Cancer is one of the major causes of death worldwide. Chemotherapeutic drugs have become a popular choice as anticancer agents. Despite the therapeutic benefits of chemotherapeutic drugs, patients often experience side effects and drug resistance. Biopolymers could be used to overcome some of the limitations of chemotherapeutic drugs, as well as be used either as anticancer agents or drug delivery vehicles. Chitosan is a biocompatible polymer derived from chitin. Chitosan, chitosan derivatives, or chitosan nanoparticles have shown their promise as an anticancer agent. Additionally, functionally modified chitosan can be used to deliver nucleic acids, chemotherapeutic drugs, and anticancer agents. More importantly, chitosan-based drug delivery systems improved the efficacy, potency, cytotoxicity, or biocompatibility of these anticancer agents. In this review, we will investigate the properties of chitosan and chemically tuned chitosan derivatives, and their application in cancer therapy.

SARS‐CoV‐2, a deadly coronavirus sparked COVID‐19 pandemic around the globe. With an increased mutation rate, this infectious agent is highly transmissible inducing an escalated rate of infections and death everywhere. Hence, the discovery of a viable antiviral therapy option is urgent. Computational approaches have offered a revolutionary framework to identify novel antimicrobial treatment regimens and allow a quicker, cost‐effective, and productive conversion into the health center by evaluating preliminary and safety investigations. The primary purpose of this research was to find plausible plant‐derived antiviral small molecules to halt the viral entrance into individuals by clogging the adherence of Spike protein with human ACE2 receptor and to suppress their genome replication by obstructing the activity of Nsp3 (Nonstructural protein 3) and 3CLpro (main protease). An in‐house library of 1163 phytochemicals were selected from the NPASS and PubChem databases for downstream analysis. Preliminary analysis with SwissADME and pkCSM revealed 149 finest small molecules from the large dataset. Virtual screening using the molecular docking scoring and the MM‐GBSA data analysis revealed that three candidate ligands CHEMBL503 (Lovastatin), CHEMBL490355 (Sulfuretin), and CHEMBL4216332 (Grayanoside A) successfully formed docked complex within the active site of human ACE2 receptor, Nsp3, and 3CLpro, respectively. Dual method molecular dynamics (MD) simulation and post‐MD MM‐GBSA further confirmed efficient binding and stable interaction between the ligands and target proteins. Furthermore, biological activity spectra and molecular target analysis revealed that all three preselected phytochemicals were biologically active and safe for human use. Throughout the adopted methodology, all three therapeutic candidates significantly outperformed the control drugs (Molnupiravir and Paxlovid). Finally, our research implies that these SARS‐CoV‐2 protein antagonists might be viable therapeutic options. At the same time, enough wet lab evaluations would be needed to ensure the therapeutic potency of the recommended drug candidates for SARS‐CoV‐2.

Supercoiled flagellar filaments function as mechanical propellers within the bacterial flagellum complex, playing a crucial role in motility. Flagellin, the building block of the filament, features a conserved inner D0/D1 core domain across different bacterial species. In contrast, approximately half of the flagellins possess additional, highly divergent outer domain(s), suggesting varied functional potential. In this study, we report atomic structures of flagellar filaments from three distinct bacterial species: Cupriavidus gilardii, Stenotrophomonas maltophilia, and Geovibrio thiophilus. Our findings reveal that the flagella from the facultative anaerobic G. thiophilus possesses a significantly more negatively charged surface, potentially enabling adhesion to positively charged minerals. Furthermore, we analyze all AlphaFold predicted structures for annotated bacterial flagellins, categorizing the flagellin outer domains into 682 structural clusters. This classification provides insights into the prevalence and experimental verification of these outer domains. Remarkably, two of the flagellar structures reported herein belong to a distinct cluster, indicating additional opportunities on the study of the functional diversity of flagellar outer domains. Our findings underscore the complexity of bacterial flagellins and open up possibilities for future studies into their varied roles beyond motility.

Purpose of Review: This review explores the complex interplay between genetic predispositions to obesity, circadian rhythms, metabolic regulation, and sleep. It highlights how genetic factors underlying obesity exacerbate metabolic dysfunction through circadian misalignment and examines promising interventions to mitigate these effects. Recent Findings: Genome-wide association Studies (GWAS) have identified numerous Single Nucleotide Polymorphisms (SNPs) associated with obesity traits, attributing 40–75% heritability to body mass index (BMI). These findings illuminate critical links between genetic obesity, circadian clocks, and metabolic processes. SNPs in clock-related genes influence metabolic pathways, with disruptions in circadian rhythms—driven by poor sleep hygiene or erratic eating patterns—amplifying metabolic dysfunction. Circadian clocks, synchronized with the 24-h light–dark cycle, regulate key metabolic activities, including glucose metabolism, lipid storage, and energy utilization. Genetic mutations or external disruptions, such as irregular sleep or eating habits, can destabilize circadian rhythms, promoting weight gain and metabolic disorders. Summary: Circadian misalignment in individuals with genetic predispositions to obesity disrupts the release of key metabolic hormones, such as leptin and insulin, impairing hunger regulation and fat storage. Interventions like time-restricted feeding (TRF) and structured physical activity offer promising strategies to restore circadian harmony, improve metabolic health, and mitigate obesity-related risks.

Determining novel therapeutic targets of Acinetobacter baumannii . Deleterious variants, causing antibiotic resistance, were identified by molecular docking and molecular dynamics simulation suggesting new therapeutic targets Oxa-376 and Oxa-530.