31 research outputs found
Antarctic microbial communities are functionally redundant, adapted and resistant to short term temperature perturbations
Climate change has the potential to induce dramatic shifts in the biodiversity and functionality of soil
microorganisms in polar hyperarid ecosystems. In these depauperate soil ecosystems, microbial communities
are vital as they represent the dominant input sources of essential nutrients. However, the
effects of changing climate on extreme edaphic environments, such as the McMurdo Dry Valleys of
Antarctica, remain poorly understood. To better understand these effects, we constructed soil microcosms
and simulated temperature shifts over a 40-day period. Soil physicochemical analysis revealed low
levels of key nutrients, with mean organic carbon and nitrogen contents of <0.1% and 11.55 ppm,
respectively. We also applied 16S rRNA gene amplicon sequencing to determine taxonomic composition
and enzyme assays to measure in situ activity. Our data showed a prevalence of ubiquitous soil taxa
(Actinobacteria, Chloroflexi and Deinococcus-Thermus), with a smaller proportion of autotrophic phyla
(i.e. Cyanobacteria). None of the major phyla showed relative abundance changes in response to temperature.
We found very low extracellular enzyme activity levels across all samples and observed no
significant differences among temperature treatments. Functional predictions (using PICRUSt) revealed
the putative presence of key genes implicated in the cycling of carbon (ppc, rbcl) and nitrogen (nifH, nirK),
in stress response and in DNA repair throughout all treatments. Overall, our results suggest that shortterm
temperature fluctuations do not alter microbial biodiversity and functionality in Antarctic soils. This
study provides the first evidence that microbial communities within this edaphic extreme environment
may be functionally redundant, adapted and resistant to short term climatic perturbations.We are grateful to the National Research Foundation (NRF)
(Grant ID 100052 SZdS, 99320 TPM, 93074 for DAC), the South
African National Antarctic Programme (SANAP e Grant ID
SNA14070974748), and the University of Pretoria (Genomics
Research Institute and the Research Development Program) for
funding. We also thank the New Zealand Antarctic Research Institute
(NZARI) for funding and Antarctica New Zealand for field and
logistics support.http://www.elsevier.com/locate/soilbio2017-12-31hb2016Genetic
Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980�2015: a systematic analysis for the Global Burden of Disease Study 2015
Background Improving survival and extending the longevity of life for all populations requires timely, robust evidence on local mortality levels and trends. The Global Burden of Disease 2015 Study (GBD 2015) provides a comprehensive assessment of all-cause and cause-specific mortality for 249 causes in 195 countries and territories from 1980 to 2015. These results informed an in-depth investigation of observed and expected mortality patterns based on sociodemographic measures. Methods We estimated all-cause mortality by age, sex, geography, and year using an improved analytical approach originally developed for GBD 2013 and GBD 2010. Improvements included refinements to the estimation of child and adult mortality and corresponding uncertainty, parameter selection for under-5 mortality synthesis by spatiotemporal Gaussian process regression, and sibling history data processing. We also expanded the database of vital registration, survey, and census data to 14�294 geography�year datapoints. For GBD 2015, eight causes, including Ebola virus disease, were added to the previous GBD cause list for mortality. We used six modelling approaches to assess cause-specific mortality, with the Cause of Death Ensemble Model (CODEm) generating estimates for most causes. We used a series of novel analyses to systematically quantify the drivers of trends in mortality across geographies. First, we assessed observed and expected levels and trends of cause-specific mortality as they relate to the Socio-demographic Index (SDI), a summary indicator derived from measures of income per capita, educational attainment, and fertility. Second, we examined factors affecting total mortality patterns through a series of counterfactual scenarios, testing the magnitude by which population growth, population age structures, and epidemiological changes contributed to shifts in mortality. Finally, we attributed changes in life expectancy to changes in cause of death. We documented each step of the GBD 2015 estimation processes, as well as data sources, in accordance with Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). Findings Globally, life expectancy from birth increased from 61·7 years (95 uncertainty interval 61·4�61·9) in 1980 to 71·8 years (71·5�72·2) in 2015. Several countries in sub-Saharan Africa had very large gains in life expectancy from 2005 to 2015, rebounding from an era of exceedingly high loss of life due to HIV/AIDS. At the same time, many geographies saw life expectancy stagnate or decline, particularly for men and in countries with rising mortality from war or interpersonal violence. From 2005 to 2015, male life expectancy in Syria dropped by 11·3 years (3·7�17·4), to 62·6 years (56·5�70·2). Total deaths increased by 4·1 (2·6�5·6) from 2005 to 2015, rising to 55·8 million (54·9 million to 56·6 million) in 2015, but age-standardised death rates fell by 17·0 (15·8�18·1) during this time, underscoring changes in population growth and shifts in global age structures. The result was similar for non-communicable diseases (NCDs), with total deaths from these causes increasing by 14·1 (12·6�16·0) to 39·8 million (39·2 million to 40·5 million) in 2015, whereas age-standardised rates decreased by 13·1 (11·9�14·3). Globally, this mortality pattern emerged for several NCDs, including several types of cancer, ischaemic heart disease, cirrhosis, and Alzheimer's disease and other dementias. By contrast, both total deaths and age-standardised death rates due to communicable, maternal, neonatal, and nutritional conditions significantly declined from 2005 to 2015, gains largely attributable to decreases in mortality rates due to HIV/AIDS (42·1, 39·1�44·6), malaria (43·1, 34·7�51·8), neonatal preterm birth complications (29·8, 24·8�34·9), and maternal disorders (29·1, 19·3�37·1). Progress was slower for several causes, such as lower respiratory infections and nutritional deficiencies, whereas deaths increased for others, including dengue and drug use disorders. Age-standardised death rates due to injuries significantly declined from 2005 to 2015, yet interpersonal violence and war claimed increasingly more lives in some regions, particularly in the Middle East. In 2015, rotaviral enteritis (rotavirus) was the leading cause of under-5 deaths due to diarrhoea (146�000 deaths, 118�000�183�000) and pneumococcal pneumonia was the leading cause of under-5 deaths due to lower respiratory infections (393�000 deaths, 228�000�532�000), although pathogen-specific mortality varied by region. Globally, the effects of population growth, ageing, and changes in age-standardised death rates substantially differed by cause. Our analyses on the expected associations between cause-specific mortality and SDI show the regular shifts in cause of death composition and population age structure with rising SDI. Country patterns of premature mortality (measured as years of life lost YLLs) and how they differ from the level expected on the basis of SDI alone revealed distinct but highly heterogeneous patterns by region and country or territory. Ischaemic heart disease, stroke, and diabetes were among the leading causes of YLLs in most regions, but in many cases, intraregional results sharply diverged for ratios of observed and expected YLLs based on SDI. Communicable, maternal, neonatal, and nutritional diseases caused the most YLLs throughout sub-Saharan Africa, with observed YLLs far exceeding expected YLLs for countries in which malaria or HIV/AIDS remained the leading causes of early death. Interpretation At the global scale, age-specific mortality has steadily improved over the past 35 years; this pattern of general progress continued in the past decade. Progress has been faster in most countries than expected on the basis of development measured by the SDI. Against this background of progress, some countries have seen falls in life expectancy, and age-standardised death rates for some causes are increasing. Despite progress in reducing age-standardised death rates, population growth and ageing mean that the number of deaths from most non-communicable causes are increasing in most countries, putting increased demands on health systems. Funding Bill & Melinda Gates Foundation. © 2016 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY licens
Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980�2015: a systematic analysis for the Global Burden of Disease Study 2015
Background Improving survival and extending the longevity of life for all populations requires timely, robust evidence on local mortality levels and trends. The Global Burden of Disease 2015 Study (GBD 2015) provides a comprehensive assessment of all-cause and cause-specific mortality for 249 causes in 195 countries and territories from 1980 to 2015. These results informed an in-depth investigation of observed and expected mortality patterns based on sociodemographic measures. Methods We estimated all-cause mortality by age, sex, geography, and year using an improved analytical approach originally developed for GBD 2013 and GBD 2010. Improvements included refinements to the estimation of child and adult mortality and corresponding uncertainty, parameter selection for under-5 mortality synthesis by spatiotemporal Gaussian process regression, and sibling history data processing. We also expanded the database of vital registration, survey, and census data to 14�294 geography�year datapoints. For GBD 2015, eight causes, including Ebola virus disease, were added to the previous GBD cause list for mortality. We used six modelling approaches to assess cause-specific mortality, with the Cause of Death Ensemble Model (CODEm) generating estimates for most causes. We used a series of novel analyses to systematically quantify the drivers of trends in mortality across geographies. First, we assessed observed and expected levels and trends of cause-specific mortality as they relate to the Socio-demographic Index (SDI), a summary indicator derived from measures of income per capita, educational attainment, and fertility. Second, we examined factors affecting total mortality patterns through a series of counterfactual scenarios, testing the magnitude by which population growth, population age structures, and epidemiological changes contributed to shifts in mortality. Finally, we attributed changes in life expectancy to changes in cause of death. We documented each step of the GBD 2015 estimation processes, as well as data sources, in accordance with Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). Findings Globally, life expectancy from birth increased from 61·7 years (95 uncertainty interval 61·4�61·9) in 1980 to 71·8 years (71·5�72·2) in 2015. Several countries in sub-Saharan Africa had very large gains in life expectancy from 2005 to 2015, rebounding from an era of exceedingly high loss of life due to HIV/AIDS. At the same time, many geographies saw life expectancy stagnate or decline, particularly for men and in countries with rising mortality from war or interpersonal violence. From 2005 to 2015, male life expectancy in Syria dropped by 11·3 years (3·7�17·4), to 62·6 years (56·5�70·2). Total deaths increased by 4·1 (2·6�5·6) from 2005 to 2015, rising to 55·8 million (54·9 million to 56·6 million) in 2015, but age-standardised death rates fell by 17·0 (15·8�18·1) during this time, underscoring changes in population growth and shifts in global age structures. The result was similar for non-communicable diseases (NCDs), with total deaths from these causes increasing by 14·1 (12·6�16·0) to 39·8 million (39·2 million to 40·5 million) in 2015, whereas age-standardised rates decreased by 13·1 (11·9�14·3). Globally, this mortality pattern emerged for several NCDs, including several types of cancer, ischaemic heart disease, cirrhosis, and Alzheimer's disease and other dementias. By contrast, both total deaths and age-standardised death rates due to communicable, maternal, neonatal, and nutritional conditions significantly declined from 2005 to 2015, gains largely attributable to decreases in mortality rates due to HIV/AIDS (42·1, 39·1�44·6), malaria (43·1, 34·7�51·8), neonatal preterm birth complications (29·8, 24·8�34·9), and maternal disorders (29·1, 19·3�37·1). Progress was slower for several causes, such as lower respiratory infections and nutritional deficiencies, whereas deaths increased for others, including dengue and drug use disorders. Age-standardised death rates due to injuries significantly declined from 2005 to 2015, yet interpersonal violence and war claimed increasingly more lives in some regions, particularly in the Middle East. In 2015, rotaviral enteritis (rotavirus) was the leading cause of under-5 deaths due to diarrhoea (146�000 deaths, 118�000�183�000) and pneumococcal pneumonia was the leading cause of under-5 deaths due to lower respiratory infections (393�000 deaths, 228�000�532�000), although pathogen-specific mortality varied by region. Globally, the effects of population growth, ageing, and changes in age-standardised death rates substantially differed by cause. Our analyses on the expected associations between cause-specific mortality and SDI show the regular shifts in cause of death composition and population age structure with rising SDI. Country patterns of premature mortality (measured as years of life lost YLLs) and how they differ from the level expected on the basis of SDI alone revealed distinct but highly heterogeneous patterns by region and country or territory. Ischaemic heart disease, stroke, and diabetes were among the leading causes of YLLs in most regions, but in many cases, intraregional results sharply diverged for ratios of observed and expected YLLs based on SDI. Communicable, maternal, neonatal, and nutritional diseases caused the most YLLs throughout sub-Saharan Africa, with observed YLLs far exceeding expected YLLs for countries in which malaria or HIV/AIDS remained the leading causes of early death. Interpretation At the global scale, age-specific mortality has steadily improved over the past 35 years; this pattern of general progress continued in the past decade. Progress has been faster in most countries than expected on the basis of development measured by the SDI. Against this background of progress, some countries have seen falls in life expectancy, and age-standardised death rates for some causes are increasing. Despite progress in reducing age-standardised death rates, population growth and ageing mean that the number of deaths from most non-communicable causes are increasing in most countries, putting increased demands on health systems. Funding Bill & Melinda Gates Foundation. © 2016 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY licens
Identifying appropriate sampling and modelling approaches for analysing distributional patterns of Antarctic terrestrial arthropods along the Victoria Land latitudinal gradient
Extended ecophysiologicalanalysis of Gomphiocephalus hodgsoni (Collembola) : flexibility in life history strategy and population response
The springtail Gomphiocephalus hodgsoni (Arthropoda: Collembola) has been the focus of extensive ecophysiological and molecular genetic work and is now arguably the most well-studied of the continental Antarctic springtails. Here, we further the ecophysiological catalogue of this species. First, we provide experimental data on G. hodgsoni from one summer season at Cape Bird (Ross Sea Region) examining dispersal ability and desiccation tolerance. Next, we expand an existing metabolic rate dataset that encompasses individual metabolic rate measurements across both temporal and spatial scales in southern Victoria Land, adding an additional season of metabolic rate measurements taken at a cooler, drier continental location (Garwood Valley). Our data show that some G. hodgsoni individuals can survive at least ten days of suspension on the surface of both fresh and sea water. This, coupled with the presence of G. hodgsoni specimens in air and pitfall traps suggests that dispersal over local scales (i.e. metres) is possible for this species. Our metabolic data show that different populations within the same Antarctic region have different average metabolic rates at both temporal and spatial scales, indicating that distinct populations may respond differently to environmental variables. We suggest that G. hodgsoni maintains a flexible life history strategy that allows its ecophysiological response(s) to be dependent on local environmental conditions. Accordingly, there may be no ‘typical’ response to environmental changes—a factor that should be considered in both future ecophysiological work and conservation approaches
Phylogeographic structure suggests multiple glacial refugia in northern Victoria Land for the endemic Antarctic springtail Desoria klovstadi (Collembola, Isotomidae).
We carried out a phylogeographic study using mtDNA (COII) for the endemic springtail Desoria klovstadi (formerly Isotoma klovstadi) from northern Victoria Land, Antarctica. Low levels of sequence divergence (≤1.6%) across 26 unique haplotypes (from 69 individuals) were distributed according to geographic location. Cape Hallett and Daniell Peninsula contained the highest nucleotide (both > 0.004) and haplotype (both > 0.9) diversity with 10 (of 16) and 8 (of 12) unique haplotypes, respectively. All other populations (Football Saddle, Crater Cirque, Cape Jones) had lower diversity with 2–4 unique haplotypes. Across the 69 individuals from five populations there was only a single haplotype shared between two populations (Daniell Peninsula and Football Saddle). Furthermore, nested clade analyses revealed that some of the Daniell Peninsula haplotypes were more closely related to Football Saddle haplotypes than to any other population. Such discrete haplotype groupings suggest historical (rare) dispersal across the Pleistocene (1.8 mya−11 kya) and Holocene (11 kya–present), coupled with repeated extinction, range contraction and expansion events, and/or incomplete sampling across the species range. The nested clade analyses reveal that a common pattern of climatic and geological history over long-term glacial habitat fragmentation has determined the geographic and haplotype distributions found for D. klovstadi
Rafting in Antarctic Collembola
Darwin was an early exponent of the importance of ‘occasional means of dispersal’ in accounting for the present-day distribution of plants and animals. This study examined the implications of capture on the water surface of meltwater and seawater for the local and long-range dispersal of Antarctic springtails. Individuals of the maritime Antarctic collembolan Cryptopygus antarcticus, were floated on tap water and seawater at 0, 5 and 10°C. LT50s on seawater were 34 (10°C), 65 (5°C) and 75 (0°C) days. On tap water, LT50s were 69 (10°C), 126 (5°C) and 239 (0°C) days. Less than 20% escaped from the water surface. A significantly greater proportion of springtails moulted on tap water and viable offspring were produced on both tap water and seawater. Comparison across treatments of survival of moulting and non-moulting individuals found significantly greater survival in moulting animals for three of the treatment combinations. It is suggested that moult exuviae facilitate survival on the water film through the simultaneous provision of a flotation aid and a source of nourishment – that is, an ‘edible raft’. A separate experiment measuring changes in haemolymph osmolality over time on tap water and seawater at 2 and 5°C found significant differences in all treatments. Causes of mortality are discussed in relation to osmoregulatory failure and starvation