Red blood cells (RBCs) are highly deformable and possess a robust membrane that can withstand shear force. Previous research showed that in diabetic patients, there is a changed RBC ultrastructure, where these cells are elongated and twist around spontaneously formed fibrin fibers. These changes may impact erythrocyte function. Ultrastructural analysis of RBCs in inflammatory and degenerative diseases can no longer be ignored and should form a fundamental research tool in clinical studies. Consequently, we investigated the membrane roughness and ultrastructural changes in type 2 diabetes. Atomic force microscopy (AFM) was used to study membrane roughness and we correlate this with scanning electron microscopy (SEM) to compare results of both the techniques with the RBCs of healthy individuals. We show that the combined AFM and SEM analyses of RBCs give valuable information about the disease status of patients with diabetes. Effectiveness of treatment regimes on the integrity, cell shape and roughness of RBCs may be tracked, as this cell’s health status is crucial to the overall wellness of the diabetic patient.
BackgroundStrokes are commonly preceded by transient ischemic attacks (TIAs). TIA is often associated with metabolic syndrome (causing chronic inflammation), resulting in a proinflammatory- and procoagulant-environment. The aim of this study was to determine whether platelet- and fibrin network-morphology or coagulation profiles of individuals that suffered a TIA in the presence of metabolic syndrome was altered when compared to healthy individuals.Materials and methodsThe study consisted of 40 voluntary participants. Twenty individuals that suffered a TIA in the previous 48 h with at least two metabolic syndrome risk factors present and twenty healthy age-matched controls. Scanning electron- and atomic force microscopy was used to study platelet- and fibrin-morphology, atomic force microscopy was used to study platelet- and fibrin fiber-elasticity and thromboelastography® for the study of coagulation profiles. Statistical analysis was performed to compare the two groups. In all cases a p-value of less than 0.05 was considered statistically significant.ResultsPlatelets of the control group appeared spherical with few pseudopodia present while the platelets of the TIA individuals presented with numerous pseudopodia and spreading, indicating activation. Platelet aggregation was also present. The fibrin networks of the healthy individuals consist of thick and thin fibers that form an organized network of fibers. The fibrin networks of the TIA individuals appeared less organized with less taut fibers. Fibrin fiber thickness was found to be significantly increased in the TIA group (p-value <0.001) when compared to healthy controls. The thicker fibers formed irregular networks with thick masses of fibrin fibers. Platelet and fibrin fiber elasticity was found to be significantly lower in the experimental group (p-value 0.0042 and p-value 0.0007 respectively). The hemostatic profiles of the diseased individuals did not differ significantly (p-value > 0.05) from the healthy controls, indicating a normal functioning coagulation cascade.ConclusionThe findings indicate that pathological clot formation is not caused by alterations in the coagulation cascade but rather by the premature activation of platelets (as a result of chronic inflammation) that in turn causes altered fibrin formation.
Atherosclerosis is a widespread disease of the arterial system that is generated by injury to the vasculature due to hypercholesterolemia, hypertension and inflammatory diseases. In the current review, we discuss the role of different risk factors, including obesity, hypertension and hypercholesterolemia in atherosclerosis, which may ultimately lead to either cardiovascular or cerebral complication. Inflammation plays a pivotal role in conjunction with obesity, hypertension and hypercholesterolemia in the etiology of atherosclerosis. We discuss the role of inflammation with regards to reactive oxygen species (ROS) linked to the specific risk factors. The role of nitric oxide (NO) in conjunction with ROS is also important. Correlations of inflammatory cytokines and their functions in the mentioned risk factors are also discussed. The risk factors may ultimately lead to ischemic events, including transient ischemic attacks (TIAs), thrombotic stroke and myocardial infarction. Importantly, it seems as if there is a combination of pathophysiological triggers that may eventually result in atherosclerosis. Therefore, atherosclerosis is not the result of only one risk factor, but a combination of various physiological processes such as homeostasis and the inflammatory response. Ultimately, each patient's risk profile is unique and determines their immediate risk for acute thrombotic events or lethal ischemia.
Water contamination with heavy metals may adversely affect our health. High metal levels lead to changes in blood coagulation processes, increasing the risk for cardiovascular disease. Exposure is not limited to a single metal but usually involves a mixture of metals. In this study 24 male Sprague-Dawley rats were exposed to cadmium (Cd) and mercury (Hg), alone and in combination, for 28 days at dosages equivalent to 1000 times the World Health Organization water limits. Scanning electron microscopy analysis revealed that both metals caused platelet activation. Cd significantly increased fibrin fibers thickness and caused aggregation and formation of dense matted deposits (DMDs). Hg reduced fibrin network formation. In the combination group, Hg appeared to augment the effect of Cd, and the presence of extensive DMDs or aggregates between the fibers, with no changes to the actual fibrin thickness, was observed.
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