Gate-Tunable Critical Current of the Three-Dimensional Niobium Nano-Bridge Josephson Junction

Recent studies have shown that the critical currents of several metallic superconducting nanowires and Dayem bridges can be locally tuned using a gate voltage {V_g}. Here, we report a gate-tunable Josephson junction structure constructed from a three-dimensional (3D) niobium nano-bridge junction (NBJ) with a voltage gate on top. Measurements up to 6 K showed that the critical current of this structure can be tuned to zero by increasing {V_g}. The critical gate voltage Vgc was reduced to 16 V and may possibly be reduced further by reducing the thickness of the insulation layer between the gate and the NBJ. Furthermore, the flux modulation generated by Josephson interference of two parallel 3D NBJs can also be tuned using {V_g} in a similar manner. Therefore, we believe that this gate-tunable Josephson junction structure is promising for superconducting circuit fabrication at high integration levels.Comment: 15 pages, 5 figure

Geometric Scaling of the Current-Phase Relation of Niobium Nano-Bridge Junctions

The nano-bridge junction (NBJ) is a type of Josephson junction that is advantageous for the miniaturization of superconducting circuits. However, the current-phase relation (CPR) of the NBJ usually deviates from a sinusoidal function which has been explained by a simplified model with correlation only to its effective length. Here, we investigated both measured and calculated CPRs of niobium NBJs of a cuboidal shape with a three-dimensional bank structure. From a sine-wave to a saw-tooth-like form, we showed that deviated CPRs of NBJs can be described quantitatively by its skewness {\Delta}{\theta}. Furthermore, the measured dependency of {\Delta}{\theta} on the critical current {I_0} from 108 NBJs turned out to be consistent with the calculated ones derived from the change in geometric dimensions. It suggested that the CPRs of NBJs can be tuned by their geometric dimensions. In addition, the calculated scaling behavior of {\Delta}{\theta} versus {I_0} in three-dimensional space was provided for the future design of superconducting circuits of a high integration level by using niobium NBJs.Comment: 20 pages, 10 figure

Helical Luttinger liquid on the edge of a 2-dimensional topological antiferromagnet

Boundary helical Luttinger liquid (HLL) with broken bulk time-reversal symmetry belongs to a unique topological class which may occur in antiferromagnets (AFM). Here, we search for signatures of HLL on the edge of a recently discovered topological AFM, MnBi2Te4 even-layer. Using scanning superconducting quantum interference device, we directly image helical edge current in the AFM ground state appearing at its charge neutral point. Such helical edge state accompanies an insulating bulk which is topologically distinct from the ferromagnetic Chern insulator phase as revealed in a magnetic field driven quantum phase transition. The edge conductance of the AFM order follows a power-law as a function of temperature and source-drain bias which serves as strong evidence for HLL. Such HLL scaling is robust at finite fields below the quantum critical point. The observed HLL in a layered AFM semiconductor represents a highly tunable topological matter compatible with future spintronics and quantum computation

Whole Genome Distribution and Ethnic Differentiation of Copy Number Variation in Caucasian and Asian Populations

Although copy number variation (CNV) has recently received much attention as a form of structure variation within the human genome, knowledge is still inadequate on fundamental CNV characteristics such as occurrence rate, genomic distribution and ethnic differentiation. In the present study, we used the Affymetrix GeneChip® Mapping 500K Array to discover and characterize CNVs in the human genome and to study ethnic differences of CNVs between Caucasians and Asians. Three thousand and nineteen CNVs, including 2381 CNVs in autosomes and 638 CNVs in X chromosome, from 985 Caucasian and 692 Asian individuals were identified, with a mean length of 296 kb. Among these CNVs, 190 had frequencies greater than 1% in at least one ethnic group, and 109 showed significant ethnic differences in frequencies (p<0.01). After merging overlapping CNVs, 1135 copy number variation regions (CNVRs), covering approximately 439 Mb (14.3%) of the human genome, were obtained. Our findings of ethnic differentiation of CNVs, along with the newly constructed CNV genomic map, extend our knowledge on the structural variation in the human genome and may furnish a basis for understanding the genomic differentiation of complex traits across ethnic groups

Luteolin Modulates SERCA2a Leading to Attenuation of Myocardial Ischemia/ Reperfusion Injury via Sumoylation at Lysine 585 in Mice

Background/Aims: The myocardial sarcoplasmic reticulum calcium ATPase (SERCA2a) is a pivotal pump responsible for calcium cycling in cardiomyocytes. The present study investigated the effect of luteolin (Lut) on restoring SERCA2a protein level and stability reduced by myocardial ischemia/reperfusion (I/R) injury. We verified a hypothesis that Lut protected against myocardial I/R injury by regulating SERCA2a SUMOylation. Methods: The hemodynamic data, myocardial infarct size of intact hearts, apoptotic analysis, mitochondrial membrane potential (ΔΨm), the level of SERCA2a SUMOylation, and the activity and expression of SERCA2a were examined in vivo and in vitro to clarify the cardioprotective effects of Lut after SUMO1 was knocked down or over-expressed. The putative SUMO conjugation sites in mouse SERCA2a were investigated as the possible regulatory mechanism of Lut. Results: Initially, we found that Lut reversed the SUMOylation and stability of SERCA2a as well as the expression of SUMO1, which were reduced by I/R injury in vitro. Furthermore, Lut increased the expression and activity of SERCA2a partly through SUMO1, thus improving ΔΨm and reducing apoptotic cells in vitro and promoting the recovery of heart function and reducing infarct size in vivo. We also demonstrated that SUMO acceptor sites in mouse SERCA2a involving lysine 585, 480 and 571. Among the three acceptor sites, Lut enhanced SERCA2a stability via lysine 585. Conclusions: Our results suggest that Lut regulates SERCA2a through SUMOylation at lysine 585 to attenuate myocardial I/R injury

A Novel NADP(H)-Dependent 7alpha-HSDH: Discovery and Construction of Substrate Selectivity Mutant by C-Terminal Truncation

7&alpha;-Hydroxysteroid dehydrogenase (7&alpha;-HSDH) plays an important role in the biosynthesis of tauroursodeoxycholic acid (TUDCA) using complex substrate chicken bile powder as raw material. However, chicken bile powder contains 4.74% taurocholic acid (TCA), and a new by-product tauroursocholic acid (TUCA) will be produced, having the risk of causing colorectal cancer. Here, we obtained a novel NADP(H)-dependent 7&alpha;-HSDH with good thermostability from Ursus thibetanus gut microbiota (named St-2-2). St-2-2 could catalyze taurochenodeoxycholic acid (TCDCA) and TCA with the catalytic activity of 128.13 and 269.39 U/mg, respectively. Interestingly, by a structure-based C-terminal truncation strategy, St-2-2&#9651;C10 only remained catalytic activity on TCDCA (14.19 U/mg) and had no activity on TCA. As a result, it can selectively catalyze TCDCA in waste chicken bile powder. MD simulation and structural analysis indicated that enhanced surface hydrophilicity and improved C-terminal rigidity affected the entry and exit of substrates. Hydrogen bond interactions between different subunits and interaction changes in Phe249 of the C-terminal loop inverted the substrate catalytic activity. This is the first report on substrate selectivity of 7&alpha;-HSDH by C-terminal truncation strategy and it can be extended to other 7&alpha;-HSDHs (J-1-1, S1-a-1)

Effect of Lipoxin A4 on Lipopolysaccharide-Induced Endothelial Hyperpermeability

Excessive oxidative stress, decreased antioxidant capacity, and enhanced cellular calcium levels are initial factors that cause endothelial cell (EC) hyperpermeability, which represents a crucial event in the pathogenesis of pre-eclampsia. Lipoxin A4 (LXA4) strongly attenuated lipopolysaccharide (LPS)-induced hyperpermeability through maintaining the normal expression of VE-cadherin and β-catenin. This effect was mainly mediated by a specific LXA4 receptor. LXA4 could also obviously inhibit LPS-induced elevation of the cellular calcium level and up-regulation of the transient receptor potential protein family C 1, an important calcium channel in ECs. At the same time, LXA4 strongly blocked LPS-triggered reactive oxidative species production, while it promoted the expression of the NF-E2 related factor 2 (Nrf2) protein. Our findings demonstrate that LXA4 could prevent the EC hyperpermeability induced by LPS in human umbilical vein endothelial cells (HUVECs), under which the possible mechanism is through Nrf2 as well as Ca2+-sensitive pathways