Demonstration of high-speed and low-complexity continuous variable quantum key distribution system with local local oscillator.

We present an experimental demonstration of the feasibility of the first 20 + Mb/s Gaussian modulated coherent state continuous variable quantum key distribution system with a locally generated local oscillator at the receiver (LLO-CVQKD). To increase the signal repetition rate, and hence the potential secure key rate, we equip our system with high-performance, wideband devices and design the components to support high repetition rate operation. We have successfully trialed the signal repetition rate as high as 500 MHz. To reduce the system complexity and correct for any phase shift during transmission, reference pulses are interleaved with quantum signals at Alice. Customized monitoring software has been developed, allowing all parameters to be controlled in real-time without any physical setup modification. We introduce a system-level noise model analysis at high bandwidth and propose a new 'combined-optimization' technique to optimize system parameters simultaneously to high precision. We use the measured excess noise, to predict that the system is capable of realizing a record 26.9 Mb/s key generation in the asymptotic regime over a 15 km signal mode fibre. We further demonstrate the potential for an even faster implementation.

Secure optical communication using a quantum alarm.

Optical fibre networks are advancing rapidly to meet growing traffic demands. Security issues, including attack management, have become increasingly important for optical communication networks because of the vulnerabilities associated with tapping light from optical fibre links. Physical layer security often requires restricting access to channels and periodic inspections of link performance. In this paper, we report how quantum communication techniques can be utilized to detect a physical layer attack. We present an efficient method for monitoring the physical layer security of a high-data-rate classical optical communication network using a modulated continuous-variable quantum signal. We describe the theoretical and experimental underpinnings of this monitoring system and the monitoring accuracy for different monitored parameters. We analyse its performance for both unamplified and amplified optical links. The technique represents a novel approach for applying quantum signal processing to practical optical communication networks and compares well with classical monitoring methods. We conclude by discussing the challenges facing its practical application, its differences with respect to existing quantum key distribution methods, and its usage in future secure optical transport network planning.

Cyclin C/cdk3 promotes Rb-dependent G0 exit.

G0 is a physiological state occupied by resting or terminally differentiated cells that have exited the cell cycle. In contrast to the well-characterized cyclin/cdk-mediated inactivation of pRb that controls the G1/S transition, little is known about regulation of the G0/G1 transition. However, pRb is likely to participate in this process because its acute somatic inactivation is sufficient for G0-arrested cells to re-enter the cell cycle. One physiological regulator of this event may be cyclin C because its highest mRNA levels occur during G0 exit. Here we show that a non-cdk8-associated cellular pool of cyclin C combines with cdk3 to stimulate pRb phosphorylation at S807/811 during the G0/G1 transition, and that this phosphorylation is required for cells to exit G0 efficiently. Thus, G1 entry is regulated in an analogous fashion to S phase entry, but involves a distinct cyclin/cdk combination.

Depletion of wild-type huntingtin in mouse models of neurologic diseases.

Huntington's disease (HD) is caused by a mutation in the gene encoding for huntingtin resulting in selective neuronal degeneration. Because HD is an autosomal dominant disorder, affected individuals have one copy of the mutant and one copy of the wild-type allele. Huntingtin has antiapoptotic properties and is critical for cell survival. However, the important role of wild-type huntingtin in both HD and other neurological diseases has not been fully recognized. We demonstrate disease-associated decreased levels of full-length huntingtin in brains of transgenic mouse models of HD, ischemia, trauma, and in spinal cord after injury. In addition, overexpression of wild-type huntingtin confers in vivo protection of neurodegeneration after ischemia. We propose that in HD, in addition to a toxic gain-of-function of mutant huntingtin, a parallel depletion of wild-type huntingtin results in a detrimental loss-of-function, playing an important role in disease progression.