Roua Mohammad Saleh Alkufeid

The widespread use of mobile phones in daily human transactions, especially those related to the medical field, leads to the spread of microbes among different communities. The microbiology student’s mobile phones could harbour various drug-resistant microbes involved in nosocomial infections to the family members. This study aimed to isolate and characterize bacteria from the mobile phones of microbiology students and other students. This cross-sectional study was performed using a random sampling technique. All data were collected using a questionnaire. Sixty samples were obtained from the surface of the mobile phones of 60 volunteers at King Saud University (KSU). Twenty-three (77%) microbiology students used their mobile phones in the toilets, compared to 23 (77%) non-microbiology students. Staphylococcus is the most prevalent organism followed by Bacillus. The isolated S. aureus was Ampicillin and polymyxin B resistant. It was intermediate against the tested Sulfamethoxazole and Bacitracin. S. aureus isolated from microbiology and non-microbiology students showed no antibiotic sensitivity changes. S. epidermidis showed resistance against Polymyxin B and exhibited an intermediate response against sulfamethoxazole and bacitracin. Bacillus sp. exhibited resistance against Erythromycin. The prevalence of bacteria was higher in microbiology students than in non-microbiology students. The mobile phones of microbiology students were contaminated with clinical pathogens. Therefore, suitable methods should be developed to prevent the outbreak of nosocomial pathogens from the laboratories.

The strong association between POPs and breast cancer in humans has been suggested in various epidemiological studies. However, the interaction of POPs with the ERα protein of breast cancer, and identification of natural and synthetic compounds to inhibit this interaction, is mysterious yet. Consequently, the present study aimed to explore the interaction between POPs and ERα using the molecular operating environment (MOE) tool and to identify natural and synthetic compounds to inhibit this association through a cluster-based approach. To validate whether our approach could distinguish between active and inactive compounds, a virtual screen (VS) was performed using actives (627 compounds) as positive control and decoys (20,818 compounds) as a negative dataset obtained from DUD-E. Comparatively, short-chain chlorinated paraffins (SCCPs), hexabromocyclododecane (HBCD), and perfluorooctanesulfonyl fluoride (PFOSF) depicted strong interactions with the ERα protein based on the lowest-scoring values of −31.946, −18.916, −17.581 kcal/mol, respectively. Out of 7856 retrieved natural and synthetic compounds, sixty were selected on modularity bases and subsequently docked with ERα. Based on the lowest-scoring values, ZINC08441573, ZINC00664754, ZINC00702695, ZINC00627464, and ZINC08440501 (synthetic compounds), and capsaicin, flavopiridol tectorgenin, and ellagic acid (natural compounds) showed incredible interactions with the active sites of ERα, even more convening and resilient than standard breast cancer drugs Tamoxifen, Arimidex and Letrozole. Our findings confirm the role of POPs in breast cancer progression and suggest that natural and synthetic compounds with high binding affinity could be more efficient and appropriate candidates to treat breast cancer after validation through in vitro and in vivo studies.