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Background: Inflammation plays a critical role in all stages of atherogenesis, including plaque destabilization leading to the rupture and local thrombosis, clinically manifested as unstable angina (UA) or myocardial infarction (MI). Recent data report enhanced expression of numerous pro-inflammatory genes in patients with acute coronary syndrome (ACS) both in plaque and in inflammatory cells. Kinins are peptides involved in vasodilation, vascular permeability, pain and inflammation. Their effects are mediated by two receptors, B1 and B2. As the role of kinins in ACS is not clear, the aim of the study was to assess the expression of the genes encoding kinin receptors in patients with ACS. Methods: The study was carried out on 40 patients with ACS and 10 age-matched healthy subjects (control (C)). To evaluate gene expression of B1 and B2 kinin receptors, total mRNA was extracted from peripheral blood mononuclear cells and the number of mRNA copies was assessed by quantitative reverse transcriptase–polymerase chain reaction. Results: In patients with MI and UA, the B1 receptor (B1R)/B2 receptor (B2R) ratio was inversed compared with healthy subjects (C group) (MI vs C: 1.54 ± 0.39 vs 0.36 ± 0.04; P < 0.01; UA vs C: 2.13 ± 0.98 vs 0.36 ± 0.04; P < 0.05 respectively). B2R gene mRNA level was markedly lower in MI group versus C group (24 216 ± 5409 copies/μg vs 39 908 ± 5309 copies/μg; P < 0.05). The difference in B1R gene expression between MI and C group was negligible. We have not observed differences in studied genes expression between UA and C groups. Conclusion: Patients with ACS show inverted B1R/B2R ratio. Such disturbance in kinin signalling may reflect increased activation of circulating mononuclears, which are important participants of atherosclerotic plaque development and eventually rupture. [ABSTRACT FROM AUTHOR]

Abstract: Matrix metalloproteinases (MMPs) are an expanding group of proteolytic enzymes that participate in numerous physiological and pathological processes including embryogenesis, connective tissue turn-over, healing, angiogenesis, etc. Disturbances in matrixin activity are observed in carcinogenesis, some degenerative processes, and in inflammation, including atherogenesis. The role of matrixins in the pathology of the cardiovascular system seems to be particularly important in two processes: (1) atherosclerotic plaque development and rupture (leading to an acute coronary event) and (2) post-infarction remodeling of myocardium, leading to heart failure. The purpose of this paper is to gather and summarize information about the role of MMPs in acute coronary syndromes (ACS), in both the processes leading to coronary artery occlusion and the “myocardial consequence” of this event. In addition, some benefits and disadvantages of pharmacological intervention into this enzymatic network will be addressed. [Copyright &y& Elsevier]

Abstract Background  Cardiac syndrome X is typically characterized by effort induced anginal pain with ST segment depression suggestive of myocardial ischemia and normal coronary arteries at angiography. The possible mechanism that may participate in the pathology of CSX is a microvascular dysfunction related to inflammatory process affecting endothelium. Interferon γ (IFN-γ) is an important cytokine in inflammatory reaction. It acts through its specific receptor composed of 2 subunits IFN-γ R1 (ligand binding) and R2 (signal transduction). The expression and proportion of these subunits influences IFN-γ activity. The aim of the study was to assess the gene expression of IFN-γ and its receptors in peripheral blood mononuclear cells (PBMC) from patients with syndrome X. Methods  The study was carried out in 36 patients aged 44–77 (average 57 years old) with cardiac syndrome X and 23 sex- and age-matched healthy subjects (control group). To evaluate gene expression of IFNγ and its receptor total mRNA was extracted from peripheral blood mononuclear cells (PBMC) and the number of mRNA copies were assessed by quantitive reverse transcriptase polymerase chain reaction (QRT-PCR). Results  We have not observed statistically significant differences in INFγ gene expression between studied group and control. Genes encoding IFNγ receptor subunits showed higher expression in PBMCs from patients with cardiac syndrome X vs control subjects (IFNγR1, 97,244  26,956 c/μg vs 12,120  2,940 c/μg, p p  Conclusion  Variation in transcriptional activity of genes encoding INF-γ receptor subunits may affect function of microvasculature and thereby participate in the pathology of cardiac syndrome X. [ABSTRACT FROM AUTHOR]

The prevalence of coronary artery disease (CAD) and acute coronary syndromes in patients with haemophilia is much lower than in general population and there is a lack of information regarding safe interventional or surgical treatment of CAD in haemophiliacs. This report presents a case of patient with moderate haemophilia A and unstable angina pectoris, who underwent successful coronary angioplasty. The patient was pretreated with factor VIII (before and after the procedure) and the incision site was sealed with vessel closure device. Additionally, the article discusses the issue of the safety of standard, postpercutaneous coronary intervention antiplatelet therapy in patients with haemophilia. [ABSTRACT FROM AUTHOR]

Abstract: Acute coronary syndromes (ACS) are one of the major causes of mortality nowadays. Although much is known about factors involved in atherogenesis and acute coronary events, there are still many cases in which a lack of classical risk factors, together with family history, suggests the presence of an unrevealed genetic predisposition and molecular mechanisms. This paper reviews genetic predisposition to ACS. It also indicates which genes are linked to the processes of destabilization and rupture of atherosclerotic plaque and thus may be potential targets for more effective prophylaxis and treatment. [Copyright &y& Elsevier]

Wstęp: Transformujący czynnik wzrostu beta (TGF-β, transforming growth factor beta) jest jedną z kluczowych cytokin biorących udział w procesie wtóknienia, w tym przebudowy miokardium po zawale serca. Celem pracy była ocena metodą mikromacierzy oligonukleotydowych profilu ekspresji genów rodziny TGF-β w miokardium chorych: po przebytym zawale, z zaawansowaną chorobą wieńcową oraz u osoby bez choroby niedokrwiennej serca. Materiał i metody: Spośród 22 283 transkryptów analizowanych za pomocą mikromacierzy HG-U133A Affymetrix badano geny związane z TGF-β i jego ścieżkami sygnałowymi. Wyłoniono następujące geny różnicujące: ENG, TGFBRII oraz NPR1 (ANP-GC-A). Wyniki: Zwiększoną ekspresję genów różnicujących stwierdzono w miokardium pozawaiowym w porównaniu z pozostałymi próbkami, potwierdzając w ten sposób rolę mechanizmów TGF-β -- zależnych w remodelingu pozawałowym. Wnioski: Uzyskane półilościową techniką mikromacierzy oligonukłeotydowych wstępne wyniki wyma-gają potwierdzenia metodą ilościowej reakcji łańcuchowej polimerazy w czasie rzeczywistym (QRT-PCR, quantitative real time polymerase chain reaction) po zebraniu odpowiednio dużej grupy chorych. [ABSTRACT FROM AUTHOR]

A continually expanding arsenal of anthropogenic and natural toxicants regulated in raw materials, food products, animal feed, in various veterinary surveillance facilities and food production facilities requires the development and implementation of accelerated methods and test systems that simultaneously determine several safety indicators. The risks associated with the safety of raw materials and food products can be attributed to contamination by anthropogenic or natural toxicants. The first include toxic elements, dioxins, synthetic plant growth regulators, substances used in animal husbandry: medicines (antibacterial, antiparasitic and hormonal drugs), phosphorus-and-chloroorganic pesticides, etc. To the second - toxins and metabolites of bacteria, fungi, plants. In order to prevent these risks, the control of these pollutants is carried out. Solving this problem will help the introduction of promising and highly effective methods. The aim of the work was to carry out an experimental and theoretical evaluation of some methods for accelerated control of anthropogenic and natural toxicants. As a result of the conducted studies, the analysis of international and Russian legal and regulatory documents on the criteria for the safety of raw materials and food products is given. The prospects of methods and test systems based on immunomicrochip technology, immunochromatographic indicator elements and PCR in "real time" mode with the use of robotics for accelerated control of anthropogenic and natural toxicants have been experimentally proved. As a result of the studies, the possibility of determining organophosphorus pesticides and pesticides from the class of imidazoles in plant foods and water has been demonstrated, based on the inhibition of acetylcholine-esterase activity with a colorimetric determination of the final result on a vertical photometer as well as immunomicrochip technology. It has been shown that immunochromatographic indicator elements with colloidal gold nanoparticles (IIEC) are promising for screening control of natural toxicants: microorganisms, toxins of bacteria and fungi. The high sensitivity of the PCR method in real time mode has been proven, and automation makes it promising for controlling bacteria in raw materials or products, especially for hard-to-grow or dangerous microorganisms (salmonella, campylobacteria, causative agents of anthrax, brucellosis, etc.) [ABSTRACT FROM AUTHOR]

Introduction. Cardiac syndrome X (CSX) is defined by typical chest pain, ST segment depression on ECG and normal coronary angiography. Pathology of CSX may involve microvascular dysfunction related to inflammation and abnormal pain sensitivity. Kinins are labile peptides participating in vasodilation, inflammation and pain. Their effects are mediated by two receptors: B1 and B2. The aim of the study was to assess gene expression of kinin receptors in peripheral blood mononuclear cells (PBMC) from patients with CSX. Methods. The study was carried out in 34 patients with cardiac syndrome X, 13 with unstable angina and ten healthy subjects. Total mRNA was extracted from PBMC and the number of mRNA copies was assessed by quantitive reverse transcriptase polymerase chain reaction. Results and Conclusion. The study showed 7-fold higher transcriptional activity of B1R in CSX vs. control and 3.5 higher vs. UA. B2R expression was 2.5-fold higher in CSX group vs. control and UA, while in the letter two groups it was similar. Such disturbance in kinin signaling may participate in local vasoconstriction and may reflect disturbances in kinin signaling leading to nociceptive disturbances in these patients. [ABSTRACT FROM AUTHOR]

Abstract: Background: Recent data report altered gene expression of numerous pro- and anti-inflammatory factors involved in pathology of acute coronary syndromes (ACS). Transforming growth factor β (TGFβ) signaling is engaged in a wide range of processes. Its effect on vessels seems to be protective due to its anti-inflammatory and anti-atherogenic action. However, it also seems to be engaged in such negative effects as neointima formation and fibrosis. The aim of the study was to assess the expression of the genes encoding TGFβ and its receptors (type I, II, and III) in patients with ACS. Methods: The study was carried out on 24 patients with acute coronary syndrome (7 with unstable angina [UA] and 17 with myocardial infarction [MI]) and 10 age-matched healthy subjects (control). To evaluate gene expression of TGFβ and its receptors total mRNA was extracted from peripheral blood mononuclear cells (PBMC) and the number of mRNA copies were assessed by quantitative reverse transcriptase polymerase chain reaction (QRT-PCR). Results: MI and UA patients demonstrated significantly lower TGFβ gene expression compared to control (2789±418 c/μg vs. 20262±2548 c/μg; p <0.001, and 3390±518 c/μg vs. 20262±2548 c/μg; p <0.001, respectively), as well as noticeably lower transcriptional activity of genes encoding its type I (3295±447 c/μg vs. 12859±1929 c/μg; p <0.001, and 3258±721 c/μg vs. 12859±1929 c/μg; p <0.01, respectively) and type II receptors (2364±346 c/μg vs. 19003±2357 c/μg; p <0.001, and 2680±522 c/μg vs. 19003±2357 c/μg; p <0.01, respectively). Also, gene expression of the type III receptor was inferior in the studied group compared to the control, although the difference was significant only for the UA group vs. control. Expressions of the studied genes did not differ between patients with MI and those with UA. Conclusion: Our report shows that the decreased activity of TGFβ in patients with ACS is at least partly due altered transcriptional activity of genes encoding both TGFβ and its receptors, what may be responsible for the evolution of atherosclerotic lesions. [Copyright &y& Elsevier]