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Thrombin Hemostatic

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141. Human megakaryocytes confer tissue factor to a subset of shed platelets to stimulate thrombin generation. (Abstract)

, and is transferred to a subset of shed platelets where it contributes to clot formation. These data were all confirmed in human CD34pos-derived megakaryocytes and in their released platelets. The effect of TF silencing in Meg-megakaryoblasts resulted in a significant reduction of TF expression in these cells and also in Meg-megakaryocytes and Meg-platelets. Moreover, the contribution of platelet-TF to the platelet hemostatic capacity was highlighted by the significant delay in the kinetic of thrombin formation (...) Human megakaryocytes confer tissue factor to a subset of shed platelets to stimulate thrombin generation. Tissue factor (TF), the main activator of the blood coagulation cascade, has been shown to be expressed by platelets. Despite the evidence that both megakaryocytes and platelets express TF mRNA, and that platelets can make de novo protein synthesis, the main mechanism thought to be responsible for the presence of TF within platelets is through the uptake of TF positive microparticles

2015 Thrombosis and haemostasis

142. Comparison of the hemostatic effects of a levonorgestrel-releasing intrauterine system and leuprolide acetate in women with endometriosis: a randomized clinical trial. (Abstract)

Comparison of the hemostatic effects of a levonorgestrel-releasing intrauterine system and leuprolide acetate in women with endometriosis: a randomized clinical trial. The hemostatic and inflammatory systems may activate each other. Endometriosis is a chronic inflammatory disease affecting 10% of women. The objective of this study was to compare the hemostatic effects of two treatments widely prescribed to women with endometriosis: the levonorgestrel intrauterine system (LNG-IUS (...) , thrombin-antithrombin complex, and prothrombin fragment 1+2. All variables were assessed before treatment and six months after treatment onset.In the LNG-IUS group, FVIII decreased 10% after six months of use. In the GnRHa group, there was a 6% increase in AT, 29% reduction in D-dimers, and 19% increase in t-PA. The LNG-IUS users exhibited a significantly greater reduction of FVIII than the GnRHa users (LNG-IUS: -6.4 ± 14.3% vs. GnRHa: 4.2 ± 12.3%, p=0.02). The women in the GnRHa group exhibited

2014 Thrombosis research Controlled trial quality: uncertain

143. Ovariectomy differential influence on some hemostatic markers of mice and rats (Full text)

Ovariectomy differential influence on some hemostatic markers of mice and rats Rodent ovariectomy is an experimental method to eliminate the main source of sexual steroids. This work explored for the first time the ovariectomy temporal changes induced in the hemostatic coagulation markers: prothrombin time (PT), activated partial thromboplastin time (aPTT), thrombin time (TT), and fibrinogen concentration (FIB) along with uterine weight on adult female CD1 mice and Wistar rats. Uterine weight (...) (Uw) was assessed before ovariectomy (control), and 1, 3, 5, 7, 9, 16, and 21 days after surgery. PT, aPTT, TT and FIB were estimated the same days, using reported standard techniques. Ovariectomy decreased Uw, since day 1; and from day 10 to 21 reached the lowest values for both species. After day 1, mice hemostatic parameters changed (PT +10%, P<0.05; aPTT +53%, P<0.05; TT -24%, P<0.05; FIB +67%, P<0.05). Rats showed significant changes only in TT and FIB (TT -13%, P<0.001; FIB +65%, P<0.001

2014 Experimental Animals PubMed abstract

144. Use of topical hemostatic agents in gynecologic surgery. (Abstract)

Use of topical hemostatic agents in gynecologic surgery. Sutures, hemoclips, and electrocautery are the primary mechanisms used to achieve hemostasis during gynecologic surgery, but in situations in which these are inadequate or not feasible, an array of hemostatic agents are available to help achieve hemostasis. These agents include physical agents such as cellulose, collagen, or gelatin products as well as biologic agents such as thrombin and fibrin products. Limited data are available (...) on many of these agents, although their use is increasing, sometimes at high costs. In gynecologic surgery, hemostatic agents are likely most effective when used in areas of oozing or slow bleeding and as an adjunct to conventional surgical methods of hemostasis.

2014 Obstetrical & Gynecological Survey

145. A combination of hemostatic agents may safely replace deep medullary suture during laparoscopic partial nephrectomy in a pig model. (Abstract)

A combination of hemostatic agents may safely replace deep medullary suture during laparoscopic partial nephrectomy in a pig model. We assessed whether a combination of the fibrin tissue adhesive Tisseel® (human fibrinogen and thrombin) plus the hemostatic matrix FloSeal® (bovine derived gelatin matrix/human thrombin) could safely replace the conventional deep medullary suture without compromising outcomes.Laparoscopic mid pole and one-third partial nephrectomy was performed on the right kidney (...) of 12 female pigs. The only difference between the 2 groups of 6 pigs each was the use of a fibrin tissue adhesive plus hemostatic matrix combination in group 2 instead of the deep medullary running suture in control group 1. Renal scans and angiograms were performed at baseline and before sacrifice at 5-week followup. Retrograde in vivo pyelogram was also done.No significant difference was seen in operative parameters or postoperative course between the groups. Renal scans revealed a statistically

2014 Journal of Urology

146. Puerarin attenuates ovalbumin-induced lung inflammation and hemostatic unbalance in rat asthma model. (Full text)

Puerarin attenuates ovalbumin-induced lung inflammation and hemostatic unbalance in rat asthma model. Aim. We aimed to investigate and evaluate the preventive activity of puerarin on the ovalbumin-induced asthma rat model. Materials and Methods. Male Wistar rats were sensitized intraperitoneally on days 0, 7, and 14 and challenged to ovalbumin intratracheally on day 21. Groups of sensitized rats were treated randomly either with placebo, puerarin, dexamethasone, or puerarin combined (...) by puerarin. Administration of puerarin also effectively rectified the coagulation disorder in asthmatic rats, such as prothrombin time (PT) (P < 0.01), thrombin time (TT) (P < 0.05), fibrinogen (FIB) (P < 0.01),the activity of factor II (FII) (P < 0.01), the activity of factor V (FV) (P < 0.05), the activity of factor VII (FVII) (P < 0.05), the activity of factor X (FX) (P < 0.05), the activity of factor VIII (FVIII) (P < 0.01), the activity of factor IX (FIX) (P < 0.05), and the activity of factor XII

2014 Evidence-based Complementary and Alternative Medicine (eCAM) PubMed abstract

147. Differential associations of oral estradiol and conjugated equine estrogen with hemostatic biomarkers. (Full text)

Differential associations of oral estradiol and conjugated equine estrogen with hemostatic biomarkers. The risk of venous thrombosis (VT) associated with oral hormone therapy (HT) may differ by type of estrogen compound.To compare the thrombotic profile of women using oral conjugated equine estrogens (CEE) with that of women using oral estradiol (E2).In postmenopausal, female, health maintenance organization (HMO) members with no history of VT, we measured thrombin generation, levels of factor (...) medroxyprogesterone acetate. Compared with E2 users, CEE users had greater thrombin generation peak values and endogenous thrombin potential, and lower total protein S (multivariate adjusted differences of 49.8 nm (95% CI, 21.0, 78.6), 175.0 nm × Min (95% CI, 54.4, 295.7) and -13.4% (95% CI, -19.8, -6.9), respectively). Factor VII and antithrombin levels were not different between E2 and CEE users. Results were similar in subgroups of users of unopposed HT, opposed HT, low-dose estrogen and standard dose

2014 Journal of Thrombosis and Haemostasis PubMed abstract

148. The hemostatic activity of cryopreserved platelets is mediated by phosphatidylserine-expressing platelets and platelet microparticles. (Abstract)

The hemostatic activity of cryopreserved platelets is mediated by phosphatidylserine-expressing platelets and platelet microparticles. Cryopreservation of platelets (PLTs) at -80°C with dimethyl sulfoxide (DMSO) can extend the shelf life from 5 days to 2 years. Cryopreserved PLTs are reported to have a greater in vivo hemostatic effect than liquid-stored PLTs. As such, the aim of this study was to understand the mechanisms responsible for the hemostatic potential of cryopreserved PLTs (...) and the contribution of the reconstitution solution to this activity.DMSO (5% final concentration) was added to buffy coat-derived PLTs, followed by prefreeze removal of DMSO and storage at -80°C. Cryopreserved PLTs (n=8 per group) were thawed at 37°C, reconstituted with either 1 unit of thawed frozen plasma or PLT additive solution (PAS-G). In vitro assays were performed before freezing and after thawing to assess the hemostatic activity of PLTs.Cryopreserved PLTs expressed high levels of phosphatidylserine

2014 Transfusion

149. Global Hemostatic Methods in Hemophilia and Von Willebrand's Disease

rather than simple concentration of a single deficient factor may correlate better with clinical phenotype in these patients. The investigators will therefore study the usefulness of global hemostatic methods (endogenous thrombin potential (ETP), overall hemostatic potential (OHP), fibrin clot structure) and microparticles in the prediction of severity of bleeding and estimation of response to the treatment in patients with hemophilia. Since hemophilia patients on prophylactic treatment virtually do (...) not bleed, additional patients who are treated on demand only will be included enabling to study possible modulatory effects of different hemostatic factors (particularly prothrombotic and thrombin activatable fibrinolysis inhibitor (TAFI)) on clinical presentation. The investigators will correlate both those factors and clinical severity with global hemostatic methods. The investigators expect to prove that individual tailoring of the treatment, which may enable lowering the prophylactic dose of factor

2014 Clinical Trials

150. Hemostatic Disorders, Nonplatelet (Diagnosis)

=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjEwNDY3LW92ZXJ2aWV3 processing > Nonplatelet Hemostatic Disorders Updated: May 12, 2016 Author: Muhammad A Mir, MD, FACP; Chief Editor: Perumal Thiagarajan, MD Share Email Print Feedback Close Sections Sections Nonplatelet Hemostatic Disorders Overview Overview Blood coagulation is triggered by the exposure of tissue factor at injury sites, leading to the generation of minute quantities of thrombin. Thrombin, in turn, activates platelets, as well as factors XI, VIII, and V, and triggers the sequential activation (...) of factors XI, IX, X, and prothrombin on the activated platelet surface, leading to the generation of sufficient thrombin to convert fibrinogen to fibrin and affect hemostasis. Platelets localize coagulation to the hemostatic thrombus and protect coagulation enzymes from inhibition by plasma and platelet inhibitors, thus preventing disseminated intravascular coagulation (DIC). Abnormalities in the coagulation cascade that are independent of the platelet protective mechanisms can affect hemostasis

2014 eMedicine.com

151. Hemostatic Disorders, Nonplatelet (Treatment)

=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjEwNDY3LW92ZXJ2aWV3 processing > Nonplatelet Hemostatic Disorders Updated: May 12, 2016 Author: Muhammad A Mir, MD, FACP; Chief Editor: Perumal Thiagarajan, MD Share Email Print Feedback Close Sections Sections Nonplatelet Hemostatic Disorders Overview Overview Blood coagulation is triggered by the exposure of tissue factor at injury sites, leading to the generation of minute quantities of thrombin. Thrombin, in turn, activates platelets, as well as factors XI, VIII, and V, and triggers the sequential activation (...) of factors XI, IX, X, and prothrombin on the activated platelet surface, leading to the generation of sufficient thrombin to convert fibrinogen to fibrin and affect hemostasis. Platelets localize coagulation to the hemostatic thrombus and protect coagulation enzymes from inhibition by plasma and platelet inhibitors, thus preventing disseminated intravascular coagulation (DIC). Abnormalities in the coagulation cascade that are independent of the platelet protective mechanisms can affect hemostasis

2014 eMedicine.com

152. Hemostatic Disorders, Nonplatelet (Overview)

=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjEwNDY3LW92ZXJ2aWV3 processing > Nonplatelet Hemostatic Disorders Updated: May 12, 2016 Author: Muhammad A Mir, MD, FACP; Chief Editor: Perumal Thiagarajan, MD Share Email Print Feedback Close Sections Sections Nonplatelet Hemostatic Disorders Overview Overview Blood coagulation is triggered by the exposure of tissue factor at injury sites, leading to the generation of minute quantities of thrombin. Thrombin, in turn, activates platelets, as well as factors XI, VIII, and V, and triggers the sequential activation (...) of factors XI, IX, X, and prothrombin on the activated platelet surface, leading to the generation of sufficient thrombin to convert fibrinogen to fibrin and affect hemostasis. Platelets localize coagulation to the hemostatic thrombus and protect coagulation enzymes from inhibition by plasma and platelet inhibitors, thus preventing disseminated intravascular coagulation (DIC). Abnormalities in the coagulation cascade that are independent of the platelet protective mechanisms can affect hemostasis

2014 eMedicine.com

153. Hemostatic Disorders, Nonplatelet (Follow-up)

=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjEwNDY3LW92ZXJ2aWV3 processing > Nonplatelet Hemostatic Disorders Updated: May 12, 2016 Author: Muhammad A Mir, MD, FACP; Chief Editor: Perumal Thiagarajan, MD Share Email Print Feedback Close Sections Sections Nonplatelet Hemostatic Disorders Overview Overview Blood coagulation is triggered by the exposure of tissue factor at injury sites, leading to the generation of minute quantities of thrombin. Thrombin, in turn, activates platelets, as well as factors XI, VIII, and V, and triggers the sequential activation (...) of factors XI, IX, X, and prothrombin on the activated platelet surface, leading to the generation of sufficient thrombin to convert fibrinogen to fibrin and affect hemostasis. Platelets localize coagulation to the hemostatic thrombus and protect coagulation enzymes from inhibition by plasma and platelet inhibitors, thus preventing disseminated intravascular coagulation (DIC). Abnormalities in the coagulation cascade that are independent of the platelet protective mechanisms can affect hemostasis

2014 eMedicine.com

154. Thrombin Generation Test in Patient With Liver Cirrhosis

Last Verified: August 2017 Keywords provided by RAWI HAZZAN, HaEmek Medical Center, Israel: Coagulation Factor cirrhosis Additional relevant MeSH terms: Layout table for MeSH terms Fibrosis Liver Cirrhosis Pathologic Processes Liver Diseases Digestive System Diseases Thrombin Hemostatics Coagulants (...) Thrombin Generation Test in Patient With Liver Cirrhosis Thrombin Generation Test in Patient With Liver Cirrhosis - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Thrombin Generation Test in Patient

2014 Clinical Trials

155. Combination of thrombin-antithrombin complex, plasminogen activator inhibitor-1, and protein C activity for early identification of severe coagulopathy in initial phase of sepsis: a prospective observational study (Full text)

Combination of thrombin-antithrombin complex, plasminogen activator inhibitor-1, and protein C activity for early identification of severe coagulopathy in initial phase of sepsis: a prospective observational study Current criteria for early diagnosis of coagulopathy in sepsis are limited. We postulated that coagulopathy is already complicated with sepsis in the initial phase, and severe coagulopathy or disseminated intravascular coagulation (DIC) becomes overt after progressive consumption (...) , fibrinogen and fibrin degradation product (FDP)); markers of thrombin generation (thrombin-antithrombin complex (TAT) and soluble fibrin); markers of anticoagulants (protein C (PC) and antithrombin); markers of fibrinolysis (plasminogen, α2-plasmin inhibitor (PI), plasmin-α2-PI complex, and plasminogen activator inhibitor (PAI)-1); and a marker of endothelial activation (soluble E-selectin) were assayed. Patients who had overt DIC at baseline were excluded, and the remaining patients were followed

2014 Critical Care PubMed abstract

156. Anti-thrombin III (ATIII) vs Placebo in Children (<7mo) Undergoing Open Congenital Cardiac Surgery

Additional relevant MeSH terms: Layout table for MeSH terms Antithrombin III Deficiency Blood Coagulation Disorders, Inherited Blood Coagulation Disorders Hematologic Diseases Blood Protein Disorders Thrombophilia Genetic Diseases, Inborn Thrombin Antithrombins Antithrombin III Hemostatics Coagulants Serine Proteinase Inhibitors Protease Inhibitors Enzyme Inhibitors Molecular Mechanisms of Pharmacological Action Anticoagulants (...) Anti-thrombin III (ATIII) vs Placebo in Children (<7mo) Undergoing Open Congenital Cardiac Surgery Anti-thrombin III (ATIII) vs Placebo in Children (<7mo) Undergoing Open Congenital Cardiac Surgery - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove

2014 Clinical Trials

157. Thrombin Generation Numerical Models Validation in Haemophilic Case

volunteers endogenous thrombin potential Additional relevant MeSH terms: Layout table for MeSH terms Hemophilia A Hemophilia B Blood Coagulation Disorders, Inherited Blood Coagulation Disorders Hematologic Diseases Coagulation Protein Disorders Hemorrhagic Disorders Genetic Diseases, Inborn Genetic Diseases, X-Linked Thrombin Hemostatics Coagulants (...) Thrombin Generation Numerical Models Validation in Haemophilic Case Thrombin Generation Numerical Models Validation in Haemophilic Case - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Thrombin Generation

2014 Clinical Trials

158. Redundancy and Interaction of Thrombin- and Collagen-Mediated Platelet Activation in Tail Bleeding and Carotid Thrombosis in Mice. (Full text)

independent, partially redundant contributions to occlusive thrombus formation in the carotid and to hemostatic clot formation in the tail under the experimental conditions examined. At face value, these results suggest that thrombin- and collagen-induced platelet activation can play partially redundant roles, despite important differences in how these agonists are made available to platelets.© 2014 American Heart Association, Inc. (...) Redundancy and Interaction of Thrombin- and Collagen-Mediated Platelet Activation in Tail Bleeding and Carotid Thrombosis in Mice. Current antiplatelet strategies to prevent myocardial infarction and stroke are limited by bleeding risk. A better understanding of the roles of distinct platelet-activating pathways is needed. We determined whether platelet activation by 2 key primary activators, thrombin and collagen, plays distinct, redundant, or interacting roles in tail bleeding and carotid

2014 Thrombosis and Vascular Biology PubMed abstract

159. Impaired thrombin generation in Reelin-deficient mice: a potential role of plasma Reelin in hemostasis. (Abstract)

Impaired thrombin generation in Reelin-deficient mice: a potential role of plasma Reelin in hemostasis. Reelin is a large extracellular glycoprotein that is present in the peripheral blood. That Reelin interacts with the coagulation components and elicits a functional role in hemostasis has not yet been elucidated.The hemostatic activity of Reelin is investigated and defined in this study.The interplay of Reelin with coagulation components was elucidated by far-Western and liposome/platelet (...) binding assays. In vivo and ex vivo hemostasis-related analyses of Reelin-deficient mice and plasma were also performed.Reelin interacted with the liposomes containing phosphatidylserine (PS) or phosphatidylcholine. Instead of interacting with known Reelin receptors (ApoE receptor 2, very low density lipoprotein receptor and integrin β1), Reelin interacted with PS of the activated platelets. The interaction between Reelin and the coagulation factors of thrombin and FXa was also demonstrated

2014 Journal of Thrombosis and Haemostasis

160. A systems approach to hemostasis: 3. Thrombus consolidation regulates intrathrombus solute transport and local thrombin activity. (Full text)

A systems approach to hemostasis: 3. Thrombus consolidation regulates intrathrombus solute transport and local thrombin activity. Hemostatic thrombi formed after a penetrating injury have a distinctive structure in which a core of highly activated, closely packed platelets is covered by a shell of less-activated, loosely packed platelets. We have shown that differences in intrathrombus molecular transport emerge in parallel with regional differences in platelet packing density and predicted (...) by computational modeling, a decrease in thrombin activity and platelet activation in the thrombus core. Collectively, these data (1) demonstrate that in addition to the activation state of individual platelets, the physical properties of the accumulated mass of adherent platelets is critical in determining intrathrombus agonist distribution and platelet activation and (2) define a novel role for integrin signaling in the regulation of intrathrombus transport rates and localization of thrombin activity. © 2014

2014 Blood PubMed abstract

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