Adult learning in veterinary education: theory to practice

This paper argues the case for the Increased application of adult learning principles to veterinary education. It encapsulates evidence from the United Kingdom, Europe, North America, and Australia to explain why it has taken veterinary schools so long to transform their curricula to best facilitate the development of lifelong learning skills, such as Independent and self-directed learning, problem solving, and critical thinking. Despite the variation in training programs In these different regions, the paper identifies common Issues-conflicting educational paradigms and the need for faculty development-and ultimately concludes that professional and continuing education should be viewed as a continuous process, supporting the adult learner's cognitive development and facilitated through experiential learnin

Recurrent subacute post-viral onset of ataxia associated with a PRF1 mutation

Inflammation is an important contributor to pediatric and adult neurodegeneration. Understanding the genetic determinants of neuroinflammation provides valuable insight into disease mechanism. We characterize a disorder of recurrent immune-mediated neurodegeneration. We report two sisters who presented with neurodegeneration triggered by infections. The proband, a previously healthy girl, presented at 22.5 months with ataxia and dysarthria following mild gastroenteritis. MRI at onset showed a symmetric signal abnormality of the cerebellar and peritrigonal white matter. Following a progressive course of partial remissions and relapses, she died at 5 years of age. Her older sister had a similar course following varicella infection, she died within 13 months. Both sisters had unremarkable routine laboratory testing, with exception of a transient mild cytopenia in the proband 19 months after presentation. Exome sequencing identified a biallelic perforin1 mutation (PRF1; p.R225W) previously associated with familial hemophagocytic lymphohistiocytosis (FHL). In contrast to FHL, these girls did not have hematopathology or cytokine overproduction. However, 3 years after disease onset, the proband had markedly deficient interleukin-1 beta (IL-1β) production. These observations extend the spectrum of disease associated with perforin mutations to immune-mediated neurodegeneration triggered by infection and possibly due to primary immunodeficiency