Waterpipe smoking is popular in many parts of the world. Micronuclei (MN) evaluation in the exfoliated oral cells of smokers is a non-invasive technique for evaluation of possible tobacco harm. We aimed to assess whether MN levels are higher in waterpipe smokers than in never smokers. We examined oral smears of 128 adult male waterpipe smokers and 78 males who never smoked tobacco in rural Egypt The total number of MN per 1000 cells per subject, and the number of MN-containing cells per individual were compared. We observed a higher level of total MN in waterpipe smokers (10 ± 4) than in never smokers (4 ± 2, p<0.001). A similar difference was found for the mean number of affected cells per individual (8 ± 3 vs. 4 ± 1.62, p < 0.001). MN levels were not significantly dose related. This study is among the first to assess the association between waterpipe smoking and a cytogenetic measure of tobacco harm. The two-fold increase in MN level is consistent with previous reports of MN in cigarette smokers. More research is needed to determine if such MN levels are predictive of future health consequences.

Aim of the work: To investigate the frequency of FoxP3+CD4+CD25+high cells (Tregs) in rheumatoid arthritis (RA) patients and their association with clinical and radiological parameters. Also to study the possible relationship between Tregs and TGF-b as an indicator of Treg function, with IL17 as an indicator of Th17 function and with the ratio between them to throw light on the imbalance between these two cytokines in RA.Patients and methods: Forty RA patients and 20 age and sex matched healthy controls were enrolled in the study. Patients underwent clinical, laboratory and radiographic assessment. The frequency of Tregs was determined by flowcytometry. Serum IL-17 and TGF-b cytokines were analyzed using ELISA.Results: The frequency of Tregs was significantly decreased among RA patients and with a parallel significant decrease in the mean fluorescence intensity (MFI) of FoxP3. Both IL-17 and TGFb were significantly increased. Tregs, IL-17 and TGF-b did not correlate with any of the clinical findings, laboratory and radiographic scores. TGFb:IL-17 ratio dropped from 15.8 ± 9.6 among controls to 5.33 ± 5 among patients with mild-to-moderate activity and 2.45 ± 1.8 among patients with severe activity.Conclusion: RA patients show a decreased frequency of Tregs that is not associated with clinical parameters or radiological damage. The five-fold increase in IL-17 and two-fold increase in TGF-b prove a disturbance in the balance of the cytokine milieu in favor of inflammation and draw attention to the importance of considering the interplay of the Treg/TH17 cytokine axis in the pathogenesis of RA; hence aiming at restoring that balance during treatment.

Sansevieria species show various bioactivities. Nevertheless, its therapeutic prospect in liver fibrosis even now is uninvestigated. The present study was conducted to analyze the metabolomic profile of Sansevieria trifasciata hort ex. Prain leaves and roots via HPLC-PAD-ESI/MS and evaluation of its hepatoprotective effect. The identified phytoconstituents were mainly steroidal saponins, phenolics and terpenoids. Sixty-one compounds were tentatively identified in StLE and fifty-nine compounds in StRE. Thioacetamide-induced liver fibrosis rat model was used to evaluate the hepatoprotective effect of Sansevieria trifasciata extracts via activation of the NRF2/ARE signaling pathway. Measurements of serum alanine transaminase (ALT), aspartate transaminase (AST) and malondialdehyde (MDA) were significantly decreased in treated groups with StLE and StRE (at doses of 200 and 100 mg/kg/day) compared with the TAA group. Also, the levels of reduced glutathione (GSH) content and hepatic mRNA levels of Nrf2, HO-1, NQO-1 and Keap-1 were markedly elevated. The prominent hepatoprotective effect was shown in StRE treated groups. Histological findings further confirmed the protective role of the plant against TAA-induced liver fibrosis. In conclusion, the abovementioned results indicated that the hepatoprotective mechanism of StLE and StRE could be achieved by activating Nrf2-ARE signaling pathways to alleviate oxidative stress and inflammation.

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