A time-domain control signal detection technique for OFDM

Transmission of system-critical control information plays a key role in efficient management of limited wireless network resources and successful reception of payload data information. This paper uses an orthogonal frequency division multiplexing (OFDM) architecture to investigate the detection performance of a time-domain approach used to detect deterministic control signalling information. It considers a type of control information chosen from a finite set of information, which is known at both transmitting and receiving wireless terminals. Unlike the maximum likelihood (ML) estimation method, which is often used, the time-domain detection technique requires no channel estimation and no pilots as it uses a form of time-domain correlation as the means of detection. Results show that when compared with the ML method, the time-domain approach improves detection performance even in the presence of synchronisation error caused by carrier frequency offset

Secret key exchange in ultra-long lasers by radio-frequency spectrum coding

We propose a new approach to the generation of an alphabet for secret key exchange relying on small variations in the cavity length of an ultra-long fiber laser. This new concept is supported by experimental results showing how the radio-frequency spectrum of the laser can be exploited as a carrier to exchange information. The test bench for our proof of principle is a 50 km-long fiber laser linking two users, Alice and Bob, where each user can randomly add an extra 1 km-long segment of fiber. The choice of laser length is driven by two independent random binary values, which makes such length become itself a random variable. The security of key exchange is ensured whenever the two independent random choices lead to the same laser length and, hence, to the same free spectral range

Activation of JNK Triggers Release of Brd4 from Mitotic Chromosomes and Mediates Protection from Drug-Induced Mitotic Stress

Some anti-cancer drugs, including those that alter microtubule dynamics target mitotic cells and induce apoptosis in some cell types. However, such drugs elicit protective responses in other cell types allowing cells to escape from drug-induced mitotic inhibition. Cells with a faulty protective mechanism undergo defective mitosis, leading to genome instability. Brd4 is a double bromodomain protein that remains on chromosomes during mitosis. However, Brd4 is released from mitotic chromosomes when cells are exposed to anti-mitotic drugs including nocodazole. Neither the mechanisms, nor the biological significance of drug-induced Brd4 release has been fully understood. We found that deletion of the internal C-terminal region abolished nocodazole induced Brd4 release from mouse P19 cells. Furthermore, cells expressing truncated Brd4, unable to dissociate from chromosomes were blocked from mitotic progression and failed to complete cell division. We also found that pharmacological and peptide inhibitors of the c-jun-N-terminal kinases (JNK) pathway, but not inhibitors of other MAP kinases, prevented release of Brd4 from chromosomes. The JNK inhibitor that blocked Brd4 release also blocked mitotic progression. Further supporting the role of JNK in Brd4 release, JNK2–/– embryonic fibroblasts were defective in Brd4 release and sustained greater inhibition of cell growth after nocodazole treatment. In sum, activation of JNK pathway triggers release of Brd4 from chromosomes upon nocodazole treatment, which mediates a protective response designed to minimize drug-induced mitotic stress

Receiver design for the uplink of base station cooperation systems employing SC-FDE modulations

The presented paper considers the uplink transmission in base station (BS) cooperation schemes where mobile terminals (MTs) in adjacent cells share the same physical channel. We consider single-carrier with frequency-domain equalization (SC-FDE) combined with iterative frequency-domain receivers based on the iterative block decision feedback equalization (IB-DFE). We study the quantization requirements when sending the received signals, from different MTs, at different BSs to a central unit that performs the separation of different MTs using iterative frequency-domain receivers. Our performance results show that a relatively coarse quantization, with only 4 bits in the in-phase and quadrature components of the complex envelope already allows close-to-optimum macro-diversity gains, as well as an efficient separation of the transmitted signals associated with each MT

A quantitative systems view of the spindle assembly checkpoint

The idle assembly checkpoint acts to delay chromosome segregation until all duplicated sister chromatids are captured by the mitotic spindle. This pathway ensures that each daughter cell receives a complete copy of the genome. The high fidelity and robustness of this process have made it a subject of intense study in both the experimental and computational realms. A significant number of checkpoint proteins have been identified but how they orchestrate the communication between local spindle attachment and global cytoplasmic signalling to delay segregation is not yet understood. Here, we propose a systems view of the spindle assembly checkpoint to focus attention on the key regulators of the dynamics of this pathway. These regulators in turn have been the subject of detailed cellular measurements and computational modelling to connect molecular function to the dynamics of spindle assembly checkpoint signalling. A review of these efforts reveals the insights provided by such approaches and underscores the need for further interdisciplinary studies to reveal in full the quantitative underpinnings of this cellular control pathway