22 research outputs found

    The use of bibliometrics for assessing research : possibilities, limitations and adverse effects

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    Researchers are used to being evaluated: publications, hiring, tenure and funding decisions are all based on the evaluation of research. Traditionally, this evaluation relied on judgement of peers but, in the light of limited resources and increased bureaucratization of science, peer review is getting more and more replaced or complemented with bibliometric methods. Central to the introduction of bibliometrics in research evaluation was the creation of the Science Citation Index (SCI)in the 1960s, a citation database initially developed for the retrieval of scientific information. Embedded in this database was the Impact Factor, first used as a tool for the selection of journals to cover in the SCI, which then became a synonym for journal quality and academic prestige. Over the last 10 years, this indicator became powerful enough to influence researchers’ publication patterns in so far as it became one of the most important criteria to select a publication venue. Regardless of its many flaws as a journal metric and its inadequacy as a predictor of citations on the paper level, it became the go-to indicator of research quality and was used and misused by authors, editors, publishers and research policy makers alike. The h-index, introduced as an indicator of both output and impact combined in one simple number, has experienced a similar fate, mainly due to simplicity and availability. Despite their massive use, these measures are too simple to capture the complexity and multiple dimensions of research output and impact. This chapter provides an overview of bibliometric methods, from the development of citation indexing as a tool for information retrieval to its application in research evaluation, and discusses their misuse and effects on researchers’ scholarly communication behavior

    Oligodendrocytes: biology and pathology

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    Oligodendrocytes are the myelinating cells of the central nervous system (CNS). They are the end product of a cell lineage which has to undergo a complex and precisely timed program of proliferation, migration, differentiation, and myelination to finally produce the insulating sheath of axons. Due to this complex differentiation program, and due to their unique metabolism/physiology, oligodendrocytes count among the most vulnerable cells of the CNS. In this review, we first describe the different steps eventually culminating in the formation of mature oligodendrocytes and myelin sheaths, as they were revealed by studies in rodents. We will then show differences and similarities of human oligodendrocyte development. Finally, we will lay out the different pathways leading to oligodendrocyte and myelin loss in human CNS diseases, and we will reveal the different principles leading to the restoration of myelin sheaths or to a failure to do so

    Mapping and Imaging the Aggressive Brain in Animals and Humans

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    GABAergic regulation of cerebellar NG2 cell development is altered in perinatal white matter injury.

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    Diffuse white matter injury (DWMI), a leading cause of neurodevelopmental disabilities in preterm infants, is characterized by reduced oligodendrocyte formation. NG2-expressing oligodendrocyte precursor cells (NG2 cells) are exposed to various extrinsic regulatory signals, including the neurotransmitter GABA. We investigated GABAergic signaling to cerebellar white matter NG2 cells in a mouse model of DWMI (chronic neonatal hypoxia). We found that hypoxia caused a loss of GABAA receptor-mediated synaptic input to NG2 cells, extensive proliferation of these cells and delayed oligodendrocyte maturation, leading to dysmyelination. Treatment of control mice with a GABAA receptor antagonist or deletion of the chloride-accumulating transporter NKCC1 mimicked the effects of hypoxia. Conversely, blockade of GABA catabolism or GABA uptake reduced NG2 cell numbers and increased the formation of mature oligodendrocytes both in control and hypoxic mice. Our results indicate that GABAergic signaling regulates NG2 cell differentiation and proliferation in vivo, and suggest that its perturbation is a key factor in DWMI

    Oligodendrocyte Development in the Absence of Their Target Axons In Vivo

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    Oligodendrocytes form myelin around axons of the central nervous system, enabling saltatory conduction. Recent work has established that axons can regulate certain aspects of oligodendrocyte development and myelination, yet remarkably oligodendrocytes in culture retain the ability to differentiate in the absence of axons and elaborate myelin sheaths around synthetic axon-like substrates. It remains unclear the extent to which the life-course of oligodendrocytes requires the presence of, or signals derived from axons in vivo. In particular, it is unclear whether the specific axons fated for myelination regulate the oligodendrocyte population in a living organism, and if so, which precise steps of oligodendrocyte-cell lineage progression are regulated by target axons. Here, we use live-imaging of zebrafish larvae carrying transgenic reporters that label oligodendrocyte-lineage cells to investigate which aspects of oligodendrocyte development, from specification to differentiation, are affected when we manipulate the target axonal environment. To drastically reduce the number of axons targeted for myelination, we use a previously identified kinesin-binding protein (kbp) mutant, in which the first myelinated axons in the spinal cord, reticulospinal axons, do not fully grow in length, creating a region in the posterior spinal cord where most initial targets for myelination are absent. We find that a 73% reduction of reticulospinal axon surface in the posterior spinal cord of kbp mutants results in a 27% reduction in the number of oligodendrocytes. By time-lapse analysis of transgenic OPC reporters, we find that the reduction in oligodendrocyte number is explained by a reduction in OPC proliferation and survival. Interestingly, OPC specification and migration are unaltered in the near absence of normal axonal targets. Finally, we find that timely differentiation of OPCs into oligodendrocytes does not depend at all on the presence of target axons. Together, our data illustrate the power of zebrafish for studying the entire life-course of the oligodendrocyte lineage in vivo in an altered axonal environment

    Emerging freeway traffic control strategies

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    Classical freeway traffic control approaches can be conveniently revisited in the light of the new technologies which have revolutionised data collection, data processing, communications and computing. In this chapter, the emerging freeway traffic control paradigms are illustrated, without claiming to be exhaustive, as the emerging control concepts are constantly evolving together with the new technologies on which they are based. The scenarios that unfold on the horizon are incredibly dense with potentialities and opportunities. Traffic data acquisition can be performed supplementing fixed sensors with probe vehicles. The overall traffic flow, even in case of mixed traffic consisting of conventional vehicles and intelligent vehicles, can be influenced by acting in a coordinated way at the level of the single intelligent vehicle. Large amounts of data can be collected, also exploiting unconventional data sources like social networks, making of paramount importance the development of traffic-oriented big data technologies, as well as efficient data mining techniques, in order to distinguish between useful and non-useful data and suitably process them. Privacy-preserving data sharing, cybersecurity, fault-tolerance and resilience concepts also play an important role in this new and challenging scenario

    Safety of drug-eluting stents

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    Drug-eluting stents (DESs) effectively reduce angiographic restenosis and the clinical need for repeat revascularization procedures as compared with bare-metal stents. Widely publicized concerns arose recently about the incidence of late and very late stent thrombosis with the use of first-generation DESs. Recent systematic reviews and large-scale registry studies demonstrated similar rates of overall mortality and myocardial infarction for patients treated with either DESs or bare-metal stents during long-term follow-up. Careful selection of stent type according to patient and lesion characteristics as well as monitoring of adherence to dual antiplatelet therapy could maximize the therapeutic potential of these devices. The purpose of the present Review is to provide the reader with an overview of the benefits and risks of first-generation DESs that could help physicians select the most appropriate stent type for each patient

    Distribution and localization of the GABAB receptor

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    The functional GABAB receptors (GABABRs) are formed by obligate heteromers composed of two principal subunits named GABAB1 and GABAB2. In Drosophila melanogaster three GABAB subunits have been identified: GB1, GB2 and GB3. The GB1 and GB2 subunits need to be co-expressed in Xenopus oocytes or in mammalian cell lines to produce functional GABABRs. A subfamily of potassium channel tetramerization domain-containing (KCTD8, 12, 12b, and 16) proteins that are constituents of native GABABRs were recently identified. KCTDs show a temporal and spatial distribution pattern that may contribute to the heterogeneity of native GABABRs and their pharmacological properties. Of several isoforms of the GABAB1 subunit identified to date, the most abundant in the brain are the isoforms 1a and 1b; they are co-expressed with the subunit GABAB2 and their expression differs across brain and neuronal populations. GABAB1a localizes to glutamatergic terminals and is necessary for hetero-receptor function. Both isoforms 1a and 1b are detected in dendrites, but only GABAB1b in spine heads. Electron microscopy studies show that in the central nervous system (CNS), GABAB1 and GABAB2 are both pre and postsynaptic, but mostly localize to postsynaptic sites. The GABAB1(a/b) and GABAB2 subunits show an overlapping pattern of distribution throughout the CNS with certain exceptions (i.e. caudate-putamen and cerebellum). GABABRs are also detected in Schwann cells, in several peripheral tissues, and in non-neuronal cells (cardiomyocytes and airway smooth muscle). The widespread distribution of GABABRs in the CNS and the periphery reflects their physiological, pathophysiological, and pharmacological relevance
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