Publications by authors named "L PETERS"

We examined how thalamocortical connectivity structure reflects children's reading performance. Diffusion-weighted MRI at 3 T and a series of reading measures were collected from 64 children (33 girls) ages 8-14 years with and without dyslexia. The topological properties of the left and right thalamus were computed based on the whole-brain white matter network and a hub-attached reading network, and were correlated with scores on several tests of children's reading and reading-related abilities.

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Objectives: Window entrapment in cats can lead to reduced blood flow to the spinal cord, muscles and nerves, resulting in ischaemic neuromyelomyopathy. The severity and duration of entrapment greatly influence clinical and neurological outcomes, as well as prognosis. The aim of the present retrospective multicentric study (2005-2022) was to describe clinical, neurological and selected clinicopathological findings, as well as the outcome of cats trapped in bottom-hung windows, presented to both first-opinion and referral-only clinics.

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The aim of this article is to take an analytical look at Social Start-Ups as organizational discourse actors of a digitalization discourse in the field of social services. The digital transformation is understood as an all-encompassing socio-cultural phenomenon that gives rise to new discourse arenas in the field of social services, in which Social Start-Ups occupy a special position. So far, however, little is known about the actual role of Social Start-Ups in the digitization discourse of social service work, although they differ from established social services and thus occupy a special spokesperson position.

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Background: Somatic Symptom Disorder (SSD) is characterized by excessive thoughts, emotions, and behaviors related to physical symptoms irrespective of their etiology. Estimates of SSD frequency assessed via self-report questionnaires range between 6.7% (general population) and 53% (specialized setting).

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Aims/hypothesis: Immunotherapeutics targeting T cells are crucial for inhibiting autoimmune disease progression proximal to disease onset in type 1 diabetes. There is an outstanding need to augment the durability and effectiveness of T cell targeting therapies by directly restraining proinflammatory T cell subsets, while simultaneously augmenting regulatory T cell (Treg) activity. Here, we present a novel strategy for preventing diabetes incidence in the NOD mouse model using a blocking monoclonal antibody targeting the type 1 diabetes risk-associated T cell co-stimulatory receptor, CD226.

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