The size of silicon transistors used in microelectronic devices is shrinking to the level where quantum effects become important 1 . While this presents a significant challenge for the further scaling of microprocessors, it provides the potential for radical innovations in the form of spin-based quantum computers 2-4 and spintronic devices 5 . An electron spin in Si can represent a well-isolated quantum bit with long coherence times 6 because of the weak spin-orbit coupling 7 and the possibility to eliminate nuclear spins from the bulk crystal 8 . However, the control of single electrons in Si has proved challenging, and has so far hindered the observation and manipulation of a single spin. Here we report the first demonstration of single-shot, time-resolved readout of an electron spin in Si. This has been performed in a device consisting of implanted phosphorus donors 9 coupled to a metal-oxide-semiconductor single-electron transistor 10,11 -compatible with current microelectronic technology. We observed a spin lifetime approaching 1 second at magnetic fields below 2 T, and achieved spin readout fidelity better than 90%. High-fidelity single-shot spin readout in Si opens the path to the development of a new generation of quantum computing and spintronic devices, built using the most important material in the semiconductor industry.The projective, single-shot readout of a qubit is a crucial step in both circuit-based and measurement-based quantum computers 12 . For electron spins in solid state, this has only been achieved in GaAs/AlGaAs quantum dots coupled to charge detectors 13-15 . The spin readout was achieved utilizing spin-dependent tunnelling, in which the electron was displaced to a different location depending on its spin state. The charge detector, electrostatically coupled to the electron site, sensed whether the charge had been displaced, thereby determining the spin state. Here we apply a novel approach to charge sensing, where the detector is not only electrostatically coupled, but also tunnel-coupled to the electron site 11 , as shown in Fig. 1a. As a charge detector we employ here the silicon single-electron transistor 10 (SET), a nonlinear nanoelectronic device consisting of a small island of electrons tunnel-coupled to source and drain reservoirs, electrostatically induced beneath an insulating SiO 2 layer. A current can flow from source to drain only when the electrochemical potential of the island assumes specific values 16 , resulting in a characteristic pattern of sharp current peaks as a function of gate voltage (Fig. 1e). The shift in electrochemical potential arising from the tunnelling of a single electron from a nearby charge centre into the SET island is large enough to switch the current from zero to its maximum value. This tunnelling event becomes spin-dependent in the presence of a large magnetic field, when the spin-up state | ↑ has a higher energy than the spin-down state | ↓ , by an amount larger than the thermal and electromagnetic broadening of electron states in the SET isla...

BackgroundCirc-ITCH is a circRNA generated from several exons of itchy E3 ubiquitin protein ligase (ITCH) and tumor suppressor served as a sponge for certain miRNAs targeting their parental transcripts of ITCH. However, the role of circ-ITCH in bladder cancer (BCa) was not reported. In the present study, we investigated the role of circ-ITCH in BCa.MethodsQuantitative real-time PCR was used to detect the expression of circ-ITCH and survival analysis was adopted to explore the association between circ-ITCH expression and the prognosis of BCa. BCa cells were stably transfected with lentivirus approach and cell proliferation, migration, invasion, cell cycle and cell apoptosis, as well as tumorigenesis in nude mice were performed to assess the effect of circ-ITCH in BCa. Biotin-coupled probe pull down assay, Biotin-coupled miRNA capture, Fluorescence in situ hybridization and Luciferase reporter assay were conducted to confirm the relationship between the circ-ITCH and the microRNA.ResultsIn the present study, we found that circ-ITCH, is down-regulated in BCa tissues and cell lines. BCa patients with low circ-ITCH expression had shortened survival. Enforced- expression of circ-ITCH inhibited cells proliferation, migration, invasion and metastasis both in vitro and in vivo. Mechanistically, we demonstrated that circ-ITCH up-regulates the expression of miR-17 and miR-224 target gene p21 and PTEN through ‘sponging’ miR-17 and miR-224, which suppressed the aggressive biological behaviors of BCa.Conclusionscirc-ITCH acts as a tumor suppressor by a novel circ-ITCH/miR-17, miR-224/p21, PTEN axis, which may provide a potential biomarker and therapeutic target for the management of BCa.Electronic supplementary materialThe online version of this article (10.1186/s12943-018-0771-7) contains supplementary material, which is available to authorized users.

Two sources of room temperature visible luminescence are identified from SiO 2 films containing ion beam synthesized Si nanocrystals. From a comparison of luminescence spectra and photoluminescence decay lifetime measurements between Xe ϩ -implanted SiO 2 films and SiO 2 films containing Si nanocrystals, a luminescence feature attributable to defects in the SiO 2 matrix is unambiguously identified. Hydrogen passivation of the films selectively quenches the matrix defect luminescence, after which luminescence attributable to Si nanocrystals is evident, with a lifetime on the order of milliseconds. The peak energy of the remaining luminescence attributable to Si nanocrystals ''redshifts'' as a function of different processing parameters that might lead to increased nanocrystal size and the intensity is directly correlated to the formation of Si nanocrystals. Upon further annealing hydrogen-passivated samples at low temperatures ͑Ͻ500°C͒, the intensity of nanocrystal luminescence increases by more than a factor of 10.

Synthesis of Ge nanocrystals in SiO 2 films is carried out by precipitation from a supersaturated solid solution of Ge in SiO 2 made by Ge ion implantation. The films exhibit strong room-temperature visible photoluminescence. The measured photoluminescence peak energy and lifetimes show poor correlations with nanocrystal size compared to calculations involving radiative recombination of quantum-confined excitons in Ge quantum dots. In addition, the photoluminescence spectra and lifetime measurements show only a weak temperature dependence. These observations strongly suggest that the observed visible luminescence in our samples is not due to the radiative recombination of quantum-confined excitons in Ge nanocrystals. Instead, observations of similar luminescence in Xe ϩ -implanted samples and reversible PL quenching by hydrogen or deuterium suggest that radiative defect centers in the SiO 2 matrix are responsible for the observed luminescence.

We have developed nanoscale double-gated field-effect-transistors for the study of electron states and transport properties of single deliberately implanted phosphorus donors. The devices provide a high-level of control of key parameters required for potential applications in nanoelectronics. For the donors, we resolve transitions corresponding to two charge states successively occupied by spin down and spin up electrons. The charging energies and the Lande g-factors are consistent with expectations for donors in gated nanostructures.

Background/Aims: CircRNAs regulate gene expression in different malignancies. However, the role of Cdr1as in the tumourigenesis of bladder cancer and its potential mechanisms remain unknown. Methods: qRT-PCR was used to detect Cdr1as and target miRNA expression in bladder cancer tissues and cell lines. Biological functional experiments were performed to detect the effects of Cdr1as on the biological behaviour of bladder cancer cells in vivo and in vitro. Bioinformatic analysis was utilised to predict potential miRNA target sites on Cdr1as. Ago2 RNA binding protein immunoprecipitation assay, RNA antisense purification assay, biotin pull down assay and RNA FISH were performed to detect the interaction between Cdr1as and target miRNAs. Western blot was used to determine the expression level of p21 in bladder cancer cells. Results: Cdr1as was significantly down-regulated in bladder cancer tissues compared with adjacent normal tissues. Overexpression of Cdr1as inhibited the proliferation, invasion and migration of bladder cancer cells in vitro and slowed down tumour growth in vivo. Cdr1as sponged multiple miRNAs in bladder cancer. Moreover, Cdr1as directly bound to miR-135a and inhibited its activity in bladder cancer. Conclusion: Cdr1as is down-regulated and sponges multiple miRNAs in bladder cancer. It exerts anti-oncogenic functions by sponging microRNA-135a.

Exacerbation of macrophage-mediated inflammation contributes to pathogenesis of various inflammatory diseases, but the immunometabolic programs underlying regulation of macrophage activation are unclear. Here we show that V-set immunoglobulin-domain-containing 4 (VSIG4), a B7 family-related protein that is expressed by resting macrophages, inhibits macrophage activation in response to lipopolysaccharide. Vsig4 −/− mice are susceptible to high-fat diet-caused obesity and murine hepatitis virus strain-3 (MHV-3)-induced fulminant hepatitis due to excessive macrophage-dependent inflammation. VSIG4 activates the PI3K/Akt–STAT3 pathway, leading to pyruvate dehydrogenase kinase-2 (PDK2) upregulation and subsequent phosphorylation of pyruvate dehydrogenase, which results in reduction in pyruvate/acetyl-CoA conversion, mitochondrial reactive oxygen species secretion, and macrophage inhibition. Conversely, interruption of Vsig4 or Pdk2 promotes inflammation. Forced expression of Vsig4 in mice ameliorates MHV-3-induced viral fulminant hepatitis. These data show that VSIG4 negatively regulates macrophage activation by reprogramming mitochondrial pyruvate metabolism.

To expand the capabilities of semiconductor devices for new functions exploiting the quantum states of single donors or other impurity atoms requires a deterministic fabrication method. Ion implantation is a standard tool of the semiconductor industry and we have developed pathways to deterministic ion implantation to address this challenge. Although ion straggling limits the precision with which atoms can be positioned, for single atom devices it is possible to use post-implantation techniques to locate favourably placed atoms in devices for control and readout. However, large-scale devices will require improved precision. We examine here how the method of ion beam induced charge, already demonstrated for the deterministic ion implantation of 14 keV P donor atoms in silicon, can be used to implant a non-Poisson distribution of ions in silicon. Further, we demonstrate the method can be developed to higher precision by the incorporation of new deterministic ion implantation strategies that employ on-chip detectors with internal charge gain. In a silicon device we show a pulse height spectrum for 14 keV P ion impact that shows an internal gain of 3 that has the potential of allowing deterministic implantation of sub-14 keV P ions with reduced straggling.