51 research outputs found
Environmental footprinting of New Zealand agricultural products and implications for food nutrition
Evaluation of two 15N methods for measuring nitrogen fixation by legumes in established pastures
Comparison of carbon footprint and water scarcity footprint of milk protein produced by cellular agriculture and the dairy industry
Purpose: This paper studies the carbon footprint and water scarcity footprint (WSF) of a milk protein, beta-lactoglobulin, produced by cellular agriculture and compares this to extracted dairy protein from milk. The calculations of the microbially produced proteins were based on a model of a hypothetical industrial-scale facility. The purpose of the study is to examine the role relative to dairy of microbially produced milk proteins in meeting future demand for more sustainably produced protein of high nutritional quality. Methods: The evaluated process considers beta-lactoglobulin production in bioreactor cultivation with filamentous fungi T. reesei and downstream processing for product purification. The model considers four production scenarios in four different locations (New Zealand, Germany, US, and Australia) with a cradle-to-gate system boundary. The scenarios consider different sources of carbon (glucose and sucrose), different options for the fungal biomass treatment (waste or animal feed) and for the purification of the product. Allocation to biomass was avoided by considering it substituting the production of general protein feed. The carbon footprint and WSF (based on AWaRe factors) modelling is compared to calculations and actual data on extracted dairy protein production in NZ. The uncertainties of modelled process were addressed with a sensitivity analysis. Results and discussion: The carbon footprint of microbially produced protein varied depending on the location (energy profile) and source of carbon used. The lowest carbon footprint (5.5 t CO2e/t protein) was found with sucrose-based production in NZ and the highest (17.6 t CO2e/t protein) in Australia with the glucose and chromatography step. The WSF results varied between 88–5030 m3 world eq./t protein, depending on the location, type of sugar and purification method used. The avoided feed production had a bigger impact on the WSF than on the carbon footprint. Both footprints were sensitive to process parameters of final titre and protein yield from sugar. The results for milk protein were of similar magnitude, c.10 t CO2e/t protein and 290–11,300 m3 world eq./t protein. Conclusions: The environmental impacts of microbially produced milk protein were of the same magnitude as for extracted dairy protein. The main contributions were sugar and electricity production. The carbon footprints of proteins produced by cellular agriculture have potential for significant reduction when renewable energy and more sustainable carbon sources are used and combined with evolving knowledge and technology in microbial production. Similarly, the carbon footprint of milk proteins can potentially be reduced through methane reduction technologies.</p
Foderproduktion och metanbildning i våmmen utgör 85-90 % av mjölkens klimatpåverkan
Klimatpåverkan från mjölkproduktionen har varit
i fokus de senaste åren, inte minst p g a djurens
utsläpp av metan. Mjölkens klimatpåverkan består
dock inte enbart av metan från foderomvandling i
våmmen. Även foderproduktionen står för en betydande
andel av växthusgaserna medan t ex transporter
och gårdens elförbrukning utgör små andelar
Beyond ruminants: discussing opportunities for alternative pasture uses in New Zealand
peer-reviewedThe New Zealand government has set ambitious goals
for primary sector growth and of zero net carbon
emissions by 2050. This presents an opportunity and
obligation to develop new ideas for grassland production
systems to increase export value and generate new job
opportunities, while reducing environmental impacts.
The aim of this paper is to draw on recent research
in Europe to investigate some of the alternative and
complementary uses for pasture as a feedstock for a
green biorefinery. A biorefinery is a facility, or a series
of processes, that convert biomass into a spectrum
of value-added products. For example, protein can
be extracted mechanically from green biomass once
harvested. The residual fibre fraction could be used
as a low-nitrogen feed for ruminants to reduce urinary
nitrogen, while the liquid protein fraction could be
processed to make it suitable for mono-gastric or human
consumption. Enzymes can promote protein extraction
and controlled conversion of insoluble plant fibres
and oligosaccharides to foster gut-health promoting
prebiotic food ingredients. Anaerobic digestion of
residues can then be used to create energy and soilimproving
products. Research and demonstration of
these approaches in practice, along with the results of
feasibility studies, will be required to see which of these
opportunities is a good fit for New Zealand pasture
systems
The value of manure - Manure as co-product in life cycle assessment
Research ArticleLivestock production is important for food security, nutrition, and landscape maintenance, but it is associated
with several environmental impacts. To assess the risk and benefits arising from livestock production, transparent
and robust indicators are required, such as those offered by life cycle assessment. A central question in
such approaches is how environmental burden is allocated to livestock products and to manure that is re-used for
agricultural production. To incentivize sustainable use of manure, it should be considered as a co-product as long
as it is not disposed of, or wasted, or applied in excess of crop nutrient needs, in which case it should be treated
as a waste. This paper proposes a theoretical approach to define nutrient requirements based on nutrient response
curves to economic and physical optima and a pragmatic approach based on crop nutrient yield adjusted for nutrient losses to atmosphere and water. Allocation of environmental burden to manure and other livestock
products is then based on the nutrient value from manure for crop production using the price of fertilizer
nutrients. We illustrate and discuss the proposed method with two case studiesinfo:eu-repo/semantics/publishedVersio
Application of life cycle assessment to sheep production systems: investigating co-production of wool and meat using case studies from major global producers
Whole-genome sequencing reveals host factors underlying critical COVID-19
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
Whole-genome sequencing reveals host factors underlying critical COVID-19
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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