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Chronic Fatigue Syndrome: HELP
Articles from Colombia
Based on 4 articles published since 2010
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These are the 4 published articles about Fatigue Syndrome, Chronic that originated from Colombia during 2010-2020.
 
+ Citations + Abstracts
1 Review Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Comprehensive Review. 2019

Cortes Rivera, Mateo / Mastronardi, Claudio / Silva-Aldana, Claudia T / Arcos-Burgos, Mauricio / Lidbury, Brett A. ·Facultad de Medicina, Grupo de Investigación Neuros, Universidad del Rosario, Bogotá 110211, Colombia. mateo.cortes@urosario.edu.co. · INPAC Research Group, Fundación Universitaria Sanitas, Bogotá 110211, Colombia. · Center for Research in Genetics and Genomics-CIGGUR, GENIUROS Research Group, School of Medicine and Health Sciences, Universidad del Rosario, Bogotá 110211, Colombia. · Group de Investigación en Psiquiatría (GIPSI), Instituto de Investigaciones Médicas, Facultad de Medicina, Universidad de Antioquia, Medellín 050002, Colombia. · The National Centre for Epidemiology and Population Health, RSPH, College of Health and Medicine, The Australian National University, Canberra ACT 2601, Australia. brett.lidbury@anu.edu.au. ·Diagnostics (Basel) · Pubmed #31394725.

ABSTRACT: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating chronic disease of unknown aetiology that is recognized by the World Health Organization (WHO) and the United States Center for Disease Control and Prevention (US CDC) as a disorder of the brain. The disease predominantly affects adults, with a peak age of onset of between 20 and 45 years with a female to male ratio of 3:1. Although the clinical features of the disease have been well established within diagnostic criteria, the diagnosis of ME/CFS is still of exclusion, meaning that other medical conditions must be ruled out. The pathophysiological mechanisms are unclear but the neuro-immuno-endocrinological pattern of CFS patients gleaned from various studies indicates that these three pillars may be the key point to understand the complexity of the disease. At the moment, there are no specific pharmacological therapies to treat the disease, but several studies' aims and therapeutic approaches have been described in order to benefit patients' prognosis, symptomatology relief, and the recovery of pre-existing function. This review presents a pathophysiological approach to understanding the essential concepts of ME/CFS, with an emphasis on the population, clinical, and genetic concepts associated with ME/CFS.

2 Article MicroRNAs hsa-miR-99b, hsa-miR-330, hsa-miR-126 and hsa-miR-30c: Potential Diagnostic Biomarkers in Natural Killer (NK) Cells of Patients with Chronic Fatigue Syndrome (CFS)/ Myalgic Encephalomyelitis (ME). 2016

Petty, Robert D / McCarthy, Neil E / Le Dieu, Rifca / Kerr, Jonathan R. ·CFS Group, St George´s University of London, Cranmer Terrace, London, United Kingdom. · Centre for Haemato-Oncology, Bart's cancer institute, Queen Mary University of London, London, United Kingdom. · Centre for Immunobiology, The Blizzard institute, Queen Mary University of London, London, United Kingdom. · Grupo de Salud Publica, Escuela de Medicine y Ciencias de la Salud, Universidad del Rosario, Quinta de Mutis, Bogotá 111221, Colombia. ·PLoS One · Pubmed #26967895.

ABSTRACT: BACKGROUND: Chronic Fatigue Syndrome (CFS/ME) is a complex multisystem disease of unknown aetiology which causes debilitating symptoms in up to 1% of the global population. Although a large cohort of genes have been shown to exhibit altered expression in CFS/ME patients, it is currently unknown whether microRNA (miRNA) molecules which regulate gene translation contribute to disease pathogenesis. We hypothesized that changes in microRNA expression in patient leukocytes contribute to CFS/ME pathology, and may therefore represent useful diagnostic biomarkers that can be detected in the peripheral blood of CFS/ME patients. METHODS: miRNA expression in peripheral blood mononuclear cells (PBMC) from CFS/ME patients and healthy controls was analysed using the Ambion Bioarray V1. miRNA demonstrating differential expression were validated by qRT-PCR and then replicated in fractionated blood leukocyte subsets from an independent patient cohort. The CFS/ME associated miRNA identified by these experiments were then transfected into primary NK cells and gene expression analyses conducted to identify their gene targets. RESULTS: Microarray analysis identified differential expression of 34 miRNA, all of which were up-regulated. Four of the 34 miRNA had confirmed expression changes by qRT-PCR. Fractionating PBMC samples by cell type from an independent patient cohort identified changes in miRNA expression in NK-cells, B-cells and monocytes with the most significant abnormalities occurring in NK cells. Transfecting primary NK cells with hsa-miR-99b or hsa-miR-330-3p, resulted in gene expression changes consistent with NK cell activation but diminished cytotoxicity, suggesting that defective NK cell function contributes to CFS/ME pathology. CONCLUSION: This study demonstrates altered microRNA expression in the peripheral blood mononuclear cells of CFS/ME patients, which are potential diagnostic biomarkers. The greatest degree of miRNA deregulation was identified in NK cells with targets consistent with cellular activation and altered effector function.

3 Article Use of single-nucleotide polymorphisms (SNPs) to distinguish gene expression subtypes of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME). 2014

Shimosako, Nana / Kerr, Jonathan R. ·CFS Group, Department of Cellular & Molecular Medicine, St George's University of London, London, UK. · CFS Group, Department of Cellular & Molecular Medicine, St George's University of London, London, UK Escuela de Medicina y Ciencias de Salud, Universidad del Rosario, Bogota, Colombia. ·J Clin Pathol · Pubmed #25240059.

ABSTRACT: AIMS: We have reported gene expression changes in patients with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) and the fact that such gene expression data can be used to identify subtypes of CFS/ME with distinct clinical phenotypes. Due to the difficulties in using a comparative gene expression method as an aid to CFS/ME disease and subtype-specific diagnosis, we have attempted to develop such a method based on single-nucleotide polymorphism (SNP) analysis. METHODS: To identify SNP allele associations with CFS/ME and CFS/ME subtypes, we tested genomic DNA of patients with CFS/ME (n=108), patients with endogenous depression (n=17) and normal blood donors (n=68) for 504 human SNP alleles located within 88 CFS-associated human genes using the SNP Genotyping GoldenGate Assay (Illumina, San Diego, California, USA). 360 ancestry informative markers (AIM) were also examined. RESULTS: 21 SNPs were significantly associated with CFS/ME compared with depression and normal groups. 148 SNP alleles had a significant association with one or more CFS/ME subtypes. For each subtype, associated SNPs tended to be grouped together within particular genes. AIM SNPs indicated that 4 subjects were of Asian origin while the remainder were Caucasian. Hierarchical clustering of AIM data revealed the relatedness between 2 couples of patients with CFS only and confirmed the overall heterogeneity of all subjects. CONCLUSIONS: This study provides evidence that human SNPs located within CFS/ME associated genes are associated with particular genomic subtypes of CFS/ME. Further work is required to develop this into a clinically useful subtype-specific diagnostic test.

4 Article Supervised selection of single nucleotide polymorphisms in chronic fatigue syndrome. 2011

Cifuentes, Ricardo A / Barreto, Emiliano. ·Escuela de Medicina y Ciencias de la Salud, Universidad del Rosario, Bogotá, DC, Colombia. ·Biomedica · Pubmed #22674373.

ABSTRACT: INTRODUCTION: The different ways for selecting single nucleotide polymorphisms have been related to paradoxical conclusions about their usefulness in predicting chronic fatigue syndrome even when using the same dataset. OBJECTIVE: To evaluate the efficacy in predicting this syndrome by using polymorphisms selected by a supervised approach that is claimed to be a method that helps identifying their optimal profile. MATERIALS AND METHODS: We eliminated those polymorphisms that did not meet the Hardy-Weinberg equilibrium. Next, the profile of polymorphisms was obtained through the supervised approach and three aspects were evaluated: comparison of prediction accuracy with the accuracy of a profile that was based on linkage disequilibrium, assessment of the efficacy in determining a higher risk stratum, and estimating the algorithm influence on accuracy. RESULTS: A valid profile (p<0.01) was obtained with a higher accuracy than the one based on linkage disequilibrium, 72.8 vs. 62.2% (p<0.01). This profile included two known polymorphisms associated with chronic fatigue syndrome, the NR3C1_11159943 major allele and the 5HTT_7911132 minor allele. Muscular pain or sinus nasal symptoms in the stratum with the profile predicted V with a higher accuracy than those symptoms in the entire dataset, 87.1 vs. 70.4% (p<0.01) and 92.5 vs. 71.8% (p<0.01) respectively. The profile led to similar accuracies with different algorithms. CONCLUSIONS: The supervised approach made it possible to discover a reliable profile of polymorphisms associated with this syndrome. Using this profile, accuracy for this dataset was the highest reported and it increased when the profile was combined with clinical data.