Flinders University

About: Flinders University is a education organization based out in Adelaide, South Australia, Australia. It is known for research contribution in the topics: Population & Health care. The organization has 12033 authors who have published 32831 publications receiving 973172 citations. The organization is also known as: Flinders University of South Australia.

A Mussel-Inspired Conductive, Self-Adhesive, and Self-Healable Tough Hydrogel as Cell Stimulators and Implantable Bioelectronics.

Abstract: A graphene oxide conductive hydrogel is reported that simultaneously possesses high toughness, self-healability, and self-adhesiveness. Inspired by the adhesion behaviors of mussels, our conductive hydrogel shows self-adhesiveness on various surfaces and soft tissues. The hydrogel can be used as self-adhesive bioelectronics, such as electrical stimulators to regulate cell activity and implantable electrodes for recording in vivo signals.

Cyto- and genotoxicity of ultrafine TiO2 particles in cultured human lymphoblastoid cells.

Abstract: Titanium dioxide is frequently used in the production of paints, paper, plastics, welding rod-coating material, and cosmetics, because of its low toxicity. However, recent studies have shown that nano-sized or ultrafine TiO(2) (UF-TiO(2)) (<100 nm in diameter) can generate pulmonary fibrosis and lung tumor in rats. Cytotoxicity induced by UF-TiO(2) in rat lung alveolar macrophages was also observed. This generates great concern about the possible adverse effects of UF-TiO(2) for humans. The cytotoxicity and genotoxicity of UF-TiO(2) were investigated using the methyl tetrazolium cytotoxicity (MTT) assay, the population growth assay, the apoptosis assay by flow cytometry, the cytokinesis block micronucleus (CBMN) assay, the comet assay, and the hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene mutation assay. WIL2-NS cells were incubated for 6, 24 and 48 h with 0, 26, 65 and 130 microg/ml UF-TiO(2). Significant decreases in viability were seen in the MTT assay at higher doses; for example, 61, 7 and 2% relative viability at 130 microg/ml for 6, 24 and 48-h exposure (P<0.01). A dose-dependent relationship was observed, while a time-dependent relationship was seen only at the highest dose (130 microg/ml) after exposure for 24 and 48 h. Treatment with 130 microg/ml UF-TiO(2) induced approximately 2.5-fold increases in the frequency of micronucleated binucleated cells (P<0.01). In addition, a significant reduction in the cytokinesis block proliferation index was observed by the CBMN assay (P<0.05). In the comet assay, treatment with 65 microg/ml UF-TiO(2) induced approximately 5-fold increases in olive tail moment (P<0.05). In the HPRT mutation assay, treatment with 130 microg/ml UF-TiO(2) induced approximately 2.5-fold increases in the mutation frequency (P<0.05). The results of this study indicate that UF-TiO(2) can cause genotoxicity and cytotoxicity in cultured human cells.

An autocrine TGF-β/ZEB/miR-200 signaling network regulates establishment and maintenance of epithelial-mesenchymal transition

Abstract: Epithelial-mesenchymal transition (EMT) is a form of cellular plasticity that is critical for embryonic development and tumor metastasis. A double-negative feedback loop involving the miR-200 family and ZEB (zinc finger E-box-binding homeobox) transcription factors has been postulated to control the balance between epithelial and mesenchymal states. Here we demonstrate using the epithelial Madin Darby canine kidney cell line model that, although manipulation of the ZEB/miR-200 balance is able to repeatedly switch cells between epithelial and mesenchymal states, the induction and maintenance of a stable mesenchymal phenotype requires the establishment of autocrine transforming growth factor-β (TGF-β) signaling to drive sustained ZEB expression. Furthermore, we show that prolonged autocrine TGF-β signaling induced reversible DNA methylation of the miR-200 loci with corresponding changes in miR-200 levels. Collectively, these findings demonstrate the existence of an autocrine TGF-β/ZEB/miR-200 signaling network that regulates plasticity between epithelial and mesenchymal states. We find a strong correlation between ZEBs and TGF-β and negative correlations between miR-200 and TGF-β and between miR-200 and ZEBs, in invasive ductal carcinomas, consistent with an autocrine TGF-β/ZEB/miR-200 signaling network being active in breast cancers.