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Background: Chronic obstructive pulmonary disease (COPD) induces an imbalance in T helper (Th) 17/regulatory T (Treg) cells that contributes to of the dysregulation of inflammation. Exercise training can modulate the immune response in healthy subjects.

Objective: We aimed to evaluate the effects of exercise training on Th17/Treg responses and the differentiation of Treg phenotypes in individuals with COPD.

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Steroids are organic compounds found in all forms of biological life. Besides their structural roles in cell membranes, steroids act as signalling molecules in various physiological processes and are used to treat inflammatory conditions. It has been hypothesised that in addition to their well-characterised genomic and non-genomic pathways, steroids exert their biological or pharmacological activities an indirect, nonreceptor-mediated membrane mechanism caused by steroid-induced changes to the physicochemical properties of cell membranes.

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Background Multiple sclerosis is a chronic, progressive, disabling disease associated with a high rate of infection, evidence of chronic inflammation, and a high mortality rate. Abnormalities of serum cytokines and changes in the activity of inflammatory cells were associated with relapsing-remitting multiple sclerosis (MS-RR). This study aims to introduce new inflammatory ratios derived from hematological and lipid indices as discriminators of T-helper (Th)-1/Th-2 activity in RR-MS.

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Glaucoma is a leading cause of irreversible blindness, often associated with elevated intraocular pressure (IOP) due to trabecular meshwork (TM) dysfunction. Diabetes mellitus (DM) is recognized as a significant risk factor for glaucoma; however, the molecular mechanisms through which hyperglycemia affects TM function remain unclear. This study investigated the impact of high glucose on gene expression in human TM (HTM) cells to uncover pathways that contribute to TM dysfunction and glaucoma pathogenesis under diabetic conditions.

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Postmenopausal osteoporosis is a chronic inflammatory disease characterized by decreased bone mass and increased bone fracture risk. Estrogen deficiency during menopause plays a major role in post-menopausal osteoporosis by influencing bone, immune, and gut cell activity. In the gut, estrogen loss decreases tight junction proteins that bind epithelial cells of the intestinal barrier together.

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