Herein, we report a robust method to fabricate expanded nanofiber scaffolds with controlled size and thickness using a customized mold during the modified gas-foaming process. The expansion of nanofiber membranes was also simulated using a computational fluid model. Expanded nanofiber scaffolds implanted subcutaneously in rats showed cellular infiltration, whereas non-expanded scaffolds only had surface cellular attachment. Compared to unexpanded nanofiber scaffolds, more CD68+ and CD163+ cells were observed within expanded scaffolds at all tested time points post-implantation. More CCR7+ cells appeared within expanded scaffolds at week 8 post-implantation. In addition, new blood vessels were present within the expanded scaffolds at week 2. The formed multinucleated giant cells within expanded scaffolds were heterogeneous expressing CD68, CCR7, or CD163 markers. Together, the present study demonstrated that the expanded nanofiber scaffolds promoted cellular infiltration/tissue integration, a regenerative response, and neovascularization after subcutaneous implantation in rats. The use of expanded electrospun nanofiber scaffolds offers a promising method for in situ tissue repair/regeneration and generation of three-dimensional tissue models/constructs.
Advances in opto-electronics are often led by discovery and development of materials featuring unique properties. Recently, the material class of transparent conductive oxides (TCO) has attracted attention for active photonic devices on-chip. In particular, indium tin oxide (ITO) is found to have refractive index changes on the order of unity. This property makes it possible to achieve electrooptic modulation of sub-wavelength device scales, when thin ITO films are interfaced with optical light confinement techniques such as found in plasmonics; optical modes are compressed to nanometer scale to create strong light-matter interactions. Here we review efforts towards utilizing this novel material for high performance and ultra-compact modulation. While high performance metrics are achieved experimentally, there are open questions pertaining to the permittivity modulation mechanism of ITO. Finally, we review a variety of optical and electrical properties of ITO for different processing conditions, and show that ITO-based plasmonic electro-optic modulators have the potential to significantly outperform diffractionlimited devices.
CTCF is an essential epigenetic regulator mediating chromatin insulation, long-range regulatory interactions, and the organization of large topological domains in the nucleus. Phenotypes of CTCF haploinsufficient mutations in humans, knockout in mice, and depletion in cells are often consistent with impaired genome stability, but a role of CTCF in genome maintenance has not been fully investigated. Here, we report that CTCF maintains genome stability, is recruited to sites of DNA damage, and promotes homologous recombination repair of DNA double-strand breaks (DSBs). CTCF depletion increased chromosomal instability, marked by chromosome breakage and end fusions, elevated genotoxic stress-induced genomic DNA fragmentation, and activated the ataxia telangiectasia mutated (ATM) kinase. We show that CTCF could be recruited to drug-induced 53BP1 foci and known fragile sites, as well as to I-SceI endonuclease-induced DSBs. Laser irradiation analysis revealed that this recruitment depends on ATM, Nijmegen breakage syndrome (NBS), and the zinc finger DNA-binding domain of CTCF. We demonstrate that CTCF knockdown impaired homologous recombination (HR) repair of DSBs. Consistent with this, CTCF knockdown reduced the formation of γ-radiation-induced Rad51 foci, as well as the recruitment of Rad51 to laser-irradiated sites of DNA lesions and to I-SceI-induced DSBs. We further show that CTCF is associated with DNA HR repair factors MDC1 and AGO2, and directly interacts with Rad51 via its C terminus. These analyses establish a direct, functional role of CTCF in DNA repair and provide a potential link between genome organization and genome stability.CTCF | chromatin | genome stability | DNA repair | homologous recombination
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