Commotio cordis: Another cardiac arrest "sine materia". The 1707 early report and interpretation by G.M. Lancisi.

Sudden death by commotio cordis is rare. It is the consequence of a blunt trauma of the chest overlying the heart. The mechanism is a cardiac arrest by ventricular fibrillation in the absence of grossly or microscopically apparent myocardial injury.

Should the annular tendon of the eye be named 'annulus of Zinn' or 'of Valsalva'?

The annular tendon is commonly named 'annulus of Zinn', from the German anatomist and botanist Johann Gottfried Zinn (1727-1759) who described this structure in his Descriptio anatomica oculi humani (Anatomical Description of the Human Eye, 1755). This structure, however, had been previously discovered not by Zinn, but by Antonio Maria Valsalva (1666-1723) some decades before the publication of Zinn, in his Dissertatio anatomica prima and Dissertatio anatomica altera (First and Second Anatomical Dissertations), inside Valsalva's Opera omnia published in 1740. We advance that this structure could be re-named such as 'annulus of Valsalva-Zinn' because Valsalva, even making a mistake in its functional interpretation, first described this anatomical structure.

Pentraxin 3 and complement cascade activation in the failure of arteriovenous fistula.

Objective: Pentraxin-3 (PTX3) has been suggested to play a role in the development of vascular pathology. Stenosis of arteriovenous fistula (AVF) leading to its failure is the major cause of morbidity in hemodialysis patients. To date, little is known on the pathogenesis of AVF stenosis.

Local activation of interleukin 6 signaling is associated with arteriovenous fistula stenosis in hemodialysis patients.

Background: Vascular access failure is the main cause of morbidity in hemodialysis patients. Stenosis of the arteriovenous fistula (AVF) is similar histologically to atherosclerosis. Recent studies showed that interleukin 6 (IL-6) has a key role in the pathogenesis of atherosclerosis by binding 2 specific receptors, gp80 and gp130.

Coagulation cascade activation causes CC chemokine receptor-2 gene expression and mononuclear cell activation in hemodialysis patients.

Priming of the coagulation cascade during hemodialysis (HD) leads to the release of activated factor X (FXa). The binding of FXa to its specific receptors, effector protease receptor-1 (EPR-1) and protease-activated receptor-2 (PAR-2), may induce the activation of peripheral blood mononuclear cells (PBMC) and promote a chronic inflammatory state that is responsible for several HD-related morbidities. In the attempt to elucidate the mechanisms underlying the coagulation-associated inflammation in HD, 10 HD patients were randomized to be treated subsequently with a cellulose acetate membrane (CA) and Ethylen-vinyl-alcohol (EVAL), a synthetic membrane that has been shown to reduce FXa generation.

In vivo modulation of soluble "antagonistic" IL-6 receptor synthesis and release in ESRD.

Soluble gp130 (sgp130) is a soluble circulating receptor of IL-6 with "antagonistic" biologic activity. It is generated independently by either shedding of the extracellular domain of membrane gp130 or alternative mRNA splicing. This study was addressed to clarify the mechanisms underlying sgp130 synthesis and release in patients who undergo regular dialysis treatment (RDT) using dialytic membranes with different biocompatibility.