Cerebrospinal fluid and plasma concentration of soluble intercellular adhesion molecule1, vascular cell adhesion molecule1 and endothelial leukocyte adhesion molecule in patients with acute ischemic b

Background. Leukocyte migration into the ischemic area is a complex process controlled by adhesion molecules (AM) in leukocytes and endothelium, by migratory capacity of leukocytes and the presence of hemotaxic agents in the tissue. In this research it was supposed that in the blood and cerebrospinal fluid (CSF) of patients in the acute phase of ischemic brain disease (IBD) there were relevant changes in the concentration of soluble AM (sICAM-1 sVCAM-1 and sE-selectin), that could have been the indicators of the intensity of damaging processes in central nervous system (CNS). Methods. The study included 45 IBD patients, 15 with transient ischemic attack (TIA) 15 with reversible ischemic attack (RIA), and 15 with brain infarction (BI) of both sexes, mean age 66±7. Control group consisted of 15 patients with radicular lesions of discal origin, subjected to diagnostic radiculography without the signs of interruption in the passage of CSF. Changes of selected biochemical parameters were determined in all patients in frame 72 hours since the occurence of an ischemic episode. Concentrations of soluble AM were determined in plasma and CSF by ELISA. Total number of leukocytes (TNL) in peripheral blood was determined by hematological analyzer. Results. The results showed that during the first 72 hrs of IBD significant increases occured in TNL and that the increase was progressive compared to the severeness of the disease. Significant increase of soluble AM concentration was shown in plasma of IBD patients. The increase was highest in BI somewhat lower in RIA and the lowest in TIA patients compared to the control. In CSF concentrations of sICAM-1, sVCAM-1 and sE-selectin demonstrated similar increasing trend as in plasma. Conclusion. TNL, as well as the soluble AM concentrations in plasma and CSF, were increased during the acute IBD phase and progressive in relation to the severeness of the disease, so that they might have been the indicators of CNS inflammatory reaction intensity. Furthermore, the results indicated their role in IBD pathogenesis and offered the possibility of researching the application of antagonists and/or activity modulators of some of them in IBD therapy

Recent views on cytohistological characteristics and pathogenic mechanisms of atherosclerotic lesions types I, II and III

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Angiotensin II receptor type 2 (AT2R) -1332 A/G gene polymorphism as a risk factor for multiple sclerosis

Multiple sclerosis (MS) is a complex inflammatory,demyelinating disease of central nervous system (CNS). All the essen-tial components of the renin-angiotensin system (RAS) are presentedin the mammalian brain. The angiotensin II (Ang II), biologicallyactive octapeptide is not only a vasoconstrictor, but also a pro-inflam-matory factor. Many of the classical and of the hypothetical functionsof brain Ang II are mediated by stimulation of AT1 receptors (AT1R).Brain AT2 receptors (AT2R) are highly expressed during development.In the adults, AT2R are restricted to areas predominantly involved inthe process of sensory information. The AT2R1332 A/G polymorph-ism was proposed to influence AT2R protein expression, and is themost studied polymorphism in this gene, in other diseases. Recently,the striking appearance of the RAS in MS brain was described.However, the role of AT2R remains to be clarified. Thus, the aim ofour study was to establish if there is an association between AT2R1332 A/G gene polymorphism and predisposition of MS Methods:Subjected group consisted of 122 female and 70 malepatients with MS and 75 female and 50 male controls from populationof Serbia. Genotyping was done by PCR and restriction digestion withEcoRI enzyme.Results:The genotype and allele frequencies for AT2R1332A/Ggene polymorphism are analyzed separately in females and males,since this gene is located on X chromosome. We detected significantoverrepresentation of1332A/G AA genotype (OR 1.6, 95% CI:1.0–2.7, p<0.05) in female patients with MS compared to female controls.In hemizygous males we didn’t found any difference between patientsand controls.Conclusion:The role of RAS genes in MS was neglected untilrecently. Than, it was shown that the role of RAS in the CNS isbeyond the regulation of cardiovascular function. Until now AT2R(1332A/G) gene polymorphism was widely studied and associatedwith hypertension and other vascular disease. Until now, there wereno studies concerning role of Ang II receptor polymorphisms in MS.This study suggest possible role of AT2R in MS. Further studies areneeded to elucidate this result.ECTRIMS : The 26th Congress of the European Committee for Treatment and Research in Multiple Sclerosis : Book of abstract

Bol i ekscitatorne aminokiseline

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Bol i ekscitatorne aminokiseline

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