Правовий режим як критерій поділу права на галузі

Стаття присвячена проблемам поділу системи права на приватне та публічне. У статті аналізуються наявні наукові теорії розподілу права з використанням різних критеріїв, серед яких автор виокремлює правовий режим, як основа утворення галузей вітчизняного законодавства. Ключові слова: приватне право, публічне право, режим, правовий режим.Статья посвящена проблемам разделения системы права на частное и публичное. В статье анализируются имеющиеся научные теории распределения права с использованием разных критериев, среди которых автор выделяет правовой режим, как основа образования отраслей отечественного законодательства. Ключевые слова: частное право, публичное право, режим, правовой режим.The article is sacred to the problems of division of the system of right on private and public. In the article the present scientific theories of distribution are analysed rights with the use of different criteria, among which an author distinguishes the legal mode, as basis of formation of industries of domestic legislation. Key words: private right, public law, mode, legal mode

Unanchored K48-Linked Polyubiquitin Synthesized by the E3-Ubiquitin Ligase TRIM6 Stimulates the Interferon-IKKε Kinase-Mediated Antiviral Response.

Type I interferons (IFN-I) are essential antiviral cytokines produced upon microbial infection. IFN-I elicits this activity through the upregulation of hundreds of IFN-I-stimulated genes (ISGs). The full breadth of ISG induction demands activation of a number of cellular factors including the IκB kinase epsilon (IKKε). However, the mechanism of IKKε activation upon IFN receptor signaling has remained elusive. Here we show that TRIM6, a member of the E3-ubiquitin ligase tripartite motif (TRIM) family of proteins, interacted with IKKε and promoted induction of IKKε-dependent ISGs. TRIM6 and the E2-ubiquitin conjugase UbE2K cooperated in the synthesis of unanchored K48-linked polyubiquitin chains, which activated IKKε for subsequent STAT1 phosphorylation. Our work attributes a previously unrecognized activating role of K48-linked unanchored polyubiquitin chains in kinase activation and identifies the UbE2K-TRIM6-ubiquitin axis as critical for IFN signaling and antiviral response

The combined effect of two mutations that alter serially homologous color pattern elements on the fore and hindwings of a butterfly

<p>Abstract</p> <p>Background</p> <p>The ability for serially homologous structures to acquire a separate identity has been primarily investigated for structures dependent on Hox gene input but is still incompletely understood in other systems. The fore and hindwings of butterflies are serially homologous structures as are the serially homologous eyespots that can decorate each of these wings. Eyespots can vary in number between fore and hindwings of the same individual and mutations of large effect can control the total number of eyespots that each of the wings displays. Here we investigate the genetics of a new spontaneous color pattern mutation, <it>Missing</it>, that alters eyespot number in the nymphalid butterfly, <it>Bicyclus anynana</it>. We further test the interaction of <it>Missing </it>with a previously described mutation, <it>Spotty</it>, describe the developmental stage affected by <it>Missing</it>, and test whether <it>Missing </it>is a mutant variant of the gene <it>Distal-less </it>via a linkage association study.</p> <p>Results</p> <p><it>Missing </it>removes or greatly reduces the size of two of the hindwing eyespots from the row of seven eyespots, with no detectable effect on the rest of the wing pattern. Offspring carrying a single <it>Missing </it>allele display intermediate sized eyespots at these positions. <it>Spotty </it>has the opposite effect of <it>Missing</it>, i.e., it introduces two extra eyespots in homologous wing positions to those affected by <it>Missing</it>, but on the forewing. When <it>Missing </it>is combined with <it>Spotty </it>the size of the two forewing eyespots decreases but the size of the hindwing spots stays the same, suggesting that these two mutations have a combined effect on the forewing such that <it>Missing </it>reduces eyespot size when in the presence of a <it>Spotty </it>mutant allele, but that <it>Spotty </it>has no effect on the hindwing. <it>Missing </it>prevents the complete differentiation of two of the eyespot foci on the hindwing. We found no evidence for any linkage between the <it>Distal-less </it>and <it>Missing </it>genes.</p> <p>Conclusion</p> <p>The spontaneous mutation <it>Missing </it>controls the differentiation of the signaling centers of a subset of the serial homologous eyespots present on both the fore and the hindwing in a dose-dependent fashion. The effect of <it>Missing </it>on the forewing, however, is only observed when the mutation <it>Spotty </it>introduces additional eyespots on this wing. <it>Spotty</it>, on the other hand, controls the differentiation of eyespot centers only on the forewing. <it>Spotty</it>, unlike <it>Missing</it>, may be under Ubx gene regulation, since it affects a subset of eyespots on only one of the serially homologous wings.</p

Tapasin's protein interactions in the rainbow trout peptide-loading complex

The final publication is available at Elsevier via http://dx.doi.org/10.1016/j.dci.2017.12.015 © 2018. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/Major histocompatibility complex (MHC) class I receptors play a key role in the immune system by presenting non-self peptides to T cell lymphocytes. In humans, the assembly of the MHC class I with a peptide is mediated by machinery in the endoplasmic reticulum referred as the peptide loading complex (PLC). Although, the identity of the PLC has been widely explored in humans, this complex has not been characterized in fish. Co-immunoprecipitation and mass spectrometry analysis revealed that the protein-protein interactions which exist in the human PLC are conserved in the monocyte/macrophage rainbow trout cell line (RTS11), in particular the interaction of tapasin with the transporter associated with antigen processing (TAP), MHC class I and ERp57. Importantly, a 20 kDa tapasin version that contains an intact C and N terminal domains was found to associate with ERp57 and form a 75 kDa heterodimer. These results suggest a possible novel alternative spliced version of tapasin may regulate the formation of the peptide-loading complex in teleosts.NSERC Discovery Grant number 217529-2008Canada Research Council Research Chair held by B

Distinct Peripheral Blood RNA Responses to Salmonella in Pigs Differing in Salmonella Shedding Levels: Intersection of IFNG, TLR and miRNA Pathways

Transcriptomic analysis of the response to bacterial pathogens has been reported for several species, yet few studies have investigated the transcriptional differences in whole blood in subjects that differ in their disease response phenotypes. Salmonella species infect many vertebrate species, and pigs colonized with Salmonella enterica serovar Typhimurium (ST) are usually asymptomatic, making detection of these Salmonella-carrier pigs difficult. The variable fecal shedding of Salmonella is an important cause of foodborne illness and zoonotic disease. To investigate gene pathways and biomarkers associated with the variance in Salmonella shedding following experimental inoculation, we initiated the first analysis of the whole blood transcriptional response induced by Salmonella. A population of pigs (n = 40) was inoculated with ST and peripheral blood and fecal Salmonella counts were collected between 2 and 20 days post-inoculation (dpi). Two groups of pigs with either low shedding (LS) or persistent shedding (PS) phenotypes were identified. Global transcriptional changes in response to ST inoculation were identified by Affymetrix Genechip® analysis of peripheral blood RNA at day 0 and 2 dpi. ST inoculation triggered substantial gene expression changes in the pigs and there was differential expression of many genes between LS and PS pigs. Analysis of the differential profiles of gene expression within and between PS and LS phenotypic classes identified distinct regulatory pathways mediated by IFN-γ, TNF, NF-κB, or one of several miRNAs. We confirmed the activation of two regulatory factors, SPI1 and CEBPB, and demonstrated that expression of miR-155 was decreased specifically in the PS animals. These data provide insight into specific pathways associated with extremes in Salmonella fecal shedding that can be targeted for further exploration on why some animals develop a carrier state. This knowledge can also be used to develop rational manipulations of genetics, pharmaceuticals, nutrition or husbandry methods to decrease Salmonella colonization, shedding and spread

Nonmarital childbearing in Russia: second demographic transition or pattern of disadvantage?

Using retrospective union, birth, and education histories that span 1980-2003, this study investigates nonmarital childbearing in contemporary Russia. We employ a combination of methods to decompose fertility rates by union status and analyze the processes that lead to a nonmarital birth. We find that the increase in the percentage of nonmarital births was driven mainly by the growing proportion of women who cohabit before conception, not changing fertility behavior of cohabitors or changes in union behavior after conception. The relationship between education and nonmarital childbearing has remained stable: the least-educated women have the highest birth rates within cohabitation and as single mothers, primarily because of their lower probability of legitimating a nonmarital conception. These findings suggest that nonmarital childbearing Russia has more in common with the pattern of disadvantage in the United States than with the second demographic transition. We also find several aspects of nonmarital childbearing that neither of these perspectives anticipates

Analysis of in vivo dynamics of influenza virus infection using a GFP reporter virus.

Influenza A virus Is being extensively studied due to its major Impact in human and animal health. However, the dynamics of Influenza virus Infection and the cell types infected In vivo are poorly understood. These characteristics are not easy to determine parUy because currently there Is no replication-competent virus expressing a fluorescent reporter gene. Here, we report the generation of a complete Influenza virus carrying a GFP reporter gene In the NS segment of its genome (NS1-GFP virus). NS1-GFP virus replicates efficiently in cell culture and shows pathogenicity In mice at levels similar to parental virus. We have analyzed the In vivo dynamics of influenza Infection progression in mice by flow cytometry and whole organ Imaging of infected lungs. Using flow cytometric analysis of infected lungs, apart from epithelial cells, we find antigen presenting cells like CD11c+, CD11b+ CD11c+, CD11b+ and B cells to be GFP positive. In addition, NK cells are susceptible to Influenza Infection. Whole organ imaging of lungs show that influenza infection starts In the respiratory tract In areas closer to large conducting airways and with time spreads to deeper sections of the lungs. We have also tested the effects of oseltamivir and amantadine on the kinetics and In vivo infection progression in mice and find Interesting differences In the effects of these antivirals. Treatment with oseltamlvlr dramatically reduces Influenza Infection in all cell types, whereas, Interestingly, amantadine treatment blocks infection In a cell type specific manner