An ethical perspective of the use of Augmented Reality in the tourism industry

This volume provides the latest outcomes of augmented reality (AR) and virtual reality (VR) research conducted in various industries

Long-term warming amplifies shifts in the carbon cycle of experimental ponds

This is the author accepted manuscript. The final version is available from Nature Research via the DOI in this record.Lakes and ponds cover only about 4% of the Earth’s non-glaciated surface1, yet they represent disproportionately large sources of methane and carbon dioxide2,3,4. Indeed, very small ponds (for example, <0.001 km2) may account for approximately 40% of all CH4 emissions from inland waters5. Understanding how greenhouse gas emissions from aquatic ecosystems will respond to global warming is therefore vital for forecasting biosphere–carbon cycle feedbacks. Here, we present findings on the long-term effects of warming on the fluxes of GHGs and rates of ecosystem metabolism in experimental ponds. We show that shifts in CH4 and CO2 fluxes, and rates of gross primary production and ecosystem respiration, observed in the first year became amplified over seven years of warming. The capacity to absorb CO2 was nearly halved after seven years of warmer conditions. The phenology of greenhouse gas fluxes was also altered, with CO2 drawdown and CH4 emissions peaking one month earlier in the warmed treatments. These findings show that warming can fundamentally alter the carbon balance of small ponds over a number of years, reducing their capacity to sequester CO2 and increasing emissions of CH4; such positive feedbacks could ultimately accelerate climate change.This study was supported by a grant from the Natural Environment Research Council of the UK (NE/H022511/1) awarded to M.T., G.Y.-D. and G.W

Pharmacokinetic and Pharmacodynamic Modeling of a Monoclonal Antibody Antagonist of Glucagon Receptor in Male ob/ob Mice

Elevated basal concentrations of glucagon and reduced postprandial glucagon suppression are partly responsible for the increased hepatic glucose production seen in type 2 diabetic patients. Recently, it was demonstrated that an antagonistic human monoclonal antibody (mAb) blocking glucagon receptor (GCGR) has profound glucose-lowering effects in various animal models. To further understand the effects on glucose homeostasis mediated by such an antibody, a pharmacokinetic-pharmacodynamic (PK-PD) study was conducted in a diabetic ob/ob mouse model. Four groups of ob/ob mice were randomized to receive single intraperitoneal administration of placebo, 0.6, 1, or 3 mg/kg of mAb GCGR, a fully human mAb against GCGR. The concentration-time data were used for noncompartmental and compartmental analysis. A semi-mechanistic PK-PD model incorporating the glucose-glucagon inter-regulation and the hypothesized inhibitory effect of mAb GCGR on GCGR signaling pathway via competitive inhibition was included to describe the disposition of glucose and glucagon over time. The pharmacokinetics of mAb GCGR was well characterized by a two-compartment model with parallel linear and nonlinear saturable eliminations. Single injection of mAb GCGR caused a rapid glucose-lowering effect with blood glucose concentrations returning to baseline by 4 to 18 days with increasing dose from 0.6 to 3 mg/kg. Elevation of glucagon concentrations was also observed in a dose-dependent manner. The results illustrated that the feedback relationship between glucose and glucagon in the presence of mAb GCGR could be quantitatively described by the developed model. The model may provide additional understanding in the underlying mechanism of GCGR antagonism by mAb