The development of printable, conductive, and biocompatible hydrogels has emerged as a promising strategy for the next generation of flexible and soft sensor platforms. In this study, we present a systematic investigation of alginate-based hydrogels incorporating different carbonaceous materials, natural graphite, carbon black (Vulcan V3), and activated carbon (PCO1000C), to evaluate their suitability for sensor applications. Hydrogels were formulated with varying concentrations of sodium alginate and a fixed loading of carbon additives. Each composite was characterized in terms of electrical conductivity under compression, rheological behavior, and mechanical strength. Printability was assessed using a custom-designed extrusion platform that allowed for the precise determination of the minimum force and optimal conditions required to extrude each formulation through a standard 20G nozzle. Among all tested systems, the alginate–graphite hydrogel demonstrated superior extrudability, shear-thinning behavior, and shape fidelity, making it well-suited for 3D printing or direct ink writing. A simple conductivity-testing device was developed to verify the electrical response of each hydrogel in the hydrated state. The effects of different drying methods on the final conductivity were also analyzed, showing that oven drying at 50 °C yielded the highest restoration of conductive pathways. Mechanical tests on printed structures confirmed their ability to maintain shape and resist compressive forces. Finally, the biocompatibility of the printed alginate–graphite hydrogel was validated using a standard cytotoxicity assay. The results demonstrated high cell viability, confirming the material’s potential for use in biomedical sensing environments. This work offers a robust framework for the development of sustainable, printable, and biocompatible conductive hydrogels. The combined performance in printability, mechanical integrity, electrical conductivity, and cytocompatibility highlights their promise for flexible biosensors and wearable sensor technologies.

The rapid advancement of 3D bioprinting is transforming possibilities in tissue engineering and personalized medicine, presenting innovative solutions to critical biomedical challenges such as organ shortages and the need for precise 3D cellular models. To fully unlock the potential of this technology, an optimized and comprehensive workflow is essential. This review provides a detailed examination of each step in the bioprinting process-from medical image acquisition to the validation of bioprinted structures-revealing key factors that influence the precision, viability, and clinical relevance of bioprinted tissues. We explore the selection of biomaterials and cell types customized for specific applications and analyze the conversion of DICOM images into 3D-printable models, emphasizing how these choices affect the functionality of the final constructs. Slicing techniques, including comparisons between planar and non-planar algorithms, are examined to highlight their impact on scaffold integrity. Furthermore, we propose advancements in algorithm development, bioprinter technology, and biomaterial optimization to enhance the reproducibility and clinical applicability of bioprinted tissues. This review offers actionable insights for researchers and practitioners aiming to refine bioprinting workflows, ultimately supporting the effective deployment of bioprinted tissues in real-world medical applications, and advancing the fields of regenerative medicine and personalized healthcare.

Chemical risk assessment ensures protection from the toxic effects of drugs and manmade chemicals. To comply with regulatory guidance, studies in complex organisms are required, as well as mechanistic studies to establish the relevance of any toxicities observed to man. Although in vitro toxicity models are improving, in vivo studies remain central to this process. Such studies are invariably time-consuming and often involve large numbers of animals. New regulatory frameworks recommend the implementation of “smart” in vivo approaches to toxicity testing that can effectively assess safety for humans and comply with societal expectations for reduction in animal use. A major obstacle in reducing the animals required is the time-consuming and complexity of the pathological endpoints used as markers of toxicity. Such endpoints are prone to inter-animal variability, subjectivity and require harmonisation between testing sites. As a consequence, large numbers of animals per experimental group are required. To address this issue, we propose the implementation of sophisticated stress response reporter mice that we have developed. These reporter models provide early biomarkers of toxic potential in a highly reproducible manner at single-cell resolution, which can also be measured non-invasively and have been extensively validated in academic research as early biomarkers of stress responses for a wide range of chemicals at human-relevant exposures. In this report, we describe a new and previously generated models in our lab, provide the methodology required for their use and discuss how they have been used to inform on toxic risk. We propose our in vivo approach is more informative (refinement) and reduces the animal use (reduction) compared to traditional toxicity testing. These models could be incorporated into tiered toxicity testing and used in combination with in vitro assays to generate quantitative adverse outcome pathways and inform on toxic potential.

Chemical risk assessment ensures protection from the toxic effects of drugs and manmade chemicals. To comply with regulatory guidance, studies in complex organisms are required, as well as mechanistic studies to establish the relevance of any toxicities observed to man. Although in vitro toxicity models are improving, in vivo studies remain central to this process. Such studies are invariably time-consuming and often involve large numbers of animals. New regulatory frameworks recommend the implementation of “smart” in vivo approaches to toxicity testing that can effectively assess safety for humans and comply with societal expectations for reduction in animal use. A major obstacle in reducing the animals required is the time-consuming and complexity of the pathological endpoints used as markers of toxicity. Such endpoints are prone to inter-animal variability, subjectivity and require harmonisation between testing sites. As a consequence, large numbers of animals per experimental group are required. To address this issue, we propose the implementation of sophisticated stress response reporter mice that we have developed. These reporter models provide early biomarkers of toxic potential in a highly reproducible manner at single-cell resolution, which can also be measured non-invasively and have been extensively validated in academic research as early biomarkers of stress responses for a wide range of chemicals at human-relevant exposures. In this report, we describe a new and previously generated models in our lab, provide the methodology required for their use and discuss how they have been used to inform on toxic risk (likelihood of chemical causing an adverse health effect). We propose our in vivo approach is more informative (refinement) and reduces the animal use (reduction) compared to traditional toxicity testing. These models could be incorporated into tiered toxicity testing and used in combination with in vitro assays to generate quantitative adverse outcome pathways and inform on toxic potential.

The development of therapies to combat neurodegenerative diseases is widely recognized as a research priority. Despite recent advances in understanding their molecular basis, there is a lack of suitable early biomarkers to test selected compounds and accelerate their translation to clinical trials. We have investigated the utility of in vivo reporters of cytoprotective pathways (e.g. NRF2, p53) as surrogate early biomarkers of the ALS degenerative disease progression. We hypothesized that cellular stress observed in a model of ALS may precede overt cellular damage and could activate our cytoprotective pathway reporters. To test this hypothesis, we generated novel ALS-reporter mice by crossing the hTDP-43tg model into our oxidative stress/inflammation (Hmox1; NRF2 pathway) and DNA damage (p21; p53 pathway) stress reporter models. Histological analysis of reporter expression in a homozygous hTDP-43tg background demonstrated a time-dependent and tissue-specific activation of the reporters in tissues directly associated with ALS, before moderate clinical signs are observed. Further work is warranted to determine the specific mechanisms by which TDP-43 accumulation leads to reporter activation and whether therapeutic intervention modulates reporters’ expression. We anticipate the reporter strategy could be of great value in developing treatments for a range of degenerative disorders.