Search

Heart rate asymmetry (HRA) refers to how asymmetrically the acceleration and deceleration patterns in heartbeat fluctuations are distributed. There is limited evidence regarding HRA changes in athletes and their association with autonomic regulation. This study aimed to compare the short-term HRA of high-performance athletes and non-athletes during an autonomic function test by calculating relevant HRA measures. This exploratory study obtained beat-to-beat RR interval time series from 15 high-performance athletes and 12 non-athletes during a standardized autonomic function test. This test includes rest, postural change, controlled respiration, prolonged orthostatism, exercise, and recovery phases. The following HRA parameters were computed from the RR time series for both groups: asymmetric spread index (ASI), slope index (SI), Porta's index (PI), Guzik's index (GI), and Ehlers' index (EI). We found significant differences (p < 0.01) in the mean value of several HRA parameters between athletes and non-athletes and across the autonomic function test phases, mainly in postural change and recovery phases. Our results indicate that high-performance athletes manifest a higher number and magnitude of cardiac decelerations than non-athletes after an orthostatic challenge, as indicated by GI and EI. In addition, lower HRA was found in athletes in the recovery phase than in non-athletes, as indicated by ASI. [ABSTRACT FROM AUTHOR]

Background: Although Down syndrome (DS) is the most frequent human chromosomal disorder and it causes mainly intellectual disability, its clinical presentation is complex and variable. Objective: We aimed to analyze and compare the transcriptome disruption in several brain areas from individuals with DS and euploid controls as a new approach to consider a global systemic differential disruption of gene expression beyond chromosome 21. Methods: We used data from a DNA microarray experiment with ID GSE59630 previously deposited in the GEO DataSet of NCBI database. The array contained log2 values of 17,537 human genes expressed in several aeras of the human brain. We calculated the differential gene expression (Z-ratio) of all genes. Results: We found several differences in gene expression along the DS brain transcriptome, not only in the genes located at chromosome 21 but in other chromosomes. Moreover, we registered the lowest Z-ratio correlation between the age ranks of 16–22 weeks of gestation and 39–42 years (R2 = 0.06) and the highest Z-ratio correlation between the age ranks of 30–39 years and 40–42 years (R2 = 0.89). The analysis per brain areas showed that the hippocampus and the cerebellar cortex had the most different gene expression pattern when compared to the brain as a whole. Conclusions: Our results support the hypothesis of a systemic imbalance of brain protein homeostasis, or proteostasis network of cognitive and neuroplasticity process, as new model to explain the important effect on the neurophenotype of trisomy that occur not only in the loci of chromosome 21 but also in genes located in other chromosomes. [ABSTRACT FROM AUTHOR]

Introduction: Skeletal muscle plasticity in exercise can be modulated by epigenomic events such as gene silencing, histone modifications and DNA methylation. In this context, our objective was to analyze the expression of genes associated with chromatin modifications in human muscle biopsies of vastus lateralis after a 20 week training program. Methods: Using data from DNA microarray experiments registered in the NCBI GEO DataSet database GSE117070, we calculated the Z ratio values as the criterion to evaluate the differential expression of genes associated with chromatin modification during aerobic training in skeletal muscle. Using the web interface GENEMANIA, we built a co-expression interaction network with the overexpressed genes. We compared Z-score values obtained from pre-trained and post-trained samples through nonparametric tests. Results: We found 10 overexpressed genes after the 20 week training program, namely, EZH1, KMT2A, KMT2D, KDM4C, KDM6A, CREBBP, HDAC10, HDAC4, DNMT3L, and H2AX. The most relevant biological processes obtained from the network included chromatin organization (FDR 9.04 × 10−9) and histone modification (FDR 9.04 × 10−9). Conclusions: In skeletal muscle, after aerobic training, there is overexpression of genes associated with the modification of the chromatin through alterations in histones and DNA, resulting in epigenetic transcriptional changes. [ABSTRACT FROM AUTHOR]

DNA methylation and histone posttranslational modifications are epigenetics processes that contribute to neurophenotype of Down Syndrome (DS). Previous reports present strong evidence that nonhistone high-mobility-group N proteins (HMGN) are epigenetic regulators. They play important functions in various process to maintain homeostasis in the brain. We aimed to analyze the differential expression of five human HMGN genes in some brain structures and age ranks from DS postmortem brain samples. Methodology: We performed a computational analysis of the expression of human HMGN from the data of a DNA microarray experiment (GEO database ID GSE59630). Using the transformed log2 data, we analyzed the differential expression of five HMGN genes in several brain areas associated with cognition in patients with DS. Moreover, using information from different genome databases, we explored the co-expression and protein interactions of HMNGs with the histones of nucleosome core particle and linker H1 histone. Results: We registered that HMGN1 and HMGN5 were significantly overexpressed in the hippocampus and areas of prefrontal cortex including DFC, OFC, and VFC of DS patients. Age-rank comparisons between euploid control and DS individuals showed that HMGN2 and HMGN4 were overexpressed in the DS brain at 16 to 22 gestation weeks. From the BioGRID database, we registered high interaction scores of HMGN2 and HMGN4 with Hist1H1A and Hist1H3A. Conclusions: Overall, our results give strong evidence to propose that DS would be an epigenetics-based aneuploidy. Remodeling brain chromatin by HMGN1 and HMGN5 would be an essential pathway in the modification of brain homeostasis in DS. [ABSTRACT FROM AUTHOR]