scholarly journals THE OCCURRENCE OF LEUCOCYTE-PLATELET THROMBOSIS IN RHEUMATIC CARDITIS

1951 ◽  
Vol 94 (6) ◽  
pp. 493-500 ◽  
Author(s):  
Chandler A. Stetson
Keyword(s):  
Rheumatic Fever ◽  
Blood Vessels ◽  
Vascular Lesions ◽  
Rheumatic Carditis ◽  
Platelet Thrombi ◽  
Coronary Blood Vessels

Leucocyte-platelet thrombi, involving the smaller branches of the coronary blood vessels, have been found in the hearts of patients with active rheumatic fever and rheumatic carditis. A consistent correlation has been observed between the existence of these vascular lesions and the presence of typical Aschoff bodies. It is suggested that these cellular thrombi may play a role in the pathogenesis of rheumatic carditis.

scholarly journals THE INDUCTION OF RHEUMATIC-LIKE CARDIAC LESIONS IN RABBITS BY REPEATED FOCAL INFECTIONS WITH GROUP A STREPTOCOCCI

1950 ◽  
Vol 91 (5) ◽  
pp. 485-498 ◽  
Author(s):  
George E. Murphy ◽  
Homer F. Swift
Keyword(s):  
Rheumatic Fever ◽  
Human Serum ◽  
Blood Vessels ◽  
Vascular Lesions ◽  
Group A Streptococci ◽  
Cardiac Valves ◽  
Striking Resemblance ◽  
Cardiac Lesions ◽  
Group A

Cardiac lesions like those characteristic of rheumatic fever in man have been induced in a small portion of rabbits that were subjected to successive focal infections with group A streptococci of several serological types. Fresh myocardial interstitial granulomata so induced bear striking resemblance to Aschoff bodies, the histologic hallmarks of human active rheumatic fever; and the fresh and healed lesions found in the cardiac valves, endocardia, epicardia, blood vessels, and aortae of some of these rabbits are homologous with those characteristic of rheumatic fever in man. These experimental myocardial and vascular lesions and those of human rheumatic fever differ in several important respects from the lesions of experimental and human serum disease.

A Device for the Production of Well-Defined Lesions of Mesenteric Blood Vessels with Resulting Platelet Thrombi

1966 ◽  
Vol 15 (03/04) ◽  
pp. 471-475 ◽  
Author(s):  
K Reber
Keyword(s):  
Blood Vessels ◽  
Microscopic Observation ◽  
Electric Stimulation ◽  
Platelet Thrombi ◽  
Reproducible Manner

SummaryWell-defined lesions of mesenteric blood vessels with resulting platelet thrombi are produced in a reproducible manner by electric stimulation with a microelectrode under microscopic observation. The apparatus used and the results obtained are described.

scholarly journals Coronary blood vessels from distinct origins converge to equivalent states during mouse and human development

2021 ◽  
Author(s):  
Ragini S Phansalkar ◽  
Josephine Krieger ◽  
Mingming Zhao ◽  
Sai Saroja Kolluru ◽  
Robert C Jones ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Cell Fate ◽  
Adult Mouse ◽  
Coronary Vessels ◽  
Lineage Tracing ◽  
Specific Gene ◽  
Cell Type ◽  
Functional Differences ◽  
Coronary Blood Vessels ◽  
Two Populations

Most cell fate trajectories during development follow a diverging, tree-like branching pattern, but the opposite can occur when distinct progenitors contribute to the same cell type. During this convergent differentiation, it is unknown if cells "remember" their origins transcriptionally or whether this influences cell behavior. Most coronary blood vessels of the heart develop from two different progenitor sources-the endocardium (Endo) and sinus venosus (SV)-but whether transcriptional or functional differences related to origin are retained is unknown. We addressed this by combining lineage tracing with single-cell RNA sequencing (scRNAseq) in embryonic and adult mouse hearts. Shortly after coronary development begins, capillary ECs transcriptionally segregated into two states that retained progenitor-specific gene expression. Later in development, when the coronary vasculature is well-established but still remodeling, capillary ECs again segregated into two populations, but transcriptional differences were related to tissue localization rather than lineage. Specifically, ECs in the heart septum expressed genes indicative of increased local hypoxia and decreased blood flow. Adult capillary ECs were more homogeneous and lacked indications of either lineage or location. In agreement, SV- and Endo-derived ECs in adult hearts displayed similar responses to injury. Finally, scRNAseq of developing human coronary vessels indicated that the human heart followed similar principles. Thus, over the course of development, transcriptional heterogeneity in coronary ECs is first influenced by lineage, then by location, until heterogeneity disappears in the homeostatic adult heart. These results highlight the plasticity of ECs during development, and the validity of the mouse as a model for human coronary development.

Abstract 237: PRMT1-p53-Slug Axis Regulates Epicardial EMT and Ventricular Development

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Olan Jackson-Weaver ◽  
Jian Wu ◽  
Yongchao Gou ◽  
Yibu Chen ◽  
Meng Li ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Heart Development ◽  
Cultured Cells ◽  
Migration And Invasion ◽  
P53 Expression ◽  
Epicardial Cells ◽  
Coronary Blood Vessels

Rationale: Epicardial epithelial-to-mesenchymal trasition (EMT) is a vital process in embryonic heart development. During EMT, epicardial cells acquire migratory and invasive properties, and differentiate into new cell types, including cardiac fibroblasts and coronary smooth muscle cells. Non-histone protein methylation is an emerging modulator of cell signaling. We have recently established a role for protein arginine methyltransferase-1 (PRMT1) in TGF-β-induced EMT in cultured cells. Objective: To determine the role of PRMT1 in epicardial EMT. Methods and Results: We investigated the role of PRMT1 in epicardial EMT in mouse epicardial cells. Embryonic day 9.5 (E9.5) tamoxifen administration of WT1-Cre ERT ;PRMT1 fl/fl ;ROSA-YFP fl/fl mouse embryos was used to delete PRMT1 in the epicardium. Epicardial PRMT1 deletion led to reduced epicardial migration into the myocardium, a thinner compact myocardial layer, and dilated coronary blood vessels at E15.5. Using the epicardial cell line MEC1, we found that PRMT1 siRNA prevented the increase in mesenchymal proteins Slug and Fibronectin and the decrease in epithelial protein E-Cadherin during TGF-β treatment-induced EMT. PRMT1 siRNA also reduced the migration and invasion of MEC1 cells. We further identified that PRMT1 siRNA also increased the expression of p53, a key regulator of the Slug degradation pathway. PRMT1 siRNA increases p53 expression by decreasing p53 degradation, and shifted p53 localization to the cytoplasm. In vitro methylation assays further demonstrated that PRMT1 methylates p53. Knockdown of p53 increased Slug levels and enhanced EMT, establishing p53 as a regulator of epicardial EMT through controlling Slug expression. Furthermore, RNAseq experiments in MEC1 cells demonstrated that 40% (545/1,351) of TGF-β-induced transcriptional changes were prevented by PRMT1 siRNA. Furthermore, when p53 and PRMT1 were simultaneously knocked down, TGF-β induced transcriptional control of 37% (201/545) of these PRMT1-dependent genes was restored. Conclusions: The PRMT1-p53-Slug pathway is necessary for epicardial EMT in cultured MEC1 cells as well as in the epicardium in vivo . Epicardial PRMT1 is required for the development of compact myocardium and coronary blood vessels.

QT dispersion in acute rheumatic fever

2006 ◽  
Vol 16 (2) ◽  
pp. 141-146 ◽  
Author(s):  
Tugcin Bora Polat ◽  
Yalim Yalcin ◽  
Celal Akdeniz ◽  
Cenap Zeybek ◽  
Abdullah Erdem ◽  
...  
Keyword(s):  
Rheumatic Fever ◽  
Acute Rheumatic Fever ◽  
Qt Dispersion ◽  
Control Group ◽  
Healthy Children ◽  
Rheumatic Carditis ◽  
Normal Children ◽  
A Value ◽  
The Mean

Background:Disturbances of conduction are well known in the setting of acute rheumatic fever. The aim of this study is to investigate the QT dispersion as seen in the surface electrocardiogram of children with acute rheumatic fever.Methods:QT dispersion was quantitatively evaluated in 88 children with acute rheumatic fever. Patients were divided into two groups based on the absence or presence of carditis. As a control group, we studied 36 healthy children free of any disease, and matched for age with both groups. Repeat echocardiographic examinations were routinely scheduled in all patients at 3 months after the initial attack to study the evolution of valvar lesions.Results:The mean QT dispersion was significantly higher in children with rheumatic carditis. But there was no statistical difference between children without carditis and normal children. Among the children with carditis, the mean dispersion was higher in those with significant valvar regurgitation. Dispersion of greater than 55 milliseconds had a sensitivity of 85%, and specificity of 70%, in predicting rheumatic carditis, while a value of 65 milliseconds or greater had sensitivity of 81% specificity of 85% in predicting severe valvar lesions in acute rheumatic carditis. At follow-up examination, a clear reduction on the QT dispersion was the main finding, reflecting an electrophysiological improvement.Conclusions:These observations suggest that QT dispersion is increased in association with cardiac involvement in children with acute rheumatic fever.

Bio-Inspired Active Electrolocation Sensors for Inspection of Tube Systems

2012 ◽  
Vol 84 ◽  
pp. 45-50 ◽  
Author(s):  
Martin Gottwald ◽  
Gerhard von der Emde
Keyword(s):  
Blood Vessels ◽  
Electric Fields ◽  
Skin Surface ◽  
Ring Electrode ◽  
Weakly Electric Fish ◽  
Atherosclerotic Lesions ◽  
Electric Image ◽  
Coronary Blood Vessels ◽  
Weakly Electric ◽  
Gnathonemus Petersii

At night, weakly electric fish Gnathonemus petersii use active electrolocation to scan their environment with self generated electric fields. Nearby objects distort the electric fields and are recognized as electric images on the electroreceptive skin surface of the animal. By analyzing the electric image, G. petersii can sense an object’s distance, dimensions and electrical properties. The principles and algorithms of active electrolocation can be applied to catheter-based sensor systems for analysing wall changes in fluid filled tube systems, for example atherosclerotic plaques of the coronary blood vessels. We used a basic atherosclerosis model of synthetic blood vessels and plaques, which were scanned with a ring electrode catheter applying active electrolocation. Based on the electric images of the plaques and the evaluation of bio-inspired image parameters, the plaque’s fine-structure could be assessed. Our results show that imaging through active electrolocation principally has the potential to detect and characterize atherosclerotic lesions.

An Angiomyomatous Hamartoma With Features of Vascular Transformation of Sinuses in the Mediastinal Lymph Node of a Beagle Dog

2020 ◽  
Vol 48 (8) ◽  
pp. 1017-1024
Author(s):  
Sophie Nelissen ◽  
Ronnie Chamanza
Keyword(s):  
Smooth Muscle ◽  
Lymph Node ◽  
Lymph Nodes ◽  
Blood Vessels ◽  
Mediastinal Lymph Node ◽  
Smooth Muscle Actin ◽  
Fibrous Tissue ◽  
Vascular Lesions ◽  
Positive Staining ◽  
Beagle Dog

Two similar benign, nonneoplastic vascular lesions have been described in the lymph nodes of humans and animals: angiomyomatous hamartoma (AMH), which is characterized by the replacement of lymphoid tissue by blood vessels, smooth muscle, and fibrous tissue, and vascular transformation of sinuses (VTS), which is considered a reactive transformation of lymph node sinuses into capillary-like vascular channels. We hereby report a lesion with features common to both lesions in the mediastinal lymph nodes of a 1-year-old beagle dog in a 1-month toxicity study. Grossly, enlargement and red discoloration were observed, while microscopically, the lesion was characterized by effacement of the lymph node parenchyma with replacement by mature blood vessels, smooth muscle, and fibrous tissue, associated with lymphoid atrophy, which is consistent with AMH. However, multifocal areas of anastomosing or plexiform capillary-like channels lined by normal to slightly plump endothelium, similar to those described for VTS, were also present. Immunohistochemistry analysis revealed abundant positive staining for smooth muscle actin and endothelial cells (von Willebrand factor/factor VIII) and the absence of proliferation (Ki67). In conclusion, these lesions most likely represent a mixture of both AMH and VTS.

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