Contrasting changes in the abundance and diversity of North American bird assemblages from 1971 to 2010

This article is based upon work from COST Action ES1101 "Harmonising Global Biodiversity Modelling" (Harmbio), supported by COST (European Cooperation in Science and Technology).Although it is generally recognized that global biodiversity is declining, few studies have examined long-term changes in multiple biodiversity dimensions simultaneously. In this study we quantified and compared temporal changes in the abundance, taxonomic diversity, functional diversity and phylogenetic diversity of bird assemblages, using roadside monitoring data of the North American Breeding Bird Survey from 1971 to 2010. We calculated 12 abundance and diversity metrics based on five year average abundances of 519 species for each of 768 monitoring routes. We did this for all bird species together as well as for four sub-groups based on breeding habitat affinity (grassland, woodland, wetland and shrubland breeders). The majority of the biodiversity metrics increased or remained constant over the study period, whereas the overall abundance of birds showed a pronounced decrease, primarily driven by declines of the most abundant species. These results highlight how stable or even increasing metrics of taxonomic, functional or phylogenetic diversity may occur in parallel with substantial losses of individuals. We further found that patterns of change differed among the species sub-groups, with both abundance and diversity increasing for woodland birds and decreasing for grassland breeders. The contrasting changes between abundance and diversity and among the breeding habitat groups underscore the relevance of a multi-faceted approach to measuring biodiversity change. Our findings further stress the importance of monitoring the overall abundance of individuals in addition to metrics of taxonomic, functional or phylogenetic diversity, thus confirming the importance of population abundance as an essential biodiversity variable.Publisher PDFPeer reviewe

Heme oxygenase-1 derived carbon monoxide suppresses Aβ1-42 toxicity in astrocytes

Neurodegeneration in Alzheimer’s disease (AD) is extensively studied, and the involvement of astrocytes and other cell types in this process has been described. However, the responses of astrocytes themselves to amyloid β peptides ((Aβ; the widely accepted major toxic factor in AD) is less well understood. Here, we show that Aβ(1-42) is toxic to primary cultures of astrocytes. Toxicity does not involve disruption of astrocyte Ca2+ homeostasis, but instead occurs via formation of the toxic reactive species, peroxynitrite. Thus, Aβ(1-42) raises peroxynitrite levels in astrocytes, and Aβ(1-42) toxicity can be inhibited by antioxidants, or by inhibition of nitric oxide (NO) formation (reactive oxygen species (ROS) and NO combine to form peroxynitrite), or by a scavenger of peroxynitrite. Increased ROS levels observed following Aβ(1-42) application were derived from NADPH oxidase. Induction of heme oxygenase-1 (HO-1) protected astrocytes from Aβ(1-42) toxicity, and this protective effect was mimicked by application of the carbon monoxide (CO) releasing molecule CORM-2, suggesting HO-1 protection was attributable to its formation of CO. CO suppressed the rise of NADPH oxidase-derived ROS caused by Aβ(1-42). Under hypoxic conditions (0.5% O2, 48h) HO-1 was induced in astrocytes and Aβ(1-42) toxicity was significantly reduced, an effect which was reversed by the specific HO-1 inhibitor, QC-15. Our data suggest that Aβ(1-42) is toxic to astrocytes, but that induction of HO-1 affords protection against this toxicity due to formation of CO. HO-1 induction, or CO donors, would appear to present attractive possible approaches to provide protection of both neuronal and non-neuronal cell types from the degenerative effects of AD in the central nervous system

Heme oxygenase-1 derived carbon monoxide suppresses Aβ1-42 toxicity in astrocytes

Neurodegeneration in Alzheimer’s disease (AD) is extensively studied, and the involvement of astrocytes and other cell types in this process has been described. However, the responses of astrocytes themselves to amyloid peptides ((A; the widely accepted major toxic factor in AD) is less well understood. Here, we show that A(1-42) is toxic to primary cultures of astrocytes. Toxicity does not involve disruption of astrocyte Ca2+ homeostasis, but instead occurs via formation of the toxic reactive species, peroxynitrite. Thus, A(1-42) raises peroxynitrite levels in astrocytes, and A(1-42) toxicity can be inhibited by antioxidants, or by inhibition of nitric oxide (NO) formation (reactive oxygen species (ROS) and NO combine to form peroxynitrite), or by a scavenger of peroxynitrite. Increased ROS levels observed following A(1-42) application were derived from NADPH oxidase. Induction of heme oxygenase-1 (HO-1) protected astrocytes from A(1-42) toxicity, and this protective effect was mimicked by application of the carbon monoxide (CO) releasing molecule CORM-2, suggesting HO-1 protection was attributable to its formation of CO. CO suppressed the rise of NADPH oxidase-derived ROS caused by A(1-42). Under hypoxic conditions (0.5% O2, 48h) HO-1 was induced in astrocytes and A(1-42) toxicity was significantly reduced, an effect which was reversed by the specific HO-1 inhibitor, QC-15. Our data suggest that A(1-42) is toxic to astrocytes, but that induction of HO-1 affords protection against this toxicity due to formation of CO. HO-1 induction, or CO donors, would appear to present attractive possible approaches to provide protection of both neuronal and non-neuronal cell types from the degenerative effects of AD in the central nervous system

Halide homogenization for low energy loss in 2-eV-bandgap perovskites and increased efficiency in all-perovskite triple-junction solar cells

Monolithic all-perovskite triple-junction solar cells have the potential to deliver power conversion efficiencies beyond those of state-of-art double-junction tandems and well beyond the detailed-balance limit for single junctions. Today, however, their performance is limited by large deficits in open-circuit voltage and unfulfilled potential in both short-circuit current density and fill factor in the wide-bandgap perovskite sub cell. Here we find that halide heterogeneity—present even immediately following materials synthesis—plays a key role in interfacial non-radiative recombination and collection efficiency losses under prolonged illumination for Br-rich perovskites. We find that a diammonium halide salt, propane-1,3-diammonium iodide, introduced during film fabrication, improves halide homogenization in Br-rich perovskites, leading to enhanced operating stability and a record open-circuit voltage of 1.44 V in an inverted (p–i–n) device; ~86% of the detailed-balance limit for a bandgap of 1.97 eV. The efficient wide-bandgap sub cell enables the fabrication of monolithic all-perovskite triple-junction solar cells with an open-circuit voltage of 3.33 V and a champion PCE of 25.1% (23.87% certified quasi-steady-state efficiency)

Assessing the suitability of diversity metrics to detect biodiversity change

This article is based upon work from COST Action ES1101 “Harmonising Global Biodiversity Modelling” (Harmbio), supported by COST (European Cooperation in Science and Technology)

Plasma Heme Oxygenase-1 Concentration in Relation to Impaired Glucose Regulation in a Non-Diabetic Chinese Population

Background: Our previous study has recently shown that plasma heme oxygenase-1 (HO-1), a stress-responsive protein, is elevated in individuals with type 2 diabetes. The current study aimed to examine the association between plasma HO-1 concentration and impaired glucose regulation (IGR) in non-diabetic individuals. Methods: We conducted a case-control study including a total of 865 subjects (262 IGR individuals and 603 healthy controls) in a Chinese population. Basic characteristics were collected by questionnaire and standardized anthropometric measurements. Plasma HO-1 concentration was determined by ELISA. Results: Plasma HO-1 concentration was significantly increased in IGR individuals compared with healthy controls (1.34 (0.81–2.29) ng/ml vs 0.98 (0.56–1.55) ng/ml, P,0.001). After adjustment for age, sex, and BMI, the ORs for IGR in the highest quartile of plasma HO-1 concentrations, compared with the lowest, was 3.42 (95 % CI 2.11–5.54; P for trend,0.001). The trend remained significant even after additional adjustment for smoking, alcohol drinking, hypertension, family history of diabetes, lipid profiles and C-reactive protein. In the receiver-operating characteristic curve analysis, addition of plasma HO-1 concentration to a model with known risk factors yielded significantly improved discriminative value for IGR (area under the curves 0.75 (95 % CI 0.71–0.78) vs. 0.72 (95 % CI 0.69–0.76); P for difference = 0.026)

Alzheimer's disease: new diagnostic and therapeutic tools

On March 19, 2008 a Symposium on Pathophysiology of Ageing and Age-Related diseases was held in Palermo, Italy. Here, the lectures of M. Racchi on History and future perspectives of Alzheimer Biomarkers and of G. Scapagnini on Cellular Stress Response and Brain Ageing are summarized. Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disease, which in Western society mainly accounts for clinica dementia. AD prevention is an important goal of ongoing research. Two objectives must be accomplished to make prevention feasible: i) individuals at high risk of AD need to be identified before the earliest symptoms become evident, by which time extensive neurodegeneration has already occurred and intervention to prevent the disease is likely to be less successful and ii) safe and effective interventions need to be developed that lead to a decrease in expression of this pathology. On the whole, data here reviewed strongly suggest that the measurement of conformationally altered p53 in blood cells has a high ability to discriminate AD cases from normal ageing, Parkinson's disease and other dementias. On the other hand, available data on the involvement of curcumin in restoring cellular homeostasis and rebalancing redox equilibrium, suggest that curcumin might be a useful adjunct in the treatment of neurodegenerative illnesses characterized by inflammation, such as AD

Lifestyle, efficiency and limits: modelling transport energy and emissions using a socio-technical approach

It is well-known that societal energy consumption and pollutant emissions from transport are influenced not only by technical efficiency, mode choice and the carbon/pollutant content of energy but also by lifestyle choices and socio-cultural factors. However, only a few attempts have been made to integrate all of these insights into systems models of future transport energy demand or even scenario analysis. This paper addresses this gap in research and practice by presenting the development and use of quantitative scenarios using an integrated transport-energy-environment systems model to explore four contrasting futures for Scotland that compare transport-related ‘lifestyle’ changes and socio-cultural factors against a transition pathway focussing on transport electrification and the phasing out of conventionally fuelled vehicles using a socio-technical approach. We found that radical demand and supply strategies can have important synergies and trade-offs between reducing life cycle greenhouse gas and air quality emissions. Lifestyle change alone can have a comparable and earlier effect on transport carbon and air quality emissions than a transition to EVs with no lifestyle change. Yet, the detailed modelling of four contrasting futures suggests that both strategies have limits to meeting legislated carbon budgets, which may only be achieved with a combined strategy of radical change in travel patterns, mode and vehicle choice, vehicle occupancy and on-road driving behaviour with high electrification and phasing out of conventional petrol and diesel road vehicles. The newfound urgency of ‘cleaning up our act’ since the Paris Agreement and Dieselgate scandal suggests that we cannot just wait for the ‘technology fix’

Internal fixation treatments for intertrochanteric fracture: A systematic review and meta-Analysis of randomized evidence

The relative effects of internal fixation strategies for intertrochanteric fracture after operation remain uncertain. We conducted a systematic review and meta-Analysis of randomized controlled trials (RCTs) to address this important issue. We searched PubMed, EMBASE and CENTRAL for RCTs that compared different internal fixation implants in patients with intertrochanteric fracture at 6-month follow-up or longer. We ultimately included 43 trials enrolling 6911 patients; most trials were small in sample sizes and events. Their risk of bias was generally unclear due to insufficient reporting. Because of these, no statistically significant differences were present from most of the comparisons across all the outcomes, and no definitive conclusions can be made. However, a number of trials compared two commonly used internal fixation strategies, gamma nail (GN) and sliding hip screw (SHS). There is good evidence suggesting that, compared to SHS, GN may increase the risk of cut out (OR = 1.87, 95% CI, 1.08 to 3.21), re-operation (OR = 1.61, 95% CI, 1.02 to 2.53), intra-operative (OR = 3.14, 95% CI, 1.34 to 7.35) and later fractures (OR = 3.67, 95% CI, 1.37 to 9.83). Future randomized trials or observational studies that are carefully designed and conducted are warranted to establish the effects of alternative internal fixation strategies for intertrochanteric fracture