| 1. |
- Gårdhagen, Roland, et al.
(författare)
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Large Eddy Simulation of Stenotic Flow for Wall Shear Stress Estimation - Validation and Application
- 2011
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Ingår i: WSEAS Transactions on Biology and Biomedicine. - 1109-9518. ; 8:3, s. 86-101
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Tidskriftsartikel (refereegranskat)abstract
- Turbulent flow in the cardiovascular system may increase the risk for severe arterial disease. This workaddresses the feasibility of Large Eddy Simulation (LES) using a general purpose code as a tool for assessmentof cardiovascular flow and investigates Wall Shear Stress (WSS) in steady as well as pulsating turbulent pipeflow. Poiseuille flow was specified at the inlet, and with a suitable ammount of perturbations at the inlet it waspossible to predict experimental data. The extent of the recirculation zone was affected by the inlet disturbances,and magnitude as well as direction of the WSS vector varied significantly at the reattachment point. For thepulsating flow, WSS shows a complex pattern with different spatial and temporal variation along the pipe. Thewall shear stress gradient was calculated on the entire post-stenotic surface and each component in the gradientwas investigated. The off-diagonal components in the gradient are usually assumed to be small, but here they werefound to be on the same order of magnitude as the diagonal terms. This work demonstrates the need for a scaleresolving simulation technique to accurately model cardiovascular flows.
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| 2. |
- Ohlsson, Susanne, et al.
(författare)
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Serum from patients with systemic vasculitis induces alternatively activated macrophage M2c polarization.
- 2014
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Ingår i: Clinical Immunology. - : Elsevier BV. - 1521-6616. ; 152:1-2, s. 10-19
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Tidskriftsartikel (refereegranskat)abstract
- Anti-neutrophil cytoplasmic antibody associated vasculitides (AAV) are conditions defined by an autoimmune small vessel inflammation. Dying neutrophils are found around the inflamed vessels and the balance between infiltrating neutrophils and macrophages is important to prevent autoimmunity. Here we investigate how sera from AAV patients may regulate macrophage polarization and function. Macrophages from healthy individuals were differentiated into M0, M1, M2a, M2b or M2c macrophages using a standardized protocol, and phenotyped according to their expression surface markers and cytokine production. These phenotypes were compared with those of macrophages stimulated with serum from AAV patients or healthy controls. While the healthy control sera induced a M0 macrophage, AAV serum promoted polarization towards the M2c subtype. No sera induced M1, M2a or M2b macrophages. The M2c subtype showed increased phagocytosis capacity compared with the other subtypes. The M2c polarization found in AAV is consistent with previous reports of increased levels of M2c-associated cytokines.
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| 3. |
- Schmitt, Roland, et al.
(författare)
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Tissue deposits of IgA-binding streptococcal M proteins in IgA nephropathy and Henoch-Schonlein purpura.
- 2010
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Ingår i: American Journal of Pathology. - : Elsevier BV. - 1525-2191 .- 0002-9440. ; 176:2, s. 608-618
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Tidskriftsartikel (refereegranskat)abstract
- IgA nephropathy (IgAN) and Henoch-Schönlein purpura (HSP) are diseases characterized by IgA deposits in the kidney and/or skin. Both may arise after upper respiratory tract infections, but the pathogenic mechanisms governing these diseases remain unclear. Patients with IgAN (n = 16) and HSP (n = 17) were included in this study aimed at examining whether IgA-binding M proteins of group A streptococci could be involved. As M proteins vary in sequence, the study focused on the IgA-binding-region (IgA-BR) of three different M proteins: M4, M22, and M60. Renal tissue from IgAN and HSP patients and skin from HSP patients were examined for deposits of streptococcal IgA-BR by immunohistochemistry and electron microscopy using specific antibodies, and a skin sample from a HSP patient was examined by mass spectrometry. IgA-BR deposits were detected in 10/16 IgAN kidneys and 7/13 HSP kidneys. Electron microscopy demonstrated deposits of IgA-BRs in the mesangial matrix and glomerular basement membrane, which colocalized with IgA. Skin samples exhibited IgA-BR deposits in 4/5 biopsies, a result confirmed by mass spectrometry in one patient. IgA-BR deposits were not detected in normal kidney and skin samples. Taken together, these results demonstrate IgA-BR from streptococcal M proteins in patient tissues. IgA-BR, would on gaining access to the circulation, encounter circulatory IgA and form a complex with IgA-Fc that could deposit in tissues and contribute to the pathogenesis of IgAN and HSP.
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