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neutrophil, thrombosis

Gemma Radley, Ina Laura Pieper, Bethan R Thomas, Karl Hawkins, Catherine A Thornton
Medical devices, such as ventricular assist devices (VADs), introduce both foreign materials and artificial shear stress to the circulatory system. The effects these have on leukocytes and the immune response are not well understood. Understanding how these two elements combine to affect leukocytes may reveal why some patients are susceptible to recurrent device-related infections and provide insight into the development of pump thrombosis. Biomaterials - DLC: diamond-like carbon coated stainless steel; Sap: single-crystal sapphire; and Ti: titanium alloy (Ti6Al4V) were attached to the parallel plates of a rheometer...
December 8, 2018: Artificial Organs
Mirta Schattner
Platelet TLR-4 activation by pathogen- or damage-associated molecular pattern molecules triggers pro-thrombotic, proinflammatory, and pro-coagulant effector responses. Moreover, platelet TLR4 has a prominent role as a sensor of high lipopolysaccharide circulating levels during sepsis and in the clearance of pathogens mediated by neutrophils. This review presents evidence pointing to TLR4 as a bridge connecting thrombosis and innate immunity.
December 4, 2018: Journal of Leukocyte Biology
Kartika R Pertiwi, Onno J de Boer, Claire Mackaaij, Dara R Pabittei, Robbert J de Winter, Xiaofei Li, Allard C van der Wal
Extracellular traps generated by neutrophils contribute to thrombus progression in coronary atherosclerotic plaques. It is not known whether other inflammatory cell types in coronary atherosclerotic plaque or thrombus also release extracellular traps. We investigated their formation by macrophages, mast cells and eosinophils in human coronary atherosclerosis, and in relation to the age of thrombus of myocardial infarction patients. Coronary arteries with thrombosed or intact plaques were retrieved from patients who died from myocardial infarction...
December 2, 2018: Journal of Pathology
Giacomo Emmi, Alessandra Bettiol, Elena Silvestri, Gerardo Di Scala, Matteo Becatti, Claudia Fiorillo, Domenico Prisco
Behçet's syndrome (BS) is a complex vasculitis, characterised by peculiar histological, pathogenetic and clinical features. Superficial venous thrombosis (SVT) and deep vein thrombosis (DVT) are the most frequent vascular involvements, affecting altogether 15-40% of BS patients. Atypical thrombosis is also an important clinical feature of BS, involving the vascular districts of the inferior and superior vena cava, suprahepatic veins with Budd-Chiari syndrome, portal vein, cerebral sinuses and right ventricle...
November 29, 2018: Internal and Emergency Medicine
Liyan Wang, Jiangang Duan, Tingting Bian, Ran Meng, Longfei Wu, Zhen Zhang, Xuxiang Zhang, Chunxiu Wang, Xunming Ji
BACKGROUND: Few studies have suggested a relationship between inflammation and cerebral venous thrombosis (CVT). This retrospective study aimed to explore the changes in inflammation in different CVT stages and the correlation between inflammation and severity and outcome of CVT. METHODS: In total, 95 suitable patients with CVT and 41 controls were compared. Patients with CVT were divided into three groups. The inflammatory factors studied included hypersensitive C-reactive protein (Hs-CRP), interleukin-6 (IL-6), and neutrophil-to-lymphocyte ratio (NLR) in the peripheral blood and immunoglobulin A (IgA), immunoglobulin M (IgM), and immunoglobulin G (IgG) in the cerebrospinal fluid (CSF)...
November 26, 2018: Journal of Neuroinflammation
Matteo Becatti, Giacomo Emmi, Alessandra Bettiol, Elena Silvestri, Gerardo Di Scala, Niccolò Taddei, Domenico Prisco, Claudia Fiorillo
Behçet's syndrome (BS) is a complex disease with different organ involvement. The vascular one is the most intriguing considering the existence of a specific group of patients suffering from recurrent vascular events involving the venous and, more rarely, the arterial vessels. There are several clinical clues suggesting the inflammatory nature of thrombosis in BS, especially of the venous involvement, thus BS is considered a model of inflammation-induced thrombosis. Unique among other inflammatory conditions, venous involvement (together with the arterial one) is currently treated with immunosuppressants, rather than with anticoagulants...
November 25, 2018: Clinical and Experimental Immunology
Jingyi Zhou, Erwen Xu, Kang Shao, Wenyan Shen, Yi Gu, Min Li, Wei Shen
Background Platelet-neutrophil aggregates (PNAs) are fundamental mechanisms linking hemostasis and inflammatory processes. Elevated level of PNAs have been reported in inflammatory diseases and coronary artery diseases. However, studies on the correlation between PNAs formation and deep venous thrombosis (DVT) are not available. Methods A total of 92 participants were involved in this study, including 32 cases with DVT and 60 cases without DVT. Blood samples coagulated by K2-EDTA or sodium citrate were prepared for blood cell count and blood smears...
November 24, 2018: Clinical Chemistry and Laboratory Medicine: CCLM
Daigo Nakazawa, Julian A Marschner, Louise Platen, Hans-Joachim Anders
During the past decade the formation of neutrophil extracellular traps (NETs) has been recognized as a unique modality of pathogen fixation (sticky extracellular chromatin) and pathogen killing (cytotoxic histones and proteases) during host defense, as well as collateral tissue damage. Numerous other triggers induce NET formation in multiple forms of sterile inflammation, including thrombosis, gout, obstruction of draining ducts, and trauma. Whether neutrophils always die along with NET release, and if they do die, how, remains under study and is most likely context dependent...
December 2018: Kidney International
François-René Bertin, Ryan N Rys, Cedric Mathieu, Sandrine Laurance, Catherine A Lemarié, Mark D Blostein
BACKGROUND: Neutrophils contribute to venous thrombosis through the release of neutrophil extracellular traps (NETs) but the mechanism triggering their formation remains unclear. In vitro data show that interferon γ (IFNγ) induces the formation of NETs. OBJECTIVES: We hypothesize that IFNγ and the transcription factor Tbet promote venous thrombosis through neutrophil activation. METHODS: Venous thrombosis was induced by flow restriction in the inferior vena cava in IFNγ deficient (-/-), Tbet-/- or wild type (WT) mice...
November 20, 2018: Journal of Thrombosis and Haemostasis: JTH
Rami Abu-Fanne, Victoria Stepanova, Rustem I Litvinov, Suhair Abdeen, Khalil Bdeir, Mohamed Higazi, Emad Maraga, Chandrasekaran Nagaswami, Alexander R Mukhitov, John W Weisel, Douglas B Cines, Abd Al-Roof Higazi
Inflammation and thrombosis are integrated, mutually reinforcing processes, but the inter-regulatory mechanisms are incompletely defined. Here, we examined the contribution of α-defensins (α-defs), antimicrobial proteins released from activated human neutrophils, on clot formation in vitro and in vivo. Activation of the intrinsic pathway of coagulation stimulates release of α-defs from neutrophils. α-defs accelerate fibrin polymerization, increase fiber density and branching, incorporate into nascent fibrin clots, and impede fibrinolysis in vitro...
November 15, 2018: Blood
Young Ho Lee, Gwan Gyu Song
AIM: We aimed to evaluate the relationship between mean platelet volume (MPV), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and Behçet's disease (BD). METHODS: We searched Medline, Embase, and Cochrane databases, and performed a meta-analysis to compare MPV, NLR, and PLR between patients with BD and healthy controls, and to evaluate these parameters in BD according to disease activity and thrombosis. RESULTS: In total, 14 studies were included...
November 11, 2018: International Journal of Rheumatic Diseases
Karl J Lackner, Nadine Müller-Calleja
Even though our understanding of the antiphospholipid syndrome (APS) has improved tremendously over the last decades, we are still not in a position to replace symptomatic anticoagulation by pathogenesis based causal treatments. Areas covered: Recent years have provided further insights into pathogenetically relevant mechanisms. These include a differentiation of pathogenic subtypes of antiphospholipid antibodies (aPL), novel mechanisms modulating disease activity, e.g. extracellular vesicles and microRNA, and novel players in pathogenesis, e...
November 9, 2018: Expert Review of Clinical Immunology
Allan K Metz, Jose A Diaz, Andrea T Obi, Thomas W Wakefield, Daniel D Myers, Peter K Henke
Deep vein thrombosis (DVT) is a common disease that carries serious ramifications for patients, including pulmonary embolism and post-thrombotic syndrome (PTS). Although standard treatment for DVT is anticoagulation, this carries an added risk of bleeding and increased medication monitoring. Identifying those at risk for DVT and PTS can be difficult, and current research with murine models is helping to illuminate the biologic changes associated with these two disorders. Potential novel biomarkers for improving the diagnosis of DVT and PTS include ICAM-1, P-selectin, and cell-free DNA...
July 2018: Methodist DeBakey Cardiovascular Journal
Keshinie Samarasekara, Janake Munasinghe
BACKGROUND: Dengue fever is a mosquito-borne viral disease with a very high incidence in Southeast Asia. Most patients with dengue fever recover following a self-limiting febrile illness, while a small proportion may progress to develop severe disease with complications such as acute liver failure, acute kidney injury, and multiorgan failure. Secondary bacterial infections and thrombotic events are very rare. CASE PRESENTATION: A 38-year-old previously healthy Sri Lankan woman from Colombo, Sri Lanka, presented with dengue shock syndrome leading to acute liver failure and kidney injury...
October 30, 2018: Journal of Medical Case Reports
Danielle H Moore, Neeral L Shah
No abstract text is available yet for this article.
December 2018: Liver Transplantation
Giampaolo Niccoli, Rocco A Montone, Vito Sabato, Filippo Crea
Inflammation is an important player both for the initiation and progression of coronary artery disease and for coronary plaque instability. Moreover, inflammation contributes to stent thrombosis and in-stent restenosis after percutaneous coronary intervention. In the past several decades, most studies evaluated the involvement of cellular effectors of classic inflammatory responses, such as monocytes/macrophages, neutrophils, and T cells. Yet, besides classic inflammation, mounting evidence derived from both experimental and clinical studies suggests an important, often unrecognized, role for effector cells of allergic inflammation in both the pathogenesis of coronary artery disease and adverse events following stent implantation...
October 16, 2018: Circulation
Sauri Hernández-Reséndiz, Mónica Muñoz-Vega, Whendy E Contreras, Gustavo E Crespo-Avilan, Julian Rodriguez-Montesinos, Oscar Arias-Carrión, Oscar Pérez-Méndez, William A Boisvert, Klaus T Preissner, Hector A Cabrera-Fuentes
One of the primary therapeutic goals of modern cardiology is to design strategies aimed at minimizing myocardial infarct size and optimizing cardiac function following acute myocardial infarction (AMI). Patients with AMI who underwent reperfusion therapy display dysfunction of the coronary endothelium. Consequently, ischemic endothelial cells become more permeable and weaken their natural anti-thrombotic and anti-inflammatory potential. Ischemia-reperfusion injury (IRI) is associated with activation of the humoral and cellular components of the hemostatic and innate immune system, and also with excessive production of reactive oxygen species (ROS), the inhibition of nitric oxide synthase, and with inflammatory processes...
August 2018: Conditioning medicine
X Feng, X F Shi
Hepatitis B remains a worldwide health problem with a high mortality rate associated with end-stage liver diseases. The Model for End-Stage Liver Disease and Child-Pugh score is still widely used as the prognostic model for liver cirrhosis and inflammatory reaction, B-type natriuretic peptide and portal vein thrombosis are independent risk factors. Many new models have been proposed for liver failure, including a new model HINAT ACLF. HINAT ACLF is better than its preceding models and increased neutrophil-to-lymphocyte ratio is a single factor to promote thyroid hormone, cholinesterase, and antiviral treatment response in this model...
August 20, 2018: Zhonghua Gan Zang Bing za Zhi, Zhonghua Ganzangbing Zazhi, Chinese Journal of Hepatology
Edoardo Elia, Fabrizio Montecucco, Piero Portincasa, Amirhossein Sahebkar, Hamid Mollazadeh, Federico Carbone
Although coronary thrombosis (CT) is integral to cardiovascular outcomes, the underlying pathophysiological mechanisms remain unclear. CT may occur in case of atherosclerotic plaque erosion/rupture, or even after stenting implantation. Platelets (PLT) activation is the keystone of atherothrombosis and depends on many dysregulated elements, including endothelial dysfunction, oxidized lipoproteins, and immune response. Besides the classical view of PLT as an effector of hemostatic response, a new repertoire of PLT activities is emerging...
March 2019: Journal of Cellular Physiology
Kandace Gollomp, Minna Kim, Ian Johnston, Vincent Hayes, John Welsh, Gowthami M Arepally, Mark Kahn, Michele P Lambert, Adam Cuker, Douglas B Cines, Lubica Rauova, M Anna Kowalska, Mortimer Poncz
Heparin-induced thrombocytopenia (HIT) is an immune-mediated thrombocytopenic disorder associated with a severe prothrombotic state. We investigated whether neutrophils and neutrophil extracellular traps (NETs) contribute to the development of thrombosis in HIT. Using an endothelialized microfluidic system and a murine passive immunization model, we show that HIT induction leads to increased neutrophil adherence to venous endothelium. In HIT mice, endothelial adherence is enhanced immediately downstream of nascent venous thrombi, after which neutrophils undergo retrograde migration via a CXCR2-dependent mechanism to accumulate into the thrombi...
September 20, 2018: JCI Insight
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