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Platelet Dysfunction

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1. Protein kinase C signaling dysfunction in von Willebrand disease (p.V1316M) type 2B platelets (Full text)

Protein kinase C signaling dysfunction in von Willebrand disease (p.V1316M) type 2B platelets von Willebrand disease (VWD) type 2B is characterized by gain-of-function mutations in von Willebrand factor (VWF), enhancing its binding affinity for the platelet receptor glycoprotein (GP)Ibα. VWD type 2B patients display a bleeding tendency associated with loss of high-molecular-weight VWF multimers and variable thrombocytopenia. We recently demonstrated that a marked defect in agonist-induced (...) ) and the adenosine 5'-diphosphate receptor P2Y12. To investigate which Rap1 signaling pathway is affected, we expressed VWF/p.V1316M by hydrodynamic gene transfer in wild-type and Caldaggef1-/- mice. Using αIIbβ3 integrin activation as a read-out, we demonstrate that platelet dysfunction in VWD (p.V1316M) type 2B affects PKC-mediated, but not CDGI-mediated, activation of Rap1. Consistently, we observed decreased PKC substrate phosphorylation and impaired granule release in stimulated VWD type 2B platelets

2018 Blood advances PubMed

2. Mean platelet volume, platelet distribution width and platelet count in erectile dysfunction: A systematic review and meta-analysis. (PubMed)

Mean platelet volume, platelet distribution width and platelet count in erectile dysfunction: A systematic review and meta-analysis. The aim of this study was to investigate the relationship between mean platelet volume (MPV), platelet distribution width (PDW), platelet count (PC) and erectile dysfunction (ED). We searched for observational studies from PubMed, EMBASE, Web of Science and CNKI up to 31 March 2016. Two reviewers independently selected the studies and extracted the data. MPV, PDW (...) , and PC and mean differences in these platelet indices between healthy subjects and ED patients were explored using the Comprehensive Meta-Analysis software package. Seven studies including 795 patients and 524 healthy subjects met the inclusion criteria. The MPV was significantly larger in patients with ED than controls with the standardised mean difference of 0.596 fL (95% CI: 0.378, 0.815, p < 0.001). In ED patients, the pooled mean difference in MPV between vasculogenic ED patients

2017 Andrologia

3. Downregulation of TREM-like transcript (TLT)-1 and collagen receptor α2 subunit, two novel RUNX1-targets, contributes to platelet dysfunction in familial platelet disorder with predisposition to acute myelogenous leukemia. (Full text)

Downregulation of TREM-like transcript (TLT)-1 and collagen receptor α2 subunit, two novel RUNX1-targets, contributes to platelet dysfunction in familial platelet disorder with predisposition to acute myelogenous leukemia. Germline RUNX1 mutations lead to thrombocytopenia and platelet dysfunction in familial platelet disorder with predisposition to acute myelogenous leukemia. Multiple aspects of platelet function are impaired in these patients, associated with altered expression of genes (...) regulated by RUNX1. We aimed to identify RUNX1-targets involved in platelet function by combining transcriptome analysis of patient and shRUNX1-transduced megakaryocytes. Downregulated genes included TREM-like transcript (TLT)-1 (TREML1) and the integrin subunit α2 (ITGA2) of collagen receptor α2β1, which are involved in platelet aggregation and adhesion, respectively. RUNX1 binding to regions enriched for H3K27Ac marks was demonstrated for both genes using chromatin immunoprecipitation. Cloning

2018 Haematologica PubMed

4. Severe platelet dysfunction in NHL patients receiving ibrutinib is absent in patients receiving acalabrutinib (Full text)

Severe platelet dysfunction in NHL patients receiving ibrutinib is absent in patients receiving acalabrutinib The Bruton tyrosine kinase (Btk) inhibitor ibrutinib induces platelet dysfunction and causes increased risk of bleeding. Off-target inhibition of Tec is believed to contribute to platelet dysfunction and other side effects of ibrutinib. The second-generation Btk inhibitor acalabrutinib was developed with improved specificity for Btk over Tec. We investigated platelet function (...) in patients with non-Hodgkin lymphoma (NHL) receiving ibrutinib or acalabrutinib by aggregometry and by measuring thrombus formation on collagen under arterial shear. Both patient groups had similarly dysfunctional aggregation responses to collagen and collagen-related peptide, and comparison with mechanistic experiments in which platelets from healthy donors were treated with the Btk inhibitors suggested that both drugs inhibit platelet Btk and Tec at physiological concentrations. Only ibrutinib caused

2017 Blood advances PubMed

5. Prophylactic platelet transfusions prior to surgery for people with a low platelet count. (Full text)

Prophylactic platelet transfusions prior to surgery for people with a low platelet count. This is a protocol for a Cochrane Review (Intervention). The objectives are as follows: To determine the clinical effectiveness and safety of prophylactic platelet transfusions prior to surgery for people with a low platelet count or platelet dysfunction (inherited or acquired).

2017 Cochrane PubMed

6. Fatal dysfunction and disintegration of thrombin-stimulated platelets. (Full text)

Fatal dysfunction and disintegration of thrombin-stimulated platelets. Platelets play a key role in formation of hemostatic clots and obstructive thrombi as well as in other biological processes. In response to physiological stimulants, including thrombin, platelets change their morphology, express adhesive molecules, undergo aggregation, and secrete bioactive substances, but their subsequent fate is largely unknown. Here we examine late-stage structural, metabolic, and functional consequences (...) of thrombin-induced platelet activation. Using a combination of confocal microscopy, scanning and transmission electron microscopy, flow cytometry, biochemical and biomechanical measurements, we show that thrombin-induced activation is followed by time-dependent platelet dysfunction and disintegration. After ~30 minutes of incubation with thrombin, unlike with collagen or ADP, human platelets underwent disintegration into cellular fragments containing organelles, such as mitochondria, glycogen granules

2019 Haematologica PubMed

7. Platelets retain inducible alpha granule secretion by P-selectin expression but exhibit mechanical dysfunction during trauma-induced coagulopathy. (PubMed)

Platelets retain inducible alpha granule secretion by P-selectin expression but exhibit mechanical dysfunction during trauma-induced coagulopathy. Trauma-induced coagulopathy (TIC) is a common and deadly bleeding disorder. Platelet dysfunction is present during TIC, but its mechanisms remain unclear. Platelets are currently thought to become "exhausted", a state in which they have released their granule contents and can no longer aggregate or contract.This prospective observational cohort study (...) tested the hypothesis that platelet exhaustion is present during TIC and characterized the early time course of platelet dysfunction. Blood was collected from 95 adult trauma patients at a Level I trauma center at time of Emergency Department arrival and several time points over 72 hours. Platelet activation state and function were characterized using CD62P (P-selectin) and PAC-1 surface membrane staining, PFA-100, aggregometry, viscoelastic platelet mapping, and, to test for exhaustion

2019 Journal of Thrombosis and Haemostasis

8. Platelet dysfunction after out of hospital cardiac arrest. Results from POHCAR: a prospective observational, cohort study. (PubMed)

Platelet dysfunction after out of hospital cardiac arrest. Results from POHCAR: a prospective observational, cohort study. Coagulation and platelet function following out of hospital cardiac arrest (OHCA) at admission to a UK cardiology centre were investigated prospectively in this observational feasibility study, and compared to that of patients receiving percutaneous coronary intervention (PCI) for ST segment elevation myocardial infarction (STEMI).Blood samples taken immediately (...) at emergency department admission from patients after OHCA of probable cardiac origin were analysed using near-patient thromboelastometry and a platelet function analyser. Physiological parameters, demographic information, bleeding rates and 30-day survival were recorded, and compared to that of patients undergoing PCI for STEMI.Thirty patients were enrolled into each group. Platelet activation with thrombin receptor stimulation was reduced in OHCA patients compared to STEMI patients; mean TRAP AUC OHCA

2019 Resuscitation

9. The association between platelet dysfunction and adverse outcomes in cardiac surgical patients. (PubMed)

The association between platelet dysfunction and adverse outcomes in cardiac surgical patients. Haemostatic activation during cardiopulmonary bypass is associated with prothrombotic complications. Although it is not possible to detect and quantify haemostatic activation directly, platelet dysfunction, as measured with point-of-care-assays, may be a useful surrogate. In this study, we assessed the association between cardiopulmonary bypass-associated platelet dysfunction and adverse outcomes (...) in 3010 cardiac surgical patients. Platelet dysfunction, as measured near the end of the rewarming phase of cardiopulmonary bypass, was calculated as the proportion of non-functional platelets after activation with collagen. Logistic regression and multivariable analyses were applied to assess the relationship between platelet dysfunction and a composite of in-hospital death; myocardial infarction; stroke; deep vein thrombosis or pulmonary embolism; and acute kidney injury (greater than a two-fold

2019 Anaesthesia

10. Adenosine, lidocaine and Mg2+ (ALM) fluid therapy attenuates systemic inflammation, platelet dysfunction and coagulopathy after non-compressible truncal hemorrhage. (Full text)

Adenosine, lidocaine and Mg2+ (ALM) fluid therapy attenuates systemic inflammation, platelet dysfunction and coagulopathy after non-compressible truncal hemorrhage. Systemic inflammation and coagulopathy are major drivers of injury progression following hemorrhagic trauma. Our aim was to examine the effect of small-volume 3% NaCl adenosine, lidocaine and Mg2+ (ALM) bolus and 0.9% NaCl/ALM 'drip' on inflammation and coagulation in a rat model of hemorrhagic shock.Sprague-Dawley rats (429±4 g (...) they were less or similar to shams. Non-ALM groups (except shams) also lost their ability to aggregate platelets, had lower plasma fibrinogen levels, and were hypocoagulable. ALM-treated animals had 50-fold higher ADP-induced platelet aggregation, and 9.3-times higher collagen-induced aggregation compared to saline-controls, and had little or no coagulopathy with significantly higher fibrinogen shifting towards baseline. Hextend® had poor outcomes.Small-volume ALM bolus/drip mounted a frontline defense

2017 PLoS ONE PubMed

11. Thrombocytopenia and Platelet Dysfunction in Acute Tropical Infectious Diseases. (PubMed)

Thrombocytopenia and Platelet Dysfunction in Acute Tropical Infectious Diseases. Thrombocytopenia is a well-known manifestation of acute tropical infectious diseases. The role of platelets in infections has received much attention recently because of their emerging activities in modulation of inflammatory responses, host defense, and vascular integrity. However, while many studies have addressed thrombocytopenia in tropical infections, abnormalities in platelet function have been largely (...) overlooked. This is an important research gap, as platelet dysfunction may contribute to the bleeding tendency that characterizes some tropical infections. The development of novel platelet function assays that can be used in thrombocytopenic conditions (e.g., flow cytometry assays) has contributed to important new insights in recent years. In this review, the importance of platelets in tropical infections is discussed with special emphasis on the underlying mechanisms and consequences

2018 Seminars In Thrombosis And Hemostasis

12. Impaired mitochondrial activity explains platelet dysfunction in thrombocytopenic cancer patients undergoing chemotherapy. (Full text)

Impaired mitochondrial activity explains platelet dysfunction in thrombocytopenic cancer patients undergoing chemotherapy. Severe thrombocytopenia (≤50×109 platelets/L) due to hematological malignancy and intensive chemotherapy is associated with an increased risk of clinically significant bleeding. Since the bleeding risk is not linked to the platelet count only, other hemostatic factors must be involved. We studied platelet function in 77 patients with acute leukemia, multiple myeloma (...) or malignant lymphoma, who experienced chemotherapy-induced thrombocytopenia. Platelets from all patients - independent of disease or treatment type - were to a variable extent compromised in Ca2+ flux, integrin a β activation and P-selectin expression when stimulated with a panelIIbof3 agonists. The patients' platelets were also impaired in spreading on fibrinogen. Whereas the Ca2+ store content was unaffected, the patients' platelets showed ongoing phosphatidylserine exposure, which was not due

2018 Haematologica PubMed

13. Mechanisms of Platelet Dysfunction in Patients with Implantable Devices. (PubMed)

Mechanisms of Platelet Dysfunction in Patients with Implantable Devices. As treatment options in modern medicine continue to expand, physicians globally have witnessed a veritable explosion in the utility of therapeutic devices. Particularly within the spheres of cardiology and critical care medicine, a plethora of devices are now available with an ever-increasing range of clinical indications. Additionally, the advent of transcatheter-mounted devices has enabled patients unsuitable for more (...) and device-induced perturbations. However, less is known about impact of mechanical surfaces on platelets and the resultant clinical complications, both hemorrhagic and thrombotic. This review will focus on exploring the pathobiology of platelet-surface interactions, contextualized within the wider hemostatic system, with a focus on the increasingly utilized technologies of transcatheter aortic-valve implantation, ventricular assist devices, and extracorporeal membrane oxygenation.Thieme Medical

2018 Seminars In Thrombosis And Hemostasis

14. Platelet Dysfunction in Blood Donors

Platelet Dysfunction in Blood Donors Platelet Dysfunction in Blood Donors - 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. Platelet Dysfunction in Blood Donors (DysPlaq) The safety and scientific validity (...) , considerable progress has been made in understanding qualitative platelet disorders. In this project, we propose to submit blood donors to a standardized hemorrhagic diathesis questionnaire and to compare the prevalence of platelet function abnormalities in blood donors with and without hemorrhagic diathesis. Condition or disease Intervention/treatment Phase Platelet Dysfunction in Blood Donors Biological: sample Not Applicable Detailed Description: Primary objective specify the prevalence of qualitative

2018 Clinical Trials

15. The Main Determinants of Diabetes Mellitus Vascular Complications: Endothelial Dysfunction and Platelet Hyperaggregation (Full text)

The Main Determinants of Diabetes Mellitus Vascular Complications: Endothelial Dysfunction and Platelet Hyperaggregation Diabetes mellitus is a common disease that affects 3⁻5% of the general population in Italy. In some countries of northern Europe or in North America, it can even affect 6⁻8% of the population. Of great concern is that the number of cases of diabetes is constantly increasing, probably due to the increase in obesity and the sedentary nature of the population. According (...) to the World Health Organization, in the year 2030 there will be 360 million people with diabetes, compared to 170 million in 2000. This has important repercussions on the lives of patients and their families, and on health systems that offer assistance to patients. In this review, we try to describe in an organized way the pathophysiological continuity between diabetes mellitus, endothelial dysfunction, and platelet hyperaggregation, highlighting the main molecular mechanisms involved

2018 International journal of molecular sciences PubMed

16. Endothelial dysfunction and platelet hyperactivity in type 2 diabetes mellitus: molecular insights and therapeutic strategies (Full text)

Endothelial dysfunction and platelet hyperactivity in type 2 diabetes mellitus: molecular insights and therapeutic strategies The incidence and prevalence of diabetes mellitus is rapidly increasing worldwide at an alarming rate. Type 2 diabetes mellitus (T2DM) is the most prevalent form of diabetes, accounting for approximately 90-95% of the total diabetes cases worldwide. Besides affecting the ability of body to use glucose, it is associated with micro-vascular and macro-vascular complications (...) . Augmented atherosclerosis is documented to be the key factor leading to vascular complications in T2DM patients. The metabolic milieu of T2DM, including insulin resistance, hyperglycemia and release of excess free fatty acids, along with other metabolic abnormalities affects vascular wall by a series of events including endothelial dysfunction, platelet hyperactivity, oxidative stress and low-grade inflammation. Activation of these events further enhances vasoconstriction and promotes thrombus formation

2018 Cardiovascular diabetology PubMed

17. Platelet Aggregometry Cannot Identify Uremic Platelet Dysfunction in Heart Failure Patients Prior to Cardiac Surgery (Full text)

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 PubMed

18. Germline variants in ETV6 underlie reduced platelet formation, platelet dysfunction and increased levels of circulating CD34+ progenitors. (Full text)

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 PubMed

19. 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)

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 PubMed

20. Can Eosinophil Count, Platelet Count, and Mean Platelet Volume Be a Positive Predictive Factor in Penile Arteriogenic Erectile Dysfunction Etiopathogenesis? (Full text)

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 PubMed

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