Investigation of X-radiation of the moon by means of the lunar satellite ''Luna-10''

Lunik-10 observations of lunar X ray

Gene family evolution: an in-depth theoretical and simulation analysis of non-linear birth-death-innovation models

BACKGROUND: The size distribution of gene families in a broad range of genomes is well approximated by a generalized Pareto function. Evolution of ensembles of gene families can be described with Birth, Death, and Innovation Models (BDIMs). Analysis of the properties of different versions of BDIMs has the potential of revealing important features of genome evolution. RESULTS: In this work, we extend our previous analysis of stochastic BDIMs. In addition to the previously examined rational BDIMs, we introduce potentially more realistic logistic BDIMs, in which birth/death rates are limited for the largest families, and show that their properties are similar to those of models that include no such limitation. We show that the mean time required for the formation of the largest gene families detected in eukaryotic genomes is limited by the mean number of duplications per gene and does not increase indefinitely with the model degree. Instead, this time reaches a minimum value, which corresponds to a non-linear rational BDIM with the degree of approximately 2.7. Even for this BDIM, the mean time of the largest family formation is orders of magnitude greater than any realistic estimates based on the timescale of life's evolution. We employed the embedding chains technique to estimate the expected number of elementary evolutionary events (gene duplications and deletions) preceding the formation of gene families of the observed size and found that the mean number of events exceeds the family size by orders of magnitude, suggesting a highly dynamic process of genome evolution. The variance of the time required for the formation of the largest families was found to be extremely large, with the coefficient of variation >> 1. This indicates that some gene families might grow much faster than the mean rate such that the minimal time required for family formation is more relevant for a realistic representation of genome evolution than the mean time. We determined this minimal time using Monte Carlo simulations of family growth from an ensemble of simultaneously evolving singletons. In these simulations, the time elapsed before the formation of the largest family was much shorter than the estimated mean time and was compatible with the timescale of evolution of eukaryotes. CONCLUSIONS: The analysis of stochastic BDIMs presented here shows that non-linear versions of such models can well approximate not only the size distribution of gene families but also the dynamics of their formation during genome evolution. The fact that only higher degree BDIMs are compatible with the observed characteristics of genome evolution suggests that the growth of gene families is self-accelerating, which might reflect differential selective pressure acting on different genes

Birth and death of protein domains: A simple model of evolution explains power law behavior

BACKGROUND: Power distributions appear in numerous biological, physical and other contexts, which appear to be fundamentally different. In biology, power laws have been claimed to describe the distributions of the connections of enzymes and metabolites in metabolic networks, the number of interactions partners of a given protein, the number of members in paralogous families, and other quantities. In network analysis, power laws imply evolution of the network with preferential attachment, i.e. a greater likelihood of nodes being added to pre-existing hubs. Exploration of different types of evolutionary models in an attempt to determine which of them lead to power law distributions has the potential of revealing non-trivial aspects of genome evolution. RESULTS: A simple model of evolution of the domain composition of proteomes was developed, with the following elementary processes: i) domain birth (duplication with divergence), ii) death (inactivation and/or deletion), and iii) innovation (emergence from non-coding or non-globular sequences or acquisition via horizontal gene transfer). This formalism can be described as a birth, death and innovation model (BDIM). The formulas for equilibrium frequencies of domain families of different size and the total number of families at equilibrium are derived for a general BDIM. All asymptotics of equilibrium frequencies of domain families possible for the given type of models are found and their appearance depending on model parameters is investigated. It is proved that the power law asymptotics appears if, and only if, the model is balanced, i.e. domain duplication and deletion rates are asymptotically equal up to the second order. It is further proved that any power asymptotic with the degree not equal to -1 can appear only if the hypothesis of independence of the duplication/deletion rates on the size of a domain family is rejected. Specific cases of BDIMs, namely simple, linear, polynomial and rational models, are considered in details and the distributions of the equilibrium frequencies of domain families of different size are determined for each case. We apply the BDIM formalism to the analysis of the domain family size distributions in prokaryotic and eukaryotic proteomes and show an excellent fit between these empirical data and a particular form of the model, the second-order balanced linear BDIM. Calculation of the parameters of these models suggests surprisingly high innovation rates, comparable to the total domain birth (duplication) and elimination rates, particularly for prokaryotic genomes. CONCLUSIONS: We show that a straightforward model of genome evolution, which does not explicitly include selection, is sufficient to explain the observed distributions of domain family sizes, in which power laws appear as asymptotic. However, for the model to be compatible with the data, there has to be a precise balance between domain birth, death and innovation rates, and this is likely to be maintained by selection. The developed approach is oriented at a mathematical description of evolution of domain composition of proteomes, but a simple reformulation could be applied to models of other evolving networks with preferential attachment

Changes in somatosensory evoked potentials in rats following transient cerebral ischemia

Background. Cerebral ischemia induced by transient middle cerebral artery occlusion is one of the most popular ischemic stroke models used to evaluate drug candidates with neuroprotective properties. The possibilities of combining this model with neurophysiological techniques (e.g., electroencephalography, electrocorticography, evoked potential registration, etc.) to assess the effectiveness of novel pharmacotherapeutic strategies appear to be of great interest to current biomedical research.The aim. Identifying specific changes in somatosensory evoked potentials occurring after cerebral ischemia induced by middle cerebral artery occlusion in rats.Materials and methods. A total number of 18 white outbred male rats were randomized into 3 groups by 6 animals in each: 1) control (presumably healthy animals); 2) ischemia-30 (30-minute middle cerebral artery occlusion); 3) ischemia-45 (45-minute occlusion). At post-surgery day 7, cortical responses to sequential electrical stimulation of left and right n. ischiadicus were registered. N1, P2, N2, P3, and N3 peak latencies and amplitudes, peak-to-peak interval durations and amplitudes were calculated. Spearman’s rank correlation coefficients were used to assess the relationship between ischemia duration and evoked potential parameters, and the Chaddock scale was used to qualitatively evaluate the strength of correlations.Results. The rats subjected to cerebral ischemia demonstrated a decrease in some of the peak amplitudes of the ipsi- and contralateral somatosensory potentials evoked by n. ischiadicus stimulation. In the injured hemisphere, decreased P2 and N3 peak and P3–N3 interval amplitudes were registered ipsilaterally, and decreased P3 peak amplitudes and N2–P3 interval durations were observed contralaterally.Conclusions. The obtained data suggest that somatosensory evoked potential registration and analysis can be used to evaluate the functional state of central nerve tracts in rats subjected to cerebral ischemia

Parameter determination of the method of directional unloading of the reservoir based on physical modelling on a true triaxial loading setup

The article presents a theoretical and experimental substantiation of the method of directional unloading of the reservoir in fields with low-permeability reservoirs. The relevance of the article is due to the reduction of hydrocarbon resources in modern conditions and the need to create new efficient environmentally friendly technologies to develop hydrocarbon deposits with hard-to-recover reserves, primarily with low-permeability reservoirs. The results of a theoretical study of the stress-strain state in the vicinity of a well, both cased and open, are presented. They are necessary to develop programs for laboratory testing of core specimens from the studied fields. A technique for physical modelling of deformation processes in the bottomhole zone with a decrease in pressure at the well bottom in a true triaxial loading unit is described in order to determine the parameters of the process impact on the formation reservoir, leading to an increase in well productivity. The method was applied to the conditions of the low-permeability reservoir at the Verkhneviluchanskoye oil and gas condensate field in the southwest of the Republic of Sakha (Yakutia). Expe-rimental studies were carried out on a unique scientific unit for true triaxial loading, created at the IPMech RAS, the Triaxial Independent Loading Test System. The directional unloading method was adapted for the studied field, the process parameters of successful application of the method were determined: the bottomhole design, the drawdown values necessary to increase the permeability of the bottomhole formation zone

Protein Evolution within a Structural Space

Understanding of the evolutionary origins of protein structures represents a key component of the understanding of molecular evolution as a whole. Here we seek to elucidate how the features of an underlying protein structural "space" might impact protein structural evolution. We approach this question using lattice polymers as a completely characterized model of this space. We develop a measure of structural comparison of lattice structures that is analgous to the one used to understand structural similarities between real proteins. We use this measure of structural relatedness to create a graph of lattice structures and compare this graph (in which nodes are lattice structures and edges are defined using structural similarity) to the graph obtained for real protein structures. We find that the graph obtained from all compact lattice structures exhibits a distribution of structural neighbors per node consistent with a random graph. We also find that subgraphs of 3500 nodes chosen either at random or according to physical constraints also represent random graphs. We develop a divergent evolution model based on the lattice space which produces graphs that, within certain parameter regimes, recapitulate the scale-free behavior observed in similar graphs of real protein structures.Comment: 27 pages, 7 figure

Межклеточные взаимоотношения и их роль в фиброгенезе при хроническом гепатите С

Introduction. The development of life-threatening complications in chronic hepatitis C (CHC) is based on progressive fibrogenesis. The developing of liver fibrosis is provided by intercellular interactions, first of all, of lymphocytes, macrophages and stellate cells (SC), the patterns of mutual influences of which have not been sufficiently studied at the moment.The objective was to study the features of intercellular interplay of nonparenchymal liver cells at different histological activity, at different stages of CHC fibrosis, and at different genotypes of the hepatitis C virus (HCV).Methods and materials. The object of the study was 64 liver biopsies of adult patients with natural course of CHC. Нistological, immunohistochemical and immunohistomorphometric methods were used.Results. The increasing histological activity is accompanied by an increase in the number and size (area) of CD68 + macrophages and SMA-alfa + SC. Correlation relationships of intercellular interactions at low and moderate histological activity had significant differences. In mild fibrosis, a relationship was found between the number of CD8 + lymphocytes, the number and area of CD68 + macrophages and SMA-alfa + SC. HCV genotype 1 is characterized by a predominance of the interactions between the number of CD8 + lymphocytes, the number and area of CD68 + macrophages in the liver, for genotype 3 – between the number of CD8 + lymphocytes, the number and area of SMA + SC.Conclusions. The maximum activation of SC and macrophages occurs even with moderate histological activity and persists with an increase. The consolidation of the immunopathological nature of the intercellular interplay between lymphocytes, macrophages and SC occurs at the stage of mild fibrosis. Intercellular interactions have significant differences depending on the HCV genotype, which can determine a poor prognosis of the disease.Введение. В основе формирования жизнеугрожающих осложнений при хроническом гепатите С (ХГС) лежит прогрессирующий фиброгенез. Процесс формирования фиброза печени обеспечивается межклеточными взаимодействиями, прежде всего, лимфоцитов, макрофагов и звездчатых клеток (ЗК), закономерности взаимных влияний которых на данный момент изучены недостаточно.Цель – изучить особенности межклеточных взаимосвязей непаренхиматозных клеток печени при различной гистологической активности, на разных стадиях фиброза ХГС и при разных генотипах вируса гепатита С (ВГС).Методы и материалы. Объект исследования – 64 биоптата печени взрослых пациентов с естественным течением ХГС. Использовали гистологический, иммуногистохимический и иммуногистоморфометрический методы.Результаты. Возрастание гистологической активности сопровождается увеличением количества и размеров (площади) CD68+-макрофагов и SMA-alfa+ ЗК. Корреляционные взаимосвязи межклеточных взаимодействий при низкой и умеренной гистологической активности имели значимые отличия. При слабо выраженном фиброзе выявлялась взаимосвязь между количеством CD8+-лимфоцитов, количеством и площадью CD68+-макрофагов и SMA-alfa+ ЗК. Для 1-го генотипа ВГС характерно преобладание взаимосвязи между содержанием CD8+-лимфоцитов, количеством и площадью CD68+-макрофагов в печени, для 3-го генотипа – между содержанием CD8+-лимфоцитов, количеством и площадью SMA+ ЗК.Заключение. Максимальная активация ЗК и макрофагов происходит уже при умеренной гистологической активности и сохраняется при ее увеличении. Закрепление иммунопатологического характера межклеточных взаимосвязей между лимфоцитами, макрофагами и ЗК происходит на стадии слабо выраженного фиброза. Межклеточные взаимосвязи имеют существенные различия в зависимости от генотипа ВГС, что может определять неблагоприятный прогноз заболевания

КЛИНИЧЕСКИЕ И ПАТОМОРФОЛОГИЧЕСКИЕ ПРОЯВЛЕНИЯ ТЯЖЕЛОЙ РЕСПИРАТОРНО-СИНЦИТИАЛЬНОЙ ВИРУСНОЙ ИНФЕКЦИИ. СЛУЧАЙ ИЗ ПРАКТИКИ

On the example of clinical observation of severe respiratory syncytial virus (RSV) infection, which occurred with the development of a specific pneumonia complicated by acute respiratory distress-syndrome and disseminated intravascular coagulation syndrome, which caused a lethal outcome in the non-term (33-34 weeks gestation) child of two months of life, the clinical and pathomorphological features of the disease are shown. Immunomorphologic study after death allowed to demonstrate the most important stages of respiratory syncytial viral infection pathogenesis and to specify reasons of long-term airway obstruction, caused by complicated respiratory syncytial viral infection. It was indicated, that bronchial obstruction may be caused by qualitative changes of epithelial lumen of different bronchi, such as direct cytophatic effect of respiratory virus or reactive changes of lumen in the form of basal squamous cell differentiation of epithelial lumen and poor regeneration of respiratory epithelium in the later stages of the disease. На примере клинического наблюдения тяжелой респираторно-синцитиальной вирусной (РСВ) инфекции, протекавшей с развитием специфической пневмонии, осложненной острым респираторным дистресс-синдромом и синдромом диссеминированного внутрисосудистого свертывания, обусловившими летальный исход у недоношенного (33–34 недели гестации) ребенка двух месяцев жизни, показаны клинические и патоморфологические особенности заболевания. Использование постмортального посмертного иммуноморфологического исследования позволило продемонстрировать важнейшие звенья патогенеза РСВ-инфекции, а также уточнить причины длительной бронхообструкции при ее тяжелом течении. Показано, что на поздних сроках заболевания в основе бронхообструкции лежат качественные изменения эпителиальной выстилки бронхов разного калибра, обусловленные как сохраняющимся цитопатическим действием РСВ, так и реактивными изменениями эпителия в виде базальной плоскоклеточной дифференцировки эпителиального пласта при слабо выраженной регенерации респираторного эпителия.

НЕИММУННЫЙ ОТЁК ПЛОДА ПРИ ВНУТРИУТРОБНОЙ ИНФЕКЦИИ

Nonimmune hydrops fetalis (NIHF) may be due to congenital infections. This article examines the congenital infections associated with NIHF – parvovirus and syphilis. Particular attention is paid to data verification infection and specificity of morphological changes in the placenta.Внутриутробная инфекция может сопровождаться неиммунным отёком плода. В данной статье приводятся практические наблюдения случаев неиммунного отёка плода при парвовирусной инфекции и сифилисе. Особое внимание уделено верификации данных инфекций и специфичности морфологических изменений в плаценте