Gaussian state-based quantum illumination with simple photodetection.

Proofs of the quantum advantage available in imaging or detecting objects under quantum illumination can rely on optimal measurements without specifying what they are. We use the continuous-variable Gaussian quantum information formalism to show that quantum illumination is better for object detection compared with coherent states of the same mean photon number, even for simple direct photodetection. The advantage persists if signal energy and object reflectivity are low and background thermal noise is high. The advantage is even greater if we match signal beam detection probabilities rather than mean photon number. We perform all calculations with thermal states, even for non-Gaussian conditioned states with negative Wigner functions. We simulate repeated detection using a Monte-Carlo process that clearly shows the advantages obtainable.

Compact multispectral pushframe camera for nanosatellites.

In this paper we present an evolution of the single-pixel camera architecture, called "pushframe," which addresses the limitations of pushbroom cameras in space-based applications. In particular, it is well-suited to observing fast-moving scenes while retaining high spatial resolution and sensitivity. We show that the system is capable of producing color images with good fidelity and scalable resolution performance. The principle of our design broadens the choice of spectral ranges that can be captured, making it suitable for wide spectral ranges of infrared imaging.

On-chip implementation of the probabilistic quantum optical state comparison amplifier.

Propagation losses in transmission media limit the transmission distance of optical signals. In the case where the signal is made up of quantum optical states, conventional deterministic optical amplification schemes cannot be used to increase the transmission distance as the copying of an arbitrary and unknown quantum state is forbidden. One strategy that can offset propagation loss is the use of probabilistic, or non-deterministic, amplification schemes - an example of which is the state comparison amplifier. Here we report a state comparison amplifier implemented in a compact, fiber-coupled femtosecond laser-written waveguide chip as opposed to the large, bulk-optical components of previous designs. This pathfinder on-chip implementation of the quantum amplifier has resulted in several performance improvements: the polarization integrity of the written waveguides has resulted in improved visibility of the amplifier interferometers; the potential of substantially-reduced losses throughout the amplifier configuration; and a more compact and environmentally-stable amplifier which is scalable to more complex networks.

Nonlocal Coherent Perfect Absorption.

Coherent absorption that occurs at two spatially separated, macroscopic lossy beam splitters is described. A superposition mode of any phase can be chosen as the absorbed or transparent mode. For a nonclassical two-photon NOON-state input, a superposition of two photons entering via one of two separate input modes, a single photon can survive the pair of beam splitters with certainty, implying nonlocal absorption of a single photon, which can be detected via the interference in the two-photon survival probability.

Stepwise activation of BAX and BAK by tBID, BIM, and PUMA initiates mitochondrial apoptosis.

While activation of BAX/BAK by BH3-only molecules (BH3s) is essential for mitochondrial apoptosis, the underlying mechanisms remain unsettled. Here we demonstrate that BAX undergoes stepwise structural reorganization leading to mitochondrial targeting and homo-oligomerization. The alpha1 helix of BAX keeps the alpha9 helix engaged in the dimerization pocket, rendering BAX as a monomer in cytosol. The activator BH3s, tBID/BIM/PUMA, attack and expose the alpha1 helix of BAX, resulting in secondary disengagement of the alpha9 helix and thereby mitochondrial insertion. Activator BH3s remain associated with the N-terminally exposed BAX through the BH1 domain to drive homo-oligomerization. BAK, an integral mitochondrial membrane protein, has bypassed the first activation step, explaining why its killing kinetics are faster than those of BAX. Furthermore, death signals initiated at ER induce BIM and PUMA to activate mitochondrial apoptosis. Accordingly, deficiency of Bim/Puma impedes ER stress-induced BAX/BAK activation and apoptosis. Our study provides mechanistic insights regarding the spatiotemporal execution of BAX/BAK-governed cell death.

Coherent Absorption of N00N States.

Recent results in deeply subwavelength thickness films demonstrate coherent control and logical gate operations with both classical and single-photon light sources. However, quantum processing and devices typically involve more than one photon and nontrivial input quantum states. Here we experimentally investigate two-photon N00N state coherent absorption in a multilayer graphene film. Depending on the N00N state input phase, it is possible to selectively choose between single- or two-photon absorption of the input state in the graphene film. These results demonstrate that coherent absorption in the quantum regime exhibits unique features, opening up applications in multiphoton spectroscopy and imaging.

Experimental implementation of a quantum optical state comparison amplifier.

We present an experimental demonstration of a practical nondeterministic quantum optical amplification scheme that employs two mature technologies, state comparison and photon subtraction, to achieve amplification of known sets of coherent states with high fidelity. The amplifier uses coherent states as a resource rather than single photons, which allows for a relatively simple light source, such as a diode laser, providing an increased rate of amplification. The amplifier is not restricted to low amplitude states. With respect to the two key parameters, fidelity and the amplified state production rate, we demonstrate significant improvements over previous experimental implementations, without the requirement of complex photonic components. Such a system may form the basis of trusted quantum repeaters in nonentanglement-based quantum communications systems with known phase alphabets, such as quantum key distribution or quantum digital signatures.

Quantum Hilbert Hotel.

In 1924 David Hilbert conceived a paradoxical tale involving a hotel with an infinite number of rooms to illustrate some aspects of the mathematical notion of "infinity." In continuous-variable quantum mechanics we routinely make use of infinite state spaces: here we show that such a theoretical apparatus can accommodate an analog of Hilbert's hotel paradox. We devise a protocol that, mimicking what happens to the guests of the hotel, maps the amplitudes of an infinite eigenbasis to twice their original quantum number in a coherent and deterministic manner, producing infinitely many unoccupied levels in the process. We demonstrate the feasibility of the protocol by experimentally realizing it on the orbital angular momentum of a paraxial field. This new non-Gaussian operation may be exploited, for example, for enhancing the sensitivity of NOON states, for increasing the capacity of a channel, or for multiplexing multiple channels into a single one.

Inactivation of ribosomal protein L22 promotes transformation by induction of the stemness factor, Lin28B.

Ribosomal protein (RP) mutations in diseases such as 5q- syndrome both disrupt hematopoiesis and increase the risk of developing hematologic malignancy. However, the mechanism by which RP mutations increase cancer risk has remained an important unanswered question. We show here that monoallelic, germline inactivation of the ribosomal protein L22 (Rpl22) predisposes T-lineage progenitors to transformation. Indeed, RPL22 was found to be inactivated in ∼ 10% of human T-acute lymphoblastic leukemias. Moreover, monoallelic loss of Rpl22 accelerates development of thymic lymphoma in both a mouse model of T-cell malignancy and in acute transformation assays in vitro. We show that Rpl22 inactivation enhances transformation potential through induction of the stemness factor, Lin28B. Our finding that Rpl22 inactivation promotes transformation by inducing expression of Lin28B provides the first insight into the mechanistic basis by which mutations in Rpl22, and perhaps some other RP genes, increases cancer risk.

Realization of quantum digital signatures without the requirement of quantum memory.

Digital signatures are widely used to provide security for electronic communications, for example, in financial transactions and electronic mail. Currently used classical digital signature schemes, however, only offer security relying on unproven computational assumptions. In contrast, quantum digital signatures offer information-theoretic security based on laws of quantum mechanics. Here, security against forging relies on the impossibility of perfectly distinguishing between nonorthogonal quantum states. A serious drawback of previous quantum digital signature schemes is that they require long-term quantum memory, making them impractical at present. We present the first realization of a scheme that does not need quantum memory and which also uses only standard linear optical components and photodetectors. In our realization, the recipients measure the distributed quantum signature states using a new type of quantum measurement, quantum state elimination. This significantly advances quantum digital signatures as a quantum technology with potential for real applications.

Context-dependent enhancement of induced pluripotent stem cell reprogramming by silencing Puma.

Reprogramming of the somatic state to pluripotency can be induced by a defined set of transcription factors including Oct3/4, Sox2, Klf4, and c-Myc [Cell 2006;126:663-676]. These induced pluripotent stem cells (iPSCs) hold great promise in human therapy and disease modeling. However, tumor suppressive activities of p53, which are necessary to prevent persistence of DNA damage in mammalian cells, have proven a serious impediment to formation of iPSCs [Nat Methods 2011;8:409-412]. We examined the requirement for downstream p53 activities in suppressing efficiency of reprogramming as well as preventing persistence of DNA damage into the early iPSCs. We discovered that the majority of the p53 activation occurred through early reprogramming-induced DNA damage with the activated expression of the apoptotic inducer Puma and the cell cycle inhibitor p21. While Puma deficiency increases reprogramming efficiency only in the absence of c-Myc, double deficiency of Puma and p21 has achieved a level of efficiency that exceeded that of p53 deficiency alone. We further demonstrated that, in both the presence and absence of p21, Puma deficiency was able to prevent any increase in persistent DNA damage in early iPSCs. This may be due to a compensatory cellular senescent response to reprogramming-induced DNA damage in pre-iPSCs. Therefore, our findings provide a potentially safe approach to enhance iPSC derivation by transiently silencing Puma and p21 without compromising genomic integrity.

Quantum optical state comparison amplifier.

It is a fundamental principle of quantum theory that an unknown state cannot be copied or, as a consequence, an unknown optical signal cannot be amplified deterministically and perfectly. Here we describe a protocol that provides nondeterministic quantum optical amplification in the coherent state basis with high gain and high fidelity and which does not use quantum resources. The scheme is based on two mature quantum optical technologies: coherent state comparison and photon subtraction. The method compares favorably with all previous nondeterministic amplifiers in terms of fidelity and success probability.

Nondemolition measurement of the vacuum state or its complement.

Measurement is integral to quantum information processing and communication; it is how information encoded in the state of a system is transformed into classical signals for further use. In quantum optics, measurements are typically destructive, so that the state is not available afterwards for further steps. Here we show how to measure the presence or absence of the vacuum in a quantum optical field without destroying the state, implementing the ideal projections onto the respective subspaces. This not only enables sequential measurements, useful for quantum communication, but it can also be adapted to create novel states of light via bare raising and lowering operators.

Hierarchical regulation of mitochondrion-dependent apoptosis by BCL-2 subfamilies.

Although the BCL-2 family constitutes a crucial checkpoint in apoptosis, the intricate interplay between these family members remains elusive. Here, we demonstrate that BIM and PUMA, similar to truncated BID (tBID), directly activate BAX-BAK to release cytochrome c. Conversely, anti-apoptotic BCL-2-BCL-X(L)-MCL-1 sequesters these 'activator' BH3-only molecules into stable complexes, thus preventing the activation of BAX-BAK. Extensive mutagenesis of BAX-BAK indicates that their activity is not kept in check by BCL-2-BCL-X(L)-MCL-1. Anti-apoptotic BCL-2 members are differentially inactivated by the remaining 'inactivator' BH3-only molecules including BAD, NOXA, BMF, BIK/BLK and HRK/DP5. BAD displaces tBID, BIM or PUMA from BCL-2-BCL-X(L) to activate BAX-BAK, whereas NOXA specifically antagonizes MCL-1. Coexpression of BAD and NOXA killed wild-type but not Bax, Bak doubly deficient cells or Puma deficient cells with Bim knockdown, indicating that activator BH3-only molecules function downstream of inactivator BH3-only molecules to activate BAX-BAK. Our data establish a hierarchical regulation of mitochondrion-dependent apoptosis by various BCL-2 subfamilies.

Single-emitter quantum key distribution over 175 km of fibre with optimised finite key rates.

Quantum key distribution with solid-state single-photon emitters is gaining traction due to their rapidly improving performance and compatibility with future quantum networks. Here we emulate a quantum key distribution scheme with quantum-dot-generated single photons frequency-converted to 1550 nm, achieving count rates of 1.6 MHz with [Formula: see text] and asymptotic positive key rates over 175 km of telecom fibre. We show that the commonly used finite-key analysis for non-decoy state QKD drastically overestimates secure key acquisition times due to overly loose bounds on statistical fluctuations. Using the tighter multiplicative Chernoff bound to constrain the estimated finite key parameters, we reduce the required number of received signals by a factor 108. The resulting finite key rate approaches the asymptotic limit at all achievable distances in acquisition times of one hour, and at 100 km we generate finite keys at 13 kbps for one minute of acquisition. This result is an important step towards long-distance single-emitter quantum networking.

Puma is an essential mediator of p53-dependent and -independent apoptotic pathways.

Puma encodes a BH3-only protein that is induced by the p53 tumor suppressor and other apoptotic stimuli. To assess its physiological role in apoptosis, we generated Puma knockout mice by gene targeting. Here we report that Puma is essential for hematopoietic cell death triggered by ionizing radiation (IR), deregulated c-Myc expression, and cytokine withdrawal. Puma is also required for IR-induced death throughout the developing nervous system and accounts for nearly all of the apoptotic activity attributed to p53 under these conditions. These findings establish Puma as a principal mediator of cell death in response to diverse apoptotic signals, implicating Puma as a likely tumor suppressor.

The Common Germline TP53-R337H Mutation Is Hypomorphic and Confers Incomplete Penetrance and Late Tumor Onset in a Mouse Model.

The TP53-R337H founder mutation exists at a high frequency throughout southern Brazil and represents one of the most common germline TP53 mutations reported to date. It was identified in pediatric adrenocortical tumors in families with a low incidence of cancer. The R337H mutation has since been found in association with early-onset breast cancers and Li-Fraumeni syndrome (LFS). To study this variability in tumor susceptibility, we generated a knockin mutant p53 mouse model (R334H). Endogenous murine p53-R334H protein was naturally expressed at high levels in multiple tissues and was functionally compromised in a tissue- and stress-specific manner. Mutant p53-R334H mice developed tumors with long latency and incomplete penetrance, consistent with many human carriers being at a low but elevated risk for cancer. These findings suggest the involvement of additional cooperating genetic alterations when TP53-R337H occurs in the context of LFS, which has important implications for genetic counseling and long-term clinical follow-up. SIGNIFICANCE: A p53-R334H knockin mouse serves as an important model for studying the most common inherited germline TP53 mutation (R337H) that is associated with variable tumor susceptibility.

Assays to measure p53-dependent and -independent apoptosis.

Paramount to the maintenance of normal tissue homeostasis is the induction of programmed cell death, otherwise known as apoptosis. Several disease states, including cancer, are characterized by an inability to remove unwanted cells due to a failure to commit to apoptosis. What is more, apoptosis is the central functional response behind many agents utilized in the treatment of cancer. Many of these antitumorigenic agents rely on the activation of the tumor suppressor p53. As the physiological "guardian of the genome," p53's normal function is to sense stressed or damaged cells and arrest proliferation, allowing time for cellular repair. However, if the damage is excessive, cells are removed prior to the onset of malignancy through apoptosis. Current chemotherapeutic strategies manipulate this property by damaging cells and turning on p53's transcriptional function, which consequently upregulates the expression of proapoptotic proteins such as Puma. We have also demonstrated that Puma is capable of inducing apoptosis independent of p53. In this regard, defects in the apoptotic machinery or in p53 function itself lead to a resistant phenotype that in cancer results in chemotherapeutic failure, and more often than not, poor prognosis. This chapter describes protocols for the determination of p53-dependent and -independent apoptosis utilizing primary cells from genetically altered mice.

From measurements to quantum friction.

We present a quantum theory of friction in which interactions with the surrounding medium are described by generalized measurements of the particle's position and momentum. The theory predicts intrinsically quantum contributions to the particle's steady-state energy and to the associated diffusion in position. We discuss the physical significance of these and demonstrate their significance in ensuring a well behaved theory.

Coherent perfect absorption in deeply subwavelength films in the single-photon regime.

The technologies of heating, photovoltaics, water photocatalysis and artificial photosynthesis depend on the absorption of light and novel approaches such as coherent absorption from a standing wave promise total dissipation of energy. Extending the control of absorption down to very low light levels and eventually to the single-photon regime is of great interest and yet remains largely unexplored. Here we demonstrate the coherent absorption of single photons in a deeply subwavelength 50% absorber. We show that while the absorption of photons from a travelling wave is probabilistic, standing wave absorption can be observed deterministically, with nearly unitary probability of coupling a photon into a mode of the material, for example, a localized plasmon when this is a metamaterial excited at the plasmon resonance. These results bring a better understanding of the coherent absorption process, which is of central importance for light harvesting, detection, sensing and photonic data processing applications.