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Martinez-Lavin M.,Instituto Nacional Of Cardiologia
Journal of Clinical Rheumatology | Year: 2013

Background: Vasovagal syncope is an acute manifestation of autonomic nervous system dysfunction. This type of syncope is often associated with other dysautonomic expressions such as migraine, gastroparesis, or postural tachycardia syndrome. Autonomic nervous system dysfunction has been proposed as a key element in the pathogenesis of fibromyalgia. Objectives: The objectives of this study were to estimate the frequency of fibromyalgia in a sample of patients with vasovagal syncope and also to correlate the presence of syncope and fibromyalgia with different dysautonomic manifestations. Methods: We studied 50 consecutive patients with vasovagal syncope seen at the Syncope Unit of the National Cardiology Institute of Mexico between June 2009 and June 2012. All individuals filled out the Composite Autonomic Symptoms and Signs questionnaire and the Fibromyalgia Impact Questionnaire. All cases underwent a head-up tilt test. A rheumatologist examined all participants to assess the presence of fibromyalgia. Results: The median age of the studied population was 21 years. Sixty-eight percent of participants were women. Eight cases (16%) had concomitant fibromyalgia. Significantly, all fibromyalgia cases were female. This subgroup of fibromyalgia subjects had more secretomotor complaints (mainly dry eyes and dry mouth) and more bowel constipation than the remainder of the group. Also in this subgroup of fibromyalgia subjects, several significant associations were found between age, blood pressure, number of syncopal episodes, constipation, insomnia, pupillomotor impairment, and disability. In contrast, no correlations were found in the subgroup of fainters without fibromyalgia. Conclusions: Fibromyalgia was relatively frequent in these women with vasovagal syncope and could be associated with dysautonomic symptoms. Therefore, it seems important to search for dysautonomic comorbidities in patients with vasovagal syncope and/or fibromyalgia, to provide a patient-centered holistic approach, instead of the often currently used therapeutic partition. Copyright © 2013 by Lippincott Williams & Wilkins. Source

Philip B.,Griffith University | Ito K.,Griffith University | Moreno-Sanchez R.,Instituto Nacional Of Cardiologia | Ralph S.J.,Griffith University
Carcinogenesis | Year: 2013

Hypoxic microenvironments frequently exist in many solid tumours with oxygen levels fluctuating temporally and spatially from normoxia to hypoxia. The response to hypoxia in human cells is mainly regulated by hypoxia-inducible factors (HIFs), a family of transcription factors which orchestrate signalling events leading to angiogenesis and tumorigenesis. Several events conspire together to lead to the stabilization of HIF-a, commonly expressed in many cancer cell types. These events can result from low oxygen tensions occurring within the expanding tumour mass to produce hypoxic microenvironments or from mutations whereby the HIFs cause changes in expression of genes involved in several cellular functions. Hypoxia-mediated HIF-a regulation has gained significant prominence in tumour biology over recent years, and the hypoxic microenvironments have been shown to facilitate and trigger major molecular and immunological processes necessary to drive the progression of tumours to malignancy. More recently, it has been realized that the hypoxic microenvironments also play significant roles in shielding tumour cells from immune attack by promoting immune suppression. In addition, the hypoxic microenvironment promotes many other oncogenic events, such as the metabolic reconfiguration of tumour cells, neovascularization, epithelial to mesenchymal transition (EMT), and cancer stem cell renewal and accumulation. This article reviews the molecular mechanisms underlying tumour hypoxia and their pro-tumour contributions, such as immune suppression, development of nascent and more permeable tumour vasculature, selective cancer stem cell renewal, accumulation, mobilization and promotion of EMT leading to tumour cell metastasis. ©The Author 2013. Published by Oxford University Press. All rights reserved. Source

Jing Z.-C.,Tongji University | Parikh K.,CARE Institute of Medical science | Pulido T.,Instituto Nacional Of Cardiologia | White R.J.,University of Rochester | And 6 more authors.
Circulation | Year: 2013

BACKGROUND-: Pulmonary arterial hypertension (PAH) is a progressive, fatal disease with no cure. Parenteral and inhaled prostacyclin analogue therapies are effective for the treatment of PAH, but complicated administration requirements can limit the use of these therapies in patients with less severe disease. This study was designed to evaluate the safety and efficacy of the oral prostacyclin analogue treprostinil diolamine as initial treatment for de novo PAH. METHODS AND RESULTS-: Three hundred forty-nine patients (intent-to-treat population) not receiving endothelin receptor antagonist or phosphodiesterase type-5 inhibitor background therapy were randomized (treprostinil, n=233; placebo, n=116). The primary analysis population (modified intent-to-treat) included 228 patients (treprostinil, n=151; placebo, n=77) with access to 0.25-mg treprostinil tablets at randomization. The primary end point was change from baseline in 6-minute walk distance at week 12. Secondary end points included Borg dyspnea index, clinical worsening, and symptoms of PAH. The week 12 treatment effect for 6-minute walk distance (modified intent-to-treat population) was 23.0 m (P=0.0125). For the intent-to-treat population, 6-minute walk distance improvements were observed at peak (26.0 m; P=0.0001) and trough (17.0 m; P=0.0025) plasma study drug concentrations. Other than an improvement in the combined 6-minute walk distance/Borg dyspnea score, there were no significant changes in secondary end points. Oral treprostinil therapy was generally well tolerated; the most common adverse events (intent-to-treat) were headache (69%), nausea (39%), diarrhea (37%), and pain in jaw (25%). CONCLUSIONS-: Oral treprostinil improves exercise capacity in PAH patients not receiving other treatment. Oral treprostinil could provide a convenient, first-line prostacyclin treatment option for PAH patients not requiring more intensive therapy. CLINICAL TRIAL REGISTRATION:-: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00325403. © 2012 American Heart Association, Inc. Source

Garcia-Contreras R.,Instituto Nacional Of Cardiologia | Maeda T.,Kyushu Institute of Technology | Wood T.K.,Pennsylvania State University
Applied and Environmental Microbiology | Year: 2013

Bacteria have the remarkable ability to communicate as a group in what has become known as quorum sensing (QS), and this trait has been associated with important bacterial phenotypes, such as virulence and biofilm formation. Bacteria also have an incredible ability to evolve resistance to all known antimicrobials. Hence, although inhibition of QS has been hailed as a means to reduce virulence in a manner that is impervious to bacterial resistance mechanisms, this approach is unlikely to be a panacea. Here we review the evidence that bacteria can evolve resistance to quorum-quenching compounds. © 2013, American Society for Microbiology. Source

Terrazas C.A.,National Autonomous University of Mexico | Gomez-Garcia L.,Instituto Nacional Of Cardiologia | Terrazas L.I.,National Autonomous University of Mexico
International Journal for Parasitology | Year: 2010

In cysticercosis, a parasitic disease caused by cestodes, the details of early interactions between parasite antigens and innate cells from the host are not well understood. In this study, the role of cestode-conditioned dendritic cells (DCs) in priming Th1 versus Th2 responses to bystander antigen was examined by using CD11c+ DCs as antigen-presenting cells and naive CD4+ DO11.10 lymphocytes specific to ovalbumin (OVA) as responding cells. No conventional maturation was induced in DCs exposed to Taenia crassiceps excreted/secreted antigens (TcES). The ability of TcES to affect Toll-like receptor (TLR)-mediated maturation and the pro-inflammatory response was analyzed by co-pulsing DCs with TcES and TLR ligands. DCs exposed to TcES blocked TLR4, TLR9 and Toxoplasma soluble antigen-induced phenotypic maturation. TcES-exposed DCs also blocked secretion of pro-inflammatory cytokines and alloreactive T cell proliferation, while preserving IL-10 production. DCs pulsed with TcES+OVA suppressed IFN-γ, whereas they induced greater IL-4 production by CD4+ DO11.10 cells. TcES with chemically-altered glycans failed to modulate TLR-mediated activation of DCs and their Th1-inhibitng ability, which was STAT6-independent. Our results reflect the capacity of TcES glyco-antigens to modulate Th1-type and inflammatory responses mediated through DC activation. © 2010 Australian Society for Parasitology Inc. Source

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