In humans prion diseases can occur sporadically, through genetic mutations, or can be transmitted from animal, human (kuru disease), or iatrogenic sources. Even though transmissible forms are the most well-known, the sporadic and heritable forms are much more frequent, accounting for about 85% of all cases. The purpose of this case report is to present an atypical variant CJD in a 26 years-old woman. The patient died secondary to infectious complications caused by an acute overdose with alcohol, beta-blockers and oral anti-diabetic drugs, and had an atypical neuropathology pattern, with absent amyloid plaques, but present focal, perivascular deposits of amyloid precursor protein and a positive immunohistochemical reaction for prp.
In the cardiac remodelling game, the casting is represented by certain players in form of four mesenchymal cells: one main player, represented by the fibroblast /and three secondary players, represented by the endothelial cell, vascular smooth muscle cell and the cardiac stem cell. The fibroblast plays a role in recruiting inflammatory cells (PMN, macrophages) in the primary secretory phase and another role in extracellular matrix remodelling in the secondary proliferative phase. Myofibroblasts are mesenchymal cells that, due to their phenotype, are often described as a bridge between fibroblasts and smooth muscle. The endothelial cells and vascular smooth muscle cells are involved in vascular remodelling, while the cardiac stem cells are involved in cardiogenesis, but at a slow rate. Last, but not least, there are transient players, in the very first moments of the game, represented by the inflammatory cells (PMN, macrophages), which clean the injured (necrobiotic) area, paving the way for the myofibroblast to cardiac remodelling. Ischemic lesions, as well as cardiac tumours produce a large variety of symptoms and changes in extracellular matrix composition.
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