| 31. |
- Marchesseau, Stephanie, et al.
(författare)
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Hybrid PET/CT and PET/MRI imaging of vulnerable coronary plaque and myocardial scar tissue in acute myocardial infarction
- 2018
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Ingår i: Journal of Nuclear Cardiology. - : SPRINGER. - 1071-3581 .- 1532-6551. ; 25:6, s. 2001-2011
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundFollowing an acute coronary syndrome, combined CT and PET with F-18-NaF can identify coronary atherosclerotic plaques that have ruptured or eroded. However, the processes behind F-18-NaF uptake in vulnerable plaques remain unclear. Methods and ResultsTen patients with STEMI were scanned after F-18-NaF injection, for 75minutes in a Siemens PET/MR scanner using delayed enhancement (LGE). They were then scanned in a Siemens PET/CT scanner for 10minutes. Tissue-to-background ratio (TBR) was compared between the culprit lesion in the IRA and remote non-culprit lesions in an effort to independently validate prior studies. Additionally, we performed a proof-of-principle study comparing TBR in scar tissue and remote myocardium using LGE images and PET/MR or PET/CT data. From the 33 coronary lesions detected on PET/CT, TBRs for culprit lesions were higher than for non-culprit lesions (TBR=2.110.45 vs 1.46 +/- 0.48; P<0.001). Interestingly, the TBR measured on the PET/CT was higher for infarcted myocardium than for remote myocardium (TBR=0.81 +/- 0.10 vs 0.71 +/- 0.05; P=0.003). These results were confirmed using the PET/MR data (TBR=0.81 +/- 0.10 for scar, TBR=0.71 +/- 0.06 for healthy myocardium, P=0.03). Conclusions We confirmed the potential of F-18-NaF PET/CT imaging to detect vulnerable coronary lesions. Moreover, we demonstrated proof-of-principle that F-18-NaF concurrently detects myocardial scar tissue.
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| 32. |
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| 33. |
- Nathanson, D, et al.
(författare)
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Reduced plasma levels of glucagon-like peptide-1 in elderly men are associated with impaired glucose tolerance but not with coronary heart disease
- 2010
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 0012-186X .- 1432-0428. ; 53:2, s. 277-280
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Tidskriftsartikel (refereegranskat)abstract
- AIMS/HYPOTHESIS: Besides the insulinotropic effects of glucagon-like peptide-1 (GLP-1) mimetics, their effects on endothelial dysfunction and myocardial ischaemia are of interest. No previous study has investigated associations between plasma levels of GLP-1 and CHD. METHODS: We investigated longitudinal relationships of fasting GLP-1 with the dynamic GLP-1 response after OGTT (difference between 60 min OGTT-stimulated and fasting GLP-1 levels [DeltaGLP-1]) and CHD in a population-based cohort of 71-year-old men. In the same cohort, we also cross-sectionally investigated the association between stimulated GLP-1 levels and: (1) cardiovascular risk factors (blood pressure, lipids, urinary albumin, waist circumference and insulin sensitivity index [M/I] assessed by euglycaemic-hyperinsulinaemic clamp); and (2) impaired glucose tolerance (IGT) and type 2 diabetes mellitus. RESULTS: During the follow-up period (maximum 13.8 years), of 294 participants with normal glucose tolerance (NGT), 69 experienced a CHD event (13.8 years), as did 42 of 141 with IGT and 32 of 74 with type 2 diabetes mellitus. DeltaGLP-1 did not predict CHD (HR 1.0, 95% CI 0.52-2.28). The prevalence of IGT was associated with DeltaGLP-1, lowest vs highest quartile (OR 0.3, 95% CI 0.12-0.58), with no such association for type 2 diabetes mellitus (OR 1.0, 95% CI 0.38-2.86). M/I was significantly associated with DeltaGLP-1 in the type 2 diabetes mellitus group (r = 0.38, p < 0.01), but not in the IGT (r = 0.11, p = 0.28) or NGT (r = 0.10, p = 0.16) groups. CONCLUSIONS/INTERPRETATION: Impaired GLP-1 secretion is associated with IGT, but not with type 2 diabetes mellitus. This finding in the latter group might be confounded by oral glucose-lowering treatment. GLP-1 does not predict CHD. Although DeltaGLP-1 was associated with insulin sensitivity in the type 2 diabetes mellitus group, GLP-1 does not seem to be a predictor of CHD in insulin-resistant patients.
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| 34. |
- Nilsson, B, et al.
(författare)
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Detection and characterization of immunoconglutinins in patients with systemic lupus erythematosus (SLE) : serial analysis in relation to disease course.
- 1992
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Ingår i: Clinical and Experimental Immunology. - 0009-9104 .- 1365-2249. ; 90:2, s. 251-255
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Tidskriftsartikel (refereegranskat)abstract
- The levels of IgA, IgG and IgM immunoconglutinins (IK) were assessed in sera from 20 patients with SLE which were followed for 8-month periods. At the time of the exacerbation, IgG IKs were significantly increased to 226 +/- 90 arbitrary units (mean +/- s.e.m.) compared with both the minimum value of 75 +/- 28 in the SLE patients and with 31 +/- 2 in healthy controls (P < 0.05). There was no difference between SLE patients and controls in the levels of IgM and IgA IKs. Most of the SLE patients in this material showed maximal IgG IK levels before exacerbation, but there was no correlation between the clinical disease index and the levels of IgG IK. The specificity of IgG IKs showed a broad diversity for microtitre-fixed C3b, iC3b, C3c and C3dg. The antibodies were of IgG1, IgG3 and in two patients, IgG4 subclass. IgG IKs were correlated to the C3d/C3 ratio which suggested that the IK responses were secondary to C3 activation. In summary, unlike other conditions associated with complement activation where elevated IgM IKs are common, an increase in IgG IK levels was observed. It is possible that this diverging IK response contributes to the pathophysiology of the disease.
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| 35. |
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| 36. |
- Nilsson, Sara, et al.
(författare)
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Genetic, molecular and functional analyses of complement factor I deficiency.
- 2009
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Ingår i: European Journal of Immunology. - : Wiley. - 1521-4141 .- 0014-2980. ; 39:1, s. 310-323
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Tidskriftsartikel (refereegranskat)abstract
- Complete deficiency of complement inhibitor factor I (FI) results in secondary complement deficiency due to uncontrolled spontaneous alternative pathway activation leading to susceptibility to infections. Current genetic examination of two patients with near complete FI deficiency and three patients with no detectable serum FI and also close family members revealed homozygous or compound heterozygous mutations in several domains of FI. These mutations were introduced into recombinant FI and the resulting proteins were purified for functional studies, while transient transfection was used to analyze expression and secretion. The G170V mutation resulted in a protein that was not expressed, whereas the mutations Q232K, C237Y, S250L, I339M and H400L affected secretion. Furthermore, the C237Y and the S250L mutants did not degrade C4b and C3b as efficiently as the WT. The truncated Q336x mutant could be expressed, in vitro, but was not functional because it lacks the serine protease domain. Furthermore, this truncated FI was not detected in serum of the patient. Structural investigations using molecular modeling were performed to predict the potential impact the mutations have on FI structure. This is the first study that investigates, at the functional level, the consequences of molecular defects identified in patients with full FI deficiency.
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| 37. |
- Nordin Fredrikson, Gunilla, et al.
(författare)
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Characterization of non-expressed C4 genes in a case of complete C4 deficiency: identification of a novel point mutation leading to a premature stop codon
- 1998
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Ingår i: Human Immunology. - 0198-8859. ; 59:11, s. 713-719
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Tidskriftsartikel (refereegranskat)abstract
- The genetic basis of complete C4 deficiency in a patient with SLE was investigated. Previous studies have demonstrated that this patient has two different major histocompatibility complex (MHC) haplotypes that each contain a major deletion and a non-expressed C4 gene. In the present study, non-expression of the C4 genes was explained by the finding of two distinct C4 gene mutations. A previously described two base pair insertion in exon 29 of the C4 gene was detected in the paternal MHC haplotype [HLA-A2, B40, SC00, DR6]. The maternal haplotype [HLA-A30, B18, F1C00, DR3] carried a C4 gene with a one base pair deletion in exon 20 generating a premature stop codon. This mutation was neither found in 10 individuals with known non-expressed C4 genes nor in 9 individuals homozygous for the complotype F1C30. The isotype and allotype specific regions of the patient's C4 genes were sequenced, and both contained C4A3a sequence. In conclusion, two different MHC haplotypes resembling the extended haplotypes [HLA-A2, B40, SC02, DR6] and [HLA-A30, B18, F1C30, DR3] both contained a non-expressed C4A gene that was due to either of two distinct mutations, demonstrating the heterogeneous genetic background of C4 deficiency.
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| 38. |
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| 39. |
- Saltzman, Katarina, 1966, et al.
(författare)
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Gardeners’ perspectives and practices in relation to plants in motion
- 2021
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Ingår i: Routledge Handbook of Biosecurity and Invasive Species. - Abingdon, Oxon ; New York, NY : Routledge, 2021. : Routledge. - 9780815354895 ; , s. 226-239
-
Bokkapitel (refereegranskat)abstract
- The establishment of introduced species in new environments is today widely acknowledged as a potential threat to biodiversity, and many plants that are known to be invasive have obviously spread from gardens. Thus, in the context of biosecurity, we need to consider how contemporary gardeners think about which plants and animals are welcome in their gardens. In this chapter we look at vegetation in motion from a cultural and social point of view, with a particular focus on some of many different ways in which people are involved in spreading of plants, both desired and undesired ones. We do this by investigating everyday practices of gardeners in Sweden, and not least the common habit of sharing plants, in order to highlight the social and cultural aspects of the spread of species. Among the gardeners in this study it is obvious that the dynamics and vitality of plants is often regarded as an asset, but also sometimes as problem, when plants simply grow too much. Understandings of the relationship between gardens and surrounding environments, as well as between nature and culture, have changed over time, and are continuously changing. As plants have the ability to multiply and spread in various ways, both on their own and with the help of humans, there is a need to acknowledge the role of human as well as non-human agencies in order to understand the complexity of these interactions. Inspired by Tim Ingold we find it useful to think about both gardeners and plants as ‘biosocial becomings’. In order to address the threat posed by invasive species, we propose that it is important to improve our understanding of what happens in everyday biosocial encounters between people, plants and other species.
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| 40. |
- Seelen, MA, et al.
(författare)
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Functional analysis of the classical, alternative, and MBL pathways of the complement system: standardization and validation of a simple ELISA
- 2005
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Ingår i: Journal of Immunological Methods. - : Elsevier BV. - 1872-7905 .- 0022-1759. ; 296:1-2, s. 187-198
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Tidskriftsartikel (refereegranskat)abstract
- Primary defence against invading microorganisms depends on a functional innate immune system and the complement system plays a major role in such immunity. Deficiencies in one of the components of the complement system can cause severe and recurrent infections, systemic diseases, such as systemic lupus erythematosus (SLE) and renal disease. Screening for complement deficiencies in the classical or alternative complement pathways has mainly been performed by haemolytic assays. Here. we describe a simple ELISA-based format for the evaluation of three pathways of complement activation. The assays are based on specific coatings for each pathway in combination with specific buffer systems. We have standardized these assays and defined cut off values to detect complement deficiencies at the different levels of the complement system. The results demonstrate the value of these ELISA-based procedures for the functional assessment of complement deficiencies in clinical practice. The assay is now available commercially in kit form.
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