Emprego e adaptação de trabalho de graduados da Universidade Russa com deficiência

The article is devoted to the analysis of the problem of social and labor adaptation and employment of university graduates with disabilities, which is relevant in modern socioeconomic conditions. As a result of the sociological research conducted by the authors, the main difficulties that arise for this category of graduates when searching and choosing a job and further employment have been identified. The analysis allows proposing, as an activation of the implementation of the principles of inclusion, an adaptation of social space for effective socialization of the increasing number of people with disabilities in recent decades and their integration into the big society, introducing promising foreign practices of the so-called supported employment of persons with disabilities.El artículo está dedicado al análisis de la problemática de la adaptación sociolaboral y el empleo de los egresados universitarios con discapacidad, que es relevante en las condiciones socioeconómicas modernas. Como resultado de la investigación sociológica realizada por los autores, se han identificado las principales dificultades que surgen para esta categoría de egresados a la hora de buscar y elegir un trabajo y un empleo posterior. El análisis permite proponer, como activación de la implementación de los principios de inclusión, una adecuación del espacio social para la socialización efectiva del creciente número de personas con discapacidad en las últimas décadas y su integración en la "gran" sociedad, introduciendo prometedoras prácticas extranjeras. del denominado "empleo con apoyo" de las personas con discapacidad.O artigo se dedica à análise da problemática, relevante nas condições socioeconômicas modernas, da adaptação social e laboral e do emprego de graduados universitários com deficiência. Como resultado da investigação sociológica realizada pelos autores, foram identificadas as principais dificuldades que surgem para essa categoria de licenciados na procura e na escolha de um emprego e de continuação do emprego. A análise permite propor, como uma ativação da implementação dos princípios da inclusão, uma adaptação do espaço social para a efetiva socialização do crescente número de pessoas com deficiência nas últimas décadas e sua inserção na grande sociedade, introduzindo práticas estrangeiras promissoras. do chamado emprego apoiado de pessoas com deficiência

The neurovirulence and neuroinvasiveness of chimeric tick-borne encephalitis/dengue virus can be attenuated by introducing defined mutations into the envelope and NS5 protein genes and the 3′ non-coding region of the genome

AbstractTick-borne encephalitis (TBE) is a severe disease affecting thousands of people throughout Eurasia. Despite the use of formalin-inactivated vaccines in endemic areas, an increasing incidence of TBE emphasizes the need for an alternative vaccine that will induce a more durable immunity against TBE virus (TBEV). The chimeric attenuated virus vaccine candidate containing the structural protein genes of TBEV on a dengue virus genetic background (TBEV/DEN4) retains a high level of neurovirulence in both mice and monkeys. Therefore, attenuating mutations were introduced into the envelope (E315) and NS5 (NS5654,655) proteins, and into the 3′ non-coding region (Δ30) of TBEV/DEN4. The variant that contained all three mutations (vΔ30/E315/NS5654,655) was significantly attenuated for neuroinvasiveness and neurovirulence and displayed a reduced level of replication and virus-induced histopathology in the brains of mice. The high level of safety in the central nervous system indicates that vΔ30/E315/NS5654,655 should be further evaluated as a TBEV vaccine

Discovery of a high-temperature antiferromagnetic state and transport signatures of exchange interactions in a Bi2Se3/EuSe heterostructure

Spatial confinement of electronic topological surface states (TSS) in topological insulators poses a formidable challenge because TSS are protected by time-reversal symmetry. In previous works formation of a gap in the electronic spectrum of TSS has been successfully demonstrated in topological insulator/magnetic material heterostructures, where ferromagnetic exchange interactions locally lifts the time-reversal symmetry. Here we report an experimental evidence of exchange interaction between a topological insulator Bi2Se3 and a magnetic insulator EuSe. Spin-polarized neutron reflectometry reveals a reduction of the in-plane magnetic susceptibility within a 2 nm interfacial layer of EuSe, and the combination of SQUID magnetometry and Hall measurements points to the formation of an antiferromagnetic layer with at least five-fold enhancement of N\'eel's temperature. Abrupt resistance changes in high magnetic fields indicate interfacial exchange coupling that affects transport in a TSS. High temperature local control of TSS with zero net magnetization unlocks new opportunities for the design of electronic, spintronic and quantum computation devices, ranging from quantization of Hall conductance in zero fields to spatial localization of non-Abelian excitations in superconducting topological qubits

Insertion of MicroRNA Targets into the Flavivirus Genome Alters Its Highly Neurovirulent Phenotype ▿

Flaviviruses such as West Nile, Japanese encephalitis, and tick-borne encephalitis (TBEV) viruses are important neurotropic human pathogens, causing a devastating and often fatal neuroinfection. Here, we demonstrate that incorporation into the viral genome of a target sequence for cellular microRNAs expressed in the central nervous system (CNS) enables alteration of the neurovirulence of the virus and control of the neuropathogenesis of flavivirus infection. As a model virus for this type of modification, we used a neurovirulent chimeric tick-borne encephalitis/dengue virus (TBEV/DEN4) that contained the structural protein genes of a highly pathogenic TBEV. The inclusion of just a single target copy for a brain tissue-expressed mir-9, mir-124a, mir-128a, mir-218, or let-7c microRNA into the TBEV/DEN4 genome was sufficient to prevent the development of otherwise lethal encephalitis in mice infected intracerebrally with a large dose of virus. Viruses bearing a complementary target for mir-9 or mir-124a were highly restricted in replication in primary neuronal cells, had limited access into the CNS of immunodeficient mice, and retained the ability to induce a strong humoral immune response in monkeys. This work suggests that microRNA targeting to control flavivirus tissue tropism and pathogenesis might represent a rational approach for virus attenuation and vaccine development

West Nile Virus Spreads Transsynaptically within the Pathways of Motor Control: Anatomical and Ultrastructural Mapping of Neuronal Virus Infection in the Primate Central Nervous System

<div><p>Background</p><p>During recent West Nile virus (WNV) outbreaks in the US, half of the reported cases were classified as neuroinvasive disease. WNV neuroinvasion is proposed to follow two major routes: hematogenous and/or axonal transport along the peripheral nerves. How virus spreads once within the central nervous system (CNS) remains unknown.</p><p>Methodology/Principal Findings</p><p>Using immunohistochemistry, we examined the expression of viral antigens in the CNS of rhesus monkeys that were intrathalamically inoculated with a wild-type WNV. The localization of WNV within the CNS was mapped to specific neuronal groups and anatomical structures. The neurological functions related to structures containing WNV-labeled neurons were reviewed and summarized. Intraneuronal localization of WNV was investigated by electron microscopy. The known anatomical connectivity of WNV-labeled neurons was used to reconstruct the directionality of WNV spread within the CNS using a connectogram design. Anatomical mapping revealed that all structures identified as containing WNV-labeled neurons belonged to the pathways of motor control. Ultrastructurally, virions were found predominantly within vesicular structures (including autophagosomes) in close vicinity to the axodendritic synapses, either at pre- or post-synaptic positions (axonal terminals and dendritic spines, respectively), strongly indicating transsynaptic spread of the virus between connected neurons. Neuronal connectivity-based reconstruction of the directionality of transsynaptic virus spread suggests that, within the CNS, WNV can utilize both anterograde and retrograde axonal transport to infect connected neurons.</p><p>Conclusions/Significance</p><p>This study offers a new insight into the neuropathogenesis of WNV infection in a primate model that closely mimics WNV encephalomyelitis in humans. We show that within the primate CNS, WNV primarily infects the anatomical structures and pathways responsible for the control of movement. Our findings also suggest that WNV most likely propagates within the CNS transsynaptically, by both, anterograde and retrograde axonal transport.</p></div

Proposed directionality of WNV spread based on the neuroanatomical connectivity and time of immunohistochemical virus detection.

<p>The connectograms illustrate most probable routes and directionality of WNV spread within the CNS in our NHP model of neuroinfection at 7 dpi (<b>A</b>) and 9/10 dpi (<b>B</b>). Construction and elements of the connectogram are described in Materials and Methods and text. Each arrow has the same color as the structure in the ring from which it originates. The circled numbers 1 to 4 represent most probable “order” of infected neurons within the corresponding anatomical structures. Solid arrows indicate most probable routes of anterograde spread; dashed arrows indicate most probable routes of retrograde spread. White lines indicate the possibility of both, anterograde and retrograde virus spread, due to existence of reciprocal connections between the same orders of neurons. <b><i>Abbreviations</i>:</b> Mthal, motor thalamus; BG, basal ganglia; CSMN, corticospinal motor neurons; SNC, substantia nigra pars compacta; RnM, red nucleus magnocellular; SMN, spinal motor neurons (C—cervical; T—thoracic; L—lumbar); CC, Clarke’s column; DCN, deep cerebellar nuclei; ACu, Accessory cuneate nucleus; IO, inferior olivary nuclear complex; MeRF, Medullary reticular formation; Ve, vestibular nuclei; PN, pontine nuclei.</p

WNV-labeled neurons in the deep cerebellar nuclei.

<p>(<b>A</b>) Low magnification overview image showing many WNV-labeled neurons in the dentate nucleus (Dt), emboliform nucleus (Emb), and globose nucleus (Glo) (9 dpi). <b>B</b> and <b>C</b> show corresponding boxed areas at higher magnification. Scale bars: 100 μm.</p

WNV-labeled neurons in the spinal cord.

<p>Representative images of WNV-labeled neurons in the cervical (<b>A</b> and <b>D</b>), thoracic (<b>B</b> and <b>E</b>), and lumbar regions (<b>C</b> and <b>F</b>) of the spinal cord are shown on indicated dpi. Approximate boundaries of the spinal cord gray matter are outlined in the overview images. Clarke’s column is shown by magenta overlay in <b>E</b>. Round insets show the corresponding circled areas at higher magnification. Note that the majority of WNV-labeled neurons occupy a medial portion of the Clarke’s column. Vh, ventral horns; CC, Clarke’s column. Bars in overview images: 1000 μm. Bars in the round insets: 100 μm.</p

WNV-labeled corticospinal motor neurons in the cortical layer 5 of the primary motor cortex.

<p>Inset shows one of the circled areas at higher magnification. Red arrowhead points to a large WNV-labeled corticospinal motor neuron (Betz cell). Note that all three circled WNV- labeled Betz cells are damaged and undergoing neuronophagia (7 dpi). Also note an adjacent long axonal profile that contains WNV-antigens (red arrows). Scale bars: 100 μm.</p