Identity and Link Reliability in Social Networks

This paper considers a non-cooperative network formation game where identity is introduced as a single dimension to capture the characteristics of a player in the network. Players access to the benefits from the link through direct and indirect connections. We consider cases where cost of link formation paid by the initiator. Each player is allowed to choose their commitment level to their identities. The cost of link formation decreases as the players forming the link share the same identity and higher commitment levels. We then introduce link imperfections to the model. We characterize the Nash networks and we find that the set of Nash networks are either singletons with no links formed or separated blocks or components with mixed blocks or connected.

Deficiency of the ferrous iron transporter FeoAB is linked with metronidazole resistance in Bacteroides fragilis

Background Metronidazole is the most commonly used antimicrobial for Bacteroides fragilis infections and is recommended for prophylaxis of colorectal surgery. Metronidazole resistance is increasing and the mechanisms of resistance are not clear.

Methods A transposon mutant library was generated in B. fragilis 638R (BF638R) to identify the genetic loci associated with resistance to metronidazole.

Results Thirty-two independently isolated metronidazole-resistant mutants had a transposon insertion in BF638R_1421 that encodes the ferrous transport fusion protein (feoAB). Deletion of feoAB resulted in a 10-fold increased MIC of metronidazole for the strain. The metronidazole MIC for the feoAB mutant was similar to that for the parent strain when grown on media supplemented with excess iron, suggesting that the increase seen in the MIC of metronidazole was due to reduced cellular iron transport in the feoAB mutant. The furA gene repressed feoAB transcription in an iron-dependent manner and disruption of furA resulted in constitutive transcription of feoAB, regardless of whether or not iron was present. However, disruption of feoAB also diminished the capacity of BF638R to grow in a mouse intraperitoneal abscess model, suggesting that inorganic ferrous iron assimilation is essential for B. fragilis survival in vivo.

Conclusions Selection for feoAB mutations as a result of metronidazole treatment will disable the pathogenic potential of B. fragilis and could contribute to the clinical efficacy of metronidazole. While mutations in feoAB are probably not a direct cause of clinical resistance, this study provides a key insight into intracellular metronidazole activity and the link with intracellular iron homeostasis.

Human body shadowing in cellular device-to-device communications: channel modeling using the shadowed κ−μ fading model

Using device-to-device communications as an underlay for cellular communications will provide an exciting opportunity to increase network capacity as well as improving spectral efficiency. The unique geometry of device-to-device links, where user equipment is often held or carried at low elevation and in close proximity to the human body, will mean that they are particularly susceptible to shadowing events caused not only by the local environment but also by the user's body. In this paper, the shadowed κ - μ fading model is proposed, which is capable of characterizing shadowed fading in wireless communication channels. In this model, the statistics of the received signal are manifested by the clustering of multipath components. Within each of these clusters, a dominant signal component with arbitrary power may exist. The resultant dominant signal component, which is formed by the phasor addition of these leading contributions, is assumed to follow a Nakagami- m distribution. The probability density function, moments, and the moment-generating function are also derived. The new model is then applied to device-to-device links operating at 868 MHz in an outdoor urban environment. It was found that shadowing of the resultant dominant component can vary significantly depending upon the position of the user equipment relative to the body and the link geometry. Overall, the shadowed κ - μ fading model is shown to provide a good fit to the field data as well as providing a useful insight into the characteristics of the received signal.

On the MIMO Capacity with Residual Transceiver Hardware Impairments

Radio-frequency (RF) impairments in the transceiver hardware of communication systems (e.g., phase noise (PN), high power amplifier (HPA) nonlinearities, or in-phase/quadrature-phase (I/Q) imbalance) can severely degrade the performance of traditional multiple-input multiple-output (MIMO) systems. Although calibration algorithms can partially compensate these impairments, the remaining distortion still has substantial impact. Despite this, most prior works have not analyzed this type of distortion. In this paper, we investigate the impact of residual transceiver hardware impairments on the MIMO system performance. In particular, we consider a transceiver impairment model, which has been experimentally validated, and derive analytical ergodic capacity expressions for both exact and high signal-to-noise ratios (SNRs). We demonstrate that the capacity saturates in the high-SNR regime, thereby creating a finite capacity ceiling. We also present a linear approximation for the ergodic capacity in the low-SNR regime, and show that impairments have only a second-order impact on the capacity. Furthermore, we analyze the effect of transceiver impairments on large-scale MIMO systems; interestingly, we prove that if one increases the number of antennas at one side only, the capacity behaves similar to the finite-dimensional case. On the contrary, if the number of antennas on both sides increases with a fixed ratio, the capacity ceiling vanishes; thus, impairments cause only a bounded offset in the capacity compared to the ideal transceiver hardware case.