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We present a novel integration technology for replacing damaged microcircuits in the rat brain with electronic neuronal networks. This technology will allow simulating important brain functions, such as memory, through the adaptive stimulating effects of neural interfaces at cellular and neuronal network levels. The proposed system includes electronic devices to register and process neuronal signals and to adaptively stimulate damaged brain areas according to the online algorithm decoding the registered neuronal activity. The stimulation algorithm is implemented in hardware neural network with memristive connections that allows both network learning and adaptive re-learning.The basic idea is to develop components of hardware neural network with memristive connections for adaptive generation of electrical signals to stimulate particular brain areas. Moreover, the uniqueness of the system is adaptive closed-loop connection between two hippocampal neuronal networks. Such a system is very promising for restoring functionality of damaged areas in the human brain to replace lost functions in patients with brain pathologies or trauma.

We propose a hybrid memristve neuromorphic system for stimulating hippocampus regions bypassing damaged areas. Synaptic plasticity properties of the system allow close-loop adaptive control of neural dynamics. We implement the simplest version of this system which consists of two neuron-like generators coupled by a memristive device, and two fiber-optic channels to transmit signals from the generators directly to living cells to stimulate hippocampus regions. The adaptive stimulation nature of the neural cells is provided by a stochastic response of the self-learning memristive device to the signal of the neuron-like generator. A biological model of impaired functioning of the perforating pathway in the rat hippocampus is implemented by damaging the CA3 region, on the base of the electrophysiological signal changes in normal and pathological conditions. The proposed adaptive stimulation technology demonstrates the possibility of restoring the functionality of the perforating pathway by introducing the neuromorphic system into the hippocampus to replace lost areas.

In the current study, biochemical abnormalities occurring in the body of children with cancer in sepsis, as well as their relationship with the new marker of sepsis and phagocytosis by presepsin, are considered. A survey enrolled 112 children who were treated at the N.N. Blokhin National Medical Research Center of Oncology. Differences in medians of a number of biochemical parameters in groups of patients who survived and died of sepsis were revealed.

The mechanisms that underlie the early loss of the male reproductive function are still unknown. Therefore, investigation of this problem is an important task. The medial preoptic nucleus takes part in the regulation of sexual behavior; however, the role of glycine transmission in this nucleus has not yet been studied. Our study focuses on these questions.

Astrocytes are involved in maintenance of synaptic microenvironment by glutamate uptake and K+ clearance. These processes are associated with net charge transfer across the membrane and therefore can be recorded as glutamate transporter (IGluT) and K+ (IK) currents. It has been previously shown that the blockade of IK with BaCl2 enhances the IGluT. Here we show that activity-dependent facilitation (5 stimuli at 50 Hz) of IGluT was not significantly different in BaCl2 compared to facilitation of IGluT isolated by post-hoc subtraction of IK. Nevertheless, BaCl2 abolished the activity-dependent prolongation of τdecay, which was observed for IGluT isolated by post-hoc subtraction of IK. This finding suggests that activity-dependent accumulation of extracellular K+ ([K+]o) causes astrocytic depolarization, which is responsible for the increase in τdecay of IGluT. The blockade of inward rectifying K+ channels (Kir) with BaCl2 makes astrocytic membrane potential insensitive to [K+]o elevation and thus abolishes this increase. Blockade of IGluT with glutamate transporter blocker, DL-threo-β-benzyloxyaspartic acid (TBOA) did not significantly affect the amplitude of IK but decreased its τdecay. However, activity dependent facilitations of both amplitude and τdecay of IK were larger in TBOA, than in the control conditions. We suggest that activity-dependent accumulation of extracellular glutamate can enhance release of K+. Thus activity-dependent changes in [K+]o can affect glutamate dwell-time in the synaptic cleft, and vice versa, extracellular glutamate accumulation can affect [K+]o time-course. Our finding is important for understanding of the astrocytic mechanisms in glutamate excitotoxicity and in diseases related to disruption of K+ homeostasis (e.g. stroke, migraine, and epilepsy).

Aim . To present rare clinical observation of successful surgical treatment of the patient with double-chamber right ventricle in combination with ventricular septal defect, subaortic fi brosis and muscular stenosis, insufficiency of the aortic valve and extrahepatic portal hypertension. Description . Patient F., 15 years old, was diagnosed with Congenital Heart Disease – double-chambered right ventricle, ventricular septal defect. Fibromuscular subaortic stenosis. Aortic valve insuffi ciency II. Circulatory failure II A., functional class III. Extrahepatic portal hypertension. Splenomegaly. Thrombocytopenia. The state after the imposition of splenorenal anastomosis in September 1998 and the imposition of mesocaval H-shaped anastomosis in 1998. Non-functioning anastomoses. Patient indicated for surgical correction of CHD, however, given the low level of platelets, expressed splenomegaly, leucopenia, the patient was referred for a preliminary treatment to Rogachev’s Pediatric Hematology, Oncology and Immunology Center. The treatment (stimulating thrombopoiesis using romiplostim) gave no signifi cant effect. Platelet count reached 70–90 A~ 10 9 . Seeing of frequent bleeding from esophageal varices, the patient underwent varix sclerosis. At the time of hospitalization – no esophageal varices. The patient appealed to V.I. Shumakov Federal Research Center of Transplantology and Artifi cial Organs where he was recommended for surgical treatment. Result . The patient performed surgery: radical correction of CHD: resection of the stenosis of the outfl ow tract of the right ventricle, subaortic stenosis resection, closure of ventricular septal defect, AV plasty under cardiopulmonary bypass. The early postoperative period was uneventful. Leukopenia was observed to 1,2 A~ 10 9 , thrombocytopenia 70–90 A~ 10 9 . Despite the low level of platelets bleeding in pre-and postoperative period was not registered. Antibiotic therapy with tienam. Good postoperative results were obtained. Liver function was not affected. Conclusion . Presented clinical case demonstrates the possibility of surgical intervention of combined heart disease with cardiopulmonary bypass in patient with extrahepatic portal hypertension.