The detection of bacteria cells and their viability in food, water and clinical samples is critical to bioscience research and biomedical practice. In this work, we present a microfluidic device encapsulating a coplanar waveguide for differentiation of live and heat-killed E.scherichiacoli cells suspended in culture media using microwave signals over the frequency range of 0.5 GHz-20 GHz. From small populations of ∼15 E. coli cells, both the transmitted (|S21|) and reflected (|S11|) microwave signals show a difference between live and dead populations, with the difference especially significant for |S21| below 10 GHz. Analysis based on an equivalent circuit suggests that the difference is due to a reduction of the cytoplasm conductance and permittivity upon cell death. The electrical measurement is confirmed by off-chip biochemical analysis: the conductivity of cell lysate from heat-killed E. coli is 8.22% lower than that from viable cells. Furthermore, protein diffusivity increases in the cytoplasm of dead cells, suggesting the loss of cytoplasmic compactness. These changes are results of intact cell membrane of live cells acting as a semipermeable barrier, within which ion concentration and macromolecule species are tightly regulated. On the other hand, the cell membrane of dead cells is compromised, allowing ions and molecules to leak out of the cytoplasm. The loss of cytoplasmic content as well as membrane integrity areis measurable by microwave impedance sensors. Since our approach allows detection of bacterial viability in the native growth environment, it is a promising strategy for rapid point-of-care diagnostics of microorganisms as well as sensing biological agents in bioterrorism and food safety threats.

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Epigenetic regulation is highly correlated with osteoarthritis (OA) development, whereas its role and detailed mechanisms remain elusive. In this study, we explored the expression of EZH2, an H3K27me3 transferase, in human OA cartilages and its roles in regulating OA pathogenesis. Here, we found EZH2 was highly expressed in both mice and human OA cartilage samples by using histological analysis and RNA sequencing (RNA-Seq). The medial meniscectomy (MMx) OA model results indicated the conditional knockout of Ezh2 deteriorated OA pathological conditions. Furthermore, we showed the positive role of Ezh2 in cartilage wound healing and inhibition of hypertrophy through activating TNFSF13B, a member of the tumor necrosis factor superfamily. Further, we also indicated that the effect of TNFSF13B, increased by Ezh2, might boost the healing of chondrocytes through increasing the phosphorylation of Akt. Taken together, our results uncovered an EZH2-positive subpopulation existed in OA patients, and that EZH2-TNFSF13B signaling was responsible for regulating chondrocyte healing and hypertrophy. Thus, EZH2 might act as a new potential target for OA diagnosis and treatment. n 956 DU ET AL. 23. Ohata J, Zvaifler NJ, Nishio M, et al. Fibroblast-like synoviocytes of mesenchymal origin express functional B cell-activating factor of the TNF family in response to proinflammatory cytokines. J Immunol. 2005;174(2):864-70. 24. Bradley EW, Carpio LR, Westendorf JJ. Histone deacetylase 3 suppression increases PH domain and leucine-rich repeat phosphatase (Phlpp)1 expression in chondrocytes to suppress Akt signaling and matrix secretion. J Biol Chem. 2013;288:9572-82. 25. Zhang S, Chuah SJ, Lai RC, JHP H, Lim SK, Toh WS. MSC exosomes mediate cartilage repair by enhancing proliferation, attenuating apoptosis and modulating immune reactivity. Biomaterials. 2018;156: 16-27. Journal of Bone and Mineral Research n 964 DU ET AL.

Electroporation of Jurkat T-lymphoma human cells was investigated using 10-MHz continuous waves and benchmarked against that at 100 kHz. Both cell poration and cell death were simultaneously monitored by fluorescence microscopy, and found to occur under approximately four times higher voltages at 10 MHz than that at 100 kHz. This weaker-than-expected increase in poration threshold could be explained by detailed analysis of the distributed effect often ignored in electroporation studies

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