Background: Nonalcoholic fatty liver disease (NAFLD) is the most abundant chronic liver disorder, because racial and ethnic differences may influence prevalence and severity of NAFLD. Objectives: This metabolomic study was conducted to identify the metabolic biomarkers and determine the mechanism of progress of NAFLD in Iranian patients. Methods: Serum samples were collected from 75 participants (37 healthy controls and 38 patients with NAFLD) after an overnight fast. The metabolome of all samples were determined by nuclear magnetic resonance (NMR) and were compared by multivariate statistical analysis. Results: Totally, 19 metabolomic biomarkers were identified by NMR. Compared to healthy controls, NAFLD patients had increased serum concentrations of glycochenodeoxycholic acid, taurocholic acid, glycocholic acid, deoxycholic acid, valine, isoleucine, succinic acid, isocitric acid, 2-ketoglutaric acid, trimethylamine, proline, hydroxyproline and tyrosine, while the concentrations of butyric acid, propionic acid, isovaleric acid, glutamine, glycine, and serine decreased. Conclusions: A robust set of biomarkers for diagnosis of NAFLD was established. Serum metabolomics biomarkers revealed changes in some amino acids and their derivatives, bile acids, short chain fatty acids, and tricarboxylic acid cycle intermediates in subjects with NAFLD compared to healthy controls. These markers could be used as indicators regarding the efficacy of therapeutic interventions.

The effects of nicotine and cigarette smoke in many diseases, notably COVID-19 infection, are being debated more frequently. The current basic data for COVID-19 is increasing and indicating the higher risk of COVID-19 infections in smokers due to the overexpression of corresponding host receptors to viral entry. However, current multi-national epidemiological reports indicate a lower incidence of COVID-19 disease in smokers. Current data indicates that smokers are more susceptible to some diseases and more protective of some other. Interestingly, nicotine is also reported to play a dual role, being both inflammatory and anti-inflammatory. In the present study, we tried to investigate the effect of pure nicotine on various cells involved in COVID-19 infection. We followed an organ-based systematic approach to decipher the effect of nicotine in damaged organs corresponding to COVID-19 pathogenesis (12 related diseases). Considering that the effects of nicotine and cigarette smoke are different from each other, it is necessary to be careful in generalizing the effects of nicotine and cigarette to each other in the conducted researches. The generalization and the undifferentiation of nicotine from smoke is a significant bias. Moreover, different doses of nicotine stimulate different effects (dose-dependent response). In addition to further assessing the role of nicotine in COVID-19 infection and any other cases, a clever assessment of underlying diseases should also be considered to achieve a guideline for health providers and a personalized approach to treatment.

Chemical warfare victims suffer from bronchiolitis and chronic pulmonary obstruction caused by sulfur mustard (SM) toxicity. Despite the mesenchymal stem cells capacity to alleviate inflammation, their low survival rate under oxidative stress severely limits their effectiveness. This study aimed to examine how natural (Crocin) and synthetic (Dexamethasone) antioxidants might affect MSC efficacy. MSCs were treated with the optimal doses of Crocin (Cr.), Dexamethasone (Dex.), and their combination. The A549 cells line was pretreated with the optimal dose of the CEES to mimic the lung disease. Then, the affected A549 cells were exposed to the preconditioned MSCs and conditioned media, and then their survival rates were estimated by MTTor2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Annexin-V PI apoptosis test was conducted for MSCs and A549 cells. Reactive Oxygen Species (ROS) assay and Enzyme-linked immunosorbent assay (ELISA) test demonstrated the percentage of production of ROS and the cytokines levels in A549/CEES, respectively. The results revealed significant increases in Cr. + Dex. treated MSCs (P < .01) and A549 cells treated with MSCs-CM/Cr/Dex (P < .01) groups’ survival. The apoptosis rate and ROS production were reduced in the MSCs-CM/Cr/Dex. Also, considerable decreases in IL-1β (P < .01) and IL-6 (P < .01) and a significant increase in IL-10 (P < .05) in treated A549/CEES by Cr/Dex and MSCs-CM/Cr/Dex supported the synergistic effects of Crocin and Dexamethasone.