Estimation of basis frequencies for time-varying SIMO channels : a second-order method

The complex exponential basis expansion model (CE-BEM) provides an accurate description for the time-varying (TV) channels encountered in mobile communications. Many blind channel identification and equalization approaches based on the CE-BEM require precise knowledge of the basis frequencies of TV channels. Existing methods for basis frequency estimation usually resort to the higher-order statistics of channel outputs and impose strict constraints on the source signal. In this paper, we propose a novel method to estimate the basis frequencies for blind identification and equalization of time-varying single-input multiple-output (SIMO) finite-impulse-response (FIR) channels. The proposed method exploits only the second-order statistics of channel outputs and does not require strong conditions on the source signal. As a result, it exhibits superior performance to the existing basis frequency estimation methods. The validity of our method is demonstrated by numerical simulations.

Water and ion channels : crucial in the initiation and progression of apoptosis in central nervous system?

Programmed cell death (PCD), is a highly regulated and sophisticated cellular mechanism that commits cell to isolated death fate. PCD has been implicated in the pathogenesis of numerous neurodegenerative disorders. Countless molecular events underlie this phenomenon, with each playing a crucial role in death commitment. A precedent event, apoptotic volume decrease (AVD), is ubiquitously observed in various forms of PCD induced by different cellular insults. Under physiological conditions, cells when subjected to osmotic fluctuations will undergo regulatory volume increase/decrease (RVI/RVD) to achieve homeostatic balance with neurons in the brain being additionally protected by the blood-brain-barrier. However, during AVD following apoptotic trigger, cell undergoes anistonic shrinkage that involves the loss of water and ions, particularly monovalent ions e.g. K+, Na+ and Cl-. It is worthwhile to concentrate on the molecular implications underlying the loss of these cellular components which posed to be significant and crucial in the successful propagation of the apoptotic signals. Microarray and real-time PCR analyses demonstrated several ion and water channel genes are regulated upon the onset of lactacystin (a proteosomal inhibitor)-mediated apoptosis. A time course study revealed that gene expressions of water and ion channels are being modulated just prior to apoptosis, some of which are aquaporin 4 and 9, potassium channels and chloride channels. In this review, we shall looked into the molecular protein machineries involved in the execution of AVD in the central nervous system (CNS), and focus on the significance of movements of each cellular component in affecting PCD commitment, thus provide some pharmacological advantages in the global apoptotic cell death.

Detection of cross-channel anomalies from multiple data channels

We identify and formulate a novel problem: crosschannel anomaly detection from multiple data channels. Cross channel anomalies are common amongst the individual channel anomalies, and are often portent of significant events. Using spectral approaches, we propose a two-stage detection method: anomaly detection at a single-channel level, followed by the detection of cross-channel anomalies from the amalgamation of single channel anomalies. Our mathematical analysis shows that our method is likely to reduce the false alarm rate. We demonstrate our method in two applications: document understanding with multiple text corpora, and detection of repeated anomalies in video surveillance. The experimental results consistently demonstrate the superior performance of our method compared with related state-of-art methods, including the one-class SVM and principal component pursuit. In addition, our framework can be deployed in a decentralized manner, lending itself for large scale data stream analysis.

Robust channel estimation algorithm for dual-hop MIMO relay channels

In conventional two-phase channel estimation algorithms for dual-hop multiple-input multiple-output (MIMO) relay systems, the relay-destination channel estimated in the first phase is used for the source-relay channel estimation in the second phase. For these algorithms, the mismatch between the estimated and the true relay-destination channel affects the accuracy of the source-relay channel estimation. In this paper, we investigate the impact of such channel state information (CSI) mismatch on the performance of the two-phase channel estimation algorithm. By explicitly taking into account the CSI mismatch, we develop a robust algorithm to estimate the source-relay channel. Numerical examples demonstrate the improved performance of the proposed algorithm. © 2012 IEEE.

ω-Conotoxin GVIA mimetics that bind and inhibit neuronal Cav2.2 ion channels

The neuronal voltage-gated N-type calcium channel (Ca_v2.2) is a validated target for the treatment of neuropathic pain. A small library of anthranilamide-derived ω-Conotoxin GVIA mimetics bearing the diphenylmethylpiperazine moiety were prepared and tested using three experimental measures of calcium channel blockade. These consisted of a ¹²⁵I-ω-conotoxin GVIA displacement assay, a fluorescence-based calcium response assay with SH-SY5Y neuroblastoma cells, and a whole-cell patch clamp electrophysiology assay with HEK293 cells stably expressing human Ca_v2.2 channels. A subset of compounds were active in all three assays. This is the first time that compounds designed to be mimics of ω-conotoxin GVIA and found to be active in the ¹²⁵I-ω-conotoxin GVIA displacement assay have also been shown to block functional ion channels in a dose-dependent manner.

‘It would be okay if they came through the proper channels’: community perceptions and attitudes toward asylum seekers in Australia

Australia's humanitarian programme contributes to UNHCR's global resettlement programme and enhances Australia's international humanitarian reputation. However, as the recent tragedy on Christmas Island has shown, the arrival of asylum seekers by boat continues to stimulate debate, discussion and reaction from the Australian public and the Australian media. In this study, we used a mixed methods community survey to understand community perceptions and attitudes relating to asylum seekers. We found that while personal contact with asylum seekers was important when forming opinions about this group of immigrants, for the majority of respondents, attitudes and opinions towards asylum seekers were more influenced by the interplay between traditional Australian values and norms, the way that these norms appeared to be threatened by asylum seekers, and the way that these threats were reinforced both in media and political rhetoric.

Distinct disulfide isomers of μ-Conotoxins KIIIA and KIIIB block voltage-gated sodium channels

In the preparation of synthetic conotoxins containing multiple disulfide bonds, oxidative folding can produce numerous permutations of disulfide bond connectivities. Establishing the native disulfide connectivities thus presents a significant challenge when the venom-derived peptide is not available, as is increasingly the case when conotoxins are identified from cDNA sequences. Here, we investigate the disulfide connectivity of μ-conotoxin KIIIA, which was predicted originally to have a [C1–C9,C2–C15,C4–C16] disulfide pattern based on homology with closely related μ-conotoxins. The two major isomers of synthetic μ-KIIIA formed during oxidative folding were purified and their disulfide connectivities mapped by direct mass spectrometric collision-induced dissociation fragmentation of the disulfide-bonded polypeptides. Our results show that the major oxidative folding product adopts a [C1–C15,C2–C9,C4–C16] disulfide connectivity, while the minor product adopts a [C1–C16,C2–C9,C4–C15] connectivity. Both of these peptides were potent blockers of NaV1.2 (Kd values of 5 and 230 nM, respectively). The solution structure for μ-KIIIA based on nuclear magnetic resonance data was recalculated with the [C1–C15,C2–C9,C4–C16] disulfide pattern; its structure was very similar to the μ-KIIIA structure calculated with the incorrect [C1–C9,C2–C15,C4–C16] disulfide pattern, with an α-helix spanning residues 7–12. In addition, the major folding isomers of μ-KIIIB, an N-terminally extended isoform of μ-KIIIA identified from its cDNA sequence, were isolated. These folding products had the same disulfide connectivities as μ-KIIIA, and both blocked NaV1.2 (Kd values of 470 and 26 nM, respectively). Our results establish that the preferred disulfide pattern of synthetic μ-KIIIA and μ-KIIIB folded in vitro is 1–5/2–4/3–6 but that other disulfide isomers are also potent sodium channel blockers. These findings raise questions about the disulfide pattern(s) of μ-KIIIA in the venom of Conus kinoshitai; indeed, the presence of multiple disulfide isomers in the venom could provide a means of further expanding the snail’s repertoire of active peptides.