This study clarified thallium-201 (Tl) kinetics in the early stage after exercise in patients with ischemic heart disease (IHD). Tl was administered for 39 patients with IHD and eight normal subjects during maximal exercise. Immediately after exercise, dynamic data were obtained using a double slant-hole collimator at one frame/2 min for a 20 min period. The data of 10 frames (20 min) were spatially smoothed, and semiquantitative segmental analyses of the uptake and kinetics of Tl were performed by computer. In eight normal subjects, Tl uptake was uniform throughout the continuous 20 min, and Tl activity was unchanged throughout the 20 min period after exercise. Among 39 patients with IHD, 39 had Tl defects in the first frame (initial defect). Among 39 initial defects, 15 (38%) showed complete or partial early redistribution as early as 20 min and Tl activity in the defect increased (10.5 +/- 1.5%) over the 20 min period. Early redistribution occurred in 10 (43%) of 23 patients with effort angina and in five (83%) of six patients with variant forms of angina, but in no patients with myocardial infarction. Patients with early redistribution showed a greater frequency either of good collateral vessels or of mild stenosis of the coronary artery, compared with those who had no early redistribution. In conclusion, analysis of Tl kinetics in the early stages after exercise can provide important information about the coronary perfusion state during recovery from transient ischemia, and early redistribution may be a sign of preserved hyperemic flow in the ischemic region.
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Am J Physiol Cell Physiol
January 2025
Departments of Surgery and Oncology, University of Calgary Arnie Charbonneau Cancer Institute, University of Calgary.
Cancer cachexia is a multifaceted metabolic syndrome characterized by muscle wasting, fat redistribution, and metabolic dysregulation, commonly associated with advanced cancer but sometimes also evident in early-stage disease. More subtle body composition changes have also been reported in association with cancer, including sarcopenia, myosteatosis, and increased fat radiodensity. Emerging evidence reveals that body composition changes including sarcopenia, myosteatosis, and increased fat radiodensity, arise from distinct biological mechanisms and significantly impact survival outcomes.
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February 2025
Human-Machine Perception Laboratory, Department of Computer Science and Engineering, University of Nevada, Reno, Reno, NV, United States.
Spaceflight-Associated Neuro-Ocular Syndrome (SANS) presents a critical risk in long-duration missions, with microgravity-induced changes that threaten astronaut vision and mission outcomes. Current SANS monitoring, limited to pre- and post-flight exams, lacks in-flight diagnostics, highlighting an urgent need for autonomous tools capable of real-time assessment. Grok, an AI platform by xAI, offers promising potential as an advanced diagnostic tool for space-based health monitoring.
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Instituto de Investigación Médica Mercedes y Martín Ferreyra, INIMEC - Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional de Córdoba, Córdoba, Argentina.
Introduction: Post-translational modifications of proteins provide cellular physiology with a broad range of adaptability to the external environment flexibly and rapidly. In the case of the protozoan parasite , the study of these modifications has gained relevance in recent years, mainly focusing on methylation and deacetylation of proteins. This study investigates the significance of acetylation in this protozoan parasite.
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January 2025
Departamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de San Luis Potosí, San Luis Potosi, Mexico.
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January 2025
Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Members of the KMT2C/D-KDM6A complex are recurrently mutated in urothelial carcinoma and in histologically normal urothelium. Here, using genetically engineered mouse models, we demonstrate that Kmt2c/d knockout in the urothelium led to impaired differentiation, augmented responses to growth and inflammatory stimuli and sensitization to oncogenic transformation by carcinogen and oncogenes. Mechanistically, KMT2D localized to active enhancers and CpG-poor promoters that preferentially regulate the urothelial lineage program and Kmt2c/d knockout led to diminished H3K4me1, H3K27ac and nascent RNA transcription at these sites, which leads to impaired differentiation.
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