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RISS 인기검색어
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- 저자 : Klaus Nielsen (검색결과 4 건)
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Rasmus K. Storm,Klaus Nielsen 글로벌지식마케팅경영학회 2023 Journal of Global Sport Management Vol.8 No.4
Research into the development and competitiveness of national elite sport systems has grown significantly in recent years. Most research concerns large or medium-sized nations whereas studies of elite sport systems in small nations are notably absent. This paper focuses on a (very) small nation and its efforts to become competitive in international elite sport. Using the nine pillars of the SPLISS framework, the study assesses the strengths and weaknesses of Greenland’s elite sport system. From a pure results perspective, Greenland performs below expectations. This is partly the result of its climatic and geographical conditions and low population density. The case study of elite sport in Greenland has intrinsic value in its analysis of a nation with extreme conditions in this respect. The case study is also used to suggest general conclusions regarding the capabilities and limitations of elite sport systems in small nations.
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Morten Løbner,Anette Walsted,Rune Larsen,Klaus Bendtzen,Claus Henrik Nielsen 한국식품영양과학회 2008 Journal of medicinal food Vol.11 No.2
The effect of consumption of Immulina, a high-molecular-weight polysaccharide extract from the cyanobac-terium Arthrospira platensis, on adaptive immune responses was investigated by evaluation of changes in leukocyte respon-siveness to two foreign recall antigens, Candida albicans(CA) and tetanus toxoid (TT), in vitro. Consumption of Immulinaby 11 healthy male volunteers caused an immediate, but temporary, increase of CA-induced CD4. T-helper (Th) cell pro-liferation (P. .02). TT-induced Th cell proliferation was increased in individuals over 50 years of age (P. .05) and corre-lated with age (P. .02). Consumption for 8 days enhanced the CA-induced B cell proliferation (P. .02), but after 56 daysa diminution was seen (P. .03). The CA-elicited production of the Th1 cytokines tumor necrosis factor (TNF)-., interleukin(IL)-2, and interferon (IFN)-. was increased after Immunlina administration for 3 days (P. .001,. .03, and. .007, re-spectively), and increased IL-2 production persisted after 56 days (P. .004). The TNF-., IFN-., and IL-6 responses to TTwere enhanced after 8 and 14 days (P. .002.05), while IL-5 responses increased significantly within 3 days (P. .04) andfell below baseline levels after 14 days (P. .008). Conversely, consumption for 3 days inhibited the IL-4 responses to bothCA and TT (P. .008 and P. .03, respectively). No effects on IL-10 responses were observed. Upon addition to normalmononuclear cells in vitro, Immulina elicited strong TNF-., IL-1., and IL-6 responses, indicating that it acts by inducing apro-inflammatory state. Taken together, the data suggest that Immulina causes an age-dependent, temporary enhancement ofadaptive immune responses.
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Li, Chunling,Shi, Yimin,Wang, Weidong,Sardeli, Chrysanthi,Kwon, Tae-Hwan,Thomsen, Klaus,Jonassen, Thomas,Djurhuus, Jens Christian,Knepper, Mark A,Nielsen, Soren,Frokiaer, Jorgen American Physiological Society 2006 American Journal of Physiology Vol.290 No.2
<P>The purpose of this study was to evaluate the effects of the anti-inflammatory hormone alpha-melanocyte-stimulating hormone (alpha-MSH) treatment on renal function and expression of aquaporins (AQPs) and Na-K-ATPase in the kidney in response to 24 h of bilateral ureteral obstruction (BUO) or release of BUO (BUO-R). In rats with 24-h BUO, immunoblotting revealed that downregulation of AQP2 and AQP3 was attenuated (AQP2: 38 +/- 5 vs. 13 +/- 4%; AQP3: 44 +/- 3 vs. 19 +/- 4% of sham levels; P < 0.05), whereas downregulation of Na-K-ATPase was prevented by alpha-MSH treatment (Na-K-ATPase: 94 +/- 7 vs. 35 +/- 5% of sham levels; P < 0.05). Immunocytochemistry confirmed the changes in AQP1 and Na-K-ATPase expression. Renal tubular cell apoptosis was confirmed in BUO kidneys, and alpha-MSH treatment virtually completely abolished apoptosis. Furthermore, we measured glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), respectively. Forty-eight hours after BUO-R demonstrated that alpha-MSH treatment almost completely prevented the decrease in GFR (nontreated: 271 +/- 50; alpha-MSH: 706 +/- 85; sham: 841 +/- 105 microl x min(-1).100 g body wt(-1), P < 0.05) and ERPF (nontreated: 1,139 +/- 217; alpha-MSH: 2,598 +/- 129; sham: 2,633 +/- 457 microl x min(-1).100 g body wt(-1), P < 0.05). alpha-MSH treatment also partly prevented the downregulation of AQP1 and Na-K-ATPase expression in rats after BUO-R for 48 h. In conclusion, alpha-MSH treatment significantly prevents impairment in renal function and also prevents downregulation of AQP2, AQP3, and Na-K-ATPase during BUO or AQP1 and Na-K-ATPase after BUO-R, demonstrating a marked renoprotective effect of alpha-MSH treatment in conditions with urinary tract obstruction.</P>
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Biphasic effects of ANP infusion in conscious, euvolumic rats: roles of AQP2 and ENaC trafficking.
Wang, Weidong,Li, Chunling,Nejsum, Lene N,Li, Hongyan,Kim, Soo Wan,Kwon, Tae-Hwan,Jonassen, Thomas E N,Knepper, Mark A,Thomsen, Klaus,Frokiaer, Jorgen,Nielsen, Soren American Physiological Society 2006 American journal of physiology. Renal physiology Vol.290 No.2
<P>Atrial natriuretic peptide (ANP) acutely promotes water and sodium excretion, whereas subchronic effects involve water retention. Renal hemodynamics, water and sodium excretion, and aquaporin-2 (AQP2) and epithelial Na channel (ENaC) subcellular trafficking were determined in response to continuous ANP infusion in conscious rats, where body sodium and fluid balance was constantly maintained. ANP (0.5 microg x kg(-1) x min(-1)) evoked a transient (peak at 10 min) fivefold diuresis followed by reduced urine production to control levels (30- to 90-min period). The fractional distal water excretion was significantly increased initially and then decreased in response to ANP. There was no change in the subcellular localization of AQP2 and AQP2 phosphorylated in PKA consensus site S256 (p-AQP2) 10 min after ANP infusion. In contrast, after 90 min a marked increase in apical labeling of AQP2 and p-AQP2 was observed in the inner and outer medullary collecting ducts but not in cortical collecting ducts. In support of this, ANP induced plasma membrane targeting of AQP2 in transiently AQP2-transfected cells. ANP infusion evoked an instant increase in renal sodium excretion, which persisted for 90 min. Ten minutes of ANP infusion induced no changes in the subcellular localization of ENaC subunits, whereas a marked increase in apical targeting of alpha- and gamma-subunits was observed after 90 min. In conclusion, 1) ANP infusion induced a sustained natriuresis and transient diuresis; 2) there were no changes in the subcellular localization of AQP2 and ENaC subunits after 10 min of ANP infusion; and 3) there was a marked increase in apical targeting of AQP2, p-AQP2, and alpha- and gamma-ENaC after 90 min of ANP infusion. The increased targeting of ENaC and AQP2 likely represents direct or compensatory effects to increase sodium and water reabsorption and to prevent volume depletion in response to prolonged ANP infusion.</P>
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