scholarly journals Mineral metabolism in various pathogenetic types of inflammation

Author(s):  
A. Tourna ◽  
R. T. Toguzov ◽  
N. A. Kolyshkina ◽  
S. N. Poyarkova

Background. A large amount of experimental and clinical data on the content and the role of chemical elements in the human body is accumulated by nowadays. However, the state of mineral metabolism, mechanisms of action and the role of chemical elements in the etiology and pathogenesis of infl ammatory, autoimmune and other diseases are to be studied. Objective. To examine the state of mineral metabolism (calcium - Ca, magnesium - Mg, iron - Fe, cobalt - Co, copper - Cu, zinc - Zn) in various pathogenetic variants of infl ammatory processes in the blood serum of patients with acute coronary syndrome, community-acquired pneumonia and rheumatoid arthritis.

2019 ◽  
Vol 10 (2) ◽  
pp. 97-100
Author(s):  
Ashok Thaned ◽  
◽  
Triveni Ayyanna ◽  
Sunil K ◽  
◽  
...  

2019 ◽  
Vol 247 ◽  
pp. 73-80 ◽  
Author(s):  
Adrienne O'Neil ◽  
C. Barr Taylor ◽  
David L. Hare ◽  
Emma Thomas ◽  
Samia R. Toukhsati ◽  
...  

2016 ◽  
Vol 218 ◽  
pp. 150-157 ◽  
Author(s):  
Markku S. Nieminen ◽  
Michael Buerke ◽  
Alain Cohen-Solál ◽  
Susana Costa ◽  
István Édes ◽  
...  

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Keiko Gomita ◽  
Kayoko Sato ◽  
Kazutaka Kitamura ◽  
Nobuhisa Hagiwara

Background: Recently, several evidences on the crucial role of adhesion molecules in the development of atherosclerosis and plaque instability have been reported. While expression of VCAM-1, ICAM-1 and L-selectin has been consistently observed in atherosclerotic plaques it is still uncertain how adhesion molecules on T cells contribute to the incidence of acute coronary syndrome (ACS). In this study, we examined whether adhesion molecules on T cells in ACS have a significant role in the plaque stability and prone to cause ACS. Methods and Results: Fresh CD4 T cells were isolated from the peripheral blood of 76 ACS patients (AMI=35, UAP=41) and 74 age-matched controls (NC). CD69, an activation marker of T cells, was strongly expressed on CD4 T cells from ACS than from NC by FACS (P<0.0001). CD4 T cells from ACS highly expressed p-selectin glycoprotein ligand-1 (PSGL-1) and integrin β (CD18), but not L-selectin by FACS (P < 0.03, P < 0.01, n.s., respectively). Soluble PSGL-1 (sPSGL-1) levels in plasma were lower in ACS patients than in NC (P=0.0001), which correlated negatively with the PSGL-1 expression on CD4 T cells (R=0.405, P<0.02). We further investigated the thrombus-aspirating device samples (n=14) and fresh CD4 T cells derived from both the coronary artery and peripheral blood from the each same patient with ACS. CD4 T cells from the coronary artery strongly expressed PSGL-1 (P<0.002), but not integrin β (CD18) and L-selectin by FACS. Finally, PSGL-1 was expressed on T cells, but not on CD68 positive macrophage, MPO positive neutrophil, or CD41 positive platelets in the thrombus-aspirating device samples. Conclusions: From these results, we demonstrated that PSGL-1-expressing CD4 T cells are enriched in the culprit coronary artery lesion of ACS, contributing to the acceleration of plaque instability and occurrence of ACS.


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