| 1. |
- Berg, Magnus, et al.
(författare)
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Förbränning av utsorterade avfallsfraktioner
- 2005
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Rapport (övrigt vetenskapligt/konstnärligt)abstract
- Projektet har visat på möjligheter och problem vid förbränning av utsorterade avfallsfraktioner bestående av papper, trä och plast i fluidbädd. Denna typ av bränslen kan antingen samförbrännas eller användas som enda bränsle i en avfallspanna. I båda fallen bör gällande gränsvärden för emissioner till luft kunna klaras men man får däremot räkna med ökade drift- och underhållskostnader, främst beroende på ökade problem med påslag och korrosion. Dessa problem är starkt kopplade till bränslets innehåll av oönskade ämnen såsom klor, alkali och vissa andra metaller. Innehållet av dessa ämnen varierar kraftigt mellan olika bränslefraktioner och därmed blir omfattningen av problemen beroende både av inblandningsgrad och av bränslets ursprung. Projektet har även visat att mängden påslag kan minskas genom tillsats av svaveladditiv samtidigt som den kemiska samansättningen i påslagen förändras på ett sådant sätt att även risken för korrosion bör minska.
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| 2. |
- Blomqvist, Evalena, et al.
(författare)
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Samförbränning av bilfluff, rötslam och avfall i en 20 MW fluidbäddpanna - Studier av bränslesammansättningens påverkan på beläggningsbildning
- 2007
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Rapport (refereegranskat)abstract
- In order to prevent a further increased use of resources and to decrease the environmental impact from landfills, organic wastes are today diverted towards material and energy recovery. This creates a waste market with an increasing number of waste fractions that needs to be treated properly. As an example, in Sweden it has recently been prohibited to landfill source separated combustible waste (2002) and organic waste (2005). Wastes as automotive shredder residue (ASR) and sewage sludge can no longer be landfilled and needs to be either material or energy recovered, which challenge the waste treatment sector. This work investigates the effects of ASR and sewage sludge co-combustion in a 20 MW Energy-from-Waste plant (bubbling fluidised bed). The long term objective of the work is to increase the fuel flexibility, the boiler availability and the power production. This report focus on boiler operation and combustion performance in terms of agglomeration, deposit rates and emissions. In addition to the tests with ASR and sewage sludge, repeated measurements were performed during normal load as a reference. The results show that the co-combusted fractions of ASR and sewage sludge, which on mass basis constituted 6 % and 15 % respectively, did not increase the risk for agglomeration or deposits on heat-exchanging surfaces. Instead, compared to the two reference cases, the deposit rates decreased when sewage sludge was added. Only minor variation in the emissions was seen between the different cases. The levels of I-TEQs were far below the legislated values in all cases.
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| 3. |
- Davidsson, Kent, 1967, et al.
(författare)
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Countermeasures against alkali-related problems during combustion of biomass in a circulating fluidized bed boiler
- 2008
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Ingår i: Chemical Engineering Science. ; 63, s. 5314-5329
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of this work was to study different ways to mitigate alkali-related problems during combustionof biomass in circulating fluidized beds. Wood chips and wood pellets were fired together withstraw pellets, while the tendency to agglomerate and form deposits was monitored. In addition to areference case, a number of countermeasures were applied in related tests. Those were addition of elementalsulphur, ammonium sulphate and kaolin to a bed of silica sand, as well as use of olivine sand andblast-furnace slag as alternative bed materials. The agglomeration temperature, composition and structureof bed-ash samples were examined. The flue-gas composition, including gaseous alkali chlorides, wasmeasured in the hot flue gases and in the stack. Particles in the flue gas were collected and analysed forsize distribution and composition. Deposits were collected on a probe in hot flue gases and their amountand composition were analysed. Addition of kaolin was found to be the best method to counteract theagglomeration problem. The deposition problem is effectively counteracted with addition of ammoniumsulphate, while kaolin is too expensive to be used commercially against deposits, and sulphur is lesseffective than ammonium sulphate.
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| 4. |
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| 5. |
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| 6. |
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| 7. |
- Elled, Anna-Lena, et al.
(författare)
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The fate of zinc during combustion of demolition wood in a fluidized bed boiler
- 2007
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Ingår i: Energy & Fuels. - : American Chemical Society. - 0887-0624 .- 1520-5029. ; 22:3
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Tidskriftsartikel (refereegranskat)abstract
- Demolition wood can be used as a fuel in heat and power plants. However, it may contain elevated amounts of zinc, originating from white paint, which can cause problems related to deposit formation and corrosion on heat transfer surfaces. In this work, combustion tests with zinc addition were carried out in a fluidized bed boiler to investigate its effect on deposit formation. Thermodynamic equilibrium calculations were performed to complement the experimental data. The results show that combustion of demolition wood only contaminated with zinc generates a modest amount of deposit. Combustion of demolition wood contaminated with both zinc and chlorine promotes the deposit formation due to the increased amount of submicron particles in the flue gas. The thermodynamic equilibrium analyses show further that reducing conditions increase the release of zinc to the flue gas. On the other hand, in the case of oxidizing conditions, the retention of zinc in the ash is strong. Zinc, in combination with chlorine, gives rise to formation of zinc chloride in the flue gas. The formation is, at reducing conditions, thermodynamically favored between 450 and 850 °C. At oxidizing conditions, the formation is initiated at 400 °C and gradually increased with the temperature.
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| 8. |
- Engström, Linda, et al.
(författare)
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Acetaminophen reduces lipopolysaccharide-induced fever by inhibiting cyclooxygenase-2
- 2013
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Ingår i: Neuropharmacology. - : Elsevier. - 0028-3908 .- 1873-7064. ; 71, s. 124-129
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Tidskriftsartikel (refereegranskat)abstract
- Acetaminophen is one of the world's most commonly used drugs to treat fever and pain, yet its mechanism of action has remained unclear. Here we tested the hypothesis that acetaminophen blocks fever through inhibition of cyclooxygenase-2 (Cox-2), by monitoring lipopolysaccharide induced fever in mice with genetic manipulations of enzymes in the prostaglandin cascade. We exploited the fact that lowered levels of a specific enzyme make the system more sensitive to any further inhibition of the same enzyme. Mice were immune challenged by an intraperitoneal injection of bacterial wall lipopolysaccharide and their body temperature recorded by telemetry. We found that mice heterozygous for Cox-2, but not for microsomal prostaglandin E synthase-1 (mPGES-1), displayed attenuated fever, indicating a rate limiting role of Cox-2. We then titrated a dose of acetaminophen that did not inhibit the lipopolysaccharide-induced fever in wild-type mice. However, when the same dose of acetaminophen was given to Cox-2 heterozygous mice, the febrile response to lipopolysaccharide was strongly attenuated, resulting in an almost normalized temperature curve, whereas no difference was seen between wild-type and heterozygous mPGES-1 mice. Furthermore, the fever to intracerebrally injected prostaglandin E2 was unaffected by acetaminophen treatment. These findings reveal that acetaminophen, similar to aspirin and other non-steroidal anti-inflammatory drugs, is antipyretic by inhibiting cyclooxygenase-2, and not by inhibiting mPGES-1 or signaling cascades downstream of prostaglandin E2.
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| 9. |
- Engström, Linda, et al.
(författare)
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Lipopolysaccharide-Induced Fever Depends on Prostaglandin E2 Production Specifically in Brain Endothelial Cells
- 2012
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Ingår i: Endocrinology. - : Endocrine Society. - 0013-7227 .- 1945-7170. ; 153:10, s. 4849-4861
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Tidskriftsartikel (refereegranskat)abstract
- Immune-induced prostaglandin E2 (PGE2) synthesis is critical for fever and other centrally elicited disease symptoms. The production of PGE2 depends on cyclooxygenase-2 and microsomal prostaglandin E synthase-1 (mPGES-1), but the identity of the cells involved has been a matter of controversy. We generated mice expressing mPGES-1 either in cells of hematopoietic or nonhematopoietic origin. Mice lacking mPGES-1 in hematopoietic cells displayed an intact febrile response to lipopolysaccharide, associated with elevated levels of PGE2 in the cerebrospinal fluid. In contrast, mice that expressed mPGES-1 only in hematopoietic cells, although displaying elevated PGE2 levels in plasma but not in the cerebrospinal fluid, showed no febrile response to lipopolysaccharide, thus pointing to the critical role of brain-derived PGE2 for fever. Immunohistochemical stainings showed that induced cyclooxygenase-2 expression in the brain exclusively occurred in endothelial cells, and quantitative PCR analysis on brain cells isolated by flow cytometry demonstrated that mPGES-1 is induced in endothelial cells and not in vascular wall macrophages. Similar analysis on liver cells showed induced expression in macrophages and not in endothelial cells, pointing at the distinct role for brain endothelial cells in PGE2 synthesis. These results identify the brain endothelial cells as the PGE2-producing cells critical for immune-induced fever.
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| 10. |
- Eskilsson, Anna, 1986-, et al.
(författare)
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Fever During Localized Inflammation in Mice Is Elicited by a Humoral Pathway and Depends on Brain Endothelial Interleukin-1 and Interleukin-6 Signaling and Central EP3 Receptors
- 2021
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Ingår i: Journal of Neuroscience. - : SOC NEUROSCIENCE. - 0270-6474 .- 1529-2401. ; 41:24, s. 5206-5218
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Tidskriftsartikel (refereegranskat)abstract
- We examined the signaling route for fever during localized inflammation in male and female mice, elicited by casein injection into a preformed air pouch. The localized inflammation gave rise to high concentrations of prostaglandins of the E species (PGE(2)) and cytokines in the air pouch and elevated levels of these inflammatory mediators in plasma. There were also elevated levels of PGE(2) in the cerebrospinal fluid, although there was little evidence for PGE(2) synthesis in the brain. Global deletion of the PGE(2) prostaglandin E receptor 3 (EP3) abolished the febrile response as did deletion of the EP3 receptor in neural cells, whereas its deletion on peripheral nerves had no effect, implying that PGE(2) action on this receptor in the CNS elicited the fever. Global deletion of the interleukin-1 receptor type 1 (IL-1R1) also abolished the febrile response, whereas its deletion on neural cells or peripheral nerves had no effect. However, deletion of the IL-1R1 on brain endothelial cells, as well as deletion of the interleukin-6 receptor a on these cells, attenuated the febrile response. In contrast, deletion of the PGE(2) synthesizing enzymes cyclooxygenase-2 and microsomal prostaglandin synthase-1 in brain endothelial cells, known to attenuate fever evoked by systemic inflammation, had no effect. We conclude that fever during localized inflammation is not mediated by neural signaling from the inflamed site, as previously suggested, but is dependent on humoral signaling that involves interleukin actions on brain endothelial cells, probably facilitating PGE(2) entry into the brain from the circulation and hence representing a mechanism distinct from that at work during systemic inflammation.
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| 11. |
- Eskilsson, Anna, et al.
(författare)
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Immune-Induced Fever Is Dependent on Local But Not Generalized Prostaglandin E-2 Synthesis in the Brain
- 2017
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Ingår i: Journal of Neuroscience. - : SOC NEUROSCIENCE. - 0270-6474 .- 1529-2401. ; 37:19, s. 5035-5044
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Tidskriftsartikel (refereegranskat)abstract
- Fever occurs upon binding of prostaglandin E-2 (PGE(2)) to EP3 receptors in the median preoptic nucleus of the hypothalamus, but the origin of the pyrogenic PGE(2) has not been clearly determined. Here, using mice of both sexes, we examined the role of local versus generalized PGE(2) production in the brain for the febrile response. In wild-type mice and in mice with genetic deletion of the prostaglandin synthesizing enzyme cyclooxygenase-2 in the brain endothelium, generated with an inducible CreER(T2) under the Slco1c1 promoter, PGE(2) levels in the CSF were only weakly related to the magnitude of the febrile response, whereas the PGE(2) synthesizing capacity in the hypothalamus, as reflected in the levels of cyclooxygenase-2 mRNA, showed strong correlation with the immune-induced fever. Histological analysis showed that the deletion of cyclooxygenase-2 in brain endothelial cells occurred preferentially in small-and medium-sized vessels deep in the brain parenchyma, such as in the hypothalamus, whereas larger vessels, and particularly those close to the neocortical surface and in the meninges, were left unaffected, hence leaving PGE(2) synthesis largely intact in major parts of the brain while significantly reducing it in the region critical for the febrile response. Furthermore, injection of a virus vector expressing microsomal prostaglandin E synthase-1 (mPGES-1) into the median preoptic nucleus of fever-refractive mPGES-1 knock-out mice, resulted in a temperature elevation in response to LPS. We conclude that the febrile response is dependent on local release of PGE(2) onto its target neurons and not on the overall PGE(2) production in the brain.
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| 12. |
- Eskilsson, Anna, et al.
(författare)
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Immune-Induced Fever Is Mediated by IL-6 Receptors on Brain Endothelial Cells Coupled to STAT3-Dependent Induction of Brain Endothelial Prostaglandin Synthesis
- 2014
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Ingår i: Journal of Neuroscience. - : Society for Neuroscience. - 0270-6474 .- 1529-2401. ; 34:48, s. 15957-15961
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Tidskriftsartikel (refereegranskat)abstract
- The cytokine IL-6, which is released upon peripheral immune challenge, is critical for the febrile response, but the mechanism by which IL-6 is pyrogenic has remained obscure. Herewegenerated mice with deletion of themembranebound IL-6 receptor alpha (IL-6R alpha) onneural cells, on peripheral nerves, on fine sensory afferent fibers, and on brain endothelial cells, respectively, and examined its role for the febrile response to peripherally injected lipopolysaccharide. We show that IL-6R alpha on neural cells, peripheral nerves, and fine sensory afferents are dispensable for the lipopolysaccharide-induced fever, whereas IL-6R alpha in the brain endothelium plays an important role. Hence deletion of IL-6R alpha on brain endothelial cells strongly attenuated the febrile response, and also led to reduced induction of the prostaglandin synthesizing enzyme Cox-2 in the hypothalamus, the temperature-regulating center in the brain, as well as reduced expression of SOCS3, suggesting involvement of the STAT signaling pathway. Furthermore, deletion of STAT3 in the brain endothelium also resulted in attenuated fever. These data show that IL-6, when endogenously released during systemic inflammation, is pyrogenic by binding to IL-6R alpha on brain endothelial cells to induce prostaglandin synthesis in these cells, probably in concerted action with other peripherally released cytokines.
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| 13. |
- Eskilsson, Anna, 1986-
(författare)
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Inflammatory Signaling Across the Blood-Brain Barrier and the Generation of Fever
- 2020
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Fever is a cardinal sign of inflammation and is evolutionary conserved. Fever is known to be beneficial during acute inflammation, but over time and if very high it can be detrimental. The signaling pathways by which fever is initiated by the brain and the peripheral mechanisms through which the temperature increase is generated were studied from several point of views. Fever is known to be dependent on prostaglandin E2 (PGE2) binding to its receptors in the median preoptic nucleus of the hypothalamus, which signals to the brainstem and through sympathetic nerves to heat conserving and heat producing effector organs. This thesis focuses on identifying the cells that produce the PGE2 critical for the fever response; showing where in the brain the critical PGE2 production takes place; demonstrating how peripheral inflammation activates these cells to produce PGE2; and finally, identifying the effector mechanisms behind the temperature elevation in fever. By using a newly developed specific antibody we showed that the enzyme responsible for the terminal step in the production of PGE2, microsomal prostaglandin E-synthase 1 (mPGES-1), is expressed in endothelial cells of brain blood vessels in mice where it is co-expressed with the enzyme cyclooxygenase-2 (Cox-2), which is known to be induced in these cells and to be rate limiting for the PGE2 production. The mPGES-1 enzyme was also expressed in several other cell types and structures which however did not express Cox-2, such as capillary-associated pericytes, astroglial cells, leptomeninges, and the choroid plexus. The role of the mPGES-1 in these other cells/structures remains unknown. Next, by using mice with selective deletion of Cox-2 in brain endothelial cells, we showed that local PGE2 production in deep brain areas, such as the hypothalamus, is critical for the febrile response to peripheral inflammation. In contrast, PGE2 production in other brain areas and the overall PGE2 level in the brain were not critical for the febrile response. Partly restoring the PGE2 synthesizing capacity in the anterior hypothalamus of mice lacking such capacity with a lentiviral vector resulted in a temperature elevation in response to an intraperitoneal injection of bacterial wall lipopolysaccharide (LPS). The data show that the febrile response is dependent on the local release of PGE2 onto its target neurons, possibly by a paracrine mechanism. Deletion of the receptor for the pyrogenic cytokine IL-6 on brain endothelial cells, but not on neurons or peripheral nerves, strongly attenuated the febrile response to LPS and reduced the induction of the Cox-2 expression in the hypothalamus. Furthermore, mice deficient of the IL- 6Rα gene in the brain endothelial cells showed a reduced SOCS3 mRNA induction, whereas IκB mRNA-levels were unaffected, suggesting that the IL-6 signaling occurs via STAT3 activation and not signaling through the transcription factor NF-κB. This idea was confirmed by the observation of attenuated fever in mice deficient of STAT3 in brain endothelial cells. These data show that IL-6, when endogenously released during systemic inflammation, is pyrogenic by binding to IL-6R on brain endothelial cells to induce prostaglandin synthesis in these cells. Finally, we demonstrate that mice with genetic deletion of uncoupling protein-1 (UCP-1), hence lacking functional brown adipose tissue, had a normal fever response to LPS, and that LPS caused no activation of brown adipose tissue in wild type mice. However, blocking peripheral cutaneous vasoconstriction resulted in a blunted fever response to LPS, suggesting that heat conservation, possibly together with shivering or non-shivering thermogenesis in the musculature, is responsible for the generation of immune-induced fever, whereas brown adipose tissue thermogenesis is not involved.
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| 14. |
- Eskilsson, Anna, et al.
(författare)
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The generation of immune-induced fever and emotional stress-induced hyperthermia in mice does not involve brown adipose tissue thermogenesis
- 2020
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Ingår i: FASEB Journal. - : WILEY. - 0892-6638 .- 1530-6860. ; 34:4, s. 5863-5876
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Tidskriftsartikel (refereegranskat)abstract
- We examined the role of brown adipose tissue (BAT) for fever and emotional stress-induced hyperthermia. Wild-type and uncoupling protein-1 (UCP-1) knockout mice were injected with lipopolysaccharide intraperitoneally or intravenously, or subjected to cage exchange, and body temperature monitored by telemetry. Both genotypes showed similar febrile responses to immune challenge and both displayed hyperthermia to emotional stress. Neither procedure resulted in the activation of BAT, such as the induction of UCP-1 or peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha) mRNA, or reduced BAT weight and triglyceride content. In contrast, in mice injected with a beta (3) agonist, UCP-1 and PGC-1 alpha were strongly induced, and BAT weight and triglyceride content reduced. Both lipopolysaccharide and the beta (3) agonist, and emotional stress, induced UCP-3 mRNA in skeletal muscle. A beta (3) antagonist did not attenuate lipopolysaccharide-induced fever, but augmented body temperature decrease and inhibited BAT activation when mice were exposed to cold. An alpha (1)/alpha (2b) antagonist or a 5HT(1A) agonist, which inhibit vasoconstriction, abolished lipopolysaccharide-induced fever, but had no effect on emotional stress-induced hyperthermia. These findings demonstrate that in mice, UCP-1-mediated BAT thermogenesis does not take part in inflammation-induced fever, which is dependent on peripheral vasoconstriction, nor in stress-induced hyperthermia. However, both phenomena may involve UCP-3-mediated muscle thermogenesis.
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| 15. |
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| 16. |
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| 17. |
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| 18. |
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| 19. |
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| 20. |
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| 21. |
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| 22. |
- Kling, Asa, et al.
(författare)
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Alkali deactivation of high-dust SCR catalysts used for NOx reduction exposed to flue gas from 100 MW-scale biofuel and peat fired boilers : Influence of flue gas composition
- 2007
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Ingår i: Applied Catalysis B. - : Elsevier BV. - 0926-3373 .- 1873-3883. ; 69:04-mar, s. 240-251
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Tidskriftsartikel (refereegranskat)abstract
- Deactivation of vanadium-titanium deNO(x) SCR (selective catalytic reduction) catalysts in high-dust position have been investigated in three 100 MW-scale boilers during biofuel and peat combustion. The deactivation of the catalyst samples has been correlated to the corresponding flue gas composition in the boilers. Too investigate the effect on catalyst deactivation a sulphate-containing additive was sprayed into one of the furnaces. Increased alkali content on the SCR catalyst samples decreased the catalytic deNO(x), activity. The study has shown a linear correlation between exposure time in the boilers and alkali concentration (mainly potassium) on the samples. The results imply that mainly alkali in ultra fine particles (< 100 nm) in the flue gas increased the alkali accumulation on the catalyst samples. Low correlation was found between particles larger than 100 nm and the catalyst deactivation. It was not possible to decrease the deactivation of the catalyst samples by the sulphate-containing additive. Although the additive had an effect in sulphating potassium chloride to potassium sulphate, it did not decrease the amount of potassium in ultra fine particles or the deactivation of the catalyst samples.
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| 23. |
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| 24. |
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| 25. |
- Matsuwaki, Takashi, 1978-, et al.
(författare)
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Involvement of interleukin-1 type 1 receptors in lipopolysaccharide-induced sickness responses
- 2017
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Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 66, s. 165-176
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Tidskriftsartikel (refereegranskat)abstract
- Sickness responses to lipopolysaccharide (LPS) were examined in mice with deletion of the interleukin (IL)-1 type 1 receptor (IL-1R1). IL-1R1 knockout (1(0) mice displayed intact anorexia and HPA-axis activation to intraperitoneally injected LPS (anorexia: 10 or 120 mu g/kg; HPA-axis: 120 mu g/kg), but showed attenuated but not extinguished fever (120 g/kg). Brain PGE2 synthesis was attenuated, but Cox-2 induction remained intact. Neither the tumor necrosis factor-alpha (TNF alpha) inhibitor etanercept nor the IL -6 receptor antibody tocilizumab abolished the LPS induced fever in IL -1R1 KO mice. Deletion of IL -1R1 specifically in brain endothelial cells attenuated the LPS induced fever, but only during the late, 3rd phase of fever, whereas deletion of IL-1R1 on neural cells or on peripheral nerves had little or no effect on the febrile response. We conclude that while IL-1 signaling is not critical for LPS induced anorexia or stress hormone release, IL-1R1, expressed on brain endothelial cells, contributes to the febrile response to LPS. However, also in the absence of IL-1R1, LPS evokes a febrile response, although this is attenuated. This remaining fever seems not to be mediated by IL-6 receptors or TNFa, but by some yet unidentified pyrogenic factor.
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| 26. |
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| 27. |
- Ruud, Johan, et al.
(författare)
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Inflammation- and tumor-induced anorexia and weight loss require MyD88 in hematopoietic/myeloid cells but not in brain endothelial or neural cells.
- 2013
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Ingår i: FASEB journal : official publication of the Federation of American Societies for Experimental Biology. - : Wiley. - 1530-6860 .- 0892-6638. ; 27:5, s. 1973-80
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Tidskriftsartikel (refereegranskat)abstract
- Loss of appetite is a hallmark of inflammatory diseases. The underlying mechanisms remain undefined, but it is known that myeloid differentiation primary response gene 88 (MyD88), an adaptor protein critical for Toll-like and IL-1 receptor family signaling, is involved. Here we addressed the question of determining in which cells the MyD88 signaling that results in anorexia development occurs by using chimeric mice and animals with cell-specific deletions. We found that MyD88-knockout mice, which are resistant to bacterial lipopolysaccharide (LPS)-induced anorexia, displayed anorexia when transplanted with wild-type bone marrow cells. Furthermore, mice with a targeted deletion of MyD88 in hematopoietic or myeloid cells were largely protected against LPS-induced anorexia and displayed attenuated weight loss, whereas mice with MyD88 deletion in hepatocytes or in neural cells or the cerebrovascular endothelium developed anorexia and weight loss of similar magnitude as wild-type mice. Furthermore, in a model for cancer-induced anorexia-cachexia, deletion of MyD88 in hematopoietic cells attenuated the anorexia and protected against body weight loss. These findings demonstrate that MyD88-dependent signaling within the brain is not required for eliciting inflammation-induced anorexia. Instead, we identify MyD88 signaling in hematopoietic/myeloid cells as a critical component for acute inflammatory-driven anorexia, as well as for chronic anorexia and weight loss associated with malignant disease.
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| 28. |
- Ruud, Johan, et al.
(författare)
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MyD88 in hematopoietic cells, but not in cerebrovascular endothelial cells or neural cells, is critical for inflammation- and cancer-induced loss of appetite
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Loss of appetite concomitant with reduced food intake is a hallmark of both acute and chronic inflammatory diseases. Yet, despite extensive investigations, the underlying mechanisms remain undefined. Here we addressed this issue using mice lacking MyD88, critical for Tolllike and IL-1 receptor family signaling, generally or in specific cell types. Ubiquitous null deletions conferred complete resistance to bacterial lipopolysaccharide (LPS) induced anorexia, but this resistance was lost when knock-out mice subjected to whole-body irradiation to delete hematopoietic cells were transplanted with wild-type bone-marrow. In line with this observation, mice lacking MyD88 in hematopoietic cells were largely protected against LPS-induced anorexia, whereas mice with abrogated MyD88 signaling in neural cells, being leaner and smaller, developed anorexia of similar magnitude as wild-type littermates. The effect of hematopoietic MyD88-deletion on feeding seemed however partially dissociated from the effect on body weight, since LPS triggered weight loss, although attenuated, in these mutants. Furthermore, MyD88 deficiency in the cerebrovascular endothelium affected neither LPS-induced anorexia nor weight loss. In a model for the cancer anorexia-cachexia syndrome, inactivation of MyD88 in hematopoietic cells strongly impaired the anorexia development and protected against body weight loss. These findings identify hematopoietic cells as a critical nexus for acute inflammatory driven anorexia as well as for chronic anorexia associated with malignant disease.
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| 29. |
- Wilhelms, Daniel Björk, et al.
(författare)
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Deletion of Prostaglandin E-2 Synthesizing Enzymes in Brain Endothelial Cells Attenuates Inflammatory Fever
- 2014
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Ingår i: Journal of Neuroscience. - : Society for Neuroscience. - 0270-6474 .- 1529-2401. ; 34:35, s. 11684-11690
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Tidskriftsartikel (refereegranskat)abstract
- Fever is a hallmark of inflammatory and infectious diseases. The febrile response is triggered by prostaglandin E-2 synthesis mediated by induced expression of the enzymes cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase 1 (mPGES-1). The cellular source for pyrogenic PGE(2) remains a subject of debate; several hypotheses have been forwarded, including immune cells in the periphery and in the brain, as well as the brain endothelium. Here we generated mice with selective deletion of COX-2 and mPGES1 in brain endothelial cells. These mice displayed strongly attenuated febrile responses to peripheral immune challenge. In contrast, inflammation-induced hypoactivity was unaffected, demonstrating the physiological selectivity of the response to the targeted gene deletions. These findings demonstrate that PGE(2) synthesis in brain endothelial cells is critical for inflammation-induced fever.
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| 30. |
- Åmand, Lars-Erik, 1957, et al.
(författare)
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Ash deposition on heat transfer tubes during combustion of demolition wood
- 2006
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Ingår i: Energy & Fuels. - : American Chemical Society (ACS). - 1520-5029 .- 0887-0624. ; 20:3, s. 1001-1007
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Tidskriftsartikel (refereegranskat)abstract
- Wood from old buildings, demolition wood, has a considerable energy value and can be used as a fuel.However, the material contains impurities that may have harmful effects. This investigation, carried out in afluidized-bed boiler, focuses on the formation of deposits on heat transfer surfaces during combustion ofdemolition wood. To avoid inhomogeneity and variations in composition of the fuel during the tests, highqualitywood was used and two substances that are suspected to contribute most to deposits, chlorine and zinc(from paint), were added in predetermined quantities. It was found that chlorine was the most harmful constituent,promoting deposits in the form of potassium chloride and also zinc chloride. The deposits from wood combustionor from wood contaminated with zinc are deemed not to be excessively harmful with respect to corrosion aslong as the chlorine concentration is low and oxidizing conditions prevail.
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| 31. |
- Åmand, Lars-Erik, 1957, et al.
(författare)
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Deposits on heat transfer tubes during co-combustion of biofuels and sewage sludge
- 2006
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Ingår i: Fuel. - 0016-2361. ; 85:10-11, s. 1313-1322
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Tidskriftsartikel (refereegranskat)abstract
- Potassium together with chlorine is the principal species that causes undesirable deposits and eventually corrosion on heat exchanger tubes in boilers fired with bio and waste fuels. It is shown here by tests in a circulating fluidized bed boiler that co-combustion of biomass with another fuel,in this case municipal sewage sludge, can remove or considerably reduce such deposits at the same time as the amount of submicron particles deceases radically. There may be at least four reasons for the beneficial impact of the additional fuel: (1) sulphur in the fuel may react withpotassium, producing sulphate and gaseous hydrogen chloride which are less harmful, (2) potassium chloride may be removed by condensation on fly ash particles added with the other fuel, or (3) potassium in gaseous form may react with alumino-silicates provided by the additional fuel, andfinally, (4) deposits may be mechanically removed by the increased ash flows caused by the additional fuel. In one of these ways or a combination of them, formation of deposits on tubes by potassium chloride could be avoided or alleviated.
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