Vol 6, No 2 (2016)

Multiple sclerosis is a common multifactorial disease in which the etiology of the interaction between external factors and structural specificities of a large number of genes plays an important role. Identification of the risk factors for multiple sclerosis and the development of an integrated pathogenesis model is a challenging task for neurology. The goal of the current review is to describe current approaches to studying the genetics of multifactorial diseases on the whole and multiple sclerosis in particular. Basic approaches to the design of the genetic epidemiological studies are described. Towards this end we discuss the gene candidate and the whole-genome methods of studying genetic associations, the statistical approaches used to combine the diverse data, namely, meta-analysis of the results of different studies, analysis of the association with groups of functionally related genes, and comparison of the genetic bases of the diseases with similar pathogenesis.

GDF11 protein, the growth differentiation factor 11, which belongs to the TGF-β superfamily (transforming growth factor β), shows marked geroprotective effects on the cardiovascular and nervous systems. The cardioprotective and myoprotective effects of the GDF11 protein are associated with its regulation of several signaling molecules, including the MAPK–p38–mioglianin pathway. GDF11 neuroprotective action is associated with the regulation of proliferation and differentiation of brain neurons by means of changing the activity of the p57 (Kip2) and p27 (Kip1) transcription factors. GDF11 may be considered a potential target for geroprotector drugs, as was demonstrated in the case of the Glu-Asp-Arg peptide possessing similar neuroprotective and myoprotective properties as GDF11. For the Glu-Asp-Arg, Ala-Glu-AspGly, and Lys-Glu peptides, binding sites were found in the promoter region of GDF11: the CCTGC, ATTTC, and GCAG motifs, respectively.

The development of the concept of an ecological optimum is discussed, and experimental data enabling its revision are analyzed. The published data on the effect of fluctuating ecological factors on various parameters of the vital activity of poikilothermic aquatic organisms and some other organisms are given. The need for terms of stationary (or static) and dynamic (or astatic) optima in modern ecology is discussed. Possible mechanisms of optimization of the vital activity of organisms under conditions of varying factors of the environment are considered.

The invasion of unicellular organisms into other organisms’ cells is widespread among bacteria, protozoa, and fungi. This phenomenon is most often manifested as intracellular parasitism, resulting in serious diseases in humans, animals, and plants. Intracellular pathogen species include about 20 bacterial taxa that can cause serious diseases in humans and animals, such as tuberculosis, leprosy, typhus, salmonellosis, brucellosis, trachoma, dysentery, and other. This review considers in detail the survival strategies of various intracellular bacterial pathogens: their mechanisms of interaction with the host cell membrane, techniques of intrusion into the host cell, survival strategies within the host cell, and mechanisms to avoid host immune responses. We also discuss the strategies of latent persistence of certain bacterial intracellular pathogens, which permit them to survive in the host organism in an inactive form for a long time under conditions of high immune pressure and become rapidly reactivated when the host immune-response levels are reduced.