This review analyzes the research results of additional effects and mechanisms of action of sugar-reducing drugs. Hence it has been suggested that asymmetric dimethylarginine may be a target molecule for metformin, vildagliptin, and combinations thereof. (For citation: Urakov AL, Gurevich KG, Sorokina IA, et al. Metformin and vildagliptin combination: a new approach of endothelial nitric oxide synthase activity regulation and metabolism in diabetes mellitus type 2. Reviews on Clinical Pharmacology and Drug Therapy. 2018;16(2):5-12. doi: 10.17816/RCF1625-12).
Aim. Search for predictors of pulmonary artery thromboembolism in patients with deep vein thrombosis among the indicators of hemostasis system. Methods. Retrospective analysis of indicators of hemostasis system was performed in 23 patients with defined pulmonary artery thromboembolism, 30 patients with deep vein thrombosis and 20 healthy volunteers. Values of platelet aggregation by Born method, concentration of circulating thrombocytic aggregates by Kohanna method, values of thromboelastometry, as well as blood levels of D-dimers and antitrombin III in arterial and venous blood were measured. Results. It was established that in patients from both thrombosis groups, haemostasis system changes are similar in nature: (1) a high value of Wu-Hoak is registered - more than 15 times higher in both arterial and venous blood compared to the control group; (2) platelet aggregation rates demonstrate hyperaggregation with all inductors, both in arterial and venous blood; (3) thromboelastography results are characterized by increased activity of thrombocytic hemostasis, prolonged clotting time, heightened clot strength compared to control in both arterial and venous blood flow. However, the difference was revealed between groups with and without pulmonary thromboembolism in venous blood levels of D-dimers and activity of antithrombin III. A function to predict pulmonary thromboembolism was constructed depending on the level of D-dimers and activity of antithrombin III in patients with deep vein thrombosis. Conclusion. The developed function for prediction of pulmonary artery thromboembolism can objectively assess the likelihood of pulmonary thromboembolism, which in turn allows minimizing risk and timely assessing the effectiveness of taken preventive measures.
Advances in modern medicine and biotechnology allow specialists to adjust the patients proteome and metabolome. Gene engineering allows us to create drugs that affect the cause of the disease at the level of gene expression. Thus, not the links of pathogenesis or the symptom of the disease are subjected to correction, but the trigger itself, a defective gene that provokes a cascade of pathological processes. According to the definition of the State Pharmacopoeia, gene therapeutic drugs are drugs whose pharmaceutical substance is a recombinant nucleic acid or includes a recombinant nucleic acid that allows for the regulation, repair, replacement, addition or removal of a genetic sequence. The article reflects all available, developed and used in real clinical practice gene therapy drugs of russian and foreign production. The mechanisms of action, features of the use of these drugs in pediatric and geriatric practice, as well as existing problems and limitations of their use, including deontological issues, are noted.
The review is devoted to revealing the connection between the intestinal microflora, diet and the effectiveness of glucose – lowering therapy in patients with type 2 diabetes. Potential targets and the effects of oral and injectable hypoglycemic agents on microbiota in this category of patients are considered. The work reflects modern views on hypoglycemic drugs from the standpoint of the science of metabolomics within the framework of personalized medicine.
Timely and effective reperfusion in ischemia and reoxygenation in hypoxia of the heart muscle prevent myocardial infarction. Delayed reperfusion and reoxygenation in myocardial ischemia and hypoxia can cause reversible damage in it, which, with a favorable outcome, disappear without a trace. Excessively late reperfusion and reoxygenation inevitably ends with irreversible damage to the myocardium, which is widely known as a myocardial infarction, and which, together with other complications of cardiac ischemia, can cause disability and death of the patient. In recent years, reperfusion injury of the ischemic heart muscle has been recognized as an independent link in the pathogenesis of myocardial infarction. The mechanisms of this link of pathogenesis have been partially studied in experimental conditions. The phenomena of preconditioning and post-conditioning have been discovered, the effects of which are currently determined fairly reliably. After determining the mechanisms of reperfusion injury of the ischemic myocardium, the search and development of pharmacological agents capable of inducing such a phenomenon as cardioprotection began. In parallel, studies of specific microRNAs that claim to be diagnostic markers are being conducted, as well as the search for drugs that affect the level of their expression is being conducted. The information about the achieved successes in this direction is given.
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