Aging in personal and social immunity: do immune traits senesce at the same rate?

How much should an individual invest in immunity as it grows older? Immunity is costly and its value is likely to change across an organism's lifespan. A limited number of studies have focused on how personal immune investment changes with age in insects, but we do not know how social immunity, immune responses that protect kin, changes across lifespan, or how resources are divided between these two arms of the immune response. In this study, both personal and social immune functions are considered in the burying beetle, Nicrophorus vespilloides. We show that personal immune function declines (phenoloxidase levels) or is maintained (defensin expression) across lifespan in nonbreeding beetles but is maintained (phenoloxidase levels) or even upregulated (defensin expression) in breeding individuals. In contrast, social immunity increases in breeding burying beetles up to middle age, before decreasing in old age. Social immunity is not affected by a wounding challenge across lifespan, whereas personal immunity, through PO, is upregulated following wounding to a similar extent across lifespan. Personal immune function may be prioritized in younger individuals in order to ensure survival until reproductive maturity. If not breeding, this may then drop off in later life as state declines. As burying beetles are ephemeral breeders, breeding opportunities in later life may be rare. When allowed to breed, beetles may therefore invest heavily in "staying alive" in order to complete what could potentially be their final reproductive opportunity. As parental care is important for the survival and growth of offspring in this genus, staying alive to provide care behaviors will clearly have fitness payoffs. This study shows that all immune traits do not senesce at the same rate. In fact, the patterns observed depend upon the immune traits measured and the breeding status of the individual.

Sum-Rate and Power Scaling of Massive MIMO Systems with Channel Aging

This paper investigates the achievable sum-rate of massive multiple-input multiple-output (MIMO) systems in the presence of channel aging. For the uplink, by assuming that the base station (BS) deploys maximum ratio combining (MRC) or zero-forcing (ZF) receivers, we present tight closed-form lower bounds on the achievable sum-rate for both receivers with aged channel state information (CSI). In addition, the benefit of implementing channel prediction methods on the sum-rate is examined, and closed-form sum rate lower bounds are derived. Moreover, the impact of channel aging and channel prediction on the power scaling law is characterized. Extension to the downlink scenario and multi-cell scenario are also considered. It is found that, for a system with/without channel prediction, the transmit power of each user can be scaled down at most by 1= p M (where M is the number of BS antennas), which indicates that aged CSI does not degrade the power scaling law, and channel prediction does not enhance the power scaling law; instead, these phenomena affect the achievable sum-rate by degrading or enhancing the effective signal to interference and noise ratio, respectively.

Retinal pigment epithelial cell multinucleation in the aging eye - a mechanism to repair damage and maintain homoeostasis

Retinal pigment epithelial (RPE) cells are central to retinal health and homoeostasis. Dysfunction or death of RPE cells underlies many age-related retinal degenerative disorders particularly age-related macular degeneration. During aging RPE cells decline in number, suggesting an age-dependent cell loss. RPE cells are considered to be postmitotic, and how they repair damage during aging remains poorly defined. We show that RPE cells increase in size and become multinucleate during aging in C57BL/6J mice. Multinucleation appeared not to be due to cell fusion, but to incomplete cell division, that is failure of cytokinesis. Interestingly, the phagocytic activity of multinucleate RPE cells was not different from that of mononuclear RPE cells. Furthermore, exposure of RPE cells in vitro to photoreceptor outer segment (POS), particularly oxidized POS, dose-dependently promoted multinucleation and suppressed cell proliferation. Both failure of cytokinesis and suppression of proliferation required contact with POS. Exposure to POS also induced reactive oxygen species and DNA oxidation in RPE cells. We propose that RPE cells have the potential to proliferate in vivo and to repair defects in the monolayer. We further propose that the conventionally accepted 'postmitotic' status of RPE cells is due to a modified form of contact inhibition mediated by POS and that RPE cells are released from this state when contact with POS is lost. This is seen in long-standing rhegmatogenous retinal detachment as overtly proliferating RPE cells (proliferative vitreoretinopathy) and more subtly as multinucleation during normal aging. Age-related oxidative stress may promote failure of cytokinesis and multinucleation in RPE cells.

Women into Non-Traditional Sectors: Addressing Gender Segregation in the Northern Ireland Workforce

The horizontal segregation of the workforce along gender lines tends to assign women to lower paid, lower status employment. Consequently, schemes to address segregation have focused on preparing women to enter non‐traditional occupations through training and development processes. This article examines models to encourage women into non‐traditional employment, focusing on the Women into Non‐Traditional Sectors (WINS) project in Belfast, Northern Ireland. However, changing women to suit a hostile work environment assumes women to be the problem, whereas it is the barriers that women face in undertaking non‐traditional jobs that need to be changed. It is concluded, therefore, that while models such as WINS can be successful in assisting women into non‐traditional sectors, change processes to make workplaces more accessible are a more pressing and appropriate approach to de‐segregating the workforce.

Effect of channel aging on the sum rate of uplink massive MIMO systems

This paper investigates the achievable sum-rate of uplink massive multiple-input multiple-output (MIMO) systems considering a practical channel impairment, namely, aged channel state information (CSI). Taking into account both maximum ratio combining (MRC) and zero-forcing (ZF) receivers at the base station, we present tight closed-form lower bounds on the sum-rate for both receivers, which provide efficient means to evaluate the sum-rate of the system. More importantly, we characterize the impact of channel aging on the power scaling law. Specifically, we show that the transmit power of each user can be scaled down by 1/√(M), which indicates that aged CSI does not affect the power scaling law; instead, it causes only a reduction on the sum rate by reducing the effective signal-to-interference-and-noise ratio (SINR).