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Platelet Dysfunction

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41. Germline variants in ETV6 underlie reduced platelet formation, platelet dysfunction and increased levels of circulating CD34+ progenitors. Full Text available with Trip Pro

Germline variants in ETV6 underlie reduced platelet formation, platelet dysfunction and increased levels of circulating CD34+ progenitors. Variants in ETV6, which encodes a transcription repressor of the E26 transformation-specific family, have recently been reported to be responsible for inherited thrombocytopenia and hematologic malignancy. We sequenced the DNA from cases with unexplained dominant thrombocytopenia and identified six likely pathogenic variants in ETV6, of which five are novel (...) with lentiviral particles encoding mutant ETV6. Reduced expression levels of key regulators of the actin cytoskeleton CDC42 and RHOA were measured. Moreover, changes in the actin structures are typically accompanied by a rounder platelet shape with a highly heterogeneous size, decreased platelet arachidonic response, and spreading and retarded clot retraction in ETV6 deficient platelets. Elevated numbers of circulating CD34+ cells were found in p.P214L and p.Y401N carriers, and two patients from different

2016 Haematologica

42. Platelet Aggregometry Cannot Identify Uremic Platelet Dysfunction in Heart Failure Patients Prior to Cardiac Surgery Full Text available with Trip Pro

Platelet Aggregometry Cannot Identify Uremic Platelet Dysfunction in Heart Failure Patients Prior to Cardiac Surgery Patients with heart failure often have concomitant renal disease which can result in uremic platelet dysfunction. Determining whether uremia has affected platelets by platelet aggregometry can be challenging in these patients since they are often on antiplatelet medications. This study was undertaken to determine if platelet aggregation studies could identify heart failure (...) of the agonists. There was a pan-decrease in platelet aggregation to all agonists in all heart failure patients.Platelet aggregometry does not appear to be useful in measuring platelet dysfunction in heart failure patients with mild to moderate renal impairment.© 2016 Wiley Periodicals, Inc.

2016 Journal of clinical laboratory analysis

43. Increased Smad2/3 Phosphorylation in Circulating Leukocytes and Platelet-Leukocyte Aggregates in a Mouse Model of Aortic Valve Stenosis: Evidence of Systemic Activation of Platelet-Derived TGF-β1 and Correlation with Cardiac Dysfunction Full Text available with Trip Pro

Increased Smad2/3 Phosphorylation in Circulating Leukocytes and Platelet-Leukocyte Aggregates in a Mouse Model of Aortic Valve Stenosis: Evidence of Systemic Activation of Platelet-Derived TGF-β1 and Correlation with Cardiac Dysfunction Transforming growth factor-β1 (TGF-β1) has been implicated in the pathogenesis of aortic valve stenosis (AS). There is, however, little direct evidence for a role of active TGF-β1 in AS due to the sensitivity of current assays. We searched for evidence (...) of plasma TGF-β1 activation by assaying Smad2/3 phosphorylation in circulating leukocytes and platelet-leukocyte aggregates (PLAs) in a mouse model of AS (Reversa).Echocardiography was used to measure AS and cardiac function. Intracellular phospho-flow cytometry in combination with optical fluorescence microscopy was used to detect PLAs and p-Smad2/3 levels.Reversa mice on a western diet developed AS, had significantly increased numbers of PLAs and more intense staining for p-Smad2/3 in both PLAs

2016 Blood cells, molecules & diseases

44. Can Eosinophil Count, Platelet Count, and Mean Platelet Volume Be a Positive Predictive Factor in Penile Arteriogenic Erectile Dysfunction Etiopathogenesis? Full Text available with Trip Pro

Can Eosinophil Count, Platelet Count, and Mean Platelet Volume Be a Positive Predictive Factor in Penile Arteriogenic Erectile Dysfunction Etiopathogenesis? Blood count parameters of patients referring with erectile dysfunction (ED) were examined in this study and it was investigated whether eosinophil count (EC), platelet count (PC), and mean platelet volume values among the suspected predictive parameters which may play a role in especially penile arteriogenic ED etiopathogenesis had (...) of 36 patients participated in the study from the penile arteriogenic ED group and 32 patients from the nonvasculogenic ED group. Compared with the nonvasculogenic ED group, the penile arteriogenic ED group's low International Index of Erectile Function score, high EC, mean platelet volume and PC values were detected to be statistically significant ( p < .001, p = .021, p = .018, p = .034, respectively). No statistically significant difference was observed among the two groups when age, white blood

2016 American journal of men's health

45. Incidence of Platelet Dysfunction by Thromboelastography–Platelet Mapping in Children Supported with ECMO: A Pilot Retrospective Study Full Text available with Trip Pro

Incidence of Platelet Dysfunction by Thromboelastography–Platelet Mapping in Children Supported with ECMO: A Pilot Retrospective Study Bleeding complications are common and decrease the odds of survival in children supported with extracorporeal membrane oxygenation (ECMO). The role of platelet dysfunction on ECMO-induced coagulopathy and resultant bleeding complications is not well understood. The primary objective of this pilot study was to determine the incidence and magnitude of platelet (...) dysfunction according to thromboelastography (TEG(®))-platelet mapping (PM) testing.Retrospective chart review of children <18 years old who required ECMO at a tertiary level hospital. We collected TEG(®)-PM and conventional coagulation tests data. We also collected demographic, medications, blood products administered, and clinical outcome data. We defined severe platelet dysfunction as <50% aggregation in response to an agonist.We identified 24 out of 46 children on ECMO, who had TEG(®)-PM performed

2016 Frontiers in pediatrics

46. Nintedanib and Sildenafil in Patients with Idiopathic Pulmonary Fibrosis and Right Heart Dysfunction. A Prespecified Subgroup Analysis of a Double-Blind Randomized Clinical Trial (INSTAGE) Full Text available with Trip Pro

Nintedanib and Sildenafil in Patients with Idiopathic Pulmonary Fibrosis and Right Heart Dysfunction. A Prespecified Subgroup Analysis of a Double-Blind Randomized Clinical Trial (INSTAGE) Nintedanib and Sildenafil in Patients With Idiopathic Pulmonary Fibrosis and Right Heart Dysfunction. A Prespecified Subgroup Analysis of a Double-Blind Randomized Clinical Trial (INSTAGE) - PubMed This site needs JavaScript to work properly. Please enable it to take advantage of the complete set of features (...) Dysfunction. A Prespecified Subgroup Analysis of a Double-Blind Randomized Clinical Trial (INSTAGE) , , , , , , , Affiliations Expand Affiliations 1 Department of Internal Medicine V, University of Munich, LMU, and Asklepios Chest Clinic Gauting, Memeber of the German Center for Lung Research, Germany. 2 McMaster University and St. Joseph's Healthcare, Hamilton, Ontario, Canada. 3 Department of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South

2020 EvidenceUpdates

47. Cathepsin K induces platelet dysfunction and affects cell signaling in breast cancer - molecularly distinct behavior of cathepsin K in breast cancer. Full Text available with Trip Pro

Cathepsin K induces platelet dysfunction and affects cell signaling in breast cancer - molecularly distinct behavior of cathepsin K in breast cancer. Breast cancer comprises clinically and molecularly distinct tumor subgroups that differ in cell histology and biology and show divergent clinical phenotypes that impede phase III trials, such as those utilizing cathepsin K inhibitors. Here we correlate the epithelial-mesenchymal-like transition breast cancer cells and cathepsin K secretion (...) target by immunodetection and specific antagonists using a fibroblast cell line derived from PARs deficient mice. Moreover, through co-culture experiments, we show that platelets activated by cathepsin K mediated the up-regulation of SHH, PTHrP, OPN, and TGFβ in epithelial-mesenchymal-like cells from patients with Luminal B breast cancer.Cathepsin K induces platelet dysfunction and affects signaling in breast cancer cells.

2016 BMC Cancer

48. Platelet Dysfunction in Patients with Chronic Myeloid Leukemia: Does Imatinib Mesylate Improve It? Full Text available with Trip Pro

Platelet Dysfunction in Patients with Chronic Myeloid Leukemia: Does Imatinib Mesylate Improve It? The aim of this study was to investigate the effects of imatinib mesylate on platelet aggregation and adenosine triphosphate (ATP) release in chronic myeloid leukemia patients.Platelet aggregation and ATP release induced by 5.0 mM adenosine diphosphate, 0.5 mM arachidonic acid, 1.0 mg/mL ristocetin, and 2 µg/mL collagen were studied by whole blood platelet lumi-aggregometer in 20 newly diagnosed (...) chronic myeloid leukemia patients before and after imatinib mesylate treatment.At the time of diagnosis, 17/20 patients had abnormal platelet aggregation results; 8 (40%) had hypoactivity, 6 (30%) had hyperactivity, and 3 (15%) had mixed hypo- and hyperactivity. Repeat platelet aggregation studies were performed after a mean of 19 months (min: 5 months-max: 35 months) in all patients who received imatinib mesylate during this period. After therapy, 18/20 (90%) patients had abnormal laboratory results

2016 Turkish Journal of Hematology

49. Platelet-Rich Fibrin Lysate Can Ameliorate Dysfunction of Chronically UVA-Irradiated Human Dermal Fibroblasts Full Text available with Trip Pro

Platelet-Rich Fibrin Lysate Can Ameliorate Dysfunction of Chronically UVA-Irradiated Human Dermal Fibroblasts To determine whether platelet-rich fibrin lysate (PRF-L) could restore the function of chronically ultraviolet-A (UVA)-irradiated human dermal fibroblasts (HDFs), we isolated and sub-cultured HDFs from six different human foreskins. HDFs were divided into two groups: those that received chronic UVA irradiation (total dosages of 10 J cm⁻²) and those that were not irradiated. We compared

2016 Yonsei medical journal

50. Platelet Dysfunction in Type 1 Diabetes: Stressing the Thromboxanes Full Text available with Trip Pro

Platelet Dysfunction in Type 1 Diabetes: Stressing the Thromboxanes 26798121 2016 06 02 2018 12 02 1939-327X 65 2 2016 Feb Diabetes Diabetes Platelet Dysfunction in Type 1 Diabetes: Stressing the Thromboxanes. 349-51 10.2337/dbi15-0032 Wisinski Jaclyn A JA Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Wisconsin-Madison, Madison, WI. Kimple Michelle E ME Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Wisconsin (...) -Madison, Madison, WI mkimple@medicine.wisc.edu. eng R01 DK102598 DK NIDDK NIH HHS United States Journal Article Comment United States Diabetes 0372763 0012-1797 0 Platelet Aggregation Inhibitors 57576-52-0 Thromboxane A2 DCR9Z582X0 Epoprostenol R16CO5Y76E Aspirin AIM IM Diabetes. 2016 Feb;65(2):503-9 26470782 Aspirin pharmacology Diabetes Mellitus, Type 1 drug therapy Epoprostenol biosynthesis Female Humans Male Platelet Activation physiology Platelet Aggregation Inhibitors pharmacology Thromboxane A2

2016 Diabetes

51. Dasatinib and Dysfunction of Platelets Full Text available with Trip Pro

Dasatinib and Dysfunction of Platelets 27408403 2016 07 13 2018 11 13 0971-4502 32 Suppl 1 2016 Jun Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion Indian J Hematol Blood Transfus Dasatinib and Dysfunction of Platelets. 246-7 10.1007/s12288-016-0659-x Sahu Kamal Kant KK Department of Clinical Haematology, Internal Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012 India. Yanamandra (...) 24;117(8):e75-87 20810928 Rinsho Ketsueki. 2014 Jan;55(1):130-2 24492046 Prostaglandins Leukot Essent Fatty Acids. 2014 Feb-Mar;90(2-3):61-8 24373610 Gan To Kagaku Ryoho. 2010 Nov;37(11):2213-5 21084830 Blood. 2009 Jul 9;114(2):261-3 19414863 Pharmacol Ther. 2014 Nov;144(2):97-113 24858060 Platelets. 2015;26(8):809-11 26029798 Leuk Lymphoma. 2015;56(8):2309-14 25563556 Biomed Res Int. 2014;2014:456569 24895576 Platelets. 2015;26(5):491-4 25025538

2016 Indian Journal of Hematology & Blood Transfusion

52. Modeling HIV-1 Induced Neuroinflammation in Mice: Role of Platelets in Mediating Blood-Brain Barrier Dysfunction Full Text available with Trip Pro

Modeling HIV-1 Induced Neuroinflammation in Mice: Role of Platelets in Mediating Blood-Brain Barrier Dysfunction The number of HIV-1 positive individuals developing some form of HIV-associated neurocognitive disorder (HAND) is increasing. In these individuals, the integrity of the blood-brain barrier (BBB) is compromised due to an increase in exposure to pro-inflammatory mediators, viral proteins, and virus released from infected cells. It has been shown that soluble CD40L (sCD40L) is released (...) associated with decreased expression of tight junction protein claudin-5, in CD40L and platelet activation-dependent manner. Treatment with an antiplatelet drug, eptifibatide, in EcoHIV-infected mice normalized BBB function, sCD40L release and platelet activity, thus implicating platelet activation and platelet-derived CD40L in virally induced BBB dysfunction. Our results also validate and underscore the importance of EcoHIV infection mouse model as a tool to explore therapeutic targets for HAND.

2016 PloS one

53. Dysfunctional epileptic neuronal circuits and dysmorphic dendritic spines are mitigated by platelet-activating factor receptor antagonism Full Text available with Trip Pro

Dysfunctional epileptic neuronal circuits and dysmorphic dendritic spines are mitigated by platelet-activating factor receptor antagonism Temporal lobe epilepsy or limbic epilepsy lacks effective therapies due to a void in understanding the cellular and molecular mechanisms that set in motion aberrant neuronal network formations during the course of limbic epileptogenesis (LE). Here we show in in vivo rodent models of LE that the phospholipid mediator platelet-activating factor (PAF) increases (...) . We suggest that over-activation of PAF-r signaling induces aberrant neuronal plasticity in LE and leads to chronic dysfunctional neuronal circuitry that mediates epilepsy.

2016 Scientific reports

54. Inherited Platelet Dysfunction and Hematopoietic Transcription Factor Mutations Full Text available with Trip Pro

Inherited Platelet Dysfunction and Hematopoietic Transcription Factor Mutations Transcription factors (TFs) are proteins that bind to specific DNA sequences and regulate expression of genes. The molecular and genetic mechanisms in most patients with inherited platelet dysfunction are unknown. There is now increasing evidence that mutations in hematopoietic TFs are an important underlying cause for the defects in platelet production, morphology, and function. The hematopoietic TFs implicated (...) . Mutations involving these TFs affect diverse aspects of megakaryocyte biology and platelet production and function, culminating in thrombocytopenia, platelet dysfunction, and associated clinical features. Mutations in TFs may occur more frequently in the patients with inherited platelet dysfunction than generally appreciated. This review focuses on the alterations in hematopoietic TFs in the pathobiology of inherited platelet dysfunction.

2016 Platelets

55. Vascular type Ehlers-Danlos syndrome is associated with platelet dysfunction and low vitamin D serum concentration Full Text available with Trip Pro

Vascular type Ehlers-Danlos syndrome is associated with platelet dysfunction and low vitamin D serum concentration The vascular type represents a very rare, yet the clinically most fatal entity of Ehlers-Danlos syndrome (EDS). Patients are often admitted due to arterial bleedings and the friable tissue and the altered coagulation contribute to the challenge in treatment strategies. Until now there is little information about clotting characteristics that might influence hemostasis decisively (...) and eventually worsen emergency situations.22 vascular type EDS patients were studied for hemoglobin, platelet volume and count, Quick and activated partial thromboplastin time, fibrinogen, factor XIII, von Willebrand disease, vitamin D and platelet aggregation by modern standard laboratory methods. Results show a high prevalence of over 50 % for platelet aggregation disorders in vascular type EDS patients, especially for collagen and epinephrine induced tests, whereas the plasmatic cascade did not show any

2016 Orphanet journal of rare diseases

56. Inherited dysfunctional platelet P2Y12 receptor mutations associated with bleeding disorders Full Text available with Trip Pro

Inherited dysfunctional platelet P2Y12 receptor mutations associated with bleeding disorders The platelet adenosine 5'-diphosphate (ADP) receptor P2Y12 (P2Y12R) plays a critical role in platelet aggregation. The present report illustrates an update of dysfunctional platelet P2Y12R mutations diagnosed with congenital lifelong bleeding problems. Described patients with heterozygous or homozygous substitution in the P2Y12R gene and qualitative abnormalities of the platelet P2Y12R are summarized (...) . Recently, a further dysfunctional variant of P2Y12R has been identified in two brothers who presented with a lifelong severe bleeding disorder. During in vitro aggregation studies, the patient´s platelets show a markedly reduced and rapid reversible ADP-promoted aggregation. A homozygous c.561T>A substitution that changes the codon for His187 to Gln (p.His187Gln) in the P2Y12R gene has been identified. This mutation causes no change in receptor expression but decreases the affinity of the ligand

2016 Hamostaseologie

57. Tranexamic acid decreases the magnitude of platelet dysfunction in aspirin-free patients undergoing cardiac surgery with cardiopulmonary bypass: a pilot study. (Abstract)

Tranexamic acid decreases the magnitude of platelet dysfunction in aspirin-free patients undergoing cardiac surgery with cardiopulmonary bypass: a pilot study. This study sought to compare the effect of tranexamic acid (TXA) administration on cardiopulmonary bypass-induced platelet dysfunction in patients who received preoperative aspirin or not. We performed a prospective, randomized, double-blind pilot study, including patients undergoing elective cardiac surgery with cardiopulmonary bypass (...) test, thrombin receptor-activating peptide test, and ASP test, at the end of CPB (P < 0.05). TXA might decrease the magnitude of platelet dysfunction in aspirin-free patients undergoing cardiac surgery. Further studies are needed to confirm these results and assess a potential relationship with clinical endpoints.

2016 Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis Controlled trial quality: uncertain

58. Desmopressin for treatment of platelet dysfunction and reversal of antiplatelet agents: a systematic review and meta-analysis of randomised controlled trials. Full Text available with Trip Pro

Desmopressin for treatment of platelet dysfunction and reversal of antiplatelet agents: a systematic review and meta-analysis of randomised controlled trials. Essentials The optimal management of patients with platelet dysfunction undergoing surgery is unclear. This meta-analysis compared perioperative administration of desmopressin to placebo. Desmopressin reduced red cell transfusions, blood loss and risk of re-operation due to bleeding. There were too few events to determine (...) if there was a change in the risk of thrombotic events.Background Platelet dysfunction, including that caused by antiplatelet agents, increases the risk of perioperative bleeding. The optimal management of patients with platelet dysfunction undergoing surgery is unclear. Objectives To assess whether desmopressin reduces perioperative allogeneic red cell transfusion and bleeding in patients with platelet dysfunction. Patients/Methods We searched for randomized controlled trials in The Cochrane Central Register

2016 Journal of thrombosis and haemostasis : JTH

59. Novel mutations in RASGRP2 encoding for CalDAG-GEFI abrogate Rap1 activation causing platelet dysfunction. Full Text available with Trip Pro

Novel mutations in RASGRP2 encoding for CalDAG-GEFI abrogate Rap1 activation causing platelet dysfunction. In addition to mutations in ITG2B or ITGB3 genes that cause defective αIIbβ3 expression and/or function in Glanzmann's thrombasthenia patients, platelet dysfunction can be a result of genetic variability in proteins that mediate inside-out activation of αIIbβ3 The RASGRP2 gene is strongly expressed in platelets and neutrophils, where its encoded protein CalDAG-GEFI facilitates (...) the activation of Rap1 and subsequent activation of integrins. We used next-generation sequencing (NGS) and whole-exome sequencing (WES) to identify 2 novel function-disrupting mutations in RASGRP2 that account for bleeding diathesis and platelet dysfunction in 2 unrelated families. By using a panel of 71 genes, we identified a homozygous change (c.1142C>T) in exon 10 of RASGRP2 in a 9-year-old child of Chinese origin (family 1). This variant led to a p.Ser381Phe substitution in the CDC25 catalytic domain

2016 Blood

60. Cytoskeletal perturbation leads to platelet dysfunction and thrombocytopenia in Glanzmann variants. Full Text available with Trip Pro

Cytoskeletal perturbation leads to platelet dysfunction and thrombocytopenia in Glanzmann variants. Several patients have been reported to have variant dominant forms of Glanzmann thrombasthenia, associated with macrothrombocytopenia and caused by gain-of-function mutations of ITGB3 or ITGA2B leading to reduced surface expression and constitutive activation of integrin αIIbβ3. The mechanisms leading to a bleeding phenotype of these patients have never been addressed. The aim of this study (...) was to unravel the mechanism by which ITGB3 mutations causing activation of αIIbβ3 lead to platelet dysfunction and macrothrombocytopenia. Using platelets from two patients carrying the β3 del647-686 mutation and Chinese hamster ovary cells expressing different αIIbβ3-activating mutations, we showed that reduced surface expression of αIIbβ3 is due to receptor internalization. Moreover, we demonstrated that permanent triggering of αIIbβ3-mediated outside-in signaling causes an impairment of cytoskeletal

2015 Haematologica

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