Andreas, Stefan

[["dc.bibliographiccitation.artnumber","7"],["dc.bibliographiccitation.journal","Respiratory Research"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Michels, Hellmuth"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:47:34Z"],["dc.date.available","2017-09-07T11:47:34Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: Systemic effects of chronic obstructive pulmonary disease (COPD) significantly contribute to severity and mortality of the disease. We aimed to develop a COPD/emphysema model exhibiting systemic manifestations of the disease. Methods: Female NMRI mice were treated 5 times intratracheally with porcine pancreatic elastase (emphysema) or phosphate-buffered saline (control). Emphysema severity was quantified histologically by mean linear intercept, exercise tolerance by treadmill running distance, diaphragm dysfunction using isolated muscle strips, pulmonary hypertension by measuring right ventricular pressure, and neurohumoral activation by determining urinary norepinephrine concentration. Results: Mean linear intercept was higher in emphysema (260.7 +/- 26.8 mu m) than in control lungs (24.7 +/- 1.7 mu m). Emphysema mice lost body weight, controls gained weight. Running distance was shorter in emphysema than in controls. Diaphragm muscle length was shorter in controls compared to emphysema. Fatigue tests of muscle strips revealed impaired relaxation in emphysema diaphragms. Maximum right ventricular pressure and norepinephrine were elevated in emphysema compared to controls. Linear correlations were observed between running distance changes and intercept, right ventricular weight, norepinephrine, and diaphragm length. Conclusion: The elastase mouse model exhibited severe emphysema with consecutive exercise limitation, and neurohumoral activation. The model may deepen our understanding of systemic aspects of COPD."],["dc.identifier.doi","10.1186/1465-9921-10-7"],["dc.identifier.gro","3143160"],["dc.identifier.isi","000263727200001"],["dc.identifier.pmid","19175913"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13854"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/643"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1465-9921"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Exercise intolerance and systemic manifestations of pulmonary emphysema in a mouse model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","273"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","280"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Renner, Bernd"],["dc.contributor.author","Kessels, Roger"],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Gerritse, Bart"],["dc.contributor.author","Tasci, Selcuk"],["dc.contributor.author","Schwab, Joerg O."],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Zenker, Dieter"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Unterberg-Buchwald, Christina"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:47:31Z"],["dc.date.available","2017-09-07T11:47:31Z"],["dc.date.issued","2009"],["dc.description.abstract","Aims The combined therapeutic impact of atrial overdrive pacing (ACIP) and cardiac resynchronization therapy (CRT) on central steep apnoea (CSA) in chronic heart failure (CHF) so far has not been investigated. We aimed to evaluate the effect of CRT alone and CRT + AOP on CSA in CHF patients and to compare the influence of CRT on CHF between CSA positive and CSA negative patients. Methods and results Thirty patients with CRT indication underwent full night polysomnography, echocardiography, exercise testing, and neurohumoral evaluation before and 3 months after CRT implantation. In CSA positive patients (60%), two additional steep studies were conducted after 3 months of CRT, with CRT alone or CRT + ACIP, in random order. Cardiac resynchronization therapy resulted in significant improvements of NYHA class, left ventricular ejection fraction, N-terminal pro-brain natriuretic peptide, VO(2)max, and quality of life irrespective of the presence of CSA. Cardiac resynchronization therapy also reduced the central apnoea-hypopnoea index (AHI) (33.6 +/- 14.3 vs. 23.8 +/- 16.9 h(-1); P < 0.01) and central apnoea index (17.3 +/- 14.1 vs. 10.9 +/- 13.9 h(-1); P < 0.01) without altering steep stages. Cardiac resynchronization therapy with atrial overdrive pacing resulted in a small but significant additional decrease of the central AHI (23.8 +/- 16.9 vs. 21.5 +/- 16.9 h(-1); P < 0.01). Conclusion In this study, CRT significantly improved CSA without altering sleep stages. Cardiac resynchronization therapy with atrial. overdrive pacing resulted in a significant but minor additional improvement of CSA. Positive effects of CRT were irrespective of the presence of CSA."],["dc.identifier.doi","10.1093/eurjhf/hfn042"],["dc.identifier.gro","3143143"],["dc.identifier.isi","000265845700008"],["dc.identifier.pmid","19147446"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/625"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Bakken Research Center, Maastricht, Netherlands"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1388-9842"],["dc.title","Cardiac resynchronization therapy and atrial overdrive pacing for the treatment of central sleep apnoea"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","118"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","American Journal of Respiratory and Critical Care Medicine"],["dc.bibliographiccitation.lastpage","122"],["dc.bibliographiccitation.volume","172"],["dc.contributor.author","Lüthje, L."],["dc.contributor.author","Unterberg-Buchwald, Christina"],["dc.contributor.author","Dajani, D."],["dc.contributor.author","Vollmann, D."],["dc.contributor.author","Hasenfuß, G."],["dc.contributor.author","Andreas, S."],["dc.date.accessioned","2017-09-07T11:54:20Z"],["dc.date.available","2017-09-07T11:54:20Z"],["dc.date.issued","2005"],["dc.description.abstract","Rationale: Atrial overdrive pacing markedly improved sleep-disordered breathing in a recent study. Objectives: Using a single-blind, randomized, crossover design, we aimed to reproduce these findings and investigate the possible underlying mechanisms. Methods: Twenty ambulatory patients with an implanted pacemaker or cardioverter defibrillator were studied by polysomnography on 3 consecutive nights in a randomized, single-blind, crossover study in which devices were programmed for nonpacing or for overdrive pacing at 7 or 15 beats/minute faster than the mean nocturnal heart rate. Ventilation and biomarkers (urinary norepinephrine excretion, amino-terminal portion of the precursor of brain natriuretic peptide, or NT-proBNP, were also evaluated. Measurements and Main Results: Neither the primary endpoint apnea-hypopnea index, nor the apnea index, oxygen desaturation, ventilation, or biomarkers were affected by the nocturnal atrial overdrive pacing. A small, clinically insignificant, rate-dependent reduction in the hypopnea index was evoked by pacing (nonpacing, 13.4 +/- 1.4; pacing 7, 12.9 +/- 1.4, pacing 15, 10.9 +/- 1.0; p < 0.01, analysis of variance). Conclusions:The lack of effect on the apnea-hypopnea index means that atrial overdrive pacing is inappropriate for treating sleep-disordered breathing."],["dc.identifier.doi","10.1164/rccm.200409-1258OC"],["dc.identifier.gro","3143824"],["dc.identifier.isi","000230102400019"],["dc.identifier.pmid","15750043"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1381"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1073-449X"],["dc.title","Atrial overdrive pacing in patients with sleep apnea with implanted pacemaker"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","19"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Sleep Medicine Reviews"],["dc.bibliographiccitation.lastpage","31"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2018-11-07T11:18:59Z"],["dc.date.available","2018-11-07T11:18:59Z"],["dc.date.issued","2008"],["dc.description.abstract","In the recent years intensive research has revealed numerous negative consequences of obstructive steep apnea (OSA) for the cardiovascular system. The pathophysiological interaction between OSA and coronary artery disease is complex and comprises neural, humoral, mechanical and haemodynamic components. One of the most important effects of OSA is an increase of sympathetic nerve traffic, which persists during the day and is thought to play a key role in the association of OSA and elevated systemic blood pressure. Nowadays, OSA is accepted as an independent risk factor for arterial hypertension. Several investigations support an association of OSA with ischemic ST-segment changes, ventricular arrhythmias, and sudden cardiac death. In line with this, a growing body of evidence strongly supports OSA having prognostic implications for cardiovascular morbidity and mortality. Continuous positive airway pressure (CPAP) has been shown to have several beneficial effects on the cardiovascular system. Uncontrolled studies indicate that it reduces cardiovascular risk in patients with severe OSA and increased risk or manifest coronary artery disease. However, ongoing studies still have to confirm this. (C) 2007 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.smrv.2007.08.002"],["dc.identifier.isi","000253349700003"],["dc.identifier.pmid","17936040"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55161"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.relation.issn","1087-0792"],["dc.title","Obstructive sleep apnea and coronary artery disease"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","215"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Pulmonary Pharmacology & Therapeutics"],["dc.bibliographiccitation.lastpage","220"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Duve, Christian"],["dc.contributor.author","Schweda, Frank"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:44:19Z"],["dc.date.available","2017-09-07T11:44:19Z"],["dc.date.issued","2011"],["dc.description.abstract","Objectives: COPD with emphysema causes marked neurohumoral activation. Angiotensin II receptors are highly expressed within the lung and interfere with mechanisms involved in the progression of emphysema. This study examined the effects of an angiotensin II receptor blocker (ARB) on pulmonary and systemic manifestations of emphysema in a mouse model. Methods: Female NMRI mice received five intratracheal instillations of porcine pancreatic elastase (emphysema; n = 11) or phosphate-buffered saline (PBS; n = 4). Emphysema severity was quantified histologically by mean linear intercept, exercise tolerance by treadmill running distance, and lung biomechanics by compliance. Following emphysema induction, 6 mice were treated with the ARB irbesartan for 8 weeks, while 5 mice receiving standard food served as controls. Results: Following emphysema induction, mean linear intercept was higher in elastase-treated than in PBS-treated lungs (103.0 +/- 6.2 mu m vs. 35.0 +/- 0.6 mu m; p = 0.043) while running distance was shorter in emphysema mice (418.6 +/- 83.5 m vs. 906.6 +/- 244.6 m, p = 0.028). Irbesartan-treated emphysema mice showed a lower mean linear intercept (90.8 +/- 3.8 mu m vs. 121.5 +/- 8.1 mu m; p = 0.005), improved compliance (163.6 +/- 55.9 mu l/cmH(2)O vs. 354.4 +/- 72.5 mu l/cmH(2)O; p = 0.063) and greater running distance (p ANOVA = 0.015) compared to emphysema mice receiving standard food. Conclusions: The ARB irbesartan elicits encouraging beneficial effects on emphysema severity, lung biomechanics and exercise capacity in an emphysema mouse model. These findings might help to understand the corresponding positive effects of angiotensin II receptor blockade noticed in patients with COPD. (C) 2010 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.pupt.2010.12.006"],["dc.identifier.gro","3142753"],["dc.identifier.isi","000289396400006"],["dc.identifier.pmid","21187155"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/192"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Sanofi-Aventis (formerly Sanofi-Synthelabo), Paris, France"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.issn","1094-5539"],["dc.title","Local and systemic effects of angiotensin receptor blockade in an emphysema mouse model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","107"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Respiratory Medicine"],["dc.bibliographiccitation.lastpage","113"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Herrmann, Peter"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:46:44Z"],["dc.date.available","2017-09-07T11:46:44Z"],["dc.date.issued","2010"],["dc.description.abstract","Objectives: Neurohumoral. activation has been shown to be present in patients with chronic obstructive pulmonary disease (COPD). The increase in respiratory muscle work might be responsible for the observed elevation of sympathetic tone via a respiratory muscle ergoreflex in these patients. The aim of this study is to investigate whether moderately increasing inspiratory resistive loading will impact on sympathetic activity in healthy subjects and COPD patients. Methods: Efferent muscle sympathetic nerve activity, blood pressure, heart rate and respiratory movements were continuously measured in 15 patients and 15 healthy control subjects. In order to increase work of breathing as evaluated by the tension-time index, inspiratory resistive loading was performed white patients were breathing through a spirometer. Results: At baseline, sympathetic nerve activity was significantly elevated in patients. Resistive loading increased work of breathing (tension-time index) by roughly 110% (COPD) and 130% (controls) but did not significantly alter blood gases or sympathetic activity in either group. Conclusions: Doubting the work of breathing does not affect sympathetic activation in COPD patients or healthy control subjects. Thus in COPD the respiratory muscle ergoreflex does not seem to play a major rote in sympathoexcitation. (C) 2009 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.rmed.2009.06.011"],["dc.identifier.gro","3143004"],["dc.identifier.isi","000274889300015"],["dc.identifier.pmid","19619996"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/471"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","W B Saunders Co Ltd"],["dc.relation.issn","0954-6111"],["dc.title","Inspiratory resistive loading does not increase sympathetic tone in COPD"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Wachter, R. Rolf"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Klemmstein, D."],["dc.contributor.author","Edelmann, F."],["dc.contributor.author","Andreas, S."],["dc.contributor.author","Pieske, Burkert M."],["dc.date.accessioned","2018-11-07T11:24:48Z"],["dc.date.available","2018-11-07T11:24:48Z"],["dc.date.issued","2009"],["dc.format.extent","833"],["dc.identifier.isi","000208702606488"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56484"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","0195-668X"],["dc.title","Impact of obstructive sleep apnea on diastolic function"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Reiter, H."],["dc.contributor.author","Hagenah, Gerrit C."],["dc.contributor.author","Delekat, A."],["dc.contributor.author","Grunewald, Rolf W."],["dc.contributor.author","Andreas, S."],["dc.date.accessioned","2018-11-07T10:46:41Z"],["dc.date.available","2018-11-07T10:46:41Z"],["dc.date.issued","2004"],["dc.format.extent","648"],["dc.identifier.isi","000224056502595"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47802"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.publisher.place","London"],["dc.relation.conference","ESC Congress 2004"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0195-668X"],["dc.title","Differential effects of theophylline on sympathetic excitation, hemodynamics and breathing in congestive heart failure"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","387"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Respiratory Journal"],["dc.bibliographiccitation.lastpage","392"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Raupach, T."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Herrmann, P."],["dc.contributor.author","Luethje, L."],["dc.contributor.author","Heusser, X."],["dc.contributor.author","Hasenfuß, G."],["dc.contributor.author","Bernardi, L."],["dc.contributor.author","Andreas, S."],["dc.date.accessioned","2017-09-07T11:48:15Z"],["dc.date.available","2017-09-07T11:48:15Z"],["dc.date.issued","2008"],["dc.description.abstract","Neurohumoral activation has been shown to be present in hypoxic patients with chronic obstructive pulmonary disease (COPD). The alms of the present study were to investigate whether there is sympathetic activation in COPD patients in the absence of hypoxia and whether slow breathing has an impact on sympathoexcitation and baroreflex sensitivity. Efferent muscle sympathetic nerve activity, blood pressure, cardiac frequency and respiratory movements were continuously measured in 15 COPD patients and 15 healthy control subjects. Baroreflex sensitivity was analysed by autoregressive spectral analysis and the alpha-angle method. At baseline, sympathetic nerve activity was significantly elevated in COPD patients and baroreflex sensitivity was decreased (5.0 +/- 0.6 versus 8.9 +/- 0.8 ms center dot mmHg(-1)). Breathing at a rate of 6 breaths.min(-1) caused sympathetic activity to drop significantly in COPD patients (from 61.3 +/- 4.6 to 53.0 +/- 4.3 bursts per 100 heartbeats) but not in control subjects (39.2 +/- 3.2 versus 37.5 +/- 3.3 bursts per 100 heartbeats). In both groups, slow breathing significantly enhanced baroreflex sensitivity. In conclusion, sympathovagal imbalance is present in normoxic chronic obstructive pulmonary disease patients. The possibility of modifying these changes by slow breathing may help to better understand and influence this systemic disease."],["dc.identifier.doi","10.1183/09031936.00109607"],["dc.identifier.gro","3143261"],["dc.identifier.isi","000258417000020"],["dc.identifier.pmid","18385175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/755"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0903-1936"],["dc.title","Slow breathing reduces sympathoexcitation in COPD"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","572"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","573"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Andreas, S."],["dc.contributor.author","Dajani, D."],["dc.contributor.author","Szych, J."],["dc.contributor.author","Hagenah, Gerrit C."],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Unterberg-Buchwald, Christine"],["dc.date.accessioned","2018-11-07T10:46:40Z"],["dc.date.available","2018-11-07T10:46:40Z"],["dc.date.issued","2004"],["dc.identifier.isi","000224056502296"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47798"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.publisher.place","London"],["dc.relation.conference","ESC Congress 2004"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0195-668X"],["dc.title","CPAP and atrial overdrive pacing in the treatment of obstructive sleep apnea syndrome"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]