Enterococci, known for their resilience, are commonly found in food, the environment, and the gastrointestinal tracts of humans and animals. In recent research, six strains of enterococcus were isolated from bat guano. These include Enterococcus mundtii SRBG1, Enterococcus gallinarum SRBG3, Enterococcus faecium SRBG2, Enterococcus casseliflavus EC1, and Enterococcus devriesei CAU 1344. Identification was done using 16S DNA analysis. Each strain underwent evaluation for its technological properties (such as tolerances to various NaCl concentrations and temperatures, as well as amylolytic, β-galactosidase, lipolytic, and proteolytic activities, and EPS production) and selected probiotic properties (including safety profile, resistance to 0.3 percent bile salts and gastric juice with a pH of 2.5, lysozyme tolerance, and antibacterial and antibiofilm activities against four foodborne pathogens). The results were analyzed using Principal Component Analysis. This analysis revealed that E. mundtii SRBG1 and E. gallinarum SRBG3, followed by E. faecium SRBG2, were most closely associated with a broad range of technological characteristics and were subsequently used for fermenting skimmed milk. The rheological properties of the samples indicated a shear-thinning or non-Newtonian behavior. Furthermore, during storage of the fermented milk at 4 °C over periods of 1, 7, 14, and 21 days, there were no significant changes in bacterial count (at around 7 log₁₀ CFU/mL) and pH when fermented with the three evaluated strains.

Cancer remains a leading cause of mortality worldwide, presenting a major challenge to global health. Quinolines, a class of nitrogen-containing heterocycles, have proven to be promising compounds for anticancer therapeutic development due to their diverse pharmacological properties, including cytotoxic, antiproliferative, pro-apoptotic, and immunomodulatory effects. This systematic review provides an updated synthesis of the anticancer applications of quinoline-based compounds, including their chemical synthesis, cytotoxic potential, clinical relevance, and biological mechanisms of action. Rigorous literature searching was conducted across multiple databases, identifying studies that evaluated quinoline derivatives using a range of methodologies, including computational modeling, cell-based cytotoxicity assays, 3D tumor spheroid models, and animal models. Quinoline-based compounds express broad-spectrum anticancer potential by acting on multiple cellular targets and pathways. Their mechanisms include inducing mitochondrial apoptosis, inhibiting key oncogenic kinases, modulating epigenetic regulators, damaging DNA, regulating autophagy, and triggering ferroptosis. Overall, this review highlights quinolines as a versatile and promising chemical scaffold for developing multi-targeted anticancer agents. Continued preclinical and clinical research is essential to optimize their efficacy and expand their therapeutic applications in oncology.

Lung cancer (LC) remains the most common malignancy in both genders and is the leading cause of cancer-related death worldwide. Despite significant advances in therapeutic approaches, radiotherapy (RT) continues to be one of the main approaches to LC treatment. However, radioresistance represents a major challenge to effective disease management and contributes significantly to treatment failure and poor prognosis. Radioresistance can be intrinsic, existing before treatment, or acquired during RT. It is a highly complex and multifactorial mechanism involving various cellular and molecular processes that are not yet fully understood. Key mechanisms contributing to radioresistance include enhanced DNA damage repair, cell cycle redistribution, inhibition of apoptosis, disruption of intracellular signaling pathways, interaction with the tumor microenvironment, autophagy-mediated survival, cancer stem cell-related resistance, and deregulation of non-coding ribonucleic acids. Understanding these pathways is essential for identifying new therapeutic targets and developing strategies to overcome resistance and improve patient outcomes. This review provides a comprehensive overview of the molecular mechanisms underlying radioresistance in LC.

The research investigates synthetic hydroxytyrosol (HT) antiviral properties against enveloped and non-enveloped viruses using in silico and in vitro methods. Molecular docking and ADMET analyses suggested favorable interactions of HT with ceramide and sphingomyelin (binding energies of −6.0 and −5.9 kcal/mol, respectively). Favorable predicted pharmacokinetics and safety profiles were also observed. In vitro tests provided preliminary evidence of the dose- and time-dependent virucidal effect of HT against several enveloped viruses, including HSV-1, West Nile virus, SARS-CoV-2 and various influenza A subtypes, which resulted in substantial viral load decreases at 1000 µg/mL. The viral titer of the measles virus decreased by 4.62 log₁₀ units during the 2 h of exposure. No virucidal activity was observed against the non-enveloped bovine rotavirus. Overall, these findings suggest that hydroxytyrosol may represent a promising candidate for further investigation as a virucidal agent, particularly against enveloped viruses.

Introduction: Colorectal cancer (CRC) is a heterogeneous and multifactorial malignancy driven by a series of genetic and epigenetic alterations. In this field, telomere/telomerase dysfunction contributes to CRC carcinogenesis by impairing genomic stability and cellular replication. Objective: This study aimed to evaluate genetic and epigenetic alterations in CRC by examining mutation rates in the human telomerase reverse transcriptase (hTERT) promoter region, relative telomere length (RTL), hTERT gene expression, and DNA methylation in the TERT hypermethylated oncological region (THOR). Methods: A total of 45 CRC and 34 adjacent normal tissue samples from Moroccan patients were analyzed using molecular approaches, such as Sanger sequencing, quantitative PCR (qPCR), reverse transcription qPCR (RT-qPCR), and methylation-specific PCR (MSP). Results: No mutations in the hTERT promoter region were identified. However, hypermethylation in the THOR region was reported in 82.2% of CRC samples and 79.4% of adjacent normal tissues. High hTERT expression was detected in 50% of CRC patients. In addition, telomere length was significantly shorter (p=0.002) in cancerous tissues (1.41 [1.36 – 1.43]) compared to normal mucosa (1.559 [1.46 – 1.63]), with an RTL ratio less than 1 (0.90 [0.86 – 0.95]). No significant differences were found between clinicopathological features and hTERT expression, THOR methylation, or RTL, except for a significant correlation between THOR hypermethylation and smaller tumor size (p=0.017) and between THOR methylation and RTL in CRC tissues (p=0.034). Conclusion: These results suggest that telomere lengthening is crucial for CRC initiation and progression, and cancer cells tend to shorten telomeres to maintain the chromosomal instability (CIN) required for tumor progression. Further research is needed to elucidate the mechanisms underlying telomere shortening in CRC and understand the role of telomerase/telomere complex in CRC initiation and progression, which could provide new diagnostic, prognostic, and therapeutic targets.