Publications by authors named "Carolina Cohen"

Background: Red blood cells from smoking donors can have more lesions from oxidative stress, decreasing the benefits of blood transfusion. We aimed to explore the effect of cigarette smoking on the oxidative status of packed red blood cells (PRBCs) prior to storage.

Materials And Methods: We compared serum vitamin C, plasmatic malondialdehyde (MDA), and non-protein thiol groups (GSH) levels in PRBCs, as well glutathione peroxidase (GPx) and glutathione s-transferase (GST) activity in PRBCs from smoking (n=36) and non-smoking (n=36) donors.

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Background And Objectives: Smokers currently have no defined restrictions for blood donation. However, cigarette smoke contains toxic substances such as carbon monoxide (CO) and trace elements that can affect the packed red blood cells (PRBCs) quality and safety of transfusion. This study evaluated the effects of smoking on the concentration of essential and trace elements and on carboxyhemoglobin (COHb) levels in PRBCs from smoker donors.

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Primary hypophysitis (PH) is a rare disease with a poorly-defined natural history. Our aim was to characterise patients with PH at presentation and during prolonged follow-up. Observational retrospective study of 22 patients was conducted from 3 centres.

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The antioxidant N-acetycysteine can turn into a prooxidant molecule in presence of iron ions. Thus, our goal was to test if the association of N-acetylcysteine (NAC) and an iron chelator (deferoxamine--DFX) in a rodent model of acute myocardial infarction (AMI) improves cardiac function. Male Wistar rats were subjected to a SHAM surgery or AMI.

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Article Synopsis
  • MicroRNAs (miRs) are crucial in regulating gene expression, and while single miR deregulation can lead to heart issues, their role in exercise-induced physiological left ventricular hypertrophy (LVH) is less understood.
  • An experiment with male Balb/c mice was conducted, dividing them into sedentary and exercise groups to analyze miR expression after 7 and 35 days of exercise training.
  • Results showed significant changes in miR levels, with multiple miRs (like miR-150, -26b, -27a, and -143) being identified as modulators of normal cardiac hypertrophy, revealing that gene pathways linked to pathological LVH remain unchanged during physiological LVH.
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Context: Elevated plasmatic microRNAs (miRs) are observed in heart failure (HF). However, the cardiac origin of these miRs remains unclear.

Objective: We calculated transcoronary gradients of miR-29b, miR-133a and miR-423-5p in 17 outpatients with stable systolic HF and in controls without structural cardiac disease.

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Background: Functional polymorphisms in the receptor for advanced glycation end-products (RAGE) gene have been implicated in several vascular diseases. However, to date, no study investigated the association of RAGE polymorphisms with heart failure (HF).

Objective: In this study we tested the hypothesis that the 63-bp insertion/deletion, the -374T>A (rs1800624) and the -429T>C (rs1800625) polymorphisms in the RAGE gene might be associated with susceptibility to HF and could predict all-cause mortality in Brazilian outpatients with left ventricular systolic dysfunction.

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Background: Endothelial nitric oxide synthase (eNOS) gene polymorphisms have been associated with the pathogenesis of cardiovascular diseases, but few studies have evaluated the role of eNOS haplotypes on the risk and prognosis of heart failure (HF). This prospective study was designed to analyze the impact of three eNOS polymorphisms (T-786C, VNTR4a/b and Glu298Asp) and their haplotypes on the susceptibility and clinical outcomes in HF outpatients with systolic dysfunction.

Methods And Results: We conducted a case-control and a cohort study in which 316 HF patients and 360 healthy controls were recruited from a tertiary care university hospital.

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Background: The role of matrix metalloproteinases (MMPs) polymorphisms on heart failure (HF) susceptibility, phenotypic characteristics, and prognosis has been poorly explored.

Methods And Results: We studied 313 HF patients with left ventricular systolic dysfunction and 367 healthy control subjects. Genotyping of MMP-1 (-1607 1G/2G), MMP-3 (-1171 5A/6A), and MMP-9 (-1562 C/T) polymorphisms was performed by polymerase chain reaction.

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