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RISS 인기검색어
- 검색키워드
- 저자 : ( Thomas Jonassen ) (검색결과 3 건)
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( Martin Skott ),( Rikke Nørregaard ),( Hanne Birke Sørensen ),( Johan Palmfeldt ),( Tae Hwan Kwon ),( Thomas Jonassen ),( Jørgen Frøkiær ),( Søren Nielsen ) 대한신장학회 2014 Kidney Research and Clinical Practice Vol.33 No.2
Background: The primary aim of the study was to investigate the cytokine/chemokine response in the kidney, lung, and liver following acute kidney injury(AKI). The secondary aim was to test whether α-melanocyte-stimulating hormone(α-MSH) could prevent a reduction in organ function, and attenuate the inflammatorycytokine/chemokine response within the kidney, lung, and liver following AKIin rats with or without preexisting chronic kidney disease (CKD). Methods: A two-stage animal model, in which AKI was induced in rats withpreexisting CKD, induced by 5/6 nephrectomy (Nx), was used. Six weeks later, AKIwas induced by intestinal ischemia and reperfusion (IIR). Sham procedures [S(Nx)and S(IIR)] were also performed. Results: Increasing levels of serum creatinine (sCr) demonstrated progressive developmentof CKD in response to Nx, and following IIR sCr levels increased furthersignificantly, except in the S(Nx) group treated with α-MSH. However, no significantdifferences in the fractional increase in sCr were observed between any of the groupsexposed to IIR. In kidney, lung, and liver tissue the levels of interleukin (IL)-1β weresignificantly higher in rats undergoing IIR when compared to the S(IIR) and control rats. The same pattern was observed for the chemokine monocyte chemoattractant protein(MCP)-1 in lung and liver tissue. Furthermore, kidney IL-1β and RANTES levels weresignificantly increased after IIR in the Nx rats compared to the S(Nx) rats. Conclusion: Both the functional parameters and the cytokine/chemokine response areas dramatic when AKI is superimposed onto CKD as onto non-CKD. No convincingprotective effect of α-MSH was detected.
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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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