| 1. |
- Henry, Anne, 1959-, et al.
(författare)
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Thick epilayers for power devices
- 2007
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Ingår i: Materials Science Forum, vol. 556-557. - : Trans Tech Publications. ; , s. 47-
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Konferensbidrag (refereegranskat)abstract
- Growth of thick epitaxial SiC layers needed for high power devices is presented for horizontal hot-wall CVD (HWCVD) reactors. We demonstrate thickness of epilayer of 100 μm and more with good morphology, low-doping with no doping variation through the whole thick layer and reasonable carrier lifetime which mainly depends on the substrate quality. Typical epidefects are described and their density can dramatically be reduced when choosing correctly the growth conditions as well as the polishing of the surface prior to the growth. The control of the doping and thickness uniformities as well as the run-to-run reproducibility is also presented. Various characterization techniques such as optical microscopy, AFM, reflectance, CV, PL and minority carrier lifetime have been used. Results of high-voltage SiC Schottky power devices are presented.
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| 2. |
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| 3. |
- Andersson, Linda, 1973, et al.
(författare)
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PLD1 and ERK2 regulate cytosolic lipid droplet formation
- 2006
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Ingår i: J Cell Sci. ; 119:Pt 11, s. 2246-57
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Tidskriftsartikel (refereegranskat)abstract
- We have previously uncovered roles for phospholipase D (PLD) and an unknown cytosolic protein in the formation of cytosolic lipid droplets using a cell-free system. In this report, PLD1 has been identified as the relevant isoform, and extracellular signal-regulated kinase 2 (ERK2) as the cytosolic protein. Increased expression of PLD1 increased lipid droplet formation whereas knockdown of PLD1 using siRNA was inhibitory. A role for ERK2 in basal lipid droplet formation was revealed by overexpression or microinjection, and ablation by siRNA knockdown or pharmacological inhibition. Similar manipulations of other Map kinases such as ERK1, JNK1 or JNK2 and p38alpha or p38beta were without effect. Insulin stimulated the formation of lipid droplets and this stimulation was inhibited by knockdown of PLD1 (by siRNA) and by inhibition or knockdown (by siRNA) of ERK2. Inhibition of ERK2 eliminated the effect of PLD1 on lipid droplet formation without affecting PLD1 activity, suggesting that PLD1 functions upstream of ERK2. ERK2 increased the phosphorylation of dynein which increased the amount of the protein on ADRP-containing lipid droplets. Microinjection of antibodies to dynein strongly inhibited the formation of lipid droplets, demonstrating that dynein has a central role in this formation. Thus dynein is a possible target for ERK2.
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| 4. |
- Aronsson, Lena, 1959-
(författare)
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När förskolan möter neurovetenskap : Kunskapsteoretiska möten i teori och i praktik
- 2019
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- This doctoral thesis in Early Childhood Education reports on encounters between the theories and practices of Swedish preschool and research-based neuroscience knowledge. Thus, this thesis concerns epistemological encounters and didactic consequences. The scientific problem pertains to the relation between scientifically generated knowledge and educational practices in preschool, with specific attention to the requirement that preschool, as the first level in the Swedish education system, should be based on scientific knowledge and verified experience-based knowledge. The didactic problem emerging from this scientific problem concerns how this might affect the daily practices of responsible preschool teachers and educators at large.The thesis adopts a relational ontology with a multi-epistemological and methodological approach, based primarily on Stengers’ (e.g., 2018) and Mols’ (e.g., 2002) respective scholarship. The aims of the thesis are to investigate, firstly; what is produced in epistemological encounters within and between the research fields of Early Childhood Education and neuroscience. Secondly; what is produced between these fields and preschool didactic practices. The focus for the latter is on the didactic practices relying on the extended language concept in the Swedish preschool curriculum.To explore these aims in more detail, a series of so-called cartography mapping exercises have been conducted. On the one hand, in the analyses of the literature aimed at bringing the two fields together. On the other hand, cartography mapping has been conducted with educators in three preschools collaboratively analyzing their literacy practices. The Deleuze-inspired (Deleuze & Guattari, 1987) methodology of cartography mapping aspire to simultaneously critically deconstruct and productively experiment with underlying lines of thinking emerging from scientific or philosophical problems that concern development and learning, and especially language development and skills of literacy during the preschool years (Lenz Taguchi, 2016a, 2016b).The knowledge that this thesis produces is summarized below. Cartography mapping can be used both as a research method and as a method in pedagogical practice. In addition, cartography mapping can accommodate issues in different epistemologies and in different practices, such as research practice and preschool didactic practice. That is, practices that are related and share an overarching aim, but which are nevertheless not the same. The method reveals the different epistemologies present and how they can operate simultaneously within preschool didactic practice. The results from the thesis support the Swedish preschool curriculum goals which encompasses a dual assignment of learning (group and individual), that require different epistemological and didactic methods to be fulfilled.A preschool practice based on scientific evidence and verified experience-based knowledge thus requires the use of a wide range of theories and epistemologies to guide preschool staff. Hence, the results of this thesis show not just the presence, but also the possibility of developing a multi-epistemological didactic repertoire in preschool development and learning practices.
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| 5. |
- Boström, Pontus, 1982, et al.
(författare)
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Cytosolic lipid droplets increase in size by microtubule-dependent complex formation
- 2005
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Ingår i: Arterioscler Thromb Vasc Biol. - 1524-4636. ; 25:9, s. 1945-51
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Adipocyte differentiation-related protein (ADRP)-containing lipid droplets have an essential role in the development of insulin resistance and atherosclerosis. Such droplets form in a cell-free system with a diameter of 0.1 to 0.4 microm, while the droplets present in cells vary in size, from small to very large, suggesting that the droplets can increase in size after being assembled. We have addressed this possibility. METHODS AND RESULTS: Experiments in NIH 3T3 cells demonstrated that the lipid droplets could increase in size independently of triglyceride biosynthesis. NIH 3T3 cells were either microinjected with ADRP-GFP (green fluorescent protein) or stained with Nile Red and followed by confocal microscopy and time-lapse recordings. The results showed that lipid droplets formed complexes with each other, with a volume equal to the sum of the merging particles. The formation of complexes could be inhibited by the nocodazole-induced depolymerization of the microtubules; thus, the process is dependent on microtubules. The presence of dynein on ADRP-containing droplets supports a role for this motor protein. CONCLUSIONS: Lipid droplets can grow after they have been assembled. This increase in size is independent of triglyceride biosynthesis and involves formation of complexes, which requires intact microtubules.
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| 6. |
- Boström, Pontus, 1982, et al.
(författare)
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SNARE proteins mediate fusion between cytosolic lipid droplets and are implicated in insulin sensitivity.
- 2007
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Ingår i: Nature cell biology. - : Springer Science and Business Media LLC. - 1465-7392 .- 1476-4679. ; 9:11, s. 1286-93
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Tidskriftsartikel (refereegranskat)abstract
- The accumulation of cytosolic lipid droplets in muscle and liver cells has been linked to the development of insulin resistance and type 2 diabetes. Such droplets are formed as small structures that increase in size through fusion, a process that is dependent on intact microtubules and the motor protein dynein. Approximately 15% of all droplets are involved in fusion processes at a given time. Here, we show that lipid droplets are associated with proteins involved in fusion processes in the cell: NSF (N-ethylmaleimide-sensitive-factor), alpha-SNAP (soluble NSF attachment protein) and the SNAREs (SNAP receptors), SNAP23 (synaptosomal-associated protein of 23 kDa), syntaxin-5 and VAMP4 (vesicle-associated membrane protein 4). Knockdown of the genes for SNAP23, syntaxin-5 or VAMP4, or microinjection of a dominant-negative mutant of alpha-SNAP, decreases the rate of fusion and the size of the lipid droplets. Thus, the SNARE system seems to have an important role in lipid droplet fusion. We also show that oleic acid treatment decreases the insulin sensitivity of heart muscle cells, and this sensitivity is completely restored by transfection with SNAP23. Thus, SNAP23 might be a link between insulin sensitivity and the inflow of fatty acids to the cell.
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| 7. |
- Boström, Pontus, 1982, et al.
(författare)
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The SNARE protein SNAP23 and the SNARE-interacting protein Munc18c in human skeletal muscle are implicated in insulin resistance/type 2 diabetes.
- 2010
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Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 59:8, s. 1870-8
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Our previous studies suggest that the SNARE protein synaptosomal-associated protein of 23 kDa (SNAP23) is involved in the link between increased lipid levels and insulin resistance in cardiomyocytes. The objective was to determine whether SNAP23 may also be involved in the known association between lipid accumulation in skeletal muscle and insulin resistance/type 2 diabetes in humans, as well as to identify a potential regulator of SNAP23. RESEARCH DESIGN AND METHODS: We analyzed skeletal muscle biopsies from patients with type 2 diabetes and healthy, insulin-sensitive control subjects for expression (mRNA and protein) and intracellular localization (subcellular fractionation and immunohistochemistry) of SNAP23, and for expression of proteins known to interact with SNARE proteins. Insulin resistance was determined by a euglycemic hyperinsulinemic clamp. Potential mechanisms for regulation of SNAP23 were also investigated in the skeletal muscle cell line L6. RESULTS: We showed increased SNAP23 levels in skeletal muscle from patients with type 2 diabetes compared with that from lean control subjects. Moreover, SNAP23 was redistributed from the plasma membrane to the microsomal/cytosolic compartment in the patients with the type 2 diabetes. Expression of the SNARE-interacting protein Munc18c was higher in skeletal muscle from patients with type 2 diabetes. Studies in L6 cells showed that Munc18c promoted the expression of SNAP23. CONCLUSIONS: We have translated our previous in vitro results into humans by showing that there is a change in the distribution of SNAP23 to the interior of the cell in skeletal muscle from patients with type 2 diabetes. We also showed that Munc18c is a potential regulator of SNAP23.
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| 10. |
- Li, Lu, 1964, et al.
(författare)
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Epigallocatechin gallate increases the formation of cytosolic lipid droplets and decreases the secretion of apoB-100 VLDL
- 2006
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Ingår i: J Lipid Res. - 0022-2275. ; 47:1, s. 67-77
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Tidskriftsartikel (refereegranskat)abstract
- Epigallocatechin gallate (EGCG) increases the formation of cytosolic lipid droplets by a mechanism that is independent of the rate of triglyceride biosynthesis and involves an enhanced fusion between lipid droplets, a process that is crucial for their growth in size. EGCG treatment reduced the secretion of both triglycerides and apolipoprotein B-100 (apoB-100) VLDLs but not of transferrin, albumin, or total proteins, indicating that EGCG diverts triglycerides from VLDL assembly to storage in the cytosol. This is further supported by the observed increase in both intracellular degradation of apoB-100 and ubiquitination of the protein (indicative of increased proteasomal degradation) in EGCG-treated cells. EGCG did not interfere with the microsomal triglyceride transfer protein, and the effect of EGCG on the secretion of VLDLs was found to be independent of the LDL receptor. Thus, our results indicate that EGCG promotes the accumulation of triglycerides in cytosolic lipid droplets, thereby diverting lipids from the assembly of VLDL to storage in the cytosol. Our results also indicate that the accumulation of lipids in the cytosol is not always associated with increased secretion of VLDL.
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