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Pharmaceuticals and Nutraceuticals from Fish and Their Activities
Published in Ramasamy Santhanam, Santhanam Ramesh, Subramanian Nivedhitha, Subbiah Balasundari, Pharmaceuticals and Nutraceuticals from Fish and Fish Wastes, 2022
Ramasamy Santhanam, Santhanam Ramesh, Subramanian Nivedhitha, Subbiah Balasundari
Anticoagulant activity: The protein isolated from this species showed anticoagulant activity by inhibiting the activated coagulation factor XII. At a concentration of 1.0 µM, this protein’s activity was recorded at 62% (Rajapakse et al., 2005).
Blood and blood component use in cardiac surgery or ‘why do cardiac surgical patients bleed?’
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
Robert R Jeffrey, Michael J Desmond
The causes of non-surgical bleeding are complex and multifactorial, and may be attributed to the period of CPB. Coagulation factor XII is activated when blood contacts the artificial surface of the CPB circuit, and activated XIIa triggers amplifying mechanisms involving coagulation, fibrinolysis, and complement activation. Platelets and white cells are also activated when they come into contact with the synthetic surfaces of the extracorporeal circuit, and are important in the systemic inflammatory response (SIRS) associated with cardiac surgery.
Plasma Protein Function in Hemostasis
Published in Genesio Murano, Rodger L. Bick, Basic Concepts of Hemostasis and Thrombosis, 2019
In considering these mechanisms as they relate to hyperacute rejections199 and en-dotoxic shock, it appears that the clot-promoting effects of phospholipids from disrupted platelets are major contributing factors. It is possible, however, that antigen-antibody complexes, in certain circumstances, may directly damage the vascular endothelium201 and that the platelet damage ensues as a consequence. Regardless of the precise sequence of events, it is apparent that the “contact phase” of coagulation (Factor XII activation) plays a major role in the pathophysiology of many syndromes.
Factor XII(a) inhibitors: a review of the patent literature
Published in Expert Opinion on Therapeutic Patents, 2021
Being an integral part of the contact activation system, blood coagulation factor XII plays an important role in pathophysiological processes such as blood coagulation and thrombosis, HAE, and (neuro)inflammation. As FXII-deficiency is practically asymptomatic, FXII zymogen, as well as its active form FXIIa, represent emerging and potentially safe drug targets. The current analysis of the patents filed by industrial and academic institutions revealed structurally and mechanistically diverse anti-FXII(a) therapeutics. These agents include small molecules [39,42–48], peptides [54,56], proteins [63,68,71–73,76,80], oligonucleotides [84], siRNAs [85,91], and mAbs [95–97,99,100,107,110]. Some of these chemical entities are active site FXIIa inhibitors, whereas others target FXII zymogen or disrupt its biosynthesis. Although many FXII(a) inhibitors are in the early preclinical stage, several already showed their efficacy in vivo animal models of thrombosis, sepsis, HAE, AD, MS, and even progressed into human clinical trials [78,103,106]. It is expected that further studies of pathophysiological functions of FXII(a) will encourage the development of new FXII(a)-targeting agents. A boost in the number of FXII(a)-related patents should be expected upon successful clinical trials of the aforementioned FXII(a)-addressing agents.
A cationic polymeric prodrug with chemotherapeutic self-sensibilization co-delivering MMP-9 shRNA plasmid for a combined therapy to nasopharyngeal carcinoma
Published in Drug Delivery, 2019
Tao Liu, Xidong Wu, Shaohua Chen, Peina Wu, Hong Han, Hongbin Zhang, Junzheng Li, Guanxue Li, Siyi Zhang
Another important concern on blood compatibility for drug carriers is the effect on the blood coagulation (Zhang et al., 2019b). Coagulation at the right time and location is necessary to maintain normal metabolism, while inappropriate coagulation will cause severe, evenfatal, risks to the living system. Therefore, the effect of Tf-PAAs-MTX/pMMP-9 on coagulation is a key factor in the blood safety evaluation. The blood coagulation cascade contains three types of pathways: intrinsic, extrinsic and common pathway. Thereinto, the performance of the intrinsic and common coagulation pathways are measured by APTT, which refers to the time needed for forming a fibrin clot after a partial thromboplastin reagent or CaCl2 is added. Meanwhile, PT measures the performance of both extrinsic and common coagulation pathways, and refers to the time taken to form a fibrin clot after tissue thromboplastin is added. The effects of the Tf-PAAs-MTX/pMMP-9 on APTT and PT are shown in Figure 7(B). Compared with the PBS control, Tf-PAAs-MTX/pMMP-9 did not significantly change the APTT and PT of the blood under the concentration of 1 mg/mL. The results indicated that Tf-PAAs-MTX/pMMP-9 under experimental concentrations had no obvious activation to coagulation factor XII in the plasma and thrombin, suggesting the blood safety in this work.
Transferrin-targeting redox hyperbranched poly(amido amine)-functionalized graphene oxide for sensitized chemotherapy combined with gene therapy to nasopharyngeal carcinoma
Published in Drug Delivery, 2019
Tao Liu, Jingzhen Li, Xidong Wu, Siyi Zhang, Zhongming Lu, Guanxue Li, Junzheng Li, Shaohua Chen
Another important concern on blood compatibility for drug carriers is the effect on the blood coagulation (Chai et al., 2017). Coagulation at the right time and location is necessary to maintain normal metabolism, while inappropriate coagulation will cause severe, even fatal, risks to the living system. Therefore, the effect of Tf-HPAA-GO on coagulation is a key factor in the blood safety evaluation. The blood coagulation cascade contains three types of pathways: intrinsic, extrinsic, and common pathway. Thereinto, the performance of the intrinsic and common coagulation pathways are measured by APTT, which refers to the time needed for forming a fibrin clot after a partial thromboplastin reagent or CaCl2 is added. Meanwhile, PT measures the performance of both extrinsic and common coagulation pathways, and refers to the time taken to form a fibrin clot after tissue thromboplastin is added. The effects of the Tf-HPAA-GO on APTT and PT are shown in Figure 10(B). Compared with the PBS control, Tf-HPAA-GO did not significantly change the APTT and PT of the blood under the concentration of 1 mg/mL. The results indicated that Tf-HPAA-GO under experimental concentrations had no obvious activation to coagulation factor XII in the plasma and thrombin, suggesting the blood safety in this work. The good blood compatibility of Tf-HPAA-GO may be attributed from its hyperbranched structure and low cationic charge density, which resulted in it showed the relative low zeta potential than other cationic polymer such as PEI, and then was avoided to interact with the proteins in the blood (Ma et al., 2014).