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Improvement of clinical and immunopathologic parameters in asthmatic children treated for concomitant chronic rhinosinusitis.
Effects of fexofenadine and other antihistamines on components of the allergic response: adhesion molecules.
Pancreatic β-cell tRNA hypomethylation and fragmentation link TRMT10A deficiency with diabetes
It is shown that tRNA guanosine 9 hypomethylation leads to t RNAGln fragmentation and that 5′-tRNAGln fragments mediate TRMT10A deficiency-induced β-cell death, which is relevant to monogenic and polygenic forms of diabetes.
DNAJC3 deficiency induces β-cell mitochondrial apoptosis and causes syndromic young-onset diabetes.
This report confirms previously described features and expands the clinical spectrum of syndromic DNAJC3 diabetes, one of the five monogenic forms of diabetes pertaining to the PERK pathway of the endoplasmic reticulum stress response.
Integrative transcriptomic and protein analysis of human bronchial BEAS-2B exposed to seasonal urban particulate matter.
Pancreatic β-cell protection from inflammatory stress by the endoplasmic reticulum proteins thrombospondin 1 and mesencephalic astrocyte-derived neutrotrophic factor (MANF)
It is shown that ER-localized THBS1 is cytoprotective to rat, mouse, and human β-cells exposed to cytokines or thapsigargin-induced ER stress and prevents the BH3-only protein BIM (BCL2-interacting mediator of cell death)-dependent triggering of the mitochondrial pathway of apoptosis.
Cytokine pattern in allergic and non‐allergic chronic rhinosinusitis in asthmatic children
This work has shown that Eosinophils and Th2 cells play a pathogenic mechanism in asthma, and the use of these cells in the treatment of rhinosinusitis is recommended.
YIPF5 mutations cause neonatal diabetes and microcephaly through endoplasmic reticulum stress
- E. De Franco, Maria Lytrivi, A. Hattersley
- Medicine, BiologyThe Journal of clinical investigation
- 9 November 2020
Neonatal diabetes is caused by single gene mutations reducing pancreatic β cell number or impairing β cell function. Understanding the genetic basis of rare diabetes subtypes highlights fundamental…
Anoctamin 1 is Apically Expressed on Thyroid Follicular Cells and Contributes to ATP- and Calcium-Activated Iodide Efflux
- Carmela Iosco, C. Cosentino, K. Rhoden
- Biology, MedicineCellular Physiology and Biochemistry
- 1 August 2014
ANO1 in thyrocytes functions as a calcium-activated channel mediating iodide efflux, and may contribute to the rapid delivery of iodide into the follicular lumen for the synthesis of thyroid hormones following activation by calcium-mobilizing stimuli.