Bottom‐up processes in a declining yellow‐footed rock‐wallaby (Petrogale xanthopus celeris) population

Populations of large herbivores are generally considered to be food limited, escaping the regulatory effects of predation through their large body size, migratory behaviour and/or the occurrence of alternate prey species. In the Australian arid and semi‐arid zones, the availability of forage biomass is considered to be the primary driver of fluctuations in kangaroo abundance. However, little is known about the population dynamics of the smaller sympatric macropods. We examined the demographic traits of a large colony of yellow‐footed rock‐wallabies (Petrogale xanthopus celeris), following a 2‐year period of above average rainfall. The population was located within a conservation reserve that was subject to a predator control program around its perimeter and on neighbouring properties. The low predator abundance provided an opportunity to gauge the strength of bottom‐up population processes. During the two years of the study, the population declined in size by 53%, resulting from both the virtual absence of juvenile recruitment and the loss of adult wallabies. Although reproductive output was high, low pouch young and juvenile survival rates resulted in few individuals progressing into the adult population. With minimal recruitment, the rate of population decline (r = 0.77) matched the observed adult survival rate (Φ = 0.76). Despite average rainfall conditions during the study, survival rates across all age‐classes were equivalent to those reported for other rock‐wallaby populations during periods of scarcity. The reduced survival rates were attributed to low levels of forage resources, particularly around the wallabies' refuge sites, suggesting the bottom‐up regulation of the colony at high densities. The data suggest that the colony was at temporarily high abundance, following a rainfall driven pulse of recruitment. Conservation management actions for this species should focus on increasing juvenile survival rates within declining populations, through the control of feral goats (Capra hircus), rabbits (Oryctolagus cuniculus) and red foxes (Vulpes vulpes).     

Genetic markers on BTA14 predictive for residual feed intake in beef steers and their effects on carcass and meat quality traits

With the high cost of feed for animal production, genetic selection for animals that metabolize feed more efficiently could result in substantial cost savings for cattle producers. The purpose of this study was to identify DNA markers predictive for differences among cattle for traits associated with feed efficiency. Crossbred steers were fed a high‐corn diet for 140 days and average daily feed intake (ADFI), average daily gain (ADG), and residual feed intake (RFI) phenotypes were obtained. A region on chromosome 14 was previously associated with RFI in this population of animals. To develop markers with the highest utility for predicting an animal's genetic potential for RFI, we genotyped additional markers within this chromosomal region. These polymorphisms were genotyped on the same animals (n = 1066) and tested for association with ADFI, ADG and RFI. Six markers within this region were associated with RFI (P ≤ 0.05). After conservative correction for multiple testing, one marker at 25.09 Mb remained significant (P = 0.02) and is responsible for 3.6% of the RFI phenotypic variation in this population of animals. Several of these markers were also significant for ADG, although none were significant after correction. Marker alleles with positive effects on ADG corresponded to lower RFI, suggesting an effect increasing growth without increasing feed intake. All markers were also assessed for their effects on meat quality and carcass traits. All of the markers associated with RFI were associated with adjusted fat thickness (AFT, P ≤ 0.009) and three were also associated with hot carcass weight (HCW, P ≤ 0.003). Marker alleles associated with lower RFI were also associated with reduced AFT, and if they were associated for HCW, the effect was an increase in weight. These markers may be useful as prediction tools for animals that utilize feed more efficiently; however, validation with additional populations of cattle is required.     

Coenzyme Q10 Protects Astrocytes from ROS-Induced Damage through Inhibition of Mitochondria-Mediated Cell Death Pathway

Coenzyme Q10 (CoQ10) acts by scavenging reactive oxygen species to protect neuronal cells against oxidative stress in neurodegenerative diseases. The present study was designed to examine whether CoQ10 was capable of protecting astrocytes from reactive oxygen species (ROS) mediated damage. For this purpose, ultraviolet B (UVB) irradiation was used as a tool to induce ROS stress to cultured astrocytes. The cells were treated with 10 and 25 μg/ml of CoQ10 for 3 or 24 h prior to the cells being exposed to UVB irradiation and maintained for 24 h post UVB exposure. Cell viability was assessed by MTT conversion assay. Mitochondrial respiration was assessed by respirometer. While superoxide production and mitochondrial membrane potential were measured using fluorescent probes, levels of cytochrome C (cyto-c), cleaved caspase-9, and caspase-8 were detected using Western blotting and/or immunocytochemistry. The results showed that UVB irradiation decreased cell viability and this damaging effect was associated with superoxide accumulation, mitochondrial membrane potential hyperpolarization, mitochondrial respiration suppression, cyto-c release, and the activation of both caspase-9 and -8. Treatment with CoQ10 at two different concentrations started 24 h before UVB exposure significantly increased the cell viability. The protective effect of CoQ10 was associated with reduction in superoxide, normalization of mitochondrial membrane potential, improvement of mitochondrial respiration, inhibition of cyto-c release, suppression of caspase-9. Furthermore, CoQ10 enhanced mitochondrial biogenesis. It is concluded that CoQ10 may protect astrocytes through suppression of oxidative stress, prevention of mitochondrial dysfunction, blockade of mitochondria-mediated cell death pathway, and enhancement of mitochondrial biogenesis.     

Phenotype Specific Analyses Reveal Distinct Regulatory Mechanism for Chronically Activated p53

The downstream functions of the DNA binding tumor suppressor p53 vary depending on the cellular context, and persistent p53 activation has recently been implicated in tumor suppression and senescence. However, genome-wide information about p53-target gene regulation has been derived mostly from acute genotoxic conditions. Using ChIP-seq and expression data, we have found distinct p53 binding profiles between acutely activated (through DNA damage) and chronically activated (in senescent or pro-apoptotic conditions) p53. Compared to the classical ‘acute’ p53 binding profile, ‘chronic’ p53 peaks were closely associated with CpG-islands. Furthermore, the chronic CpG-island binding of p53 conferred distinct expression patterns between senescent and pro-apoptotic conditions. Using the p53 targets seen in the chronic conditions together with external high-throughput datasets, we have built p53 networks that revealed extensive self-regulatory ‘p53 hubs’ where p53 and many p53 targets can physically interact with each other. Integrating these results with public clinical datasets identified the cancer-associated lipogenic enzyme, SCD, which we found to be directly repressed by p53 through the CpG-island promoter, providing a mechanistic link between p53 and the ‘lipogenic phenotype’, a hallmark of cancer. Our data reveal distinct phenotype associations of chronic p53 targets that underlie specific gene regulatory mechanisms.     

Pectenotoxin and okadaic acid-based toxin profiles in Dinophysis acuta and Dinophysis acuminata from New Zealand

The major pectenotoxin and okadaic acid group toxins in Dinophysis acuta and Dinophysis acuminata cell concentrates, collected from various locations around the coast of the South Island of New Zealand (NZ), were determined by liquid chromatography–tandem mass spectrometry (LC–MS/MS). PTX2 and PTX11 were the major polyether toxins in all Dinophysis spp. cell concentrates. D. acuta contained PTX11 and PTX2 at concentrations of 4.7–64.6 and 32.5–107.5 pg per cell, respectively. The amounts of PTX11 and PTX2 in D. acuminata were much lower at 0.4–2.1 and 2.4–25.8 pg per cell, respectively. PTX seco acids comprised only 4% of the total PTX content of both D. acuta and D. acuminata. D. acuta contained low levels of OA (0.8–2.7 pg per cell) but specimens from the South Island west coast also contained up to 10 times higher levels of OA esters (7.0–10.2 pg per cell). Esterified forms of OA were not observed in D. acuta specimens from the Marlborough Sounds. D. acuta did not contain any DTX1 though all D. acuminata specimens contained DTX1 at levels of 0.1–2.4 pg per cell. DTX2 was not present in any New Zealand Dinophysis spp. specimens. Although the total toxin content varied spatially and temporally, the relative proportions of the various toxins in different specimens from the same location appeared to be relatively stable. The total PTX/total OA ratios in different isolates of D. acuta were very similar (mean±S.E.: 14.9±1.9), although the Marlborough Sounds D. acuminata isolates had a higher total PTX/total OA ratio (mean±S.E.: 22.7±2.4) than the Akaroa Harbour isolates (8.0). No evidence of azaspiracids were detected in these specimens. These results show that the LC–MS/MS monitoring of plankton for PTX group toxins (e.g. PTX2) and their derivatives (e.g. PTX2 seco acid) may provide a sensitive, semi-quantitative, indicator of the presence of more cryptic OA group toxins (e.g. OA esters).     

Changes in ponderal index and body mass index across childhood and their associations with fat mass and cardiovascular risk factors at age 15

Background

Little is known about whether associations between childhood adiposity and later adverse cardiovascular health outcomes are driven by tracking of overweight from childhood to adulthood and/or by vascular and metabolic changes from childhood overweight that persist into adulthood. Our objective is to characterise associations between trajectories of adiposity across childhood and a wide range of cardiovascular risk factors measured in adolescence, and explore the extent to which these are mediated by fat mass at age 15.

Methods and Findings

Using data from the Avon Longitudinal Study of Parents and Children, we estimated individual trajectories of ponderal index (PI) from 0–2 years and BMI from 2–10 years using random-effects linear spline models (N = 4601). We explored associations between PI/BMI trajectories and DXA-determined total-body fat-mass and cardiovascular risk factors at 15 years (systolic and diastolic blood pressure, fasting LDL- and HDL-cholesterol, triglycerides, C-reactive protein, glucose, insulin) with and without adjustment for confounders. Changes in PI/BMI during all periods of infancy and childhood were associated with greater DXA-determined fat-mass at age 15. BMI changes in childhood, but not PI changes from 0–2 years, were associated with most cardiovascular risk factors in adolescence; associations tended to be strongest for BMI changes in later childhood (ages 8.5–10), and were largely mediated by fat mass at age 15.

Conclusion

Changes in PI/BMI from 0–10 years were associated with greater fat-mass at age 15. Greater increases in BMI from age 8.5–10 years are most strongly associated with cardiovascular risk factors at age 15, with much of these associations mediated by fat-mass at this age. We found little evidence supporting previous reports that rapid PI changes in infancy are associated with future cardiovascular risk. This study suggests that associations between early overweight and subsequent adverse cardiovascular health are largely due to overweight children tending to remain overweight.     

Contexts,developing ideas and emerging issues in the conservation management of the RSPB Abernethy Forest Reserve

Summary

Native pinewoods are fragmentary in extent and floristic integrity. In maintaining and extending these remnants, managers should recognise the diversity of potential communities and the unique mix of species in their flora. At the RSPB Abernethy Forest Reserve management aims to develop a self sustaining forest of natural character over the potential woodland area. A present-natural forest provides one model for the attributes and processes, which this forest should contain. Habitat management experiments have recently commenced investigating ways of increasing blaeberry Vaccinium myrtillus in forest areas, and increasing tree regeneration at the forest edge. The possible wider role of management intervention in pinewoods is discussed.     

Identification of interferon-stimulated gene 15 as an antiviral molecule during Sindbis virus infection in vivo

The innate immune response, and in particular the alpha/beta interferon (IFN-alpha/beta) system, plays a critical role in the control of viral infections. Interferons alpha and beta exert their antiviral effects through the induction of hundreds of interferon-induced (or -stimulated) genes (ISGs). While several of these ISGs have characterized antiviral functions, their actions alone do not explain all of the effects mediated by IFN-alpha/beta. To identify additional IFN-induced antiviral molecules, we utilized a recombinant chimeric Sindbis virus to express selected ISGs in IFN-alpha/beta receptor (IFN-alpha/betaR)(-/-) mice and looked for attenuation of Sindbis virus infection. Using this approach, we identified a ubiquitin homolog, interferon-stimulated gene 15 (ISG15), as having antiviral activity. ISG15 expression protected against Sindbis virus-induced lethality and decreased Sindbis virus replication in multiple organs without inhibiting the spread of virus throughout the host. We establish that, much like ubiquitin, ISG15 requires its C-terminal LRLRGG motif to form intracellular conjugates. Finally, we demonstrate that ISG15's LRLRGG motif is also required for its antiviral activity. We conclude that ISG15 can be directly antiviral.     

In vivo progestin treatments inhibit nitric oxide and endothelin-1-induced bovine endometrial prostaglandin (PG) E (PGE) secretion in vitro

Synchronization of estrus with progestins in cows has been reported to inhibit nitric oxide (NO) and endothelin-1 (ET-1)-stimulated bovine luteal PGE secretion without affecting prostaglandin F2alpha (PGF2alpha) secretion in vitro [Weems YS, Randel RD, Tatman S, Lewis A, Neuendorff DA, Weems CW. Does estrous synchronization affect corpus luteum (CL) function? Prostaglandins Other Lipid Mediat 2004;74:45-59]. Two experiments were conducted to determine the effects of NO donors, endothelin-1 (ET-1), and NO synthase (NOS) inhibitors on bovine caruncular endometrial secretion of PGE and PGF2alpha in vitro. In Experiment 1, estrus was synchronized in Brahman cows with Synchromate-B ear implants, which contained the synthetic progestin norgestamet. Days 14-15 caruncular endometrial slices were weighed, diced, and incubated in vitro with treatments. Treatments (100 ng/ml) were: Vehicle (control), l-NAME (NOS inhibitor), l-NMMA (NOS inhibitor), DETA (control), DETA-NONOate (NO donor), sodium nitroprusside (NO donor), or ET-1. In Experiment 2, estrus was synchronized in Brahman cows with either Lutalyse (PGF2alpha) or a controlled intravaginal drug releasing device (CIDR-containing progesterone) or estrus was not synchronized. Days 14-15 caruncular endometrial slices were weighed, diced, and incubated in vitro with treatments. Treatments (100 ng/ml) were: vehicle, l-NAME, l-NMMA, DETA, DETA-NONOate, sodium nitroprusside, SNAP (NO donor) or ET-1. Tissues were incubated in M-199 for 1h without treatments and with treatments for 4 and 8h in both experiments. Media were analyzed for concentrations of PGE and PGF2alpha by radioimmunoassay (RIA). Hormone data in Experiments 1 and 2 were analyzed by 2x7 and 3x2x8 factorial design for ANOVA, respectively. Concentrations of PGE and PGF2alpha in media increased (P< or =0.05) from 4 to 8 h regardless of treatment group in Experiment 1, but did not differ (P> or =0.05) among treatments. In Experiment 2, concentrations of PGE and PGF2alpha increased (P< or =0.05) with time in all treatment groups of all three synchronization regimens. DETA-NONOate, SNAP, and sodium nitroprusside (NO donors) and ET-1 increased caruncular endometrial (P< or =0.05) secretion of PGE2 in unsynchronized and Lutalyse synchronized cows, but not when estrus was synchronized with a CIDR (P> or =0.05). No treatment increased (P> or =0.05) PGF2alpha in any synchronization regimen. It is concluded that norgestamet in Synchromate-B ear implants or progesterone in a CIDR alters NO or ET-1-induced secretion of PGE by bovine caruncular endometrium and could interfere with implantation by altering the PGE:PGF2alpha ratio resulting in increased embryonic losses during early pregnancy.     

The effect of fragment area on site‐level biodiversity

Habitat fragmentation accompanies habitat loss, and drives additional biodiversity change; but few global biodiversity models explicitly analyse the effects of both fragmentation and loss. Here we propose and test the hypothesis that, as fragment area increases, species density (the number of species in a standardised plot) will scale with an exponent given by the difference between the exponents of the species–area relationships for islands (z ~ 0.25) and in contiguous habitat (z ~ 0.15), and test whether scaling varies between land uses. We also investigate the scaling of overall abundance and rarefaction‐based richness, as some mechanisms make different predictions about how fragment area should affect them. The relevant data from the taxonomically and geographically broad PREDICTS database were used to model the three diversity measures, testing their scaling with fragment area and whether the scaling exponent varied among land uses (primary forest, secondary forest, plantation forest, cropland and pasture). In addition, the consistency of the response of species density to fragment area was tested across three well represented taxa (Magnoliopsida, Hymenoptera and ‘herptiles’). Species density and total abundance showed area‐scaling exponents of 0.07 and 0.16, respectively, and these exponents did not vary significantly among land uses; rarefaction‐based richness by contrast did not increase consistently with area. These results suggest that the area‐scaling of species density is driven by the area‐scaling of total abundance, with additive edge effects (species moving into the small fragments from the surroundings) opposing – but not fully overcoming – the effect of fragment area on overall density of individuals. The interaction between fragment area and higher taxon (plants, vertebrates and invertebrates), which remained in the rarefied richness model, indicates that mechanisms may vary among groups.