Soil quality is a factor which is directly related to the sustainability of agricultural production and can be compromised through the use of inadequate management practices. In this work, soil edaphic respiration and changes in microbial biomass promoted by cover crops in an integrated crop-livestock system (ICLS) were evaluated using soil quality indicators by the respirometry method. The design used was completely randomized in a 3x6 factorial scheme and multivariate principal components analysis (PCA) was performed according to MANOVA. The edaphic respiration was determined based on the respirometry technique. From the results, it was found that edaphic soil respiration was significant in the nine evaluation periods, demonstrating the importance of grass cover on this edaphic respiration arising from the biological activity of microorganisms, which is directly related to the amount of organic carbon in the soil. It was concluded that the use of cover crops contributed to producing organic matter in the soil and consequently greater microbial respiratory activity.

Coral reefs are declining worldwide due to global changes in the marine environment. The increasing frequency of massive bleaching events in the tropics is highlighting the need to better understand the stages of coral physiological responses to extreme conditions. Moreover, like many other coastal regions, coral reef ecosystems are facing additional localized anthropogenic issues such as nutrient loading, increased turbidity, and coastal development. Different strategies have been developed to measure the health status of a damaged reef, ranging from the resolution of individual polyps to an entire coral community, but techniques for measuring coral physiology in situ are not yet widely implemented. For instance, while there are many studies of the coral holobiont response in single or limited-number multiple stressor experiments, they provide only partial insights to metabolic performance under more complex temporally and spatially variable natural conditions. Here, we discuss the current status of coral reefs and their global and local stressors in the context of experimental techniques that measure core processes in coral metabolism (respiration, photosynthesis, and biocalcification) in situ, and their role in indicating the health status of colonies and communities. We highlight the need to improve the capability of in situ studies in order to better understand the resilience and stress response of corals under multiple global and local scale stressors.

Microglia are the resident immune cells of the central nervous system. Upon stimulus presentation microglia polarize from a resting to an activated state. Microglial translocator protein 18 kDa (TSPO) is considered as a marker of inflammation. Here, we characterized the role of TSPO by investigating the impact of TSPO deficiency on human microglia. We used TSPO knockout (TSPO-/-) variants of the human C20 microglia cell line. We found a significant reduction in the TSPO-associated protein VDAC1 in TSPO-/- compared to control cells. Moreover, we assessed the impact of TSPO deficiency on calcium levels and the mitochondrial membrane potential. Cytosolic and mitochondrial calcium concentrations were increased in TSPO-/- cell lines, whereas the mitochondrial membrane potential tended to be lower. Assessment of the mitochondrial DNA copy number via RT-PCR revealed a decreased amount of mtDNA in the TSPO-/- cells when compared to controls. Moreover, metabolic profiles of C20 cells were strongly dependent on the glycolytic pathway. However, TSPO depletion did not affect the cellular metabolic profile. Measurement of the mRNA expression levels of the pro-inflammatory mediators revealed an attenuated response to proinflammatory stimuli in TSPO-depleted cells, implying a role of the TSPO protein in the process of microglial polarization.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is an enigmatic condition characterized by exacerbation of symptoms after exertion (post-exertional malaise or “PEM”), and by fatigue whose severity and associated requirement for rest are excessive and disproportionate to the fatigue-inducing activity. There is no definitive molecular marker or known underlying pathological mechanism for the condition. Increasing evidence for aberrant energy metabolism suggests a role for mitochondrial dysfunction in ME/CFS. Our objective was therefore to measure mitochondrial function and cellular stress sensing in actively metabolising patient blood cells. We immortalized lymphoblasts isolated from 51 ME/CFS patients diagnosed according to the Canadian Consensus Criteria and an age- and gender-matched control group. Parameters of mitochondrial function and energy stress sensing were assessed by Seahorse extracellular flux analysis, proteomics, and an array of additional biochemical assays. As a proportion of the basal oxygen consumption rate (OCR), the rate of ATP synthesis by Complex V was significantly reduced in ME/CFS lymphoblasts, while significant elevations were observed in Complex I OCR, maximum OCR, spare respiratory capacity, nonmitochondrial OCR and “proton leak” as a proportion of the basal OCR. This was accompanied by a reduction of mitochondrial membrane potential, chronically hyperactivated TOR Complex I stress signalling and upregulated expression of mitochondrial respiratory complexes, fatty acid transporters and enzymes of the β-oxidation and TCA cycles. By contrast, mitochondrial mass and genome copy number, as well as glycolytic rates and steady state ATP levels were unchanged. Our results suggest a model in which ME/CFS lymphoblasts have a Complex V defect accompanied by compensatory upregulation of their respiratory capacity that includes the mitochondrial respiratory complexes, membrane transporters and enzymes involved in fatty acid β-oxidation. This homeostatically returns ATP synthesis and steady state levels to “normal” in the resting cells, but may leave them unable to adequately respond to acute increases in energy demand as the relevant homeostatic pathways are already activated.

In the past decade, a growing demand for sustainable cosmetic ingredients has yielded numerous biodegradation protocols. While OECD (Organization for Economic Co-operation and Development) aquatic assays are suitable for water-borne chemicals, it is crucial for the personal care industry to consider the persistence of plastics in soil, compost, and municipal sludge. Adopting this cradle-to-grave holistic approach would strengthen product appeal, while increasing the accuracy and ethical integrity of green-product labeling. Our study employs quantitative CO2 detection and thermophilic composting protocols specified in ASTM D5338, along with pass level criteria outlined in ASTM D6400, to assess the mineralization of plastics commonly formulated into personal care products. The results indicate that many cellulose ethers, cationic guars, starches, and labile polyesters demonstrate satisfactory disintegration, biodegradation, and seed germination rates to secure an ASTM D6400 compostability claim. In contrast, macromolecules designed with carbon-carbon backbones resisted acceptable mineralization in composting experiments, suggesting that unadulterated municipal compost lacks the microbial diversity to enzymatically digest many synthetically derived resins. Additionally, polymers that demonstrated acceptable biodegradability in internal and published OECD aquatic studies—including chitosan and polyvinyl alcohol—exhibited limited fragmentation in local municipal compost; hence, untested correlations between aquatic, soil, and compost testing outcomes should never be assumed.

The stability of twenty seven composts and organic substrates (including raw, less stable and stable materials) was assessed using two different liquid phase tests were carried out. One of the tests was introduced in 1998 and was based on the calculation of a Specific Oxygen Uptake Rate (SOUR). The newly introduced liquid phase test presented here is simpler to set-up and to perform that the older liquid phase test. It is based on the quantification of oxygen consumption in the headspace of a BOD bottle that contains the liquid-solid solution. The results indicate that a marginal correlation does exist between the main indices calculated from both tests. The correlation was stronger for the indices calculated for stable-processed organics than for the raw (unprocessed materials). The SOUR ranged from 1520 to 3650mg O₂/kg VS-h for the raw materials and from 110 to 1150 mg O₂/kg VS-h for the processed materials, respectively. The corresponding stability rate related index (LSRI₂₄) of the new liquid phase test introduced here ranged from 240 to 1180 mg O₂/dry kg-h for the raw materials and from 64 to 792 mg O₂/dry kg-h for the processed ones.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a devastating illness whose biomedical basis is now beginning to be elucidated. We reported previously that, after recovery from frozen storage, lymphocytes (peripheral blood monocytic cells, PBMCs) from ME/CFS patients die faster in culture medium than those from healthy controls. We also found that lymphoblastoid cell lines (lymphoblasts) derived from these PBMCs exhibit multiple abnormalities in mitochondrial respiratory function and signalling activity by the cellular stress-sensing kinase TORC1. These differences were correlated with disease severity, as measured by the Richardson and Lidbury Weighted Standing Test. The clarity of the differences between these cells derived from ME/CFS patient blood and those from healthy controls suggested that they may provide useful biomarkers for ME/CFS. Here we report a preliminary investigation into that possibility using a variety of analytical classification tools, including linear discriminant analysis, logistic regression and Receiver Operating Characteristic (ROC) curve analysis. We found that results from three different tests, lymphocyte death rate, mitochondrial respiratory function and TORC1 activity could each individually serve as biomarker with better than 90% sensitivity but only modest specificity vís a vís healthy controls. However, in combination they provided a cell-based biomarker with sensitivity and specificity approaching 100% in our sample. This level of sensitivity and specificity was almost equalled by a suggested protocol in which the frozen lymphocyte death rate was used as a highly sensitive test to triage positive samples to the more time consuming and expensive tests measuring lymphoblast respiratory function and TORC1 activity. This protocol provides a promising biomarker that could assist in more rapid and accurate diagnosis of ME/CFS.