| 1. |
- Ahlsson, Anders, 1962-, et al.
(författare)
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Patients with postoperative atrial fibrillation have a doubled cardiovascular mortality
- 2009
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Ingår i: Scandinavian cardiovascular journal : SCJ. - : Informa UK Limited. - 1651-2006 .- 1401-7431. ; 43:5, s. 330-336
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To investigate the impact of postoperative AF on late mortality and cause of death in CABG patients.DESIGN: All CABG patients without preoperative AF surgically treated between January 1, 1997 and June 30, 2000 were included (N = 1419). Altogether, 419 patients (29.5%) developed postoperative AF. After a median follow-up of 8.0 years, survival data were obtained, causes of death were compared and Cox proportional hazard analysis was used to determine predictors of late mortality.RESULTS: The total mortality was 140 deaths/419 patients (33.4%) in postoperative AF patients and 191 deaths/1 000 patients (19.1%) in patients without AF. Death due to cerebral ischemia (2.6% vs. 0.5%), myocardial infarction (7.4% vs. 3.0%), sudden death (2.6% vs. 0.9%), and heart failure (6.7% vs. 2.7%) was more common among postoperative AF patients. Postoperative AF was an age-independent risk indicator for late mortality with a hazard ratio (HR) of 1.56 (95% confidence interval 1.23-1.98).CONCLUSIONS: Postoperative AF is an age-independent risk factor for late mortality in CABG patients, explained by an increased risk of cardiovascular death.
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| 2. |
- Ahlsson, Anders, 1962-, et al.
(författare)
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Postoperative atrial fibrillation in patients undergoing aortocoronary bypass surgery carries an eightfold risk of future atrial fibrillation and a doubled cardiovascular mortality
- 2010
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Ingår i: European Journal of Cardio-Thoracic Surgery. - : Oxford University Press (OUP). - 1010-7940 .- 1873-734X. ; 37:6, s. 1353-1359
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: This article presents a study of postoperative atrial fibrillation (AF) and its long-term effects on mortality and heart rhythm.METHODS: The study cohort consisted of 571 patients with no history of AF who underwent primary aortocoronary bypass surgery from 1999 to 2000. Postoperative AF occurred in 165/571 patients (28.9%). After a median follow-up of 6 years, questionnaires were obtained from 91.6% of surviving patients and an electrocardiogram (ECG) from 88.6% of all patients. Data from hospitalisations due to arrhythmia or stroke during follow-up were analysed. The causes of death were obtained for deceased patients.RESULTS: In postoperative AF patients, 25.4% had atrial fibrillation at follow-up compared with 3.6% of patients with no AF at surgery (p<0.001). An episode of postoperative AF was the strongest independent risk factor for development of late AF, with an adjusted risk ratio of 8.31 (95% confidence interval (CI) 4.20-16.43). Mortality was 29.7% (49 deaths/165 patients) in the AF group and 14.8% (60 deaths/406 patients) in the non-AF group (p<0.001). Death due to cerebral ischaemia was more common in the postoperative AF group (4.2% vs 0.2%, p<0.001), as was death due to myocardial infarction (6.7% vs 3.0%, p=0.041). Postoperative AF was an age-independent risk factor for late mortality, with an adjusted hazard ratio of 1.57 (95% CI 1.05-2.34).CONCLUSIONS: Postoperative AF patients have an eightfold increased risk of developing AF in the future, and a doubled long-term cardiovascular mortality.
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| 3. |
- Heins, Nico, et al.
(författare)
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Derivation, characterization, and differentiation of human embryonic stem cells.
- 2004
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Ingår i: Stem cells (Dayton, Ohio). - 1066-5099. ; 22:3, s. 367-76
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Tidskriftsartikel (refereegranskat)abstract
- The derivation of human embryonic stem (hES) cells establishes a new avenue to approach many issues in human biology and medicine for the first time. To meet the increased demand for characterized hES cell lines, we present the derivation and characterization of six hES cell lines. In addition to the previously described immunosurgery procedure, we were able to propagate the inner cell mass and establish hES cell lines from pronase-treated and hatched blastocysts. The cell lines were extensively characterized by expression analysis of markers characteristic for undifferentiated and differentiated hES cells, karyotyping, telomerase activity measurement, and pluripotency assays in vitro and in vivo. Whereas three of the cell lines expressed all the characteristics of undifferentiated pluripotent hES cells, one cell line carried a chromosome 13 trisomy while maintaining an undifferentiated pluripotent state, and two cell lines, one of which carried a triploid karyotype, exhibited limited pluripotency in vivo. Furthermore, we clonally derived one cell line, which could be propagated in an undifferentiated pluripotent state.
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| 4. |
- Krank, Benjamin, et al.
(författare)
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Tuning spot weld models for vehicle body structural dynamics
- 2012
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Ingår i: Proceedings Of International Conference On Noise And Vibration Engineering (ISMA2012) / International Conference On Uncertainty In Structural Dynamics (USD2012). - : Katholieke Universiteit Leuven. - 9789073802896 ; , s. 3915-3926
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Konferensbidrag (refereegranskat)abstract
- Efforts focussing on modelling of spot welds in typical automotive structures have been spent during the last decades resulting in a number of different modelling techniques. One of the crucial aspects common to all these approaches is the difficulties related to the local complexity of the modelling of the actual connections. In order to handle this complexity, spot weld models are often dependent on parameters tuning their characteristics. This paper discusses the tuning of two different spot weld models with respect to certain parameters; the RBE3-Hexa-RBE3 model (also known as the ACM 2) and the Spider2 model available in the pre-processor Ansa. With the current trend towards increasingly refined finite element model meshes, current guide lines need to be updated and elaborated further in order to identify the best performing models. In this paper, model studies are discussed targeting tuning of spot weld parameters together with a new proposal for an exact method for updating the Young's modulus and density of isotropic shell structures analytically using an initial FE calculation.
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| 5. |
- Svensson, Per Anders, 1959, et al.
(författare)
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Identification of genes predominantly expressed in human macrophages
- 2004
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Ingår i: Atherosclerosis. - : Elsevier BV. ; 177, s. 287-290
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Tidskriftsartikel (refereegranskat)abstract
- Identification of cell and tissue specific genes may provide novel insights to signaling systems and functions. Macrophages play a key role in many diseases including atherosclerosis. Using DNA microarrays we compared the expression of approximately 10,000 genes in 56 human tissues and identified 23 genes with predominant expression in macrophages. The identified genes include both genes known to be macrophage specific and genes previously not well described in this cell type. Tissue distribution of two genes, liver X receptor (LXR) alpha and interleukin-1 receptor antagonist (IL1RN), was verified by real-time RT-PCR. We conclude that comparison of expression profiles from a large number of tissues can be used to identify genes that are predominantly expressed in certain tissues. Identification of novel macrophage specific genes may increase our understanding of the role of this cell in different diseases.
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| 6. |
- Svensson, Per-Arne, 1969, et al.
(författare)
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Regulation and splicing of scavenger receptor class B type I in human macrophages and atherosclerotic plaques
- 2005
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Ingår i: BMC Cardiovasc Disord. - : Springer Science and Business Media LLC. - 1471-2261. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The protective role of high-density lipoprotein (HDL) in the cardiovascular system is related to its role in the reverse transport of cholesterol from the arterial wall to the liver for subsequent excretion via the bile. Scavenger receptor class B type I (SR-BI) binds HDL and mediates selective uptake of cholesterol ester and cellular efflux of cholesterol to HDL. The role of SR-BI in atherosclerosis has been well established in murine models but it remains unclear whether SR-BI plays an equally important role in atherosclerosis in humans. The aim of this study was to investigate the expression of SR-BI and its isoforms in human macrophages and atherosclerotic plaques. METHODS: The effect of hypoxia and minimally modified low-density lipoprotein (mmLDL), two proatherogenic stimuli, on SR-BI expression was studied in human monocyte-derived macrophages from healthy subjects using real-time PCR. In addition, SR-BI expression was determined in macrophages obtained from subjects with atherosclerosis (n = 15) and healthy controls (n = 15). Expression of SR-BI isoforms was characterized in human atherosclerotic plaques and macrophages using RT-PCR and DNA sequencing. RESULTS: SR-BI expression was decreased in macrophages after hypoxia (p < 0.005). In contrast, SR-BI expression was increased by exposure to mmLDL (p < 0.05). There was no difference in SR-BI expression in macrophages from patients with atherosclerosis compared to controls. In both groups, SR-BI expression was increased by exposure to mmLDL (p < 0.05). Transcripts corresponding to SR-BI and SR-BII were detected in macrophages. In addition, a third isoform, referred to as SR-BIII, was discovered. All three isoforms were also expressed in human atherosclerotic plaque. Compared to the other isoforms, the novel SR-BIII isoform was predicted to have a unique intracellular C-terminal domain containing 53 amino acids. CONCLUSION: We conclude that SR-BI is regulated by proatherogenic stimuli in humans. However, we found no differences between subjects with atherosclerosis and healthy controls. This indicates that altered SR-BI expression is not a common cause of atherosclerosis. In addition, we identified SR-BIII as a novel isoform expressed in human macrophages and in human atherosclerotic plaques.
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