Pathology of the central nervous system in children of early age, due mainly hypoxic-ischemic brain damage in the antenatal period and delivery, which occupies a leading place among all factors of perinatal nervous system lesions in infants, is one of the most actual problems of modern medicine. Despite favourable demographic state, the improvement of the quality of perinatal care and medical care of newborns with a weight at birth from 500 grams, the tendency to reduction in the incidence of perinatal lesions of the central nervous system didn’t observed. On the contrary, there is progression of their course, which determines the subsequent mental and physical development of the child - from minimal brain dysfunction and gross motor and intellectual disorders, often resulting in disability. Purpose of the study is to evaluate the clinical features of central nervous system pathology in children of early age by means of neurobiochemistry markers and to develop prognostic criteria for the course and pathogenetic therapy regimens. Materials and methods. Comprehensive survey of 134 children (61 boys and 73 girls ) aged from 0 to 9 months was carried out with the assessment of neurological status and biochemical markers. Results of study. In formation of gravity of perinatal lesions all the studied markers participated, but to a greater extent – the parameters of neurotrophic lesions and endothelial dysfunction. The first component of the nervous tissue of the brain, responding to hypoxia, is microglial environment, which is caused by the growth of lesions S100- protein (i.e., the neuron at the stage of 0-1 months didn’t been metabolic changes – this is evidence of low levels of SOD and MDA).

Aim. To study the role of markers of endothelial dysfunction, oxidative and cellular stress in the prediction of myocardial infarction (MI) in comorbid patients with stable coronary heart disease (CHD). Material and methods. The study involved 336 patients with a diagnosis of CHD. The presence of CHD was confirmed by diagnostic coronary angiography with the calculation of the Gensini index. All patients were divided into 2 groups: group 1288 patients without a history of MI, group 248 patients with a history of MI. All patients were assessed for the levels of oxidized modified proteins, high-sensitivity C-reactive protein (hs-CRP), homocysteine, heat shock protein (HSP70), and superoxide dismutase activity. Results. All patients were comparable in age. For other clinical and anthropometric characteristics, we saw significant differences (according to the MannWhitney criterion): patients with previous MI had higher BMI, waist circumference, and blood pressure. The correlation analysis revealed positive significant average strength relationships between past MI and the Gensini index, low-density lipoprotein level, total cholesterol level, homocysteine level, hs-CRP level, and the level of oxidized modified proteins; and negative significant average strength relationships between past MI and SOD activity level (r=-0.374, p=6.4 E-07) and HSP70 level (r=-0.563, p=2.6 E-15). The ROC analysis revealed that not all markers were significant in predicting the risk of MI. It is shown that the most expected characteristics were shown by the hs-СRP. However, further analysis of the predictive significance of the markers demonstrated that the addition of HSP70 to hs-CRP increases the predictive significance of hs-CRP in relation to the risk of developing MI. Conclusion. We have demonstrated that a strategy using a cumulative risk assessment consisting of 2 biomarkers (individually involved in inflammation and stress-induced cellular responses) can identify patients with an established diagnosis of CHD who have an increased risk of acute MI.

The study established a pattern of changes in neurovascular biomarkers in children who underwent perinatal hypoxia in order to optimize the prognosis of neurological disorders in children in the long term. Materials and methods. 419 patients aged 1 to 6 months were examined, 2 age groups 1-3 and 4-6 months were identified, the physical and psychomotor development of each subject was analyzed, and groups of mild, medium and severe forms of lesion were identified; a quantitative assessment of the biochemical markers of the neurovascular component of the pathogenesis of CNS lesion was carried out with the identification of the boundaries of the formation of processes. Results. The direct dependence of changes in indicators of biochemical markers on the degree of CNS damage was established.

To simulate acute lung injury (ALI) in SD male rats they we administered intratracheally with lipopolysaccharide (LPS) followed by hyperventilation of the lungs (HVL), which lead to functional changes in the respiratory system and an increase in the blood serum concentration of inflammatory cytokines. LPS + HVL after 4 h lead to pronounced histological signs of lung damage. We have studied the effectiveness of Derinat® when administered intramuscularly at dose of 7.5 mg/kg for 8 days in the ALI model. Derinat® administration lead to an increase in the concentration of most of the studied cytokines in a day. In the ALI model the administration of Derinat® returned the concentration of cytokines to its original values already 48 h after LPS + HVL, and also normalized the parameters of pulmonary respiration in comparison with animals without treatment. By the eighth day after LPS + HVL, respiratory parameters and cytokine levels, as well as biochemical and hematological parameters did not differ between groups, while histological signs of residual effects of lung damage were found in all animals, and were more pronounced in Derinat® group, which may indicate stimulation of the local immune response. Thus, the administration of Derinat® stimulates the immune response, has a pronounced protective effect against cytokinemia and respiratory failure caused by ALI, has immunomodulatory effect, and also stimulates a local immune response in lung tissues. Thus, Derinat® is a promising treatment for ALI.

Inherited metabolic disorders have a specific place among cases of sudden deterioration of the newborn’s condition. Therapies have been developed for some of these disorders. Accurate verification of the diagnosis is extremely important for choosing an optimal treatment strategy. However, treatment is not always successful due to the rapid progression of symptoms. We report a case of citrullinemia diagnosed in a newborn in Vidnoye Perinatal Center.

The true picture of the severity and the degree of central nervous system (CNS) in children of the first months of life, doesn´t is always reflected. The outcome of the disease, including unfavorable, is obvious only to the 9-12 months of age due to the features that are assessed as the phenomena of self-defense. A lot of attention in modern Russian and foreign literature is given to the biochemical risk factors for the development of various diseases and their complications, in particular the indicators of oxidative stress, lipid peroxidation, oxidative modification of proteins and antioxidant defense, neurospecific factors involved in the processes of maturation, differentiation and maintain the viability of brain neurons. However, the diagnostic potential of the investigated markers in children didn´t revealed. Purpose of this study is determination of markers of neurological deficits in infants on the basis of neurotrophic factors, indicators of oxidative stress and endothelial dysfunction. Materials and methods. Comprehensive survey of 134 children (61 boys and 73 girls) aged from 0 to 9 months was carried out with the assessment of neurological status and biochemical markers. Results of study. The first component of the nervous tissue of the brain, responding to hypoxia, is microglial environment, which is caused by the growth of lesions S100- protein (i.e., the neuron at the stage of 0-1 months didn´t been metabolic changes - this is evidence of low levels of SOD and MDA).

This study reports an assessment of adaptive possibilities of the central nervous system (CNS) in infants. The study shows how the homocysteine level depends on the severity of neurological deficit (ND) in infants, and how the serum homocysteine level changes during the various treatment regimens. (International Journal of Biomedicine. 2017;7(4):286-288.)

The high incidence of stable coronary heart disease, the increasing frequency of myocardial infarction, disability and mortality determine the relevance of the search for new risk markers and laboratory criteria for predicting this severe complication. The aim of the study was to develop an information panel for diagnosing the risk of myocardial infarction in patients with stable coronary heart disease, including significant generally accepted and potentially possible new laboratory parameters characterizing various pathogenetic links of coronary atherosclerosis. The study included 168 patients who were divided into 2 groups: Group 1 - with a history of myocardial infarction, Group 2 - without a history of myocardial infarction. In addition to the standard laboratory and instrumental examination, all patients were identified parameters of endothelial dysfunction, oxidative stress and chaperone activity as potential markers of myocardial infarction in patients with stable coronary heart disease. Assessment of the risk of myocardial infarction in patients with stable coronary heart disease was carried out using a logical and mathematical model, which combined the most informative laboratory indicators of oxidative stress, endothelial dysfunction, and chaperone activity, which are important in the occurrence and progression of coronary atherosclerosis, according to the results of preliminary comparative and correlation analysis. The basis for the development of the information panel was the method of decision trees. The study confirmed the relationship between the severity of coronary atherosclerosis and the occurrence of myocardial infarction. Comparative analysis of the selected groups of patients showed a higher level of oxidative stress, serum homocysteine concentrations and lower values of chaperone activity in Group 1. In patients with a history of myocardial infarction, C-reactive protein was significantly higher than in Group 2, indicating a more pronounced inflammatory response in patients with large atherosclerotic lesions. The study suggests the possibility of using mathematical information panels based on decision trees as a system for assessing the risk of acute myocardial infarction in patients with stable coronary heart disease. As a result of the analysis of the obtained model, laboratory biochemical factors of high risk of myocardial infarction were identified. Such factors were chaperone activity, serum homocysteine level, serum C-reactive protein concentration and superoxide dismutase activity.