Ethylene based on woody biomass—what are environmental key issues of a possible future Swedish production on industrial scale

Purpose

In order to reduce its environmental impact, the chemical industry no longer produces base chemicals such as ethylene, solely from fossil, but also from biomass-based feedstocks. However, a biomass option suitable for one region might not be as suitable for another region due to, e.g., long transport and the related environmental. Therefore, local biomass alternatives and the environmental impact related to the production of chemicals from these alternatives need to be investigated. This study assesses the environmental impact of producing ethylene from Swedish wood ethanol.

Methods

The study was conducted following the methodology of life cycle assessment. The life cycle was assessed using a cradle-to-gate perspective for the production of 50,000 tonnes ethylene/year for the impact categories global warming, acidification (ACP), photochemical ozone creation, and eutrophication (EP).

Results and discussion

The production of enzymes used during the life cycle had a significant effect on all investigated impacts. However, reduced consumption of enzyme product, which could possibly be realized considering the rapid development of enzymes, lowered the overall environmental impact of the ethylene. Another approach could be to use alternative hydrolyzing agents. However, little information on their environmental impact is available. An additional key contributor, with regard to ACP, EP, and POCP, was the ethanol production. Therefore, further improvements with regard to the process’ design may have beneficial effects on its environmental impact.

Conclusions

The study assessed the environmental impact of wood ethylene and pointed to several directions for improvements, such as improved enzyme production and reduced consumption of enzyme products. Moreover, the analysis showed that further investigations into other process options and increase of ethylene production from biomass are worth continued research.     

Inhibition of Phosphoinositide 3-Kinase p110delta Does Not Affect T Cell Driven Development of Type 1 Diabetes Despite Significant Effects on Cytokine Production

Type 1 diabetes is caused by the destruction of insulin producing beta cells by the immune system. The p110δ isoform of PI3K is expressed primarily in cells of haematopoietic origin and the catalytic activity of p110δ is important for the activation of these cells. Targeting of this pathway offers an opportunity to reduce immune cell activity without unwanted side effects. We have explored the effects of a specific p110δ isoform inhibitor, IC87114, on diabetogenic T cells both in vitro and in vivo, and find that although pharmacological inhibition of p110δ has a considerable impact on the production of pro-inflammatory cytokines, it does not delay the onset of diabetes after adoptive transfer of diabetogenic cells. Further, we demonstrate that combination treatment with CTLA4-Ig does not improve the efficacy of treatment, but instead attenuates the protective effects seen with CTLA4-Ig treatment alone. Our results suggest that decreased IL-10 production by Foxp3⁺ CD4⁺ T cells in the presence of IC87114 negates individual anti-inflammatory effects of IC8114 and CTLA4-Ig.     

Arsenic alters global histone modifications in lymphocytes in vitro and in vivo

Arsenic, an established carcinogen and toxicant, occurs in drinking water and food and affects millions of people worldwide. Arsenic appears to interfere with gene expression through epigenetic processes, such as DNA methylation and post-translational histone modifications. We investigated the effects of arsenic on histone residues in vivo as well as in vitro. Analysis of H3K9Ac and H3K9me3 in CD4+ and CD8+ sorted blood cells from individuals exposed to arsenic through drinking water in the Argentinean Andes showed a significant decrease in global H3K9me3 in CD4+ cells, but not CD8+ cells, with increasing arsenic exposure. In vitro studies of inorganic arsenic-treated T lymphocytes (Jurkat and CCRF-CEM, 0.1, 1, and 100 μg/L) showed arsenic-related modifications of H3K9Ac and changes in the levels of the histone deacetylating enzyme HDAC2 at very low arsenic concentrations. Further, in vitro exposure of kidney HEK293 cells to arsenic (1 and 5 μM) altered the protein levels of PCNA and DNMT1, parts of a gene expression repressor complex, as well as MAML1. MAML1 co-localized and interacted with components of this complex in HEK293 cells, and in silico studies indicated that MAML1 expression correlate with HDAC2 and DNMT1 expression in kidney cells. In conclusion, our data suggest that arsenic exposure may lead to changes in the global levels of H3K9me3 and H3K9Ac in lymphocytes. Also, we show that arsenic exposure affects the expression of PCNA and DNMT1—proteins that are part of a gene expression silencing complex.     

Recruitment of chromatin remodelling factors during gene activation via the glucocorticoid receptor N-terminal domain

We have shown that yeast mutants with defects in the Ada adaptor proteins are defective in hormone-dependent gene activation by ectopically expressed human glucocorticoid receptor (GR). Others have shown that the Ada2 protein is required for physical interactions between some activation domains and TBP (TATA-binding protein), whereas the Gcn5 (Ada4) protein has a histone acetyltransferase (HAT) activity. Although all HAT enzymes are able to acetylate histone substrates, some also acetylate non-histone proteins. Taken together, these observations suggest that the Ada proteins have the ability to effect different steps in the process of gene activation. It has recently been shown that the Ada proteins are present in two distinct protein complexes, the Ada complex and a larger SAGA complex. Our recent work has focused on determining (1) which of the Ada-containing complexes mediates gene activation by GR, (2) whether the HAT activity encoded by GCN5 is required for GR-dependent gene activation, (3) whether the Ada proteins contribute to GR-mediated activation at the level of chromatin remodelling and (4) how the role of these HAT complexes is integrated with other chromatin remodelling activities during GR-mediated gene activation. Our results suggest a model in which GR recruits the SAGA complex and that this contributes to chromatin remodelling via a mechanism involving the acetylation of histones. Furthermore, recruitment of the SWI/SNF remodelling complex also has a role in GR-mediated activation that is independent of the role of SAGA. These complexes are similar to analogous mammalian complexes and therefore these results are likely to be relevant to the human system.     

Effect of nutrient enrichment on the distribution and sedimentation of polychlorinated biphenyls (PCBs) in seawater

The effect of nutrient enrichment on the distribution of polychlorinated biphenyl's (PCBs) in the microbial food web and the residence time of PCBs in seawater was studied in an experimental mesocosm system. Two 5 m high temperature and light controlled mesocosm tubes (⊘ = 0,5 m) were filled with seawater from the northern Baltic Sea. Inorganic phosphorus and nitrogen were added daily to one mesocosm, while the other served as a control. Experiments were conducted at 5, 10 and 20°>C. Three ¹⁴C-labelled PCBs of different degree of chlorination were added to subsamples of the mesocosms: 4 chlorobiphenyl (MCB), IUPAC # 3; 2,2′,5,5′-tetrachlorobiphenyl (TCB), IUPAC # 52 and 2,2′, 4,4′,5,5′-hexachlorobiphenyl (HCB) IUPAC # 153. The biomasses and growth rates of the microorganisms as well as the sedimentation rate of particulate organic material increased with nutrient enrichment. The size distribution of the microorganisms changed with nutrient status, from dominance of picoplankton (< 2 μm) in the control towards increased importance of micro (> 10 μm) and nanoplankton (2– 10 μm) in nutrient enrichment. The specific growth rate of the bacterial community was found to be more temperature dependent than that of the phytoplankton community. The relative proportion of PCBs in the >2 μm fraction was observed to be in the order MCB < TCB < HCB, while the opposite distribution prevailed in the < 2 μm fraction. We hypothesize that this is due to the combined effect of the different Kow values of the PCBs and a different composition of the particulate organic carbon in the > 2 μm and < 2 μm fractions (e.g. different lipid composition). The residence time of the PCBs in the mesocosm generally decreased with nutrient enrichment, but was dependent on the degree of chlorination of the PCB. Our results indicate that the transport of organic pollutants up through the food web is more important in nutrient poor than in nutrient rich waters and that the importance of sedimentation is higher in eutrophic ecosystems. This revised version was published online in July 2006 with corrections to the Cover Date.     

Short-term adaptation during propagation improves the performance of xylose-fermenting <Emphasis Type="Italic">Saccharomyces cerevisiae</Emphasis> in simultaneous saccharification and co-fermentation

Background

Inhibitors that are generated during thermochemical pretreatment and hydrolysis impair the performance of microorganisms during fermentation of lignocellulosic hydrolysates. In omitting costly detoxification steps, the fermentation process relies extensively on the performance of the fermenting microorganism. One attractive option of improving its performance and tolerance to microbial inhibitors is short-term adaptation during propagation. This study determined the influence of short-term adaptation on the performance of recombinant Saccharomyces cerevisiae in simultaneous saccharification and co-fermentation (SSCF). The aim was to understand how short-term adaptation with lignocellulosic hydrolysate affects the cell mass yield of propagated yeast and performance in subsequent fermentation steps. The physiology of propagated yeast was examined with regard to viability, vitality, stress responses, and upregulation of relevant genes to identify any links between the beneficial traits that are promoted during adaptation and overall ethanol yields in co-fermentation.

Results

The presence of inhibitors during propagation significantly improved fermentation but lowered cell mass yield during propagation. Xylose utilization of adapted cultures was enhanced by increasing amounts of hydrolysate in the propagation. Ethanol yields improved by over 30 % with inhibitor concentrations that corresponded to ≥2.5 % water-insoluble solids (WIS) load during the propagation compared with the unadapted culture. Adaptation improved cell viability by >10 % and increased vitality by >20 %. Genes that conferred resistance against inhibitors were upregulated with increasing amounts of inhibitors during the propagation, but the adaptive response was not associated with improved ethanol yields in SSCF. The positive effects in SSCF were observed even with adaptation at inhibitor concentrations that corresponded to 2.5 % WIS. Higher amounts of hydrolysate in the propagation feed further improved the fermentation but increased the variability in fermentation outcomes and resulted in up to 20 % loss of cell mass yield.

Conclusions

Short-term adaptation during propagation improves the tolerance of inhibitor-resistant yeast strains to inhibitors in lignocellulosic hydrolysates and improves their ethanol yield in fermentation and xylose-fermenting capacity. A low amount of hydrolysate (corresponding to 2.5 % WIS) is optimal, whereas higher amounts decrease cell mass yield during propagation.