Optical coherent state discrimination using a closed-loop quantum measurement

Quantum mechanics hinders our ability to determine the state of a physical system in two ways: individual measurements provide only partial information about the observed system (because of Heisenberg uncertainty), and measurements are themselves invasive-meaning that little or no refinement is achieved by further observation of an already measured system. Theoretical methods have been developed to maximize the information gained from a quantum measurement while also minimizing disturbance, but laboratory implementation of optimal measurement procedures is often difficult. The standard class of operations considered in quantum information theory tends to rely on superposition-basis and entangled measurements, which require high-fidelity implementation to be effective in the laboratory. Here we demonstrate that real-time quantum feedback can be used in place of a delicate quantum superposition, often called a 'Schr?dinger cat state', to implement an optimal quantum measurement for discriminating between optical coherent states. Our procedure actively manipulates the target system during the measurement process, and uses quantum feedback to modify the statistics of an otherwise sub-optimal operator to emulate the optimal cat-state measurement. We verify a long-standing theoretical prediction and demonstrate feedback-mediated quantum measurement at its fundamental quantum limit over a non-trivial region of parameter space.     

LKB1 modulates lung cancer differentiation and metastasis

Germline mutation in serine/threonine kinase 11 (STK11, also called LKB1) results in Peutz-Jeghers syndrome, characterized by intestinal hamartomas and increased incidence of epithelial cancers. Although uncommon in most sporadic cancers, inactivating somatic mutations of LKB1 have been reported in primary human lung adenocarcinomas and derivative cell lines. Here we used a somatically activatable mutant Kras-driven model of mouse lung cancer to compare the role of Lkb1 to other tumour suppressors in lung cancer. Although Kras mutation cooperated with loss of p53 or Ink4a/Arf (also known as Cdkn2a) in this system, the strongest cooperation was seen with homozygous inactivation of Lkb1. Lkb1-deficient tumours demonstrated shorter latency, an expanded histological spectrum (adeno-, squamous and large-cell carcinoma) and more frequent metastasis compared to tumours lacking p53 or Ink4a/Arf. Pulmonary tumorigenesis was also accelerated by hemizygous inactivation of Lkb1. Consistent with these findings, inactivation of LKB1 was found in 34% and 19% of 144 analysed human lung adenocarcinomas and squamous cell carcinomas, respectively. Expression profiling in human lung cancer cell lines and mouse lung tumours identified a variety of metastasis-promoting genes, such as NEDD9, VEGFC and CD24, as targets of LKB1 repression in lung cancer. These studies establish LKB1 as a critical barrier to pulmonary tumorigenesis, controlling initiation, differentiation and metastasis.     

Anaphase initiation is regulated by antagonistic ubiquitination and deubiquitination activities

The spindle checkpoint prevents chromosome mis-segregation by delaying sister chromatid separation until all chromosomes have achieved bipolar attachment to the mitotic spindle. Its operation is essential for accurate chromosome segregation, whereas its dysregulation can contribute to birth defects and tumorigenesis. The target of the spindle checkpoint is the anaphase-promoting complex (APC), a ubiquitin ligase that promotes sister chromatid separation and progression to anaphase. Using a short hairpin RNA screen targeting components of the ubiquitin-proteasome pathway in human cells, we identified the deubiquitinating enzyme USP44 (ubiquitin-specific protease 44) as a critical regulator of the spindle checkpoint. USP44 is not required for the initial recognition of unattached kinetochores and the subsequent recruitment of checkpoint components. Instead, it prevents the premature activation of the APC by stabilizing the APC-inhibitory Mad2-Cdc20 complex. USP44 deubiquitinates the APC coactivator Cdc20 both in vitro and in vivo, and thereby directly counteracts the APC-driven disassembly of Mad2-Cdc20 complexes (discussed in an accompanying paper). Our findings suggest that a dynamic balance of ubiquitination by the APC and deubiquitination by USP44 contributes to the generation of the switch-like transition controlling anaphase entry, analogous to the way that phosphorylation and dephosphorylation of Cdk1 by Wee1 and Cdc25 controls entry into mitosis.     

Information sharing and strategic signaling in supply chains

Information sharing in procurement occurs in rich and varied industry contexts in which managerial decisions are made and organizational strategy is formulated. We explore how information sharing ought to work in procurement contexts that involve investments in inter-organizational information systems (IOS) and collaborative planning, forecasting and replenishment (CPFR) practices. How and under what circumstances does a firm that plays the role of a supply chain buyer decide to share information on key variables, such as point-of-sale consumer demand data with its supplier, up the supply chain? This is a key issue that crosses the boundary between supply chain management and information systems (IS) management. The answers that we provide are based on our use of a game-theoretic signaling model of buyer and supplier strategy in the presence of uncertainties about final consumer demand. We also explore the connection between operational costs that are associated with the firm’s information sharing and information withholding strategies. Our results provide normative guidance to supply chain buyers about how to interpret different demand uncertainty scenarios to improve their decisions and generate high value. From the IS management perspective, we show the impacts on the firm of different information sharing approaches that are made possible by present day technologies.