This study employs a comprehensive approach combining protein retrieval, sequence alignment, and molecular dynamics simulations to investigate the structural dynamics and stability of wild-type KRas and its mutated variants (G12C, G12D, G12V, and G13D). The selected protein structures were retrieved from the Protein Data Bank (PDB) and prepared by using visual molecular dynamics (VMD) software. Sequence alignment using Clustal Omega provided a detailed comparison of the amino acid sequences, focusing on key mutation sites. Molecular dynamics simulations, performed with Gromacs, revealed distinct conformational changes and stability patterns in the wild-type and mutated KRas proteins over 100 ns. Clustering analysis identified higher conformational changes in the second α-helix of the mutated variants. The root-mean-square deviation (RMSD) distribution analysis showed variant-specific conformational dynamics, with G12V and G12D exhibiting slightly higher average RMSD values. Furthermore, clustering and RMSD analyses of specific amino acid residues (12, 13, 51, and 118) highlighted their roles in maintaining overall stability and influencing structural dynamics. The results indicate that mutations at positions 12 and 13 disrupt normal cycling between wild and mutated variants, leading to the persistent activation of KRas. Additionally, principal component analysis (PCA) elucidated unique conformational dynamics in mutated variants. Free energy landscape (FEL) analysis revealed alterations in the thermodynamic stability of mutated variants compared with the wild type. Overall, this study provides a detailed understanding of the structural changes associated with oncogenic mutations in KRas, offering insights crucial for targeted therapeutic strategies in KRas-driven cancers.

Recent advancements in neuroendocrinology challenge the long‐held belief that hormonal effects are confined to perivascular tissues and do not extend to the central nervous system (CNS). This paradigm shift, propelled by groundbreaking research, reveals that synthetic hormones, notably in anti‐inflammatory medications, significantly influence steroid psychosis, behavioural, and cognitive impairments, as well as neuropeptide functions. A seminal development in this field occurred in 1968 with McEven's proposal that rodent brains are responsive to glucocorticoids, fundamentally altering the understanding of how anxiety impacts CNS functionality and leading to the identification of glucocorticosteroids and mineralocorticoids as distinct corticotropic receptors. This paper focuses on the intricate roles of the neuroendocrine, immunological, and CNS in fostering stress resilience, underscored by recent animal model studies. These studies highlight active, compensatory, and passive strategies for resilience, supporting the concept that anxiety and depression are systemic disorders involving dysregulation across both peripheral and central systems. Resilience is conceptualized as a multifaceted process that enhances psychological adaptability to stress through adaptive mechanisms within the immunological system, brain, hypothalamo–pituitary–adrenal axis, and ANS Axis. Furthermore, the paper explores oxidative stress, particularly its origin from the production of reactive oxygen species (ROS) in mitochondria. The mitochondria's role extends beyond ATP production, encompassing lipid, heme, purine, and steroidogenesis synthesis. ROS‐induced damage to biomolecules can lead to significant mitochondrial dysfunction and cell apoptosis, emphasizing the critical nature of mitochondrial health in overall cellular function and stress resilience. This comprehensive synthesis of neuroendocrinological and cellular biological research offers new insights into the systemic complexity of stress‐related disorders and the imperative for multidisciplinary approaches in their study and treatment.

Liquid biopsy represents a transformative approach in oncology, enabling noninvasive disease detection and monitoring through epigenetic signals in circulating tumor DNA (ctDNA), nucleosomes, and noncoding RNAs. Tumor initiation is driven by epigenetic modifications, including DNA methylation, histone alterations, and dysregulated noncoding RNAs, which disrupt gene regulation, cell cycle control, DNA repair, and metastatic processes. This review systematically examines recent evidence on DNA methylation, histone marks (e.g., H3K27me3, H3K18ac), and noncoding RNAs (miRNAs, lncRNAs) as biomarkers for early cancer detection, prognosis, and therapeutic response. Particular focus is placed on aberrant DNA methylation (e.g., hypermethylation of CDKN2A, RASSF1A) and altered histone modifications (e.g., EZH2‐mediated silencing) as indicators of tumor heterogeneity and evolution. Stable and specific in biofluids, noncoding RNAs such as oncogenic miR‐21, tumor‐suppressive miR‐34a, and metastasis‐associated MALAT1/HOTAIR further enhance clinical applicability. Recent detection methods, including bisulfite sequencing, ChIP‐seq, and RNA‐seq, have advanced biomarker profiling, though challenges remain in standardization and low‐abundance detection. With over 12 active clinical studies validating their utility, integration of epigenetic markers with AI and multiomics holds promise for individualized, dynamically guided oncology care. Future innovations, such as chromatin accessibility analysis and cfDNA fragmentation profiling, may further refine diagnostic precision and therapeutic monitoring.

This review explores the application of induced pluripotent stem cells (iPSCs) in regenerative medicine. The therapeutic significance of iPSC-derived cell therapy within regenerative medicine, emphasizes their reprogramming process and crucial role in cellular differentiation while setting the purpose and scope for the comprehensive exploration of iPSC-derived cell therapy. The subsequent sections intricately examine iPSC-derived cell therapy, unravelling the diverse derivatives of iPSCs and striking a delicate balance between advantages and limitations in therapeutic applications. Mechanisms of action, revealing how iPSC-derived cells seamlessly integrate into tissues, induce regeneration, and contribute to disease modeling and drug screening advancements is discussed. The analysis extends to clinical trials, shedding light on outcomes, safety considerations, and ethical dimensions. Challenges and concerns, including the risk of tumorigenesis and scalability issues, are explored. The focus extends to disease-specific applications, showcasing iPSC-derived cell therapy as a promising avenue for various medical conditions, supported by illustrative case studies. Future directions and research needs are outlined, identifying areas for further exploration, safety considerations and potential enhancements that will shape the future landscape of iPSC-derived therapies. In conclusion, this review provides significant understanding of iPSC-derived cell therapy’s status, that contemplates the implications for regenerative medicine and personalized treatment using iPSCs, offering a comprehensive perspective on the evolving field within the confines of a dynamic and promising scientific frontier. Export

Zein, a corn‐derived prolamine protein, has become a powerful ally in the fight against cancer, particularly non‐small cell lung cancer (NSCLC.) Its unique attributes, enriched by modifiable hydroxyl and amino groups, have led to the development of advanced functionalised drug delivery systems. Innovative techniques like chemical crosslinking, desolvation, dispersion and micromixing have led to the creation of zein‐based nanoparticles, revolutionising cancer therapy. Central to this examination is the remarkable ability of zein NPs to enhance drug stability, optimise oral bioavailability and improve targeted drug delivery, specifically tailored to combat NSCLC. This represents not just a technological breakthrough but a paradigm shift, ushering in a new era of precise, personalised and effective cancer treatment. Zein, a hydrophobic nanoparticle, is a promising drug for cancer treatment. However, its journey to the clinic is challenging due to its hydrophobic nature and the need for advanced evaluative platforms. This review emphasises the need for rigorous research to align zein's potential with real‐world applications. It offers a synthesis of methodologies, applications, and obstacles, aiming to see zein nanoparticles as a central element in cancer therapy innovations. The review encourages researchers, clinicians and industry professionals to embrace the potential of zein and promote the convergence of laboratory innovation and clinical application.