Human impacts and Anthropocene environmental change at Lake Kutubu, a Ramsar wetland in Papua New Guinea.

The impacts of human-induced environmental change that characterize the Anthropocene are not felt equally across the globe. In the tropics, the potential for the sudden collapse of ecosystems in response to multiple interacting pressures has been of increasing concern in ecological and conservation research. The tropical ecosystems of Papua New Guinea are areas of diverse rainforest flora and fauna, inhabited by human populations that are equally diverse, both culturally and linguistically. These people and the ecosystems they rely on are being put under increasing pressure from mineral resource extraction, population growth, land clearing, invasive species, and novel pollutants. This study details the last ∼90 y of impacts on ecosystem dynamics in one of the most biologically diverse, yet poorly understood, tropical wetland ecosystems of the region. The lake is listed as a Ramsar wetland of international importance, yet, since initial European contact in the 1930s and the opening of mineral resource extraction facilities in the 1990s, there has been a dramatic increase in deforestation and an influx of people to the area. Using multiproxy paleoenvironmental records from lake sediments, we show how these anthropogenic impacts have transformed Lake Kutubu. The recent collapse of algal communities represents an ecological tipping point that is likely to have ongoing repercussions for this important wetland's ecosystems. We argue that the incorporation of an adequate historical perspective into models for wetland management and conservation is critical in understanding how to mitigate the impacts of ecological catastrophes such as biodiversity loss.

Concentration-Dependent Solar Thermochemical CO2/H2O Splitting Performance by Vanadia-Ceria Multiphase Metal Oxide Systems.

The effects of V and Ce concentrations (each varying in the 0-100% range) in vanadia-ceria multiphase systems are investigated for synthesis gas production via thermochemical redox cycles of CO2 and H2O splitting coupled to methane partial oxidation reactions. The oxidation of prepared oxygen carriers is performed by separate and sequential CO2 and H2O splitting reactions. Structural and chemical analyses of the mixed-metal oxides revealed important information about the Ce and V interactions affecting their crystal phases and redox characteristics. Pure CeO2 and pure V2O5 are found to offer the lowest and highest oxygen exchange capacities and syngas production performance, respectively. The mixed-oxide systems provide a balanced performance: their oxygen exchange capacity is up to 5 times higher than that of pure CeO2 while decreasing the extent of methane cracking. The addition of 25% V to CeO2 results in an optimum mixture of CeO2 and CeVO4 for enhanced CO2 and H2O splitting. At higher V concentrations, cyclic carbide formation and oxidation result in a syngas yield higher than that for pure CeO2.

Assessment of metal concentrations in the SOD1G93A mouse model of amyotrophic lateral sclerosis and its potential role in muscular denervation, with particular focus on muscle tissue.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is among the most common of the motor neuron diseases, and arguably the most devastating. During the course of this fatal neurodegenerative disorder, motor neurons undergo progressive degeneration. The currently best-understood animal models of ALS are based on the over-expression of mutant isoforms of Cu/Zn superoxide dismutase 1 (SOD1); these indicate that there is a perturbation in metal homeostasis with disease progression. Copper metabolism in particular is affected in the central nervous system (CNS) and muscle tissue. METHODS: This present study assessed previously published and newly gathered concentrations of transition metals (Cu, Zn, Fe and Se) in CNS (brain and spinal cord) and non-CNS (liver, intestine, heart and muscle) tissues from transgenic mice over-expressing the G93A mutant SOD1 isoform (SOD1G93A), transgenic mice over-expressing wildtype SOD1 (SOD1WT) and non-transgenic controls. RESULTS: Cu accumulates in non-CNS tissues at pre-symptomatic stages in SOD1G93A tissues. This accumulation represents a potentially pathological feature that cannot solely be explained by the over-expression of mSOD1. As a result of the lack of Cu uptake into the CNS there may be a deficiency of Cu for the over-expressed mutant SOD1 in these tissues. Elevated Cu concentrations in muscle tissue also preceded the onset of symptoms and were found to be pathological and not be the result of SOD1 over-expression. CONCLUSIONS: It is hypothesized that the observed Cu accumulations may represent a pathologic feature of ALS, which may actively contribute to axonal retraction leading to muscular denervation, and possibly significantly contributing to disease pathology. Therefore, it is proposed that the toxic-gain-of-function and dying-back hypotheses to explain the molecular drivers of ALS may not be separate, individual processes; rather our data suggests that they are parallel processes.

Longitudinal assessment of metal concentrations and copper isotope ratios in the G93A SOD1 mouse model of amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a motor neuron disease, which involves progressive motor neuron degeneration in the central nervous system (CNS). The G93A SOD1 mouse model simulates one of the most common causes of familial ALS through the overexpression of a mutated form of the human gene encoding copper/zinc superoxide dismutase (SOD1). Transition metals, particularly Cu and Zn, have been shown to behave abnormally in the disease context and have been hypothesized to contribute to and potentially trigger the disease. In this study, concentrations of Cu, Zn and Fe, as well as Cu isotope ratios were assessed in keystone tissues of ALS, including the brain, spinal cord, muscle and whole blood, from transgenic mutant SOD1G93A mice and non-transgenic controls. While no consistent Cu isotope signal was found to be related to the disease state, concentrations of Cu, Zn and Fe were significantly elevated in muscle tissue of the transgenic mice, even at pre-symptomatic time points. In brain and muscle tissue, in both animal groups, a time-dependent Cu isotope signal was observed. We hypothesize that the early and significant elevation in metal concentration in muscle tissue from SOD1 transgenic mice could facilitate the development of ALS, without affecting the overall signal from well-buffered CNS tissues. Ageing may be recorded isotopically as a shift from a neonatal Cu pool as inherited from the mother, through dietary Cu and recycling processes.