Publications by authors named "Dana Bronte-Tinkew"
Vitamin D deficiency enhances expression of autophagy-regulating miR-142-3p in mouse and "involved" IBD patient intestinal tissues.
Am J Physiol Gastrointest Liver Physiol
August 2021
Vitamin D deficiency is an environmental factor involved in the pathogenesis of inflammatory bowel disease (IBD); however, the mechanisms surrounding its role remain unclear. Previous studies conducted in an intestinal epithelial-specific vitamin D receptor (VDR) knockout model suggest that a lack of vitamin D signaling causes a reduction in intestinal autophagy. A potential link between vitamin D deficiency and dysregulated autophagy is microRNA (miR)-142-3p, which suppresses autophagy.
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- A study analyzed blood samples from 1005 children with inflammatory bowel diseases (IBDs) to assess the prevalence of single-gene variants, known as monogenic IBD.
- The researchers found rare variants associated with monogenic IBD in 31 children, representing about 3% of the cohort, with distinct symptoms and earlier onset in those affected.
- Key findings included specific symptoms linked to different types of monogenic IBD and a notable correlation between early onset, family history of autoimmune disease, and extra-intestinal manifestations.
Helicobacter pylori (H. pylori) is the causative agent of gastric cancer, making it the only bacterium to be recognized as a Class I carcinogen by the World Health Organization. The virulence factor cytotoxin associated gene A (CagA) is a known oncoprotein that contributes to the development of gastric cancer.
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- Peroxisome biogenesis disorders (PBDs) are metabolic issues caused by the loss of peroxisomes, often due to mutations in genes responsible for a complex (AAA-complex) involved in protein import.
- Instead of halting matrix protein import, loss of the AAA-complex leads to increased degradation of peroxisomes via a process called pexophagy.
- By inhibiting autophagy, researchers can restore peroxisome numbers and function, highlighting the potential for new treatments for PBDs based on these findings.
Background & Aims: Severe malnutrition in young children is associated with signs of hepatic dysfunction such as steatosis and hypoalbuminemia, but its etiology is unknown. Peroxisomes and mitochondria play key roles in various hepatic metabolic functions including lipid metabolism and energy production. To investigate the involvement of these organelles in the mechanisms underlying malnutrition-induced hepatic dysfunction we developed a rat model of malnutrition.
View Article and Find Full Text PDFPersistent infection with Helicobacter pylori confers an increased risk for the development of gastric cancer. However, the exact mechanisms whereby this bacterium causes carcinogenesis have not been completely elucidated. Recent evidence indicates that aberrant activation of the signal transducers and activators of transcription 3 (STAT3) signaling pathway may play a role in gastric carcinogenesis.
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