The concept of limiting irreversible damage due to ischemic arrest by inhibiting nucleoside breakdown was tested in the isolated perfused rat heart. Functional recovery measurements were combined with continuous high-energy phosphate measurements by means of 31P nuclear magnetic resonance (NMR) and with nucleoside release measurements in the reperfusion period. The adenosine deaminase inhibitors erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA) and 2'-deoxycoformycin (DCF) were given 5 min before ischemia and for the first 5 min of reperfusion. These treated groups were compared with a control, untreated group. These were further compared with a group of hearts arrested with potassium and to a group combining potassium arrest and EHNA. It was found that all treated groups recovered mechanical function significantly better than the untreated group. DCF, K+, and K+ + EHNA slowed ATP decline and resulted in better ATP recovery than untreated or EHNA-treated, and all treatments decreased nucleoside base release. Intracellular pH fell equally in all groups and recovered to preischemic values. Thus, these adenosine deaminase inhibitors improve functional recovery following ischemia, although this improvement was not well correlated with purine losses observed during reperfusion.
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http://dx.doi.org/10.1097/00005344-198311000-00019 | DOI Listing |
World J Surg Oncol
January 2025
Department of Hepatobiliary and Pancreas, Affiliated Hospital of Qingdao University, NO.1677 Wutaishan Road, Qingdao, Shandong Province, 266555, China.
Background: With the rising diagnostic rate of gallbladder polypoid lesions (GPLs), differentiating benign cholesterol polyps from gallbladder adenomas with a higher preoperative malignancy risk is crucial. This study aimed to establish a preoperative prediction model capable of accurately distinguishing between gallbladder adenomas and cholesterol polyps using machine learning algorithms.
Materials And Methods: We retrospectively analysed the patients' clinical baseline data, serological indicators, and ultrasound imaging data.
Methods Enzymol
January 2025
Department of Chemistry, Washington University in St. Louis, MO, United States. Electronic address:
Adenosine-to-inosine (A-to-I) editing, catalyzed by adenosine deaminases acting on RNA (ADARs), is a prevalent post-transcriptional modification that is vital for numerous biological functions. Given that this modification impacts global gene expression, RNA localization, and innate cellular immunity, dysregulation of A-to-I editing has unsurprisingly been linked to a variety of cancers and other diseases. However, our current understanding of the underpinning mechanisms that connect dysregulated A-to-I editing and disease processes remains limited.
View Article and Find Full Text PDFMethods Enzymol
January 2025
Medical University of Vienna, Center of Anatomy and Cell Biology, Division of Cell and Developmental Biology, Schwarzspanier Strasse, Vienna, Austria. Electronic address:
Adenosine to inosine deaminases acting on RNA (ADARs) enzymes are found in all metazoa. Their sequence and protein organization is conserved but also shows distinct differences. Moreover, the number of ADAR genes differs between organisms, ranging from one in flies to three in mammals.
View Article and Find Full Text PDFMethods Enzymol
January 2025
Natural Products Research Center, Chengdu Institute of Biology, Chinese Academy of Science, Chengdu, P.R. China. Electronic address:
As a promising therapeutic approach, the RNA editing process can correct pathogenic mutations and is reversible and tunable, without permanently altering the genome. RNA editing mediated by human ADAR proteins offers unique advantages, including high specificity and low immunogenicity. Compared to CRISPR-based gene editing techniques, RNA editing events are temporary, which can reduce the risk of long-term unintended side effects, making off-target edits less concerning than DNA-targeting methods.
View Article and Find Full Text PDFMethods Enzymol
January 2025
Raymond and Beverly Sackler School of Physics and Astronomy, Tel Aviv University, Tel Aviv, Israel. Electronic address:
A-to-I RNA editing is an RNA modification that alters the RNA sequence relative to the its genomic blueprint. It is catalyzed by double-stranded RNA-specific adenosine deaminase (ADAR) enzymes, and contributes to the complexity and diversification of the proteome. Advancement in the study of A-to-I RNA editing has been facilitated by computational approaches for accurate mapping and quantification of A-to-I RNA editing based on sequencing data.
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