Capacity and resource allocation of cooperative MIMO in ad hoc networks

Cooperative MIMO (Multiple Input–Multiple Output) allows multiple nodes share their antennas to emulate antenna arrays and transmit or receive cooperatively. It has the ability to increase the capacity for future wireless communication systems and it is particularly suited for ad hoc networks. In this study, based on the transmission procedure of a typical cooperative MIMO system, we first analyze the capacity of single-hop cooperative MIMO systems, and then we derive the optimal resource allocation strategy to maximize the end-to-end capacity in multi-hop cooperative MIMO systems. The study shows three implications. First, only when the intra-cluster channel is better than the inter-cluster channel, cooperative MIMO results in a capacity increment. Second, for a given scenario there is an optimal number of cooperative nodes. For instance, in our study an optimal deployment of three cooperative nodes achieve a capacity increment of 2 bps/Hz when compared with direct transmission. Third, an optimal resource allocation strategy plays a significant role in maximizing end-to-end capacity in multi-hop cooperative MIMO systems. Numerical results show that when optimal resource allocation is applied we achieve more than 20% end-to-end capacity increment in average when compared with an equal resource allocation strategy.

Maximizing the Localized Relaxation: The Origin of the Outstanding Oxygen Storage Capacity of kappa-Ce2Zr2O8

Pretty vacant: The excellent oxygen storage capacity (OSC) of ?-Ce2Zr2O8 (see picture; Ce gray, Zr green, O red) is shown to be a result of its unique structural features; after removing oxygen atoms, the structural relaxation is local (vacancy shown in brown), and both the localized structural relaxation and the number of localized structural relaxations are maximized.

hVps34 is a nutrient-regulated lipid kinase required for activation of p70 S6 kinase

Mammalian cells respond to nutrient deprivation by inhibiting energy consuming processes, such as proliferation and protein synthesis, and by stimulating catabolic processes, such as autophagy. p70 S6 kinase (S6K1) plays a central role during nutritional regulation of translation. S6K1 is activated by growth factors such as insulin, and by mammalian target of rapamycin (mTOR), which is itself regulated by amino acids. The Class IA phosphatidylinositol (PI) 3-kinase plays a well recognized role in the regulation of S6K1. We now present evidence that the Class III PI 3-kinase, hVps34, also regulates S6K1, and is a critical component of the nutrient sensing apparatus. Overexpression of hVps34 or the associated hVps15 kinase activates S6K1, and insulin stimulation of S6K1 is blocked by microinjection of inhibitory anti-hVps34 antibodies, overexpression of a FYVE domain construct that sequesters the hVps34 product PI(3) P, or small interfering RNA-mediated knock-down of hVps34. hVps34 is not part of the insulin input to S6K1, as it is not stimulated by insulin, and inhibition of hVps34 has no effect on phosphorylation of Akt or TSC2 in insulin-stimulated cells. However, hVps34 is inhibited by amino acid or glucose starvation, suggesting that it lies on the nutrient-regulated pathway to S6K1. Consistent with this, hVps34 is also inhibited by activation of the AMP-activated kinase, which inhibits mTOR/S6K1 in glucose-starved cells. hVps34 appears to lie upstream of mTOR, as small interfering RNA knock- down of hVps34 inhibits the phosphorylation of another mTOR substrate, eIF4E-binding protein-1 (4EBP1). Our data suggest that hVps34 is a nutrient-regulated lipid kinase that integrates amino acid and glucose inputs to mTOR and S6K1.

An exploratory study of Principal Investigator roles in UK University Proof-of-Concept processes: an Absorptive capacity perspective

The increasing emphasis on academic entrepreneurship, technology transfer and research commercialisation within UK universities is predicated on basic research being developed by academics into commercial entities such as university spin-off companies or licensing arrangements. However, this process is fraught with challenges and risks, given the degree of uncertainty regarding future returns. In an attempt to minimise such risks, the Proof-of-Concept (PoC) process has been developed within University Science Park Incubators (USIs) to test the technological, business and market potential of embryonic technology. The key or the pivotal stakeholder within the PoC is the Principal Investigator (PI), who is usually the lead academic responsible for the embryonic technology. Within the current literature, there appears to be a lack of research pertaining to the role of the PI in the PoC process. Moreover, Absorptive Capacity (ACAP) has emerged within the literature as a theoretical framework or lens for exploring the development and application of new knowledge and technology, where the USI is the organisation considered in the current study. Therefore, the aim of this paper is to explore the role and influence of the PI in the PoC process within a USI setting using an ACAP perspective. The research involved a multiple case analysis of PoC applications within a UK university USI. The results demonstrate the role of the PI in developing practices and routines within the PoC process. These practices and processes were initially tacit and informal in nature but became more explicit and formal over time so that knowledge was retained within the USI after the PIs had completed the PoC process. © 2010 The Authors. R&D Management © 2010 Blackwell Publishing Ltd.

p63 maintains keratinocyte proliferative capacity through regulation of Skp2-p130 levels

p63 is a master regulator of proliferation and differentiation in stratifying epithelia, and its expression is frequently altered in carcinogenesis. However, its role in maintaining proliferative capacity remains unclear. Here, we demonstrate that hypoproliferation and loss of differentiation in organotypic raft cultures of primary neonatal human foreskin keratinocytes (HFKs) depleted of the a and ß isoforms of p63 result from p53-p21-mediated accumulation of retinoblastoma (Rb) family member p130. Hypoproliferation in p63-depleted HFKs can be rescued by depletion of p53, p21(CIP1) or p130. Furthermore, we identified the gene encoding S-phase kinase-associated protein 2 (Skp2), the recognition component of the SCF(Skp2) E3 ubiquitin ligase, as a novel target of p63, potentially influencing p130 levels. Expression of Skp2 is maintained by p63 binding to a site in intron 2 and mRNA levels are downregulated in p63-depleted cells. Hypoproliferation in p63-depleted cells can be restored by re-expression of Skp2. Taken together, these results indicate that p63 plays a multifaceted role in maintaining proliferation in the mature regenerating epidermis, in addition to being required for differentiation.

Approaching near-capacity on a multi-antenna channel using successive decoding and interference cancellation receivers

In this paper, we address the problem of designing multirate codes for a multiple-input and multiple-output (MIMO) system by restricting the receiver to be a successive decoding and interference cancellation type, when each of the antennas is encoded independently. Furthermore, it is assumed that the receiver knows the instantaneous fading channel states but the transmitter does not have access to them. It is well known that, in theory, minimum-mean-square error (MMSE) based successive decoding of multiple access (in multi-user communications) and MIMO channels achieves the total channel capacity. However, for this scheme to perform optimally, the optimal rates of each antenna (per-antenna rates) must be known at the transmitter. We show that the optimal per-antenna rates at the transmitter can be estimated using only the statistical characteristics of the MIMO channel in time-varying Rayleigh MIMO channel environments. Based on the results, multirate codes are designed using punctured turbo codes for a horizontal coded MIMO system. Simulation results show performances within about one to two dBs of MIMO channel capacity.