Reduced graphene oxide nanosheets decorated with ZnS and ZnS-Ag nanoparticles are successfully prepared via a facile one-step chemical approach consisting of reducing the metal precursors on a rGO surface. Prepared rGO-ZnS nanocomposite is employed as an adsorbent material against two model dyes: malachite green (MG) and ethyl violet (EV). The adsorptive behavior of the nanocomposite was tuned by monitoring some parameters, such as the time of contact between the dye and the adsorbent, and the adsorbent dose. Experimental data were also simulated with kinetic models to evaluate the adsorption behavior, and the results confirmed that the adsorption of both dyes followed a pseudo 2nd order kinetic mode. Moreover, the adsorbent was also regenerated in a suitable media for both dyes (HCl for MG and ethanol for EV), without any significant loss in removal efficiency. Ag doped rGO-ZnS nanocomposite was also utilized as a photocatalyst for the degradation of the selected organic contaminant, resorcinol. The complete degradation of the phenolic compound was achieved after 60 min with 200 mg of rGO-ZnS-Ag nanocomposite under natural sunlight irradiation. The photocatalytic activity was studied considering some parameters, such as the initial phenol concentration, the photocatalyst loading, and the pH of the solution. The degradation kinetics of resorcinol was carefully studied and found to follow a linear Langmuir–Hinshelwood model. An additional advantage of rGO-ZnS and rGO-ZnS-Ag nanocomposites was antibacterial activity against Gram-negative bacterium, E. coli, and the results confirmed the significant performance of the nanocomposites in destroying harmful pathogens.

The genesis of cancer is a precisely organized process in which normal cells undergo genetic alterations that cause the cells to multiply abnormally, colonize, and metastasize to other organs such as the liver, lungs, colon, and brain. Potential drugs that could modify these carcinogenic pathways are the ones that will be used in clinical trials as anti-cancer drugs. Resveratrol (RES) is a polyphenolic natural antitoxin that has been utilized for the treatment of several diseases, owing to its ability to scavenge free radicals, control the expression and activity of antioxidant enzymes, and have effects on inflammation, cancer, aging, diabetes, and cardioprotection. Although RES has a variety of pharmacological uses and shows promising applications in natural medicine, its unpredictable pharmacokinetics compromise its therapeutic efficacy and prevent its use in clinical settings. RES has been encapsulated into various nanocarriers, such as liposomes, polymeric nanoparticles, lipidic nanocarriers, and inorganic nanoparticles, to address these issues. These nanocarriers can modulate drug release, increase bioavailability, and reach therapeutically relevant plasma concentrations. Studies on resveratrol-rich nano-formulations in various cancer types are compiled in the current article. Studies relating to enhanced drug stability, increased therapeutic potential in terms of pharmacokinetics and pharmacodynamics, and reduced toxicity to cells and tissues are the main topics of this research. To keep the readers informed about the current state of resveratrol nano-formulations from an industrial perspective, some recent and significant patent literature has also been provided. Here, the prospects for nano-formulations are briefly discussed, along with machine learning and pharmacometrics methods for resolving resveratrol’s pharmacokinetic concerns.

The COVID-19 infection caused by SARS-CoV-2 in late 2019 posed unprecedented global health challenges of massive proportions. The persistent effects of COVID-19 have become a subject of significant concern amongst the medical and scientific community. This article aims to explore the probability of a link between the COVID-19 infection and the risk of lung cancer development. First, this article reports that SARS-CoV-2 induces severe inflammatory response and cellular stress, potentially leading to tumorigenesis through common pathways between SARS-CoV-2 infection and cancer. These pathways include the JAK/STAT3 pathway which is activated after the initiation of cytokine storm following SARS-CoV-2 infection. This pathway is involved in cellular proliferation, differentiation, and immune homeostasis. The JAK/STAT3 pathway is also hyperactivated in lung cancer which serves as a link thereof. It predisposes patients to lung cancer through myriad molecular mechanisms such as DNA damage, genomic instability, and cell cycle dysregulation. Another probable pathway to tumorigenesis is based on the possibility of an oncogenic nature of SARS-CoV-2 through hijacking the p53 protein, leading to cell oxidative stress and interfering with the DNA repair mechanisms. Finally, this article highlights the overexpression of the SLC22A18 gene in lung cancer. This gene can be overexpressed by the ZEB1 transcription factor, which was found to be highly expressed during COVID-19 infection.

This work relates to the discovery of safer and more potent triazole-pyridazinone hybrid (TP) compounds as an inhibitor of sterol 14α-demethylase (SDM). The chemical structures of thirty-three TPs (TP1 to TP33) were designed. The docking scores (DS) of TPs were determined by molecular docking software utilizing three different proteins of SDM (PDB IDs: 3LD6, 5FSA, and 5TZ1). The ProTox II web server predicted TPs' oral LD50 and toxicity class (TC), whereas the Swiss-ADME database anticipated their pharmacokinetic parameters. Based on the in silico study data, four TPs (TP18, TP22, TP27, and TP33) were synthesized and evaluated for their in vitro antifungal activity against seven fungi. The DS (kcal/mol) of TP18 (3LD6 = -8.27; 5FSA = -9.07; 5TZ1 = -9.42), TP22 (3LD6 = -8.23; 5FSA = -8.93; 5TZ1 = -9.57), TP27 (3LD6 = -8.31; 5FSA = -9.12; 5TZ1 = -9.38), and TP33 (3LD6 = -8.19; 5FSA = -8.98; 5TZ1 = -9.94) were better than the DS of fluconazole (3LD6 = -8.18; 5FSA = -8.79; 5TZ1 = -9.18) and ketoconazole (3LD6 = -8.16; 5FSA = -8.86; 5TZ1 = -9.06) implying high potency of TP18, TP22, TP27 and TP33 than fluconazole and ketoconazole against SDM. The anticipated LD50 and toxicity class (TC) of TP18 (500 mg/kg; TC 4), TP22 (500 mg/kg; TC 4), TP27 (1000 mg/kg; TC 4), and TP33 (1000 mg/kg; TC 4) was better than ketoconazole (166 mg/kg; TC 3). The Swiss-ADME database results revealed that TP18, TP22, TP27, and TP33 passed Lipinski’s drug-likeliness rule and demonstrated high oral absorption and bioavailability comparable to ketoconazole and fluconazole. The synthesized compounds' spectral data (FTIR, 1H-NMR, 13C-NMR, and Mass) aligned to their designed chemical structure. The antifungal activity data implies that TP18, TP22, TP27, and TP33 were better antifungal agents than fluconazole and ketoconazole against tested fungi. These findings concurred with the DS of TP18, TP22, TP27, and TP33. In conclusion, TP18, TP22, TP27, and TP33 represent a new chemical template for developing safer and better SDM inhibitors as antifungal agents.