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Background: Thyroid nodules are epidemic in certain countries. Advancements in imaging technology and increased healthcare screening have led to a notable rise in their detection. This surge in detection has also sparked a renewed focus on understanding their pathophysiology. Limited research exists regarding involvement of proinflammatory cytokines in thyroid disorders. We studied the presence of these proinflammatory cytokines in preoperative serum samples from the tissue of interest (colloid) retrieved during surgery, and postoperative serum samples.
Materials And Methods: We performed a prospective study including patients having solitary thyroid nodule (colloid goiter) undergoing surgery. A total of 3 mL each of preoperative serum sample, aspirated colloid from thyroid specimen, and postoperative serum sample 4 weeks after surgery were collected. The quantification of supernatant cytokines (IL-1, IL-4, IL-6, IL-10, IL-12, IL-17A, IFN-γ, TNF-α, and TGF-β) was done by ELISA. Standard protocols for ELISA were followed, and all assays were performed in duplicate to ensure accuracy.
Results: The study included 40 patients with a median age of 32.5 years (27-48.5 years). The majority of our participants were female, reflecting the higher prevalence of thyroid nodules in women. On analyzing the levels of proinflammatory cytokines, significant differences were seen between the preoperative serum sample, colloid sample, and postoperative serum sample. Colloid had considerably higher levels of proinflammatory cytokines (IL-1, IL-4, IL-6, IL-10, IL-12, IL-17A, IFN-γ, TNF-α, and TGF-β) when compared to both pre- and postoperative serum samples (p < 0.05).
Conclusion: Markedly elevated levels of proinflammatory cytokines seen in colloid obtained during surgery compared to both the pre- and postoperative serum samples suggest that the inflammatory milieu of thyroid tissue is different to that of the systemic circulation. These findings provide a foundation for further research into the inflammatory mechanisms.
Research Registry Registration: No: 8638 dated January 22, 2023.
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http://dx.doi.org/10.1002/wjs.12643 | DOI Listing |
J Neurochem
September 2025
Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Microglia, the resident immune cells of the central nervous system (CNS), are involved in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD), Dementia with Lewy Bodies (DLB), and Parkinson's disease (PD). 14-3-3 proteins act as molecular hubs to regulate protein-protein interactions, which are involved in numerous cellular functions, including cellular signaling, protein folding, and apoptosis. We previously revealed decreased 14-3-3 levels in the brains of human subjects with neurodegenerative diseases.
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Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Aims: Sustained neuroinflammation following ischemic stroke impedes post-injury tissue repairment and neurological functional recovery. Developing innovative therapeutic strategies that simultaneously suppress detrimental inflammatory cascades and facilitate neurorestorative processes is critical for improving long-term rehabilitation outcomes.
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Schizophr Bull
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Department of Psychiatry, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
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September 2025
State Key Laboratory of Southwestern Chinese Medicine Resources, College of Modern Chinese Medicine Industry, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by joint inflammation, damage, and disability. Activated fibroblast-like synoviocytes (FLSs), abundant in RA synovium, crucially facilitate disease progression. These activated FLSs drive RA pathogenesis by upregulating adhesion molecules, proinflammatory cytokines, chemokines, and major histocompatibility complex class II (MHC-II).
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Department of Medicine, UMass Chan Medical School, Worcester, MA, USA; Department of Genetic and Cellular Medicine, UMass Chan Medical School, Worcester, MA, USA; Horae Gene Therapy Center, UMass Chan Medical School, Worcester, MA, USA; Li Weibo Institute for Rare Diseases Research, UMass Chan Medic
The interleukin (IL)-1 pathway is a key mediator of inflammation and innate immune responses. Its dysregulation contributes to rheumatoid arthritis (RA) and autoinflammatory diseases (AIDs). In this study, we develop a recombinant adeno-associated virus (rAAV)-based gene therapy to deliver an inflammation-inducible, secreted human IL-1 receptor antagonist (sIL-1Ra) as a complementary approach to existing IL-1 blockers.
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