Окремі проблеми імплементації європейського досвіду використання нетрадиційних та відновлювальних джерел енергії в Україні

Рибнікова Е. Ю. Окремі проблеми імплементації європейського досвіду використання нетрадиційних та відновлювальних джерел енергії в Україні / Е. Ю. Рибнікова // Актуальні проблеми держави і права : зб. наук. пр. / редкол.: В. В. Завальнюк (голов. ред.) [та ін.]. – Одеса : Видавничий дім "Гельветика", 2017. – Вип. 78. – С. 135-142.У статті зроблена спроба висвітлити деякі аспекти використання нетрадиційних та відновлювальних джерел енергії, проаналізовано вітчизняну та європейську нормативно-правову базу у галузі альтернативної енергетики. Запропоновано пропозиції щодо спрощення процедури приєднання об’єктів альтернативної енергії до електричних мереж, а також надані рекомендації стосовно імплементації досвіду країн ЄС щодо використання "зелених" тарифівОтдельные проблемы имплементации европейского опыта использования нетрадиционных и возобновляемых источников энергии в Украине. В статье сделана попытка осветить некоторые аспекты использования нетрадиционных и возобновляемых источников энергии, проанализированы отечественную и европейскую нормативно-правовую базу в области альтернативной энергетики. Предложено предложения по упрощению процедуры присоединения объектов альтернативной энергии к электрическим сетям, а также даны рекомендации относительно имплементации опыта стран ЕС по использованию "зеленых" тарифов.Some problems of implementation of European experience in using non-traditional and renewable energy sources in Ukraine. The value of non-traditional and renewable sources of energy have been concerned in the article. Applying of such sources is an indicator of economic and energy well-being of countries through out the world. Ukraine has a great potential for usage of alternative energy sources but imperfection of the legal framework doesn’t allow to achieve the desired level of development of renewable sources. Recommendations for improving of procedure of commissioning of enterprises which use alternative energy are given. Also analysis of experience of the European countries in this area was made, especially in the sphere of using of such economic incentives as "feed-in tariff"

Transcriptional landscape of bone marrow-derived very small embryonic-like stem cells during hypoxia

<p>Abstract</p> <p>Background</p> <p>Hypoxia is a ubiquitous feature of many lung diseases and elicits cell-specific responses. While the effects of hypoxia on stem cells have been examined under <it>in vitro </it>conditions, the consequences of <it>in vivo </it>oxygen deprivation have not been studied.</p> <p>Methods</p> <p>We investigated the effects of <it>in vivo </it>hypoxia on a recently characterized population of pluripotent stem cells known as very small embryonic-like stem cells (VSELs) by whole-genome expression profiling and measuring peripheral blood stem cell chemokine levels.</p> <p>Results</p> <p>We found that exposure to hypoxia in mice mobilized VSELs from the bone marrow to peripheral blood, and induced a distinct genome-wide transcriptional signature. Applying a computationally-intensive methodology, we identified a hypoxia-induced gene interaction network that was functionally enriched in a diverse array of programs including organ-specific development, stress response, and wound repair. Topographic analysis of the network highlighted a number of densely connected hubs that may represent key controllers of stem cell response during hypoxia and, therefore, serve as putative targets for altering the pathophysiologic consequences of hypoxic burden.</p> <p>Conclusions</p> <p>A brief exposure to hypoxia recruits pluripotent stem cells to the peripheral circulation and actives diverse transcriptional programs that are orchestrated by a selective number of key genes.</p

Differential Neuregulin 1 Cleavage in the Prefrontal Cortex and Hippocampus in Schizophrenia and Bipolar Disorder: Preliminary Findings

Neuregulin 1 (NRG1) is a key candidate susceptibility gene for both schizophrenia (SCZ) and bipolar disorder (BPD). The function of the NRG1 transmembrane proteins is regulated by cleavage. Alteration of membrane bound-NRG1 cleavage has been previously shown to be associated with behavioral impairments in mouse models lacking expression of NRG1-cleavage enzymes such as BACE1 and gamma secretase. We sought to determine whether alterations in NRG1 cleavage and associated enzymes occur in patients with SCZ and BPD.Using human postmortem brain, we evaluated protein expression of NRG1 cleavage products and enzymes that cleave at the external (BACE1, ADAM17, ADAM19) and internal (PS1-gamma secretase) sides of the cell membrane. We used three different cohorts (Controls, SCZ and BPD) and two distinct brain regions: BA9-prefrontal cortex (Controls (n = 6), SCZ (n = 6) and BPD (n = 6)) and hippocampus (Controls (n = 5), SCZ (n = 6) and BPD (n = 6)). In BA9, the ratio of the NRG1 N-terminal fragment relative to full length was significantly upregulated in the SCZ cohort (Bonferroni test, p = 0.011). ADAM17 was negatively correlated with full length NRG1 levels in the SCZ cohort (r = -0.926, p = 0.008). In the hippocampus we found significantly lower levels of a soluble 50 kDa NRG1 fragment in the two affected groups compared the control cohort (Bonferroni test, p = 0.0018). We also examined the relationship of specific symptomatology criteria with measures of NRG1 cleavage using the Bipolar Inventory of Signs and Symptoms Scale (BISS) and the Montgomery Åsberg Depression Rating Scale (MADRS). Our results showed a positive correlation between ADAM19 and psychosis (r = 0.595 p = 0.019); PS1 and mania (r = 0.535, p = 0.040); PS1 and depression (r = 0.567, p = 0.027) in BA9, and BACE1 with anxiety (r = 0.608, p = 0.03) in the hippocampus.Our preliminary findings suggest region-specific alterations in NRG1 cleavage in SCZ and BPD patients. These changes may be associated with specific symptoms in these psychiatric disorders

Adaptive preconditioning in neurological diseases -­ therapeutic insights from proteostatic perturbations

International audienceIn neurological disorders, both acute and chronic neural stress can disrupt cellular proteostasis, resulting in the generation of pathological protein. However in most cases, neurons adapt to these proteostatic perturbations by activating a range of cellular protective and repair responses, thus maintaining cell function. These interconnected adaptive mechanisms comprise a 'proteostasis network' and include the unfolded protein response, the ubiquitin proteasome system and autophagy. Interestingly, several recent studies have shown that these adaptive responses can be stimulated by preconditioning treatments, which confer resistance to a subsequent toxic challenge - the phenomenon known as hormesis. In this review we discuss the impact of adaptive stress responses stimulated in diverse human neuropathologies including Parkinson´s disease, Wolfram syndrome, brain ischemia, and brain cancer. Further, we examine how these responses - and the molecular pathways they recruit - might be exploited for therapeutic gai

Circadian Rhythm and Sleep Disruption: Causes, Metabolic Consequences and Countermeasures.

Circadian (∼ 24 hour) timing systems pervade all kingdoms of life, and temporally optimize behaviour and physiology in humans. Relatively recent changes to our environments, such as the introduction of artificial lighting, can disorganize the circadian system, from the level of the molecular clocks that regulate the timing of cellular activities to the level of synchronization between our daily cycles of behaviour and the solar day. Sleep/wake cycles are intertwined with the circadian system, and global trends indicate that these too are increasingly subject to disruption. A large proportion of the world's population is at increased risk of environmentally-driven circadian rhythm and sleep disruption, and a minority of individuals are also genetically predisposed to circadian misalignment and sleep disorders. The consequences of disruption to the circadian system and sleep are profound and include myriad metabolic ramifications, some of which may be compounded by adverse effects on dietary choices. If not addressed, the deleterious effects of such disruption will continue to cause widespread health problems; therefore, implementation of the numerous behavioural and pharmaceutical interventions that can help restore circadian system alignment and enhance sleep will be important

A rare loss-of-function variant of ADAM17 is associated with late-onset familial Alzheimer disease

Common variants of about 20 genes contributing to AD risk have so far been identified through genome-wide association studies (GWAS). However, there is still a large proportion of heritability that might be explained by rare but functionally important variants. One of the so far identified genes with rare AD causing variants is ADAM10. Using whole-genome sequencing we now identified a single rare nonsynonymous variant (SNV) rs142946965 [p.R215I] in ADAM17 co-segregating with an autosomal-dominant pattern of late-onset AD in one family. Subsequent genotyping and analysis of available whole-exome sequencing data of additional case/control samples from Germany, UK, and USA identified five variant carriers among AD patients only. The mutation inhibits pro-protein cleavage and the formation of the active enzyme, thus leading to loss-of-function of ADAM17 alpha-secretase. Further, we identified a strong negative correlation between ADAM17 and APP gene expression in human brain and present in vitro evidence that ADAM17 negatively controls the expression of APP. As a consequence, p.R215I mutation of ADAM17 leads to elevated Aß formation in vitro. Together our data supports a causative association of the identified ADAM17 variant in the pathogenesis of AD

Effect of inescapable stress in rodent models of depression and posttraumatic stress disorder on CRH and vasopressin immunoreactivity in the hypothalamic paraventricular nucleus

The present study was designed to reveal possible common and specific neuroendocrine mechanisms of depressionand anxiety-like states in rodents. Animal models of depression and anxiety (in particular, posttraumatic stress disorder, PTSD) were applied including the learned helplessness and the stress-restress paradigms, respectively. Immunocytochemical staining revealed that depressive- and anxiety-like states in animals were accompanied by the rise in corticotropin-releasing hormone (CRH) immunoreactivity in the parvocellular division of the hypothalamic paraventricular nucleus (PVN). Decrease in vasopressin-immunoreactivity in early period of depressive-like state development was followed by the normalization of vasopressin content in the hypothalamic PVN in delayed period. Increased CRH and vasopressin immunoreactivity in the magnocellular part of the PVN in delayed period of anxiety-like state development was detected only in the stress-restress paradigm. These results suggest that CRH hyperdrive in the parvocellular PVN appears to be a common neuroendocrine abnormality for depressive- and anxiety-like states in animals, while over-expression of CRH and vasopressin in the magnocellular PVN represents a specific feature of anxiety/PTSD-like state