Mapping arctic tundra vegetation communities using field spectroscopy and multispectral satellite data in North Alaska, USA

The Arctic is currently undergoing intense changes in climate; vegetation composition and productivity are expected to respond to such changes. To understand the impacts of climate change on the function of Arctic tundra ecosystems within the global carbon cycle, it is crucial to improve the understanding of vegetation distribution and heterogeneity at multiple scales. Information detailing the fine-scale spatial distribution of tundra communities provided by high resolution vegetation mapping, is needed to understand the relative contributions of and relationships between single vegetation community measurements of greenhouse gas fluxes (e.g., ~1 m chamber flux) and those encompassing multiple vegetation communities (e.g., ~300 m eddy covariance measurements). The objectives of this study were: (1) to determine whether dominant Arctic tundra vegetation communities found in different locations are spectrally distinct and distinguishable using field spectroscopy methods; and (2) to test which combination of raw reflectance and vegetation indices retrieved from field and satellite data resulted in accurate vegetation maps and whether these were transferable across locations to develop a systematic method to map dominant vegetation communities within larger eddy covariance tower footprints distributed along a 300 km transect in northern Alaska. We showed vegetation community separability primarily in the 450-510 nm, 630-690 nm and 705-745 nm regions of the spectrum with the field spectroscopy data. This is line with the different traits of these arctic tundra communities, with the drier, often non-vascular plant dominated communities having much higher reflectance in the 450-510 nm and 630-690 nm regions due to the lack of photosynthetic material, whereas the low reflectance values of the vascular plant dominated communities highlight the strong light absorption found here. High classification accuracies of 92% to 96% were achieved using linear discriminant analysis with raw and rescaled spectroscopy reflectance data and derived vegetation indices. However, lower classification accuracies (~70%) resulted when using the coarser 2.0 m WorldView-2 data inputs. The results from this study suggest that tundra vegetation communities are separable using plot-level spectroscopy with hand-held sensors. These results also show that tundra vegetation mapping can be scaled from the plot level (<1 m) to patch level (<500 m) using spectroscopy data rescaled to match the wavebands of the multispectral satellite remote sensing. We find that developing a consistent method for classification of vegetation communities across the flux tower sites is a challenging process, given thespatial variability in vegetation communities and the need for detailed vegetation survey data for training and validating classification algorithms. This study highlights the benefits of using fine-scale field spectroscopy measurements to obtain tundra vegetation classifications for landscape analyses and use in carbon flux scaling studies. Improved understanding of tundra vegetation distributions will also provide necessary insight into the ecological processes driving plant community assemblages in Arctic environments

Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: A systematic analysis for the Global Burden of Disease Study 2015

Background: The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. Methods: We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). Findings: Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6–58·8) of global deaths and 41·2% (39·8–42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa. Interpretation: Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden. Funding: Bill & Melinda Gates Foundation

Setting shrinkage strains of chemical-cured glass ionomer-based dental restorative materials

Shrinkage strains are exhibited by the current formulations of chemical-cured dental restorative systems. In resin-modified glass ionomer systems, these have been linked to filler contents, types and quantity of monomer. Post-gelation rigid contraction that follows onset of cure leading to marginal defects is a clinically significant factor, although flow is noted to compensate for shrinkage effects during pre-gelation phase. The bonded-disk technique was employed to study the shrinkage strains of chemical-cured and light-activated glass polyalkenoate-based cements at two clinical temperatures of 37EC and 60EC over a period of 2 hours. Magnitudes of shrinkage strains obtained were subjected to one-way ANOVA and Schefe's 0.5 significant level statistical analysis. The time-dependent shrinkage strain data characteristic of the materials indicated a linear initial rigid and rapid contraction, which is appropriately represented by the Kohlrausch-Williams-Watts stretched exponential decay curve. The kinetics of shrinkage was expressed by the overall time constant and the initial contraction strains at 30 s, following the onset of cure. Data obtained after 15 minutes up to 2 hours indicated high contraction strains at 60EC compared to that at the intra-oral temperature, 37EC. There is a relatively slow development of contraction strains in glass ionomer-based systems compared to resin-based ones. This is, however, a positive quality for the glassy materials in their use as marginal seals. Nevertheless, contraction strains in dental restorative systems with their destructive shrinkage stresses remain unresolved. JOURNAL OF THE GHANA SCIENCE ASSOCIATION Volume 2 No. 3 (2000) pp. 103-11

Statin therapy improves brachial artery endothelial function in nephrotic syndrome

Background: Patients with nephrotic syndrome have impaired endothelial function probably related to dyslipidemia. This study evaluated the effects of statin therapy on dyslipidemia and endothelial function in patients with nephrotic syndrome. Methods: A sequential, open-label study of the effects of statins on endothelial dysfunction in 10 nephrotic patients treated with an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II (Ang II) receptor antagonist. Endothelial function was assessed at baseline, after 12 weeks of treatment with statins, and after an 8-week washout. Brachial artery endothelial function was measured as post-ischemic flow-mediated dilation (FMD) using ultrasonography. Endothelium-independent, glyceryl trinitrate-mediated vasodilation (GTNMD) also was measured. Results: Serum lipids were significantly lower following statin: total cholesterol mean 8.2 ± 0.4 (standard error) mmol/L versus 5.2 ± 0.3 mmol/L, triglycerides 2.6 ± 0.4 mmol/L versus 1.6 ± 0.2 mmol/L, non-HDL-cholesterol 6.7 ± 0.4 mmol/L versus 3.7 ± 0.2 mmol/L (all P < 0.001). There was a trend to an increase in serum albumin (31.0 ± 1.3 g/L vs. 33.8 ± 1.5 g/L; P = 0.078) and FMD improved significantly following treatment (3.7 ± 1.1% vs. 7.0 ± 0.8%, P < 0.01). After washout, FMD deteriorated significantly to 3.5 ± 1.4% (P < 0.05) versus week 12 FMD. GTNMD was unchanged. In multivariate regression, reduction in non-high-density lipoprotein (HDL)-cholesterol (β - 0.736, P = 0.027) and increase in serum albumin (β 0.723, P = 0.028), but not the on-treatment level of non-HDL-cholesterol, were significant independent predictors of improvement in FMD after adjusting for change in resting brachial artery diameter. Changes in serum lipoprotein and albumin concentrations off treatment were not associated with deterioration in FMD. Conclusion: Statin therapy significantly improves dyslipidemia and brachial artery endothelial function in patients with nephrotic syndrome. Improvement in brachial artery endothelial function may be in part related to a non-lipid effect of statins. The findings also suggest a role for dyslipidemia in endothelial dysfunction and the risk for cardiovascular disease in nephrotic syndrome

Hypercoagulability in chronic kidney disease is associated with coagulation activation but not endothelial function

Introduction Patients with chronic kidney disease exhibit features of a hypercoagulable state and have endothelial dysfunction, which may contribute to their increased cardiovascular risk. We examined the relationship between coagulation activation and vascular function in patients with chronic kidney disease. Materials and Methods We measured parameters of the tissue factor pathway of blood coagulation (tissue factor, factor VIIc and factor X); natural inhibitors (tissue factor pathway inhibitor, protein C, free and total protein S, antithrombin III) and markers of coagulation activation (thrombin-antithrombin complexes, prothrombin fragment 1 + 2) in 66 stage 4&5 chronic kidney disease patients and 36 healthy controls. Their relationship with markers of vascular function (flow mediated dilatation, soluble E-selectin and thrombomodulin) and a mediator of inflammation (interleukin-6) was determined. Results Up-regulation of the tissue factor pathway (increased tissue factor and factor VIIc), increased prothrombin fragment 1 + 2 and significant reductions in antithrombin III and the ratio of free protein S: total protein S were found in patients compared to healthy controls. Increased tissue factor antigen was significantly and independently correlated with creatinine and interleukin-6 (P < 0.001). Factor X and antithrombin III were both reduced in chronic kidney disease and correlated (r = 0.58; P < 0.001). Changes in coagulation and anti-coagulation were independent of all measures of endothelial function. Conclusions Significant activation of the TF pathway of coagulation and depletion or reduction of some natural anticoagulants in chronic kidney disease was correlated with the degree of renal dysfunction, but not correlated with the abnormalities of vascular function. These data are consistent with a hypercoagulable state in chronic kidney disease that may be independent of endothelial based regulation but associated with an inflammatory state

Insulin resistance, dyslipidaemia, inflammation and endothelial function in nephrotic syndrome

Background. Nephrotic syndrome (NS) is associated with an increased risk of cardiovascular disease (CVD). We have shown previously that endothelial function, measured by post‐ischaemic flow‐mediated dilatation (FMD) of the brachial artery, is impaired in NS. In this study our aim was to assess the potential roles of insulin resistance, plasma non‐esterified fatty acids (NEFAs) and inflammation in endothelial dysfunction in NS patients. Methods. FMD was compared between NS patients (n=19) and controls (CS, n=19). Plasma glucose, insulin and NEFAs were measured. Insulin resistance was calculated using the Homeostasis Model Assessment (HOMA) score. C‐reactive protein (CRP), interleukin‐6 (IL‐6), tumour necrosis factor α (TNFα) and fibrinogen were measured as markers of inflammation. Results. FMD was significantly lower in the NS group (mean±standard error, NS 5.1±0.7%, CS 7.3±0.7%, P=0.02). Fasting insulin (NS 12.5±1.5 mU/l, CS 6.8±0.7 mU/l, P<0.01), fasting glucose (NS 5.3±0.2, CS 4.8±0.1, P=0.02) and the HOMA score (NS 3.0±0.4, CS 1.5±0.2, P=0.001) were significantly higher in NS. These differences persisted after adjusting for waist circumference. Of the inflammatory markers, only fibrinogen (P<0.01) and IL‐6 (P=0.01) were significantly increased in NS. Despite significantly lower plasma NEFAs in NS, the NEFA:albumin ratio showed a non‐significant trend to higher levels in NS (NS 10.7±0.1 µmol/g, CS 8.7±0.1 µmol/g, P=0.06). Within the NS group, multivariate backward regression analysis showed that NEFAs (P<0.01) and low‐density lipoprotein (LDL) cholesterol (P=0.05) were significant negative independent predictors of FMD. Conclusion. Endothelial function in NS is inversely correlated with plasma concentrations of NEFAs and LDL cholesterol. Dyslipoproteinaemia and NEFAs probably contribute to the increased risk of CVD seen in NS. We also postulate that in NS, hypoalbuminaemia increases the delivery of NEFAs to endothelial cells thereby impairing the synthesis and release of nitric oxide

Vascular function of the peripheral circulation in patients with nephrosis

Background. Nephrotic syndrome is associated with abnormal lipoprotein metabolism and increased risk of coronary heart disease. Endothelial dysfunction, an early phase of atherogenesis that manifests as impaired flow-mediated dilation (FMD) of the peripheral circulation, may link these associations. Methods. We examined endothelial function of the brachial artery and forearm resistance arteries in 15 patients with nephrosis (NP), 15 patients with primary hyperlipidemia (HL) alone, and 15 normolipidemic, nonproteinuric subjects (NC) matched for age, sex, and weight. The NP and HL groups had similar serum cholesterol and triglyceride concentrations. Postischemic FMD (endothelium-dependent) and glyceryl trinitrate-mediated dilation (GTNMD; endothelium-independent) of the brachial artery were studied using ultrasonography and computerized edge detection software. Postischemic forearm blood flow was also measured using plethysmography. Results. Postischemic FMD of the brachial artery was significantly lower in the NP and HL groups compared with NC group (mean ± SE): NP 4.91 ± 0.8%, HL 4.53 ± 0.6%, NC 8.45 ± 0.5% (P < 0.001). There were no significant differences among the groups in baseline diameter and GTNMD of the brachial artery, nor in maximal forearm blood flow and flow debt repayment of the forearm microcirculation. Significant differences in FMD among the groups were principally related to differences in serum low-density lipoprotein cholesterol. Conclusions. Patients with NP have abnormal endothelium-dependent but preserved endothelium-independent dilation of the brachial artery following an ischemic stimulus. Postischemic forearm microcirculatory function is unimpaired. Dyslipoproteinemia is probably the principal cause of endothelial dysfunction of conduit arteries in patients with NP and the basis for their increased risk of cardiovascular disease

The cost-effectiveness of coronary calcium score-guided statin therapy initiation for Australians with family histories of premature coronary artery disease

Objectives: To compare the cost-effectiveness of coronary artery calcium (CAC) score-guided statin therapy criteria and American College of Cardiology/American Heart Association (ACC/AHA) guidelines (10-year pooled cohort equation [PCE] risk ≥ 7.5%) with selection according to Australian guidelines (5-year absolute cardiovascular disease risk [ACVDR] ≥ 10%), for people with family histories of premature coronary artery disease. Study design, setting: Markov microsimulation state transition model based on data from the Coronary Artery calcium score: Use to Guide management of Hereditary Coronary Artery Disease (CAUGHT-CAD) trial and transition probabilities derived from published statin prescribing and adherence outcomes and clinical data. Participants: 1083 people with family histories of premature coronary artery disease but no symptomatic cardiovascular disease. Main outcome measures: Relative cost-effectiveness over fifteen years, from the perspective of the Australian health care system, compared with usual care (Australian guidelines), assessed as incremental cost-effectiveness ratios (ICERs), with a notional willingness-to-pay threshold of $50 000 per quality-adjusted lifeyear (QALY) gained. Results: Applying the Australian guidelines, 77 people were eligible for statin therapy (7.1$33 108 (CAC ≥ 100) and $53 028 per QALY gained (CAC > 0); the ACC/AHA guidelines approach (ICER,$909 241 per QALY gained) was not cost-effective. CAC score-guided selection (CAC ≥ 100) was cost-effective for people with 5-year ACVDR of at least 5%. Conclusion: Expanding the number of people at low to intermediate CVD risk eligible for statin therapy should selectively target people with subclinical atherosclerosis identified by CAC screening. This approach can be more cost-effective than simply lowering treatment eligibility thresholds.Prasanna Venkataraman, Amanda L Neil, Geoffrey K Mitchell, Tony Stanton, Stephen Nicholls, Andrew M Tonkin, Gerald F Watts, Thomas H Marwic