This study evaluated whether statin therapy changed a diagnostic validity of lipid and inflammatory markers in ischemic heart disease (IHD) patients. Levels of lipids, lipoproteins, apolipoproteins, inflammatory markers, and atherogenic indexes were determined in 49 apparently healthy men and women, 82 patients having stable angina pectoris (SAP), 80 patients with unstable angina (USAP), and 106 patients with acute ST-elevation myocardial infarction (STEMI) treated or not treated with statins. Diagnostic accuracy of markers was determined by ROC curve analysis. Significantly lower apoA-I in all statin-treated groups and significantly higher apoB in statin-treated STEMI group compared to non-statin-treated groups were observed. CRP showed the best ROC characteristics in the assessment of STEMI patients. Lp(a) is better in the evaluation of SAP and USAP patients, considering that Lp(a) showed the highest area under the curve (AUC). Regarding atherogenic indexes, the highest AUC in SAP group was obtained for TG/apoB and in USAP and STEMI patients for TG/HDL-c. Statins lowered total cholesterol, LDL-c, and TG but fail to normalize apoA-I in patients with IHD.
The role of nitrosative stress in the early pathogenesis of neuroinflammation and demyelination is undoubtedly wide. This review summarizes and integrates the results, found in previously performed studies, which have evaluated nitrosative stress participation in neuroinflammation. The largest number of studies indicates that the supply of nitrosative stress inhibitors has led to the opposite clinical effects in experimental studies. Some results claim that attributing the protective role to nitric oxide, outside the total changes of redox oxidative processes and without following the clinical and paraclinical correlates of neuroinflammation, is an overrated role of this mediator. The fact is that the use of nitrosative stress inhibitors would be justified in the earlier phases of neuroinflammation. The ideal choice would be a specific inducible nitric oxide synthase (iNOS) inhibitor, because its use would preserve the physiological features of nitric oxide produced by the effects of constitutive NOS. This review discusses the antinitrosative therapy as a potential mode of therapy that aims to control neuroinflammation in early phases, delaying its later phases, which are accompanied with irreversible neurological disabilities. Some parameters of nitrosative stress might serve as surrogate biomarkers for neuroinflammation intensity and its radiological and clinical correlates.
Abstract Background: Glucocorticoids (GCs) exert a wide range of anti-inflammatory, immunosuppressive, and antineoplastic activities. The aim of our investigation was to elucidate the effect of dexamethasone, a synthetic GC, on polyamine metabolism in the rat thymus. Methods: Male albino Wistar rats, weighing 180–230 g, were divided into two groups: control and experimental. The experimental group received dexamethasone intraperitoneally for 3 days, in a daily dose of 4 mg/animal. The last dose of the hormone was applied on the 3rd day, 1 h before killing. The control group received 0.9% NaCl instead of the hormone. The animals were killed by decapitation. The thymus was removed quickly and rinsed with ice-cold saline. Polyamines were extracted using butanol. The amount of polyamines was investigated by electrophoresis. For the estimation of polyamine oxidase (PAO) activity, 10% water homogenate was prepared. Results: Our results suggested that dexamethasone supplementation of experimental animals for 3 days significantly decreased the spermine (Sp) and spermidine (Spd) levels in rat thymus tissue (Sp Control, 362.56±25.33 nmol/g wet weight; Sp Exp. Group, 313.01±21.16 nmol/g wet weight; Spd Control, 673.81±30.95 nmol/g wet weight; Spd Exp. Group, 410.21±17.26 nmol/g wet weight). PAO activity significantly decreased under hormone influence in comparison with the control group (PAO Control, 0.449±0.121 U/mg prot.; PAO Exp. Group, 0.312±0.096 U/mg prot.). Conclusions: The decrease in polyamine amounts in the rat thymus is not due to the change in PAO activity.
Article Thymus as a target tissue of glucocorticoid action: What are the consequences of glucocorticoids thymectomy? was published on June 1, 2009 in the journal Journal of Basic and Clinical Physiology and Pharmacology (volume 20, issue 2).
Summary Cardiac troponins have a crucial role in diagnosing acute myocardial infarction, but have been considered by some authors to have a high false positive rate. Such opinions may decrease the confidence in troponin with important clinical consequences. The aim of the paper is to analyze three different meanings of the phrase »false positive troponin«: A) analytic (technical) false positive, with no real myocardial damage; B) false positive considering AMI: cardiac injury is present, but there is no AMI; C) false positive considering CAD: there is myocardial damage, but no CAD. The most frequent and the most important source of misunderstanding is the confusion between aspects A) and B). Namely, there has been a relatively small percentage of false positive troponin elevations due to analytic reasons. On the contrary, there has been a re - latively large percentage of »false positive« results in patients with myocardial necrosis due to causes other than AMI; for them - instead of »FP troponin elevation« - another phrase ought to be used, e.g., »non-AMI troponin elevation « until the etiopathogenesis in an individual patient is recognized. The phrase »false positive troponin« should be restricted to the artificial increase in troponin due to preanalytic and analytic reasons. By doing so, we may decrease the degree of confusion about troponin and increase the confidence in this highly specific marker of myocardial injury. The possibility of an analytic false positive result should always be kept in mind when one interprets elevated troponin.