Additive manufacturing also known as 3D printing is being utilised in electrochemistry to reproducibly develop complex geometries with conductive properties. In this study, we explored if the electrochemical behavior of 3D printed acrylonitrile butadiene styrene (ABS)/carbon black electrodes was influenced by printing direction. The electrodes were printed in both horizontal and vertical directions. The horizsontal direction resulted in a smooth surface (HPSS electrode) and a comparatively rougher surface (HPRS electrode) surface. Electrodes were characterized using cyclic voltammetry, electrochemical impedance spectroscopy and chronoamperometry. For various redox couples, the vertical printed (VP) electrode showed enhanced current response when compared the two electrode surfaces generated by horizontal print direction. No differences in the capacitive response was observed, indicating that the conductive surface area of all types of electrodes were identical. The VP electrode had reduced charge transfer resistance and uncompensated solution resistance when compared to the HPSS and HPRS electrodes. Overall, electrodes printed in a vertical direction provide enhanced electrochemical performance and our study indicates that print orientation is a key factor that can be used to enhance sensor performance.
Cancer progression is driven by coordinated dysregulation of signaling and gene-expression programs that sustain multiple hallmarks of malignancy. Eukaryotic initiation factor 4E (eIF4E) has emerged as an important determinant of this translational reprogramming by preferentially enhancing the synthesis of proteins that support oncogenic phenotypes. This review critically examines the mechanistic evidence linking eIF4E-dependent translation to major cancer hallmarks, including sustained proliferative signaling, evasion of apoptosis, tumor-promoting inflammation, angiogenesis, invasion, and metastasis. We discuss how dysregulated eIF4E activity, driven in part by the PI3K/AKT/mTOR and MAPK/MNK pathways, promotes selective translation of oncogenic, survival, stress-response, hypoxia-, and epithelial-mesenchymal transition-associated factors. We further examine evidence implicating eIF4E in the regulation of p53- and telomerase reverse transcriptase (TERT)-dependent pathways, highlighting potential links to genomic instability and replicative immortality. Finally, we evaluate pharmacological strategies targeting eIF4E and discuss the opportunities and challenges of exploiting eIF4E-dependent translational and metabolic vulnerabilities for cancer therapy. Collectively, the evidence supports eIF4E as a therapeutically relevant translational regulator whose functional activity, rather than expression alone, may help define tumor dependencies and inform mechanism-based therapeutic strategies.