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Search results for: Human Thrombin

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#32644199   2020/07/09 To Up

The effect of hyperoxia on inflammation and platelet responses in an ex vivo extracorporeal membrane oxygenation circuit.

Use of extracorporeal membrane oxygenation (ECMO) is expanding, however it is still associated with significant morbidity and mortality. Activation of inflammatory and innate immune responses and hemostatic alterations contribute to complications. Hyperoxia may play a role in exacerbating these responses. Nine ex vivo ECMO circuits were tested using fresh healthy human whole blood, with two oxygen levels: 21% inspired fraction of oxygen (FiO ; mild hyperoxia; n=5) and 100% FiO (severe hyperoxia; n=4). Serial blood samples were taken for analysis of platelet aggregometry, leukocyte activation, inflammatory and oxidative stress markers. ECMO resulted in reduced adenosine diphosphate- (p<0.05) and thrombin receptor activating peptide-induced (p<0.05) platelet aggregation, as well as increasing levels of the neutrophil activation marker, neutrophil elastase (p=0.013). Additionally, levels of the inflammatory chemokine interleukin-8 were elevated (p<0.05) and the activity of superoxide dismutase, a marker of oxidative stress, was increased (p=0.002). Hyperoxia did not augment these responses, with no significant differences detected between mild and severe hyperoxia. Our ex vivo model of ECMO revealed that the circuit itself triggers a pro-inflammatory and oxidative stress response however exposure to supra-physiologic oxygen does not amplify that response. Extended-duration studies and inclusion of an endothelial component could be beneficial in characterizing longer-term changes.
Margaret R Passmore, Katrina K Ki, Chris Hh Chan, Talvin Lee, Mahé Bouquet, Emily S Wood, Sainath Raman, Sacha Rozencwajg, Aidan Jc Burrell, Charles I McDonald, Daman Langguth, Kiran Shekar, Maximilian V Malfertheiner, John F Fraser, Jacky Y Suen

2841 related Products with: The effect of hyperoxia on inflammation and platelet responses in an ex vivo extracorporeal membrane oxygenation circuit.

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#32641132   2020/07/08 To Up

Phospho-Tyr705 of STAT3 is a therapeutic target for sepsis through regulating inflammation and coagulation.

Sepsis is an infection-induced aggressive and life-threatening organ dysfunction with high morbidity and mortality worldwide. Infection-associated inflammation and coagulation promote the progression of adverse outcomes in sepsis. Here, we report that phospho-Tyr705 of STAT3 (pY-STAT3), not total STAT3, contributes to systemic inflammation and coagulopathy in sepsis.
Shunyao Xu, Xiaojun Pan, Lingjie Mao, Hao Pan, Wenwei Xu, Yufeng Hu, Xueshu Yu, Zhiqiang Chen, Songzan Qian, Yincai Ye, Yueyue Huang, Jingye Pan

1555 related Products with: Phospho-Tyr705 of STAT3 is a therapeutic target for sepsis through regulating inflammation and coagulation.

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#32638089   2020/07/07 To Up

Photoelectrochemical aptasensor for thrombin based on Au-rGO-CuS as signal amplification elements.

A photoelectrochemical platform for thrombin determination was developed based on Au-rGO-CuS as multiple signal amplification elements. CuInS QDs was used to sensitize burr-shape TiO (b-TiO) to obtain a strong photocurrent. Under the specific recognition between aptamer and thrombin, a sandwichlike structure was formed and the Au-rGO-CuS-labeled aptamer ([email protected]) was immobilized on the electrode surface. This induced a sharp decrease in photocurrent. The phenomenon is mainly due to the fact that CuS NPs can competitively consume the light energy and electron donor with CuInS/b-TiO. The rGO can increase the amount of CuS NPs and the Au NPs can accelerate charge transferring which depress the recombination of photogenerated electrons and holes in CuS to further enhance the competitive capacity of CuS. The sandwichlike structure has a steric hindrance effect. Therefore, the [email protected] has a multiple signal amplification function for thrombin determination. Under optimal conditions, the PEC aptasensor exhibited a wide linear concentration range from 0.1 pM to 10 nM with a low detection limit of 30 fM (S/N = 3) for thrombin. Besides, the designed aptasensor performed well in the assay of human serum sample, indicating good potential for the determination of thrombin in real samples. Graphical abstract.
Lina Zou, Lingxi Yang, Yi Zhan, Di Huang, Baoxian Ye

2547 related Products with: Photoelectrochemical aptasensor for thrombin based on Au-rGO-CuS as signal amplification elements.

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#32612531   2020/06/16 To Up

LCTX-F2, a Novel Potentiator of Coagulation Factors From the Spider Venom of .

Spider venoms contain many functional proteins/peptides such as proteinases, serine/cysteine proteinase inhibitors, insecticidal toxins, and ion channel toxins. However, to date, no peptide toxin with procoagulant activities has been identified from spider venom. In this study, a novel toxin LCTX-F2 with coagulation-promoting activity was identified and characterized in the venom of the spider (). LCTX-F2 significantly shortened activated partial thromboplastin time (APTT), clotting time, and plasma recalcification time. This toxin directly interacted with several coagulation factors such as FXIIa, kallikrein, thrombin, and FXa and increased their protease activities. In liver bleeding and tail bleeding mouse models, LCTX-F2 significantly decreased the number of blood cells and bleeding time in a dose-dependent manner. At the same dosage, LCTX-F2 exhibited a more significant procoagulant effect than epsilon aminocaproic acid (EACA). Moreover, LCTX-F2 showed no cytotoxic or hemolytic activity against either normal cells or red blood cells. Our results suggested that LCTX-F2 is a potentiator of coagulation factors with the potential for use in the development of procoagulant drugs.
Pengpeng Li, Zhongzhe Zhang, Qiong Liao, Er Meng, James Mwangi, Ren Lai, Mingqiang Rong

2887 related Products with: LCTX-F2, a Novel Potentiator of Coagulation Factors From the Spider Venom of .

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#32603422   // To Up

Flow studies on human GPVI-deficient blood under coagulating and noncoagulating conditions.

The role of glycoprotein VI (GPVI) in platelets was investigated in 3 families bearing an insertion within the GP6 gene that introduces a premature stop codon prior to the transmembrane domain, leading to expression of a truncated protein in the cytoplasm devoid of the transmembrane region. Western blotting and flow cytometry of GP6hom (homozygous) platelets confirmed loss of the full protein. The level of the Fc receptor γ-chain, which associates with GPVI in the membrane, was partially reduced, but expression of other receptors and signaling proteins was not altered. Spreading of platelets on collagen and von Willebrand factor (which supports partial spreading) was abolished in GP6hom platelets, and spreading on uncoated glass was reduced. Anticoagulated whole blood flowed over immobilized collagen or a mixture of von Willebrand factor, laminin, and rhodocytin (noncollagen surface) generated stable platelet aggregates that express phosphatidylserine (PS). Both responses were blocked on the 2 surfaces in GP6hom individuals, but adhesion was not altered. Thrombin generation was partially reduced in GP6hom blood. The frequency of the GP6het (heterozygous) variant in a representative sample of the Chilean population (1212 donors) is 2.9%, indicating that there are ∼4000 GP6hom individuals in Chile. These results demonstrate that GPVI supports aggregation and PS exposure under flow on collagen and noncollagen surfaces, but not adhesion. The retention of adhesion may contribute to the mild bleeding diathesis of GP6hom patients and account for why so few of the estimated 4000 GP6hom individuals in Chile have been identified.
Magdolna Nagy, Gina Perrella, Amanda Dalby, M Francisca Becerra, Lourdes Garcia Quintanilla, Jeremy A Pike, Neil V Morgan, Elizabeth E Gardiner, Johan W M Heemskerk, Lorena Azócar, Juan Francisco Miquel, Diego Mezzano, Steve P Watson

2621 related Products with: Flow studies on human GPVI-deficient blood under coagulating and noncoagulating conditions.

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#32581015   // To Up

Coagulation Panel in Patients with SARS-CoV2 Infection (COVID-19).

The 2019 novel coronavirus (SARS-CoV2) is the causal agent of the newly-termed Coronavirus Disease 2019 (COVID-19). In January 2020, the World Health Association (WHO) declared the CO-VID-19 as an epidemic. Abnormal coagulation parameters in COVID-19 patients currently are considered as prognostic factors of severity. Our aim is to summarize the current data available in the literature.
Kerbi Alejandro Guevara-Noriega, Gustavo Adolfo Lucar-Lopez, Giselle Nuñez, Luis Rivera-Aguasvivas, Ishit Chauhan

2156 related Products with: Coagulation Panel in Patients with SARS-CoV2 Infection (COVID-19).

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#32580633   2020/06/25 To Up

Role of PAR1-Egr1 in the Initiation of Thoracic Aortic Aneurysm in Fbln4-Deficient Mice.

Remodeling of the extracellular matrix plays a vital role in cardiovascular diseases. Using a mouse model of postnatal ascending aortic aneurysms (termed ), we have reported that abnormal mechanosensing led to aneurysm formation in with an upregulation of the mechanosensitive transcription factor, Egr1 (Early growth response 1). However, the role of Egr1 and its upstream regulator(s) in the initiation of aneurysm development and their relationship to an aneurysmal microenvironment are unknown. Approach and Results: To investigate the contribution of Egr1 in the aneurysm development, we deleted in mice and generated double knockout mice (, ; ). Aneurysms were prevented in mice (42.8%) and ; mice (26%). Ingenuity Pathway Analysis identified PAR1 (protease-activated receptor 1) as a potential Egr1 upstream gene. Protein and transcript levels of PAR1 were highly increased in aortas at postnatal day 1 before aneurysm formed, together with active thrombin and MMP (matrix metalloproteinase)-9, both of which serve as a PAR1 activator. Concordantly, protein levels of PAR1, Egr1, and thrombin were significantly increased in human thoracic aortic aneurysms. In vitro cyclic stretch assays (1.0 Hz, 20% strain, 8 hours) using mouse primary vascular smooth muscle cells induced marked expression of PAR1 and secretion of prothrombin in response to mechanical stretch. Thrombin was sufficient to induce Egr1 expression in a PAR1-dependent manner.
Seung Jae Shin, Huynh Thuy Hang, Bui Quoc Thang, Tomonari Shimoda, Hiroaki Sakamoto, Motoo Osaka, Yuji Hiramatsu, Yoshito Yamashiro, Hiromi Yanagisawa

2966 related Products with: Role of PAR1-Egr1 in the Initiation of Thoracic Aortic Aneurysm in Fbln4-Deficient Mice.

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