The future of tokenizing : art industry in decentralized space

The time being spent online is becoming more important, encouraging companies and industries to follow consumers into the digital space. Along with that, technologies, systems of values, and business models are adopting. The dissertation aims to study the vectors of the Rare Digital Art market development and answer questions about what processes and players will shape this emerging branch of the art industry. This work presents an alternative Value Chain model tailored to Crypto art projects, and concludes that the project cycle will become faster and more activities will fully or partially migrate online. Our research suggests that the rare crypto art market will inherit the technological capabilities of a DeFi market, while maintaining creativity and aesthetics of the art industry. We conclude that validation activities and players will gain an even stronger position in this emerging market, while managerial positions will weaken. Digital Art will move the art industry towards innovative blockchain applications and sophisticated DRM use cases.O tempo passado online está se tornando cada vez mais importante, incentivando empresas e indústrias a seguirem os consumidores no espaço digital, junto com isso estão surgindo tecnologias, sistemas de valores e modelos de negócio. A dissertação tem como objetivo estudar os vetores de desenvolvimento do mercado de Arte Digital Rara, e responder a perguntas sobre quais processos e personagens moldarão este ramo emergente da indústria da arte. Este trabalho apresenta um modelo alternativo de Cadeia de Valor adaptado aos projetos de arte Crypto, e conclui que o ciclo do projeto se tornará mais rápido à medida que mais atividades migrarão total ou parcialmente para online. Nossa pesquisa sugere que o raro mercado de arte criptográfica herdará as capacidades tecnológicas de um Mercado financeiro descentralizado, mantendo a criatividade e a estética da indústria da arte. Concluímos que as atividades de validação e os personagens ganharão uma posição ainda mais forte nesse mercado emergente, enquanto as áreas gerenciais enfraquecer-se-ão. A Arte Digital levará a indústria de arte para aplicativos inovadores de Blockchain e casos de uso sofisticados de DRM

SVM-based texture classification in optical coherence tomography

This paper describes a new method for automated texture classification for glaucoma detection using high resolution retinal Optical Coherence Tomography (OCT). OCT is a non-invasive technique that produces cross-sectional imagery of ocular tissue. Here, we exploit information from OCT im-ages, specifically the inner retinal layer thickness and speckle patterns, to detect glaucoma. The proposed method relies on support vector machines (SVM), while principal component analysis (PCA) is also employed to improve classification performance. Results show that texture features can improve classification accuracy over what is achieved using only layer thickness as existing methods currently do. Index Terms — classification, support vector machine, optical coherence tomography, texture 1

Enhancement of visual cortex plasticity by dark exposure

Dark rearing is known to delay the time course of the critical period for ocular dominance plasticity in the visual cortex. Recent evidence suggests that a period of dark exposure (DE) may enhance or reinstate plasticity even after closure of the critical period, mediated through modification of the excitatory–inhibitory balance and/or removal of structural brakes on plasticity. Here, we investigated the effects of a week of DE on the recovery from a month of monocular deprivation (MD) in the primary visual cortex (V1) of juvenile mice. Optical imaging of intrinsic signals revealed that ocular dominance in V1 of mice that had received DE recovered slightly more quickly than of mice that had not, but the level of recovery after three weeks was similar in both groups. Two-photon calcium imaging showed no significant difference in the recovery of orientation selectivity of excitatory neurons between the two groups. Parvalbumin-positive (PV+) interneurons exhibited a smaller ocular dominance shift during MD but again no differences in subsequent recovery. The percentage of PV+ cells surrounded by perineuronal nets, a structural brake on plasticity, was lower in mice with than those without DE. Overall, DE causes a modest enhancement of mouse visual cortex plasticity

The optical detection of retinal ganglion cell damage

We provide an overview of developments in the use OCT imaging for the detection of retinal ganglion cell damage in vivo that avoid use of any exogenous ligands to label cells. The method employs high resolution OCT using broad spectral light sources to deliver axial resolution of under 5 microns. The resolution approximates that of cellular organelles, which undergo degenerative changes that progress to apoptosis as a result of axon damage. These degenerative changes are manifest as the loss of retinal ganglion cell dendrites and fragmentation of the subcellular network of organelles, in particular, the mitochondria that support dendritic structure. These changes can alter the light scattering behaviour of degenerating neurons. Using OCT imaging techniques to identify these signals in cultured neurons, we have demonstrated changes in cultured cells and in retinal explants. Pilot studies in human glaucoma suggest that similar changes are detectable in the clinical setting. High resolution OCT can be used to detect optical scatter signals that derive from the retinal ganglion cell layer and are associated with neuronal damage. These findings suggest that OCT instruments can be used to derive quantitative measurements of retinal ganglion cell damage. Critically, these signals can be detected at an early stage of retinal ganglion cell degeneration when cells could be protected or remodeled to support visual recovery

Opa1 deficiency leads to diminished mitochondrial bioenergetics with compensatory increased mitochondrial motility

Purpose: Retinal ganglion cells (RGCs) are susceptible to mitochondrial deficits and also the major cell type affected in patients with mutations in the OPA1 gene in autosomal dominant optic atrophy (ADOA). Here, we characterized mitochondria in RGCs in vitro from a heterozygous B6; C3-Opa1Q285STOP (Opa1+/−) mouse model to investigate mitochondrial changes underlying the pathology in ADOA. Methods: Mouse RGCs were purified from wild-type and Opa1+/− mouse retina by two-step immunopanning. The mitochondria in neurites of RGCs were labeled with MitoTracker Red for structure and motility measurement by time-lapse imaging. Mitochondrial bioenergetics were determined by the real-time measurement of oxygen consumption rate using a Seahorse XFe 96 Extracellular Flux Analyzer. Results: We observed a significant decrease in mitochondrial length in Opa1+/− RGCs with a remarkably higher proportion and density of motile mitochondria along the neurites. We also observed an increased transport velocity with a higher number of contacts between mitochondria in Opa1+/− RGC neurites. The oxygen consumption assays showed a severe impairment in basal respiration, Adenosine triphosphate-linked (ATP-linked) oxygen consumption, as well as reserve respiratory capacity, in RGCs from Opa1+/− mouse retina. Conclusions: Opa1 deficiency leads to significant fragmentation of mitochondrial morphology, activation of mitochondrial motility and impaired respiratory function in RGCs from the B6; C3-Opa1Q285STOP mouse model. This highlights the significant alterations in the intricate interplay between mitochondrial morphology, motility, and energy production in RGCs with Opa1 deficiency long before the onset of clinical symptoms of the pathology

A perspective on accelerated ageing caused by genetic deficiency of the metabolic protein, OPA1

Autosomal Dominant Optic Atrophy (ADOA) is an ophthalmological condition associated primarily with mutations in the OPA1 gene. It has variable onset, sometimes juvenile, but in other patients, the disease does not manifest until adult middle age despite the presence of a pathological mutation. Thus, individuals carrying mutations are considered healthy before the onset of clinical symptoms. Our research, nonetheless, indicates that on the cellular level pathology is evident from birth and mutant cells are different from controls. We argue that the adaptation and early recruitment of cytoprotective responses allows normal development and functioning but leads to an exhaustion of cellular reserves, leading to premature cellular aging, especially in neurons and skeletal muscle cells. The appearance of clinical symptoms, thus, indicates the overwhelming of natural cellular defenses and break-down of native protective mechanisms

Optophysiological characterisation of inner retina responses with high-resolution optical coherence tomography

Low coherence laser interferometry has revolutionised quantitative biomedical imaging of optically transparent structures at cellular resolutions. We report the first optical recording of neuronal excitation at cellular resolution in the inner retina by quantifying optically recorded stimulus-evoked responses from the retinal ganglion cell layer and comparing them with an electrophysiological standard. We imaged anaesthetised paralysed tree shrews, gated image acquisition, and used numerical filters to eliminate noise arising from retinal movements during respiratory and cardiac cycles. We observed increases in contrast variability in the retinal ganglion cell layer and nerve fibre layer with flash stimuli and gratings. Regions of interest were subdivided into three-dimensional patches (up to 5-15μm in diameter) based on response similarity. We hypothesise that these patches correspond to individual cells, or segments of blood vessels within the inner retina. We observed a close correlation between the patch optical responses and mean electrical activity of afferent visual neurons. While our data suggest that optical imaging of retinal activity is possible with high resolution OCT, the technical challenges are not trivial

OPA1 deficiency accelerates hippocampal synaptic remodelling and age-related deficits in learning and memory

A healthy mitochondrial network is essential for the maintenance of neuronal synaptic integrity. Mitochondrial and metabolic dysfunction contributes to the pathogenesis of many neurodegenerative diseases including dementia. OPA1 is the master regulator of mitochondrial fusion and fission and is likely to play an important role during neurodegenerative events. To explore this, we quantified hippocampal dendritic and synaptic integrity and the learning and memory performance of aged Opa1 haploinsufficient mice carrying the Opa1Q285X mutation (B6; C3-Opa1Q285STOP; Opa1+/−). We demonstrate that heterozygous loss of Opa1 results in premature age-related loss of spines in hippocampal pyramidal CA1 neurons and a reduction in synaptic density in the hippocampus. This loss is associated with subtle memory deficits in both spatial novelty and object recognition. We hypothesize that metabolic failure to maintain normal neuronal activity at the level of a single spine leads to premature age-related memory deficits. These results highlight the importance of mitochondrial homeostasis for maintenance of neuronal function during ageing

Профессиональное «выгорание» как актуальная проблема управления персоналом авиационных предприятий

The results of research of the "risks" in the professional conduct of aviation professionals, leading to professional burnout syndrome. Comparative analysis of the propensity for "burnout" among different categories of aviation personnel,is given, the category with a clear tendency to "burnout" is istentified and directions for prevention of this syndrome are suggested.Представлены результаты исследования «рисков» в профессиональном поведении авиационных специалистов, приводящих к синдрому профессионального «выгорания». Дан сравнительный анализ склонности к «выгоранию» у разных категорий авиационного персонала, выявлены категории с явно выраженной склонностью к «выгоранию» и предложены направления профилактики данного синдрома