Exposure of rats with experimental diabetes mellitus to wide-band electromagnetic radiation generated by He-Ne laser and modulated by the pancreas and spleen is informing and phenomenological method prolonging animal life span, normalizing blood glucose level, and promoting regeneration of the pancreas.

The aim of the study was to define the role of brain-derived and glial cell line-derived neurotrophic factors (BDNF and GDNF) in realization of compensative and adaptive mechanisms of a neonatal organism to hypoxia. Materials and Methods. The experiments in vivo have been carried out on pregnant C57BL/6 mice (n=36). Chronic hypobaric hypoxia has been modeled in different pregnancy trimesters. On gestation days E19-20, concentration of BDNF and GDNF in the blood of the pregnant females was determined by enzyme immunoassay. Further, the number of neonatal mice, their weight and body length parameters have been assessed. Parturient mothers (n=88) and their newborn babies followed up at the Clinic of Obstetrics and Gynecology of Pavlov University took part in the clinical investigations. Concentration of BDNF, GDNF, neuron-specific enolase (NSE), and hypoxia-inducible factor (HIF-1β) in the fetal cord blood has been determined by ELISA. The obtained data were retrospectively compared with cardiotocography, dopplerometry, presence of meconium-stained amniotic fluid and the neonate state at birth, assessment according to the Apgar score, and the course of adaptation period. Results. Chronic hypobaric hypoxia in pregnant mice in trimester I and II resulted in the significant decrease of BDNF and GDNF level, decrease in the number of embryos, and in significant changes in weight/height characteristics of the newborn pups. According to the clinical observations, an increased expression of the neurotrophic factors BDNF, GDNF provides protection to a neonate even if hypoxia factors are present and realized. A low content of BDNF and GDNF was observed in the group of infants with a high risk of developing unfavorable hypoxic damaging effects.

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It was found that acute exposure to ionizing radiation at doses of 7.5 and 8 Gy leads to the development of bone marrow syndrome of acute radiation sickness in mice. On the 7th day after exposure at doses of 7.5 Gy and 8 Gy, the mortality rate of animals was 66.7%, on the 10th day 83.3 and 86.7%, and by the 14th day it reached 91.7 and 100%, respectively. Prophylactic exposure to electromagnetic radiation from a helium-neon laser modulated with preparations with the tissue of the hypothalamic structures of the brain, spleen and bone marrow of a newborn mouse (P1-4) before X-ray irradiation at doses of 7.5 and 8 Gy contributed to a decrease in the mortality of animals from acute radiation sickness during the first 14 days, which was 28.6 and 50%, respectively. However, with this method of protective action, by the 22nd day after the radiation damage of 7.5 Gy, the mortality rate reached 64.3%, and 8 Gy-90%. On the contrary, with a therapeutic and preventive method of exposure to electromagnetic radiation by a helium-neon laser modulated by drugs with tissue from hypothalamic structures of the brain, spleen and bone marrow of a newborn mouse (R1-4) after a radiation lesion at a dose of 7.5 Gy, the mortality on the 25th day was 23.3%, and 8 Gy 30% and remained at this level for more than 30 days. We believe that the increase in the resistance of mice to ionizing radiation and the different nature of the course of acute radiation sickness with preventive and therapeutic methods of exposure is due to several factors. On the one hand, it is the realization of antihypoxic, antioxidant effects when exposed to electromagnetic radiation modulated by drugs with tissue from hypothalamic structures of the brain, spleen and bone marrow of a newborn mouse. On the other hand, the effect of electromagnetic radiation modulated by the preparation of the bone marrow and spleen of a newborn mouse has a cytoprotective effect on the bone marrow cells of mice with acute radiation sickness. It is also possible that this effect contributes to adequate neuroimmune regulation in the development of acute radiation sickness in mice.

The constant frequent incidents of fetal hypoxia during pregnancy and childbirth remain the leading unsolved problem in modern practical obstetrics. In some cases, the onset of a pathological process can be diagnosed earlier due to the on-time monitoring of functional disorders of the fetus. However, the existing diagnostic methods do not show the compensatory and adaptive capabilities of the fetus; do not lead to an in-depth understanding of the pathophysiology of this condition and do not contribute to the implementation of evidence-based therapy. This review summarizes current knowledge about the diagnosis of functional disorders of the fetus and discusses possible ways of assessing adaptive mechanisms in response to stress during pregnancy and childbirth. The article shows the development of biochemical methods for diagnosing functional disorders of the fetus. The putative biochemical markers for assessing the compensatory capabilities of the fetus during pregnancy and childbirth are presented.