Publications by authors named "R J Bridges"
Article Synopsis
- There is a significant need for new treatments targeting diseases caused by premature termination codons (PTCs), which lead to faulty proteins.
- Splice-switching antisense oligonucleotides (ASOs) can help by inducing exon skipping, effectively removing PTCs from mRNA and potentially restoring protein function if the remaining exons are in the correct reading frame.
- The research focuses on the cystic fibrosis transmembrane regulator (CFTR) gene, demonstrating that ASOs can restore CFTR function in airway cells from individuals with PTC-causing mutations, showing the potential for ASO therapies across similar multi-exon genes.
Background & Aims: Endoscopic retrograde cholangiopancreatography (ERCP)-related adverse events (AEs) are associated with morbidity, mortality, and health care expenditure. We aimed to assess incidences and comparisons of ERCP AEs.
Methods: We included studies performed after 2000 reporting on ERCP AEs from database inception through March 12, 2024.
Introduction: Clinically significant post-endoscopic retrograde cholangiopancreatography (ERCP) bleeding (CSPEB) is common. Contemporary estimates of risk are lacking. We aimed to identify risk factors of and outcomes after CSPEB.
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- Clinically significant post-endoscopic retrograde cholangiopancreatography (ERCP) bleeding (CSPEB) occurs in about 1.5% of procedures, often following higher-risk interventions like sphincterotomies, with patients frequently needing endoscopy and transfusions.
- Key risk factors for CSPEB include the use of antiplatelet medications (like P2Y12 inhibitors) and anticoagulants (like warfarin and dabigatran), which significantly increase the likelihood of bleeding.
- The study suggests that endoscopists may underestimate the bleeding risks associated with these medications, emphasizing the need for improved management of antithrombotic therapy during the periprocedural period to enhance
Cystic fibrosis results from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel, ultimately leading to diminished transepithelial anion secretion and mucociliary clearance. CFTR correctors are therapeutics that restore the folding/trafficking of mutated CFTR to the plasma membrane. The large-conductance calcium-activated potassium channel (BKCa, KCa1.
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