Josephson junction in cobalt-doped BaFe2As2 epitaxial thin films on (La, Sr)(Al, Ta)O3 bicrystal substrates

Josephson junctions were fabricated in epitaxial films of cobalt-doped BaFe2As2 on [001]-tilt (La,Sr)(Al,Ta)O3 bicrystal substrates. 10m-wide microbridges spanning a 30-degrees-tilted bicrystal grain boundary (BGB bridge) exhibited resistively-shunted-junction (RSJ)-like current-voltage characteristics up to 17 K, and the critical current was suppressed remarkably by a magnetic field. Microbridges without a BGB did not show the RSJ-like behavior, and their critical current densities were 20 times larger than those of BGB bridges, confirming BGB bridges display a Josephson effect originating from weakly-linked BGB

Biaxially textured cobalt-doped BaFe2As2 films with high critical current density over 1 MA/cm2 on MgO-buffered metal-tape flexible substrates

High critical current densities (Jc) > 1 MA/cm2 were realized in cobalt-doped BaFe2As2 (BaFe2As2:Co) films on flexible metal substrates with biaxially-textured MgO base-layers fabricated by an ion-beam assisted deposition technique. The BaFe2As2:Co films showed small in-plane crystalline misorientations (delta fai BaFe2As2:Co) of ~3o regardless of doubly larger misorientaions of the MgO base-layers (delta fai MgO = 7.3o), and exhibited high self-field Jc up to 3.5 MA/cm2 at 2 K. These values are comparable to that on MgO single crystals and the highest Jc among iron pnictide superconducting tapes and wires ever reported. High in-field Jc suggests the existence of c-axis correlated vortex pinning centers.Comment: Published in Appl. Phys. Let

Aurora-A controls pre-replicative complex assembly and DNA replication by stabilizing geminin in mitosis

Geminin, an essential factor for DNA replication, directly binds to the licensing factor Cdt1 and inhibits pre-replicative complex formation to prevent re-replication. In G1, geminin levels are controlled by the anaphase-promoting complex/cyclosome (APC/C) ubiquitin ligase complex, which targets geminin for proteasomal degradation to allow pre-replicative complex formation. Conversely, from S to G2, geminin is stabilized due to APC/C ubiquitin ligase complex inhibition, ensuring the inhibition of pre-replicative complex formation. However, mitotic regulation of geminin has hitherto not been described. Here we show that Aurora-A phosphorylates geminin on Thr25 during M phase, and this event induces geminin stabilization by preventing its APC/C ubiquitin ligase complex-mediated degradation during mitosis. In turn, stabilized geminin inhibits SCFSkp2-mediated degradation of Cdt1 to ensure pre-replicative complex formation in the ensuing S phase. The Aurora-A–geminin–Cdt1 axis therefore represents a critical regulator of proper DNA replication

DC superconducting quantum interference devices fabricated using bicrystal grain boundary junctions in Co-doped BaFe2As2 epitaxial films

DC superconducting quantum interference devices (dc-SQUIDs) were fabricated in Co-doped BaFe2As2 epitaxial films on (La, Sr)(Al, Ta)O3 bicrystal substrates with 30deg misorientation angles. The 18 x 8 micro-meter^2 SQUID loop with an estimated inductance of 13 pH contained two 3 micro-meter wide grain boundary junctions. The voltage-flux characteristics clearly exhibited periodic modulations with deltaV = 1.4 micro-volt at 14 K, while the intrinsic flux noise of dc-SQUIDs was 7.8 x 10^-5 fai0/Hz^1/2 above 20 Hz. The rather high flux noise is mainly attributed to the small voltage modulation depth which results from the superconductor-normal metal-superconductor junction nature of the bicrystal grain boundary

Odontogenic stem cells

Epithelial cell rests of Malassez (ERM) are quiescent epithelial remnants of the Hertwig’s epithelial root sheath (HERS) that are involved in the formation of tooth roots. ERM cells are unique epithelial cells that remain in periodontal tissues throughout adult life. They have a functional role in the repair/regeneration of cement or enamel. Here, we isolated odontogenic epithelial cells from ERM in the periodontal ligament, and the cells were spontaneously immortalized. Immortalized odontogenic epithelial (iOdE) cells had the ability to form spheroids and expressed stem cell-related genes. Interestingly, iOdE cells underwent osteogenic differentiation, as demonstrated by the mineralization activity in vitro in mineralization-inducing media and formation of calcification foci in iOdE cells transplanted into immunocompromised mice. These findings suggest that a cell population with features similar to stem cells exists in ERM and that this cell population has a differentiation capacity for producing calcifications in a particular microenvironment. In summary, iOdE cells will provide a convenient cell source for tissue engineering and experimental models to investigate tooth growth, differentiation, and tumorigenesis

Influence of dosing times on cisplatin-induced peripheral neuropathy in rats

Background: Although cis-diamminedichloro-platinum (CDDP) exhibits strong therapeutic effects in cancer chemotherapy, its adverse effects such as peripheral neuropathy, nephropathy, and vomiting are dose-limiting factors. Previous studies reported that chronotherapy decreased CDDP-induced nephropathy and vomiting. In the present study, we investigated the influence of dosing times on CDDP-induced peripheral neuropathy in rats. Methods: CDDP (4 mg/kg) was administered intravenously at 5:00 or 17:00 every 7 days for 4 weeks to male Sprague-Dawley rats, and saline was given to the control group. To assess the dosing time dependency of peripheral neuropathy, von-Frey test and hot-plate test were performed. Results: In order to estimate hypoalgesia, the hot-plate test was performed in rats administered CDDP weekly for 4 weeks. On day 28, the withdrawal latency to thermal stimulation was significantly prolonged in the 17:00-treated group than in the control and 5:00-treated groups. When the von-Frey test was performed to assess mechanical allodynia, the withdrawal threshold was significantly lower in the 5:00 and 17:00-treated groups than in the control group on day 6 after the first CDDP dose. The 5:00-treated group maintained allodynia throughout the experiment with the repeated administration of CDDP, whereas the 17:00-treated group deteriorated from allodynia to hypoalgesia. Conclusions: It was revealed that the severe of CDDP-induced peripheral neuropathy was inhibited in the 5:00-treated group, whereas CDDP-treated groups exhibited mechanical allodynia. These results suggested that the selection of an optimal dosing time ameliorated CDDP-induced peripheral neuropathy

Analysis of a pair of END+ and END- viruses derived from the same bovine viral diarrhea virus stock reveals the amino acid determinants in N-pro responsible for inhibition of type I interferon production

The Exaltation of Newcastle disease virus (END) phenomenon is induced by the inhibition of type I interferon in pestivirus-infected cells in vitro, via proteasomal degradation of cellular interferon regulatory factor (IRF)-3 with the property of the viral autoprotease protein N-pro. Reportedly, the amino acid residues in the zinc-binding TRASH motif of N-pro determine the difference in characteristics between END-phenomenon-positive (END) and END-phenomenon-negative (END-) classical swine fever viruses (CSFVs). However, the basic mechanism underlying this function in bovine viral diarrhea virus (BVDV) has not been elucidated from the genomic differences between END+ and END- viruses using reverse genetics till date. In the present study, comparison of complete genome sequences of a pair of END+ and END- viruses isolated from the same virus stock revealed that there were only four amino acid substitutions (D136G, I2623V, D3148G and D3502Y) between two viruses. Based on these differences, viruses with and without mutations at these positions were generated using reverse genetics. The END assay, measurements of induced type I interferon and IRF-3 detection in cells infected with these viruses revealed that the aspartic acid at position 136 in the zinc-binding TRASH motif of N-pro was required to inhibit the production of type I interferon via the degradation of cellular IRF-3, consistently with CSFV