Unlabelled: Te aim of the study was to evaluate the temporal dynamics of brain CD68+ and stabilin-1+ macrophage infltration in patients with fatal myocardial infarction (MI) type 1.
Materials And Methods: Te study included 31 patients with fatal MI type I. Te control group comprised 10 patients of 18-40 age group who died from injuries incompatible with life. Patients with MI were divided into two groups. Group 1 comprised patients who died during the frst 72 hours of MI, group 2 comprised patients who died on days 4‒28. Macrophage infltration in the brain was assessed by immunohistochemical analysis. We used CD68 as a marker for the cells of the macrophage lineage and stabilin-1 as an M2-like macrophage biomarker.
Results: In group 1 the number of brain CD68+ macrophages was signifcantly higher than in the control group. In group 2 the intensity of brain CD68+ cells infltration was lower than in group 1 and higher than in the control group. Tere was a small amount of stabilin-1+ macrophages in the brain of healthy people, as well as of patients who died from MI. Tere were no signifcant differences in the number of stabilin-1+ cells between group 1 and group 2. Correlation analysis revealed the presence of positive correlation between the number of CD68 + macrophages in the infarct, peri-infarct, and non-infarct areas of the myocardium and the number of CD68+ macrophages in the brain in patients with MI. Tere were not correlations between the number of CD68 + and stabilin-1+ cells and the presence of diabetes mellitus, history of stroke, history of MI, and pre-infarction angina.
Conclusion: Te number of brain CD68+ macrophages signifcantly increased during the frst three days of MI. Te number of brain stabilin-1+ macrophages did not increase and did not differ from the control values. We observed a positive correlation between the number of CD68+ macrophages in the brain and myocardium.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.18087/cardio.2584 | DOI Listing |
J Neuroinflammation
January 2025
Spinal Cord and Brain Injury Research Center, Department of Physiology, College of Medicine, University of Kentucky, Lexington Kentucky, USA.
Objective: Therapeutic translation is challenging in spinal cord injury (SCI) and large animal models with high clinical relevance may accelerate therapeutic development. Pigs have important anatomical and physiological similarities to humans. Intraspinal inflammation mediates SCI pathophysiology.
View Article and Find Full Text PDFFront Immunol
January 2025
Institute for Experimental Immunology and Imaging, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Post-stroke early activation of neutrophils contributes to intensive neuroinflammation and worsens disease outcomes. Other pre-existing patient conditions can modify the extent of their activation during disease, especially hypercholesterolemia. However, whether and how increased circulating cholesterol amounts can change neutrophil activation responses very early after stroke has not been studied.
View Article and Find Full Text PDFTransl Lung Cancer Res
December 2024
Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China.
Background: Differences in the immune microenvironment and responses to immunotherapy may exist between primary non-small cell lung cancer (NSCLC) and brain metastases (BMs). This study aimed to investigate discrepancies in programmed death-ligand 1 (PD-L1) expression, tumor-infiltrating lymphocytes (TILs), tertiary lymphoid structures (TLS), and tumor mutational burden (TMB) between matched BMs and primary tumors (PTs) in NSCLC.
Methods: Twenty-six pairs of surgically resected BMs and corresponding PTs from NSCLC patients were collected.
Alzheimers Res Ther
January 2025
Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, A1B 3V6, Canada.
Background: Alzheimer's disease (AD) remains incurable, yet its long prodromal phase offers a crucial window for early intervention. Pretangle tau, a precursor to neurofibrillary tangles, plays a key role in early AD pathogenesis. Intervening in pretangle tau pathology could significantly delay the progression of AD.
View Article and Find Full Text PDFIntroduction: CLN8-Batten disease is a rare neurodegenerative disorder characterized phenotypically by progressive deterioration of motor and cognitive abilities, visual symptoms, epileptic seizures, and premature death. Mutations in CLN8 result in characteristic Batten disease symptoms and brain-wide pathology including accumulation of lysosomal storage material, gliosis, and neurodegeneration. Recent investigations of other subtypes of Batten disease (CLN1, CLN3, CLN6) have emphasized the influence of biological sex on disease and treatment outcomes; however, little is known about sex differences in the CLN8 subtype.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!