| 1. |
- Andersson, Maria, 1975, et al.
(författare)
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Differential global gene expression response patterns of human endothelium exposed to shear stress and intraluminal pressure
- 2005
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Ingår i: J Vasc Res. - : S. Karger AG. - 1018-1172. ; 42:5, s. 441-52
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Tidskriftsartikel (refereegranskat)abstract
- We investigated the global gene expression response of endothelium exposed to shear stress and intraluminal pressure and tested the hypothesis that the two biomechanical forces induce a differential gene expression response pattern. Intact living human conduit vessels (umbilical veins) were exposed to normal or high intraluminal pressure, or to low or high shear stress in combination with a physiological level of the other force in a unique vascular ex vivo perfusion system. Gene expression profiling was performed by the Affymetrix microarray technology on endothelial cells isolated from stimulated vessels. Biomechanical forces were found to regulate a very large number of genes in the vascular endothelium. In this study, 1,825 genes were responsive to mechanical forces, which corresponds to 17% of the expressed genes. Among pressure-responsive genes, 647 genes were upregulated and 519 genes were down regulated, and of shear stress-responsive genes, 133 genes were upregulated and 771 down regulated. The fraction of genes that responded to both pressure and shear stimulation was surprisingly low, only 13% of the regulated genes. Our results indicate that the two different stimuli induce distinct gene expression response patterns, which can also be observed when studying functional groups. Considering the low number of overlapping genes, we suggest that the endothelial cells can distinguish between shear stress and pressure stimulation.
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| 2. |
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| 3. |
- Bayati, Zahra, 1958, et al.
(författare)
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Nytt centrum mot rasism får fel vetenskaplig inriktning
- 2015
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Ingår i: Göteborgs Posten. - 1103-9345. ; :2015-06-14
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Tidskriftsartikel (populärvet., debatt m.m.)abstract
- När rasism ska förstås som något som kan lösas genom att lära ut tolerans undergrävs förtroendet för regeringens satsning. Dessutom saknas det etnisk/rasifierad mångfald bland forskargruppen.
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| 4. |
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| 5. |
- Karlsson, Lena, 1964, et al.
(författare)
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Outcome after intensive reinduction therapy and allogeneic stem cell transplant in paediatric relapsed acute myeloid leukaemia
- 2017
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Ingår i: British Journal of Haematology. - : WILEY. - 0007-1048 .- 1365-2141. ; 178:4, s. 592-602
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Tidskriftsartikel (refereegranskat)abstract
- Given that 30-40% of children with acute myeloid leukaemia (AML) relapse after primary therapy it is important to define prognostic factors and identify optimal therapy. From 1993 to 2012, 543 children from the Nordic countries were treated according to two consecutive protocols: 208 children relapsed. The influence of disease characteristics, first line treatment, relapse therapy and duration of first remission on outcome was analysed. Second complete remission (CR2) was achieved in 146 (70%) patients. Estimated 5-year overall survival (OS5y) was 39 +/- 4% for the whole group and 43 +/- 4% for the 190 patients given re-induction therapy, of whom 76% received regimens that included fludarabine, cytarabine (FLA) +/- anthracyclines, 18% received Nordic Society for Paediatric Haematology and Oncology (NOPHO) upfront blocks and 5% received other regimens. Late relapse >= 1 year from diagnosis, no allogeneic stem cell transplantation (SCT) in first remission and core binding factor AML were independent favourable prognostic factors for survival. For the 128 children (124 in CR2) that received SCT as consolidation therapy after relapse, OS5y was 61 +/- 5%. Four of 19 children (21%) survived without receiving SCT as part of relapse therapy. Our data show that intensive re-induction followed by SCT can give cure rates of 40% in children with relapsed AML.
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| 6. |
- Karlsson, Lena, 1964, et al.
(författare)
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Risk of Recurrent Stroke in Patients with Symptomatic Mild (20-49% NASCET) Carotid Artery Stenosis
- 2016
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Ingår i: European Journal of Vascular and Endovascular Surgery. - : Elsevier BV. - 1078-5884. ; 52:3, s. 287-294
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Tidskriftsartikel (refereegranskat)abstract
- Objective: The objective of this study was to evaluate the risk of recurrent ischaemic stroke in patients with ultrasound assessed symptomatic mild carotid artery stenosis (20-49% NASCET) treated solely with modern medical treatment. Method: This was a retrospective, observational register cohort study. Three groups of patients were recruited from a database of all carotid Doppler ultrasound examinations performed in the Gothenburg region between 2004 and 2009. Patients with symptomatic mild carotid artery stenosis (n = 162) were compared with patients with asymptomatic carotid artery stenosis (n = 301) of equal degree and a group of patients with surgically (CEA) treated symptomatic moderate or severe carotid artery stenosis (n = 220). Kaplan-Meier estimates and Cox proportional hazard models were used to compare the primary outcome (ipsilateral ischaemic stroke) between groups. Results: After a 3 year follow up, the cumulative incidence of recurrent ipsilateral stroke in patients with symptomatic mild carotid artery stenosis was 7.4%. Patients with symptomatic mild carotid artery stenosis had a substantially increased risk of recurrent ipsilateral stroke compared with asymptomatic patients with equal degree of stenosis (HR 5.5. 95% CI 1.8-17.1; p = .003) as also compared with patients with CEA treated symptomatic moderate or severe stenosis (HR 7.8. 95% CI 1.62-37.8; p = .011). Conclusions: The present study on patients with symptomatic mild carotid artery stenosis, as determined by Doppler ultrasound, shows that there is still a substantial risk of recurrent stroke in this group. (C) 2016 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.
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| 7. |
- Bengtsson, Anders, 1964-, et al.
(författare)
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Acquisitions 2014 : exposé
- 2015
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Ingår i: Art Bulletin of Nationalmuseum Stockholm. - Stockholm : Nationalmuseum. - 2001-9238. ; 21:2014, s. 65-122
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 8. |
- Bergh, Niklas, 1979, et al.
(författare)
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A new biomechanical perfusion system for ex vivo study of small biological intact vessels
- 2005
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Ingår i: Ann Biomed Eng. - : Springer Science and Business Media LLC. - 0090-6964. ; 33:12, s. 1808-18
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Tidskriftsartikel (refereegranskat)abstract
- The vascular endothelium transduces physical stimuli within the circulation into physiological responses, which influence vascular remodelling and tissue homeostasis. Therefore, a new computerized biomechanical ex vivo perfusion system was developed, in which small intact vessels can be perfused under well-defined biomechanical forces. The system enables monitoring and regulation of vessel lumen diameter, shear stress, mean pressure, variable pulsatile pressure and flow profile, and diastolic reversal flow. Vessel lumen measuring technique is based on detection of the amount of flourescein over a vessel segment. A combination of flow resistances, on/off switches, and capacitances creates a wide range of pulsatile pressures and flow profiles. Accuracy of the diameter measurement was evaluated. The diameters of umbilical arteries were measured and compared with direct ultrasonographic measurement of the vessel diameter. As part of the validation the pulsatile pressure waveform was altered, e.g., in terms of pulse pressure, frequency, diastolic shape, and diastolic reversal flow. In a series of simulation experiments, the hemodynamic homeostasis functions of the system were successfully challenged by generating a wide range of vascular diameters in artificial and intact human vessels. We conclude that the system presented may serve as a methodological and technical platform when performing advanced hemodynamic stimulation protocols.
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| 9. |
- Bergh, Niklas, 1979, et al.
(författare)
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Effects of two complex hemodynamic stimulation profiles on hemostatic genes in a vessel-like environment
- 2008
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Ingår i: Endothelium. - : Informa UK Limited. - 1029-2373 .- 1062-3329. ; 15:5-6, s. 231-8
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Tidskriftsartikel (refereegranskat)abstract
- Endothelial cells are the main sensors of changes in the biomechanical flow environment and play a pivotal role in vascular homeostasis. An in vitro perfusion model was developed to study the regulatory effect on gene expression by different flow and pressure profiles. Human umbilical vein endothelial cells were grown to confluence inside capillary microslides or silicone tubes. Thereafter, they were exposed to different levels of shear stress or different levels of static or pulsatile pressure. Genes representing various hemostasis functions of the endothelial cells were analyzed. Shear stress was a more effortful stimulus than static or pulsatile tensile stress. Although shear stress affected mRNA expression of all six studied genes (tissue-type plasminogen activator [t-PA], plasminogen activator inhibitor [PAI]-1, Thrombomodulin [TM], urokinase-type plasminogen activator [u-PA], vascular cell adhesion molecule [VCAM-1], and endothelial nitric oxide synthase [eNOS]), none of the genes was found regulated by pressure. Shear stress down-regulated t-PA and VCAM-1 in a dose response-dependent way, and up-regulated TM. u-PA, eNOS, and PAI-1 were up-regulated by shear stress, but there was no obvious dose-response effect for these genes. These findings suggest that shear stress has a more powerful gene regulatory effect on endothelial gene expression than tensile stress. Low shear stress induced a more proatherogenic endothelial surface but preserved t-PA gene expression levels compared to high shear stress.
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| 10. |
- Brogren, Helén, 1977, et al.
(författare)
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Heterogeneous glycosylation patterns of human PAI-1 may reveal its cellular origin.
- 2008
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Ingår i: Thrombosis research. - : Elsevier BV. - 0049-3848. ; 122:2, s. 271-81
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Tidskriftsartikel (refereegranskat)abstract
- The main inhibitor of intravascular fibrinolysis is plasminogen activator inhibitor 1 (PAI-1) which binds to and irreversibly inhibits tissue plasminogen activator (tPA). PAI-1 is present in blood, both in platelets and in plasma, and PAI-1 levels are associated with risk of atherothrombosis. Several tissues express PAI-1 but the source of plasma PAI-1 is not known. We recently found that platelets can de novo synthesize PAI-1 and the amount synthesized in vitro in 24 hours is 35-fold higher than required to maintain normal plasma levels. Recombinant human PAI-1 expressed in different cell types or secreted naturally by human cell lines, exhibit heterogeneous glycosylation patterns. The aim of this study was to investigate the hypothesis that platelets might be the source of plasma PAI-1 and that the cellular source of PAI-1 can be determined by its tissue-specific glycosylation pattern. PAI-1 was isolated from platelets, macrophages, endothelial cells, adipose tissue, as well as plasma from lean and obese subjects. The glycosylation was analyzed by nanoLC-MS/MS. PAI-1 isolated from cell lysates and conditioned media from macrophages, endothelial cells, and adipose tissue expressed heterogeneous glycosylation patterns. By contrast, no glycans were detected on PAI-1 isolated from plasma or platelets from healthy lean individuals. Hence, our data suggest that platelets may be the main source of plasma PAI-1 in lean individuals. Interestingly, plasma PAI-1 from obese subjects had a glycan composition similar to that of adipose tissue suggesting that obese subjects with elevated PAI-1 levels may have a major contribution from other tissues.
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