Firoz Ahmad

Pancreatic cancer remains one of the most lethal malignancies, characterised by aggressive progression, metabolic adaptation, and resistance to therapy. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a critical mechanism influencing tumour survival and therapeutic response. However, the role of ferroptosis suppressor genes (FSGs) in pancreatic cancer remains incompletely understood. In this study, FSGs were systematically retrieved from FerrDb V2 and subjected to multi-step filtering to identify a curated set of 196 protein-coding genes. Genomic alteration analysis using cBioPortal across 21 pancreatic cancer studies (n = 5189 samples) identified seven recurrently altered genes (TP53, HSF1, PARP10, ZFP36, SIRT2, ECH1, and ENPP2) with alteration frequencies ≥ 3%. Co-occurrence analysis revealed predominantly cooperative alteration patterns among these genes, suggesting functional complementarity. Survival analysis demonstrated that alterations in FSGs were significantly associated with reduced overall survival in pancreatic cancer, with several genes (ECH1, ZFP36, SIRT2, and ENPP2) showing particularly strong adverse prognostic effects. In contrast, no significant survival associations were observed in oesophageal and gastric cancers, indicating a tumour-specific dependency on ferroptosis-related mechanisms. KEGG pathway enrichment analysis of the broader FSG set revealed significant involvement in pathways related to metabolic regulation (AMPK-mTOR signalling), autophagy, hypoxia response (HIF-1 signalling), and oncogenic signalling (PI3K-Akt pathway). Integration of these findings suggests that ferroptosis suppressor genes contribute to pancreatic cancer progression by promoting metabolic adaptation and resistance to oxidative stress. In conclusion, this study identifies key ferroptosis suppressor genes with prognostic relevance in pancreatic cancer and highlights their integration within critical metabolic and stress-response pathways. The tumour-specific nature of these associations underscores the importance of biological context and supports the potential of FSGs as prognostic biomarkers and potential therapeutic targets in ferroptosis-based strategies.

Corticosteroids are among the most widely prescribed medications in modern medicine, valued for their potent anti-inflammatory and immunosuppressive properties. Despite their therapeutic benefits, corticosteroids are frequently associated with adverse neuropsychiatric manifestations that range from mild mood disturbances to severe psychosis. These side effects, although often under recognized, can significantly impair quality of life and complicate clinical management. The incidence of steroid-induced psychiatric symptoms varies widely, from 5 to 20%, depending on dosage, duration of therapy, and patient vulnerability. The underlying mechanisms involve dysregulation of the hypothalamicpituitary–adrenal (HPA) axis, alterations in neurotransmitter systems, neuroinflammation, and structural changes in brain regions such as the hippocampus, amygdala, and prefrontal cortex. Clinically, corticosteroid-induced neuropsychiatric effects manifest across a spectrum, including depression, mania, anxiety, psychosis, cognitive deficits, and behavioral disturbances. Risk factors such as high cumulative dose, rapid administration, older age, female sex, and pre-existing psychiatric illness increase susceptibility. Timely recognition and differentiation from primary psychiatric disorders are crucial for effective intervention. Management strategies encompass pharmacological approaches such as dose reduction, antipsychotics, antidepressants, and mood stabilizers, as well as non-pharmacological interventions including psychotherapy, lifestyle modification, and preventive monitoring protocols. This review synthesizes current evidence on the pathophysiology, clinical spectrum, risk factors, diagnostic considerations, and management of corticosteroid-induced neuropsychiatric manifestations. It also highlights research gaps and future directions aimed at mitigating these complications while preserving the therapeutic utility of corticosteroids. Understanding this complex interplay between corticosteroid therapy and neuropsychiatric health is essential for clinicians to optimize patient outcomes.

Introduction: Brain disorders, including Parkinson’s disease, epilepsy, traumatic brain injury, and psychiatric illnesses, continue to pose substantial clinical and societal burdens. Traditional treatment approaches are often limited by poor targeting efficiency and the complexity of neural networks. Neuroengineering combines principles of engineering, materials science, and neuroscience to develop innovative tools capable of monitoring and modulating brain activity. Advances in neural interfaces, neurostimulation technologies, and bioengineered therapeutic systems are enabling more precise and minimally invasive treatment strategies, offering new possibilities for restoring neurological function and improving patient outcomes. Short summary: Brain disorders represent one of the greatest challenges in modern medicine, demanding innovative approaches that integrate neuroscience, engineering, and technology. Neuroengineering has emerged as a transformative discipline that bridges these domains, offering new strategies for diagnosis, monitoring, and therapeutic intervention. This review discusses recent advances in neuroengineering technologies, including neural interfaces, neurostimulation systems, nanotechnology-based therapeutics, and tissue engineering approaches supported by artificial intelligence for precision brain disorder management. Conclusion: Neuroengineering represents a rapidly evolving field with the potential to transform brain healthcare through innovative diagnostic and therapeutic technologies. Continued interdisciplinary collaboration and technological refinement are essential to overcome translational challenges and achieve widespread clinical implementation.

Glioblastoma (GB) remains a major challenge owing to its extremely aggressive nature and resistance to conventional therapies. This review focuses on the intricate roles of progenitor cells, microglia, and non-coding RNAs (ncRNAs) in orchestrating GB pathogenesis and therapy resistance. Glioma stem cells (GSCs), derived from progenitor cells, are important drivers of tumor initiation and recurrence and exhibit remarkable plasticity and resistance to treatment. Microglia, the immune cells of the brain, are hijacked by GB cells to create an immunosuppressive microenvironment that supports tumor growth and resistance to therapy. Non-coding RNAs, including microRNAs and long noncoding RNAs, regulate multiple resistance mechanisms by modulating gene expression and influencing the interactions between progenitor cells and microglia. This review highlights new insights into these interconnected signaling pathways and explores potential therapeutic strategies targeting these molecular players to overcome treatment resistance and improve outcomes in patients with GB.