Neurophysiological and transcriptomic predictors of chronic low back pain: towards precision pain management (NEAT Study)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA671156 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome-wide expression profiling was performed on 50 core needle biopsies from 18 breast cancer patients using Affymetrix GeneChip Human Genome Plus 2.0 Arrays. Global profiles of expression were characterized using unsupervised clustering methods and variance components models. Precision of predictors of breast cancer biology and clinical outcome were evaluated by interclass correlation.
2010-08-12 | E-GEOD-23593 | biostudies-arrayexpress
Project description:We performed genome-wide DNA methylation analysis of 850,000 CpG sites in women and men with chronic Low Back Pain (LBP) and pain free-controls. T cells were isolated (Discovery Cohort, n=32) and used to identify differentially methylated CpG sites, and gene ontologies and molecular pathways were identified.T cells were isolated (Discovery Cohort, n=32) and used to identify differentially methylated CpG sites, and gene ontologies and molecular pathways were identified. A polygenic DNA methylation score for LBP was generated in both women and men. Validation was performed in an independent cohort (Validation Cohort, n=63) of chronic LBP and healthy controls. Analysis with the Discovery Cohort revealed a total of 2,496 and 419 differentially methylated CpGs in women and men, respectively. The majority of these sites were hypo-methylated in women and enriched in genes with functions in the extracellular matrix, the immune system (i.e. cytokines) or in epigenetic processes. In men, we identified a unique chronic LBP DNA methylation signature characterized by significant enrichment for genes from the major histocompatibility complex. A sex-specific polygenic DNA methylation score was generated to evaluate the pain status of each individual and confirmed in The Validation Cohort using pyrosequencing.
2021-11-10 | GSE162350 | GEO
Project description:Epigenetic Signature of Chronic Low Back Pain in Human T Cells
| PRJNA681581 | ENA
Project description:Towards precision medicine for pain: diagnostic biomarkers and repurposed drugs
| PRJNA524343 | ENA
Project description:HEAL PRECISION: Penn Human Precision Pain Center (HPPC): Discovery and Functional Evaluation of Human Primary Somatosensory Neurons at Baseline and Chronic Pain Conditions
| PRJNA1084178 | ENA
Project description:We endeavored to identify objective blood biomarkers for pain, a subjective sensation with a biological basis, using a stepwise discovery, prioritization, validation, and testing in independent cohorts design. We studied psychiatric patients, a high risk group for co-morbid pain disorders and increased perception of pain. For discovery, we used a powerful withinsubject longitudinal design. We were successful in identifying blood gene expression biomarkers that were predictive of pain state, and of future emergency department (ED) visits for pain, more so when personalized by gender and diagnosis.
2019-02-27 | GSE127208 | GEO
Project description:Not all patients with nerve injury develop neuropathic pain. The extent of nerve damage and age at the time of injury are two of the few risk factors identified to date. In addition, preclinical studies show that neuropathic pain variance is heritable. To define such factors further, we performed a large-scale gene profiling experiment which plotted global expression changes in the rat dorsal root ganglion in three peripheral neuropathic pain models. This resulted in the discovery that the potassium channel alpha subunit KCNS1, involved in neuronal excitability, is constitutively expressed in sensory neurons and markedly downregulated following nerve injury. KCNS1 was then characterized by an unbiased network analysis as a putative pain gene, a result confirmed by single nucleotide polymorphism association studies in humans. A common amino acid changing allele, the 'valine risk allele', was significantly associated with higher pain scores in five of six independent patient cohorts assayed (total of 1359 subjects). Risk allele prevalence is high, with 18-22% of the population homozygous, and an additional 50% heterozygous. At lower levels of nerve damage (lumbar back pain with disc herniation) association with greater pain outcome in homozygote patients is P = 0.003, increasing to P = 0.0001 for higher levels of nerve injury (limb amputation). The combined P-value for pain association in all six cohorts tested is 1.14 E-08. The risk profile of this marker is additive: two copies confer the most, one intermediate and none the least risk. Relative degrees of enhanced risk vary between cohorts, but for patients with lumbar back pain, they range between 2- and 3-fold. Although work still remains to define the potential role of this protein in the pathogenic process, here we present the KCNS1 allele rs734784 as one of the first prognostic indicators of chronic pain risk. Screening for this allele could help define those individuals prone to a transition to persistent pain, and thus requiring therapeutic strategies or lifestyle changes that minimize nerve injury. Microarrays were run on mRNA extracted from adult rat L4 and L5 DRGs cells after 3,7,21,40 hours after three different sciatic nerve lesions [Spared Nerve Injury (SNI); Chronic Constriction Injury (CCI); Spinal Nerve Ligation (Ch) with Sham controls (SH)].
2011-07-14 | E-GEOD-30691 | biostudies-arrayexpress
Project description:We used transcriptome-wide data to investigate the molecular pathophysiological mechanisms in peripheral blood immune cells at the transcriptome-wide level that underlie the transition of acute to chronic low back pain.
2022-04-21 | GSE177034 | GEO
Project description:BackgroundSelf-management (SM) is a key recommended strategy for managing chronic low back pain (CLBP). However, SM programmes generate small to moderate benefits for reducing pain and disability in patients with CLBP. The benefits of the SM programme can potentially be optimised by identifying specific subgroups of patients who are the best responders. To date, no longitudinal study has examined the predictive relationships between SM and biopsychosocial factors in patients with CLBP. The aim was to determine whether biopsychosocial factors predict SM and its change over time in patients with CLBP.MethodsIn this multi-centre longitudinal cohort study, we recruited 270 working-age patients with CLBP (mean age 43.74, 61% female) who consulted outpatient physiotherapy for their CLBP. Participants completed self-reported validated measures of pain intensity, disability, physical activity, kinesiophobia, catastrophising, depression and SM at baseline and six months. SM constructs were measured using eight subscales of the Health Education Impact Questionnaire (heiQ), including Health Directed Activity (HDA), Positive and Active Engagement in Life (PAEL), Emotional Distress (ED), Self-Monitoring and Insight (SMI), Constructive Attitudes and Approaches (CAA), Skill and Technique Acquisition (STA), Social Integration and Support (SIS) and Health Service Navigation (HSN). Data were analysed using General Linear Model (GLM) regression.ResultsPhysical activity and healthcare use (positively) and disability, depression, kinesiophobia, catastrophising (negatively) predicted (p < 0.05, R2 0.07-0.55) SM constructs at baseline in patients with CLBP. Baseline depression (constructs: PAEL, ED, SMI, CAA and STA), kinesiophobia (constructs: CAA and HSN), catastrophising (construct: ED), and physical disability (constructs: PAEL, CAA and SIS) negatively predicted a range of SM constructs. Changes over six months in SM constructs were predicted by changes in depression, kinesiophobia, catastrophising, and physical activity (p < 0.05, R2 0.13-0.32).ConclusionsSelf-reported disability, physical activity, depression, catastrophising and kinesiophobia predicted multiple constructs of SM measured using the heiQ subscales in working-age patients with CLBP. Knowledge of biopsychosocial predictors of SM may help triage patients with CLBP into targeted pain management programmes.Trial registrationThe study protocol was registered at ClinicalTrials.gov on 22 December 2015 (ID: NCT02636777).
| S-EPMC9727914 | biostudies-literature
Project description:Genomics of Pain - Resilience to Pain
| PRJNA498368 | ENA