Luda B. Diatchenko

This study shows that translational control in spinal cord neurons, particularly in inhibitory and PV+ interneurons, significantly influences gene expression and pain hypersensitivity during the chronic phase of neuropathic pain.

The paper identifies a causal link between chronic pain genetics and late-onset asthma through the nervous system using genome-wide association and Mendelian randomization analyses.

The paper identifies a paradoxical inflammation state in FM neutrophils that are unresponsive to LPS, linked to NF-κB suppression, and suggests bryostatin as a potential therapeutic target.

This paper identifies cell-type-specific genetic variants associated with chronic pain using GWAS and scRNA-seq data from brain and dorsal root ganglia tissues.

The paper creates a database of pain-related transcriptomic data, identifies shared pathways, RNA biomarkers, and shows differential expression genes are more informative than tissue-specific genes in heritability analyses.

This study identifies genetic risk factors for chronic post-surgical pain through GWAS across five surgery types, finding immune-related genes contribute significantly to heritability.

This study finds that fibromyalgia patients with higher anti-satellite glia cell IgG antibodies have more severe symptoms, suggesting these antibodies may contribute to disease severity.

The paper introduces a graph-embedded topic model to analyze UK Biobank data, identifying pain phenotypes and revealing cardiovascular-related medication and condition patterns.

The paper identifies primate sensory neuron types associated with human chronic pain using transcriptomics and maps human pain heritability to these neuronal types.

This study uses single-cell RNA sequencing to analyze spinal cord microglia responses to nerve injury, identifying sex- and time-specific changes and a role for ApoE in neuropathic pain.