The 3-dimensional (3D) printing technologies, referred to as additive manufacturing (AM) or rapid prototyping (RP), have acquired reputation over the past few years for art, architectural modeling, lightweight machines, and tissue engineering applications. Among these applications, tissue engineering field using 3D printing has attracted the attention from many researchers. 3D bioprinting has an advantage in the manufacture of a scaffold for tissue engineering applications, because of rapid-fabrication, high-precision, and customized-production, etc. In this review, we will introduce the principles and the current state of the 3D bioprinting methods. Focusing on some of studies that are being current application for biomedical and tissue engineering fields using printed 3D scaffolds.

Radiation exposure is a threat to public health because it causes many diseases, such as cancers and birth defects, due to genetic modification of cells. Compared with the past, a greater number of people are more frequently exposed to higher levels of radioactivity today, not least due to the increased use of diagnostic and therapeutic radiation-emitting devices. In this study, ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS)-based metabolic profiling was used to investigate radiation- induced metabolic changes in human fibroblasts. After exposure to 1 and 5 Gy of γ-radiation, the irradiated fibroblasts were harvested at 24, 48, and 72 h and subjected to global metabolite profiling analysis. Mass spectral peaks of cell extracts were analyzed by pattern recognition using principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA). The results showed that the cells irradiated with 1 Gy returned to control levels at 72 h post radiation, whereas cells irradiated with 5 Gy were quite unlike the controls; therefore, cells irradiated with 1 Gy had recovered, whereas those irradiated with 5 Gy had not. Lipid and amino acid levels increased after the higher-level radiation, indicating degradation of membranes and proteins. These results suggest that MS-based metabolite profiling of γ-radiation-exposed human cells provides insight into the global metabolic alterations in these cells.

Metformin is one of the most effective therapies for treating type 2 diabetes and has been shown to also attenuate aging and age-related disorders. In this study, we explored the relationship between metformin and DNA damage repair in ionizing radiation (IR)-induced damage of human aortic endothelial cells (HAECs). Metformin treatment suppressed IR-induced senescence phenotypes, such as increased senescent-associated β-galactosidase (SA β-gal) activity and decreased tube formation and proliferation. Moreover, metformin increased BRCA1-associated RING domain protein 1 (BARD1) and RAD51 expression in both aging and IR-exposed cells. Metformin-treated cells exhibited higher levels of the BRCA1-BARD1-RAD51 complex during irradiation, even in the presence of compound C, an AMP-activated protein kinase inhibitor. BARD1 knockdown confirmed its critical role in metformin-mediated inhibition of endothelial senescence. Metformin increased blood vessel sprouting and decreased SA β-gal activity in mouse aortas. Collectively, our findings provide new insights into how metformin can prevent endothelial cell senescence by promoting BARD1-related DNA damage repair, suggesting that metformin may be an effective anti-aging agent and a promising therapeutic for protecting against radiation-induced cardiotoxicity.

Three in vitro dose calibration curves for biodosimetry such as dicentric chromosome assay, fluorescence in situ hybridization (FISH) assay for translocation, and micronuclei (MNs) in binucleated cell assay were established after exposure to ionizing radiation. Peripheral blood lymphocyte samples obtained from healthy donors were irradiated with ⁶⁰Co source at a dose rate of 0.5 Gy/min to doses of 0.1–6 Gy. The results from three in vitro dose calibration curves for biodosimetry were analyzed to understand the relationship among biodosimetry assay techniques. Our comparison demonstrates that there is a very strong positive correlation among the dicentric assay, FISH, and MNs analysis, and these three biodosimetry assays strongly support the in vitro dose reconstruction and the emergency preparedness of public or occupational radiation overexposure.

Background: this study aimed to conduct a biological assessment of the potential exposure to carcinogenic substances in current semiconductor workers. Methods: A cross-sectional study was conducted on 306 semiconductor workers. The assessed biomarkers were as follows: (benzene) urine S-phenylmercapturic, trans,trans-muconic acid, blood benzene; (trichloroethylene) urine trichloroacetic acid; (2-ethoxyethanol) 2-ethoxyacetic acid; (arsine) urine arsenic3+, arsenic5+, monomethylarsonic, dimethylarsinic acid, arsenobetaine; (shift work) 6-hydroxymelatonin; (smoking) cotinine, and (radiation). The detection rate of these materials is defined as more than the biological exposure index (BEI) or the previous reference value. Results: Some workers exposed to trans,trans-muconic acid, trichloroacetic acid, and arsenic5+ showed high BEI levels. Generally, there was no difference according to job categories, and workers were suspected to be exposed to other sources. The melatonin concentration tended to decrease when working at night, and cotinine was identified as an excellent surrogate marker for smoking. In the case of radiation exposure, there was no significant difference in the number of stable chromosome translocation in 19 semiconductor workers. Their estimated radiation exposure level was below the limit of detection (LOD) or near the LOD level. Conclusion: In this study, most carcinogens were below the BEI level, but verification through re-measurement was needed for workers who were identified to have a high BEI level. For continuous monitoring, a prospective cohort is necessary to deal with the healthy worker effect and assess additional materials.