ripk3–/– mice lacking GSDMD survived a C. rodentium infection, suggesting that pyroptosis was not crucial for the protective functions of canonical inflammasomes in these mice. Taken together, our mouse genetic experiments revealed an essential cooperation between caspase-8 signaling and GSDMD-independent canonical inflammasome signaling to establish intestinal and systemic host defense against gastrointestinal C. rodentium infection

Vorming, training en opleiding als middel om langer te blijven werken. Een kwalitatief onderzoek in de Vlaamse voedingssector /

Master of Science in de handelswetenschappe

Unique human immune signature of Ebola virus disease in Guinea.

Despite the magnitude of the Ebola virus disease (EVD) outbreak in West Africa, there is still a fundamental lack of knowledge about the pathophysiology of EVD. In particular, very little is known about human immune responses to Ebola virus. Here we evaluate the physiology of the human T cell immune response in EVD patients at the time of admission to the Ebola Treatment Center in Guinea, and longitudinally until discharge or death. Through the use of multiparametric flow cytometry established by the European Mobile Laboratory in the field, we identify an immune signature that is unique in EVD fatalities. Fatal EVD was characterized by a high percentage of CD4(+) and CD8(+) T cells expressing the inhibitory molecules CTLA-4 and PD-1, which correlated with elevated inflammatory markers and high virus load. Conversely, surviving individuals showed significantly lower expression of CTLA-4 and PD-1 as well as lower inflammation, despite comparable overall T cell activation. Concomitant with virus clearance, survivors mounted a robust Ebola-virus-specific T cell response. Our findings suggest that dysregulation of the T cell response is a key component of EVD pathophysiology