Mechanisms and Mitigation of Agglomeration during Fluidized Bed Combustion of Biomass: A Review

A key issue associated with fluidized bed combustion of biomass is agglomeration. The presence of high quantities of alkali metal species in biomass ash leads to the formation of sticky alkali silicate liquid phases during combustion, and consequently the adhesion and agglomeration of bed material. This review examines probable mechanisms of agglomeration and the effects of operational variables in reducing its severity. Additionally, an overview of monitoring and prediction of agglomerate formation is given. Two key mechanisms of agglomeration are apparent in literature, and both may occur concurrently dependending on fuel composition. Coating-induced agglomeration is defined by the interaction of alkali metals in fuel ash with silica in the bed material to form an alkali silicate melt. Melt-induced agglomeration is defined by the presence of sufficient amounts of alkali metals and silica in the fuel ash which together form a eutectic melt. Physical mechanisms, such as tumble agglomeration and sintering, may further enhance either of the coating-induced or melt-induced mechanisms. Of the operational variables examined in this review, temperature, fluidizing gas velocity, fuel, bed material and additives have been shown to have the greatest effect on agglomeration severity. Prediction of agglomeration propensity may be attempted with mathematical correlations or lab-scale fuel testing before use in the boiler, or with in-situ methods, which are typically focused on temperature or pressure analysis. The review of the literature has highlighted the need for further research in several areas, including: mechanisms when using alternate bed materials, use of dual-fuel biomass blends, technical and economic optimisation of the use of alternative bed materials and additives, and further modelling of coating growth behaviours

Bio-CCS: co-firing of established greenfield and novel, brownfield biomass resources under air, oxygen-enriched air and oxy-fuel conditions

As demand for electricity and atmospheric CO concentrations rise technologies that reduce the environmental impact of generating electricity are sought. Within the many options a combination of co-firing of biomass and carbon capture and storage (Bio-CCS) could present a negative-emission process. This work investigates co-firing of a novel brownfield and two conventional greenfield biomass reserves with coal in oxygen-enriched conditions which may enhance the efficiency of post-combustion capture units. A 20kW furnace is used to assess combustion characteristics in a range of scenarios. Results suggest oxidant staging during oxygen-enriched co-firing can exhibit lower NO emissions while achieving high combustion efficiencies

Reactivity during bench-scale combustion of biomass fuels for carbon capture and storage applications

Reactivities of four biomass samples were investigated in four combustion atmospheres using non-isothermal thermogravimetric analysis (TGA) under two heating rates. The chosen combustion atmospheres reflect carbon capture and storage (CCS) applications and include O2O2 and CO2CO2-enrichment. Application of the Coats–Redfern method assessed changes in reactivity. Reactivity varied due to heating rate: the reactivity of char oxidation was lower at higher heating rates while devolatilisation reactions were less affected. In general, and particularly at the higher heating rate, increasing [O2O2] increased combustion reactivity. A lesser effect was observed when substituting N2N2 for CO2CO2 as the comburent; in unenriched conditions this tended to reduce char oxidation reactivity while in O2O2-enriched conditions the reactivity marginally increased. Combustion in a typical, dry oxyfuel environment (30% O2O2, 70% CO2CO2) was more reactive than in air in TGA experiments. These biomass results should interest researchers seeking to understand phenomena occurring in larger scale CCS-relevant experiments

Efficacy and micro-characterization of pathophysiological events on caries-affected dentin treated with glass-ionomer cements

The aim of this study was to evaluate if mechanical cycling influences bioactivity and bond strength at the glass-ionomer cement-dentin interface, after load cycling. Microtensile bond strength (MTBS) was assessed with Ketac-Bond (conventional glass ionomer/GIC) or Vitrebond Plus (resin-modified/RMGIC), in sound dentin or in cariesaffected dentin (CAD). Debonded dentin surfaces were studied by field emission scanning electron microscopy (FESEM), and remineralization was evaluated through nanohardness (Hi) and Young’s modulus (Ei), Raman spectroscopy, and Masson's trichrome staining technique. Load cycling did not affect MTBS, except when Ketac- Bond was applied on sound dentin, which attained 100% pretesting failures. Minerals precipitated in porous platforms. GIC promoted total occlusion of tubules, and RMGIC originated empty or partial occluded tubules. In sound dentin, load cycling produced an increase of the relative presence of crystalline minerals after using Ketac-Bond (Phosphate peak, from 18.04 up to 81.29 cm-1 at hybrid layer, and from 19.28 up to 108.48 cm-1 at the bottom of the hybrid layer; Carbonate peak, from 8.06 up to 15.43 cm-1 at the hybrid layer, and from 7.22 up to 19.07 cm-1 at the bottom of the hybrid layer). Vitrebond Plus, in sound dentin, attained opposite outcomes. In CAD treated with Ketac- Bond, the highest Hi (1.11 GPa) and Ei (32.91 GPa) values were obtained at the hybrid layer after load cycling. This GIC showed increased and immature mineral components (an average of 25.82 up to 30.55 cm-1), higher frequencies of crosslinking (considering the pyridinium ring at hybrid layer, from 4.1 up to 6.86 cm-1; at bottom of the hybrid layer, from 7.55 up to 8.58 cm-1) and worst collagen quality (considering the ratio amide I/AGEs-pentosidine at the hybrid layer, from 0.89 up to 0.69 cm-1; at the bottom of the hybrid layer, from 1.39 up to 1.29 cm-1) after load cycling, at the interface of the CAD samples. Both Hi and Ei of CAD treated with RMGIC were not affected 4 after load cycling, though phosphates, carbonates and crystallinity increased. The organic components showed a dissimilar crosslinking and an improvement of the nature of collagen. Trichrome staining showed lower signs of demineralization or exposed proteins after mechanical loading, though Vitrebond Plus exhibited a slight increment in red intensity at the interface. The null hypothesis to be tested is that bond strength, chemical bonding and mechanical performance of the tested ionomer-based cements would not be influenced by the application of load cycling on restorations of sound and caries-affected dentin substrates.Project MAT2014-52036-P supported by the Ministery of Economy and Competitiveness (MINECO) and European Regional Development Fund (FEDER)

Modulation of Mrp1 (ABCc1) and Pgp (ABCb1) by Bilirubin at the Blood-CSF and Blood-Brain Barriers in the Gunn Rat

Accumulation of unconjugated bilirubin (UCB) in the brain causes bilirubin encephalopathy. Pgp (ABCb1) and Mrp1 (ABCc1), highly expressed in the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB) respectively, may modulate the accumulation of UCB in brain. We examined the effect of prolonged exposure to elevated concentrations of UCB on expression of the two transporters in homozygous, jaundiced (jj) Gunn rats compared to heterozygous, not jaundiced (Jj) littermates at different developmental stages (2, 9, 17 and 60 days after birth). BBB Pgp protein expression was low in both jj and Jj pups at 9 days (about 16–27% of adult values), despite the up-regulation in jj animals (2 and 1.3 fold higher than age matched Jj animals at P9 and P17–P60, respectively); Mrp1 protein expression was barely detectable. Conversely, at the BCSFB Mrp1 protein expression was rather high (60–70% of the adult values) in both jj and Jj at P2, but was markedly (50%) down-regulated in jj pups starting at P9, particularly in the 4th ventricle choroid plexuses: Pgp was almost undetectable. The Mrp1 protein down regulation was accompanied by a modest up-regulation of mRNA, suggesting a translational rather than a transcriptional inhibition. In vitro exposure of choroid plexus epithelial cells obtained from normal rats to UCB, also resulted in a down-regulation of Mrp1 protein. These data suggest that down-regulation of Mrp1 protein at the BSCFB, resulting from a direct effect of UCB on epithelial cells, may impact the Mrp1-mediated neuroprotective functions of the blood-cerebrospinal fluid barrier and actually potentiate UCB neurotoxicity

Molecular biology of the blood-brain and the blood-cerebrospinal fluid barriers: similarities and differences

Efficient processing of information by the central nervous system (CNS) represents an important evolutionary advantage. Thus, homeostatic mechanisms have developed that provide appropriate circumstances for neuronal signaling, including a highly controlled and stable microenvironment. To provide such a milieu for neurons, extracellular fluids of the CNS are separated from the changeable environment of blood at three major interfaces: at the brain capillaries by the blood-brain barrier (BBB), which is localized at the level of the endothelial cells and separates brain interstitial fluid (ISF) from blood; at the epithelial layer of four choroid plexuses, the blood-cerebrospinal fluid (CSF) barrier (BCSFB), which separates CSF from the CP ISF, and at the arachnoid barrier. The two barriers that represent the largest interface between blood and brain extracellular fluids, the BBB and the BCSFB, prevent the free paracellular diffusion of polar molecules by complex morphological features, including tight junctions (TJs) that interconnect the endothelial and epithelial cells, respectively. The first part of this review focuses on the molecular biology of TJs and adherens junctions in the brain capillary endothelial cells and in the CP epithelial cells. However, normal function of the CNS depends on a constant supply of essential molecules, like glucose and amino acids from the blood, exchange of electrolytes between brain extracellular fluids and blood, as well as on efficient removal of metabolic waste products and excess neurotransmitters from the brain ISF. Therefore, a number of specific transport proteins are expressed in brain capillary endothelial cells and CP epithelial cells that provide transport of nutrients and ions into the CNS and removal of waste products and ions from the CSF. The second part of this review concentrates on the molecular biology of various solute carrier (SLC) transport proteins at those two barriers and underlines differences in their expression between the two barriers. Also, many blood-borne molecules and xenobiotics can diffuse into brain ISF and then into neuronal membranes due to their physicochemical properties. Entry of these compounds could be detrimental for neural transmission and signalling. Thus, BBB and BCSFB express transport proteins that actively restrict entry of lipophilic and amphipathic substances from blood and/or remove those molecules from the brain extracellular fluids. The third part of this review concentrates on the molecular biology of ATP-binding cassette (ABC)-transporters and those SLC transporters that are involved in efflux transport of xenobiotics, their expression at the BBB and BCSFB and differences in expression in the two major blood-brain interfaces. In addition, transport and diffusion of ions by the BBB and CP epithelium are involved in the formation of fluid, the ISF and CSF, respectively, so the last part of this review discusses molecular biology of ion transporters/exchangers and ion channels in the brain endothelial and CP epithelial cells