Individual features of geometric figures discrimination by three species of reptiles

Background (context). The individual characteristics of reptiles have been studied less than that of other classes of animals. One of the basic properties of their individuality, impulsivity, on which behavior and the solution of cognitive tasks in humans and animals significantly depend, has not been practically investigated. Objective. To study manifestations of impulsivity in decision-making in visual recognition in three types of reptiles. Design. In ten experiments, each of six individuals of three reptile species chose one of two paths in the task of distinguishing geometric shapes in mazes. The indicators of the percentage of erroneous choices and the average time for making choices were evaluated relative to the corresponding median values, similar to the study of a person’s impulsivity when choosing among similar visual images in the Kagan test. Results. Among the individuals of each species, four individual typological groups were distinguished: impulsive, slow — accurate, fast — accurate, and slow — inaccurate. This confirmed the authors’ hypothesis based on their study of color recognition in common grass snakes. In slow — accurate and slow — inaccurate individuals, repeated turns to the stimuli being compared were observed before they made a decision, apparently reflecting the expanded analysis of visual information, unlike in most impulsive and fast-accurate individuals. Conclusions. The four individual-typological groups identified in the three types of reptiles in the task of visual recognition are similar in terms of impulsivity to the known groups of people identified in a similar task. The differences in the behavioral reactions of individuals of the four typological groups of reptiles before making a decision correspond to the different psychological content of such a choice in these groups. Our results, which were obtained for reptiles for the first time, confirm the concept of impulsivity as one of the fundamental biologically determined characteristics of individuality, which is valid for other species of animals and humans. In the future it would be useful to find out: 1. Whether the following methods of studying impulsivity evaluate the same individual characteristic of animals: the well-known method of choosing the type of reinforcement and the auto method of choosing the path in the labyrinth with visual discrimination; 2. Do the assessments of impulsivity by these methods correlate with assessments of courage in reactions to a new object, territory and food? The practical significance of the work lies in the fact that knowledge of the individual characteristics of reptiles allows us to develop scientifically based recommendations for maintaining their well-being in zoos and nurseries

Low Density Lipoprotein-Containing Circulating Immune Complexes : Role in Atherosclerosis and Diagnostic Value

Peer reviewe

Genome-Wide Association Study Identifies CDKN1A as a Novel Locus Associated with Muscle Fiber Composition

departmental bulletin pape

Send Orders for Reprints to [email protected] Mitochondrial Genome Sequencing in Atherosclerosis: What's Next?

Abstract: Cardiovascular diseases are currently a basic cause of mortality in highly developed countries. The major reason for genesis and development of cardiovascular diseases is atherosclerosis. At the present time high technology methods of molecular genetic diagnostics can significantly simplify early presymptomatic recognition of patients with atherosclerosis, to detect risk groups and to perform a family analysis of this pathology. A Next-Generation Sequencing (NGS) technology can be characterized by high productivity and cheapness of full genome analysis of each DNA sample. We suppose that in the nearest future NGS methods will be widely used for scientific and diagnostic purposes, including personalized medicine. In the present review article literature data on using NGS technology were described in studying mitochondrial genome mutations associated with atherosclerosis and its risk factors, such as mitochondrial diabetes, mitochondrial cardiomyopathy, diabetic nephropathy and left ventricular hypertrophy. With the use of the NGS technology it proved to be possible to detect a range of homoplasmic and heteroplasmic mutations and mitochondrial genome haplogroups which are associated with these pathologies. Meanwhile some mutations and haplogroups were detected both in atherosclerosis and in its risk factors. It conveys the suggestion that there are common pathogenetic mechanisms causing these pathologies. What comes next? New paradigm of crosstalk between non-pharmaceutical (including molecular genetic) and true pharmaceutical approaches may be developed to fill the niche of effective and pathogenically targeted pretreatment and treatment of preclinical and subclinical atherosclerosis to avoid the development of chronic life-threatening disease

Mitochondrial aging : focus on mitochondrial DNA damage in atherosclerosis : a mini-review

Atherosclerosis is a complex disease which can be described as an excessive fibrofatty, proliferative, inflammatory response to damage to the artery wall involving several cell types such as smooth muscle cells, monocyte-derived macrophages, lymphocytes, dendritic cells and platelets. On the other hand, atherosclerosis is a typical age-related degenerative pathology, which is characterized by signs of cell senescence in the arterial wall including reduced cell proliferation, irreversible growth arrest and apoptosis, increased DNA damage, the presence of epigenetic modifications, shortening of telomere length and mitochondrial dysfunction. The most prominent characteristics of mitochondrial aging are their structural alterations and mitochondrial DNA damage. The mechanisms of mitochondrial genome damage in the development of chronic age-related diseases such as atherosclerosis are not yet well understood. This review focuses on the latest findings from studies of those mutations of the mitochondrial genome which may play an important role in the development of atherosclerosis and which are, at the same time, also markers of mitochondrial aging and cell senescence

Association of mutations in the mitochondrial genome with the subclinical carotid atherosclerosis in women

The importance of the study of an association of mitochondrial DNA mutations with asymptomatic atherosclerosis in women is undeniable. In the present study, a series of PCR with primers for mutation region and further amplificate pyrosequencing were carried out to identify point substitutions or microdeletions of the mitochondrial genome. The results obtained were processed using the original method of estimating the level of heteroplasmy. Five mutations in the mitochondrial genome, namely C3256T, G14709A, G12315A, G13513A and G14846A, in which the heteroplasmy level was associated with the degree of preclinical atherosclerosis in women, were identified. The data obtained in the study showed that C3256T, G14709A and G12315A mutations have a positive correlation with atherosclerosis while G13513A and G14846A mutations have a negative correlation with atherosclerotic lesions. Total mutational load of the mitochondrial genome for C3256T, G14709A, G12315A, G13513A and G14846A mutations explains 68% of the variability of thickness of the carotid intima-medial layer, while the complex of traditional risk factors for cardiovascular diseases explains only 8% of the IMT variability. Data on the correlation between heteroplasmy levels of C3256T, G14709A, G12315A, G13513A and G14846A mutations prompt a suggestion that these mutations may be present on the same haplotypes of mitochondrial genome, associated with atherosclerosis

Quantitative Assessment of Heteroplasmy of Mitochondrial Genome: Perspectives in Diagnostics and Methodological Pitfalls

The role of alterations of mitochondrial DNA (mtDNA) in the development of human pathologies is not understood well. Most of mitochondrial mutations are characterized by the phenomenon of heteroplasmy which is defined as the presence of a mixture of more than one type of an organellar genome within a cell or tissue. The level of heteroplasmy varies in wide range, and the expression of disease is dependent on the percent of alleles bearing mutations, thus allowing consumption that an upper threshold level may exist beyond which the mitochondrial function collapses. Recent findings have demonstrated that some mtDNA heteroplasmic mutations are associated with widely spread chronic diseases, including atherosclerosis and cancer. Actually, each etiological mtDNA mutation has its own heteroplasmy threshold that needs to be measured. Therefore, quantitative evaluation of a mutant allele of mitochondrial genome is an obvious methodological challenge, since it may be a keystone for diagnostics of individual genetic predisposition to the disease. This review provides a comprehensive comparison of methods applicable to the measurement of heteroplasmy level of mitochondrial mutations associated with the development of pathology, in particular, in atherosclerosis and its clinical manifestations

Analysis of mitochondrial DNA heteroplasmic mutations A1555G, C3256T, T3336C, C5178A, G12315A, G13513A, G14459A, G14846A and G15059A in CHD patients with the history of myocardial infarction

The present study was undertaken in order to advance our earlier studies directed to define genetic risk of atherosclerotic vascular lesion development on a base on the analysis of sets of mutational load relevant to the mitochondrial genome mutations. A comparative evaluation of the two study participants’ populations (that included coronary heart disease (CHD) patients who underwent myocardial infarction and apparently healthy donors with no clinical manifestations of coronary heart disease) on heteroplasmy levels of nine mutations of the mitochondrial genome (A1555G, C3256T, T3336C, С5178А, G12315A, G13513A, G14459A, G14846А and G15059A) that were shown previously to be associated with risk factors for atherosclerosis was performed. Close associations with the risk of cardiovascular disease were confirmed for mutation C3256T (gene MT-TL1), G12315A (gene MT-TL2), G13513A (gene MT-ND5) and G15059A (gene MT-CYB) by RT-PCR