Quantum random number generationXiongfeng Ma, Xiao Yuan, Zhu Cao et al.|npj Quantum Information|2016 Abstract Quantum physics can be exploited to generate true random numbers, which have important roles in many applications, especially in cryptography. Genuine randomness from the measurement of a quantum system reveals the inherent nature of quantumness—coherence, an important feature that differentiates quantum mechanics from classical physics. The generation of genuine randomness is generally considered impossible with only classical means. On the basis of the degree of trustworthiness on devices, quantum random number generators (QRNGs) can be grouped into three categories. The first category, practical QRNG, is built on fully trusted and calibrated devices and typically can generate randomness at a high speed by properly modelling the devices. The second category is self-testing QRNG, in which verifiable randomness can be generated without trusting the actual implementation. The third category, semi-self-testing QRNG, is an intermediate category that provides a tradeoff between the trustworthiness on the device and the random number generation speed.
CD39/CD73 upregulation on myeloid-derived suppressor cells via TGF-β-mTOR-HIF-1 signaling in patients with non-small cell lung cancerCD39/CD73-adenosine pathway has been recently defined as an important tumor-induced immunosuppressive mechanism. We here documented a fraction of CD11b+CD33+ myeloid-derived suppressor cells (MDSCs) in peripheral blood and tumor tissues from non-small cell lung cancer (NSCLC) patients expressed surface ectonucleotidases CD39 and CD73. Tumor TGF-β stimulated CD39 and CD73 expression, thereby inhibited T cell and NK cell activity, and protected tumor cells from the cytotoxic effect of chemotherapy through ectonucleotidase activity. Mechanistically, TGF-β triggered phosphorylation of mammalian target of rapamycin, and subsequently activated hypoxia-inducible factor-1α (HIF-1α) that induced CD39/CD73 expression on MDSCs. CD39 and CD73 on MDSCs, therefore, link their immunosuppressive and chemo-protective effects to NSCLC progression, providing novel targets for chemo-immunotherapeutic intervention.