Progress in sustainability science: lessons learnt from current methodologies for sustainability assessment: Part 1

Purpose

Sustainability Science (SS) is considered an emerging discipline, applicative and solution-oriented whose aim is to handle environmental, social and economic issues in light of cultural, historic and institutional perspectives. The challenges of the discipline are not only related to better identifying the problems affecting sustainability but to the actual transition towards solutions adopting an integrated, comprehensive and participatory approach. This requires the definition of a common scientific paradigm in which integration and interaction amongst sectorial disciplines is of paramount relevance. In this context, life cycle thinking (LCT) and, in particular, life cycle-based methodologies and life cycle sustainability assessment (LCSA) may play a crucial role. The paper illustrates the main challenges posed to sustainability assessment methodologies and related methods in terms of ontology, epistemology and methodology of SS. The aims of the analysis are twofold: (1) to identify the main features of methodologies for sustainability assessment and (2) to present key aspects for the development of robust and comprehensive sustainability assessment.

Methods

The current debate on SS addressing ontological, epistemological and methodological aspects has been reviewed, leading to the proposal of a conceptual framework for SS. In addition, a meta-review of recent studies on sustainability assessment methodologies and methods, focusing those life cycle based, supports the discussion on the main challenges for a comprehensive and robust approach to sustainability assessment. Starting from the results of the meta-review, we identified specific features of sustainable development-oriented methods: firstly, highlighting key issues towards robust methods for SS and, secondly, capitalising on the findings of each review’s paper. For each issue, a recommendation towards a robust sustainability assessment method is given. Existing limitations of sectorial academic inquiries and proposal for better integration and mainstreaming of SS are the key points under discussion.

Discussion

In the reviewed papers, LCT and its basic principles are acknowledged as relevant for sustainability assessment. Nevertheless, LCT is not considered as a reference approach in which other methods could also find a place. This aspect has to be further explored, addressing the lack of multi-disciplinary exchange and putting the mainstreaming of LCT as a priority on the agenda of both life cycle assessment and sustainability assessment experts. Crucial issues for further developing sustainability assessment methodologies and methods have been identified and can be summarised as follows: holistic and system wide approaches, shift from multi- towards trans-disciplinarity; multi-scale (temporal and geographical) perspectives; and better involvement and participation of stakeholders.

Conclusions

Those are also the main challenges posed to LCSA in terms of progress of ontology, epistemology and methodology in line with the progress of SS. The life cycle-based methodologies should be broadened from comparing alternatives and avoiding negative impacts, to also proactively enhancing positive impacts, and towards the achievement of sustainability goals.     

Evidence for oxylipin synthesis and induction of a new polyunsaturated fatty acid hydroxylase activity in Chondrus crispus in response to methyljasmonate

Signaling cascades involving oxygenated derivatives (oxylipins) of polyunsaturated fatty acids (PUFAs) are known to operate in response to external stimuli. The marine red alga Chondrus crispus uses both oxygenated derivatives of C18 (octadecanoids) and C20 (eicosanoids) PUFAs as developmental or defense hormones. The present study demonstrates that methyljasmonate (MeJA) triggers a cascade of oxidation of PUFAs leading to the synthesis of prostaglandins and other oxygenated fatty acids. As a result of a lipoxygenase-like activation, MeJA induces a concomitant accumulation of 13-hydroxy-9Z,11E-octadecadienoic acid (13-HODE) and 13-oxo-9Z,11E-octadecadienoic acid (13-oxo-ODE) in a dose-dependent manner in C. crispus. Furthermore, MeJA increases the level of mRNA encoding a gluthatione S-transferase and induces the activity of a new enzyme catalyzing the regio- and stereoselective bisallylic hydroxylation of polyunsaturated fatty acids from C(18) to C(22). The enzyme selectively oxidized the omega minus 7 carbon position (omega-7) and generated the stereoselective (R)-hydroxylated metabolites with a large enantiomeric excess. The enzyme specificity for the fatty acid recognition was not dependent of the position of double bonds but at least requires a methylene interrupted double bond 1,4-pentadiene motif involving the omega-7 carbon.     

Epigenetic control of the critical region for premature ovarian failure on autosomal genes translocated to the X chromosome: a hypothesis

Chromosomal rearrangements in Xq are frequently associated to premature ovarian failure (POF) and have contributed to define a POF “critical region” from Xq13.3 to Xq26. Search for X-linked genes responsible for the phenotype has been elusive as most rearrangements did not interrupt genes and many were mapped to gene deserts. We now report that ovary-expressed genes flanked autosomal breakpoints in four POF cases analyzed whose X chromosome breakpoints interrupted a gene poor region in Xq21, where no ovary-expressed candidate genes could be found. We also show that the global down regulation in the oocyte and up regulation in the ovary of X-linked genes compared to the autosomes is mainly due to genes in the POF “critical region”. We thus propose that POF, in X;autosome balanced translocations, may not only be caused by haploinsufficiency, but also by a oocyte-specific position effect on autosomal genes, dependent on dosage compensation mechanisms operating on the active X chromosome in mammals.     

A message emerging from development: the repression of mitochondrial β-F1-ATPase expression in cancer

Mitochondrial research has experienced a considerable boost during the last decade because organelle malfunctioning is in the genesis and/or progression of a vast array of human pathologies including cancer. The renaissance of mitochondria in the cancer field has been promoted by two main facts: (1) the molecular and functional integration of mitochondrial bioenergetics with the execution of cell death and (2) the implementation of ¹⁸FDG-PET for imaging and staging of tumors in clinical practice. The latter, represents the bed-side translational development of the metabolic hallmark that describes the bioenergetic phenotype of most cancer cells as originally predicted at the beginning of previous century by Otto Warburg. In this minireview we will briefly summarize how the study of energy metabolism during liver development forced our encounter with Warburg’s postulates and prompted us to study the mechanisms that regulate the biogenesis of mitochondria in the cancer cell.     

How can LCA include prospective elements to assess emerging technologies and system transitions? The 76th LCA Discussion Forum on Life Cycle Assessment, 19 November 2020

This paper summarizes the 76th LCA Discussion Forum end its main findings. Main issues when addressing emerging technologies identified were: the lack of primary data, the need for (shared) future background scenarios and (guidlines for) a common methodology. The following recommendations have been derived by the organizers: 1) Specific foreground inventories are always tailor-made, but consistency can be improved through lists of mandatory considerations. 2) Continue sharing (future) technology data and proxy processes, that can be readily replicated to new studies and assist in developing inventories. 3) Streamline and unify the process of including scenarios for background systems. New approaches may provide first important solutions to efficiently include consistent future scenarios in prospective LCA.

     

Seasonal changes in substrate utilization patterns by bacterioplankton in the Amundsen Gulf (western Arctic)

Due to logistic difficulties, biological processes along the Arctic winter remain poorly known. In particular, carbon sources used by bacterioplankton have not been identified. A previous study in Franklin Bay suggested that polymers were one of the main substrates used by bacteria. During the Circumpolar Flaw Lead System Study, we analyzed metabolic capabilities of the heterotrophic bacterioplankton using Biolog MT2 MicroPlates^® amended with custom-selected substrates. Our purpose was to test whether the use of polymers was a peculiarity of Franklin Bay or a robust feature of the Arctic winter community. Seventeen stations were sampled in the Amundsen Gulf (western Arctic), a very dynamic area with heterogeneous ice conditions, from February to July 2008, at the surface (0–12 m), intermediate depths (20–70 m), and near the bottom (200 m). In winter, when nutrients and chlorophyll a concentrations were low, the number of substrates used was close to zero. In early spring, when the levels of chlorophyll a increased, so did the number of substrates used. This was followed by a 1-month period with no substrates used in April and May. Finally, the activity recovered toward the summer. Amino acids were occasionally used. However, the group of substrates most commonly used at all depths was carbohydrates, especially cellobiose, maltose, N-acetyl-d-glucosamine and glycogen. All these are either polymers or monomers derived from polymers. These results confirm that the heterotrophic bacterial assemblage relies heavily on polysaccharides for subsistence during the Arctic winter.     

Impact of Risk Factors on Different Interval Cancer Subtypes in a Population-Based Breast Cancer Screening Programme

Background

Interval cancers are primary breast cancers diagnosed in women after a negative screening test and before the next screening invitation. Our aim was to evaluate risk factors for interval cancer and their subtypes and to compare the risk factors identified with those associated with incident screen-detected cancers.

Methods

We analyzed data from 645,764 women participating in the Spanish breast cancer screening program from 2000–2006 and followed-up until 2009. A total of 5,309 screen-detected and 1,653 interval cancers were diagnosed. Among the latter, 1,012 could be classified on the basis of findings in screening and diagnostic mammograms, consisting of 489 true interval cancers (48.2%), 235 false-negatives (23.2%), 172 minimal-signs (17.2%) and 114 occult tumors (11.3%). Information on the screening protocol and women''s characteristics were obtained from the screening program registry. Cause-specific Cox regression models were used to estimate the hazard ratios (HR) of risks factors for interval cancer and incident screen-detected cancer. A multinomial regression model, using screen-detected tumors as a reference group, was used to assess the effect of breast density and other factors on the occurrence of interval cancer subtypes.

Results

A previous false-positive was the main risk factor for interval cancer (HR = 2.71, 95%CI: 2.28–3.23); this risk was higher for false-negatives (HR = 8.79, 95%CI: 6.24–12.40) than for true interval cancer (HR = 2.26, 95%CI: 1.59–3.21). A family history of breast cancer was associated with true intervals (HR = 2.11, 95%CI: 1.60–2.78), previous benign biopsy with a false-negatives (HR = 1.83, 95%CI: 1.23–2.71). High breast density was mainly associated with occult tumors (RRR = 4.92, 95%CI: 2.58–9.38), followed by true intervals (RRR = 1.67, 95%CI: 1.18–2.36) and false-negatives (RRR = 1.58, 95%CI: 1.00–2.49).

Conclusion

The role of women''s characteristics differs among interval cancer subtypes. This information could be useful to improve effectiveness of breast cancer screening programmes and to better classify subgroups of women with different risks of developing cancer.     

Fatty Acid Transport Protein 1 (FATP1) Localizes in Mitochondria in Mouse Skeletal Muscle and Regulates Lipid and Ketone Body Disposal

FATP1 mediates skeletal muscle cell fatty acid import, yet its intracellular localization and metabolic control role are not completely defined. Here, we examine FATP1 localization and metabolic effects of its overexpression in mouse skeletal muscle. The FATP1 protein was detected in mitochondrial and plasma membrane fractions, obtained by differential centrifugation, of mouse gastrocnemius muscle. FATP1 was most abundant in purified mitochondria, and in the outer membrane and soluble intermembrane, but not in the inner membrane plus matrix, enriched subfractions of purified mitochondria. Immunogold electron microscopy localized FATP1-GFP in mitochondria of transfected C2C12 myotubes. FATP1 was overexpressed in gastrocnemius mouse muscle, by adenovirus-mediated delivery of the gene into hindlimb muscles of newborn mice, fed after weaning a chow or high-fat diet. Compared to GFP delivery, FATP1 did not alter body weight, serum fed glucose, insulin and triglyceride levels, and whole-body glucose tolerance, in either diet. However, fatty acid levels were lower and β-hydroxybutyrate levels were higher in FATP1- than GFP-mice, irrespective of diet. Moreover, intramuscular triglyceride content was lower in FATP1- versus GFP-mice regardless of diet, and β-hydroxybutyrate content was unchanged in high-fat-fed mice. Electroporation-mediated FATP1 overexpression enhanced palmitate oxidation to CO2, but not to acid-soluble intermediate metabolites, while CO2 production from β-hydroxybutyrate was inhibited and that from glucose unchanged, in isolated mouse gastrocnemius strips. In summary, FATP1 was localized in mitochondria, in the outer membrane and intermembrane parts, of mouse skeletal muscle, what may be crucial for its metabolic effects. Overexpressed FATP1 enhanced disposal of both systemic fatty acids and intramuscular triglycerides. Consistently, it did not contribute to the high-fat diet-induced metabolic dysregulation. However, FATP1 lead to hyperketonemia, likely secondary to the sparing of ketone body oxidation by the enhanced oxidation of fatty acids.