| 1. |
- Ringdahl, Ulrika, et al.
(författare)
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A role for the fibrinogen-binding regions of streptococcal M proteins in phagocytosis resistance
- 2000
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Ingår i: Molecular Microbiology. - : Wiley. - 1365-2958 .- 0950-382X. ; 37:6, s. 1318-1326
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Tidskriftsartikel (refereegranskat)abstract
- All virulent group A streptococcal isolates bind fibrinogen, a property that is closely linked to expression of type-specific antiphagocytic surface molecules designated M proteins. Here we show that although the M proteins from two different strains, M1 and M5, both bind fibrinogen with high affinity, they interact with different regions in the ligand. Moreover, mapping experiments demonstrated that the fibrinogen-binding regions in the M1 and M5 proteins are quite dissimilar at the amino acid sequence level and that they bind to different regions in the plasma protein. In spite of these differences, the fibrinogen-binding regions of M1 and M5 could both be shown to contribute to streptococcal survival in human blood, providing evidence for the distinct function of a plasma protein interaction in bacterial pathogenesis.
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| 2. |
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| 3. |
- Bjarnegård, Mattias, 1970, et al.
(författare)
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Endothelium-specific ablation of PDGFB leads to pericyte loss and glomerular, cardiac and placental abnormalities
- 2004
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Ingår i: DEVELOPMENT. - : The Company of Biologists. - 0950-1991 .- 1477-9129. ; 131:8, s. 1847-1857
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Tidskriftsartikel (refereegranskat)abstract
- Platelet-derived growth factor-B (PDGFB) is necessary for normal cardiovascular development, but the relative importance of different cellular sources of PDGFB has not been established. Using Cre-lox techniques, we show here that genetic ablation of Pdgfb in endothelial cells leads to impaired recruitment of pericytes to blood vessels. The endothelium-restricted Pdgfb knockout mutants also developed organ defects including cardiac, placental and renal abnormalities. These defects were similar to those observed in Pdgfb null mice. However, in marked contrast to the embryonic lethality of Pdgfb null mutants, the endothelium-specific mutants survived into adulthood with persistent pathological changes, including brain microhemorrhages, focal astrogliosis, and kidney glomerulus abnormalities. This spectrum of pathological changes is reminiscent of diabetic microangiopathy, suggesting that the endothelium-restricted Pdgfb knockouts may serve as models for some of the pathogenic events of vascular complications to diabetes. Key words: PDGFB, Endothelium, Cre, loxP, Pericytes, Microaneurysm
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| 4. |
- Enge, Maria, 1970, et al.
(författare)
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Endothelium-specific platelet-derived growth factor-B ablation mimics diabetic retinopathy.
- 2002
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Ingår i: The EMBO journal. - : Wiley. - 0261-4189 .- 1460-2075. ; 21:16, s. 4307-16
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Tidskriftsartikel (refereegranskat)abstract
- Loss of pericytes from the capillary wall is a hallmark of diabetic retinopathy, however, the pathogenic significance of this phenomenon is unclear. In previous mouse gene knockout models leading to pericyte deficiency, prenatal lethality has so far precluded analysis of postnatal consequences in the retina. We now report that endothelium-restricted ablation of platelet-derived growth factor-B generates viable mice with extensive inter- and intra-individual variation in the density of pericytes throughout the CNS. We found a strong inverse correlation between pericyte density and the formation of a range of retinal microvascular abnormalities strongly reminiscent of those seen in diabetic humans. Proliferative retinopathy invariably developed when pericyte density was <50% of normal. Our data suggest that a reduction of the pericyte density is sufficient to cause retinopathy in mice, implying that pericyte loss may also be a causal pathogenic event in human diabetic retinopathy.
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| 5. |
- Flood, Christofer, 1974, et al.
(författare)
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Molecular mechanism for changes in proteoglycan binding on compositional changes of the core and the surface of low-density lipoprotein-containing human apolipoprotein B100
- 2004
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Ingår i: Arterioscler Thromb Vasc Biol. - 1524-4636. ; 24:3, s. 564-70
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The aim of this study was to investigate the molecular mechanism for changes in proteoglycan binding and LDL receptor affinity on two compositional changes in LDL that have been associated with atherosclerosis: cholesterol enrichment of the core and modification by secretory group IIA phospholipase A2 (sPLA2) of the surface. METHODS AND RESULTS: Transgenic mice expressing recombinant apolipoprotein (apo) B and sPLA2 were generated. Recombinant LDL were isolated and tested for their proteoglycan and LDL receptor-binding activity. The results show site A (residues 3148-3158) in apoB100 becomes functional in sPLA2-modified LDL and that site A acts cooperatively with site B (residues 3359-3369), the primary proteoglycan-binding site in native LDL, in the binding of sPLA2-modified LDL to proteoglycans. Our results also show that cholesterol enrichment of LDL is associated with increased affinity for proteoglycans and for the LDL receptor. This mechanism is likely mediated by a conformational change of site B and is independent of site A in apoB100. CONCLUSIONS: Site A in apoB100 becomes functional in sPLA2-modified LDL and acts cooperatively with site B resulting in increased proteoglycan-binding activity. The increased binding for proteoglycans of cholesterol-enriched LDL is solely dependent on site B.
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| 6. |
- Frick, Inga-Maria, et al.
(författare)
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Uptake and intracellular transportation of a bacterial surface protein in lymphoid cells.
- 2002
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Ingår i: Molecular Microbiology. - : Wiley. - 1365-2958 .- 0950-382X. ; 44:4, s. 917-934
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Tidskriftsartikel (refereegranskat)abstract
- Some strains of the human pathogen Streptococcus pyogenes express a surface protein called protein H, which is released from the streptococcal surface by a cysteine proteinase produced by the bacteria. Here, we find that soluble protein H binds to the surface of lymphocytes and granulocytes, and that the molecule is taken up by lymphocytes and transported to the perinuclear region. The translocation over the cell membrane is rapid, and the uptake and intracellular transportation is not dependent on actin polymerization. Protein H could be immunoprecipitated from cell extracts and nuclear preparations of lymphocytes, and analysis of molecular interactions between pro-tein H and proteins of different cellular compart-ments demonstrated a binding to nucleophosmin/ B23, a protein known to shuttle between the cytoplasm and the nucleus, and to the nuclear proteins SET and hnRNP A2/B1. Nucleophosmin/B23 was co-immunoprecipitated with protein H from cell and nuclear extracts, and binding experiments, including kinetic analyses, suggest that protein H dissociating from nucleophosmin/B23 complexes in the perinuclear region or in the nucleus binds to proteins SET and hnRNP A2/B1. Finally, the uptake and intracellular transportation of protein H was found to result in a cytostatic effect on B and T lymphocytes.
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| 7. |
- Gaspari, Martina, et al.
(författare)
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The mitochondrial RNA polymerase contributes critically to promoter specificity in mammalian cells.
- 2004
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Ingår i: The EMBO journal. - : Wiley. - 0261-4189 .- 1460-2075. ; 23:23, s. 4606-14
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Tidskriftsartikel (refereegranskat)abstract
- Initiation of transcription in mammalian mitochondria depends on three proteins: mitochondrial RNA polymerase (POLRMT), mitochondrial transcription factor A (TFAM) and mitochondrial transcription factor B2 (TFB2M). We show here that the recombinant mouse and human transcription machineries are unable to initiate transcription in vitro from the heterologous light-strand promoter (LSP) of mitochondrial DNA. This species specificity is dependent on the interaction of TFAM and POLRMT with specific distal and proximal promoter elements. A sequence element localized from position -1 to -2 relative to the transcription start site in LSP functionally interacts with POLRMT. The POLRMT/TFB2M heterodimer is unable to interact with promoter elements and initiate even abortive transcription in the absence of TFAM. TFAM is thus an integral part of the mammalian transcription machinery, and we propose that TFAM induces a structural change of the promoter that is required for POLRMT-dependent promoter recognition.
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| 8. |
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| 9. |
- Gustafsson, Ewa, 1955, et al.
(författare)
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The use of information technology among young adults--experience, attitudes and health beliefs
- 2003
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Ingår i: Appl Ergon. - : Pergamon. - 0003-6870 .- 1872-9126. ; 34:6, s. 565-70
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to explore attitudes, coherence and health beliefs among young adults, related to their use and experience of information technology (IT). A qualitative approach was used and the data were collected through individual thematised interviews with 25 young IT users, aged 18-24. The interviews were analysed in line with the grounded theory method with a constructivist approach. The main findings were the young adults' experience of the two sides of being social, efficient and independent here and now. They described almost unlimited opportunities in connection with IT, but they also had misgivings, and perceived risks regarding IT use. Feelings of freedom and being efficient were countered by feelings of restrictions on living space and of intangibility. Knowledge concerning these attitudes, coherence and health beliefs can be considered when designing epidemiological and ergonomic studies aimed at risk identification.
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| 10. |
- Gustafsson, Ingegerd, et al.
(författare)
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Bacteria with increased mutation frequency and antibiotic resistance are enriched in the commensal flora of patients with high antibiotic usage
- 2003
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Ingår i: Journal of Antimicrobial Chemotherapy. - : Oxford University Press (OUP). - 0305-7453 .- 1460-2091. ; 52:4, s. 645-650
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: We examined how prolonged antibiotic treatment affected the resistance and mutation frequency of human microflora isolated from intestine (Escherichia coli, enterococci spp.), pharynx (alpha-streptococci) and nostril (coagulase-negative staphylococci, CoNS).METHODS: Samples were collected from patients at the Center of Cystic Fibrosis (n=18) and the haematology ward (n=18) of the University Hospital, Uppsala, Sweden. The individually used amount of antibiotics for 1 year was recorded as the defined daily dose (DDD). Primary health care patients (n=30), with no antibiotic treatment for 1 year before sampling, were used as controls. Three isolates of each bacterium from each patient were examined. Antibiotic susceptibilities were determined by disc diffusion. Mutation frequencies to rifampicin resistance were measured on 30 independent cultures of each bacterial species from each individual by plating on rifampicin agar plates. For alpha-streptococci the mutation frequency to streptomycin resistance was also determined.RESULTS: Isolates from patients with high antibiotic use showed a pronounced shift towards increased resistance and a small but significant increase in the mutation frequency compared with isolates from the controls. For E. coli, enterococci and CoNS the increase in geometric mean mutation frequency in the patient group was 3-, 1.8- and 1.5-fold, respectively (P values 0.0001, 0.016 and 0.012). For alpha-streptococci there was a significant difference in geometric mean mutation frequency between patient and control groups for streptomycin resistance (P=0.024) but not for rifampicin resistance (P=0.74).CONCLUSIONS: High antibiotic use selected for commensals with highly increased resistance and a slight increase in mutation frequency.
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| 11. |
- Gustafsson, Jan, et al.
(författare)
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APSI - svår autoimmun sjukdom med endokrina och icke-endokrina symtom
- 2004
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Ingår i: Läkartidningen. - 0023-7205 .- 1652-7518. ; 101:24, s. 2096-2103
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Tidskriftsartikel (refereegranskat)abstract
- Autoimmune polyglandular syndrome type I (APS I) is an autosomal recessive disorder characterized by a combination of autoimmune manifestations affecting endocrine and non-endocrine organs. APS I usually presents in childhood. The three most common manifestations are chronic mucocutaneous candidiasis, hypoparathyroidism and Addison's disease. At least two of these must be present to fulfill the diagnostic criteria of this syndrome. The spectrum of other associated diseases includes gonadal insufficiency, alopecia, vitiligo and chronic active hepatitis. APS I is caused by a mutation in the AIRE-gene (autoimmune regulator) located on chromosome 21. Analysis of specific autoantibodies against intracellular enzymes, particularly enzymes in the synthesis of steroids and neurotransmittors, can be used in the diagnosis of APS I and to predict different manifestations of the disease.
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| 12. |
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| 13. |
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| 14. |
- Gustafsson, Maria, 1976, et al.
(författare)
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Mechanism of lipoprotein retention by the extracellular matrix
- 2004
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Ingår i: Curr Opin Lipidol. - 0957-9672. ; 15:5, s. 505-14
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE OF REVIEW: Considerable evidence suggests that the subendothelial retention of atherogenic lipoproteins is a key early step in atherogenesis. In humans and experimental animals, elevated levels of plasma lipoproteins are associated with increased atherosclerosis, and lipoproteins with higher affinity for arterial proteoglycans are more atherogenic. Here we discuss the molecular mechanisms underlying lipoprotein retention in the arterial wall and how this interaction can be modulated. RECENT FINDINGS: Functional proteoglycan binding sites in lipoproteins containing apolipoprotein B have been identified and shown to have atherogenic potential in vivo. In addition to apolipoprotein B, novel bridging molecules, those that can interact with both proteoglycans and lipoproteins, have been identified that mediate the retention of atherogenic particles in the vessel wall. The interaction between lipoproteins and proteoglycans can be enhanced by the modification of lipoproteins in the circulation and in the arterial wall, by alterations in the subendothelium, and by changes in proteoglycan synthesis that result in a more atherogenic profile. The retention of atherogenic lipoproteins is a potential target for therapies to reverse atherosclerosis, and in-vitro studies have identified compounds that decrease the affinity of proteoglycans for lipoproteins. SUMMARY: Considerable progress has been made in understanding the association between lipoproteins and cardiovascular disease. This review highlights the importance of the interaction between lipoproteins and the arterial matrix.
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| 15. |
- Gustafsson, Maria, 1976, et al.
(författare)
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Retention of atherogenic lipoproteins in atherogenesis
- 2004
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Ingår i: Cell Mol Life Sci. - : Springer Science and Business Media LLC. - 1420-682X. ; 61:1, s. 4-9
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Tidskriftsartikel (refereegranskat)abstract
- Atherosclerosis is a multifactorial disease whose pathogenesis is still unclear. Mounting evidence, however, supports the concept that subendothelial retention of apoB100-containing lipoproteins is the initiating event in atherogenesis. Subsequently, a series of biological responses to this retained material leads to specific molecular and cellular processes that promote lesion formation.
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| 16. |
- Gustafsson, Maria, 1976
(författare)
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Retention of atherogenic lipoproteins in atherogenesis
- 2004
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Atherosclerosis is the most common cause of death in the industrialized world. The diseaseis characterized by lipid accumulation and inflammation in the arterial wall, which may leadto obstruction of the blood flow. Lipoprotein retention is a key step in the pathogenesis of thedisease and it has been debated that this is the initiating step of atherosclerosis. Accumulationof lipids in the arterial wall can provoke all known features seen in atherogenesis.In this thesis we have investigated how hyperlipidemia induces the pathobiological changesthat lead to atherosclerosis. The aim was to investigate the mechanisms for lipid retention inthe initiation and progress of atherosclerosis and to elucidate the proteoglycan affinity ofmodified low density lipoprotein (LDL). First we identified site B in apolipoprotein (apo)B100 as the important feature for retention in early atherosclerosis. By creating transgenicmice expressing proteoglycan binding defective LDL we demonstrated that lipoproteinretention is an early step of atherosclerosis. This effect was abrogated by apoE, which showedthat apoE has the potential to retain lipoproteins in vivo. Furthermore, apoB48, which lackssite B, was demonstrated to contain a proteoglycan binding site in the amino-terminal. Thepresence of a proteoglycan binding site in the amino-terminal region of apoB may explainwhy apoB48- and apoB100-containing lipoproteins are equally atherogenic. In addition, theresults implicate that this site is masked in apoB100 and therefore non-functional. Theinteraction between LDL and proteoglycans can be modulated by changes in the composition(both surface and core lipids) of the particles. We identified site A in apoB100 to be responsiblefor the increased interaction with proteoglycans seen in secretory group IIA phospholipaseA2 (sPLA2) modified LDL. However, site A was dependent on site B to increase the affinityfor proteoglycans. In addition, cholesterol enriched LDL has been shown to be moreatherogenic than triglyceride-rich LDL. We demonstrated that the increased atherogenicitycould be due to an enhanced affinity for proteoglycans, which probably is dependent onconformational changes of apoB100. In the last study we investigated the lipid retention inadvanced lesions. We demonstrated an increased retention in atherosclerotic plaques, whichcould partly be explained by an alteration in the proteoglycan phenotype. In addition, wewere able to demonstrate that the retention was increased by facilitated interaction mediatedby bridging molecules including lipoprotein lipase (LpL) in the arterial wall. Finally, thepro-atherogenic effect of LpL seen in the vessel wall was shown to be dependent on its noncatalyticalfunction.Taken together, the results presented in this thesis reinforce the importance of retention ofapoB-containing lipoproteins in early and advanced atherosclerosis.
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| 17. |
- Gustafsson, Tomas, et al.
(författare)
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Synthesis of a C-glycoside analogue of β-D -galactosyl threonine
- 2003
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Ingår i: Journal of Organic Chemistry. - : American Chemical Society (ACS). - 0022-3263 .- 1520-6904. ; 68:6, s. 2506-2509
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Tidskriftsartikel (refereegranskat)abstract
- A C-linked analogue of β-d-galactosylthreonine has been prepared from 2,3,4,6-tetra-O-benzyl-d-galactopyranolactone (1) in 14 steps. Three stereogenic centers were created during the synthesis, with the anomeric center of the C-glycoside being generated first by addition of a Grignard reagent to 1 and subsequent reduction of the intermediate hemiacetal with triethylsilane. The two stereogenic centers in the threonine moiety were both established by alkylation of Evans' chiral N-acyloxazolidinone enolates.
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| 18. |
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| 19. |
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| 20. |
- Lindén, Daniel, 1971, et al.
(författare)
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Influence of peroxisome proliferator-activated receptor alpha agonists on the intracellular turnover and secretion of apolipoprotein (Apo) B-100 and ApoB-48.
- 2002
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Ingår i: The Journal of biological chemistry. - 0021-9258. ; 277:25, s. 23044-53
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Tidskriftsartikel (refereegranskat)abstract
- The peroxisome proliferator-activated receptor (PPAR) alpha agonist WY 14,643 increased the secretion of apolipoprotein (apo) B-100, but not that of apoB-48, and decreased triglyceride biosynthesis and secretion from primary rat hepatocytes. These effects resulted in decreased secretion of apoB-100-very low density lipoprotein (VLDL) and an increased secretion of apoB-100 on low density lipoproteins/intermediate density lipoproteins. ApoB-48-VLDL was also replaced by more dense particles. The proteasomal inhibitor lactacystin did not influence the recovery of apoB-100 or apoB-48 in primary rat hepatocytes, indicating that co-translational (proteasomal) degradation is of less importance in these cells. Treatment with WY 14,643 made the recovery of apoB-100 sensitive to lactacystin, most likely reflecting the decreased biosynthesis of triglycerides. The PPAR alpha agonist induced a significant increase in the accumulation of pulse-labeled apoB-100 even after a short pulse (2-5 min). There was also an increase in apoB-100 nascent polypeptides, indicating that the co-translational degradation of apoB-100 was inhibited. However, a minor influence on an early posttranslation degradation cannot be excluded. This decreased co-translational degradation of apoB-100 explained the increased secretion of the protein. The levels of apoB-48 remained unchanged during these pulse-chase experiments, and albumin production was not affected, indicating a specific effect of PPAR alpha agonists on the co-translational degradation of apoB-100. These findings explain the difference in the rate of secretion of the two apoB proteins seen after PPAR alpha activation. PPAR alpha agonists increased the expression and biosynthesis of liver fatty acid-binding protein (LFABP). Increased expression of LFABP by transfection of McA-RH7777 cells increased the secretion of apoB-100, decreased triglyceride biosynthesis and secretion, and increased PPAR alpha mRNA levels. These findings suggest that PPAR alpha and LFABP could interact to amplify the effect of endogenous PPAR alpha agonists on the assembly of VLDL.
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| 21. |
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| 22. |
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| 23. |
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| 24. |
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| 25. |
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| 26. |
- Ringvall, Maria, 1969-
(författare)
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Functions of Heparan Sulfate During Mouse Development : Studies of Mice with Genetically Altered Heparan Sulfate Biosynthesis
- 2004
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Heparan sulfate (HS) is a ubiquitous polysaccharide on the cell surface and in the extracellular matrix. HS is an important actor in the regulation of cell signaling, especially in the developing embryo. In combination with cell culture and biochemical experiments, in vivo studies of genetically modified animals have pointed out the sulfation pattern of HS as highly important for binding of ligands, their receptors and other signaling modulators.The sulfation pattern of an HS chain is gained by several modifying steps, performed by multiple enzymes during biosynthesis in the Golgi apparatus. By alterations of sulfation pattern, and the amount of sulfate groups, a cell can regulate the binding properties of its HS to different molecules. The most highly sulfated form of HS is called heparin, and can only be found intracellularly in mast cells.This thesis describes the phenotypes and the alterations in HS/heparin biosynthesis of two genetically modified mouse strains deficient in N-deacetylase/N-sulfotransferase-1 (NDST1) and -2 (NDST2) respectively. We have found NDST1 to be important for correct sulfation of HS and that NDST2 is crucial in heparin biosynthesis. NDST2 deficient mice completely lack heparin and therefore have a severe mast cell phenotype. NDST1 deficient mice produce undersulfated HS and show several developmental disturbances. Some NDST1 embryos die in utero while the rest die neonatally due to breathing difficulties. Defect brain, eye and skeletal development has also been observed while some organs, such as the liver, appear to be largely unaffected. Several phenotypes are similar to defects seen in other mouse strains with impaired fibroblast growth factor and bone morphogenetic protein signaling, among others. This suggests the phenotypes of NDST1 deficient embryos to be of a multi factorial origin, in complete accordance to the many signaling pathways HS is suggested to modulate.
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| 27. |
- Soto Thompson, Marcelo, et al.
(författare)
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Photodynamic therapy and diagnostic measurements of basal cell carcinomas using esterified and non-esterified delta-aminolevulinic acid
- 2001
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Ingår i: Journal of Porphyrins and Phthalocyanines. - 1099-1409. ; 5:2, s. 147-147
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Tidskriftsartikel (refereegranskat)abstract
- Various optical techniques were used to investigate relevant parameters involved in photodynamic therapy (PDT) of human basal cell carcinomas (BCCs). The aim of the study was to compare the diagnostic and therapeutic outcome when using topically applied methyl-esterified delta -aminolevulinic acid (ALA-ME) and delta -aminolevulinic acid (ALA). A total of 35 pathologically verified BCCs in 14 patients were investigated. A diode laser. emitting continuous light at 633 nm, was used to induce PDT. The diagnostic measurements were performed before, during, and after PDT. Laser-induced fluorescence (LIF) was used to monitor the build-up of the ALA/ALA-ME-induced protoporphyrin IX (PpIX), The superficial tissue perfusion was measured with laser-Doppler perfusion imaging (LDPI) and the temperature of the lesion and the surrounding tissue was imaged with an IR-camera. A clear demarcation between the lesion and the normal skin was detected with LIF before the treatment for both PpIX precursors. The fluorescence measurements suggest that PpIX builds up to a higher degree and more selectively in the tumour following ALA-ME as compared to ALA. The LDPI measurements indicate a local transient restriction in blood perfusion immediately post-PDT. The measurement with the IR-camera revealed a temperature rise of about 1-2 degreesC during the treatment.
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| 28. |
- Stockeld, Dag, et al.
(författare)
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A Swedish study of chemoradiation in squamous cell carcinoma of the esophagus
- 2001
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Ingår i: Acta Oncologica. - : Informa UK Limited. - 1651-226X .- 0284-186X. ; 40, s. 566-
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Tidskriftsartikel (refereegranskat)abstract
- This multicenter study describes the development of a chemoradiation protocol for the treatment of non-metastatic squamous cell carcinoma of the esophagus. Eighty patients were treated with three courses of chemotherapy (cisplatinum and 5-fluorouracil) with concomitant radiotherapy (40 Gy) during the last two courses of chemotherapy. Esophagectomy was performed, when feasible. If no operation was performed, patients were planned to receive a target dose of 64 Gy. Toxicity was mainly attributable to hematological impairment and led to two adjustments of the treatment protocol (addition of filgrastim and lowering of the 5-fluorouracil dose). These changes made it possible to administer the planned treatment in a gradually higher proportion of patients (13/23 [57%] before changes of treatment compared with 30/36 [83%] after changes). Treatment-related mortality was 3.75% (3 patients, associated with leucopenic septicemia after chemotherapy). Fifty-four patients were resected. No per- or postoperative mortality was encountered. The complete response (pathological CR) rate in operated patients was 46% (27/59 patients) after chemoradiation. In the whole series the CR rate (including clinical CR for non-resected patients) was 44%. With a minimum follow-up of 37 months, the 3-year survival for the whole group was 31% compared with 57% for the CR patients. Total 5-year survival thus far (July 1999) is 26%.
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| 29. |
- Svanborg, Catharina, et al.
(författare)
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Adhesion, signal transduction and mucosal inflammation
- 2002
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Ingår i: Bacterial Adhesion to Host Tissues. - Cambridge : Cambridge University Press. - 9780521801072 - 0521801079 ; , s. 223-246
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 30. |
- Söderbergh, Annika, et al.
(författare)
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Prevalence and clinical associations of 10 defined autoantibodies in autoimmune polyendocrine syndrome type I
- 2004
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 89:2, s. 557-562
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Tidskriftsartikel (refereegranskat)abstract
- The prevalence of autoantibodies against nine intracellular enzyme autoantigens, namely 21-hydroxylase, side-chain cleavage enzyme (SCC), 17 alpha-hydroxylase, glutamic acid decarboxylase 65, aromatic L-amino acid decarboxylase, tyrosine phosphatase-like protein IA-2, tryptophan hydroxylase (TPH), tyrosine hydroxylase, cytochrome P450 1A2, and against the extracellular calcium-sensing receptor, was assessed in 90 patients with autoimmune polyendocrine syndrome type I. A multivariate logistic regression analysis was performed for the presence of autoantibodies as independent predictors for different disease manifestations. Reactivities against 21-hydroxylase and SCC were associated with Addison's disease with odds ratios (ORs) of 7.8 and 6.8, respectively. Hypogonadism was exclusively associated with autoantibodies against SCC with an OR of 12.5. Autoantibodies against tyrosine phosphatase-like protein IA-2 were associated with insulin-dependent diabetes mellitus with an OR of 14.9, but with low sensitivity. Reactivities against TPH and, surprisingly, glutamic acid decarboxylase 65, were associated with intestinal dysfunction, with ORs of 3.9 and 6.7, respectively. TPH reactivity was the best predictor for autoimmune hepatitis, with an OR of 27.0. Hypoparathyroidism was not associated with reactivity against any of the autoantigens tested. No reactivity against the calcium-sensing receptor was found. Analysis of autoantibodies in autoimmune polyendocrine syndrome type I patients is a useful tool for establishing autoimmune manifestations of the disease as well as providing diagnosis in patients with suspected disease.
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| 31. |
- Tuomas, Göran, et al.
(författare)
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Evaluation of ground thermal conductivity from drilling data
- 2004
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Ingår i: International Journal of Rock Mechanics And Mining Sciences. - : Elsevier BV. - 1365-1609 .- 1873-4545. ; 41:Suppl 1, s. 241-247
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Tidskriftsartikel (refereegranskat)abstract
- In this paper a new method for evaluating ground thermal conductivity is suggested. The principle is based on ordinary drilling where energy is injected into the borehole in the form of pressurised fluid, mechanical torque, and mechanical feed force, which all dissipate into heat. Part of the heat leaves the borehole with the fluid while the rest is mainly transferred into the formation. By determining the energy flows, ground thermal conductivity can be estimated. This new measurement method would have many advantages. Ground conductivity values would be continuously estimated along the borehole, meaning that values are obtained through the formation. This quality could, for example, be used during production drilling in a mine to instantly detect lithological boundaries, resulting in increased ore extraction efficiency. Energy storage systems could be dynamically designed since the system capacity could be recognized and verified during drilling. Presented simulation results, where realistic drilling parameters were used, show that the method has the potential to be practically applied.
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| 32. |
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| 33. |
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| 34. |
- Vikström, Maria, et al.
(författare)
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Dagvattendammars avskiljningsförmåga – påverkande faktorer och metodik för bedömning
- 2004
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Rapport (övrigt vetenskapligt/konstnärligt)abstract
- Rapporten beskriver hur numeriska modeller, främst MIKE 21, använts för att ta fram en generell beräkningsmetodik för bedömning av dagvattendammars avskiljningsförmåga. En modellbaserad fallstudie har genomförts för att studera de påverkansfaktorer som styr avskiljningen i en dagvattendamm.
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