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Artykuły w czasopismach na temat "TREK1"

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Levitz, Joshua, Perrine Royal, Yannick Comoglio, Brigitte Wdziekonski, Sébastien Schaub, Daniel M. Clemens, Ehud Y. Isacoff i Guillaume Sandoz. "Heterodimerization within the TREK channel subfamily produces a diverse family of highly regulated potassium channels". Proceedings of the National Academy of Sciences 113, nr 15 (28.03.2016): 4194–99. http://dx.doi.org/10.1073/pnas.1522459113.

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Twik-related K+ channel 1 (TREK1), TREK2, and Twik-related arachidonic-acid stimulated K+ channel (TRAAK) form the TREK subfamily of two-pore-domain K+ (K2P) channels. Despite sharing up to 78% sequence homology and overlapping expression profiles in the nervous system, these channels show major differences in their regulation by physiological stimuli. For instance, TREK1 is inhibited by external acidification, whereas TREK2 is activated. Here, we investigated the ability of the members of the TREK subfamily to assemble to form functional heteromeric channels with novel properties. Using single-molecule pull-down (SiMPull) from HEK cell lysate and subunit counting in the plasma membrane of living cells, we show that TREK1, TREK2, and TRAAK readily coassemble. TREK1 and TREK2 can each heterodimerize with TRAAK, but do so less efficiently than with each other. We functionally characterized the heterodimers and found that all combinations form outwardly rectifying potassium-selective channels but with variable voltage sensitivity and pH regulation. TREK1-TREK2 heterodimers show low levels of activity at physiological external pH but, unlike their corresponding homodimers, are activated by both acidic and alkaline conditions. Modeling based on recent crystal structures, along with mutational analysis, suggests that each subunit within a TREK1-TREK2 channel is regulated independently via titratable His. Finally, TREK1/TRAAK heterodimers differ in function from TRAAK homodimers in two critical ways: they are activated by both intracellular acidification and alkalinization and are regulated by the enzyme phospholipase D2. Thus, heterodimerization provides a means for diversifying functionality through an expansion of the channel types within the K2P channels.
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Kim, Seong-Seop, Jimin Park, Eunju Kim, Eun Mi Hwang i Jae-Yong Park. "β-COP Suppresses the Surface Expression of the TREK2". Cells 12, nr 11 (29.05.2023): 1500. http://dx.doi.org/10.3390/cells12111500.

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K2P channels, also known as two-pore domain K+ channels, play a crucial role in maintaining the cell membrane potential and contributing to potassium homeostasis due to their leaky nature. The TREK, or tandem of pore domains in a weak inward rectifying K+ channel (TWIK)-related K+ channel, subfamily within the K2P family consists of mechanical channels regulated by various stimuli and binding proteins. Although TREK1 and TREK2 within the TREK subfamily share many similarities, β-COP, which was previously known to bind to TREK1, exhibits a distinct binding pattern to other members of the TREK subfamily, including TREK2 and the TRAAK (TWIK-related acid-arachidonic activated K+ channel). In contrast to TREK1, β-COP binds to the C-terminus of TREK2 and reduces its cell surface expression but does not bind to TRAAK. Furthermore, β-COP cannot bind to TREK2 mutants with deletions or point mutations in the C-terminus and does not affect the surface expression of these TREK2 mutants. These results emphasize the unique role of β-COP in regulating the surface expression of the TREK family.
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Bai, Xilian, George J. Bugg, Susan L. Greenwood, Jocelyn D. Glazier, Colin P. Sibley, Philip N. Baker, Michael J. Taggart i Gregor K. Fyfe. "Expression of TASK and TREK, two-pore domain K+ channels, in human myometrium". Reproduction 129, nr 4 (kwiecień 2005): 525–30. http://dx.doi.org/10.1530/rep.1.00442.

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Two-pore domain K+channels are an emerging family of K+channels that may contribute to setting membrane potential in both electrically excitable and non-excitable cells and, as such, influence cellular function. The human uteroplacental unit contains both excitable (e.g. myometrial) and non-excitable cells, whose function depends upon the activity of K+channels. We have therefore investigated the expression of two members of this family, TWIK (two-pore domain weak inward rectifying K+channel)-related acid-sensitive K+channel (TASK) and TWIK-related K+channel (TREK) in human myometrium. Using RT-PCR the mRNA expression of TASK and TREK isoforms was examined in myometrial tissue from pregnant women. mRNAs encoding TASK1, 4 and 5 and TREK1 were detected whereas weak or no signals were observed for TASK2, TASK3 and TREK2. Western blotting for TASK1 gave two bands of approximately 44 and 65 kDa, whereas TREK1 gave bands of approximately 59 and 90 kDa in myometrium from pregnant women. TASK1 and TREK1 immunofluorescence was prominent in intracellular and plasmalemmal locations within myometrial cells. Therefore, we conclude that the human myometrium is a site of expression for the two-pore domain K+channel proteins TASK1 and TREK1.
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Afzali, Ali M., Tobias Ruck, Alexander M. Herrmann, Janette Iking, Claudia Sommer, Christoph Kleinschnitz, Corinna Preuβe i in. "The potassium channels TASK2 and TREK1 regulate functional differentiation of murine skeletal muscle cells". American Journal of Physiology-Cell Physiology 311, nr 4 (1.10.2016): C583—C595. http://dx.doi.org/10.1152/ajpcell.00363.2015.

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Two-pore domain potassium (K2P) channels influence basic cellular parameters such as resting membrane potential, cellular excitability, or intracellular Ca2+-concentration [Ca2+]i. While the physiological importance of K2P channels in different organ systems (e.g., heart, central nervous system, or immune system) has become increasingly clear over the last decade, their expression profile and functional role in skeletal muscle cells (SkMC) remain largely unknown. The mouse SkMC cell line C2C12, wild-type mouse muscle tissue, and primary mouse muscle cells (PMMs) were analyzed using quantitative PCR, Western blotting, and immunohistochemical stainings as well as functional analysis including patch-clamp measurements and Ca2+ imaging. Mouse SkMC express TWIK-related acid-sensitive K+ channel (TASK) 2, TWIK-related K+ channel (TREK) 1, TREK2, and TWIK-related arachidonic acid stimulated K+ channel (TRAAK). Except TASK2 all mentioned channels were upregulated in vitro during differentiation from myoblasts to myotubes. TASK2 and TREK1 were also functionally expressed and upregulated in PMMs isolated from mouse muscle tissue. Inhibition of TASK2 and TREK1 during differentiation revealed a morphological impairment of myoblast fusion accompanied by a downregulation of maturation markers. TASK2 and TREK1 blockade led to a decreased K+ outward current and a decrease of ACh-dependent Ca2+ influx in C2C12 cells as potential underlying mechanisms. K2P-channel expression was also detected in human muscle tissue by immunohistochemistry pointing towards possible relevance for human muscle cell maturation and function. In conclusion, our findings for the first time demonstrate the functional expression of TASK2 and TREK1 in muscle cells with implications for differentiation processes warranting further investigations in physiologic and pathophysiologic scenarios.
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Blin, Sandy, Ismail Ben Soussia, Eun-Jin Kim, Frédéric Brau, Dawon Kang, Florian Lesage i Delphine Bichet. "Mixing and matching TREK/TRAAK subunits generate heterodimeric K2P channels with unique properties". Proceedings of the National Academy of Sciences 113, nr 15 (28.03.2016): 4200–4205. http://dx.doi.org/10.1073/pnas.1522748113.

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The tandem of pore domain in a weak inwardly rectifying K+ channel (Twik)-related acid-arachidonic activated K+ channel (TRAAK) and Twik-related K+ channels (TREK) 1 and TREK2 are active as homodimers gated by stretch, fatty acids, pH, and G protein-coupled receptors. These two-pore domain potassium (K2P) channels are broadly expressed in the nervous system where they control excitability. TREK/TRAAK KO mice display altered phenotypes related to nociception, neuroprotection afforded by polyunsaturated fatty acids, learning and memory, mood control, and sensitivity to general anesthetics. These channels have emerged as promising targets for the development of new classes of anesthetics, analgesics, antidepressants, neuroprotective agents, and drugs against addiction. Here, we show that the TREK1, TREK2, and TRAAK subunits assemble and form active heterodimeric channels with electrophysiological, regulatory, and pharmacological properties different from those of homodimeric channels. Heteromerization occurs between all TREK variants produced by alternative splicing and alternative translation initiation. These results unveil a previously unexpected diversity of K2P channels that will be challenging to analyze in vivo, but which opens new perspectives for the development of clinically relevant drugs.
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Hermanstyne, T. O., K. Markowitz, L. Fan i M. S. Gold. "Mechanotransducers in Rat Pulpal Afferents". Journal of Dental Research 87, nr 9 (wrzesień 2008): 834–38. http://dx.doi.org/10.1177/154405910808700910.

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The hydrodynamic theory suggests that pain associated with stimulation of a sensitive tooth ultimately involves mechanotransduction as a consequence of fluid movement within exposed dentinal tubules. To determine whether putative mechanotransducers could underlie mechanotransduction in pulpal afferents, we used a single-cell PCR approach to screen retrogradely labeled pulpal afferents. The presence of mRNA encoding BNC-1, ASIC3, TRPV4, TRPA1, the α, β, and γ subunits of ENaC, and the two pore K+ channels (TREK1, TREK2) and TRAAK were screened in pulpal neurons from rats with and without pulpal inflammation. ASIC3, TRPA1, TREK1, and TREK2 were present in ~67%, 64%, 14%, and 10% of pulpal neurons, respectively. There was no detectable influence of inflammation on the proportion of neurons expressing these mechanotransducers. Given that the majority of pulpal afferents express ASIC3 and TRPA1, our results raise the possibility that these channels may be novel targets for the treatment of dentin sensitivity.
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Peng, Yuanzhi, Qingqing Zhang, Hao Cheng, Saie Shen i Xiaojian Weng. "Activation of TREK1 Channel in the Anterior Cingulate Cortex Improves Neuropathic Pain in a Rat Model". Computational Intelligence and Neuroscience 2022 (30.09.2022): 1–6. http://dx.doi.org/10.1155/2022/1372823.

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Objective. To explore the biological function and mechanism of TREK1 in neuropathic pain. Thirty-two healthy rats and rats with sciatic nerve chronic press-fitting model (chronic constriction injury of the sciatic nerve, CCI) were selected. Western blot, immunofluorescence staining, and patch clamp technique were performed to explore the biological functions of TREK1. The expression of TREK1 was decreased in the CCI model. The TREK1 channel current in the CCI model was decreased. After local administration of TREK1 channel activator in the anterior cingulate cortex area, the pain behavior of CCI rats and the expression of TREK1 protein were reversed. The expression of TREK1 was downregulated in the ACC area of CCI rats and the current of TREK1 was decreased, which played an important role in the regulation of neuropathic pain.
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Kim, Seong-Seop, Yeonju Bae, Osung Kwon, Seung-Hae Kwon, Jong Bok Seo, Eun Mi Hwang i Jae-Yong Park. "β-COP Regulates TWIK1/TREK1 Heterodimeric Channel-Mediated Passive Conductance in Astrocytes". Cells 11, nr 20 (21.10.2022): 3322. http://dx.doi.org/10.3390/cells11203322.

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Mature astrocytes are characterized by a K+ conductance (passive conductance) that changes with a constant slope with voltage, which is involved in K+ homeostasis in the brain. Recently, we reported that the tandem of pore domains in a weak inward rectifying K+ channel (TWIK1 or KCNK1) and TWIK-related K+ channel 1 (TREK1 or KCNK2) form heterodimeric channels that mediate passive conductance in astrocytes. However, little is known about the binding proteins that regulate the function of the TWIK1/TREK1 heterodimeric channels. Here, we found that β-coat protein (COP) regulated the surface expression and activity of the TWIK1/TREK1 heterodimeric channels in astrocytes. β-COP binds directly to TREK1 but not TWIK1 in a heterologous expression system. However, β-COP also interacts with the TWIK1/TREK1 heterodimeric channel in a TREK1 dependent manner and enhances the surface expression of the heterodimeric channel in astrocytes. Consequently, it regulates TWIK1/TREK1 heterodimeric channel-mediated passive conductance in astrocytes in the mouse brain. Taken together, these results suggest that β-COP is a potential regulator of astrocytic passive conductance in the brain.
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Royal, Perrine, Pablo Ávalos Prado, Brigitte Wdziekonski i Guillaume Sandoz. "Canaux potassiques à deux domaines P (K2P) et migraine". Biologie Aujourd'hui 213, nr 1-2 (2019): 51–57. http://dx.doi.org/10.1051/jbio/2019020.

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La migraine est un désordre neurologique qui affecte 15 % de la population mondiale. Les crises migraineuses sont liées, entre autres, à l’hyperexcitabilité électrique des neurones trigéminaux. Leur activité électrique est contrôlée par les canaux potassiques à deux domaines P (K2P) dont l’importance dans l’induction du contrôle de l’excitabilité a récemment été mise en évidence par la découverte d’une version mutée de l’un d’eux TRESK, le mutant TRESK-MT, qui est lié à la migraine. Cette découverte a été controversée à la suite du séquençage d’autres canaux TRESK mutés non fonctionnels qui ne sont pas liés à la migraine. Notre étude montre que les mutations délétères du gène TRESK impliquées dans la migraine entraînent la formation de deux protéines au lieu d’une (comme attendu du gène non muté), via un nouveau mécanisme appelé fsATI (initiation alternative de la traduction induite par déplacement du cadre de lecture). L’une est inactive et l’autre, en ciblant d’autres canaux K2P, TREK1 et TREK2, stimule fortement l’activité électrique des neurones provoquant ainsi des crises migraineuses. Cette découverte a permis l’identification de deux nouvelles cibles dans le traitement de la migraine, TREK1 et TREK2, et suggère que les mutations induisant une traduction alternative due à un déplacement du cadre de lecture (fsATI) doivent être considérées comme une classe distincte de mutations lors de l’étude des mutations impliquées dans les pathologies humaines.
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Brohawn, Stephen G. "How ion channels sense mechanical force: insights from mechanosensitive K2P channels TRAAK, TREK1, and TREK2". Annals of the New York Academy of Sciences 1352, nr 1 (31.08.2015): 20–32. http://dx.doi.org/10.1111/nyas.12874.

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Rozprawy doktorskie na temat "TREK1"

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Walsh, Yvonne. "Pharmacological regulation of TREK1, TREK2 and TRESK two pore domain potassium channels". Thesis, University of Kent, 2017. https://kar.kent.ac.uk/68081/.

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Introduction: Two pore domain potassium (K2P) channels are responsible for background currents that regulate membrane potential and neuronal excitability. Compounds which alter the activity of these channels are predicted to have therapeutic potential in treating CNS disorders. Members of the TREK family of K2P channels (TREK1 and TREK2) have been shown to play an active role in neuroprotection, depression and pain, whilst TRESK, with high expression in sensory neurons, has a role in nociception. Sipatrigine, a neuroprotective agent and a derivative of the anticonvulsant lamotrigine, is a known antagonist of TREK channels whilst lamotrigine is thought to primarily inhibit TRESK channels. A new compound, Cen-092-C, has also been developed which is structurally similar to lamotrigine. However, its effects on K2P channels are unknown. To understand the mechanism of channel inhibition by drugs, the structure of TREK2 was solved and was co-crystallised with norfluoxetine. This showed that fenestration sites were important in channel and current inhibition. Furthermore, TRESK docking studies showed that F145 and F352 function in a similar way to TREK2 fenestration site, as the bulky phenylalanine faces into the pore, and are thought to be important for compound binding. The aim of this study is to clarify to differences in the inhibitory effect of these compounds on the selected K2P channels and to investigate the mechanism by which these compounds inhibit the channels current. Methods: Wild-type (WT) and mutated human K2P channels were transiently expressed in tsA-201 cells. The currents were measured using whole-cell patch-clamp electrophysiology. Results: Sipatrigine was shown to inhibit both TREK1 and TREK2 current. Lamotrigine was also found to inhibit TREK1 and to a lesser extent TREK2. Cen-092-C was found to be less effective on TREK1 and TRESK current compared to sipatrigine, but similar to lamotrigine results. The sipatrigine inhibitory effect, but not lamotrigine, was reduced by mutations on the M4 region at the fenestration site of TREK1 and TREK2 (L286 and L320). This sensitivity is selective at this site as other mutations in the central cavity showed no change in sipatrigine inhibition. Interestingly, the gain-of-function mutation (TREK1 E306A) on the C terminus showed a reduced sipatrigine inhibition. The effect of sipatrigine on TREK2 showed an over-recovery of current following wash-off of the compound. The wash-off current increase was not seen if the N-terminus length is forced into intermediate and short isoform. Sipatrigine inhibition was significantly decreased when the N-terminus was truncated. Sipatrigine has been shown to strongly inhibit TRESK. Lamotrigine was seen to inhibit TRESK current, however significantly less effective compared to sipatrigine. Furthermore, lamotrigine did show state dependent inhibition when TRESK is in the fixed activated state. Cen-092-C was also found to inhibit TRESK to a similar degree to lamotrigine, however there was no state dependent inhibition on TRESK current. The effects of these antagonists on TRESK has been shown to be abolished by mutations on two sites at the central cavity (F145 and F352). Conclusion: Lamotrigine was found not to be TRESK selective, contrary to other studies. Sipatrigine and lamotrigine inhibition works through binding to the channel. The fenestration site in both TREK1 and TREK2 has been found to be an important binding site of sipatrigine, differing from lamotrigine. This suggests that the structurally similar compounds bind to different regions of the TREK channels. Furthermore, the over recovery of TREK2 current after sipatrigine wash off is believed to show the compound's biphasic effect, where the underlying enhancement of current is hidden by the action of inhibition. The N-terminus is therefore believed to be important in regulating sipatrigine action on TREK2. It remains unclear whether the TRESK potential binding sites (F1452 and F352) are important in compound binding as the inserted mutation is believed to shift the channel to constant active state. The newly developed compound Cen-092-C shows a significantly greater degree of inhibition of TRESK when compared to TREK1. Cen-092-C and lamotrigine inhibition of TRESK is not significantly different. Lamotrigine inhibition of TRESK current is state dependent whereas sipatrigine and Cen-092-C inhibition of TRESK current is shown as state independent. All of this together could lead to a better understanding of how neuroprotective agents effect TREK and TRESK channels and could contribute to the design of more efficient ligands.
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SATO, Jun, Kazue MIZUMURA, Ken TAKAHASHI, Kimiaki KATANOSAKA i Yasuko KOZAKI. "Increased C-fiber Activities to Cold in Adjuvant-monoarthritic Rats was not Accompanied by Increased Expression of TREK1 and CMR1 mRNAs(RIEM Conference II, 2002)". Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2809.

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Dolcemascolo, Axel. "Laser à semi-conducteur pour modéliser et contrôler des cellules et des réseaux excitables". Thesis, Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4208/document.

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Les systèmes « excitables » sont omniprésents dans la nature, le plus paradigmatique d'entre eux étant le neurone, qui répond de façon « tout ou rien » aux perturbations externes. Cette particularité étant clairement établie comme l'un des points clé pour le fonctionnement des systèmes nerveux, son analyse dans des systèmes modèles (mathématiques ou physiques) peut d'une part aider à la compréhension de la dynamique d'ensembles de neurones couplés et d'autre part ouvrir des voies pour un traitement neuromimétique de l'information. C'est dans cette logique que s'inscrit la préparation de cette thèse de doctorat. Dans ce mémoire, nous utilisons des systèmes basés sur des lasers à semiconducteur pour d'une part modéliser des systèmes excitables ou des ensembles de systèmes neuromimétiques couplés et d'autre part pour contrôler (grâce à l'optogénétique) des canaux ioniques impliqués dans l'émission de potentiels d'action par des neurones de mammifères. Le long du premier chapitre, nous présentons de manière synthétique les concepts dynamiques sur lesquels nous nous appuierons dans la suite du manuscrit. Par la suite, nous décrivons brièvement le contexte de ce travail du point de vue de la synchronisation, notamment de cellules excitables. Enfin, nous discutons le contexte applicatif potentiel de ces travaux, c’est-à-dire l'utilisation de systèmes photoniques dits « neuromimétiques » dans le but de traiter de l'information. Dans le chapitre 2, nous analysons tout d'abord du point de vue théorique et bibliographique le caractère excitable d'un laser à semiconducteur sous l'influence d'un forçage optique cohérent. Par la suite, nous détaillons nos travaux expérimentaux d'abord, puis numériques et théoriques, sur la réponse de ce système « neuromimétique » à des perturbations répétées dans le temps. Tandis que le modèle mathématique simplifié prévoit un comportement de type intégrateur en réponse a des perturbations répétées, nous montrons que le comportement est en fait souvent résonateur, ce qui confère à ce système la propriété étonnante d'émettre une impulsion seulement s'il reçoit deux perturbations séparées d'un intervalle de temps bien précis. Nous montrons également que ce système peut convertir des perturbations de différente intensité en une série d'impulsions toutes identiques mais dont le nombre dépend de l'intensité de la perturbation incidente. Dans le chapitre 3, nous analysons (de nouveau expérimentalement, puis numériquement et théoriquement) le comportement dynamique d'un réseau de lasers à semiconducteur couplés dans un régime de chaos lent-rapide. Nous nous basons sur une étude antérieure montrant qu'un seul de ces éléments peut présenter une dynamique neuromimétique (en particulier l'émission chaotique d'impulsions originant du phénomène de canard). De façon surprenante pour un système ayant un si grand nombre de degrés de liberté, nous observons une dynamique qui semble chaotique de basse dimension. Nous examinons l'impact des propriétés statistiques de la population considérée sur la dynamique et relions nos observations expérimentales et numériques à l'existence d'une variété critique calculable analytiquement pour le champ moyen et près duquel converge la dynamique grâce au caractère lent-rapide du système. Dans le chapitre 4 enfin, nous présentons une brève étude expérimentale de la réponse de cellules biologiques à des perturbations lumineuses. En effet, les techniques optogénétiques permettent de rendre des cellules (en particulier des neurones) sensibles à la lumière grâce au contrôle optique de l'ouverture et de la fermeture de canaux ioniques. Ainsi, après avoir étudié dans les chapitres précédents des systèmes optiques sur la base de considérations provenant de systèmes biologiques, nous amenons matériellement un système laser vers un système biologique
Excitable systems are everywhere in Nature, and among them the neuron, which responds to an external stimulus with an all-or-none type of response, is often regarded as the most typical example. This excitability behaviour is clearly established as to be one of the underlying operating mechanisms of the nervous system and its analysis in model systems (being them mathematical of physical) can, from one hand, shed some light on the dynamics of neural networks, and from the other, open novel ways for a neuro-mimetic treatment of information. The work presented in this PhD thesis was realized in this perspective. In this dissertation we will consider systems based on semiconductor lasers both for modelling excitable systems or coupled neuromorphic networks and for controlling (in an optogenetic outlook) ionic channels that are involved in the emission of action potentials of neurons in mammals. During the first chapter, we will briefly present the dynamical concepts on which we will build our understanding for the rest of the manuscript. Thereafter, we will describe the context of this work from the point of view of synchronized systems, in particular excitable cells. Finally, we will discuss in this context the applications potential of this work, namely the possibility of using “neuromimetic” photonic systems as a was to treat information. In chapter 2 we will firstly analyse from a theoretical and bibliographical standpoint the excitable character of a laser with coherent injection. Later, we will firstly detail our results, firstly experimental and subsequently numerical and theoretical, on the response of this “neuromimetic” system to perturbations repeated in time. Whereas the simplified mathematical model envisions an integrator behaviour in response to repeated perturbations, we will show that the system often acts as a resonator, thus imparting the remarkable property of being able to emit a single pulse only if it receives two perturbations that are separated by a specific time interval. We will also illustrate how this system can convert perturbations of different intensity in a series of all identical pulses whose number depends on the intensity of the incoming perturbation. In the third chapter we will analyse, first experimentally and later numerically and theoretically, the dynamical behaviour of a network of coupled semiconductor lasers in a slow-fast chaotic regime. We will rely on a previous study documenting that a single such element can present a neuromimetic dynamics (in particular, the emission of chaotic pulses originating from a canard phenomenon). Surprisingly for a system having such a large number of degrees of freedom, we observe a dynamics which seems low dimensional chaotic. We will examine the impact of statistical properties of the selected population on the dynamics, and we will link our experimental and numerical observations to the existence of a slow manifold for the mean field, computable analytically, and towards whom the dynamics converges thanks to the slow-fact nature of the system. Finally, in chapter 4 we will present a short experimental study on the response of biological cells to light perturbations. Indeed, optogenetic techniques enables to render the cells (in particular neurons) sensitive to light due to the optical control of the opening and closing of ionic channels. Hence, after having studied in the previous chapters optical systems on the basis of observations derived from biological systems, we will physically transfer an optical system towards a biological one. Here we lay the groundwork of a photonic system which allows, with a moderate complexity, to realize cell measurements in response to spatially localized optical perturbations
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Schön, Anna. "Utopia Trek : utopibegreppets resa genom Star Trek". Thesis, Linköping University, Department of Thematic Studies, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-2539.

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Humanity has always dreamed about a better world. These dreams has manifested themselves in the vision of Utopia - the good place, but also the non-existing place. Up until World War II man still wrote optimistic descriptions of this ideal world, and spread the idea through literature. In the aftermath of the atomic bomb and under the influence of the cold war, these publications seized to surface in literary surroundings. Despite this utopia did not die - it has only changed. Today you can find utopia, not primarily in books, but in Science Fiction. TV’s biggest Science Fiction-series, Star Trek, is perhaps the best example of this. The Master's thesis "Utopia Trek - a travel through Star Trek with the concept of utopia" takes you through the history of utopia and into its new habitat, Star Trek, where the essence of a utopia for the 21th century is found, discussed and reevaluated.


Mänskligheten har alltid drömt om en bättre värld. Dessa drömmar har manifesterats i visionen om Utopia - den goda platsen, men också platsen som inte existerar. Fram till andra världskriget skrev man fortfarande optimistiska beskrivningar av denna idealvärld, och spred idén via litteraturen. Efter hotet från atombomben och under påverkan av det kalla kriget, slutade dessa publikationer att dyka uppi litterära sammanhang. Trots detta dog inte drömmen utopia - det har bara förändrats. Idag kan man finna utopia, inte företrädesvis i böcker, utan i science fiction. Tv:s största science fiction-serie, Star Trek, är kanske det bästa exemplet på detta. Magisteruppsatsen "Utopia Trek - utopibegreppets resa genom Star Trek" tar dig genom utopias historia och in i dess nya hemvist, Star Trek, där essensen av ett utopia för 2000-talet upptäcks, diskuteras och omvärderas.

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Geraghty, Lincoln. "Living with Star Trek : utopia, community, self-improvement and the Star Trek universe". Thesis, University of Nottingham, 2005. http://eprints.nottingham.ac.uk/10982/.

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Living with Star Trek investigates the connections between Star Trek fandom and the Star Trek text. This study identifies and examines the American themes of utopia, community and self-improvement inherent within the fictional text which also form the thematic framework for letters written by fans to express their affection for the series. These letters represent a `network of support', whereby a community of fans is able to communicate with each other through written correspondence sent to producers, edited collections, and fan magazines. In talking about the series, fans confess and share intimate stories, often based around trauma or bereavement, and at the same time describe how Star Trek has played an important and inspirational part in their daily lives; Star Trek's utopian vision and communal spirit has given them the impetus to enact positive change. Drawing together the themes identified in the text and fan letters, the first half of the thesis examines Star Trek's use of history, narrative and myth to tell its futuristic stories. In particular, I examine how Star Trek has used the distinctive literary tradition of the Puritan American Jeremiad to create a didactic narrative that emphasises the attainment of utopia through communal effort and personal change. The second half of the thesis continues this inquiry by examining a range of letters that describe how fans are able to tap into the open nature of the Star Trek text and use it to fulfil needs and desires in their own daily lives. In particular, I stress how the letters are not just examples of fan affection but also represent a reciprocal relationship where fans can criticise and engage with the programme as well as use it as a form of motivation.
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Valverde, Estrella Lorena. "TREX1 and SAMHD1, and Aicardi-Goutières Syndrome". Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/291940.

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Aicardi-Goutières Syndrome (AGS) is a rare encephalopathy which mimics a viral intrauterine infection and is characterized by calcifications of the basal ganglia, cerebral atrophy and IFN-a in the cerebrospinal fluid. AGS is a heterogenic disease associated with mutations in the gene of the exonuclease TREX1, in any of the genes codifying for the ribonuclease H2, in the phosphohydrolase SAMHD1, in the deaminase ADAR1 or in the cytoplasmic sensor MDA5. The knowledge of these functions is basic for the comprehension of the beginning of the pathogenesis of AGS. In this thesis we focused in the mechanism of Samhd1 transcription. We have seen that Samhd1 is induced by pro-inflammatory stimuli but neither by anti-inflammatory stimuli nor TNF-a, and that the induction of Samhd1 is through STAT1 pathway. We wanted to know a bit more about Samhd1 induction so we focused on the study of its promoter. We did a construct in a luciferase-reporter vector with 1500bp of Samhd1 promoter, and we saw that this region of the promoter is enough to induce luciferase expression. From this construct, we did new plasmids and when deleting a specific region, the luciferase expression was abolished, indicating that in Samhd1 promoter, 161bp are critical for Samhd1 induction. EMSA assays showed that Samhd1 expression is repressed in basal conditions by an unknown protein, and ChIP assays also showed that IRF1 is involved in Samhd1 induction by IFN-.. We hypothesized that the regulation mechanism is depending in an STAT1-depending pathway, through IRF1, and also in an STAT1-independing pathway, through an unknown mechanism up to date. We checked with proteomics analysis the protein which might be involved in Samhd1 repression but the results were not significant. We also constructed a conditional KO mouse for TREX1, and now we are crossing it with different CRE­Socs2 expressing strands. Homozygous KO expressing CRElitter, show a similar phenotype to TREX1 total KO. We are in the process to obtain homozygous KO expressing CRELysM, but due to problems with the penetrance of this CRE allele we have some difficulties. All together, the results of this thesis will shed light in the inner operation of AGS.
La síndrome d'Aicardi-Goutières (AGS), és una malaltia autoimmunitària recessiva que mimetitza una infecció vírica intrauterina, i la qual és caracteritzada per calcificacions intracranials, atròfia cerebral i augment d'IFN-alfa al líquid cefaloraquidi. L'AGS és una malaltia genètica heterogènia associada amb mutacions al gen que codifica per a l'exonucleasa TREX1, a qualsevol dels gens codificants per a les components de la ribonucleasa RNASE H2, a la fosfo­hidrolasa SAMHD1, a la deaminasa ADAR1 o al sensor citoplasmàtic MDA5. El coneixement d'aquestes funcions és fonamental per tal d'entendre la patogènesi de l'AGS. En aquesta tesi s'ha aprofundit en el coneixement del mecanisme regulador de la transcripció de Samhd1. Hem vist que Samhd1 es troba expressat en diferents òrgans sense necessitat de cap estímul previ, com el pàncrees, l’intestí prim i els macròfags derivats de moll d’os, i en diferents quantitats en altres òrgans de ratolí. Donada la important afectació que té l’AGS al cervell, també es va analitzar la seva expressió en neurones i cèl·lules de la micròglia. També hem vist que Samhd1 es troba induït en presència de citocines proinflamatòries, però no es troba afectada la seva expressió en presència de citocines antiinflamatòries així com tampoc en presència de TNF-gamma. Utilitzant macròfags derivats de ratolins deficients en STAT1, hem pogut demostrar que l’expressió de Samhd1 per IFN-alfa és a través d’STAT1, ja que la seva expressió es troba completament reprimida en aquestes cèl·lules. Ens vam centrar en la inducció de Samhd1 i per la seva comprensió vam focalitzar en l’estudi del seu promotor. Es van clonar 1500 parells de bases del promotor de Samhd1 en un plasmidi reporter de luciferasa, i es va veure que aquest fragment era suficient per induir l’expressió de luciferasa. A partir d’aquest constructe, es van realitzar llavors noves construccions delecionant cada vegada una regió del promotor. Es va veure que en delecionar una regió específica de 161pb, l’expressió de luciferasa es trobava completament reprimida, indicant que aquesta regió del promotor és crítica per a la inducció de Samhd1. Experiments de retard en gel (EMSA) van mostrar que Samhd1 es troba reprimit en condicions basals per una proteïna que no hem arribat a caracteritzar, i experiments de precipitació de cromatina (ChIP) van mostrar que IRF1 es troba involucrada en la inducció de Samhd1 per IFN-alfa. La nostra hipòtesi doncs, és que l’expressió de Samhd1 té un mecanisme de regulació doble: en condicions basals es troba reprimit i en presència d’IFN-alfa s’indueix una via de senyalització independent d’STAT1 que fa saltar el complex repressor del promotor, i també s’indueix una via de senyalització dependent d’STAT1, que indueix l’expressió d’IRF1 i que activa la transducció de Samhd1. Fins ara no hem caracteritzat la proteïna o complex de proteïnes que reprimeix l’expressió de Samhd1 en condicions basals, però s’està investigant mitjançant anàlisis proteòmics. En aquesta tesi també s’ha fet la construcció d’un ratolí KO condicional per a TREX1. Una vegada aconseguit aquest animal condicional, el qual conté el gen de Trex1 flanquejat per dues dianes LoxP, aquest s’està encreuant amb diferents soques que expressen CRE sota regulació de diferents Socs2 promotors. Els ratolins homozigots KO i que expressen CRE, tenen un fenotip similar al fenotip que mostren els ratolins KO totals de TREX1. Estem en el procés d’obtenció de ratolins homozigots KO i que expressen CRELysM però, donat a problemes amb la penetrància d’aquest al·lel, hem tingut algunes dificultats. Els resultats d’aquesta tesi en conjunt poden ajudar a entendre una mica més el funcionament de l'AGS.
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Roy, André 1963. "Une lecture politique de Star trek /". Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61800.

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Hawkey, Kate. "Beginning and becoming : a narrative trek". Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.684911.

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In chapter one I present a history and critique of the articles which comprise my PhD looking at each article in turn. There are two main sets of articles included and I set out how one area of interest developed into the next. The work focuses on the theme of mentoring and then history education. Together they represent my concern with a community of.practice within the history teaching profession. In chapter one I explain the contextual history in the development of my ideas and thinking between the articles and demonstrate how together they form a coherent whole. The chapter is presented as a story, something of a personal narrative, placing my own development over the years of my PhD at the centre. The chapter also includes a critical update on the themes raised in the articles along with my ongoing critical reflections. In chapter two I examine the ontology, epistemology and methodology which underpin my PhD articles. Again I present the story of my own introduction to educational research to assist in explaining the approaches adopted. The shift from history graduate and history teacher to researcher in education is examined and the place of story and narrative in educational research is also examined.
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Lyons, Reneé C. "Trips and Treks: Teaching Endangered Species Through Literature". Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etsu-works/2367.

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Innamaa, Anni. "Expression and function of the two pore potassium (K2P) channels TREK-1, TREK-2 and TASK-3 in ovarian cancer". Thesis, University of Nottingham, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606812.

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Aberrant expression of potassium (K+) channels contributes to cancer cell proliferation and in certain circumstances channel blockade has been shown to inhibit cell proliferation. Two pore potassium (K2P) channels are the most recently identified group of K+ channels. K2P channels have been found to play a role in several cancers including prostate and breast cancer. We investigated the K2P channels TREK-1, TREK-2 and TASK-3, in ovarian cancer and normal ovaries and described the effect of channel blockade on cell proliferation, the cell cycle and apoptosis. Immunofluorescence confirmed expression in the cell lines (n=3) normal ovaries (n=4) and ovarian cancer (n=4). Western blotting quantified channel expression in normal ovaries (n=6) and cancer (n=22). There appeared to be a significant increase in expression of TREK-1 (P=O.0019) and TASK-3 (P=O.0047) in cancer when compared to normal ovaries. Immunohistochemistry further established expression in ovarian cancer (TREK-1 and -2, n=69) and normal ovaries (n=9) and in the TMA (TASK-3 n=230). Increased TASK-3 immunostaining conferred a significant survival advantage (P=O.001). There was a significant (P
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Książki na temat "TREK1"

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Trek. London: Corgi, 2007.

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Paul, Stewart. Trek. London: Cape, 1991.

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Trek. Rearsby: W F Howes, 2009.

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London, Jack. Serdt︠s︡a trekh. Kharʹkov: Folio, 1998.

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Norris, Dorothy Tinnin. Tinnin treks. Houston, Mo: D.T. Norris, 1989.

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Dunham, Judith. Backcountry treks. Singapore: Discovery Communications, 2000.

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Merezhkovsky, Dmitry Sergeyevich. Taĭna trekh. Moskva: Izd-vo "Respublika", 1999.

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Judith, Dunham, red. Backcountry treks. Bethesda, MD: Discovery Communications, 2000.

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Dunham, Judith. Backcountry treks. Singapore: Discovery Communications, 2000.

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Chernomorskiĭ flot v trekh voĭnakh i trekh revoli︠u︡t︠s︡ii︠a︡kh. Moskva: AST, 2007.

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Części książek na temat "TREK1"

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Šiljak, Harun. "Normed Trek". W Murder on the Einstein Express and Other Stories, 3–10. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-29066-9_1.

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Dewdney, Alexander Keewatin. "The Trek". W The Planiverse, 83–106. New York, NY: Springer New York, 2000. http://dx.doi.org/10.1007/978-1-4613-0199-8_6.

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Tahan, Mary R. "Snow Trek". W Roald Amundsen’s Sled Dogs, 387–414. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-02692-9_29.

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Artzt, Karen, i Jiang I. Wu. "Star Trek". W Advances in Experimental Medicine and Biology, 1–24. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7005-3_1.

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Hark, Ina Rae. "Trekker’s Log, Stardate 1908200.7". W Star Trek, 1–7. London: British Film Institute, 2008. http://dx.doi.org/10.1007/978-1-349-92226-0_1.

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Hark, Ina Rae. "Course Plotted and Laid In". W Star Trek, 8–20. London: British Film Institute, 2008. http://dx.doi.org/10.1007/978-1-349-92226-0_2.

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Hark, Ina Rae. "Star Trek: This Side of Paradise". W Star Trek, 21–57. London: British Film Institute, 2008. http://dx.doi.org/10.1007/978-1-349-92226-0_3.

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Hark, Ina Rae. "Star Trek: The Next Generation: The Best of Both Worlds". W Star Trek, 58–87. London: British Film Institute, 2008. http://dx.doi.org/10.1007/978-1-349-92226-0_4.

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Hark, Ina Rae. "Star Trek: Deep Space Nine: Necessary Evil". W Star Trek, 88–115. London: British Film Institute, 2008. http://dx.doi.org/10.1007/978-1-349-92226-0_5.

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Hark, Ina Rae. "Star Trek: Voyager: Time and Again". W Star Trek, 116–34. London: British Film Institute, 2008. http://dx.doi.org/10.1007/978-1-349-92226-0_6.

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Streszczenia konferencji na temat "TREK1"

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Fickas, Stephen, McKay Sohlberg i Jason Prideaux. "TREK". W the 7th international conference. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1463689.1463717.

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Marques, Leonardo, Mauro Amazonas, Thais Castro, Willian Assuncao, Luciana Zaina, Bruno Gadelha i Tayana Conte. "UX trek". W IHC '20: XIX Brazilian Symposium on Human Factors in Computing Systems. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3424953.3426547.

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Sinnott, Richard O. "Cloud Trek". W UCC '17: 10th International Conference on Utility and Cloud Computing. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3147213.3155014.

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Horta, Edson, Ho-Ren Chuang, Naarayanan Rao VSathish, Cesar Philippidis, Antonio Barbalace, Pierre Olivier i Binoy Ravindran. "Xar-trek". W Middleware '21: 22nd International Middleware Conference. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3464298.3493388.

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Balan, V. "CMP-Stack Trek". W 2016 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 2016. http://dx.doi.org/10.7567/ssdm.2016.k-2-01.

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Datz, Suzanne. "Star Trek---the experience". W ACM SIGGRAPH 97 Visual Proceedings: The art and interdisciplinary programs of SIGGRAPH '97. New York, New York, USA: ACM Press, 1997. http://dx.doi.org/10.1145/259081.259492.

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Dudak, Celal, Emrah Oncu, Koray Karakus, Neslin Ismailoglu i Volkan Akan. "Variations on the theme of TREKS-823". W 2013 6th International Conference on Recent Advances in Space Technologies (RAST). IEEE, 2013. http://dx.doi.org/10.1109/rast.2013.6581297.

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Shimizu, Suguru. "Active polarimeter system for TREK experiment". W 2009 KAON International Conference. Trieste, Italy: Sissa Medialab, 2010. http://dx.doi.org/10.22323/1.083.0016.

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Djalali, Chaden, i TREK Collaboration. "The TREK program at J-PARC". W IX LATIN AMERICAN SYMPOSIUM ON NUCLEAR PHYSICS AND APPLICATIONS. AIP, 2012. http://dx.doi.org/10.1063/1.3688817.

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Kohl, M., i TREK Collaboration. "The TREK/E36 experiment at J-PARC". W WORKSHOP TO EXPLORE PHYSICS OPPORTUNITIES WITH INTENSE, POLARIZED ELECTRON BEAMS AT 50-300 MEV. AIP, 2013. http://dx.doi.org/10.1063/1.4829396.

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Raporty organizacyjne na temat "TREK1"

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Bruce Ohme. Deep Trek High Temperature Electronics Project. Office of Scientific and Technical Information (OSTI), lipiec 2007. http://dx.doi.org/10.2172/923033.

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Bruce Ohme i Michael Johnson. Deep Trek Re-configurable Processor for Data Acquisition (RPDA). Office of Scientific and Technical Information (OSTI), czerwiec 2009. http://dx.doi.org/10.2172/982893.

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Desilets, Y., M. Fafard, M. Lasserre, S. Lebeau, M J Manore i B. Ramsay. RADARSAT Helps High-Tech Trek to the Magnetic North Pole. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1996. http://dx.doi.org/10.4095/218978.

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Kohl, Michael. Closeout Report - Search for Time Reversal Symmetry Violation with TREK at J-PARC. Office of Scientific and Technical Information (OSTI), kwiecień 2015. http://dx.doi.org/10.2172/1212319.

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Kevin D. Edgley, Fred L. Sabins i Larry T. Watters. Supercement for Annular Seal and Long-Term Integrity in Deep, Hot Wells "Deep Trek". Office of Scientific and Technical Information (OSTI), sierpień 2005. http://dx.doi.org/10.2172/908315.

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Frykman, P. N., E. A. Harman, J. F. Patton, P. K. Opstad i R. W. Hoyt. Effects of a World Record Unsupported Ski Trek Across Greenland (The G2 Expedition) on Physical Performance and Body Composition. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2001. http://dx.doi.org/10.21236/ada396385.

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Njå, Ove, i Kirsti Russell Vastveit. Norske kommuners planlegging, gjennomføring og bruk av risiko- og sårbarhetsanalyse i forbindelse med samfunnssikkerhetsarbeidet. University of Stavanger, październik 2016. http://dx.doi.org/10.31265/usps.164.

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I prosjektet; «Helhetlig ROS-analyse i norske kommuner» analyserer vi hvordan kommuner utvikler, bruker og oppdaterer ROS-analyser og risikoforestillinger i sitt samfunnssikkerhetsarbeid. Det legges vekt på hvordan kommuner integrerer ROS-arbeidet og risikoforestillinger i eksisterende plan- og arbeidsprosesser. Hvilke utfordringer opplever kommunene i dette arbeidet? Etter å ha jobbet med risiko og sikkerhet i mer enn 20 år, og en vesentlig del av disse opp mot kommuner, er det etter vårt syn et gjennomgående trekk at kommunalt ansatte som jobber med sikkerhet og beredskap har stor skepsis til akademikere på dette feltet. Den teoretiske «verden» er ikke i stand til å kommunisere med den praktiske og vice versa. Denne utfordringen mener vi står sterkt også i dag, og dermed ble det i prosjektet viktig å finne ut hvordan begrepene ble brukt i kommunene. Hvor kritiske er begrepene for omfanget av bruken av analysene? Står vi ved et markant skille nå med innføring av ny veileder for helhetlig ROS-analyse i kommuner? Eller, er arbeidet omkring samfunnssikkerhet og beredskap fastnet i en praksis uten påvirkning fra ROS-analyse? Datamateriale fra 26 kommuner er inkludert i studien. Kommunene dekker alle landsdelene og de har varierte demografiske og geografiske profiler. Blant deltagerne er kommuner med storulykkesindustri, større bykommuner, mindre øykommuner og grensekommuner. Opptil fem personer med ulikt ansvar for samfunnssikkerhets- og beredskapsarbeidet er intervjuet i hver kommune. En viktig del av prosjektet er forholdet mellom ROS-analyser på ulike forvaltningsnivåer, hvordan ROS-analysene kommuniserer risikoforestillinger og hvordan kommunene kan bygge på og hente innspill fra hverandre i ROS-analysearbeidet. Siden 2010 har Lov om kommunal beredskapsplikt, sivile beskyttelsestiltak og Sivilforsvaret (sivilbeskyttelsesloven) og underliggende Forskrift om kommunal beredskapsplikt stilt krav til kommunenes ROS-analyse og samfunnssikkerhetsarbeid i stort. Likevel er det ikke opplagt hva det innebærer. Forskriften snakker om begreper og konsepter som; - Jobbe systematisk og helhetlig med samfunnssikkerhet; - Forankring i kommunestyret; - Eksisterende og fremtidige risiko- og sårbarhetsfaktorer; - Særlige utfordringer; - Langsiktige mål, strategier, prioriteringer og plan for oppfølging av samfunnssikkerhets- og beredskapsarbeidet; - Vurdere forhold som bør integreres i planer og prosesser; og - Overordnet beredskapsplan. Det stiller store krav til kommunens ansattes kunnskap og kompetanse til å fortolke hva alle disse konseptene skal bety for kommunen og hvordan ansatte skal jobbe med kravene. Her ligger kjernen av vår studie. Studien vår viser at det legges betydelig med ressurser og arbeid ned i kommuners helhetlige ROS-analyser, samfunnssikkerhets og beredskapsarbeid. Risikoinformert styring og risikotenkning er en krevende filosofi, hvor det forutsettes at de ansatte med ansvar for kommunens systemer og samfunnssikkerhets- og beredskapsarbeidet har høy kompetanse på området. I kommunene som deltok i studien synes det å være enklere for kommunene å konkretisere hvordan de arbeidet med beredskap enn med samfunnssikkerhet. Kommunene hadde i varierende grad oversikt over hvordan beredskapsarbeidet var satt i system på tvers av etater. Materialet ble analysert ut fra fire forhold: - Begrepsforståelser og bruk av begreper for å uttrykke samfunnssikkerhet - Planlegging og gjennomføring av ROS-analyseprosesser - Presentasjon av resultater fra ROS-analysearbeidet - Implementering av analyseresultatene i kommunens aktiviteter Datamaterialet viser at kommunene og de fleste respondentene våre er i liten grad bekymret over begrepene de bruker. I hovedsak er det risiko, ROS-analyse (eller andre koplinger av ROS), hendelser, akseptkriterier, beredskap, kriseplaner og tiltak som er konseptene i bruk. Usikkerhet var et begrep som fulgte med, men det var i liten grad reflektert over utover at det var en egenskap med hele ROS-analyseprosessene. Samfunnssikkerhet, ytelse av beredskapstiltak, sårbarhet, resiliens, barrierer, system er begreper som får lite eller ingen omtale i kommunenes befatning med samfunnssikkerhet og beredskap. Kommunene er veldige instrumentelle i arbeidet med å utvikle produktene (helhetlig) ROS-analyse og beredskap- og kriseplaner. Beslutningsprosessene som den helhetlige ROS-analysen er en del av, trekkes ikke frem som førende for hvordan ROS-analyser og samfunnssikkerhetsarbeidet gjøres. Fylkesmannen sin rolle som pådriver, rådgiver og tilsynsmyndighet var for de aller fleste kommunene beskrevet med positive fortegn. Alle analysene vi har hatt tilgang til er utført som grovanalyser (hazid-gjennomganger, scenariobeskrivelser, gruppediskusjoner), men med relativt små variasjoner innenfor hvordan risiko måles og uttrykkes. Enkelte kommuner inspireres av innholdet i FylkesROS-analyse eller Nasjonalt Risikobilde, mens andre har et større fokus på lokale forhold og hendelser. I forbindelse med bruk av tiltak fra helhetlig ROS-analyse var det en klar trend at kommunene synes det var vanskelig å sikre implementering av tiltak. Dette skyldes blant annet at det var utfordrende å sikre at den ansvarlige etat tok ansvar for tiltak, at beredskapskoordinatorer ikke anså tiltak som skulle implementeres i enkeltetater som sitt ansvar og at kommunene i mange tilfeller ikke hadde midler til gjennomføring av tiltak. Problemet kan trolig også spores til at helhetlig ROS-analyse ikke var et dokument som var i aktiv bruk i hverdagen til kommunenes ansatte, og som det i de fleste tilfeller ikke ble laget aksjonsplaner for å følge opp. På tiltakssiden var det også tydelig at flere kommuner gjorde det vanskelig for seg selv, ettersom de beskrev svært generelle tiltak i rapportene sine, tiltak som egentlig var på plass i den ansvarlige etat og som var dekket av andre internkontrollrutiner, eller som andre offentlige etater var ansvarlige for. Kommunene i prosjektet hadde i varierende grad koblet beredskapsplanene sine opp mot de helhetlige ROS-analysene. En annen utfordring i forbindelse med «bruk» til beredskapsplanlegging var at kommunene ikke var sikre på hvordan dette skulle tolkes. Skulle man lage øvelser basert på hendelsene som var brukt i helhetlig ROS-analyse, skulle det lages tiltakskort som passet til scenarioene i helhetlig ROS-analyse? Enkelte kommuner hadde inkludert hendelser fra helhetlig ROS-analyse i beredskapsplanverket sitt, mens andre hadde fokusert mer på felles kapasiteter i helhetlig ROS-analyse. Å se sammenhengen mellom helhetlig ROS-analyse og beredskapsplanlegging var et vanskelig tema for kommunene. Beredskapsanalyse og vurdering av «godheten» av beredskapstiltak er også en stor utfordring. Den største utfordringen og det viktigste funnet som har kommet fram gjennom studiet er at prinsippene i risikobasert styring er nærmest fraværende i kommunene. Funksjonelle krav til sikkerhet mangler, en levende diskusjon om samfunnssikkerhet og beredskap mangler, og analysene brukes i svært liten grad. ROS-analyse og intensjoner om risikobasert styring har vært i norske kommuner i mer enn 20 år, og basert på dette mener vi at det er kompetanse og reguleringsregimet det må gjøres noe med, heller enn å innføre nye veiledere og tilsynsaktiviteter. Ansvaret for kommunens samfunnssikkerhets- og beredskapsarbeid må knyttes opp mot spesifikk kompetanse. Det krever at kommunene endrer praksis på i den administrative ledelsen og virksomhetene som eier systemene, tjenestene og aktivitetene, så vel som i kommunikasjonen mellom administrativ og politisk ledelse når det gjelder samfunnssikkerhet og beredskap. Vi mener at politikeren fra bykommune 1 langs kysten i Nord-Norge illustrerer behovet på en betegnende måte: «Veldig få i beredskapsrådet har lest dokumentene. I vårt fylke tror jeg vi er noen av de som har kommet lengst, og det sier etter mitt skjønn sitt». «Vi må involvere oss på et mye tidligere stadium. Skaffe oss oversikt over hva som er beredskapsplanene, og hvor flaskehalsene er. Det tror jeg at jeg deler med veldig mange. Vi strykes med hårene i alt for stor grad. Vi får for mye ros.»
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