Experimental Studies of Humoral and Cellular Immunological Parameters of Viral Heart Disease

1993 ◽  
pp. 233-274
Author(s):  
B. Maisch ◽  
M. Herzum
2017 ◽  
Vol 13 (3) ◽  
pp. 241-253
Author(s):  
Mohammed Khalifa Khudair ◽  
◽  
Mohammed Abdul Diam saleh ◽  
Naseer Hafedh Ibrahim

2004 ◽  
Vol 193 (2-3) ◽  
pp. 65-69 ◽  
Author(s):  
Matthias Pauschinger ◽  
Kumaran Chandrasekharan ◽  
Michel Noutsias ◽  
Uwe K�hl ◽  
Lothar Peter Schwimmbeck ◽  
...  

ESC CardioMed ◽  
2018 ◽  
pp. 44-49
Author(s):  
José M. Pérez-Pomares ◽  
José L. de la Pompa

The heart is the first functional organ of the vertebrate embryo, beginning to beat at around 4 weeks of gestation in humans. Tissue interactions orchestrate the complex patterning, proliferation, and differentiation processes that transform the embryonic cardiac primordium into the adult heart. During heart embryogenesis, cardiac mesoderm progenitor cells originate bilaterally during gastrulation and move rostrally to form the primitive heart tube, which will then loop towards the right and initiate septation to give rise to the mature four-chambered heart. Experimental studies in animal models have revealed the crucial role that a number of highly conserved signalling pathways, involving active molecular cross-talk between adjacent tissues, play in cardiac development, and how the alterations in these signalling mechanisms may cause congenital heart disease affecting the neonate or adult. Here, we describe briefly the knowledge gained on the molecular and cellular mechanisms underlying cardiac chamber and valve development and its implication in disease. This knowledge will ultimately facilitate the design of diagnostic and therapeutic strategies to treat congenital heart disease.


1984 ◽  
pp. 95-98 ◽  
Author(s):  
C. L. Miklozek ◽  
P. C. Come ◽  
H. D. Royal ◽  
C. S. Crumpacker ◽  
W. H. Abelmann

1995 ◽  
Vol 16 (suppl O) ◽  
pp. 25-27 ◽  
Author(s):  
P. Liu ◽  
J. Penninger ◽  
K. Aitken ◽  
M. Sole ◽  
T. Mak

2016 ◽  
pp. 99-113
Author(s):  
Bruce M. McManus ◽  
Michael Seidman ◽  
Karin Klingel ◽  
Honglin Luo

2019 ◽  
Author(s):  
Doa’a Al-u’datt ◽  
Bruce G Allen ◽  
Stanley Nattel

Abstract Heart diseases are a major cause of morbidity and mortality world-wide. Lysyl oxidase (LOX) and related LOX-like (LOXL) isoforms play a vital role in remodelling the extracellular matrix (ECM). The LOX family controls ECM formation by cross-linking collagen and elastin chains. LOX/LOXL proteins are copper-dependent amine oxidases that catalyse the oxidation of lysine, causing cross-linking between the lysine moieties of lysine-rich proteins. Dynamic changes in LOX and LOXL protein-expression occur in a variety of cardiac pathologies; these changes are believed to be central to the associated tissue-fibrosis. An awareness of the potential pathophysiological importance of LOX has led to the evaluation of interventions that target LOX/LOXL proteins for heart-disease therapy. The purposes of this review article are: (i) to summarize the basic biochemistry and enzyme function of LOX and LOXL proteins; (ii) to consider their tissue and species distribution; and (iii) to review the results of experimental studies of the roles of LOX and LOXL proteins in heart disease, addressing involvement in the mechanisms, pathophysiology and therapeutic responses based on observations in patient samples and relevant animal models. Therapeutic targeting of LOX family enzymes has shown promising results in animal models, but small-molecule approaches have been limited by non-specificity and off-target effects. Biological approaches show potential promise but are in their infancy. While there is strong evidence for LOX-family protein participation in heart failure, myocardial infarction, cardiac hypertrophy, dilated cardiomyopathy, atrial fibrillation and hypertension, as well as potential interest as therapeutic targets, the precise involvement of LOX-family proteins in heart disease requires further investigation.


2008 ◽  
Vol 33 (6) ◽  
pp. 1269-1283 ◽  
Author(s):  
Rob M. van Dam

Numerous epidemiological studies have evaluated the association between coffee consumption and risk of type 2 diabetes, coronary heart disease, and various cancers. This paper briefly reviews the evidence for a relation between coffee consumption and these conditions, with particular attention to methodological issues. Several early studies suggested that coffee consumption could result in a marked increase in risk of coronary heart disease and several types of cancer. However, more recent prospective cohort studies that are less prone to selection and information bias have not confirmed these findings. High consumption of unfiltered types of coffee, such as French press and boiled coffee, has been shown to increase low-density-lipoprotein-cholesterol concentrations. In addition, limiting caffeinated coffee intake during pregnancy seems a prudent choice. However, evidence has been accumulating that frequent consumption of coffee may reduce risk of type 2 diabetes and liver cancer. Further experimental studies are warranted to elucidate the underlying mechanisms and possibly identify the components in coffee that are responsible for these putative effects. In sum, the currently available evidence on coffee and risk of cardiovascular diseases and cancer is largely reassuring, and suggests that, for the general population, addressing other health-related behaviors has priority for the prevention of chronic diseases.


Pathology ◽  
1993 ◽  
Vol 25 (3) ◽  
pp. 326
Author(s):  
Bruce Warren

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