1,721,100 research outputs found
Editorial: New Insights Into Oxidative Stress and Inflammation in the Pathophysiology and Treatment of Cardiovascular Diseases
Modulation of gut microbiota through nutritional interventions in Behçet’s syndrome patients (the MAMBA study): study protocol for a randomized controlled trial
Background: Behçet's syndrome (BS) is a systemic inflammatory disorder of unknown etiology, characterized by a wide range of potential clinical manifestations. Recent evidences suggest that the gut microbiota (GM) in BS shows low biodiversity with a significant depletion in butyrate producers. The aim of the present project is to investigate whether a dietary intervention could ameliorate the clinical manifestations and modulate the GM of individuals with BS.
Methods: This is a randomized, open, cross-over study involving 90 BS individuals who will be randomized to follow a 3-months dietary profile with either: lacto-ovo-vegetarian diet (VD), Mediterranean diet (MD) or Mediterranean diet supplemented with butyrate (MD-Bt). The VD will contain inulin and resistant starch-rich foods, eggs and dairy, in addition to plant-based food, but will not contain meat, poultry or fish. The MD will contain all food categories and will provide 2 portions per week of fish and 3 portions per week of fresh and processed meat. The MD-Bt will be similar to the MD but supplemented with 1.8 g/day of oral butyrate. The three different dietary patterns will be isocaloric and related to participants’ nutritional requirements. Anthropometric measurements, body composition, blood and fecal samples will be obtained from each participant at the beginning and at the end of each intervention phase. The primary outcomes will be represented by the change from baseline of the BS gastrointestinal and systemic symptoms. Changes from baseline of GM composition, SCFA production, inflammatory and antioxidant profile will be considered as secondary outcomes.
Discussion: BS is a rare disease, and, actually, not all the available treatments are target therapies. A supportive treatment based on dietary and lifestyle issues, able to restore immune system homeostasis, could have a high impact on costs sustainability for the treatment of such a chronic and disabling inflammatory condition
SIRT1 activity is decreased in lesional psoriatic skin
Dear Editor,
Psoriasis is a chronic immune-mediated hyperproliferative
inflammatory skin disease of unknown etiology characterized
by the appearance of sore patches of thick, red skin
with silvery scales. It affects about up to 3 % of the world
population and it is equally prevalent in both genders,
although results from a recent study have shown that on
average, men have more severe forms of the disease.
Psoriasis treatment often requires a varied team of
clinicians with a range of expertise due to the fact that high
prevalence, chronicity, disfiguration, disability, and associated
comorbidity characterize the disease. The deep
understanding of the role of immune function in psoriasis
permits the management of this complex disease, which
dramatically affects patients far beyond the skin
Repeated low-dose courses of rituximab in SLE-associated antiphospholipid syndrome: Data from a tertiary dedicated centre
WereadwithinteresttherecentarticlebyWangandLiu [1],
describing theirexperiencewithrituximab(RTX)in6systemic
lupus erythematosus(SLE)-associatedantiphospholipidsyndrome
(APS) patients.Thesedatasupporttheideathat,inlinewith
previoussporadiccasesreportedinliterature,RTXatdifferent
regimensisabletoreducethromboticrecurrencesandtoimprove
SLE activity,withanoverallgoodsafetyprofile. Moreover,they
confirm thedisappearance/decreaseoftiterofantiphospholipid
antibodies afterRTX [1]
Vascular Behçet's syndrome: an update
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. On the other hand, arterial involvement, although affecting only 3-5% of patients, represents a unique feature of BS, with aneurysms potentially affecting peripheral, visceral and pulmonary arteries. Vascular events in BS are promoted by inflammation, with neutrophils playing a key role in the pathogenesis of thrombotic events; in turn, coagulative components such as fibrinogen, thrombin, factor Xa and factor VIIa amplify the inflammatory cascade. Understanding the contribution of inflammatory and coagulation components in the pathogenesis of BS vascular events is crucial to define the most effective therapeutic strategy. Control of vascular thrombosis is achieved with immunosuppressants drugs rather than anticoagulants. In particular, use of azathioprine and cyclosporine in association with low-dose corticosteroids should be considered in DVT and SVT cases, while treatment with cyclophosphamide together with anti-TNF-α agents can be effectively used in arterial involvement. More recently, the anti-TNF-α drugs have also been reported as a valid alternative for the treatment also of venous events, especially DVT. An exception to the use of anticoagulant in BS could be represented by cerebral veins thrombosis. In this review, we will depict the main characteristics of the vascular involvement in BS, briefly describing histological and pathogenetic features, while focusing on the clinical and therapeutical approaches of the vascular manifestations of BS
Erythrocyte oxidative stress and thrombosis
Thrombosis is a common disorder with a relevant burden of morbidity and mortality worldwide, particularly among elderly patients. Growing evidence demonstrated a direct role of oxidative stress in thrombosis, with various cell types contributing to this process. Among them, erythrocytes produce high quantities of intracellular reactive oxygen species (ROS) by NADPH oxidase activation and haemoglobin autoxidation. Concomitantly, extracellular ROS released by other cells in the blood flow can be uptaken and accumulate within erythrocytes. This oxidative milieu can alter erythrocyte membrane structure, leading to an impaired erythrocyte function, and promoting erythrocytes lysis, binding to endothelial cells, activation of platelet and of coagulation factors, phosphatidylserine exposure and release of microvesicles. Moreover, these abnormal erythrocytes are able to adhere to the vessel wall, contributing to thrombin generation within the thrombus. This process results in accelerated haemolysis and in a hypercoagulable state, in which structurally impaired erythrocytes contribute to increase thrombus size, to reduce its permeability and susceptibility to lysis. However, the wide plethora of mechanisms by which oxidised erythrocytes contribute to thrombosis is not completely elucidated. This review discusses the main biochemical aspects linking erythrocytes, oxidative stress and thrombosis, addressing their potential implication for clinical and therapeutic management
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Detection of allergen-ige interaction in allergic children through combined impedance and ros measurements
The aim of this paper is to provide an alternative and more efficient screening test for allergy with respect to traditional UNICAP and prick skin tests, which are commercially available nowadays. The proposed test is aimed at monitoring the interaction of the IgE protein with the allergen in an allergic subject. The idea relies on the fact that the interaction between the IgE and the corresponding allergen happens through binding mechanisms between the IgE and the allergen structure, changing the ionic content of the serum. This latter can be monitored by impedance measurements and confirmed by reactive oxygen species (ROS) evaluation in leukocyte subpopulations. Therefore, in this paper we propose a novel system for the detection of allergies based on impedance measurements and confirmed by ROS measurements. This type of measurement approach has never been presented in the literature for this purpose. A measurement protocol has been developed to guarantee reproducibility and repeatability of the assay. This paper describes both the instrument-specifically designed for impedance evaluation-and the measurement protocols for both methodologies, defining univocally, in this way, the overall measurement technique
Oxidative Stress as a Thrombophilic Factor in Behçet Syndrome
Behçet syndrome (BS) is a multisystemic disease that includes a heterogeneous variety of different organ manifestations. The disease is sustained by an inflammatory state, which mediates different types of involvement, among which vascular is one. The vascular manifestations of BS usually involve the venous and, more rarely, the arterial branches, with inflammation-induced thrombosis being a common event. Notably, vascular involvement related to this syndrome is treated with immunosuppressant agents, rather than with anticoagulant treatments.
To date, the mechanisms sustaining the pathophysiology of thrombo-inflammation in BS are poorly described. Recent findings suggest a possible role of modification of fibrinogen, a protein involved both in inflammatory processes and in the fibrin network formation and in platelet aggregation. Fibrinogen undergoes different posttranslational modifications and is responsible for its structural and functional changes, which are mainly mediated by reactive oxygen species (ROS). In BS, fibrinogen oxidation and thrombus formation seem to be mediated by neutrophils, which are pivotal in the pathogenetic mechanisms leading to BS-related damages.
Understanding the molecular mechanisms that sustain inflammation-induced thrombosis in BS may help to identify potential targets for new therapeutic strategies
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