Dextran-sulfate-adsorption of atherosclerotic lipoproteins from whole blood or separated plasma for lipid-apheresis—Comparison of performance characteristics with DALI and lipidfiltration

2007 ◽  
Vol 22 (4) ◽  
pp. 215-223 ◽  
Author(s):  
Ulrich Julius ◽  
Klaus G. Parhofer ◽  
Andreas Heibges ◽  
Stefan Kurz ◽  
Reinhard Klingel ◽  
...  
2013 ◽  
Vol 14 (1) ◽  
pp. 157-160 ◽  
Author(s):  
S. Kopprasch ◽  
S.R. Bornstein ◽  
P.E.H. Schwarz ◽  
S. Bergmann ◽  
U. Julius ◽  
...  

1992 ◽  
Vol 67 (02) ◽  
pp. 219-225 ◽  
Author(s):  
Walter A Wuillemin ◽  
Miha Furlan ◽  
Hans Stricker ◽  
Bernhard Lämmle

SummaryThe plasma of a healthy woman was found to contain half normal factor XII (FXII) antigen level (0.46 U/ml) without any FXII clotting activity (<0.01 U/ml). The variant FXII in this plasma, denoted as FXII Locarno, was partially characterized by immunological and functional studies on the proposita’s plasma. FXII Locarno is a single chain molecule with the same size (M r = 80 kDa) as normal FXII. Isoelectric focusing suggested an excess of negative charge in the variant FXII as compared to normal FXII. In contrast to FXII in normal plasma, FXII Locarno was not proteolytically cleaved upon prolonged incubation of proposita’s plasma with dextran sulfate. Adsorption to kaolin was similar for both, abnormal and normal FXII. Incubation of the proposita’s plasma with dextran sulfate and exogenous plasma kallikrein showed normal cleavage of FXII Locarno outside of the tentative disulfide loop Cys340-Cys467, but only partial cleavage within this disulfide loop. Furthermore, plasma kallikrein-cleaved abnormal FXII showed neither amidolytic activity nor proteolytic activity against factor XI and plasma prekallikrein.These results suggest a structural alteration of FXII Locarno, affecting the plasma kallikrein cleavage site Arg353-Val354 and thus formation of activated FXII (a-FXIIa).


2021 ◽  
Author(s):  
Yuya Tabuchi ◽  
Masao Katsushima ◽  
Yuri Nishida ◽  
Mirei Shirakashi ◽  
Hideaki Tsuji ◽  
...  

Abstract Background: Spondyloarthritis (SpA) is an autoimmune and autoinflammatory musculoskeletal disease characterised by systemic enthesitis. Recent research has focused on subclinical inflammatory bowel disease (IBD) in SpA pathogenesis. SKG mice, harbouring the Zap70 W163C mutation, increase autoreactive Th17 cells intrinsically, and show SpA features, including enteritis, after peritoneal injection of β-1,3- glucan under SPF conditions. In a conventional environment, they exhibit spontaneous arthritis with fungal factors. This study aimed to clarify whether oral dextran sulfate sodium (DSS) administration, utilised in IBD model mice, can provoke SpA features in SKG mice under SPF conditions, focusing on the relationship between gut microorganisms and SpA pathogenesis.Methods: SKG and BALB/c mice were administered oral DSS, and their body weights, arthritis, and enthesitis scores were recorded. In another cohorts, antibiotics (meropenem and vancomycin) or an anti-fungal agent (amphotericin B) were administered orally before DSS administration. The splenic Th1 and Th17 cell populations were examined before and after DSS administration using flow cytometry. Furthermore, the amount of circulating bacterial DNA in whole blood was measured by absolute quantitative polymerase chain reaction (qPCR), and the number and characteristics of bacterial species corresponding to these circulating DNA were analised by next-generation sequencing (NGS).Results: Ankle enthesitis as a peripheral SpA feature was elicited in half of DSS-administered SKG mice, and none of the BALB/c mice. Pre-administration of antibiotics suppressed enthesitis, whilst an anti-fungal agent could not. Th1 and Th17 cell levels in the spleen increased after DSS administration, and this was suppressed by pre-administration of antibiotics. SKG mice have a larger amount of bacterial DNA in whole blood than BALB/c mice before and one day after the initiation of DSS administration. The number of bacterial species in whole blood increased after DSS administration in SKG and BALB/c mice. Some genera and species significantly specific to the DSS-treated SKG mice group were also detected. Conclusion: Oral DSS administration alone elicited peripheral enthesitis in SKG mice with bacterial translocation accompanied by increased splenic Th1 and Th17 cell levels. Pre-administration of antibiotics ameliorated these DSS-induced SpA features. These findings suggest that intestinal bacterial leakage plays a pivotal role in SpA pathogenesis.


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