The cold extraction method was used to obtain the aqueous extract of Vitex leucoxylon leaves in a ratio of 1:10. Iron nanoparticles (FeNPs) were synthesized using aqueous leaf extract of V. leucoxylon as a reducing agent. The phytoreducing approach was used to make FeNPs by mixing 1 mL of plant extract with 1 mM of ferric sulfate. Scanning electron microscopy (SEM), Fourier-transform infrared spectroscopy (FTIR), Ultraviolet–visible spectroscopy (UV-Vis), and energy-dispersive X-ray spectroscopy were used to examine the synthesized FeNPs. The reducing reaction was shown by a change in the color of the solution, and the formation of black color confirms that FeNPs have been formed. The greatest absorption peak (max) was found at 395 nm in UV-Vis spectral analysis. The FTIR spectra of V. leucoxylon aqueous leaf extract showed shifts in some peaks, namely 923.96 cm⁻¹ and 1709.89 cm⁻¹, with functional groups carboxylic acids, unsaturated aldehydes, and ketones, which were lacking in the FTIR spectra of FeNPs and are responsible for FeNPs formation. FeNPs with diameters between 45 and 100 nm were observed in SEM images. The creation of FeNPs was confirmed by EDX, which shows a strong signal in the metallic iron region at 6–8 Kev. XRD revealed a crystalline nature and an average diameter of 136.43 nm. Antioxidant, anti-inflammatory, cytotoxic, and wound healing in vitro tests reported significant activity of the FeNPs. The cumulative findings of the present study indicate that the green synthesis of FeNPs boosts its biological activity and may serve as a possible dermal wound-healing agent and cytotoxic agent against cancer. Future study is needed on the identification of mechanisms involved in the synthesis of FeNPs by V. leucoxylon and its biomedical applications.

The applications of bioactive compounds from medicinal plants as therapeutic drugs are largely increasing. The present study selected the bioactive compounds from Acacia concinna (A. concinna) and Citrus limon (C. limon) to assess their phytochemicals, proteins, and biological activity. The plant material was collected, and extraction performed as per the standard procedure. Qualitative analysis was undertaken, and identification of functional organic groups was performed by FTIR and HPLC. Antibacterial, anticancer, antioxidant, antihyperglycemic, antihyperlipidemic, and inhibition kinetics studies for enzymes were performed to assess the different biological activities. Flavonoids and phenols were present in a significant amount in both the selected plants. A. concinna showed significant antimicrobial activity against Z. mobilis, E. coli, and S. aureus, with minimum inhibition zones (MIZ) of 24, 22, and 20 mm, respectively. C. limon strongly inhibited all the tested pathogenic bacteria with maximum and minimum MIZ of 32 and 17 mm. A. concinna silver nanoparticles also exhibited potent antimicrobial activity. Both extracts showed substantial antioxidant, antihyperlipidemic, antidiabetic, anticancer (MCF-7), and anti-urease (antiulcer) properties. To conclude, these plants can be used to treat hyperlipidemia, diabetes, cancer, and gastrointestinal ulcers. They can also serve as antimicrobial and antioxidant agents. Thus, the studied plants must be exploited cost-effectively to generate therapeutic drugs for various diseases.

Background: Primary Ciliary Dyskinesia (PCD) is also known as immotile-cilia syndrome, an autosomal recessive disorder of ciliary function, leading to mucus retention in the respiratory system in childhood. Our knowledge in the pathophysiological aspect of this devastating disorder is increasing with the advancement of genetic and molecular testing. Case presentation: Here in, we report two siblings with a classical clinical and radiological presentation of PCD. Using whole exome sequencing we identified a homozygous truncating variant (c.3402 T > A); p.(Tyr1134*) in the NEK10 gene. Western bolt analysis revealed a decrease in the expression of NEK10 protein in the patient cells. Conclusions: NEK10 plays a central role in the post-mitotic process of cilia assembly, regulating ciliary length and functions during physiological and pathological status. This study highlights the challenges of identifying disease-causing variants for a highly heterogeneous disorder and reports on the identification of a novel variant in NEK10 which recently associated with PCD.

Background: Accurate assessment of drug cytotoxicity in vitro is essential for preclinical evaluation of anticancer agents. Methodological parameters such as cell density and solvent concentrations can significantly influence the reproducibility and reliability of cell-based assay results. Objective: This study aims to optimize cell seeding density and evaluate the cytotoxic effects of common solvents (DMSO and ethanol) on different cancer cell lines, complemented by in silico analysis to elucidate underlying mechanisms. Materials and Methods: Six cancer cell lines (HepG2, Huh7, HT29, SW480, MCF-7, and MDA-MB-231) were seeded at different densities to determine the optimal cell seeding number ideal for cell viability assay at 24, 48, and 72 h. The cytotoxicity of DMSO and ethanol was assessed in these cell lines using an MTT assay at multiple time points. In silico docking studies were conducted to investigate the interactions between solvents and key proteins involved in apoptosis, membrane function, and metabolism. Results: A cell density of 2000 cells per well yielded consistent linear viability across cell lines and time points. DMSO at 0.3125% showed minimal cytotoxicity across all cell lines (except MCF-7) and time points; the cytotoxic effect at higher concentrations is variable depending on cell type and exposure duration. Ethanol exhibited rapid and concentration-dependent cytotoxicity, reducing viability by more than 30% at as low as 0.3125% concentration after 24 h. Docking analyses revealed that DMSO binds specifically to apoptotic and membrane proteins, suggesting a role in inducing apoptosis. In contrast, ethanol primarily interacts with metabolic proteins, consistent with its effect on membrane disruption and rapid cell death. Conclusion: DMSO at 0.3125% is a good choice as a solvent since it has low toxicity in most tested cell lines; however, the safe concentration limit is dependent on cell type and exposure duration. Ethanol exhibited higher cytotoxicity, necessitating careful concentration management. The in silico analysis supports these findings, indicating that DMSO interacts with apoptosis-related proteins, whereas ethanol primarily affects metabolic processes. These results highlight the importance of precise cell density optimization and solvents for reliable cytotoxicity assessment in cell-based assays.

CDC42 (cell division cycle protein 42) belongs to the Rho GTPase family that is known to control the signaling axis that regulates several cellular functions, including cell cycle progression, migration, and proliferation. However, the functional characterization of the CDC42 gene in mammalian physiology remains largely unclear. Here, we report the genetic and functional characterization of a non-consanguineous Saudi family with a single affected individual. Clinical examinations revealed poor wound healing, heterotopia of the brain, pancytopenia, and recurrent infections. Whole exome sequencing revealed a de novo missense variant (c.101C > A, p.Pro34Gln) in the CDC42 gene. The functional assays revealed a substantial reduction in the growth and motility of the patient cells as compared to the normal cells control. Homology three-dimensional (3-D) modeling of CDC42 revealed that the Pro34 is important for the proper protein secondary structure. In conclusion, we report a candidate disease-causing variant, which requires further confirmation for the etiology of CDC42 pathogenesis. This represents the first case from the Saudi population. The current study adds to the spectrum of mutations in the CDC42 gene that might help in genetic counseling and contributes to the CDC42-related genetic and functional characterization. However, further studies into the molecular mechanisms that are involved are needed in order to determine the role of the CDC42 gene associated with aberrant cell migration and immune response.

The interplay between genetics and cancer has been a focal point of research for decades, leading to profound understandings into the molecular mechanisms driving tumorigenesis. In this comprehensive review article, we explore the genetic basis of cancer, encompassing the diverse array of alterations that underline oncogenic transformation. From oncogenes to tumor suppressor genes, and from point mutations to chromosomal rearrangements, we delve into the molecular hallmarks of cancer and their implications for diagnosis, treatment, and prevention. Drawing on recent advancements in genomic technologies, we discuss the role of next-generation sequencing, single-cell sequencing, and computational modeling in unraveling the complexity of cancer genetics. Furthermore, we examine the clinical implications of genetic predisposition to cancer, highlighting the importance of genetic testing and counselling in cancer risk assessment and management. Through an exploration of tumor heterogeneity, clonal evolution, and therapeutic resistance, we underscore the challenges and opportunities in precision oncology. Finally, we discuss future directions in cancer genetics research, including precision prevention strategies and ethical considerations.Keywords: Cancer Genetics; Oncogenes; Tumor Suppressor Genes; Genetic Alterations; Precision Oncology; Clonal Evolution