How to Trip Rapid Review

Step 1: Select articles relevant to your search (remember the system is only optimised for single intervention studies)

Step 2: press

Step 3: review the result, and maybe amend the or if you know better! If we're unsure of the overall sentiment of the trial we will display the conclusion under the article title. We then require you to tell us what the correct sentiment is.

282 results for

Intrinsic Clotting Pathway

by
...
Latest & greatest
Alerts

Export results

Use check boxes to select individual results below

SmartSearch available

Trip's SmartSearch engine has discovered connected searches & results. Click to show

1. Abnormal clotting of the intrinsic/contact pathway in Alzheimer disease patients is related to cognitive ability (PubMed)

Abnormal clotting of the intrinsic/contact pathway in Alzheimer disease patients is related to cognitive ability Alzheimer disease (AD) is a neurodegenerative disorder characterized by extracellular β-amyloid (Aβ) deposition. Although peripheral inflammation and cerebrovascular pathology are reported in AD, there is a lack of plasma biomarkers in this field. Because the contact system is triggered in patient plasma, we hypothesized that the hemostasis profile could be a novel biomarker in AD (...) . Here, we assessed the clotting profile in plasma from AD patients and age-matched controls. Utilizing clinically relevant assays, thromboelastography and activated partial thromboplastin time, we found impaired clot initiation and formation rate in AD patient plasma. These coagulation end points correlated with cerebrospinal fluid neurofilament-light levels and cognition and were more profound in younger AD patients. Ex vivo intrinsic clotting of plasma from AD mice expressing human amyloid

Full Text available with Trip Pro

2018 Blood advances

2. Intrinsic Clotting Pathway

Intrinsic Clotting Pathway Intrinsic Clotting Pathway Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Intrinsic Clotting Pathway (...) Intrinsic Clotting Pathway Aka: Intrinsic Clotting Pathway , Intrinsic Clotting Cascade II. Pathophysiology Initiated by negatively charged surface III. Physiology: Pathway Factor XII converted to Factor XIIa ors PK HMWK Inhibitors Factor XI converted to Factor XIa Factor IX converted to Factor IXa ors: Factor VIII von Willebrand's factor (vWF) carries Factor VIII Inhibitors Protein C Protein S Factor X converted to Factor Xa Joins Images: Related links to external sites (from Bing) These images

2018 FP Notebook

3. A kallikrein-targeting RNA aptamer inhibits the intrinsic pathway of coagulation and reduces bradykinin release. (PubMed)

A kallikrein-targeting RNA aptamer inhibits the intrinsic pathway of coagulation and reduces bradykinin release. Essentials Kallikrein amplifies contact activation and is a potential target for preventing thrombosis. We developed and characterized a kallikrein aptamer using convergent evolution and kinetic assays. Kall1-T4 prolongs intrinsic clotting time by inhibiting factor XIIa-mediated prekallikrein activation. Kall1-T4 decreases high-molecular-weight kininogen cleavage and bradykinin (...) release.Background Plasma kallikrein is a serine protease that plays an integral role in many biological processes, including coagulation, inflammation, and fibrinolysis. The main function of kallikrein in coagulation is the amplification of activated factor XII (FXIIa) production, which ultimately leads to thrombin generation and fibrin clot formation. Kallikrein is generated by FXIIa-mediated cleavage of the zymogen prekallikrein, which is usually complexed with the non-enzymatic cofactor high molecular weight

Full Text available with Trip Pro

2017 Journal of Thrombosis and Haemostasis

4. Clotting Pathway

are not activated and Clotting Cascade does not occur inhibits the cyclic interconversion of to a reduced form, thereby keeping it and dependent factors inactive Procoagulant Factors (Mnemonic: 1972) Factor 10 (half life 36 hours) Factor 9 (half life 24 hours) Factor 7 (half life 7 hours) Factor 2 (half life 50 hours) Factors Protein C (half life 8 hours) Protein S (half life 30 hours) IV. Labs (PTT) Measures intrinsic pathway Prolonged by ( ) ( ) (PT) Measures extrinsic pathway Affecting both and Factor X (...) Clotting Pathway Clotting Pathway Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Clotting Pathway Clotting Pathway Aka: Clotting

2018 FP Notebook

5. How to Optimize Activated Partial Thromboplastin Time (APTT) Testing: Solutions to Establishing and Verifying Normal Reference Intervals and Assessing APTT Reagents for Sensitivity to Heparin, Lupus Anticoagulant, and Clotting Factors. (PubMed)

How to Optimize Activated Partial Thromboplastin Time (APTT) Testing: Solutions to Establishing and Verifying Normal Reference Intervals and Assessing APTT Reagents for Sensitivity to Heparin, Lupus Anticoagulant, and Clotting Factors. The activated partial thromboplastin time (APTT) assay is a very common coagulation test, used for several reasons. The test is conventionally used for assessing the contact factor (intrinsic) pathway of blood coagulation, and thus for screening deficiencies (...) in this pathway, most typically factors VIII, IX, and XI. The APTT is also sensitive to contact factor deficiencies, including factor XII, prekallikrein, and high-molecular-weight kininogen. The APTT may also be elevated in a variety of conditions, including liver disease, vitamin K deficiency, and disseminated intravascular coagulation. The APTT can also be used for monitoring unfractionated heparin (UFH) therapy, as well as for screening lupus anticoagulant (LA) or for assessing thrombosis risk. Which

2019 Seminars In Thrombosis And Hemostasis

6. Intrinsic Clotting Pathway

Intrinsic Clotting Pathway Intrinsic Clotting Pathway Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Intrinsic Clotting Pathway (...) Intrinsic Clotting Pathway Aka: Intrinsic Clotting Pathway , Intrinsic Clotting Cascade II. Pathophysiology Initiated by negatively charged surface III. Physiology: Pathway Factor XII converted to Factor XIIa ors PK HMWK Inhibitors Factor XI converted to Factor XIa Factor IX converted to Factor IXa ors: Factor VIII von Willebrand's factor (vWF) carries Factor VIII Inhibitors Protein C Protein S Factor X converted to Factor Xa Joins Images: Related links to external sites (from Bing) These images

2015 FP Notebook

7. Integrating platelet and coagulation activation in fibrin clot formation (PubMed)

the secretion of (anti)coagulation factors, as well as surface exposure of phosphatidylserine, thereby catalysing thrombin generation. This procoagulant platelet response is also facilitated by the adhesive complexes glycoprotein Ib-V-IX and integrin αIIbβ3. In the buildup of a platelet-fibrin thrombus, the extrinsic, tissue factor-driven coagulation pathway is predominant in early stages, while the intrinsic, factor XII pathway seems to promote at later time points. Already early generation of thrombin (...) Integrating platelet and coagulation activation in fibrin clot formation Platelets interact with the coagulation system in a multitude of ways, not only during the phases of thrombus formation, but also in specific areas within a formed thrombus. This review discusses current concepts of platelet control of thrombin generation, fibrin formation and structure, and anticoagulation. Indicated are how combined signalling via the platelet receptors for collagen (glycoprotein VI) and thrombin induces

Full Text available with Trip Pro

2018 Research and Practice in Thrombosis and Haemostasis

8. Histidine-rich glycoprotein binds DNA and RNA and attenuates their capacity to activate the intrinsic coagulation pathway. (PubMed)

via the intrinsic pathway and shortens the clotting time. Their effect on the clotting time is seven- to 14-fold greater in HRG-deficient plasma than in control plasma. Investigations into the mechanisms of activation reveal that nucleic acids a) promote FXII activation in the presence of prekallikrein- and high molecular weight kininogen (HK), and b) enhance thrombin-mediated FXI activation by 10- to 12-fold. Surface plasmon resonance studies show that DNA and RNA bind FXII, FXIIa, HK, FXI, FXIa (...) Histidine-rich glycoprotein binds DNA and RNA and attenuates their capacity to activate the intrinsic coagulation pathway. When triggered by factor (F) XII and nucleic acids, we showed that thrombosis in HRG-deficient mice is accelerated compared with that in wild-type mice. In this study, we set out to identify the mechanisms by which nucleic acids promote contact activation, and to determine whether HRG attenuates their effects. DNA or RNA addition to human plasma enhances thrombin generation

2015 Thrombosis and haemostasis

9. Maggot excretion products from the blowfly Lucilia sericata contain contact phase/intrinsic pathway-like proteases with procoagulant functions. (PubMed)

and kininogen as well as factor IX, thereby providing kallikrein-bypassing and factor XIa-like activities, both in plasma and in isolated systems. In plasma samples deficient in contact phase proteins, MEP restored full clotting activity, whereas in plasma deficient in either factor VII, IX, X or II no effect was seen. The observed procoagulant/intrinsic pathway-like activity was mediated by (chymo-) trypsin-like proteases in total MEP, which were significantly blocked by C1-esterase inhibitor or other (...) Maggot excretion products from the blowfly Lucilia sericata contain contact phase/intrinsic pathway-like proteases with procoagulant functions. For centuries, maggots have been used for the treatment of wounds by a variety of ancient cultures, as part of their traditional medicine. With increasing appearance of antimicrobial resistance and in association with diabetic ulcers, maggot therapy was revisited in the 1980s. Three mechanisms by which sterile maggots of the green bottle fly Lucilia

2015 Thrombosis and haemostasis

10. Saliva-Induced Clotting Captures Streptococci: Novel Roles for Coagulation and Fibrinolysis in Host Defense and Immune Evasion (PubMed)

pathways, entrapping the bacteria in fibrin clots. The bacteria escape the clots by activating host plasminogen. Our results identify a potential function for the intrinsic pathway of coagulation in host defense and a corresponding role for fibrinolysis in streptococcal immune evasion.Copyright © 2016 Wollein Waldetoft et al. (...) Saliva-Induced Clotting Captures Streptococci: Novel Roles for Coagulation and Fibrinolysis in Host Defense and Immune Evasion Streptococcal pharyngitis is among the most common bacterial infections, but the molecular mechanisms involved remain poorly understood. Here we investigate the interactions among three major players in streptococcal pharyngitis: streptococci, plasma, and saliva. We find that saliva activates the plasma coagulation system through both the extrinsic and the intrinsic

Full Text available with Trip Pro

2016 Infection and immunity

11. Alteration of blood clotting and lung damage by protamine are avoided using the heparin and polyphosphate inhibitor UHRA. (PubMed)

Alteration of blood clotting and lung damage by protamine are avoided using the heparin and polyphosphate inhibitor UHRA. Anticoagulant therapy-associated bleeding and pathological thrombosis pose serious risks to hospitalized patients. Both complications could be mitigated by developing new therapeutics that safely neutralize anticoagulant activity and inhibit activators of the intrinsic blood clotting pathway, such as polyphosphate (polyP) and extracellular nucleic acids. The latter strategy (...) could reduce the use of anticoagulants, potentially decreasing bleeding events. However, previously described cationic inhibitors of polyP and extracellular nucleic acids exhibit both nonspecific binding and adverse effects on blood clotting that limit their use. Indeed, the polycation used to counteract heparin-associated bleeding in surgical settings, protamine, exhibits adverse effects. To address these clinical shortcomings, we developed a synthetic polycation, Universal Heparin Reversal Agent

Full Text available with Trip Pro

2016 Blood

12. Inhibiting the intrinsic pathway of coagulation with a factor XII-targeting RNA aptamer. (PubMed)

targeting FXII/activated FXII (FXIIa) that dose dependently prolongs fibrin clot formation and thrombin generation in clinical coagulation assays. This aptamer functions as a potent anticoagulant by inhibiting the autoactivation of FXII, as well as inhibiting intrinsic pathway activation (FXI activation). However, the aptamer does not affect the FXIIa-mediated activation of the proinflammatory kallikrein-kinin system (plasma kallikrein activation).We have generated a specific and potent FXII/FXIIa (...) Inhibiting the intrinsic pathway of coagulation with a factor XII-targeting RNA aptamer. Exposure of the plasma protein factor XII (FXII) to an anionic surface generates activated FXII that not only triggers the intrinsic pathway of blood coagulation through the activation of FXI but also mediates various vascular responses through activation of the plasma contact system. While deficiencies of FXII are not associated with excessive bleeding, thrombosis models in factor-deficient animals have

Full Text available with Trip Pro

2013 Journal of Thrombosis and Haemostasis

13. Clotting Pathway

are not activated and Clotting Cascade does not occur inhibits the cyclic interconversion of to a reduced form, thereby keeping it and dependent factors inactive Procoagulant Factors (Mnemonic: 1972) Factor 10 (half life 36 hours) Factor 9 (half life 24 hours) Factor 7 (half life 7 hours) Factor 2 (half life 50 hours) Factors Protein C (half life 8 hours) Protein S (half life 30 hours) IV. Labs (PTT) Measures intrinsic pathway Prolonged by ( ) ( ) (PT) Measures extrinsic pathway Affecting both and Factor X (...) Clotting Pathway Clotting Pathway Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Clotting Pathway Clotting Pathway Aka: Clotting

2015 FP Notebook

14. The missense Thr211Pro mutation in the factor X activation peptide of a bleeding patient causes molecular defect in the clotting cascade. (PubMed)

The missense Thr211Pro mutation in the factor X activation peptide of a bleeding patient causes molecular defect in the clotting cascade. Factor X (FX) is a vitamin K-dependent coagulation zymogen, which upon activation to factor Xa assembles into the prothrombinase complex to activate prothrombin to thrombin. FX can be activated by either factor VIIa-tissue factor or factor IXa-factor VIIIa in extrinsic and intrinsic pathways, respectively. In this study, we identified a bleeding patient (...) with moderate FX deficiency who exhibits a clotting defect only in the intrinsic pathway. Exome sequencing revealed that the patient carries a novel homozygous missense mutation that results in substitution of Thr211 with Pro in the activation peptide of FX. Thr211 is the site of an O-linked glycosylation in the activation peptide of FX. We postulated that the lack of this post-translational modification specifically impacts the activation of FX by intrinsic Xase, thereby impairing thrombin generation

Full Text available with Trip Pro

2013 Thrombosis and haemostasis

15. The Epidemiology of Bleeding and Clotting in Patients Undergoing Heart Transplantation, Coronary Artery Bypass Graft Surgery,or Implantation of Left Ventricular Assist Devices

Go to Brief Summary: The purpose of this study is to obtain data or information on how blood clotting factors are activated during open heart surgery. In particular, the investigators are interested in how blood clotting factors are activated by the heart-lung bypass machine and by left ventricular assist devices (LVAD). Patients on these two machines have an increased risk of bleeding and blood clot formation. This is because both machines stimulate the intrinsic coagulation pathway, one (...) of the chemical pathways that cause blood to clot. The process of surgery itself also stimulates the "extrinsic coagulation pathway," the other chemical pathway that causes blood to clot. Stimulating these coagulation pathways can use up the body's clotting factors. As a result, patients may be at risk for both bleeding and blood clot formation. The investigators would like to study how the blood factors are activated during and after surgery, to help develop treatments to prevent bleeding and clot formation

2011 Clinical Trials

16. Inhibition of Intrinsic Xase by Protein S: A Novel Regulatory Role of Protein S Independent of Activated Protein C. (PubMed)

Inhibition of Intrinsic Xase by Protein S: A Novel Regulatory Role of Protein S Independent of Activated Protein C. Protein S is a vitamin K-dependent plasma protein that functions in the feedback regulation of thrombin generation. Our goal was to determine how protein S regulates the intrinsic pathway of blood coagulation.We used plasma, including platelet-rich plasma, and in vitro methods to determine how the intrinsic pathway of blood coagulation is regulated by protein S. We obtained (...) the following results: (1) activated partial thromboplastin time assays with protein S-supplemented plasma confirmed that protein S prolongs clotting time; (2) a modified activated partial thromboplastin time assay with factor IX (fIX)-deficient plasma confirmed that protein S affects fIX-initiated clotting; (3) a fIXa/factor VIIIa (fVIIIa)-mediated thrombin generation assay with either platelet-rich plasma or factor-deficient plasma, initiated with a limiting amount of tissue factor, was regulated

Full Text available with Trip Pro

2012 Thrombosis and Vascular Biology

17. Acute Kidney Injury (AKI)

or haemodiafiltration in patients with AKI meet the microbial standards for fluids used for chronic haemodialysis. (1A) Guideline 9.3 - Vascular access for RRT We recommend that: ? veno-venous access is used for acute renal replacement therapy. (1A) ? dialysis catheters should be of an adequate length to minimise the risk of premature filter clotting and access recirculation. (1C) ? access should be placed by experienced or appropriately supervised staff. Real-time ultrasound guidance should be used to aid (...) descriptives (e.g. ‘pre-renal’ and ‘renal / intrinsic’) to pathophysiological ones (‘functional change’ and ‘kidney damage’, respectively) [34]. Given the momentum of current training and educational endeavours, particularly across the UK, a change in nomenclature, we feel, would be counterproductive at this stage. Paediatric considerations (to be read in conjunction with adult guidance, above) Clinical Assessment; History, Examination Rationale As discussed above in relation to adult disease, the early

2019 Renal Association

To help you find the content you need quickly, you can filter your results via the categories on the right-hand side >>>>