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To support higher education institutions, the Flemish Support Center for Inclusive Higher Education conducts research on inclusive higher education and studying with a disability. This article is about the insider's perspective of 8 students with a disability. Their experience on studying in higher education is questioned trough qualitative interviews. The results from the interviews are categorized in 5 themes: the higher education institution, the disability, studying, support and the power of the student. We can draw three main conclusions. First, the students experience a discrepancy between two aspects of inclusion: the structure and the culture. Second, the decision of students to disclose depends on the structural advantages and the negative consequences this may entail. Third, students experience that they often have to arrange their own support, which we can frame in a medical perspective on disability. [ABSTRACT FROM AUTHOR]

Plasminogen activator inhibitor type 1 (PAI-1) is a central regulator of fibrinolysis and tissue remodelling. PAI-1 belongs to the serpin superfamily and unlike other inhibitory serpins undergoes a spontaneous inactivation process under physiological conditions, termed latency transition. During latency transition the solvent exposed reactive centre loop is inserted into the central β-sheet A of the molecule, and is no longer accessible to reaction with the protease. More than three decades of research on mammalian PAI-1 has not been able to clarify the evolutionary advantage and physiological relevance of latency transition. In order to study the origin of PAI-1 latency transition, we produced PAI-1 from Spiny dogfish shark (Squalus acanthias) and African lungfish (Protopterus sp.), which represent central species in the evolution of vertebrates. Although human PAI-1 and the non-mammalian PAI-1 variants share only approximately 50 % sequence identity, our results showed that all tested PAI-1 variants undergo latency transition with a similar rate. Since the functional stability of PAI-1 can be greatly increased by substitution of few amino acid residues, we conclude that the ability to undergo latency transition must have been a specific selection criterion for the evolution of PAI-1. It appears that all PAI-1 molecules must harbour latency transition to fulfil their physiological function, stressing the importance to further pursue a complete understanding of this molecular phenomenon with possible implication to pharmacological intervention. Our results provide the next step in understanding how the complete role of this important protease inhibitor evolved along with the fibrinolytic system.