| 1. |
- Rydén, Magnus, 1975, et al.
(author)
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Fe2O3 on Ce-, Ca- or Mg-stabilized ZrO2 as oxygen carrier for chemical-looping combustion using NiO as additive
- 2010
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In: AICHE Journal. - : Wiley. - 1547-5905 .- 0001-1541. ; 56:8, s. 2211-2220
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Journal article (peer-reviewed)abstract
- Oxygen-carrier particles for chemical-looping combustion have been manufactured by freeze granulation. The particles consisted of 60 wt % Fe2O3 as active phase and 40 wt % stabilized ZrO2 as support material. Ce, Ca, or Mg was used to stabilize the ZrO2. The hardness and porosity of the particles were altered by varying the sintering temperature. The oxygen carriers were examined by redox experiments in a batch fluidized- bed reactor at 800–950°C, using CH4 as fuel. The experiments showed good reactivity between the particles and CH4. NiO was used as an additive and was found to reduce the fraction of unconverted CH4 with up to 80%. The combustion efficiency was 95.9% at best and was achieved using 57 kg oxygen carrier per MW fuel. Most produced oxygen carriers appear to have been decently stable, but using Ca as stabilizer resulting in uneven results. Further, particles sintered at high temperatures had a tendency to defluidize.
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| 2. |
- Rydén, Magnus, 1975, et al.
(author)
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Ilmenite with addition of NiO as oxygen carrier for chemical-looping combustion
- 2010
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In: Fuel. - : Elsevier BV. - 0016-2361. ; 89:11, s. 3523-3533
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Journal article (peer-reviewed)abstract
- The naturally occurring mineral ilmenite, FeTiO3, has been examined as oxygen carrier for chemical-loopingcombustion. NiO-based particles have been used as an additive, in order to examine if it is possible toutilize the catalytic properties of metallic Ni to facilitate decomposition of hydrocarbons into more reactivecombustion intermediates such as CO and H2. Firstly, ilmenite was examined by oxidation and reductionexperiments in a batch fluidized-bed reactor. These experiments indicated moderate reactivitybetween ilmenite and CH4, which was used as reducing gas. However, adding 5 wt.% of NiO-based particlesto the ilmenite improved the conversion of CH4 greatly, resulting in an increase in combustion efficiencywith a factor of 3. Secondly, 83 h of chemical-looping combustion experiments were conducted ina small circulating fluidized-bed reactor, using ilmenite as oxygen carrier and natural gas as fuel. A widerange of process parameters and different levels of NiO addition were examined. Occasionally, there wereproblems with the circulation of solids between the air reactor and fuel reactor, but most of the time theexperiments worked well. The products were mostly CO2, H2O and unconverted CH4. Adding smallamounts of NiO-based particles to the reactor increased the conversion of the fuel considerably. Forthe base case conducted at 900, the combustion efficiency was 76% for pure ilmenite and 90% for thecorresponding experiments with 1 wt.% NiO-based particles added to the reactor. The properties ofilmenite were found to change considerably during operation. Used particles had lower density, weremore reactive and more porous than fresh particles. These changes appear to have been physical, andno unexpected chemical phases could be identified.
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| 3. |
- Sayin, Volkan I., 1983, et al.
(author)
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Zfp148 Deficiency Causes Lung Maturation Defects and Lethality in Newborn Mice That Are Rescued by Deletion of p53 or Antioxidant Treatment
- 2013
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In: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 8:2
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Journal article (peer-reviewed)abstract
- The transcription factor Zfp148 (Zbp-89, BFCOL, BERF1, htβ) interacts physically with the tumor suppressor p53 and is implicated in cell cycle control, but the physiological role of Zfp148 remains unknown. Here we show that Zfp148 deficiency leads to respiratory distress and lethality in newborn mice. Zfp148 deficiency prevented structural maturation of the prenatal lung without affecting type II cell differentiation or surfactant production. BrdU analyses revealed that Zfp148 deficiency caused proliferation arrest of pulmonary cells at E18.5–19.5. Similarly, Zfp148-deficient fibroblasts exhibited proliferative arrest that was dependent on p53, raising the possibility that cell stress is part of the underlying mechanism. Indeed, Zfp148 deficiency lowered the threshold for activation of p53 under oxidative conditions. Moreover, both in vivo and cellular phenotypes were rescued on Trp53+/− or Trp53−/− backgrounds and by antioxidant treatment. Thus, Zfp148 prevents respiratory distress and lethality in newborn mice by attenuating oxidative stress–dependent p53-activity during the saccular stage of lung development. Our results establish Zfp148 as a novel player in mammalian lung maturation and demonstrate that Zfp148 is critical for cell cycle progression in vivo.
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| 4. |
- Berndt, Sonja I., et al.
(author)
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Genome-wide meta-analysis identifies 11 new loci for anthropometric traits and provides insights into genetic architecture
- 2013
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In: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 45:5, s. 501-U69
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Journal article (peer-reviewed)abstract
- Approaches exploiting trait distribution extremes may be used to identify loci associated with common traits, but it is unknown whether these loci are generalizable to the broader population. In a genome-wide search for loci associated with the upper versus the lower 5th percentiles of body mass index, height and waist-to-hip ratio, as well as clinical classes of obesity, including up to 263,407 individuals of European ancestry, we identified 4 new loci (IGFBP4, H6PD, RSRC1 and PPP2R2A) influencing height detected in the distribution tails and 7 new loci (HNF4G, RPTOR, GNAT2, MRPS33P4, ADCY9, HS6ST3 and ZZZ3) for clinical classes of obesity. Further, we find a large overlap in genetic structure and the distribution of variants between traits based on extremes and the general population and little etiological heterogeneity between obesity subgroups.
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| 5. |
- Everard, A., et al.
(author)
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Microbiome of prebiotic-treated mice reveals novel targets involved in host response during obesity
- 2014
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In: Isme Journal. - : Springer Science and Business Media LLC. - 1751-7362 .- 1751-7370. ; 8:10, s. 2116-2130
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Journal article (peer-reviewed)abstract
- The gut microbiota is involved in metabolic and immune disorders associated with obesity and type 2 diabetes. We previously demonstrated that prebiotic treatment may significantly improve host health by modulating bacterial species related to the improvement of gut endocrine, barrier and immune functions. An analysis of the gut metagenome is needed to determine which bacterial functions and taxa are responsible for beneficial microbiota-host interactions upon nutritional intervention. We subjected mice to prebiotic (Pre) treatment under physiological (control diet: CT) and pathological conditions (high-fat diet: HFD) for 8 weeks and investigated the production of intestinal antimicrobial peptides and the gut microbiome. HFD feeding significantly decreased the expression of regenerating islet-derived 3-gamma (Reg3g) and phospholipase A2 group-II (PLA2g2) in the jejunum. Prebiotic treatment increased Reg3g expression (by similar to 50-fold) and improved intestinal homeostasis as suggested by the increase in the expression of intectin, a key protein involved in intestinal epithelial cell turnover. Deep metagenomic sequencing analysis revealed that HFD and prebiotic treatment significantly affected the gut microbiome at different taxonomic levels. Functional analyses based on the occurrence of clusters of orthologous groups (COGs) of proteins also revealed distinct profiles for the HFD, Pre, HFD-Pre and CT groups. Finally, the gut microbiota modulations induced by prebiotics counteracted HFD-induced inflammation and related metabolic disorders. Thus, we identified novel putative taxa and metabolic functions that may contribute to the development of or protection against the metabolic alterations observed during HFD feeding and HFD-Pre feeding.
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| 6. |
- Herz, Marcus, 1978-, et al.
(author)
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Avslutning
- 2012. - 1
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In: Kritiskt socialt arbete. - Malmö : Liber. - 9789147096886 ; , s. 169-180
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Book chapter (other academic/artistic)
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| 7. |
- Johansson, Maria E, 1977, et al.
(author)
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alpha 7 Nicotinic Acetylcholine Receptor Is Expressed in Human Atherosclerosis and Inhibits Disease in Mice-Brief Report
- 2014
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In: Arteriosclerosis Thrombosis and Vascular Biology. - : Ovid Technologies (Wolters Kluwer Health). - 1079-5642 .- 1524-4636. ; 34:12, s. 2632-2636
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Journal article (peer-reviewed)abstract
- Objective-Cholinergic pathways of the autonomic nervous system are known to modulate inflammation. Because atherosclerosis is a chronic inflammatory condition, we tested whether cholinergic signaling operates in this disease. We have analyzed the expression of the alpha 7 nicotinic acetylcholine receptor (alpha 7nAChR) in human atherosclerotic plaques and studied its effects on the development of atherosclerosis in the hypercholesterolemic Ldlr(-/-) mouse model. Approach and Results-alpha 7nAChR protein was detected on T cells and macrophages in surgical specimens of human atherosclerotic plaques. To study the role of alpha 7nAChR signaling in atherosclerosis, male Ldlr(-/-) mice were lethally irradiated and reconstituted with bone marrow from wild-type or alpha 7nAChR-deficient animals. Ablation of hematopoietic cell alpha 7nAChR increased aortic atherosclerosis by 72%. This was accompanied by increased aortic interferon-gamma mRNA, implying increased Th1 activity in the absence of a7nAChR signaling. Conclusions-The present study shows that signaling through hematopoietic alpha 7nAChR inhibits atherosclerosis and suggests that it operates by modulating immune inflammation. Given the observation that alpha 7nAChR is expressed by T cells and macrophages in human plaques, our findings support the notion that cholinergic regulation may act to inhibit disease development also in man.
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| 8. |
- Levin, Malin, 1973, et al.
(author)
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Rip2 deficiency leads to increased atherosclerosis despite decreased inflammation.
- 2011
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In: Circulation research. - 1524-4571. ; 109:11, s. 1210-8
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Journal article (peer-reviewed)abstract
- The innate immune system and in particular the pattern-recognition receptors Toll-like receptors have recently been linked to atherosclerosis. Consequently, inhibition of various signaling molecules downstream of the Toll-like receptors has been tested as a strategy to prevent progression of atherosclerosis. Receptor-interacting protein 2 (Rip2) is a serine/threonine kinase that is involved in multiple nuclear factor-κB (NFκB) activation pathways, including Toll-like receptors, and is therefore an interesting potential target for pharmaceutical intervention.
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| 9. |
- Lind, Marcus, 1975-
(author)
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Determinants of adverse events during oral anticoagulant treatment
- 2012
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Doctoral thesis (other academic/artistic)abstract
- Treament with oral anticoagulation is highly effective in reducing the burden of thromboembolic complications in several clinical conditions. The number of patients receiving oral anticoagulation is growing steadily. InSwedenabout 1.5 percent of the population receives treatment. Although the treatment is highly effective in preventing thromboembolic complications, it is also associated with a substantial increase in the risk of bleeding. In clinical practice every physician has to balance the potential benefit of treatment against the risk of bleeding complications in the individual patient. To aid in this decision making, risk scores addressing the likelihood of thromboembolic events, as well as the risk of bleeding complications, have been developed. These scores are imperfect and, to some degree limited by the fact that the risk factors predictive of thromboembolic events are also often associated with bleeding complications. The addition of biomarkers has the potential to increase the predictive ability of risk scores and further enhance the net benefit of oral anticoagulant treatment in the individual patient. In this thesis several potential biomarkers for thromoboembolic and haemorrhagic complications of anticoagulant therapy have been investigated in a longitudinal cohort study of 719 patients with a median follow-up time of 4.2 years. Thrombomodulin is a key component in the generation of activated protein C and hence, a coagulation inhibitor. Conversely, it is also a key component in the inhibition of fibrinolysis by activation of trombin-activated fibrinolysis inhibitor. In warfarin-treated patients we demonstrate that thrombomodulin predicts an increased risk of bleeding complications, but not cardiovascular events. Thus, thrombomodulin has potential as a biomarker specifically for bleeding complications. Von Willebrand factor plays a central and intricate role in the aggregation of platelets and low levels of VWF have been associated with bleeding as a manifestation of von Willebrand’s disease. In our study we noted that high levels of von Willebrand factor predict an increased risk of cardiovascular as well as all-cause mortality, possibly as an expression of endothelial dysfunction. We also noted that high levels of WVF seem to be associated with serious bleeding complications. Decreased renal function is usually measured by an increase in the levels of creatinine and cystatin C, or a decrease in the calculated glomerular filtration rate. A decrease in kidney function is regarded as a marker of an increased risk of bleeding complications. We investigated all the mentioned markers of kidney function and no association with bleeding complications became apparent. However, a clear association between a decrease in kidney function and mortality was noted. Our findings indicate that the emphasis on impaired kidney function as a risk marker needs to be shifted from bleeding complications toward thromboembolic events. Fibrinolysis is important in containing coagulation and several constituents of the fibrinolytic pathway have been shown to predict cardiovascular events and mortality. We found that fibrinolytic factors seem to predict cardiovascular events in patients with oral anticoagulation and that D-dimer also predicts bleeding complications. In conclusion, we have found several biomarkers which exhibit different predictive abilities in patients with oral anticoagulation. It is likely that biomarkers, either alone, in combination, or as ancillary components of risk scores, can contribute to improved risk stratification in patients with oral anticoagulation.
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| 10. |
- Lindwall, Magnus, 1975, et al.
(author)
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Dynamic associations of change in physical activity and change in cognitive function: Coordinated analyses of four longitudinal studies
- 2012
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In: Journal of Aging Research. - : Hindawi Limited. - 2090-2204 .- 2090-2212. ; 2012
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Journal article (peer-reviewed)abstract
- The present study used a coordinated analyses approach to examine the association of physical activity and cognitive change in four longitudinal studies. A series of multilevel growth models with physical activity included both as a fixed (between-person) and time-varying (within-person) predictor of four domains of cognitive function (reasoning, memory, fluency, and semantic knowledge) was used. Baseline physical activity predicted fluency, reasoning and memory in two studies. However, there was a consistent pattern of positive relationships between time-specific changes in physical activity and time-specific changes in cognition, controlling for expected linear trajectories over time, across all four studies. This pattern was most evident for the domains of reasoning and fluency.
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| 11. |
- Perman Sundelin, Jeanna, et al.
(author)
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Increased Expression of the Very Low-Density Lipoprotein Receptor Mediates Lipid Accumulation in Clear-Cell Renal Cell Carcinoma
- 2012
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In: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 7:11
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Journal article (peer-reviewed)abstract
- Clear-cell renal cell carcinoma (RCC) is, in most cases, caused by loss of function of the tumor suppressor gene von Hippel-Lindau, resulting in constitutive activation of hypoxia-inducible factor (HIF)-1 alpha and expression of hypoxia-induced genes in normoxic conditions. Clear-cell RCC cells are characterized histologically by accumulation of cholesterol, mainly in its ester form. The origin of the increased cholesterol remains unclear, but it is likely explained by an HIF-1 alpha-driven imbalance between cholesterol uptake and excretion. Here, we showed that expression of the very low-density lipoprotein receptor (VLDL-R) was significantly increased in clear-cell RCC human biopsies compared with normal kidney tissue. Partial knockdown of HIF-1 alpha in clear-cell RCC cells significantly reduced the VLDL-R expression, and knockdown of either HIF-1 alpha or VLDL-R reduced the increased lipid accumulation observed in these cells. We also showed increased uptake of fluorescently labeled lipoproteins in clear-cell RCC cells, which was significantly reduced by knockdown of HIF-1 alpha or VLDL-R. Taken together, our results support the concept that the pathological increase of HIF-1 alpha in clear-cell RCC cells upregulates VLDL-R, which mediates increased uptake and accumulation of lipids. These results explain the morphological characteristics of clear-cell RCC, and open up novel possibilities for detection and treatment of clear-cell RCC.
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| 12. |
- Svensk, Emma, et al.
(author)
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PAQR-2 Regulates Fatty Acid Desaturation during Cold Adaptation in C. elegans
- 2013
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In: Plos Genetics. - : Public Library of Science (PLoS). - 1553-7404. ; 9:9
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Journal article (peer-reviewed)abstract
- C. elegans PAQR-2 is homologous to the insulin-sensitizing adiponectin receptors in mammals, and essential for adaptation to growth at 15 degrees C, a low but usually acceptable temperature for this organism. By screening for novel paqr-2 suppressors, we identified mutations in genes involved in phosphatidylcholine synthesis (cept-1, pcyt-1 and sams-1) and fatty acid metabolism (ech-7, hacd-1, mdt-15, nhr-49 and sbp-1). We then show genetic evidence that paqr-2, phosphatidylcholines, sbp-1 and Delta 9-desaturases form a cold adaptation pathway that regulates the increase in unsaturated fatty acids necessary to retain membrane fluidity at low temperatures. This model is supported by the observations that the paqr-2 suppressors normalize the levels of saturated fatty acids, and that low concentrations of detergents that increase membrane fluidity can rescue the paqr-2 mutant.
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