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The processes of the liberalization of tariffs for cargo handling in the sea ports of Ukraine by deregulation of rates for loading and unloading. The expediency of introducing tools of controlling tariffs for cargo handling in the sea ports, that is to determine the reasonable value of the discount rate applicable at the time of tariffs for loading and unloading services ports. A methodical approach was developed to control tariffs transshipment at the sea ports for the calculation of each cargo traffic that is served in a port value economically justified tariff considering the demand for port cargo handling, regulation of tariffs in the sea ports of Ukraine and achieve maximum profit from the port transshipment. Availability of the proposed methodological approach to optimize tariff policy seaports of Ukraine confirmed by the example of calculating the amount of discounts on the existing tariffs transshipment cargo flows for the three that are served in Izmail seaport. [ABSTRACT FROM AUTHOR]

The article reveals inapplicability of classical models of optimisation of the period and volume of supply of reserves when managing reserves at water transport ships due to a discrete nature of supplies, due to which scheduled supplies of reserves should be done during arrival/departure of the ship into/out of the port. The article justifies a possibility of gaining additional economic effect when introducing the factor of cost of money in time by means of maximisation of flows of money payment into classical logistical models of optimisation of a consignment of orders when organising supplies of reserves. It develops a logistical approach to optimisation of supplies of reserves at water transport ships with consideration of a pronounced discrete character of supplies. It justifies that the optimal period of supply of ship reserves, which minimise costs of supplies of reserves and maximise money receipts from the use of ship reserves, is the time of ship's stay in ports visited, which maximum value of the indicator of intensity of money flow corresponds to. [ABSTRACT FROM AUTHOR]

Subcellular localization of ion channels is crucial for the transmission of electrical signals in the nervous system. Here we show that Discs-Large (DLG), a member of the MAGUK (membrane-associated guanylate kinases) family in Drosophila, co-localizes with Shaker potassium channels (Sh Kch) in most synaptic areas of the adult brain and in the outer membrane of photoreceptors. However, DLG is absent from axonal tracts in which Sh channels are concentrated. Truncation of the C-terminal of Sh (including the PDZ binding site) disturbs its pattern of distribution in both CNS and retina, while truncation of the guanylate kinase/C-terminal domain of DLG induces ectopic localization of these channels to neuronal somata in the CNS, but does not alter the distribution of channels in photoreceptors. I mmunocytochemical, membrane fractionation and detergent solubilization analysis indicate that the C-terminal of Sh Kch is required for proper trafficking to its final destination. Thus, several major conclusions emerge from this study. First, DLG plays a major role in the localization of Sh channels in the CNS and retina. Second, localization of DLG in photoreceptors but not in the CNS seems to depend on its interaction with Sh. Third, the guanylate kinase/C-terminal domain of DLG is involved in the trafficking of Shaker channels but not of DLG in the CNS. Fourth, different mechanisms for the localization of Sh Kch operate in different cell types. [ABSTRACT FROM AUTHOR]

The article reveals inapplicability of classical models of optimisation of the period and volume of supply of reserves when managing reserves at water transport ships due to a discrete nature of supplies, due to which scheduled supplies of reserves should be done during arrival/departure of the ship into/out of the port. The article justifies a possibility of gaining additional economic effect when introducing the factor of cost of money in time by means of maximisation of flows of money payment into classical logistical models of optimisation of a consignment of orders when organising supplies of reserves. It develops a logistical approach to optimisation of supplies of reserves at water transport ships with consideration of a pronounced discrete character of supplies. It justifies that the optimal period of supply of ship reserves, which minimise costs of supplies of reserves and maximise money receipts from the use of ship reserves, is the time of ship’s stay in ports visited, which maximum value of the indicator of intensity of money flow corresponds to.Выявлена неприменимость классических моделей оптимизации периода и объема поставки запасов при управлении запасами на судах водного транспорта вследствие дискретного характера поставок, в связи с которым очередные поставки запасов должны осуществляться в период прибытия/отбытия судна в порт/из порта. Обоснована возможность получения дополнительного экономического эффекта при введении в классические логистические модели оптимизации партии заказов фактора стоимости денег во времени за счет максимизации потоков денежных платежей при организации поставок запасов. Разработан логистический подход к оптимизации поставок запасов на судах водного транспорта с учетом выраженного дискретного характера поставок. Обосновано, что оптимальным периодом поставки судовых запасов, минимизирующим затраты поставки запасов и максимизирующим денежные поступления от использования судовых запасов, является время пребывания судна в портах следования, которому соответствует максимальное значение показателя интенсивности денежного потока.

Arc/Arg3.1 is required for synaptic plasticity and cognition, and mutations in this gene are linked to autism and schizophrenia. Arc bears a domain resembling retroviral/retrotransposon Gag-like proteins, which multimerize into a capsid that packages viral RNA. The significance of such a domain in a plasticity molecule is uncertain. Here, we report that the Drosophila Arc1 protein forms capsid-like structures that bind darc1 mRNA in neurons and is loaded into extracellular vesicles that are transferred from motorneurons to muscles. This loading and transfer depends on the darc1-mRNA 3' untranslated region, which contains retrotransposon-like sequences. Disrupting transfer blocks synaptic plasticity, suggesting that transfer of dArc1 complexed with its mRNA is required for this function. Notably, cultured cells also release extracellular vesicles containing the Gag region of the Copia retrotransposon complexed with its own mRNA. Taken together, our results point to a trans-synaptic mRNA transport mechanism involving retrovirus-like capsids and extracellular vesicles., (Copyright © 2017 Elsevier Inc. All rights reserved.)

A pivotal feature of long-lasting synaptic plasticity is the localization of RNAs and the protein synthesis machinery at synaptic sites. How and where ribonucleoprotein (RNP) transport granules that support this synthetic activity are formed is of fundamental importance. The prevailing model poses that the nuclear pore complex (NPC) is the sole gatekeeper for transit of cellular material in and out of the nucleus. However, insights from the nuclear assembly of large viral capsids highlight a back door route for nuclear escape, a process referred to nuclear envelope (NE) budding. Recent studies indicate that NE budding might be an endogenous cellular process for the nuclear export of very large RNPs and protein aggregates. In Drosophila, this mechanism is required for synaptic plasticity, but its role may extend beyond the nervous system, in tissues where local changes in translation are required. Here we discuss these recent findings and a potential relationship between NE budding and the NPC., (Copyright © 2017. Published by Elsevier Inc.)

In this issue of Neuron, Newman et al. (2017) image calcium events at single synapses of unanesthetized Drosophila larvae. Synaptic plasticity and homeostatic regulation of synapses is established to be input specific. Furthermore, plasticity forms involve selective recruitment of previously active or silent synapses., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Defective RNA metabolism and transport are implicated in aging and degeneration [1, 2], but the underlying mechanisms remain poorly understood. A prevalent feature of aging is mitochondrial deterioration [3]. Here, we link a novel mechanism for RNA export through nuclear envelope (NE) budding [4, 5] that requires A-type lamin, an inner nuclear membrane-associated protein, to accelerated aging observed in Drosophila LaminC (LamC) mutations. These LamC mutations were modeled after A-lamin (LMNA) mutations causing progeroid syndromes (PSs) in humans. We identified mitochondrial assembly regulatory factor (Marf), a mitochondrial fusion factor (mitofusin), as well as other transcripts required for mitochondrial integrity and function, in a screen for RNAs that exit the nucleus through NE budding. PS-modeled LamC mutations induced premature aging in adult flight muscles, including decreased levels of specific mitochondrial protein transcripts (RNA) and progressive mitochondrial degradation. PS-modeled LamC mutations also induced the accelerated appearance of other phenotypes associated with aging, including a progressive accumulation of polyubiquitin aggregates [6, 7] and myofibril disorganization [8, 9]. Consistent with these observations, the mutants had progressive jumping and flight defects. Downregulating marf alone induced the above aging defects. Nevertheless, restoring marf was insufficient for rescuing the aging phenotypes in PS-modeled LamC mutations, as other mitochondrial RNAs are affected by inhibition of NE budding. Analysis of NE budding in dominant and recessive PS-modeled LamC mutations suggests a mechanism by which abnormal lamina organization prevents the egress of these RNAs via NE budding. These studies connect defects in RNA export through NE budding to progressive loss of mitochondrial integrity and premature aging., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

The nuclear envelope (NE) physically separates the cytoplasmic and nuclear compartments. While this barrier provides advantages, it also presents a challenge for the nuclear export of large ribonucleoprotein (RNP) complexes. Decades-old dogma holds that all such border-crossing is via the nuclear pore complex (NPC). However, the diameter of the NPC central channel limits the passage of large cargos. Here, we review evidence that such large RNPs employ an endogenous NE-budding pathway, previously thought to be exclusive to the nuclear egress of Herpes viruses. We discuss this and other models proposed, the likelihood that this pathway is conserved, and the consequences of disrupting NE-budding for synapse development, localized translation of synaptic mRNAs, and laminopathies inducing accelerated aging., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Functional neural competence and integrity require interactive exchanges among sensory and motor neurons, interneurons and glial cells. Recent studies have attributed some of the tasks needed for these exchanges to extracellular vesicles (such as exosomes and microvesicles), which are most prominently involved in shuttling reciprocal signals between myelinating glia and neurons, thus promoting neuronal survival, the immune response mediated by microglia, and synapse assembly and plasticity. Such vesicles have also been identified as important factors in the spread of neurodegenerative disorders and brain cancer. These extracellular vesicle functions add a previously unrecognized level of complexity to transcellular interactions within the nervous system.

An important mechanism underlying synapse development and plasticity is the localization of mRNAs that travel from the nucleus to synaptic sites. Here we demonstrate that the giant nuclear-associated Nesprin1 (dNesp1) forms striated F-actin-based filaments, which we dubbed "railroad tracks," that span from muscle nuclei to postsynaptic sites at the neuromuscular junction in Drosophila. These railroad tracks specifically wrap around immature boutons formed during development and in response to electrical activity. In the absence of dNesp1, mRNAs normally localized at postsynaptic sites are lacking and synaptic maturation is inhibited. This dNesp1 function does not depend on direct association of dNesp1 isoforms with the nuclear envelope. We also show that dNesp1 functions with an unconventional myosin, Myo1D, and that both dNesp1 and Myo1D are mutually required for their localization to immature boutons. These studies unravel a novel pathway directing the transport of mRNAs from the nucleus to postsynaptic sites during synaptic maturation. VIDEO ABSTRACT., (Copyright © 2015 Elsevier Inc. All rights reserved.)