CanopyShotNoise - An individual-based tree canopy modelling framework for projecting remote-sensing data and ecological sensitivity analysis

Very few spatially explicit tree models have so far been constructed with a view to project remote-sensing data directly. To fill this gap, we introduced the prototype of the CanopyShotNoise model, an individual-based model specifically designed for projecting airborne laser scanning (ALS) data. Given the nature of ALS data, the model focuses on the dynamics of individual-tree canopies in forest ecosystems, that is, spatial tree interaction and resulting growth, birth and death processes. In this study, CanopyShotNoise was used to analyse the long-term effects of the processes crown plasticity (C) and superorganism formation (S) on spatial tree canopy patterns that are likely to play an important role in ongoing climate change. We designed a replicated computer experiment involving the four scenarios C0S0, C1S0, C0S1 and C1S1 where 0 and 1 imply that the preceding process was switched off and on, respectively. We hypothesized that C and S are antagonistic processes, specifically that C would lead to increasing regularity of tree locations and S would result in clustering. Our simulation results confirmed that in the long run intertree distances decreased and canopy gap size increased when superorganisms were encouraged to form. At the same time, the overlap and packing of tree crowns increased. The long-term effect of crown plasticity increased the regularity of tree locations; however, this effect was much weaker than that of superorganism formation. As a result, gap patterns remained more or less unaffected by crown plasticity. In scenario C1S1, both processes interestingly interacted in such a way that crown plasticity even increased the effect of superorganism formation. Our simulation results are likely to prove helpful in recognizing patterns of facilitation with ongoing climate change

Remote Sensing Technologies for Assessing Climate-Smart Criteria in Mountain Forests

Peer reviewe

Developing a dual-wavelength full-waveform terrestrial laser scanner to characterise forest canopy structure

The development of a dual-wavelength full-waveform terrestrial laser scanner to measure the three-dimensional structure of forest canopies is described, and field measurements used to evaluate and test the instrument measurement characteristics. The Salford Advanced Laser Canopy Analyser (SALCA) measures the full-waveform of backscattered radiation at two laser wavelengths, one in the near-infrared (1063 nm) and one in the shortwave infrared (1545 nm). The instrument is field-portable and measures up to nine million waveforms, at the two wavelengths, across a complete hemisphere above the instrument. SALCA was purpose-built to measure structural characteristics of forest canopies and this paper reports the first results of field-based data collection using the instrument. Characteristics of the waveforms, and waveform data processing are outlined, applications of dual wavelength measurements are evaluated, and field deployment of the instrument at a forest test site described. Preliminary instrument calibration results are presented and challenges in extracting useful information on forest structure are highlighted. Full-waveform multiple-wavelength terrestrial laser scanners are likely to provide more detailed and more accurate forest structural measurement in the future. This research demonstrates how SALCA provides a key step to develop, test and apply this new technology in a range of forest-related problems

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Waveform lidar over vegetation : An evaluation of inversion methods for estimating return energy

Full waveform lidar has a unique capability to characterise vegetation in more detail than any other practical method. The reflectance, calculated from the energy of lidar returns, is a key parameter for a wide range of applications and so it is vital to extract it accurately. Fifteen separate methods have been proposed to extract return energy (the amount of light backscattered from a target), ranging from simple to mathematically complex, but the relative accuracies have not yet been assessed. This paper uses a simulator to compare all methods over a wide range of targets and lidar system parameters. For hard targets the simplest methods (windowed sum, peak and quadratic) gave the most consistent estimates. They did not have high accuracies, but low standard deviations show that they could be calibrated to give accurate energy. This may be why some commercial lidar developers use them, where the primary interest is in surveying solid objects. However, simulations showed that these methods are not appropriate over vegetation. The widely used Gaussian fitting performed well over hard targets (0.24% root mean square error, RMSE), as did the sum and spline methods (0.30% RMSE). Over vegetation, for large footprint (15 m) systems, Gaussian fitting performed the best (12.2% RMSE) followed closely by the sum and spline (both 12.7% RMSE). For smaller footprints (33 cm and 1 cm) over vegetation, the relative accuracies were reversed (0.56% RMSE for the sum and spline and 1.37% for Gaussian fitting). Gaussian fitting required heavy smoothing (convolution with an 8 m Gaussian) whereas none was needed for the sum and spline. These simpler methods were also more robust to noise and far less computationally expensive than Gaussian fitting. Therefore it was concluded that the sum and spline were the most accurate for extracting return energy from waveform lidar over vegetation, except for large footprint (15 m), where Gaussian fitting was slightly more accurate. These results suggest that small footprint (≪ 15 m) lidar systems that use Gaussian fitting or proprietary algorithms may report inaccurate energies, and thus reflectances, over vegetation. In addition the effect of system pulse length, sampling interval and noise on accuracy for different targets was assessed, which has implications for sensor design

Genome-wide associations for birth weight and correlations with adult disease

Birth weight (BW) is influenced by both foetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease1. These lifecourse associations have often been attributed to the impact of an adverse early life environment. We performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where foetal genotype was associated with BW (P <5x10-8). Overall, ˜15% of variance in BW could be captured by assays of foetal genetic variation. Using genetic association alone, we found strong inverse genetic correlations between BW and systolic blood pressure (rg-0.22, P =5.5x10-13), T2D (rg-0.27, P =1.1x10-6) and coronary artery disease (rg-0.30, P =6.5x10-9) and, in large cohort data sets, demonstrated that genetic factors were the major contributor to the negative covariance between BW and future cardiometabolic risk. Pathway analyses indicated that the protein products of genes within BW-associated regions were enriched for diverse processes including insulin signalling, glucose homeostasis, glycogen biosynthesis and chromatin remodelling. There was also enrichment of associations with BW in known imprinted regions (P =1.9x10-4). We have demonstrated that lifecourse associations between early growth phenotypes and adult cardiometabolic disease are in part the result of shared genetic effects and have highlighted some of the pathways through which these causal genetic effects are mediated

Genome-wide associations for birth weight and correlations with adult disease

Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW ($\textit{P}$  < 5 × 10$^{-8}$). Overall, approximately 15% of variance in BW was captured by assays of fetal genetic variation. Using genetic association alone, we found strong inverse genetic correlations between BW and systolic blood pressure ($\textit{R}$ $_{g}$ = -0.22, $\textit{P}$  = 5.5 × 10$^{-13}$), T2D ($\textit{R}$ $_{g}$ = -0.27, $\textit{P}$  = 1.1 × 10$^{-6}$) and coronary artery disease ($\textit{R}$ $_{g}$ = -0.30, $\textit{P}$  = 6.5 × 10$^{-9}$). In addition, using large -cohort datasets, we demonstrated that genetic factors were the major contributor to the negative covariance between BW and future cardiometabolic risk. Pathway analyses indicated that the protein products of genes within BW-associated regions were enriched for diverse processes including insulin signalling, glucose homeostasis, glycogen biosynthesis and chromatin remodelling. There was also enrichment of associations with BW in known imprinted regions ($\textit{P}$ = 1.9 × 10$^{-4}$). We demonstrate that life-course associations between early growth phenotypes and adult cardiometabolic disease are in part the result of shared genetic effects and identify some of the pathways through which these causal genetic effects are mediated.For a full list of the funders pelase visit the publisher's website and look at the supplemetary material provided. Some of the funders are: British Heart Foundation, Cancer Research UK, Medical Research Council, National Institutes of Health, Royal Society and Wellcome Trust

Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors.

Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.The Fenland Study is funded by the Medical Research Council (MC_U106179471) and Wellcome Trust