According to previous studies, many neuroanatomical alterations have been detected in patients with tinnitus. However, few studies have reported on the morphological changes observed following sound therapy. To explore the brain anatomical alterations in patients with idiopathic tinnitus using voxel-based morphometry (VBM) analysis before and after effective 12 weeks sound therapy. The protocol was registered on ClinicalTrials.gov, ID: NCT02774122. In this study, we collected data from 27 matched healthy control (HC) individuals and 27 idiopathic tinnitus patients before and after 12 weeks of sound therapy by using adjusted narrow band sound. 3.0T MRI system and high-resolution 3D structural images were acquired with a 3D-BRAVO pulse sequence. Structural image data preprocessing was performed using the VBM8 toolbox. The Tinnitus Handicap Inventory (THI) score was acquired in the tinnitus group to assess the severity of tinnitus and tinnitus-related distress. Mann-Whitney U Test, Wilcoxon Signed-Ranks test, and Pearson's correlation analysis were used in the statistical analysis. We found significantly decreased gray matter (GM) volume in the left thalami, right thalami, and cochlear nucleus among the tinnitus patients before sound therapy (baseline) compared to the HC group. However, we did not find significant differences in brain regions between the 12-week treatment and HC groups. According to the results of Wilcoxon Signed-Ranks test, the 12-week sound therapy group demonstrated significant greater brain volume compared with the baseline group among these brain regions. Decreased THI score and changed GM volume were not correlated. This is a useful study for observing the characteristics of neuroanatomical changes in patients with idiopathic tinnitus before and after sound treatment. The study characterized the effect of sound therapy on brain volume. It found that sound therapy had a normalizing effect on the bilateral thalami and cochlear nucleus.
Background: Ulcerative colitis (UC), a subtype of inflammatory bowel disease (IBD), has been found to be associated with colorectal cancer (CRC) in observational studies, but there is no evidence to support a causal relationship or reverse causality between the two diseases.Methods: We employed two-sample bidirectional Mendelian randomization to estimate an unconfounded bidirectional causal relationship between IBD (including UC and Crohn’s disease (CD)) and colorectal cancer. After searching IEU GWAS database and filtering SNPs, we applied a variety of MR methods including IVW method using qualified instrumental variables, and conducted sensitivity analysis to detect the heterogeneity and pleiotropy of instrumental variables.Results: After using three groups of SNPs (CD: 106, UC: 113, IBD: 70), the IVW method MR analysis showed that the results were not significant (result for UC: odds ratio (OR) [95% Confidence Interval (CI)]: 0.9998 [0.9991–1.0005], p value: 0.58; result for CD: OR [95%CI]: 0.99962 [0.99912–1.00012], p value: 0.14; results for IBD: OR [95%CI]: 0.99959 [0.99869–1.00048], p value: 0.36). MR-Egger regression, WM method and MR-RAPS method reached the same conclusion. Sensitivity analysis did not reveal heterogeneity and pleiotropy. Bidirectional MR analysis was performed using the same procedure, and the results of IVW MR analysis were also not significant (result for CD: OR [95%CI]: 1.07985 [0.00049–2372.38304], p value 0.98; result for UC: OR [95%CI]: 0.27117 [0.00014–528.3707], p value: 0.74; result for IBD: OR [95%CI]: 0.47101 [0.0001–2242.94159], p value: 0.86). MR-Egger regression, WM method and MR-RAPS method also reached the same conclusion. Sensitivity analysis did not find any evidence of heterogeneity and pleiotropy.Conclusion: Contrary to the conclusions of previous observational studies, a two-sample MR analysis did not find a causal relationship or reverse causal relationship between IBD and CRC. Sporadic CRC (sCRC) may differ in pathogenesis from IBD-related CRC.
Background and Aims: Although observational studies have reported correlations between inflammatory bowel disease (IBD) and aging, there is no evidence supporting causal relationships between the two. Methods: Summary data from the Genome-Wide Association Study (GWAS) were subjected to two-sample and bidirectional Mendelian randomization (MR) to assess the causal relationships between biomarkers of IBD and aging. Following IEU GWAS database screening and single nucleotide polymorphism filtering, various MR methods, including the inverse-variance weighted method, were applied to qualified instrumental variables. The heterogeneity and pleiotropy of the instrumental variables were verified by sensitivity analyses. Results: Ulcerative colitis (UC) was associated with a 0.10 standard deviation (SD) unit increase in DNA methylation PhenoAge acceleration (adjusted P-value=0.010). SD unit increases in intrinsic epigenetic age acceleration were associated with increases in the probability of Crohn’s disease (CD) and IBD of 0.05 (adjusted P-value=0.032) and 0.04 (adjusted P-value=0.039), respectively. SD unit increases in physical activity and DNA methylation PhenoAge acceleration increased the probabilities of IBD by 0.03 and 0.04 (adjusted P-value=0.039), respectively. CD was associated with shorter telomere length; UC was associated with increased DNA methylation PhenoAge acceleration; and IBD was associated with decreased appendicular lean mass. Four factors associated with aging showed causal relationships: telomere length, DNA methylation GrimAge acceleration, DNA methylation Hannum age acceleration, and usual walking pace, with IBD ruled out. Conclusion: These findings provide new evidence for the causal relationship between IBD and aging in European populations, as well as providing suggestions for the prevention and treatment of IBD.
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