One of the most common causes of morbidity and mortality worldwide is ischemic stroke. Historically, an animal model used to stimulate ischemic stroke involves middle cerebral artery occlusion (MCAO). Infarct zone, brain edema and blood-brain barrier (BBB) breakdown are measured as parameters that reflect the extent of brain injury after MCAO. A significant limitation to this method is that these measurements are normally obtained in different rat brain samples, leading to ethical and financial burdens due to the large number of rats that need to be euthanized for an appropriate sample size. Here we present a method to accurately assess brain injury following MCAO by measuring infarct zone, brain edema and BBB permeability in the same set of rat brains. This novel technique provides a more efficient way to evaluate the pathophysiology of stroke.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.3791/61309 | DOI Listing |
Front Neurol
January 2025
Department of Neurosurgery, Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Objective: The relationship between small subcortical ischemic infarction remains poorly characterized. Therefore, the present study aimed to investigate the association between artery-to-artery embolization and small subcortical infarctions.
Methods: This retrospective observational cross-sectional study enrolling 230 patients with acute middle cerebral artery (MCA) stroke classified into the microembolic signals-positive (MES+) and MES-negative (MES-) groups.
Eur J Pharmacol
January 2025
Department of Basic Medicine, Institute of Respiratory Diseases Xiamen Medical College, Xiamen Medical College, Xiamen, Fujian 361023, P. R. China; State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin Medical University, Harbin, Heilongjiang 150081, P. R. China. Electronic address:
ITFG2 is an intracellular protein known to modulate the immune response of T-cells. Our previous investigation revealed that ITFG2 specifically targets ATP5b to regulate ATP energy metabolism and maintain mitochondrial function, thereby protecting the heart from ischemic injury. However, the role of ITFG2 in ischemic ventricular arrhythmias and its underlying mechanisms have not been previously reported.
View Article and Find Full Text PDFAm J Emerg Med
January 2025
Instituto Nacional de Cardiología Ignacio Chávez, Coronary Care Unit, Juan Badiano 1, Sección XVI, Tlalpan 14080, Ciudad De México, Mexico.
Introduction: Earthquakes are unpredictable natural events that can elicit acute physiological responses, potentially triggering cardiovascular events. This study investigates the association between seismic activity and ST-elevation myocardial infarction (STEMI) admissions in a tertiary care hospital in an earthquake-prone region over 19 years.
Methods: We analyzed STEMI admissions at a tertiary center in Mexico City from October 2005 to August 2024.
Acta Pharmacol Sin
January 2025
Department of Pharmacology, National Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Medicine Research, Ministry of Education, College of Pharmacy, Harbin Medical University, Harbin, 150086, China.
Eukaryotic translation initiation factor 4A1 (eIF4A1) is an ATP-dependent RNA helicase that participates in a variety of biological and pathological processes such as cell proliferation and apoptosis, and cancer. In this study we investigated the role of eIF4A1 in ischemic heart disease. The myocardial ischemia/reperfusion (I/R) model was established in mice by ligation of the left anterior descending artery for 45 min with the subsequent reperfusion for 24 h; cultured neonatal mouse ventricular cardiomyocytes (NMVCs) treated with HO (200 μM) or H/R (12 h hypoxia and 12 h reoxygenation) were used for in vitro study.
View Article and Find Full Text PDFCurr Issues Mol Biol
January 2025
Institute of Experimental Medicine, Almazov National Medical Research Centre, 15B Parkhomenko Street, 194021 Saint Petersburg, Russia.
Myocardial ischemia-reperfusion injury increases myocardial microvascular permeability, leading to enhanced microvascular filtration and interstitial fluid accumulation that is associated with greater microvascular obstruction and inadequate myocardial perfusion. A burst of reactive oxygen species and inflammatory mediators during reperfusion causes myosin light chain kinase (MLCK)-dependent endothelial hyperpermeability, which is considered a preventable cause of reperfusion injury. In the present study, a single intravenous injection of MLCK peptide inhibitor PIK7 (2.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!