Determinants of reproductive success in voles: space use in relation to food and litter size manipulation

Spacing behaviour of female mammals is suggested to depend on the distribution and abundance of food. In addition, food limitation has been found to constrain the reproductive success of females. However, whether females maximize their reproductive success by adjusting space use in relation to current food availability and reproductive effort (e.g. litter size) has not been experimentally studied. We examined these questions by manipulating simultaneously food resources (control vs. food supplementation) and litter sizes (control vs. plus two pups) of territorial female bank voles (Clethrionomys glareolus) in large outdoor enclosures. Females with supplementary food had smaller home ranges (foraging area) and home range overlaps than control females, whereas litter size manipulation had no effect on space use. In contrast, the size of territory (exclusive area) was not affected by food supplementation or litter size manipulation. As we have previously shown elsewhere, extra food increases the reproductive success of bank vole females in terms of size and proportion of weaned offspring. According to the present data, greater overlap of female home ranges had a negative effect on reproductive success of females, particularly on survival of offspring. We conclude that higher food availability increases the reproductive success of bank vole females, and this effect may be mediated through lower vulnerability of offspring to direct killing and/or detrimental effects from other females in the population. Moreover, it seems that when density of conspecifics is controlled for, home range sizes of females, but not territoriality, is related to food resources in Clethrionomys voles.     

Pentraxin 3 (PTX3) Is Associated with Severe Sepsis and Fatal Disease in Emergency Room Patients with Suspected Infection: A Prospective Cohort Study

Background

Early diagnostic and prognostic stratification of patients with suspected infection is a difficult clinical challenge. We studied plasma pentraxin 3 (PTX3) upon admission to the emergency department in patients with suspected infection.

Methods

The study comprised 537 emergency room patients with suspected infection: 59 with no systemic inflammatory response syndrome (SIRS) and without bacterial infection (group 1), 67 with bacterial infection without SIRS (group 2), 54 with SIRS without bacterial infection (group 3), 308 with sepsis (SIRS and bacterial infection) without organ failure (group 4) and 49 with severe sepsis (group 5). Plasma PTX3 was measured on admission using a commercial solid-phase enzyme-linked immunosorbent assay (ELISA).

Results

The median PTX3 levels in groups 1–5 were 2.6 ng/ml, 4.4 ng/ml, 5.0 ng/ml, 6.1 ng/ml and 16.7 ng/ml, respectively (p<0.001). The median PTX3 concentration was higher in severe sepsis patients compared to others (16.7 vs. 4.9 ng/ml, p<0.001) and in non-survivors (day 28 case fatality) compared to survivors (14.1 vs. 5.1 ng/ml, p<0.001). A high PTX3 level predicted the need for ICU stay (p<0.001) and hypotension (p<0.001). AUC^ROC in the prediction of severe sepsis was 0.73 (95% CI 0.66–0.81, p<0.001) and 0.69 in case fatality (95% CI 0.58–0.79, p<0.001). PTX3 at a cut-off level for 14.1 ng/ml (optimal cut-off value for severe sepsis) showed 63% sensitivity and 80% specificity. At a cut-off level 7.7 ng/ml (optimal cut-off value for case fatality) showed 70% sensitivity and 63% specificity in predicting case fatality on day 28.In multivariate models, high PTX3 remained an independent predictor of severe sepsis and case fatality after adjusting for potential confounders.

Conclusions

A high PTX3 level on hospital admission predicts severe sepsis and case fatality in patients with suspected infection.     

Idle slow as you grow old: longitudinal age-related metabolic decline in a wild passerine

Physiological changes due to aging are intensively studied as they have far-reaching implications for the mechanistic and evolutionary theories of senescence. In this respect, metabolic rate has been suggested to play a role for the deterioration and damage of cells and tissues with age, partly due to the generation of reactive oxygen species. To mitigate such damage, individuals can be predicted to reduce basal metabolic rate (BMR) with age. This prediction has been verified in humans and some laboratory animals but never in wild animal populations. We analyzed the change in BMR within individuals across years in two wild populations of great tit (Parus major) differing in BMR. Great tits, living under stressful conditions towards the northern limit of their distribution, decreased their BMR as they aged whereas no such decrease was found in a southern population. Thus, we found a clear decline only in the population with the highest BMR levels. This study provides the first evidence of an age-related decline in BMR for a wild homeotherm.     

Poisson Regression with Change‐Point Prior in the Modelling of Disease Risk around a Point Source

Bayesian estimation of the risk of a disease around a known point source of exposure is considered. The minimal requirements for data are that cases and populations at risk are known for a fixed set of concentric annuli around the point source, and each annulus has a uniquely defined distance from the source. The conventional Poisson likelihood is assumed for the counts of disease cases in each annular zone with zone‐specific relative risk and parameters and, conditional on the risks, the counts are considered to be independent. The prior for the relative risk parameters is assumed to be piecewise constant at the distance having a known number of components. This prior is the well‐known change‐point model. Monte Carlo sampling from the posterior results in zone‐specific posterior summaries, which can be applied for the calculation of a smooth curve describing the variation in disease risk as a function of the distance from the putative source. In addition, the posterior can be used in the calculation of posterior probabilities for interesting hypothesis. The suggested model is suitable for use in geographical information systems (GIS) aimed for monitoring disease risks. As an application, a case study on the incidence of lung cancer around a former asbestos mine in eastern Finland is presented. Further extensions of the model are discussed.     

Size of environmental grain and resource matching

For most animals their foraging environment consists of a patch network. In random environments there are no spatial autocorrelation at all, while in fine-grained systems positive autocorrelations flip to negative ones and back again against distance. With increasing grain size the turnover rate of spatial autocorrelation slows down. Using a cellular automaton with foragers having limited information about their feeding environment we examined how well consumer numbers matched resource availability, also known as the ideal free distribution. The match is the better the smaller the size of the environmental grain. This is somewhat contrary to the observation that in large-grained environments the spatial autocorrelation is high and positive over long distances. In such an environment foragers, by knowing a limited surrounding, should in fact know a much larger area because of the spatially autocorrelated resource pattern. Yet, when foragers have limited knowledge, we observed that the degree of undermatching (i.e., more individuals in less productive patches than expected) increases with increasing grain size.     

Mortality in Iraq Associated with the 2003–2011 War and Occupation: Findings from a National Cluster Sample Survey by the University Collaborative Iraq Mortality Study

Background

Previous estimates of mortality in Iraq attributable to the 2003 invasion have been heterogeneous and controversial, and none were produced after 2006. The purpose of this research was to estimate direct and indirect deaths attributable to the war in Iraq between 2003 and 2011.

Methods and Findings

We conducted a survey of 2,000 randomly selected households throughout Iraq, using a two-stage cluster sampling method to ensure the sample of households was nationally representative. We asked every household head about births and deaths since 2001, and all household adults about mortality among their siblings. We used secondary data sources to correct for out-migration. From March 1, 2003, to June 30, 2011, the crude death rate in Iraq was 4.55 per 1,000 person-years (95% uncertainty interval 3.74–5.27), more than 0.5 times higher than the death rate during the 26-mo period preceding the war, resulting in approximately 405,000 (95% uncertainty interval 48,000–751,000) excess deaths attributable to the conflict. Among adults, the risk of death rose 0.7 times higher for women and 2.9 times higher for men between the pre-war period (January 1, 2001, to February 28, 2003) and the peak of the war (2005–2006). We estimate that more than 60% of excess deaths were directly attributable to violence, with the rest associated with the collapse of infrastructure and other indirect, but war-related, causes. We used secondary sources to estimate rates of death among emigrants. Those estimates suggest we missed at least 55,000 deaths that would have been reported by households had the households remained behind in Iraq, but which instead had migrated away. Only 24 households refused to participate in the study. An additional five households were not interviewed because of hostile or threatening behavior, for a 98.55% response rate. The reliance on outdated census data and the long recall period required of participants are limitations of our study.

Conclusions

Beyond expected rates, most mortality increases in Iraq can be attributed to direct violence, but about a third are attributable to indirect causes (such as from failures of health, sanitation, transportation, communication, and other systems). Approximately a half million deaths in Iraq could be attributable to the war. Please see later in the article for the Editors'' Summary     

Removal of GABA(A) receptor γ2 subunits from parvalbumin neurons causes wide-ranging behavioral alterations

We investigated the behavioral significance of fast synaptic inhibition by αβγ2-type GABA(A) receptors on parvalbumin (Pv) cells. The GABA(A) receptor γ2 subunit gene was selectively inactivated in Pv-positive neurons by Cre/loxP recombination. The resulting Pv-Δγ2 mice were relatively healthy in the first postnatal weeks; but then as Cre started to be expressed, the mice progressively developed wide-ranging phenotypic alterations including low body weight, motor deficits and tremor, decreased anxiety levels, decreased pain sensitivity and deficient prepulse inhibition of the acoustic startle reflex and impaired spatial learning. Nevertheless, the deletion was not lethal, and mice did not show increased mortality even after one year. Autoradiography with t-butylbicyclophosphoro[(35)S]thionate suggested an increased amount of GABA(A) receptors with only α and β subunits in central nervous system regions that contained high levels of parvalbumin neurons. Using BAC-transgenesis, we reduced some of the Pv-Δγ2 phenotype by selectively re-expressing the wild-type γ2 subunit back into some Pv cells (reticular thalamic neurons and cerebellar Pv-positive neurons). This produced less severe impairments of motor skills and spatial learning compared with Pv-Δγ2 mice, but all other deficits remained. Our results reveal the widespread significance of fast GABAergic inhibition onto Pv-positive neurons for diverse behavioral modalities, such as motor coordination, sensorimotor integration, emotional behavior and nociception.