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paniculata (C.B. Clarke) Munir Leaves on Various Gastric Aggressive Factors
Published in Parimelazhagan Thangaraj, Phytomedicine, 2020
P. S. Sreeja, K. Arunachalam, Parimelazhagan Thangaraj
Prostaglandins are small lipid molecules that have biological actions in various tissues and processes in the body, such as platelet aggregation, renal function, release of neurotransmitters, modulation of the immune response (Tarnawski et al. 2013), and an important role in the defense of the gastric mucosa. The endogenous prostaglandins originate from arachidonic acid through the oxidation by the constitutive COX-1, as well as by the induced isoform (COX-2); these are described as catalysts for the conversion of the arachidonic acid for the endoperoxide H2 (PGH2) and prostaglandin that serve as substrates for the biosynthesis of prostanoids (PGE2, PGF2α, PGD2, PGI2, and Thromboxane A2 (TXA2) (Hata and Breyer 2004).
Red Blood Cell and Platelet Mechanics
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
Platelet adhesion, activation, and aggregation together form a multistep process that requires multiple platelet receptor–ligand interactions, as shown in Figure 8.11. After damage to the vessel wall, circulating platelets undergo a rapid deceleration, which is mainly mediated by the interaction of the platelet-specific glycoprotein (GP) Ib-V-IX complex and immobilized von Willebrand factor (vWF) bound to exposed collagen (Savage et al. 1998). However, the binding of GPIb to vWF has a fast off-rate and is therefore insufficient to mediate stable adhesion, but it rather maintains the platelet in close contact with the vessel wall. Finally, the translocating platelets establish contact with the thrombogenic protein collagen through the receptor glycoprotein VI (Dutting et al. 2012). This protein, though a low-affinity receptor for collagen and thus unable to mediate firm adhesion, triggers intracellular signaling, which results in a shift of platelet integrins from a low- to a high-affinity state. Subsequently, the platelet activation process is reinforced by the local production of thrombin and the release and synthesis, of the secondary mediators adenosine diphosphate (ADP) and thromboxane A2, respectively, which, in turn, activate G-protein-coupled receptors (Gq, Gi, and G12/13) (Offermanns 2006). These signaling pathways finally induce full platelet activation, resulting in shape change due to extensive cytoskeletal rearrangement, release of granule contents, and coagulant activity. The stabilization of a newly formed thrombus is essential to stop bleeding; therefore, the final thrombus is embedded in a fibrin network to withstand shear forces generated by the blood flow. In addition, outside-in signaling-mediated clot retraction through integrin αIIbβ3 plays a critical role in thrombus stabilization, and an increasing number of other receptors have been identified to be potentially involved in thrombus perpetuation as well as in limiting thrombus growth (Nieswandt et al. 2011). Recently, it was described that not all platelets in a thrombus are activated to the same extent, but platelet activation is rather heterogeneous. While some platelets undergo a full activation response, others display only minimal signs of activation. Thus, a thrombus consists of a core with fully activated, densely packed platelets, a shell of less activated and packed platelets, and a transition zone between these two layers (Stalker et al. 2014). A better understanding of the mechanisms involved in thrombus growth and the thrombus architecture will have important implications for the understanding of new and existing antiplatelet agents and their potential side effects.
Kinetic study of NTPDase immobilization and its effect of haemocompatibility on polyethylene terephthalate
Published in Journal of Biomaterials Science, Polymer Edition, 2019
Balaji Ramachandran, Vignesh Muthuvijayan
Heparin is one of the widely studied bioactive molecules on various material surfaces to improve haemocompatibility [5]. Despite heparin-mediated inhibition of thrombin formation, researchers have explored the inhibition of early stages of thrombus formation through inhibiting platelet activation. Upon adhesion to the foreign material surfaces, platelets can lead to activation and release of pro-coagulant agonists from dense granules such as thromboxane A2, ADP, serotonin [6]. For platelet-specific improvement of haemocompatibility of material surfaces, many molecules such as nitric oxide, dipyridamole, hirudin had been explored [7,8]. Apyrase/ecto-nucleoside triphosphate diphosphohydrolase (E-NTPDase/CD39) is also one such molecule which can be used for enhancing haemocompatibility of the material surface [9,10]. NTPDase is an important transmembrane protein that phosphohydrolyses ATP to ADP and then to AMP, thereby regulating ADP-dependent platelet activation and adhesion [11,12]. Coating of modified apyrase on the material surface shows improved blood compatibility [13,14]. Clinical studies showed that the platelet adhesion and activation vary between healthy individuals and patients with cardiovascular artery disease [15]. Hence, the coating of the NTPDase should be based on the end user application. This can be only achieved by studying the kinetics of the attached biomolecules.
Calcium content mediated hemostasis of calcium-modified oxidized microporous starch
Published in Journal of Biomaterials Science, Polymer Edition, 2018
Junxia Yu, Huantong Su, Shuda Wei, Fangping Chen, Changsheng Liu
Pseudopodia and flattening were observed on the surface of the activated platelets, resulting in an increase in the roughness of the platelet surface, thereby causing extensive platelet aggregation, the release of abundant procoagulant substances, and ultimately the acceleration of clot formation. The initial adhesion can generate intracellular signals responsible for the activation of GPIIb/IIIa and release of thromboxane A2/ADP, which further promotes platelet spreading, thus strengthening the stability of adhesion [35]. The morphology of platelets spread flattening and extended into irregular shapes indicating the activation of platelets. Figure 7(B) distinctly showed platelet aggregation on the surfaces of MS, OMS3 and CaOMS3. Owing to its poor water absorption capacity, MS showed little platelet aggregation. The other two modified starch-based materials showed remarkable aggregation, pseudopodia and flattening of adhered platelets. Physiologically unstimulated platelets maintained a very low cytosolic free Ca2+ concentration of approximately 0.1 μM. When exposed to blood, CaOMS3 released Ca2+, giving rise to a significant increase in cytosolic free Ca2+. All these mechanisms facilitated subsequent events, including GPIIb/IIIa expression and fibrinogen binding to platelets, leading to platelet activation [31].
Computational modeling of blast induced whole-body injury: a review
Published in Journal of Medical Engineering & Technology, 2018
Arnab Chanda, Christian Callaway
Blunt, ballistic, and blast effects cause significant injury to the CNS, however, primary blast was found to be the major cause of Traumatic Brain Injury (TBI) among military personnel and soldiers [79]. To date, theories such as direct blast wave propagation through the brain, pressure wave propagation through the great vessels and secondarily to the brain, and blast under pressure followed by cavitation together with blast electromagnetic pulses have been suggested to account for TBI. In 1994, 1303 patients who were injured by explosive munitions in extremity wounds were admitted to the Military Medical Academy in Belgrade, and a cohort study was performed to investigate CNS injuries [80]. 51% patients were detected with symptoms of primary blast injury with a much higher blood thromboxane A2 (TxA2), prostacyclin (PGI2) and sulfide-peptide leukotrienes then a sampling of patients without blast symptoms. Also, 30% of those with primary blast injury had long-term symptoms for at least a year and signs of CNS disorders, whereas only 4% of those without blast injury had indications of CNS disorders. These changes in chemical compounds, experienced by those with blast injury indicate that blast causes major physiologic stress and could be responsible for post-traumatic stress disorder (PTSD) [80].