Sarah J. Richardson

The paper confirms non-neuronal Tau expression in multiple tissues of humans and mice using validated antibodies and tissue microarrays.

This study uses histopathological scoring and AI analysis to map the progression of pancreatic changes in cystic fibrosis across age, identifying key fibrotic and fatty tissue transformations linked to exocrine and endocrine dysfunction.

This study performs a genome-wide association study of T1D stratified by HLA DR3 and DR4 status, revealing genetic and biological heterogeneity in T1D progression.

Image analysis of 262,832 pancreatic endocrine objects across 220 donors reveals that small beta-cell-only clusters are abundant in early childhood but virtually absent in type 1 diabetes.

This study shows that EVs deplete GGA2 in beta cells, causing Golgi acidification and altering the MHC class I immunopeptidome through premature cathepsin activation.

This study characterizes native human pancreatic mesenchymal stromal cells (npMSCs) in type 1 diabetes, finding increased npMSC density around insulin-containing islets and reduced density around insulin-deficient islets in diabetic individuals.

This study shows that IFN-α increases HLA-B-restricted antigen presentation in pancreatic β-cells, potentially influencing T1D pathogenesis.

The paper quantifies DNA methylation changes in human fetal pancreas development, identifying developmental differentially methylated positions and their genomic distribution.

This paper evaluates 53 Tau antibodies for Western blot and immunohistochemistry, identifying those with high specificity and sensitivity for detecting Tau, including low-level and modified forms.

The paper identifies non-coding mutations in a regulatory element of HK1 that lead to inappropriate expression in pancreatic beta-cells and cause congenital hyperinsulinism.