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Background: Inflammation and maladaptive immune mechanisms have been substantiated as integral components in the critical pathological processes of the injury cascade in ischemic stroke (IS). This study aimed to explore the associations between six systemic inflammatory indices and IS in a Chinese population.

Methods: This was a case-control study based on the retrospective review of electronic medical records from two hospitals in Shandong Province, China.

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Despite immense interest in biomarker applications of extracellular vesicles (EVs) from blood, our understanding of circulating EVs under physiological conditions in healthy humans remains limited. Using imaging and multiplex bead-based flow cytometry, we comprehensively quantified circulating EVs with respect to their cellular origin in a large cohort of healthy blood donors. We assessed coefficients of variations to characterize their biological variation and explored demographic, clinical, and lifestyle factors contributing to observed variation.

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Objective: To study the associations of genetic markers influencing the residual reactivity of platelets during antiplatelet therapy with acetylsalicylic acid, and clinical and laboratory parameters, including parameters of the platelet hemostasis, in patients with non-cardioembolic ischemic stroke (IS) for a deeper understanding of the pathogenetic mechanisms and prediction of response to therapy and clinical outcome.

Material And Methods: The study included 296 patients (average age 64.65 [55; 76] years) undergoing treatment at the City Clinical Hospital named after.

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Tris (2-chloroethyl) phosphate (TCEP), recognized as an emerging pollutant, has been frequently detected in human blood. Maintenance of blood homeostasis is indispensable for regulating various physiological states and overall health, yet hematological toxicology of TCEP has not been extensively investigated. Platelets, a vital component of blood, are fundamental in the processes of hemostasis and thrombosis through their activation; thus, this study was designed to elucidate the effects and underlying mechanisms of TCEP on platelet activation.

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Cognitive dysfunction has become the second leading cause of death among the diabetic patients. In pre-diabetic stage, blood-brain barrier (BBB) injury occurs and induced the microvascular complications of diabetes, especially, diabetes-associated cognitive dysfunction (DACD). Endothelial cells are the major component of BBB, on which the increased expression of CD40 could mediate BBB dysfunction in diabetics.

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