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BackgroundHepatocellular carcinoma (HCC) is one of the most common cancers worldwide. It has been widely established that the early detection of HCC enables more treatment options with improvements in prognosis and survival.ObjectivesThe aim of this study was to assess the diagnostic accuracy of both circulating miR-215 and squamous cell carcinoma antigen-IgM (SCCA-IgM) as serum biomarkers for HCC by examining their diagnostic sensitivity, specificity, accuracy, and predictive values in hepatitis C virus (HCV)-induced HCC patients.Subjects and methodsThis study included 60 patients with HCV-related HCC. In addition, 60 patients with HCV-related liver cirrhosis (LC) and 60 apparently healthy subjects were involved, and served as diseased and healthy control groups, respectively. The relative expression levels of miR-215 were detected using quantitative real-time PCR. SCCA-IgM levels in serum were measured by enzyme immunoassay. We used receiver operating characteristic (ROC) curve to calculate the diagnostic accuracy against alpha-fetoprotein (AFP).ResultsRelative miR-215 expression levels increased the most in HCC patients compared to that in healthy or diseased controls (P<0.001). Serum concentration of SCCA-IgM was significantly higher in HCC group than that in the two control groups. We performed multivariate analysis using AFP level, focal lesion size, and portal vein thrombosis as independent variables. ROC curves showed that the optimum diagnostic miR-215 cutoff value for identifying HCC patients from cirrhotic ones was 417 (sensitivity, 97%; specificity, 91%) and for SCCA-IgM was 95 AU/mL (sensitivity, 92%; specificity, 98%). Moreover, the superiority of both miR-215 and SCCA-IgM to AFP is obvious in our study and this superiority is more evident in distinguishing HCC with AFP levels <200 ng/mL and HCC patients with small-sized focal lesions from cirrhotic patients.ConclusionCell-free miR-215 and serum SCCA-IgM could be used for early diagnosis of HCC either each one as a single marker or with AFP complement measurement.

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Autism Spectrum Disorder (ASD) and learning disabilities are neurodevelopmental disabilities characterized by dramatically increasing incidence rates, yet the exact etiology for these disabilities is not identified. Impairment in tryptophan metabolism has been suggested to participate in the pathogenesis of ASD, however, further validation of its involvement is required. Additionally, its role in learning disabilities is still uninvestigated. Our objective was to evaluate some aspects of tryptophan metabolism in ASD children (N = 45) compared to children with learning disabilities (N = 44) and healthy controls (N = 40) by measuring the expression levels of the MAOA, HAAO and AADAT genes using real-time RT-qPCR. We also aimed to correlate the expression patterns of these genes with parental ages at the time of childbirth, levels of serum iron, and vitamin D3 and zinc/copper ratio, as possible risk factors for ASD. Results demonstrated a significant decrease in the expression of the selected genes within ASD children (p < 0.001) relative to children with learning disabilities and healthy controls, which significantly associated with the levels of our targeted risk factors (p < 0.05) and negatively correlated to ASD scoring (p < 0.001). In conclusion, this study suggests that the expression of the MAOA, HAAO and AADAT genes may underpin the pathophysiology of ASD.

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Background:Active Rheumatoid Arthritis (RA) is associated with considerable changes in body composition, lipids, adipokines and insulin sensitivity. RA is an independent risk factor for CVD. The mechanisms leading to synovial inflammation are similar to those found in unstable atherosclerotic plaque. Irisin is a metabolic hormone and a novel adipomyokine related to insulin resistance and endothelial functions (1).Objectives:To investigate the relationship between serum irisin levels, disease activity and cardiovascular risk in RA patients, and to test its performance in predicting subclinical atherosclerosis in RA patients.Methods:60 RA patients fulfilling the 2010 ACR/EULAR RA Classification Criteria and 30 healthy controls were recruited for serological testing of irisin levels. BMI was calculated. Waist/hip ratio was measured. RA disease activity was assessed by DAS28-ESR. Disability was assessed by HAQ-DI in its Arabic version. Serum ESR, CRP, glycated hemoglobin (HbA1c), lipid profile (serum level of cholesterol, triglyceride, HDL, LDL and cholesterol/ LDL ratio), insulin levels were measured in all patients and controls. Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) was used to calculate insulin resistance. Carotid intimal medial thickness (C-IMT), an indicator of atherosclerosis, was measured by carotid doppler ultrasonography. Echocardiography was performed to assess cardiac abnormalities. Our RA patients were classified twice; first, according to cardiovascular abnormalities and second, according to cut-off values of DAS28.Results:Serum irisin levels were significantly lower in RA patients (9.84 ± 10.56)ng/ml compared to controls (20.48±13.82)ng/ml (p<0.001). BMI values were significantly higher in all patients than controls (P= 0.035), while waist/hip ratio in female patients only were significantly higher (P= 0.007).We found a negative correlation between serum irisin and DAS28-ESR (r = -0.455, P-value 0.005)& HAQ-DI (r = -0.309, P-value 0.016). There was a negative correlation between serum irisin level and parameters of cardiovascular risk including anthropometric measurements (BMI and waist/hip ratio), HOMA-IR (r=−0.371, p=0.009) and C-IMT (r=−0.511, p<0.001). No correlation could be detected between irisin and lipid profile. The frequency of cardiovascular (CV) involvement in RA patients was 45% (27 patients) (11.6 % with echocardiographic abnormalities and 40% having increased C-IMT). Patients with CV involvement showed lower serum irisin level, increased disease activity assessed by DAS28 and increased disease disability assessed by HAQ-DI with statistically significant difference (P < 0.001, P < 0.05 and P < 0.001 respectively). Classifying the patients based on cut-off values of DAS28 into 3 groups (low disease activity, moderate and high disease activity), we found a statistically significant difference between the irisin levels of the 3 groups, being lowest among highly active patients (P= 0.014). c-IMT values were significantly higher in highly active patients (P= 0.04). Assessing the biomarker’s performance as an independent indicator of subclinical atherosclerosis in RA patients using ROC curve, it showed an excellent ability (AUC 0.8, P <0.001). As regarding its ability to differentiate patients with high disease activity, it showed a very good performance (AUC 0.73, P <0.001).Conclusion:In RA patients, serum irisin level was significantly lower and perform better than traditional yardsticks in identifying disease activity. It may act as an independent indicator of subclinical atherosclerosis in RA patients. Serum irisin level may be responsible for increased cardiovascular risk in those patients.References:[1]Chen JQ, Huang YY, Gusdon AM, Qu S.Irisin: a new molecular marker and target in metabolic disorder. Lipids Health Dis. 2015 Jan 14; 14:2.Disclosure of Interests:None declared

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing interstitial respiratoryillness with an unknown origin, which leads to inevitably fatal outcomes in the majority of cases. The pro-inflammatory cytokine interferon lambda-3 (IFN-λ3) has been recently identified as a risk factor for the development of lung fibrosis in scleroderma patients. In this study, we examined the involvement of IFN-λ3 in IPF by utilizing the mouse model of BLM-induced pulmonary fibrosis. Our study identifies a remarkable overexpression in the mRNA of IFNL3, and a positive significant correlation between the IFNL3 mRNA levels and the various proinflammatory cytokines for instance NF-kB, TNF-α, IL-1β and TGF-β throughout the threeweeks study. These findings have proven the impact of IFNL3 on BLM-induced pulmonary fibrosis occurrence and progression. Moreover, the data suggest that the pro-inflammatory and pro-fibrotic capacities of IFNL3 may be provoked by additional pro-inflammatory cytokines In conclusion, IFN-λ3 looks like a promising target in the therapeutic development of new drug candidates for pulmonary fibrosis.