Background Cognitive impairment has received attention as an important problem in patients with end-stage renal disease, although end-stage renal disease patients with secondary hyperparathyroidism have not been studied. Purpose To assess the pattern of brain volume changes in end-stage renal disease patients with secondary hyperparathyroidism by using voxel-based morphometry and correlating these measures with clinical markers and the Montreal Cognitive Assessment scores. Material and Methods Fifty end-stage renal disease patients with no anatomical abnormalities in conventional MRI (25 patients with secondary hyperparathyroidism, 14 men, mean age 42.20 ± 7.53 years; 25 patients without secondary hyperparathyroidism, 15 men, mean age 41.96 ± 6.17 years) were selected in this study. All patients underwent laboratory tests, neuropsychological tests, and MRI. Voxel-based morphometry analysis was performed to detect regional gray matter volume differences between the two groups. The relationships between abnormal gray matter volume and clinical markers and Montreal Cognitive Assessment scores were investigated. Results Voxel-based morphometry revealed increased gray matter volume in end-stage renal disease patients with secondary hyperparathyroidism in the bilateral caudate and bilateral thalamus compared with non- secondary hyperparathyroidism end-stage renal disease patients ( P < 0.05, FWE corrected). Regarding the laboratory and neuropsychological tests, we found significant correlations between volume in these brain regions and intact parathyroid hormone levels and negative correlations with the Montreal Cognitive Assessment scores. There were no significant associations between brain volume changes and other clinical data (disease duration, urea, creatinine, and uric acid levels). Conclusion Our results showed significantly increased gray matter volume in end-stage renal disease patients with secondary hyperparathyroidism, which was associated with intact parathyroid hormone levels and cognitive impairment. Serum intact parathyroid hormone levels may be a risk factor for cognitive impairment in end-stage renal disease patients with secondary hyperparathyroidism.
This study aims to identify potential microRNAs (miRNAs) contribute to liver fibrosis progression and investigate how the miRNA is involved. We recruited totally 58 patients. Magnetic resonance imaging (MRI) was employed to detect fibrosis. Classification of liver fibrosis was carried out by Ishak scoring system. Cell viability was tested using cell counting kit-8. Measurements of mRNA and protein expressions were conducted using real-time quantitative polymerase chain reaction and western blotting. Luciferase reporter assay was recruited for determination of miR-29b-3p targets. We found that relative enhancement (RE) values were reduced with the increases of fibrosis stages and was negatively associated with Ishak scores. In comparison with patients without liver fibrosis, miR-29b-3p level was remarkably reduced in those with liver fibrosis. Its level was found to be positively associated with RE values. Transforming growth factor beta 1 (TGF-β1)-induced hepatic stellate cell (HSC) activation significantly decreased miR-29b-3p expression. However, miR-29b-3p overexpression repressed TGF-β1-induced collagen I protein and alpha-smooth muscle actin (α-SMA) expression. As expected, its overexpression also reduced cell viability. We found that miR-29b-3p directly bind to signal transducer and activator of transcription 3 (STAT3) and suppressed its expression. Our study demonstrates that low expression of miR-29b-3p may contribute to the progression of liver fibrosis by suppressing STAT3.
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