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.