IntroductionPatients with sickle cell anemia (SCA) may present chronic hemolytic anemia, vaso-occlusion and respiratory tract infection (RTI) episodes. Galectin-3 (GAL-3) is a multifunctional protein involved in inflammation, apoptosis, adhesion and resistance to reactive oxygen species. Studies point to a dual role for GAL-3 as both a circulation damage-associated molecular pattern and a cell membrane associated pattern recognition receptor.ObjectiveTo investigate associations between the SNPs of GAL-3 gene (LGALS3) and serum levels with RTI and vaso-occlusive crisis (VOC) in children with SCA.Materials and MethodsSNPs +191 and +292 in LGALS3 were studied using the TaqMan real-time PCR system; GAL-3 serum levels were measured by ELISA. The study included 79 children with SCA ranging from 2 to 12 years old.ResultsGAL-3 serum levels were associated with LGALS3 +191 and +292 genotypes (p <0.0001; p = 0.0169, respectively). LGALS3 +191, AA genotype was associated with low and CC with higher levels of GAL-3. For LGALS3 +292, the CC genotype was associated with lower GAL-3 and AA with higher levels. Patients with Frequency of RTI (FRTI) ≥1 presented higher frequency of +191AA (p = 0.0263) and +292AC/CC genotypes (p = 0.0320). SNP +292 was associated with Frequency of VOC (FVOC) (p = 0.0347), whereas no association was shown with SNP +191 and FVOC. However, CA/AC and AA/CC genotypes with lower GAL-3 levels showed a higher frequency in patients with FRTI ≥1 (p = 0.0170; p = 0.0138, respectively). Also, patients with FVOC ≥1 presented association with CA/AC (p = 0.0228). LGALS3 +191 and +292 combined genotypes related to low (p = 0.0263) and intermediate expression (p = 0.0245) were associated with FRTI ≥1. Lower GAL-3 serum levels were associated with FRTI ≥1 (p = 0.0426) and FVOC ≥1 (p = 0.0012).ConclusionVariation of GAL-3 serum levels related to SNPs at +191 and +292 may constitute a susceptibility factor for RTI and VOC frequency.
The SOD2 polymorphism Val16Ala T→C influences the antioxidative response. This study investigated the association of the SOD2 polymorphism and superoxide dismutase (SOD) activity with the vaso-occlusive crisis (VOC) and acute splenic sequestration (ASS) in children with sickle cell anemia (SCA). One hundred ninety-five children with SCA aged 1–9 years old were analyzed. The TC and CC genotypes were associated with lower SOD activity compared with the TT genotype (p=0.0321; p=0.0253, respectively). Furthermore, TC and CC were more frequent in patients with VOC or ASS (p=0.0285; p=0.0090, respectively). These results suggest that the SOD2 polymorphism associated with low SOD activity could be a susceptibility factor for the occurrence of VOC and ASS.
Introduction
Warfarin continues to be the most widely used anticoagulant in clinical practice around the world for the prevention of thromboembolic events in patients with atrial fibrillation (AF). The evaluation of the quality of anticoagulation control, estimated by time in therapeutic range (TTR), is accepted as a good method to evaluate the quality of anticoagulation. The variability of TTR can be explained by the presence of variants of the
CYP2C9
and
VKORC1
genes.
Methods
This study examined the association between polymorphisms of the
CYP2C9
and
VKORC1
genes and control of oral anticoagulation, through TTR, in patients with AF. A cross-sectional study was conducted within a cohort follow-up. The study comprised of 317 patients with AF, using warfarin, who were followed up for one year. The genotyping of genes
CYP2C9
(rs1057910), (rs1799853) and
VKORC1
(rs923231) was performed by PCR in real time, using TaqMan probes.
Results
Patients who had variant genotypes for the
CYP2C9*3
gene (rs1057910) presented higher TTR (TTR 81–100%) when compared to when compared to the <45% and 46–60% TTR groups (
p
=0.005 and
p
=0.002, respectively). Regarding
VKORC1
(rs923231), patients who had the variant genotype for the
VKORC1
(rs923231) gene also presented a higher TTR (TTR 81–100%), when when compared to the <45% and 46–60% TTR groups (
p
=0.005 and
p
=0.004, respectively). In a multivariate model,
VKORC1
(rs923231) remained associated for comparisons with the TTR groups (<45% vs 81–100% groups,
p
=0.01; and 46–60% vs 81–100% groups,
p
=0.01).
Conclusion
The genotypes of the
CYP2C9*3
(AA) and
VKORC1
-1639 (GG) genes were associated with the worst quality of anticoagulation control (TTR) in patients with AF using warfarin in the northeast of Brazil.
Objective: to analyze the nursing care strategies employed in pain management in children with sickle cell anemia. Method: integrative literature review on the topic in the virtual databases Scielo, Lilacs, PubMed, MEDLINE and BDENF in the months of January and February. Results: 17 articles were selected and two analytical categories were identified: knowledge of professionals and education of children and family members about the pathological process of pain and pharmacological and non-pharmacological treatment for pain management. Conclusions: as strategies for coping with pain in children, there is adequate pharmacological and non-pharmacological treatment, in addition to nursing knowledge that prevents complications, as well as the education of children and family members about the disease, which favors improvement and adaptation to symptoms.
Background: Atrial fibrillation (AF) is the most common type of sustained arrhythmia in clinical practice. Biochemical markers and imaging tests have been used with the aim of stratifying the risk and detecting atrial fibrosis. Speckle-tracking echocardiography (STE) is used for the detection of atrial fibrosis and Gal-3 provides an important prognostic value. The objective of the study was to assess the association between atrial fibrosis markers and serum levels, genetic polymorphisms and genic expression of galectin-3.
Methods: Two hundred and six patients with permanent AF and 70 patients with paroxysmal AF were included in the study. Real time PCR (TaqMan) system was used to study SNPs rs4652 and 4644 of the gene LGALS3. Serum levels of Gal-3 were determined by ELISA and STE was performed to assess fibrosis.
Results: Mean age of individuals with permanent AF was 66.56±12 years. As for the echocardiography results, those patients showed an increase in the following parameters: left atrial diameter (LAD) (p=0.007), LA volume (p=0.02) and volume indexed to the body surface area (p=0.04). And a decrease in values of peak atrial longitudinal strain (PALS) (p=0.002) when compared to the same parameters from the paroxysmal AF group of patients. There was a correlation between serum levels of Gal-3 and PALS in the group of patients with permanent AF; the lower the levels of gal-3, the lower the LA strain (r=0.24; p=0.01).
Conclusions: Echocardiographic findings showed association with the groups, and with serum levels of Gal-3 in patients with permanent AF. The distribution of allelic and genotypic frequencies, and of the haplotypes of polymorphism LGALS3 rs4652 and rs4644 did not present statistical variation, which suggests that those SNPs are not associated with the AF clinical forms (permanent and paroxysmal).
Introduction:
Alcoholic Cardiomyopathy (ACM) is a disease with a difficult diagnosis.
The real mechanisms related to its pathophysiology are not fully understood.
Objective:
The aims of this study were to investigate whether miR-133b and miR-138 could be associated
with ACM.
Method:
Forty-four patients were included comprising 24 with ACM and 20 with cardiomyopathies
of different etiologies (control group). Real-time PCR was performed to verify the relative expression
among the studied groups. In the statistical analysis, the quantitative variables t-student Mann-
Whitney and correlation of Pearson tests were carried out, while the qualitative variable comprised
the chi-square test, with p<0.05 being considered statistically significant.
Results:
There was no association between clinical and sociodemographic characteristics of the
groups. The patients with ACM presented downregulation of miR-133b in comparison with control
patients (p=0.004). On the other hand, for the miR-138, there was no association when the ACM
group was compared with the control group. The presence of miR-133b among cases and controls
was not correlated with any of the echocardiographic parameters. However, the increase in the expression
of miR-138 was correlated with an increase in the ejection fraction (r=0.28, p=0.01) and the
diameter of the left atrium (r=0.23, p=0.04) in patients with ACM.
Conclusion:
The downregulation of miR-133b might be a marker for ACM and, in addition, miR-
138 could be used to correlate the increase in ejection fraction with and normalization of the diameter
of the left atrium diameter in patients with this disease.
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