17 research outputs found
Pets as Sentinels of Human Exposure to Neurotoxic Metals
The idea that animals may be used as sentinels of environmental hazards
pending over humans and the associated public health implications is not a new one.
Nowadays pets are being used as bioindicators for the effects of environmental contaminants
in human populations. This is of paramount importance due to the large
increase in the worldwide distribution of synthetic chemicals, particularly in the
built environment. Companion animals share the habitat with humans being simultaneously
exposed to and suffering the same disease spectrum as their masters.
Moreover, their shorter latency periods (due to briefer lifespans) enable them to act
as early warning systems, allowing timely public health interventions. The rise on
ethical constraints on the use of animals and, consequently, on the sampling they
can be subjected to has led to the preferential use of noninvasive matrices, and in
this case we are looking into hair. This chapter focuses in three non-essential metals:
mercury, lead, and cadmium, due to their ubiquitous presence in the built environment
and their ability of affecting the mammal nervous system. There is a fairly
short amount of studies reporting the concentrations of these metals in pets’ hair,
particularly for cats. These studies are characterized, and the metal concentrations
corresponding to different parameters (e.g., age, sex, diet, rearing) are described in
order to provide the reader with a general vision on the use of this noninvasive
matrix on the studies conducted since the last two decades of the twentieth
century.publishe
Platelet Function and Coronary Microvascular Dysfunction
The ability of platelets to activate and aggregate to form blood clots in response to endothelial injury is well established. They are therefore critical contributors to ischaemia in atherothrombosis [1]. However, their role in cardiovascular disease is not limited to end-stage thrombosis in large vessels [2]. Abundant experimental evidence has established that activated platelets are also important mediators of microvascular thrombosis and promote the inflammatory response during ischaemia-reperfusion (IR) injury [3–5]. While platelets do not physically interact with the healthy endothelium, they can bind to the wall of hypoxic microvessels and release a plethora of inflammatory mediators that further enhance the activation of the endothelial monolayer and the recruitment of circulating leukocytes (monocytes, neutrophils, T-cells) [2]. In addition, deposition of platelets to the dysfunctional endothelium can lead to vasoconstriction which accelerates microvascular occlusion, thereby impairing tissue perfusion [3]. In this chapter, we discuss the role of platelets in promoting microvascular dysfunction and inflammation during IR injury. Focus is placed on the cross-talk between platelets and other cell types (endothelial cells [ECs] and leukocytes) via platelet adhesion receptors and platelet-derived proinflammatory mediators. We also consider new paradoxical functionalities of platelets promoting cardiac recovery after myocardial infarction (MI)