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BackgroundAlzheimer’s disease (AD) is a debilitating neurodegenerative disease. Early diagnosis of AD and its precursor, mild cognitive impairment (MCI), is crucial for timely intervention and management. Magnetic resonance imaging (MRI) radiomics showed a promising result for diagnosing and classifying AD, and MCI from normal subjects. Thus, we aimed to systematically evaluate the diagnostic performance of the MRI radiomics for this task.Methods and materialsA comprehensive search of the current literature was conducted using relevant keywords in PubMed/MEDLINE, Embase, Scopus, and Web of Science databases from inception to October 17, 2022. Original studies discussing the diagnostic performance of MRI Radiomics for the classification of AD, MCI, and normal subjects were included. Method quality was evaluated with the Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2), and the Radiomic Quality Score tool (RQS).ResultsWe identified 10 studies that met the inclusion criteria, involving a total of 3446 participants. The overall quality of the included studies was moderate to high. The pooled sensitivity and specificity of MRI radiomics for differentiating AD from normal subjects were 0.8822 (95% CI 0.7888-0.9376), and 0.8849 (95% CI 0.7978-0.9374), respectively. The pooled sensitivity and specificity of MRI radiomics for differentiating MCI from normal subjects were 0.7882 (95% CI 0.6272-0.8917) and 0.7736 (95% CI 0.6480-0.8639), respectively. Also, the pooled sensitivity and specificity of MRI radiomics for differentiating AD from MCI were 0.6938 (95% CI 0.6465-0.7374) and 0.8173 (95% CI 0.6117-0.9270), respectively.ConclusionMRI radiomics has promising diagnostic performance in differentiating AD, MCI, and normal subjects. It can potentially serve as a non-invasive and reliable tool for early diagnosis and classification of AD and MCI.

Background: The aim of this study was to evaluate the status of anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with transverse myelitis (TM) and compare the clinical and imaging characteristics of MOG immunoglobulin G (IgG)-positive with negative cases. Methods: This cohort study enrolled 71 patients diagnosed with new-onset of TM who were being followed at a referral university clinic in Isfahan, Iran, from November 2016 to January 2019. Magnetic resonance imaging (MRI) images and blood samples for anti-MOG, anti-aquaporin 4 (anti-AQP4) (using the cell-based technique), and vasculitis-related antibodies were collected from patients. Outcomes were assessed by the evolution of the Expanded Disability Status Scale(EDSS) score and brain and spinal cord imaging findings within three months. All patients underwent imaging and clinical assessment during a mean period of one year as a follow-up. We compared the characteristics of clinical and radiological outcomes in MOG-IgG-positive and negative cases. Results: Of the total population studied, there were 26.8% men and 73.2% women, with a mean age of 33 ± 10 years. 12 (16.9%) patients were seropositive for MOG antibody and 17 (89.5%) were positive for anti-AQP4 antibodies. There was no significant association between anti-MOG antibody seropositivity and age, gender distribution, the presence of other autoimmune diseases, and number and interval of relapses. However, the involvement site of the spine at first imaging was significantly different between seronegative and seropositive patients. Conclusion: In patients with MOG antibody disease (MOG-AD) TM, the MRI findings suggest a preferential involvement of the cervical-thoracic section in seropositive cases which may help differentiate from non-MOG demyelination TM.

Background Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder of unknown etiology; although infection and inflammation have recently been considered as important etiologic agents. A recent meta-analysis showed correlations between cytokine [interleukin-10 (IL-10) and tumor necrosis factor (TNF)] gene polymorphisms and IBS; however, it is still unknown whether patients with IBS have different cytokine profiles compared to healthy population. Methods To determine the relationships between serum/plasma levels or mucosal expression of IL-10/TNF-α and IBS, we conducted a systematic review and meta-analysis based on case–control studies retrieved from PubMed and EMBASE search through August 2013. Standardized mean difference (SMD) was generated by using the inverse variance method. Heterogeneity was assessed based on I2 values. Key Results Serum/plasma levels of TNF-α tended to be higher in IBS vs controls (p = 0.09); this reached significance in IBS subtypes vs controls and in female patients with IBS. However, serum/plasma levels of IL-10 were not significantly different in IBS patients vs controls. Further analysis of serum/plasma IL-10 levels in IBS subtypes did not show any difference; however, analysis based on gender showed a significantly lower serum/plasma IL-10 levels in male patients with IBS vs male controls (p = 0.02). Colonic IL-10 mRNA had a significantly lower expression in IBS vs control (p = 0.001). Conclusions & Inferences There is an imbalance of proinflammatory TNF-α, and anti-inflammatory IL-10, cytokines in IBS. Stratifying IBS patients based on cytokine profile may represent an opportunity for personalized treatment of this condition.

The real pathophysiology of Crohn’s disease is unknown. The higher prevalence of Crohn’s disease in Caucasian and Jewish ethnicities, as well as its familial aggregation and higher concordance among monozygotic twins, suggest some roles for genes in its development, clinical progression, and outcome. Recent original studies have indicated DLG5113G/A gene polymorphism as a risk factor for Crohn’s disease. Meanwhile, the results of these studies are not consistent. We performed the current meta-analysis to understand whether there is any association between DLG5 gene polymorphism and the risk of Crohn’s disease. PubMed was searched to find the case-control studies on DLG5 gene polymorphisms and Crohn’s disease. This search compiled 65 articles and based on our criteria. 11 articles were included in this meta-analysis. The association between the DLG5 113G/A polymorphism and the risk of disease was assessed using odds ratio (OR) and 95% confidence interval (95% CI). Heterogeneity was evaluated based on I2 values. Random and fixed-effect models were used when I2>50% and I2≤50%, respectively. Eleven studies with a total of 4648 cases and 5677 controls were pooled. Based on our meta-analysis, DLG5113G/A gene polymorphism both at genotypic and allelic levels were not associated with the risk of Crohn’s disease. Pooled data indicated no significant association between DLG5113G/A gene polymorphism and the development of Crohn’s disease. In order to achieve a superior conclusion, multicenter studies on larger number of patients are recommended.

Cystic fibrosis (CF) is a common autosomal recessive disorder with different clinical manifestations, mainly in the gastrointestinal and respiratory tracts. This study was performed to access the effect of probiotics in the status of intestinal inflammation in a group of children with CF by measuring the calprotectin level in the fecal samples. Forty-seven patients with CF were enrolled in this study. The fecal calprotectin levels were measured by enzyme linked immunosorbent assay. In a randomized systematic method, the children were divided into two groups - one group received probiotic powder and another received placebo for four weeks. After this period, fecal calprotectin was re-measured. Thirty-one of 47 enrolled patients (65.9%) had abnormal fecal calprotectin levels (50 g/g). After the intervention, the fecal calprotectin levels decreased in 29 patients (21 patients in the drug group, and only 8 patients in the placebo group; p0.001). This study showed that about two-thirds of patients with CF had intestinal inflammation based on fecal calprotectin levels. Probiotic administration was shown to decrease calprotectin concentrations and subsequently intestinal inflammation in CF patients.

Background Low-grade inflammation has been increasingly implicated in the pathophysiology of irritable bowel syndrome (IBS). Imbalances of pro- and anti-inflammatory cytokines and polymorphisms in cytokine genes have been reported in IBS; however, these findings have not been consistently observed. This may be due to small sample sizes and differences in ethnicities. Therefore, we performed a meta-analysis on the studies that investigated cytokine gene polymorphisms in IBS patients compared to healthy controls. Methods A PubMed and EMBASE search was performed, and cytokine gene polymorphisms, which had been investigated in at least two case-control studies, were evaluated. Pooled odds ratios (OR) for the genotypes were calculated using random- or fixed-effects models. Key Results Five studies that investigated interleukin-10 (IL-10; −1082 G/A), transforming growth factor-β1 (TGF-β1; +869 T/C and +915 G/C) and tumor necrosis factor (TNF; −308 G/A) polymorphisms in IBS patients and controls were included. High producer IL-10 (−1082 G/G; OR: 0.64 [95% CI: 0.48–0.87]) was significantly associated with a decreased risk of IBS. The intermediate producer TGF-β1 (+915 G/C) genotype showed a tendency toward decreasing the risk of IBS. No associations were found between TNF (−308 G/A) genotypes and IBS in the whole meta-analysis although an analysis of Asian studies revealed an association between TNF (−308 G/A and G/G) genotypes and IBS (OR: 0.50 [95% CI: 0.29–0.85]), and 1.82 [95% CI: 1.08–3.07], respectively). Conclusions & Inferences This meta-analysis indicates a role for IL-10 polymorphisms in IBS in general and TNF in Asian populations. Whether or not gene polymorphisms are associated with alterations in cytokine levels leading to functional effects at the level of the gut needs further investigation.

Background: Irritable bowel syndrome (IBS) is a highly prevalent functional gastrointestinal (GI) disorder. Although the mucosal histology of the GI tract is normal, low grade inflammation is considered as an underlyingmechanism in IBS. Imbalances in proand anti-inflammatory cytokines and polymorphisms of cytokines genes have been observed in some studies. However, studies on cytokine gene polymorphisms have not revealed consistent genetic features in these patients, possibily due to lack of statistical power, small sample sizes and differences in ethnicities. To overcome this problem, we performed a systematic review and meta-analysis on the case-control studies which investigated cytokine gene polymorphisms in IBS patients vs. healthy controls. Methods: A MEDLINE and EMBASE search of the literature was performed. Cytokine gene polymorphisms which had been investigated in at least 2 published studies were included. Pooled odds ratios (OR) with 95% confidence interval (95%CI) for the genotypes and allelic distributions were calculated using randomor fixed-effects models. Results: Five case-control studies were identified. IL-10 (−1082 G/ A), TGF-β1 (+869T/C and +915G/C) and TNF-α (−308G/A) were investigated in 5, 3 and 4 studies, respectively. A total of 529 IBS patients and 860 controls were included. High producer IL-10 (−1082 G/G) (OR: 0.68 [95%CI: 0.50-0.91]), intermediate producer TGFβ1 (+869T/C) (OR: 0.64 [95%CI: 0.45-0.91]) and intermediate producer TGF-β1 (+915G/ C) (OR: 0.55 [95%CI: 0.32-0.97]) genotypes were associated with a decreased risk of IBS. No associations were found between IBS and TNF-α (-308G/A) genotypes. Moreover, there was no significant association between the frequency of alleles of each polymorphism and IBS. Conclusion: Results from this meta-analysis suggest a role for IL-10 and TGF-β1 polymorphisms in IBS. Whether the changes in IL-10 and TGF-β1 producer genes translate to alterations in the levels of these cytokines in the gut wall and the nature of their protective role need further investigations.