The worldwide prevalence of obesity more than doubled between 1980 and 2014. The obesity pandemic is tightly linked to an increase in energy availability, sedentariness and greater control of ambient temperature that have paralleled the socioeconomic development of the past decades. The most frequent cause which leads to the obesity development is a dysbalance between energy intake and energy expenditure. The gut microbiota as an environmental factor which influence whole-body metabolism by affecting energy balance but also inflammation and gut barrier function, integrate peripheral and central food intake regulatory signals and thereby increase body weight. Probiotics have physiologic functions that contribute to the health of gut microbiota, can affect food intake and appetite, body weight and composition and metabolic functions through gastrointestinal pathways and modulation of the gut bacterial community.

Basic part of the current standard treatment of organophosphate (OP) agent poisoning is administration of cholinesterase reactivators. It includes different types of oximes with a similar basic structure differing by the number of pyridinium rings and by the position of the oxime group in the pyridinium ring. Oximes hydrolytically cleave the organophosphates from acetylcholinesterase (AChE), restoring enzymatic function. This reactivation of AChE is dependent on the type of the agent and, on the reactivator used. From the common oximes, mono- and bisquaternary pyridinium oximes are more or less frequently used in clinical practice such as pralidoxime, obidoxime, trimedoxime, and HI-6. Though there are data on a good therapeutic effects of reactivators, some attempts to undermine the role of reactivators as effective antidotes against OP poisoning have been made. Some arguments on the necessity of their administration following OP poisoning are discussed with the aim to resolve the question on their effective use, possible repeated administration in the treatment of OP poisoning, their peripheral and central effects including questions on their penetration through the blood brain barrier as well as a possibility to achieve their effective concentration for AChE reactivation in the brain. Reactivation of cholinesterases in the peripheral and central nervous system is described and it is underlined its importance for the survival or death of the organism poisoned with OP. An universality of oximes able to reactivate AChE inhibited by all OP is questioned and trends (molecular modelling using neural network, structure-activity relationship, combination of reactivation and anticholinergic properties in one molecule) for future research are characterized.

Prophylactic approaches against intoxication with organophosphates (OP)/nerve agents can be based on following principles: keeping acetylcholinesterase (AChE), the key enzyme for toxic action of OP/nerve agents, intact (protection of cholinesterases) is a basic requirement for effective prophylaxis. It can be reached using simple chemicals such as reversible inhibitors (preferably carbamates), which are able to inhibit AChE reversibly. AChE inhibited by carbamates is resistant to OP/nerve agent inhibition. After spontaneous recovery of the activity, normal AChE serves as a source of the active enzyme. Detoxification is realised by administration of the enzymes splitting the OP or exploitating specific enzymes (cholinesterases). OP/nerve agent is bound to the exogenously administered proteins (enzymes) and, thus, the agent level in the organism is decreased ("scavenger" effect). The antidotes currently used for the treatment of OP poisoning (also simple chemicals) can be tested as prophylactics. This principle can be considered as a treatment "in advance". The problem with their use is the timing, duration and achievement of sufficient levels of these antidotes after the administration. At present, PYRIDOSTIGMINE seems to be common prophylactic antidote; prophylactics PANPAL (tablets with pyridostigmine, trihexyphenidyle and benactyzine), TRANSANT (transdermal patch containing HI-6) are other means introduced into different armies as prophylactics. Future development will be focused on scavengers (cholinesterases and other enzymes) acting before the binding of nerve agent to the target sites, and on other drugs reversible cholinesterase inhibitors (e.g. huperzine A, physostigmine, acridine derivatives etc.) including non-traditional routes of administration.

Deamination of 7-(Me3N)-nido-7,8,9-C3B8H10 (1a) leads either to the parent tricarbollide anion [nido-7,8,9-C3B8H11]- (2 - ) or to the neutral tricarbaborane nido-7,8,9-C3B8H12 (2a), together with a small amount of 8-Me-nido-7,8,9-C3B8H11 (2b). Di- and trisubstituted derivatives of 2a, 7-(Bu t MeN)-10-Me-nido-7,8,9-C3B8H10 (2c), and 7-(Bu t MeN)-10,11-Me2-nido-7,8,9- C3B8H9 (2d) were obtained as byproducts from the methylation of both 7-(Bu t NH2)-nido-7,8,9-C3B8H10 (1b) and 7-(Bu t MeNH)-nido-7,8,9- C3B8H10 (1c) with MeI in THF under reflux. Heating of 1a and 2 - at 350 °C resulted in the rearrangement of the carbons on the open-face to give high yields of the isomeric tricarbollides 10-(Me3N)-nido-7,8,10-C3B8H10 (3a) and [nido -7,8,10-C3B8H11]- (4 - ), respectively. The structure of 3a was determined by an X-ray diffraction analysis, and the geometries of the parent compounds 2 - , 2a, and 4 - were optimized at the ab initio MP2(fc)/6-31G* level. The structures of all compounds also were secured by the excellent agreement between the experimental data and the IGLO/NMR calculations of the 11B chemical shifts for the parent compounds at the DZ//6-31G*, DZ//MP2/6-31G*, and II‘//MP2/6-31G* levels.