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RISS 인기검색어
- 검색키워드
- 저자 : Ottersen, G. (검색결과 3 건)
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Major pathways by which climate may force marine fish populations
Ottersen, G.,Kim, S.,Huse, G.,Polovina, J.J.,Stenseth, N.Chr. Elsevier 2010 Journal of marine systems Vol.79 No.3
Climate may affect marine fish populations through many different pathways, operating at a variety of temporal and spatial scales. Climate impacts may work their way bottom up through the food web or affect higher trophic levels more directly. In this review we try to disentangle and summarize some of the current knowledge made available through the rapidly increasing literature on the topic, with particular emphasis on the work within the Global Ocean Ecosystems Dynamics (GLOBEC) programme. We first consider different classification schemes and hypotheses relating climate through physical features of the ocean to population patterns. The response of a population or community to climate may be linear or non-linear, direct or indirect. The hypotheses may be classified according to the form of physical features in operation as being related to mixing, advection or temperature. The bulk of the paper is devoted to a region-by-region presentation and discussion of examples relating climate variability to marine fish populations. It is slanted towards the North Atlantic and North Pacific, but the tropical Pacific is also covered. By means of different categorization methods we compare climate responses between ecosystems. We conclude that the use of such classification schemes allows for a more precise description of the various ecosystems particular properties and facilitates inter-regional comparison.
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On the processes linking climate to ecosystem changes
Drinkwater, K.F.,Beaugrand, G.,Kaeriyama, M.,Kim, S.,Ottersen, G.,Perry, R.I.,Portner, H.O.,Polovina, J.J.,Takasuka, A. Elsevier 2010 Journal of marine systems Vol.79 No.3
While documentation of climate effects on marine ecosystems has a long history, the underlying processes have often been elusive. In this paper we review some of the ecosystem responses to climate variability and discuss the possible mechanisms through which climate acts. Effects of climatological and oceanographic variables, such as temperature, sea ice, turbulence, and advection, on marine organisms are discussed in terms of their influence on growth, distribution, reproduction, activity rates, recruitment and mortality. Organisms tend to be limited to specific thermal ranges with experimental findings showing that sufficient oxygen supply by ventilation and circulation only occurs within these ranges. Indirect effects of climate forcing through effects on the food web are also discussed. Research and data needs required to improve our knowledge of the processes linking climate to ecosystem changes are presented along with our assessment of our ability to predict ecosystem responses to future climate change scenarios.
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PKCδ-dependent p47<i>phox</i> activation mediates methamphetamine-induced dopaminergic neurotoxicity
Dang, Duy-Khanh,Shin, Eun-Joo,Kim, Dae-Joong,Tran, Hai-Quyen,Jeong, Ji Hoon,Jang, Choon-Gon,Ottersen, Ole Petter,Nah, Seung-Yeol,Hong, Jau-Shyong,Nabeshima, Toshitaka,Kim, Hyoung-Chun PERGAMON PRESS 2018 FREE RADICAL BIOLOGY AND MEDICINE Vol.115 No.-
<P><B>Abstract</B></P> <P>Protein kinase C (PKC) has been recognized to activate NADPH oxidase (PHOX). However, the interaction between PKC and PHOX <I>in vivo</I> remains elusive. Treatment with methamphetamine (MA) resulted in a selective increase in PKCδ expression out of PKC isoforms. PKCδ co-immunoprecipitated with p47<I>phox</I>, and facilitated phosphorylation and membrane translocation of p47<I>phox</I>. MA-induced increases in PHOX activity and reactive oxygen species were attenuated by knockout of p47<I>phox</I> or PKCδ. In addition, MA-induced impairments in the Nrf-2-related glutathione synthetic system were also mitigated by knockout of p47<I>phox</I> or PKCδ. Glutathione-immunoreactivity was co-localized in Iba-1-labeled microglial cells and in NeuN-labeled neurons, but not in GFAP-labeled astrocytes, reflecting the necessity for self-protection against oxidative stress by mainly microglia. Buthionine-sulfoximine, an inhibitor of glutathione biosynthesis, potentiated microglial activation and pro-apoptotic changes, leading to dopaminergic losses. These neurotoxic processes were attenuated by rottlerin, a pharmacological inhibitor of PKCδ, genetic inhibitions of PKCδ <B>[</B>i.e., PKCδ knockout mice (KO) and PKCδ antisense oligonucleotide (ASO)<B>]</B>, or genetic inhibition of p47<I>phox</I> (i.e., p47<I>phox</I> KO or p47<I>phox</I> ASO). Rottlerin did not exhibit any additive effects against the protective activity offered by genetic inhibition of p47<I>phox</I>. Therefore, we suggest that PKCδ is a critical regulator for p47<I>phox</I> activation induced by MA, and that Nrf-2-dependent GSH induction via inhibition of PKCδ or p47<I>phox</I>, is important for dopaminergic protection against MA insult.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Interplay between PKC and PHOX <I>in vivo</I> in the neurotoxic condition remains unclear. </LI> <LI> PKCδ co-immunoprecipitated with p47<I>phox</I> and facilitated the potential of p47<I>phox.</I> </LI> <LI> Methamphetamine-induced Nrf-2 system was mitigated by inhibition of p47<I>phox</I> or PKCδ. </LI> <LI> BSO potentiated microgliosis and apoptotic changes, leading to dopaminergic losses. </LI> <LI> PKCδ is a critical regulator for p47<I>phox</I> activation induced by methamphetamine. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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