The Utilisation of biomass as a fuel for chemical looping combustion

Development of a commercially viable carbon capture and sequestration (CCS) technology for fossil fuel power generation is vital if the anticipated effects of global warning are to be avoided. Chemical-looping combustion (CLC) is an indirect combustion process that utilises a regenerable solid oxygen sorbent (oxygen carrier, OC), typically a metal oxide, to transfer oxygen from the combustion air to the fuel such that direct contact between air and fuel is avoided. CLC is a variant on an oxy-fuel carbon capture system that offers the potential for a much lower energy penalty as CO2 separation is achieved intrinsically such that additional energy-intensive gas separation steps are avoided. Our research focuses on the development and optimisation of OCs for CLC systems using biomass and biomass derived fuels. The development of a CLC process utilising biomass is of particular interest as it has the potential to result in negative CO2 emissions i.e. a net removal of CO2 from the atmosphere. Thermochemical conversion of biomass typically results in the formation of significant quantities of refractory tar compounds which are difficult to combust and can lead to reduced fuel conversion efficiencies. Decomposition of the tars on the surface of the OC can result in severe coking and temporary deactivation. Coking of the OC also limits the overall CO2 capture efficiency of the process as regeneration of the OC in air produces CO2 which cannot be captured. This thesis documents the progress made towards the development of a robust laboratory based system for testing the effects of biomass tars on the long term performance of a chemical-looping combustion process. The work completed in this thesis can be divided into two main areas: the first involved developing optimised fabrication strategies for the production of inexpensive iron-based oxygen carrier particles of high reactivity and robust physical characteristics that could be used in CLC systems utilising biomass as the fuel. The second research focus involved the development of a reactor and analysis protocol for studying the interactions between biomass pyrolysis tars and the cheap, synthetic iron-based oxygen carrier materials. A range of pure iron oxide and iron oxide supported with 40 wt.% Al2O3 oxygen carrier materials were prepared via simple scalable fabrication techniques based on wet granulation for use in CLC systems utilising biomass or gasified biomass as a fuel. The oxygen carrier particles were subjected to rigorous testing using a range of analytical methods to assess their physical and chemical properties and suitability for use in large-scale systems. The effect of fabrication method and alumina precursor material used for producing the supported iron oxide materials were found to have a considerable effect on the physical characteristics and reactivity of the oxygen carrier material. The reduction kinetics (the rate limiting step in the CLC of gaseous fuels) of the different OC materials prepared in this work were assessed using a thermogravimetric analyser (TGA). A simple particle model based on the concept of effectiveness factor was applied to determine the intrinsic kinetic information. Preparation of the Al2O3 supported iron oxide oxygen carrier material using a Al(OH)3 alumina precursor gave the most porous oxygen carrier material with the highest surface area. This oxygen carrier was also the most reactive particularly at temperatures above 973 K and demonstrated very good thermal stability at temperatures up to 1173 K. The activation energy of the oxygen carrier was found to increase from 73 kJ mol-1 for the temperature range 823-1073 K to 123 kJ mol-1 at temperatures of 1073-1173 K. The increase in the activation energy was attributed to further conversion of Fe3O4 to FeAl2O4 which was more pronounced at the higher temperature range. Here we propose that the formation of FeAl2O4 was beneficial, acting to enhance the thermal stability, reactivity and oxygen transfer capacity of the iron oxide based oxygen carrier material. A new 500W laboratory-scale, two-stage fixed-bed reactor for simulating CLC with ex situ solid fuel gasification has been designed and constructed. Preliminary studies of the interactions between OC materials consisting of pure iron oxide and 60 wt.% Fe2O3 iron oxide supported on Al2O3 and a gas stream produced from the pyrolysis of biomass to emulate a fuel gas containing large quantities of tars were carried out. The presence of both OC materials at 973 K was found to significantly reduce the amount of biomass tars by up to 71 wt.% in the case of the 60 wt.% Fe2O3/40 wt.% Al2O3 OC material compared with analogous experiments in which the biomass tars were exposed to an inert bed of sand. Exposing the pyrolysis vapours to the oxygen carriers in their oxidised form favoured the production of CO2. The production of CO was favoured when the oxygen carriers were in their reduced forms. Both oxygen carrier materials were affected by carbon deposition. Carbon deposition was removed in the subsequent oxidation phase with no obvious deleterious effects on the reactivity of the oxygen carrier materials after exposure to the pyrolysis gases and vapours.Open Acces

Assessing Models using Monte Carlo Simulations

We establish a framework for assessing the validity of a given model using Monte Carlo simulations and inferences based on sampling distributions. Using this framework, we show that geometric brownian motion alone cannot generate a majority of the patterns in the distribution of stock returns and wealth creation. Our paper represents an often overlooked departure from the traditional way of validating asset pricing models, in which implications are derived, parameters calibrated, and magnitudes compared to empirical data. Instead, we seek to leverage the power of large numbers by conducting numerous simulations and assessing the probability that they contain our realized stock market

Hydrogen production by sorption enhanced steam reforming (SESR) of biomass in a fluidised-bed reactor using combined multifunctional particles

The performance of combined CO2-sorbent/catalyst particles for sorption enhanced steam reforming (SESR), prepared via a simple mechanical mixing protocol, was studied using a spout-fluidised bed reactor capable of continuous solid fuel (biomass) feeding. The influence of particle size (300–500 and 710–1000 µm), CaO loading (60–100 wt %), Ni-loading (10–40 wt %) and presence of dicalcium silicate support (22.6 wt %) on SESR process performance were investigated. The combined particles were characterised by their density, porosity and CO2 carrying capacity with the analysis by thermogravimetric analysis (TGA), Brunauer-Emmett-Teller (BET), Barrett-Joyner-Halenda (BJH) and mercury intrusion porosimetry (MIP). All experiments were conducted with continuous oak biomass feeding at a rate of 0.9 g/min ± 10%, and the reactor was operated at 660 ± 5 °C, 1 atm and 20 ± 2 vol % steam which corresponds to a steam-to-carbon ratio of 1.2:1. Unsupported combined particles containing 21.0 wt % Ni and 79 wt % CaO were the best performing sorbent/catalyst particle screened in this study, when accounting for the cost of Ni and the improvement in H2 produced by high Ni content particles. SESR tests with these combined particles produced 61 mmol H2/gbiomass (122 g H2/kgbiomass) at a purity of 61 vol %. Significant coke formation within the feeding tube and on the surfaces of the particles was observed which was attributed to the low steam to carbon ratio utilised

Superoxide dismutase downregulation in osteoarthritis progression and end-stage disease

Oxidative stress is proposed as an important factor in osteoarthritis (OA). To investigate the expression of the three superoxide dismutase (SOD) antioxidant enzymes in OA. SOD expression was determined by real-time PCR and immunohistochemistry using human femoral head cartilage. SOD2 expression in Dunkin–Hartley guinea pig knee articular cartilage was determined by immunohistochemistry. The DNA methylation status of the SOD2 promoter was determined using bisulphite sequencing. RNA interference was used to determine the consequence of SOD2 depletion on the levels of reactive oxygen species (ROS) using MitoSOX and collagenases, matrix metalloproteinase 1 (MMP-1) and MMP-13, gene expression. All three SOD were abundantly expressed in human cartilage but were markedly downregulated in end-stage OA cartilage, especially SOD2. In the Dunkin–Hartley guinea pig spontaneous OA model, SOD2 expression was decreased in the medial tibial condyle cartilage before, and after, the development of OA-like lesions. The SOD2 promoter had significant DNA methylation alterations in OA cartilage. Depletion of SOD2 in chondrocytes increased ROS but decreased collagenase expression. This is the first comprehensive expression profile of all SOD genes in cartilage and, importantly, using an animal model, it has been shown that a reduction in SOD2 is associated with the earliest stages of OA. A decrease in SOD2 was found to be associated with an increase in ROS but a reduction of collagenase gene expression, demonstrating the complexities of ROS function

The integrins of the urochordate Ciona intestinalis provide novel insights into the molecular evolution of the vertebrate integrin family

BACKGROUND: Integrins are a functionally significant family of metazoan cell surface adhesion receptors. The receptors are dimers composed of an alpha and a beta chain. Vertebrate genomes encode an expanded set of integrin alpha and beta chains in comparison with protostomes such as drosophila or the nematode worm. The publication of the genome of a basal chordate, Ciona intestinalis, provides a unique opportunity to gain further insight into how and when the expanded integrin supergene family found in vertebrates evolved. RESULTS: The Ciona genome encodes eleven α and five β chain genes that are highly homologous to their vertebrate homologues. Eight of the α chains contain an A-domain that lacks the short alpha helical region present in the collagen-binding vertebrate alpha chains. Phylogenetic analyses indicate the eight A-domain containing α chains cluster to form an ascidian-specific clade that is related to but, distinct from, the vertebrate A-domain clade. Two Ciona α chains cluster in laminin-binding clade and the remaining chain clusters in the clade that binds the RGD tripeptide sequence. Of the five Ciona β chains, three form an ascidian-specific clade, one clusters in the vertebrate β1 clade and the remaining Ciona chain is the orthologue of the vertebrate β4 chain. CONCLUSION: The Ciona repertoire of integrin genes provides new insight into the basic set of these receptors available at the beginning of vertebrate evolution. The ascidian and vertebrate α chain A-domain clades originated from a common precursor but radiated separately in each lineage. It would appear that the acquisition of collagen binding capabilities occurred in the chordate lineage after the divergence of ascidians

A Novel Form of Chondrocyte Stress is Triggered by a COMP Mutation Causing Pseudoachondroplasia

Pseudoachondroplasia (PSACH) results from mutations in cartilage oligomeric matrix protein (COMP) and the p.D469del mutation within the type III repeats of COMP accounts for approximately 30% of PSACH. To determine disease mechanisms of PSACH in vivo, we introduced the Comp D469del mutation into the mouse genome. Mutant animals were normal at birth but grew slower than their wild-type littermates and developed short-limb dwarfism. In the growth plates of mutant mice chondrocyte columns were reduced in number and poorly organized, while mutant COMP was retained within the endoplasmic reticulum (ER) of cells. Chondrocyte proliferation was reduced and apoptosis was both increased and spatially dysregulated. Previous studies on COMP mutations have shown mutant COMP is co-localized with chaperone proteins, and we have reported an unfolded protein response (UPR) in mouse models of PSACH-MED (multiple epiphyseal dysplasia) harboring mutations in Comp (T585M) and Matn3, Comp etc (V194D). However, we found no evidence of UPR in this mouse model of PSACH. In contrast, microarray analysis identified expression changes in groups of genes implicated in oxidative stress, cell cycle regulation, and apoptosis, which is consistent with the chondrocyte pathology. Overall, these data suggest that a novel form of chondrocyte stress triggered by the expression of mutant COMP is central to the pathogenesis of PSACH. Hum Mutat 33:218–231, 2012. © 2011 Wiley Periodicals, Inc

Reduced cell proliferation and increased apoptosis are significant pathological mechanisms in a murine model of mild pseudoachondroplasia resulting from a mutation in the C-terminal domain of COMP

Pseudoachondroplasia (PSACH) is one of the more common skeletal dysplasias and results from mutations in cartilage oligomeric matrix protein (COMP). Most COMP mutations identified to date cluster in the TSP3 repeat region of COMP and the mutant protein is retained in the rough endoplasmic reticulum (rER) of chondrocytes and may result in increased cell death. In contrast, the pathomolecular mechanism of PSACH resulting from C-terminal domain COMP mutations remain largely unknown. This study describes the generation and analysis of a murine model of mild PSACH resulting from a p.Thr583Met mutation in the C-terminal globular domain (CTD) of COMP. Mutant animals are normal at birth, but grow slower than their wild-type littermates and by 9 weeks of age they have mild short-limb dwarfism. Furthermore, by 16 months of age mutant animals exhibit severe degeneration of articular cartilage, which is consistent with early onset osteoarthritis seen in PSACH patients. In the growth plates of mutant mice the chondrocyte columns are sparser and poorly organized. Mutant COMP is secreted into the extracellular matrix, but its localization is disrupted along with the distribution of several COMP-binding proteins. Although mutant COMP is not retained within the rER there is an unfolded protein/cell stress response and chondrocyte proliferation is significantly reduced, while apoptosis is both increased and spatially dysregulated. Overall, these data suggests a mutation in the CTD of COMP exerts a dominant-negative effect on both intra- and extracellular processes. This ultimately affects the morphology and proliferation of growth plate chondrocytes, eventually leading to chondrodysplasia and reduced long bone growth

Development and techno-economic analyses of a novel hydrogen production process via chemical looping

In this work, a novel hydrogen production process (Integrated Chemical Looping Water Splitting “ICLWS”) has been developed. The modelled process has been optimised via heat integration between the main process units. The effects of the key process variables (i.e. the oxygen carrier-to-fuel ratio, steam flow rate and discharged gas temperature) on the behaviour of the reducer and oxidiser reactors were investigated. The thermal and exergy efficiencies of the process were studied and compared against a conventional steam-methane reforming (SMR) process. Finally, the economic feasibility of the process was evaluated based on the corresponding CAPEX, OPEX and first-year plant cost per kg of the hydrogen produced. The thermal efficiency of the ICLWS process was improved by 31.1% compared to the baseline (Chemical Looping Water Splitting without heat integration) process. The hydrogen efficiency and the effective efficiencies were also higher by 11.7% and 11.9%, respectively compared to the SMR process. The sensitivity analysis showed that the oxygen carrier–to-methane and -steam ratios enhanced the discharged gas and solid conversions from both the reducer and oxidiser. Unlike for the oxidiser, the temperature of the discharged gas and solids from the reducer had an impact on the gas and solid conversion. The economic evaluation of the process indicated hydrogen production costs of $1.41 and$1.62 per kilogram of hydrogen produced for Fe-based oxygen carriers supported by ZrO2 and MgAl2O4, respectively - 14% and 1.2% lower for the SMR process H2 production costs respectively

Cartilage-specific ablation of XBP1 signaling in mouse results in a chondrodysplasia characterized by reduced chondrocyte proliferation and delayed cartilage maturation and mineralization

SummaryObjectiveTo investigate the in vivo role of the IRE1/XBP1 unfolded protein response (UPR) signaling pathway in cartilage.DesignXbp1flox/flox.Col2a1-Cre mice (Xbp1CartΔEx2), in which XBP1 activity is ablated specifically from cartilage, were analyzed histomorphometrically by Alizarin red/Alcian blue skeletal preparations and X-rays to examine overall bone growth, histological stains to measure growth plate zone length, chondrocyte organization, and mineralization, and immunofluorescence for collagen II, collagen X, and IHH. Bromodeoxyuridine (BrdU) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analyses were used to measure chondrocyte proliferation and cell death, respectively. Chondrocyte cultures and microdissected growth plate zones were analyzed for expression profiling of chondrocyte proliferation or endoplasmic reticulum (ER) stress markers by Quantitative PCR (qPCR), and of Xbp1 mRNA splicing by RT-PCR to monitor IRE1 activation.ResultsXbp1CartΔEx2 displayed a chondrodysplasia involving dysregulated chondrocyte proliferation, growth plate hypertrophic zone shortening, and IRE1 hyperactivation in chondrocytes. Deposition of collagens II and X in the Xbp1CartΔEx2 growth plate cartilage indicated that XBP1 is not required for matrix protein deposition or chondrocyte hypertrophy. Analyses of mid-gestation long bones revealed delayed ossification in Xbp1CartΔEx2 embryos. The rate of chondrocyte cell death was not significantly altered, and only minimal alterations in the expression of key markers of chondrocyte proliferation were observed in the Xbp1CartΔEx2 growth plate. IRE1 hyperactivation occurred in Xbp1CartΔEx2 chondrocytes but was not sufficient to induce regulated IRE1-dependent decay (RIDD) or a classical UPR.ConclusionOur work suggests roles for XBP1 in regulating chondrocyte proliferation and the timing of mineralization during endochondral ossification, findings which have implications for both skeletal development and disease