Publications by authors named "Camila De Oliveira Vaz"

Background: Antiphospholipid syndrome (APS) is an acquired autoimmune disorder characterized by distinct pathophysiological mechanisms leading to heterogeneous manifestations, including venous and arterial thrombosis. Despite the lack of specific markers of thrombosis risk in APS, some of the mechanisms responsible for thrombosis in APS may overlap with those of other thromboembolic diseases. Understanding these similarities is important for improving the assessment of thrombosis risk in APS.

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Diabetes-associated atherosclerosis involves excessive immune cell recruitment and plaque formation. However, the mechanisms remain poorly understood. Transcriptomic analysis of the aortic intima in Ldlr mice on a high-fat, high-sucrose-containing (HFSC) diet identifies a macrophage-enriched nuclear long noncoding RNA (lncRNA), MERRICAL (macrophage-enriched lncRNA regulates inflammation, chemotaxis, and atherosclerosis).

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Coronavirus disease 2019 (COVID-19) is an acute respiratory infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The uncontrolled systemic inflammatory response, resulting from the release of large amounts of pro-inflammatory cytokines, is the main mechanism behind severe acute respiratory syndrome and multiple organ failure, the two main causes of death in COVID-19. Epigenetic mechanisms, such as gene expression regulation by microRNAs (miRs), may be at the basis of the immunological changes associated with COVID-19.

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Article Synopsis
  • The study retrospectively analyzed thrombotic events in patients hospitalized with acute respiratory distress syndrome (ARDS) related to COVID-19 from March to July 2020, comparing them to patients not infected with the virus.
  • Both COVID-19-positive and negative patients had similar rates of clinically relevant thrombotic events, with 10.2% of non-COVID-19 and 8.7% of COVID-19 patients experiencing such events.
  • The findings suggest that the thrombotic risk associated with ARDS is similar regardless of the specific respiratory infection, indicating that infection-induced ARDS carries an inherent thrombotic risk.
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Thrombotic primary antiphospholipid syndrome (t-PAPS) is an acquired condition characterized by heterogeneous thrombotic manifestations, which is intriguing since venous and arterial thrombosis appear to have distinct pathogenesis. Gene expression analysis may constitute a new approach to evaluate potential similarities or differences between the clinical manifestations of t-PAPS. Recently, dysregulation of the , and genes has been associated with both arterial and venous thrombosis in the general population.

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Thrombotic risk in antiphospholipid syndrome (APS) is conferred by the association of antiphospholipid (aPL) antibodies (first hit) with additional pro-coagulant stimulus (second hit), such as inflammation. Among inflammatory responses, the production of large amounts of interferon (IFN)-I by plasmacytoid dendritic cells (pDCs) is at the basis of the pathophysiology of systemic autoimmune disorders, which raises the hypothesis that this mechanism could also be associated with vascular manifestations of APS. Here, we determined the association of pDCs and IFN-I production with thrombotic APS.

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Background: The release of neutrophil extracellular traps (NETs) is the basis of immune-mediated thrombosis. Data on the clinical relevance of NETs in antiphospholipid syndrome-related thrombosis are scarce.

Objective: The aim of this study was to evaluate whether the NET regulator proteins PADI4, ELANE, and MPO are associated with thrombosis in APS.

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Although dyslipidemia is associated with poorer prognosis in antiphospholipid syndrome (APS), the management of lipid disorders can be challenging. While statins may increase the bleeding risk associated with anticoagulation, the effectiveness of hypolipid diet (HD) has not yet been established in patients with autoimmune disorders. In this study, we evaluated whether HD is associated with decreases in cholesterol levels in patients with thrombotic primary APS (t-PAPS) and dyslipidemia.

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Purpose: Primary antiphospholipid syndrome (PAPS) is a chronic autoimmune disorder clinically characterized by thromboembolic events or obstetric complications. Prolonged anticoagulation therapy with vitamin K antagonists (VKA) is the treatment of choice for PAPS patients with thrombosis. However, the efficacy of VKA therapy depends on laboratory monitoring, dose adjustment, adequate lifestyle and adherence to treatment.

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Tissue factor (TF) is a procoagulant protein associated with increased risk of thrombotic events in antiphospholipid syndrome (t-APS). The mechanisms by which TF levels are increased in APS have not yet been established. The aim of this study was to investigate whether TF mRNA expression is associated with TF levels and thrombosis in APS.

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