Andrew M. Roberts

TL;DR: It is suggested that bacterial amyloid functions as a trigger to initiate AS aggregation through cross-seeding and also primes responses of the innate immune system.

TL;DR: Experimental data, which demonstrate the effects of Fg causing vascular dysfunction and possible mechanisms for these effects are discussed, which could exacerbate microcirculatory complications during cardiovascular diseases accompanied by increased Fg content.

TL;DR: A review discusses the relationship between ROS, RNS, P-selectin, and platelet–arteriolar wall interactions and proposes a hypothesis for their role in microvascular responses during pulmonary IR.

TL;DR: Increased cerebrovascular leakage in the MMP-9-/- + histamine group showed that microvascular permeability could still increase by a mechanism independent of M MP-9, suggesting that Hcy increases microv vascular permeability, in part, through MMPs activation.

TL;DR: Elevated un-degraded Fg may be a factor causing microvascular permeability that typically accompanies cardiovascular and cerebrovascular disorders, and formation of F-actin and gaps may be the mechanism for increased albumin leakage through the EC monolayer.