{"entity": "journal", "iuid": "4967cc7b8cda49a584e3032b501fba55", "timestamp": "2026-08-07T18:41:56.215Z", "links": {"self": {"href": "https://publications.scilifelab.se/journal/Pain.json"}, "display": {"href": "https://publications.scilifelab.se/journal/Pain"}}, "title": "Pain", "issn": "1872-6623", "issn-l": "0304-3959", "publications_count": 3, "publications": [{"entity": "publication", "iuid": "92002a39d15d4eb59d1072b72eb9c387", "links": {"self": {"href": "https://publications.scilifelab.se/publication/92002a39d15d4eb59d1072b72eb9c387.json"}, "display": {"href": "https://publications.scilifelab.se/publication/92002a39d15d4eb59d1072b72eb9c387"}}, "title": "Hepatocyte growth factor, colony-stimulating factor 1, CD40, and 11 other inflammation-related proteins are associated with pain in diabetic neuropathy: exploration and replication serum data from the Pain in Neuropathy Study.", "authors": [{"family": "B\u00e4ckryd", "given": "Emmanuel", "initials": "E", "orcid": "0000-0003-4420-418", "researcher": {"href": "https://publications.scilifelab.se/researcher/90b0eb424bac489e9436cc0ff3941463.json"}}, {"family": "Themistocleous", "given": "Andreas", "initials": "A", "orcid": "0000-0002-1089-1543", "researcher": {"href": "https://publications.scilifelab.se/researcher/753e444361b0448e8f28785e1af434e5.json"}}, {"family": "Larsson", "given": "Anders", "initials": "A", "orcid": "0000-0003-3161-0402", "researcher": {"href": "https://publications.scilifelab.se/researcher/2276de26382b402aa384ac231f30f156.json"}}, {"family": "Gordh", "given": "Torsten", "initials": "T"}, {"family": "Rice", "given": "Andrew S C", "initials": "ASC", "orcid": "0000-0001-9533-5636", "researcher": {"href": "https://publications.scilifelab.se/researcher/44710ccc1b084269956e6bc4b0163b3a.json"}}, {"family": "Tesfaye", "given": "Solomon", "initials": "S", "orcid": "0000-0003-1190-1472", "researcher": {"href": "https://publications.scilifelab.se/researcher/cb0fe693dd2b47c98c2681bc9d73d343.json"}}, {"family": "Bennett", "given": "David L", "initials": "DL", "orcid": "0000-0002-7996-2696", "researcher": {"href": "https://publications.scilifelab.se/researcher/0b0c988bc8344ca8b1711325ad16a85b.json"}}, {"family": "Gerdle", "given": "Bj\u00f6rn", "initials": "B", "orcid": "0000-0002-4316-1264", "researcher": {"href": "https://publications.scilifelab.se/researcher/1d3d1896af4848e2bb6054dc1c2da715.json"}}], "type": "journal article", "published": "2022-05-01", "journal": {"title": "Pain", "issn": "1872-6623", "volume": "163", "issue": "5", "pages": "897-909", "issn-l": "0304-3959"}, "abstract": "One in 5 patients with diabetes suffers from chronic pain with neuropathic characteristics, but the pathophysiological mechanisms underlying the development of neuropathic pain in patients with diabetic distal symmetrical polyneuropathy (DSP) are poorly understood. Systemic low-grade inflammation has been implicated, but there is still a considerable knowledge gap concerning its scope and meaning in this context. The aim of the study was to establish the broad inflammatory signature of painful diabetic DSP in serum samples from the Pain in Neuropathy Study, an observational cross-sectional multicentre study in which participants underwent deep phenotyping. In the present two cohorts exploration-replication study (180 participants in each cohort), serum samples from Pain in Neuropathy Study participants were analyzed with the Olink INFLAMMATION panel (Olink Bioscience, Uppsala, Sweden) that enables the simultaneous measurement of 92 inflammation-related proteins (mainly cytokines, chemokines, and growth factors). In both the exploration and the replication cohort, we identified a high-inflammation subgroup where 14 inflammation-related proteins in particular were associated with more neuropathy and higher pain intensity. The top 3 proteins were hepatocyte growth factor, colony-stimulating factor 1, and CD40 in both cohorts. In the exploratory cohort, additional clinical data were available, showing an association of inflammation with insomnia and self-reported psychological distress. Hence, this cross-sectional exploration-replication study seems to confirm that low-grade systemic inflammation is related to the severity of neuropathy and neuropathic pain in a subgroup of patients with diabetic DSP. The pathophysiological relevance of these proteins for the development of neuropathic pain in patients with diabetic DSP must be explored in more depth in future studies.", "doi": "10.1097/j.pain.0000000000002451", "pmid": "34433766", "labels": {"Affinity Proteomics Uppsala": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC9009322"}, {"db": "pii", "key": "00006396-202205000-00014"}], "notes": [], "created": "2022-12-02T09:02:32.019Z", "modified": "2022-12-02T09:02:32.203Z"}, {"entity": "publication", "iuid": "179d461633984a84b5056070367e2884", "links": {"self": {"href": "https://publications.scilifelab.se/publication/179d461633984a84b5056070367e2884.json"}, "display": {"href": "https://publications.scilifelab.se/publication/179d461633984a84b5056070367e2884"}}, "title": "High levels of cerebrospinal fluid chemokines point to the presence of neuroinflammation in peripheral neuropathic pain: a cross-sectional study of 2 cohorts of patients compared with healthy controls.", "authors": [{"family": "B\u00e4ckryd", "given": "Emmanuel", "initials": "E"}, {"family": "Lind", "given": "Anne-Li", "initials": "AL"}, {"family": "Thulin", "given": "M\u00e5ns", "initials": "M"}, {"family": "Larsson", "given": "Anders", "initials": "A"}, {"family": "Gerdle", "given": "Bj\u00f6rn", "initials": "B"}, {"family": "Gordh", "given": "Torsten", "initials": "T"}], "type": "comparative study", "published": "2017-12-00", "journal": {"title": "Pain", "issn": "1872-6623", "issn-l": "0304-3959", "volume": "158", "issue": "12", "pages": "2487-2495"}, "abstract": "Animal models suggest that chemokines are important mediators in the pathophysiology of neuropathic pain. Indeed, these substances have been called \"gliotransmitters,\" a term that illustrates the close interplay between glial cells and neurons in the context of neuroinflammation and pain. However, evidence in humans is scarce. The aim of the study was to determine a comprehensive cerebrospinal fluid (CSF) inflammatory profile of patients with neuropathic pain. Our hypothesis was that we would thereby find indications of a postulated on-going process of central neuroinflammation. Samples of CSF were collected from 2 cohorts of patients with neuropathic pain (n = 11 and n = 16, respectively) and healthy control subjects (n = 11). The samples were analyzed with a multiplex proximity extension assay in which 92 inflammation-related proteins were measured simultaneously (Proseek Multiplex Inflammation I; Olink Bioscience, Uppsala, Sweden). Univariate testing with control of false discovery rate, as well as orthogonal partial least squares discriminant analysis, were used for statistical analyses. Levels of chemokines CXCL6, CXCL10, CCL8, CCL11, CCL23 in CSF, as well as protein LAPTGF-beta-1, were significantly higher in both neuropathic pain cohorts compared with healthy controls, pointing to neuroinflammation in patients. These 6 proteins were also major results in a recent similar study in patients with fibromyalgia. The findings need to be confirmed in larger cohorts, and the question of causality remains to be settled. Because it has been suggested that prevalent comorbidities to chronic pain (eg, depression, anxiety, poor sleep, and tiredness) also are associated with neuroinflammation, it will be important to determine whether neuroinflammation is a common mediator.", "doi": "10.1097/j.pain.0000000000001061", "pmid": "28930774", "labels": {"Clinical Biomarkers": "Service", "Affinity Proteomics Stockholm": "Service", "Affinity Proteomics Uppsala": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC5690569"}, {"db": "pii", "key": "00006396-201712000-00022"}], "notes": [], "created": "2020-01-23T15:08:27.848Z", "modified": "2023-04-14T13:56:08.522Z"}, {"entity": "publication", "iuid": "a8a647fae4e14476b12653f6b774884b", "links": {"self": {"href": "https://publications.scilifelab.se/publication/a8a647fae4e14476b12653f6b774884b.json"}, "display": {"href": "https://publications.scilifelab.se/publication/a8a647fae4e14476b12653f6b774884b"}}, "title": "Pain sensitivity and opioid analgesia: a pharmacogenomic twin study.", "authors": [{"family": "Angst", "given": "Martin S", "initials": "MS"}, {"family": "Phillips", "given": "Nicholas G", "initials": "NG"}, {"family": "Drover", "given": "David R", "initials": "DR"}, {"family": "Tingle", "given": "Martha", "initials": "M"}, {"family": "Ray", "given": "Amrita", "initials": "A"}, {"family": "Swan", "given": "Gary E", "initials": "GE"}, {"family": "Lazzeroni", "given": "Laura C", "initials": "LC"}, {"family": "Clark", "given": "J David", "initials": "JD"}], "type": "journal article", "published": "2012-07-00", "journal": {"volume": "153", "issn": "1872-6623", "issue": "7", "pages": "1397-1409", "title": "Pain", "issn-l": "0304-3959"}, "abstract": "Opioids are the cornerstone medication for the management of moderate to severe pain. Unfortunately, vast inter-individual differences in dose requirements complicate their effective and safe clinical use. Mechanisms underlying such differences are incompletely understood, are likely multifactorial, and include genetic and environmental contributions. While accumulating evidence suggests that variants of several genes account for some of the observed response variance, the relative contribution of these factors remains unknown. This study used a twin paradigm to provide a global estimate of the genetic and environmental contributions to inter-individual differences in pain sensitivity and analgesic opioid effects. Eighty one monozygotic and 31 dizygotic twin pairs successfully underwent a computer-controlled infusion with the \u03bc-opioid agonist alfentanil in a single occasion, randomized, double-blind and placebo-controlled study design. Pain sensitivity and analgesic effects were assessed with experimental heat and cold pressor pain models along with important covariates including demographic factors, depression, anxiety, and sleep quality. Significant heritability was detected for cold pressor pain tolerance and opioid-mediated elevations in heat and cold pressor pain thresholds. Genetic effects accounted for 12-60% of the observed response variance. Significant familial effects accounting for 24-32% of observed variance were detected for heat and cold pressor pain thresholds and opioid-mediated elevation in cold pressor pain tolerance. Significant covariates included age, gender, race, education, and anxiety. Results provide a strong rationale for more detailed molecular genetic studies to elucidate mechanisms underlying inter-individual differences in pain sensitivity and analgesic opioid responses. Such studies will require careful consideration of the studied pain phenotype.", "doi": "10.1016/j.pain.2012.02.022", "pmid": "22444188", "labels": {"Mutation Analysis Facility (MAF)": null}, "xrefs": [{"db": "pii", "key": "S0304-3959(12)00098-X"}, {"db": "pmc", "key": "PMC3377769"}, {"db": "mid", "key": "NIHMS365869"}], "notes": [], "created": "2017-05-04T15:03:33.760Z", "modified": "2017-05-30T12:45:10.575Z"}], "created": "2017-05-09T09:12:48.181Z", "modified": "2020-11-27T13:14:07.369Z"}