Self-passivated freestanding superconducting oxide film for flexible electronics

The integration of high-temperature superconducting YBa2Cu3O6+x (YBCO) into flexible electronic devices has the potential to revolutionize the technology industry. The effective preparation of high-quality flexible YBCO films therefore plays a key role in this development. We present a novel approach for transferring water-sensitive YBCO films onto flexible substrates without any buffer layer. Freestanding YBCO film on a polydimethylsiloxane substrate is extracted by etching the Sr3Al2O6 sacrificial layer from the LaAlO3 substrate. In addition to the obtained freestanding YBCO thin film having a Tc of 89.1 K, the freestanding YBCO thin films under inward and outward bending conditions have Tc of 89.6 K and 88.9 K, respectively. A comprehensive characterization involving multiple experimental techniques including high-resolution transmission electron microscopy, scanning electron microscopy, Raman and X-ray Absorption Spectroscopy is conducted to investigate the morphology, structural and electronic properties of the YBCO film before and after the extraction process where it shows the preservation of the structural and superconductive properties of the freestanding YBCO virtually in its pristine state. Further investigation reveals the formation of a YBCO passivated layer serves as a protective layer which effectively preserves the inner section of the freestanding YBCO during the etching process. This work plays a key role in actualizing the fabrication of flexible oxide thin films and opens up new possibilities for a diverse range of device applications involving thin-films and low-dimensional materials.Comment: 22 pages,4 figures,references adde

Attenuation of Vaccinia Tian Tan Strain by Removal of Viral TC7L-TK2L and TA35R Genes

Vaccinia Tian Tan (VTT) was attenuated by deletion of the TC7L-TK2L and TA35R genes to generate MVTT3. The mutant was generated by replacing the open reading frames by a gene encoding enhanced green fluorescent protein (EGFP) flanked by loxP sites. Viruses expressing EGFP were then screened for and purified by serial plaque formation. In a second step the marker EGFP gene was removed by transfecting cells with a plasmid encoding cre recombinase and selecting for viruses that had lost the EGFP phenotype. The MVTT3 mutant was shown to be avirulent and immunogenic. These results support the conclusion that TC7L-TK2L and TA35R deletion mutants can be used as safe viral vectors or as platform for vaccines

Immune responses induced by vaccination.

<p>Ten 6-week-old BALB/c mice received 5×10⁴ PFU MVTT1, MVTT2 or MVTT3 by intramuscular route and three weeks later received booster of the same dose in 0.1 ml of PBS. The serum were harvested on weeks 3 and 5 post infection (i.m.). Shown were induced IL-2, IL-4, IL-10 and IFN-γsystemic immune responses in the two vaccinated cohorts as measured by mouse ELISA kit analysis. All measurements were performed in triplicate. Data were presented as mean ± SD.</p

Virus titer of mutants in five cell lines tested.

<p>PK(15), MDCK, HeLa, BHK-21 and Vero cells infected with 0.05 MOI of VTT and the mutants, and then the viruses were harvested and titrated in BHK-21 cells. Virus titer was determined by measuring the plaque assays.</p

Schematic representation of the MVTT3 genome and identification of mutants.

<p>(A) The TC7L-TK2L and TA35R genomic deletions were found in the viral genome. (B) EGFP was expressed by mutants MVTT1-EGFP, MVTT2-EGFP, or MVTT3-EGFP in the BHK-21 cells. The virus-infected cells were visualized by isolated fluorescent plaque, which was recognized in the same visual fields. Non-fluorescent plaques appeared because of recombinant MVTT1, MVTT2, or MVTT3 in the BHK-21 cells. All photos were taken at 200× magnification.</p

Protection of mice against pathogenic vaccinia VTT strain challenge.

<p>Groups of ten BALB/c mice (3-week-old) were vaccinated with 5×10⁴ PFU MVTT1, MVTT2 or MVTT3 via intramuscular routes. Mice received PBS were included as controls. Four weeks post-immunization, the mice were challenged intranasally with 500×LD₅₀ VTT strain. Cross marks indicate the mice that were killed because of a 30% weight loss. Data show average percent change in pre-challenge weigh. The error bar indicates the standard deviation (SD) of animals from each group.</p

Protection from lethal challenge.

<p>Six 3-week-old mice in each dilution group were inoculated intracranially with 10⁵, 10⁶, and 10⁷ pfu of MVTT3 and VTT (A), and MVTT1 and MVTT2 (B). The survival rate of animals were observed for 14 d. All mice inoculated with MVTT1, MVTT3 and10⁵ pfu of MVTT2 survived. All mice infected with 10⁶ and 10⁷ pfu of MVTT2 and VTT died.</p

Characterization of virulence of strains intradermally injected in rabbits.

<p>Each rabbit was inoculated intradermally on the dorsal spine with a 10-fold dilution of MVTT1, MVTT2, MVTT3, or VTT (10⁶, 10⁷, and 10⁸ pfu). The central size diameters were recorded 18 d after inoculation. The diameters when erythemas reached their peak for each rabbit (A and C) are presented. The average difference is shown between lesion diameter produced by each recombinant and that by VTT (B). The data represents the mean ± SD of three lesions. The mean lesion sizes produced by MVTT1 and MVTT2 were significantly smaller than those formed by parental VTT. Lesions did not develop after inoculation with MVTT3 at the three doses.</p

PCR analysis results of the TC7L-TK2L and TA35R genes of the isolated mutant.

<p>Diagnostic PCR was performed to identify the final mutant. The deletion of the TC7L-TK2L and TA35R genes was investigated by PCR 72 h after infection of BHK-21 cells with 0.01 MOI of wild-type VTT. Approximately 366 bp (TC7L-TK2L; A, lane 1) and 353 bp (TA35R; A, lane 3) were detected by ethidium bromide staining. In addition, the TC7L-TK2L and TA35R fragments were missing in the mutants MVTT1-EGFP (TC7L-TK2L; A, lane 2), MVTT2-EGFP (TA35R; A, lane 4), and MVTT3-EGFP (TC7L-TK2L and TA35R; A, lane 5 and lane 6). The genes 431 bp flanking the TC7L-TK2L regions (B, MVTT1, lane 1; and MVTT3, lane 3) and the genes 1142 bp flanking the TA35R regions (B, MVTT2, lane 2; and MVTT3, lane 4) were investigated to identify non-EGFP-expressing virus. Evaluation of the genetic stability in the BHK-21 cells after 2, 4, 6, 8 and 10 passages. TC7L-TK2L gene of MVTT1 (C, lanes 2–6), TA35R gene of MVTT2 (D, lane 2–6), TC7L-TK2L gene of MVTT3 (G, lanes 3–7), and TA35R gene of MVTT3 (G, lanes 8–12) produced negative results, comparing to positive PCR results. The genes of MVTT1 flanking the TC7L-TK2L regions (E), the genes of MVTT2 flanking the TA35R regions (F), and the genes of MVTT3 flanking the TC7L-TK2L regions (H, lanes 1–5) or TA35R regions (H, lanes 6–10) were detected correctly.</p