Carrion subsidies provided by fishermen increase predation of beach-nesting bird nests by facultative scavengers

© 2014 The Zoological Society of London. Many predators are also scavengers that feed on carrion and human refuse. Therefore, the availability of carrion can elevate the abundance or activity of facultative scavengers, amplifying predation pressure on prey. On Australian beaches, fishermen often discard fish carcasses that could attract facultative scavengers, both native, such as Australian ravens Corvus coronoides, and invasive, such as European red foxes Vulpes vulpes, and result in elevated rates of predation on wildlife. We tested whether the presence of fish carcasses increased the risk of depredation for nearby nests of beach-nesting birds by deploying artificial nests in 12 subsidized and 12 control patches, spaced 1 km apart, on a beach. We placed a fish carcass in each subsidized patch, but not at control patches. In each patch, we placed two artificial nests, which resembled red-capped plover Charadrius ruficapillus nests, 80 m apart and 40m from carcasses at subsidized patches. Nest predators were identified from tracks and predator activity near subsidized and control nests was measured by counting tracks crossing a straight transect (220m). The activity of a native predator, the Australian raven, was 17 times higher near (<80m) nests with fish carcasses than nests without carcasses. After 72h, 96% of nests near carcasses were depredated compared with 30% of nests without carcasses. Ravens were identified as the culprit for 80% of depredated nests. Although other predators were present in the study area, they did not depredate artificial nests in this experiment. Previous studies have highlighted the effects of permanent and/or large-scale food resources on scavenger abundance and impact. A key management implication of our study is that even small, sparsely distributed, temporally irregular food subsidies, provided by humans, can elevate the activity and predatory impacts of facultative scavengers

triSPIM: light sheet microscopy with isotropic super-resolution

We propose a three-objective light sheet microscopy geometry which, through a combination of skewed lattice light sheet excitation through two objectives and the computational fusion of images taken from two separate lens pairings, would allow for isotropic super-resolution in mesoscopic samples. We also show that simultaneous coherent excitation through two excitation objectives could further substantially increase resolution. Simulations demonstrate that our design could achieve a resolution of 120 nm for EGFP imaging while minimizing photodamage.Engineering and Physical Sciences Research Council (EPSRC) Sensor CDT (EP/L015889/1); MedImmune

Measuring multiple 17O–13C J-couplings in naphthalaldehydic acid: a combined solid state NMR and density functional theory approach

A combined multinuclear solid state NMR and gauge included projected augmented wave, density functional theory (GIPAW DFT) computational approach is evaluated to determine the four heteronuclear 1J(13C,17O) couplings in solid 17O enriched naphthalaldehydic acid. Direct multi-field 17O magic angle spinning (MAS), triple quantum MAS (3QMAS) and double rotation (DOR) experiments are initially utilised to evaluate the accuracy of the DFT approximations used in the calculation of the isotropic chemical shifts (diso), quadrupole coupling constants (CQ) and asymmetry (ZQ) parameters. These combined approaches give diso values of 313, 200 and 66 ppm for the carbonyl (CQO), ether (–O–) and hydroxyl (–OH) environments, respectively, with the corresponding measured quadrupole products (PQ) being 8.2, 9.0 and 10.6 MHz. The geometry optimised DFT structure derived using the CASTEP code gives firm agreement with the shifts observed for the ether (diso = 223, PQ = 9.4 MHz) and hydroxyl (diso = 62, PQ = 10.5 MHz) environments but the unoptimised experimental XRD structure has better agreement for the carbonyl group (diso = 320, PQ = 8.3 MHz). The determined diso and ZQ values are shown to be consistent with bond lengths closer to 1.222 Å (experimental length) rather than the geometry optimised length of 1.238 Å. The geometry optimised DFT 1J(13C,17O) coupling to the hydroxyl is calculated as 20 Hz and the couplings to the ether were calculated to be 37 (O–CQO) and 32 (O–C–OH) Hz. The scalar coupling parameters for the unoptimised experimental carbonyl group predict a 1J(13C,17O) value of 28 Hz, whilst optimisation gives a value of 27 Hz. These calculated 1J(13C,17O) couplings, together with estimations of the probability of each O environment being isotopically labelled (determined by electrospray ionisation mass spectrometry) and the measured refocussable transverse dephasing (T2 0) behaviour, are combined to simulate the experimental decay behaviour. Good agreement between the measured and calculated decay behaviour is observed

Measuring compensation in neurodegeneration using MRI

PURPOSE OF REVIEW: Despite signs of cortical and subcortical loss, patients with prodromal and early-stage neurodegenerative disease are able to perform at a level comparable to the normal population. It is presumed that the onset of compensatory processes, that is changes in brain activation within a function-specific network or in the recruitment of a region outside of the task-network, underlies this maintenance of normal performance. However, in most studies to date, increased brain activity is not correlated with indices of both disease and performance and what appears to be compensation could simply be a symptom of neurodegeneration. RECENT FINDINGS: MRI studies have explored compensation in neurodegenerative disease, claiming that compensation is evident across a number of disorders, including Alzheimer's and Parkinson's disease, but generally always in early stages; after this point, compensation is generally no longer able to operate under the severe burden of disease. However, none of these studies explicitly adopted a particular model of compensation. Thus, we also discuss our recent attempts to operationalize compensation for empirical testing. SUMMARY: There is clear evidence of compensatory processes in the early stages of neurodegenerative disease. However, for a more complete understanding, this requires more explicit empirical modelling

Multimodal characterization of the visual network in Huntington's disease gene carriers

Objective A sensorimotor network structural phenotype predicted motor task performance in a previous study in Huntington’s disease (HD) gene carriers. We investigated in the visual network whether structure – function – behaviour relationship patterns, and the effects of the HD mutation, extended beyond the sensorimotor network. Methods We used multimodal visual network MRI structural measures (cortical thickness and white matter connectivity), plus visual evoked potentials and task performance (Map Search; Symbol Digit Modalities Test) in healthy controls and HD gene carriers. Results Using principal component (PC) analysis, we identified a structure – function relationship common to both groups. PC scores differed between groups indicating white matter disorganization (higher RD, lower FA) and slower, and more disperse, VEP signal transmission (higher VEP P100 latency and lower VEP P100 amplitude) in HD than controls while task performance was similar. Conclusions HD may be associated with reduced white matter organization and efficient visual network function but normal task performance. Significance These findings indicate that structure – function relationships in the visual network, and the effects of the HD mutation, share some commonalities with those in the sensorimotor network. However, implications for task performance differ between the two networks suggesting the influence of network specific factors

β2-adrenergic signalling promotes cell migration by upregulating expression of the metastasis-associated molecule LYPD3

Metastasis is associated with poor prognosis in breast cancer. Although some studies suggest beta-blockers increase survival by delaying metastasis, others have been discordant. This study provides both insights into the anomalous findings and identifies potential biomarkers that may be treatment targets. Cell line models of basal-type and oestrogen receptor-positive breast cancer were profiled for basal levels of adrenoceptor gene/protein expression, and β2-adrenoceptor mediated cell behaviour including migration, invasion, adhesion, and survival in response to adrenoceptor agonist/antagonist treatment. Protein profiling and histology identified biomarkers and drug targets. Baseline levels of adrenoceptor gene expression are higher in basal-type rather than oestrogen receptor-positive cancer cells. Norepinephrine (NE) treatment increased invasive capacity in all cell lines but did not increase proliferation/survival. Protein profiling revealed the upregulation of the pro-metastatic gene Ly6/PLAUR Domain-Containing Protein 3 (LYPD3) in norepinephrine-treated MDA-MB-468 cells. Histology confirmed selective LYPD3 expression in primary and metastatic breast tumour samples. These findings demonstrate that basal-type cancer cells show a more aggressive adrenoceptor-β2-activated phenotype in the resting and stimulated state, which is attenuated by adrenoceptor-β2 inhibition. This study also highlights the first association between ADRβ2 signalling and LYPD3; its knockdown significantly reduced the basal and norepinephrine-induced activity of MCF-7 cells in vitro. The regulation of ADRβ2 signalling by LYPD3 and its metastasis promoting activities, reveal LYPD3 as a promising therapeutic target in the treatment of breast and other cancers

‘Do i care?’ young adults' recalled experiences of early adolescent overweight and obesity: a qualitative study

&lt;p&gt;Objective: Individual behaviour change to reduce obesity requires awareness of, and concern about, weight. This paper therefore describes how young adults, known to have been overweight or obese during early adolescence, recalled early adolescent weight-related awareness and concerns. Associations between recalled concerns and weight-, health- and peer-related survey responses collected during adolescence are also examined.&lt;/p&gt; &lt;p&gt;Design: Qualitative semi-structured interviews with young adults; data compared with responses to self-report questionnaires obtained in adolescence.&lt;/p&gt; &lt;p&gt;Participants: A total of 35 participants, purposively sub-sampled at age 24 from a longitudinal study of a school year cohort, previously surveyed at ages 11, 13 and 15. Physical measures during previous surveys allowed identification of participants with a body mass index (BMI) indicative of overweight or obesity (based on British 1990 growth reference) during early adolescence. Overall, 26 had been obese, of whom 11 had BMI99.6th centile, whereas 9 had been overweight (BMI=95th–97.9th centile).&lt;/p&gt; &lt;p&gt;Measures: Qualitative interview responses describing teenage life, with prompts for school-, social- and health-related concerns. Early adolescent self-report questionnaire data on weight-worries, self-esteem, friends and victimisation (closed questions).&lt;/p&gt; &lt;p&gt;Results: Most, but not all recalled having been aware of their overweight. None referred to themselves as having been obese. None recalled weight-related health worries. Recollection of early adolescent obesity varied from major concerns impacting on much of an individual's life to almost no concern, with little relation to actual severity of overweight. Recalled concerns were not clearly patterned by gender, but young adult males recalling concerns had previously reported more worries about weight, lower self-esteem, fewer friends and more victimisation in early adolescence; no such pattern was seen among females. Conclusion: The popular image of the unhappy overweight teenager was not borne out. Many obese adolescents, although well aware of their overweight recalled neither major dissatisfaction nor concern. Weight-reduction behaviours are unlikely in such circumstances.&lt;/p&gt

Gene expression and matrix turnover in overused and damaged tendons

Chronic, painful conditions affecting tendons, frequently known as tendinopathy, are very common types of sporting injury. The tendon extracellular matrix is substantially altered in tendinopathy, and these changes are thought to precede and underlie the clinical condition. The tendon cell response to repeated minor injuries or “overuse” is thought to be a major factor in the development of tendinopathy. Changes in matrix turnover may also be effected by the cellular response to physical load, altering the balance of matrix turnover and changing the structure and composition of the tendon. Matrix turnover is relatively high in tendons exposed to high mechanical demands, such as the supraspinatus and Achilles, and this is thought to represent either a repair or tissue maintenance function. Metalloproteinases are a large family of enzymes capable of degrading all of the tendon matrix components, and these are thought to play a major role in the degradation of matrix during development, adaptation and repair. It is proposed that some metalloproteinase enzymes are required for the health of the tendon, and others may be damaging, leading to degeneration of the tissue. Further research is required to investigate how these enzyme activities are regulated in tendon and altered in tendinopathy. A profile of all the metalloproteinases expressed and active in healthy and degenerate tendon is required and may lead to the development of new drug therapies for these common and debilitating sports injuries

Compensation in Preclinical Huntington's Disease: Evidence From the Track-On HD Study

BACKGROUND: Cognitive and motor task performance in premanifest Huntington's disease (HD) gene-carriers is often within normal ranges prior to clinical diagnosis, despite loss of brain volume in regions involved in these tasks. This indicates ongoing compensation, with the brain maintaining function in the presence of neuronal loss. However, thus far, compensatory processes in HD have not been modeled explicitly. Using a new model, which incorporates individual variability related to structural change and behavior, we sought to identify functional correlates of compensation in premanifest-HD gene-carriers. METHODS: We investigated the modulatory effects of regional brain atrophy, indexed by structural measures of disease load, on the relationship between performance and brain activity (or connectivity) using task-based and resting-state functional MRI. FINDINGS: Consistent with compensation, as atrophy increased performance-related activity increased in the right parietal cortex during a working memory task. Similarly, increased functional coupling between the right dorsolateral prefrontal cortex and a left hemisphere network in the resting-state predicted better cognitive performance as atrophy increased. Such patterns were not detectable for the left hemisphere or for motor tasks. INTERPRETATION: Our findings provide evidence for active compensatory processes in premanifest-HD for cognitive demands and suggest a higher vulnerability of the left hemisphere to the effects of regional atrophy