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- Abrahamson, Magnus
(författare)
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Att förlåta det oförlåtliga
- 2002
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Ingår i: Budbäraren. ; :21, s. 12-
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Tidskriftsartikel (populärvet., debatt m.m.)
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| 2. |
- Abrahamson, Magnus, et al.
(författare)
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Cystatins.
- 2003
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Ingår i: Biochemical Society Symposia. - 0067-8694. ; 70, s. 179-199
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Tidskriftsartikel (refereegranskat)
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| 3. |
- Abrahamson, Magnus, 1972-
(författare)
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Jesu uppståndelse som historiskt problem : En studie av Rudolf Bultmanns och Wolfhart Pannenbergs tolkningar
- 2001
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The main purpose of this study is to make a critical examination of Rudolf Bultmann´s (1884–1976) and Wolfhart Pannenberg´s (b. 1928) interpretations of the resurrection of Jesus. Bultmann is best known for seeking to demythologize the miracles of the New Testament. Pannenberg has gained much attention for arguing that the resurrection of Jesus is an event in chronological history. In this thesis I first present Bultmann´s and Pannenberg´s interpretations of the resurrection of Jesus. In order to help the reader understand the context in which these interpretations were made, I give a brief sketch of the German theological setting. Second, I compare the theologies of Bultmann and Pannenberg from the concept of background theory, principles of interpretation, exegetical reasoning, the meaning of the resurrection and what it means to accept the resurrection. Third, I categorize different ways that the resurrection could be interpreted today. Fourth, I critically discuss the way that Bultmann and Pannenberg argue and give some proposals for how their theologies can be developed. Developing the theology of Bultmann I give more attention to chronological history than he does. I also make alterations in the way he understands God´s action. Concerning Pannenberg I discuss the importance of rational arguments in his theology. I argue that the resurrection should be interpreted from the perspective of a faith or an interpretation which seeks understanding.
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| 4. |
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| 5. |
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| 6. |
- Abrahamson, Magnus
(författare)
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Wolfhart Pannenberg och Jesu uppståndelse
- 2004
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Ingår i: Tro & Liv: Tidskrift för kristen tro och förkunnelse. ; 63:3-4, s. 13-21
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 7. |
- Ahuja, Sat pal, et al.
(författare)
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Glutathione S-transferase µ(GST) modifies activities of proteases and levels of cystatin C secreted by mouse retinal explants
- 2004
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Ingår i: Investigative Ophthalmology & Visual Science. - 1552-5783. ; 45, s. 352-352
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Konferensbidrag (refereegranskat)abstract
- Purpose: In one form of human autosomal recessive retinitis pigmentosa and in retinal degeneration (rd1) mouse, mutation occurs in the genes encoding ß subunit of rod photoreceptor cGMP phosphodiesterase. Therefore, rd1 mutant mouse is an appropriate model for human inherited retinal degeneration studies. Retinal explants are successfully cultured in serum free chemically defined R16 medium to evaluate effects of various rescue factors and retinal conditioned medium (RCM) for secreted molecules like proteases and their inhibitors. Cysteine protease inhibitor cystatin C has recently been identified in rodent neuroretina and RPE. RCM of explants treated with GST were analyzed for proteases and cystatin C to explain, in part, mode of action of GST in protection of degenerating retina. Methods: Postnatal day 2 (PN2) and PN7 control (wt) and rd1 were cultured with (10 ng / ml GST) and without GST in R16 medium, respectively, for 26 and 21 days in vitro (div). Retinal extracts (RE) and RCM were analyzed by fluorometry using casein green fluorescent labeled with BODIPY–FL (Molecular Probes) for total proteases; Z–Phe–Arg–NMec or Z–Arg–Arg–NMec for cysteine proteases and by ELISA for cystatin C, respectively, for levels and secretion of proteases and cystatin C. The protein content of RE was measured. Results: Protein content (µg) of RE from wt and rd1 retinal extracts respectively increased and decreased with age. Cystatin C (ng/ml RCM) content in wt and rd1 RE increased with age (was always higher in wt) up to PN14 and then decreased but was higher than that at PN2. Progressive secretion of cystatin C by PN2 explants was lower than that by PN7 explants; and that by rd1 PN2 and PN7 explants was initially lower up to in vitro age of PN19 and subsequently it was higher than that by wt explants. Secretion of total cystatin C by PN2 and PN7 wt and rd1 explants was similar and was increased by GST. During initial stage of culture total protease activity ({Delta} F / 100 µl RCM) in RCM of rd1 PN2 and PN7 explants was higher and was decreased in GST treated explants. Conclusions: Cystatin C content and secretion by wt RE is always higher and that of proteases is lower than that of rd1. Treatment with GST increases content of cystatin C and consequently decreases that of proteases especially cysteine proteases.
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| 8. |
- Brage, Monica, et al.
(författare)
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Osteoclastogenesis is decreased by cysteine proteinase inhibitors.
- 2004
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Ingår i: Bone. - : Elsevier BV. - 8756-3282 .- 1873-2763. ; 34:3, s. 412-24
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Tidskriftsartikel (refereegranskat)abstract
- The effects of cystatin C and other cysteine proteinase inhibitors on osteoclast formation and differentiation have been investigated. Cystatin C decreased osteoclast formation stimulated by parathyroid hormone (PTH), 1,25(OH)2-vitamin D3 or interleukin-6 (IL-6) (in the presence of its soluble receptor) as assessed by the number of tartrate-resistant acid phosphatase (TRAP+) multinucleated cells in mouse bone marrow cultures. The inhibitory effect was associated with decreased mRNA expression for the calcitonin receptor as well as decreased number of specific binding sites for 125I-calcitonin, and without any effect on the mRNA expression of receptor activator of nuclear factor kappaB (NF-kappaB) ligand (RANKL). Similarly, the cysteine proteinase inhibitors leupeptin, E-64 and benzyloxycarbonyl-Phe-Ala-diazomethane (Z-FA-CHN2) decreased PTH-stimulated formation of TRAP+ multinucleated cells and binding of 125I-calcitonin. A peptidyl derivative synthesized to mimic part of the proteinase-binding site of cystatin C (benzyloxycarbonyl-Arg-Leu-Val-Gly-diazomethane, or Z-RLVG-CHN2) also decreased PTH-stimulated osteoclast formation. In a 9-day culture, addition of cystatin C during the last 5 days was sufficient to cause substantial inhibition of osteoclast formation. Cystatin C-induced decrease of osteoclast formation was associated with enhanced number of F4/80-positive macrophages and increased mRNA expression of the macrophage receptor c-fms in the bone marrow culture. Osteoclast formation in mouse bone marrow cultures as well as in mouse spleen cell cultures, stimulated by macrophage colony-stimulating factor (M-CSF) and RANKL was also decreased by different cysteine proteinase inhibitors. In addition, cystatin C inhibited M-CSF/RANKL induction of calcitonin receptor mRNA in spleen cell cultures. The inhibitory effect by cystatin C in spleen cells was associated with decreased mRNA expression of RANK and the transcription factor NFAT2. It is concluded that cysteine proteinase inhibitors decrease formation of osteoclasts by interfering at a late stage of pre-osteoclast differentiation.
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| 9. |
- Eksandh, Louise, et al.
(författare)
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Different clinical expressions in two families with Stargardt's macular dystrophy (STGD1)
- 2001
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Ingår i: Acta Ophthalmologica Scandinavica. - : Wiley. - 1395-3907. ; 79:5, s. 524-530
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: To describe the clinical expressions, with emphasis on electrophysiological examinations, in two Swedish families with Stargardt's macular dystrophy (STGD1). Methods. Two pairs of siblings with STGD1, for whom diagnosis had been confirmed by genetic linkage to the ABCA4 gene region, were examined regarding visual acuity, kinetic perimetry, fundus photography, full-field ERG and multifocal ERG (MERG). Possible disease-causing mutations were screened for by DNA sequencing of selected regions of the ABCA4 gene. Results. All STGD1 patients, had visual acuity 0.07-0.1. The two families presented different fundus appearances, MERGs and implicit times on. 30 Hz flicker white light full-field ERGs. Genetic analysis revealed one unique sequence variation in exon 19 of the ABCA4 gene, in one allele from the patients of one of the families. This point mutation causes the amino acid substitution T972N in the ABCR protein. Conclusion. Two pairs of siblings with STGD1 presented two different expressions of the disease regarding the distribution of the retinal dysfunction. One possible molecular explanation to the different clinical expressions may be the T972N substitution present in the ABCR protein in one of the STGD1 families investigated.
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| 10. |
- Ekström, Ulf, et al.
(författare)
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Expression of an LDL receptor allele with two different mutations (E256K and I402T)
- 2000
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Ingår i: Molecular Pathology. - 1366-8714. ; 53:1, s. 31-36
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: To investigate the disease causing event in patients with familial hypercholesterolaemia, carrying two mutations each, E256K in exon 6 and I402T in exon 9, of the gene encoding the low density lipoprotein (LDL) receptor. It was not known whether the mutations were positioned in cis or trans, or if they were each pathogenic separately or only when present together. METHODS: Polymerase chain reaction, denaturing gradient gel electrophoresis and sequencing were used to characterise the LDL receptor locus of the patients and family members. The different LDL receptor mutants, constructed in vitro by oligonucleotide directed mutagenesis, were expressed in LDL receptor deficient Chinese hamster ovary (CHO1d1A7) cells, to determine the effects of the mutations on LDL receptor function. RESULTS: The two mutations were located on the same allele of the LDL receptor gene. All mutant constructs resulted in the production of a detectable protein in CHO cells. The cells expressing only the I402T mutation, or the combination of I402T and E256K mutations, were seriously affected in mediating uptake and degradation of LDL. Contrary to initial predictions, the cells expressing only the E256K mutation showed essentially the same binding, uptake, and degradation of 125I labelled LDL as cells transfected with normal LDL receptor cDNA. These results suggest that the pathogenic mutation in the patients heterozygous for the E256K/I402T allele is the I402T mutation, and that E256K alone is a rare sequence variation, which does not affect LDL receptor protein function. E256K was not detected either in DNA from a healthy population or in DNA from other hypercholesterolaemic patients studied. CONCLUSIONS: Despite the information available on the structure-function relations between the LDL receptor and LDL receptor like proteins, predictions about the disease causing potential of a mutation are not reliable. These results suggest that the I402T mutation is pathogenic and that the substitution of E256K alone is a rare sequence variation, without a detectable phenotype modulating effect.
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