The development of human intellectual abilities in these periods is associated with the maximum speed of the formation of synaptic connections between neurons, which requires a large amount of different information. When there is its insufficient flow, the child experiences data starvation that causes a state of discomfort.

CML), the accepting inhibitors tyrosine of kinases (TKI) I and the II generations (TKI1 and TKI2 respectively), and development of arterial hypertension.Material and methods. Examination of 137 patients with CML in the chronic phase (CP) is conducted, the median of age — 47 years. 24 of them were with for the first time the verified diagnosis of CML and earlier did not accept TKI, they have made group of control. Other patients accepted TKI: 39 patients — imatinib 400 mg/day, 36 — dasatinib 100 mg/day, 38 — nilotinib 800 mg/day) more than 6 months. In biochemical analysis of blood indicators of lipidic range were defined. Level detection of ET-1 and VEGF was made by means of enzyme immunoassay. To all patients measurement of the heart rate (HR) and the arterial blood pressure (ABP) on both hands at an interval of 2 minutes from previous was once taken.Results. In group of patients from CML accepting nilotinib authentically significant increase in levels of systolic and diastolic ABP (р<0,001) in comparison with group of control, with group of the patients accepting imatinib and dasatinib is noted. The most serious changes of lipidic range are noted at the patients accepting nilotinib. In all groups statistically significant increase in level of C-reactive protein, fibrinogen, homocysteine, endothelin-1 and VEGF in comparison with group of control is revealed. The most expressed changes are found in group of the patients accepting nilotinib, values of parameters of C-reactive protein, fibrinogen, homocysteine, endothelin-1 and VEGF are changed authentically (р<0,001) and statistically significantly differ in comparison with group for the first time of the revealed patients with CML and groups of reception of imatinib and dazatinib.Conclusion. As a result of the conducted research endothelium variation of a function at patients from CML accepting TKI1 and TKI2 is revealed. The above-stated indicators can be used as additional diagnostic criteria for assessment of risk of development of arterial hypertension in patients with CML at reception of TKI.

From the standpoint of evidence - based medicine, the ability of various drugs to induce the development of gastroesophageal reflux disease and esophagitis is considered. Thus, all known drugs can be divided into 3 groups: drugs that have the ability to reduce pressure in the lower esophageal sphincter, for example, β-adrenoreceptor agonists, α-adrenoreceptor antagonists, anticholinergics, calcium channel blockers, nitrates, benzodiazepines (diazepam), estrogen, progesterone, aminophylline (theophylline), tricyclic antidepressants, selective serotonin reuptake inhibitors, glucocorticosteroids; means providing a direct damaging effect on the esophageal mucosa, as well as lowering its resistance reflyuktatu, e.g., bisphosphonates, acetylsalicylic acid / non - steroidal anti - inflammatory agents, anticoagulants, antiplatelet drugs, iron preparations, ascorbic acid, potassium chloride, quinidine, phenytoin, calcium dobesilate, 131I sodium iodide, antibiotics (tetracycline, doxycycline, clindamycin, ciprofloxacin, ornidazole, clindamycin, rifampicin), antitumor agents; drugs that impede gastric emptying: calcium channel blockers, anticholinergics. These data can be used in practice in the choice of treatment tactics, especially in individuals with a diagnosis of gastroesophageal reflux disease or heartburn.

Aim - to explore the features of comorbidity and multimorbidity of infiltrative pulmonary tuberculosis (IPT), peptic ulcer (PU), HIV infection in modern conditions. Materials and methods. The study involved 392 patients with IPT aged 20-44 years, HIV-positive with CD4 200500/pl, suffering from uncomplicated ulcer. Results. Peptic ulcer disease was diagnosed in 20.5% of patients with IPT and 19.5% patients with HIV infection in stage C2 and IPT, complaining of dyspepsia. The multimorbid combination of IPT, HIV infection and PU is characterized by: oligosymptomatic onset of tuberculosis; the clinical picture shows the dominance of asthenic syndrome, manifestations of gastric and intestinal dyspepsia, weight loss (2-4 times more frequently than in patients without HIV infection), less prominent destructive process in the lung tissue (2 times less than in patients without HIV infection). H.pylori is the aetiological factor of PU in 62.5% of patients with IPT and 58.7% patients with HIV infection in stage C2 and IPT. The combination of H.pylori-negative PU and IPT has significantly more unfavorable prognosis compared to comorbidity of H.pylori-positive peptic ulcer and IPT. Conclusion. Diagnosis of PU, HIV infection and H.pylori-status allows defining multiple categories of comorbidity (patients with IPT and dyspeptic syndrome, patients with IPT and H.pylori-associated peptic ulcer, patients with IPT and H.pylori-negative ulcer) and multimorbidity (HIV-infected patients with IPT and H.pylori-associated ulcer, HIV-infected patients with IPT and H.pylori-negative ulcer).

In the present review the cardiovascular complications in patients with chronic myeloid leukemia (CML) receiving tyrosine kinase inhibitors (TKI) are discussed. It covers current views on pathogenesis of TKI cardiovascular toxicity. The pathophysiology of cardiovascular diseases (CVD) is considered as a part of the so-called pathophysiological continuum, i.e. a complex of processes developing at the molecular and cellular levels before clinical symptoms of the above diseases occur. Cardiovascular toxicity of certain TKIs can contribute to progression of pathophysiological processes in CML patients. The study of mechanisms underlying cardiovascular complications of TKI-based therapy is essential for evaluating the risks of their development in each patient. Identification of CVD predictors during TKI-based therapy can allow to elaborate a scheme for cardiovascular monitoring and safe patient management under consideration of individual risks and to avoid severe life-threatening complications.