Buchwald, Arnd B.

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.lastpage","74"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Scheschonka, A."],["dc.contributor.author","Bleich, S."],["dc.contributor.author","Buchwald, A. B."],["dc.contributor.author","Ruther, E."],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2017-09-07T11:44:38Z"],["dc.date.available","2017-09-07T11:44:38Z"],["dc.date.issued","2002"],["dc.description.abstract","In this report, we will describe the first case of obsessive-compulsive behaviour following oral corticosteroid treatment in a 75-year old adult male patient with pulmonal disease, but without previous psychiatric symptoms or organic brain disorder. We will also discuss the clinical and pathophysiological considerations."],["dc.identifier.doi","10.1055/s-2002-25022"],["dc.identifier.gro","3151718"],["dc.identifier.pmid","11951148"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8538"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0176-3679"],["dc.title","Development of Obsessive-Compulsive Behaviour Following Cortisone Treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","413"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Zeitschrift für Gastroenterologie"],["dc.bibliographiccitation.lastpage","418"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Opitz, T."],["dc.contributor.author","Buchwald, Arnd B."],["dc.contributor.author","Lorf, Thomas"],["dc.contributor.author","Awuah, David"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Nolte, W."],["dc.date.accessioned","2018-11-07T10:39:30Z"],["dc.date.available","2018-11-07T10:39:30Z"],["dc.date.issued","2003"],["dc.description.abstract","We present a 40-year-old female patient with epigastric pain, ascites, and progressive liver failure, caused by Budd-Chiari syndrome (BCS) with thrombotic occlusion of the right and middle hepatic veins. As underlying diseases, essential thrombocythemia and resistance to activated protein C (APC) due to heterozygote factor V Leiden were found. Initial therapy with heparin caused thrombocytopenia (HIT) type 11 culminating in thrombosis of the last patent left hepatic vein and further deterioration of liver function. The decision against a surgical shunt and liver transplantation by our surgeons on the basis of the risks involved, prompted us to insert a transjugular intrahepatic portosystemic stent-shunt (TIPS). There was no measurable flow signal in the doppler sonography of the portal vein presumably due to thrombosis. A further evaluation with magnetic resonance tomography and angiography was impossible due to movement artefacts. TIPS initially served as a diagnostic tool allowing direct angiography-diagnosed thrombosis of the portal vein, the superior mesenteric and the splenic vein respectively. However, insertion of the TIPS shunt and subsequent fragmentation led to an effective hepatic decompression and full recanalisation of the portal vein. In the present case TIPS simultaneously allowed the diagnosis of portal vein thrombosis and served as rescue therapy of complicated Budd-Chiari syndrome. The potential development of HIT type II should be kept in mind when heparin is given, especially to patients with thrombophilia."],["dc.identifier.isi","000183193200007"],["dc.identifier.pmid","12772054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46063"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0044-2771"],["dc.title","The transjugular intrahepatic portosystemic stent-shunt (TIPS) as rescue therapy for complete Budd-Chiari syndrome and portal vein thrombosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1632"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","1636"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Binder, L."],["dc.contributor.author","Hruska, N."],["dc.contributor.author","Luthe, Hilmar"],["dc.contributor.author","Buchwald, Arnd B."],["dc.date.accessioned","2018-11-07T08:36:53Z"],["dc.date.available","2018-11-07T08:36:53Z"],["dc.date.issued","2000"],["dc.description.abstract","OBJECTIVES The purpose of this study was to evaluate the prevalence and diagnostic utility of cardiac troponin I to identify patients with right ventricular (RV) dysfunction in pulmonary embolism. BACKGROUND Right ventricular overload resulting from elevated pulmonary resistance is a common finding in major pulmonary embolism. However, biochemical markers to assess the degree of RV dysfunction have not been evaluated so far. METHODS In this prospective, double-blind study we included 36 study patients diagnosed as having acute pulmonary embolism. RESULTS Among the whole study population, 14 patients (39%) had positive troponin I tests. Ten of 16 patients (62.5%) with RV dilatation had increased serum troponin I levels, while only 4 of 14 patients (28.6%) with elevated troponin I values had a normal RV diameter as assessed by echocardiography, indicating that positive troponin I tests were significantly associated with RV dilatation (p = 0.009). Patients with positive troponin I tests had significantly more segmental defects in ventilation/perfusion lung scans than patients with normal serum troponin I (p = 0.0002). CONCLUSIONS Our data demonstrate that more than one-third of patients clinically diagnosed as having pulmonary embolism presented with elevated serum troponin I concentrations. Troponin I tests helped to identify patients with RV dilatation who had significantly more segmental defects in lung scans. Thus, troponin I assays are useful to detect minor myocardial damage in pulmonary embolism. (C) 2000 by the American College of Cardiology."],["dc.identifier.doi","10.1016/S0735-1097(00)00905-0"],["dc.identifier.isi","000165171500028"],["dc.identifier.pmid","11079669"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18410"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0735-1097"],["dc.title","Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","PII S0735-1097(01)01797-1"],["dc.bibliographiccitation.firstpage","732"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","738"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Webel, Christian"],["dc.contributor.author","Hecker, Markus"],["dc.contributor.author","Buchwald, Arnd B."],["dc.contributor.author","Wagner, Andreas H."],["dc.date.accessioned","2021-06-01T10:50:17Z"],["dc.date.available","2021-06-01T10:50:17Z"],["dc.date.issued","2002"],["dc.description.abstract","OBJECTIVES We sought to demonstrate, in an appropriate animal model, that co-medication with a transcription factor-blocking agent limits restenosis after percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND Enhanced synthesis in the vessel wall of endothelin-1 (ET-1), a powerful co-mitogen for vascular smooth muscle cells, appears to be one mechanism that promotes restenosis after PTCA. Deformation-induced expression of prepro-ET-1 is governed by the transcription factor, activator protein-1 (AP-1). METHODS An anti-AP-1 decoy oligodeoxynucleotide (dODN) strategy was devised in which the dODN-containing solution (20 nmol) was administered locally through a Dispatch catheter into the coronary arteries of hypercholesterolemic minipigs at the time of PTCA (AVE-GFX stent). RESULTS Treatment with an AP-1 dODN, mimicking the consensus binding site of the transcription factor, significantly reduced neointimal formation in the coronary arteries of hypercholesterolemic minipigs (n = 10 to 12), compared with vehiclc-treated coronary arteries, after four weeks of follow-up (neointimal area 2.64 +/- 0.33 vs. 4.81 +/- 1.04 mm(2) [mean +/- SEM]; p < 0.05). This effect was maintained after eight weeks (neointimal area 2.04 +/- 0.22 mm(2); n = 3) and correlated with a reduction in both nuclear translocation of AP-1 and ET-1 synthesis in the vessel wall 48 h after PTCA (n = 4). In contrast, an AP-1 mutant dODN, to which the transcription factor does not bind, showed no effect on neointimal formation at either time point (n = 3 to 7). Moreover, a consensus dODN directed against CCAAT/enhancer binding protein (C/EBP), another deformation-sensitive transcription factor, did not significantly affect neointimal formation after four weeks (n = 3), CONCLUSIONS These findings demonstrate the feasibility, efficacy and specificity of the anti-AP-1 dODN approach to the treatment of restenosis, which principally but not exclusively targets deformation-induced ET-1 synthesis in the vessel wall. Provided that these findings can be extrapolated to the situation of patients with coronary artery disease, the observed extent of the inhibitory effect of the AP-1 dODN treatment suggests that this co-medication may greatly reduce the incidence of in-stent restenosis. (C) 2002 by the American College of Cardiology."],["dc.identifier.doi","10.1016/S0735-1097(01)01797-1"],["dc.identifier.isi","000173904800026"],["dc.identifier.pmid","11849876"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86602"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0735-1097"],["dc.title","Decoy oligodeoxynucleotide againstactivator protein-1 reducesneointimal proliferation after coronaryangioplasty in hypercholesterolemic minipigs"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","477"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Interventional Cardiac Electrophysiology"],["dc.bibliographiccitation.lastpage","485"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Stevens, J."],["dc.contributor.author","Buchwald, Arnd B."],["dc.contributor.author","Unterberg, Christina"],["dc.date.accessioned","2018-11-07T11:21:38Z"],["dc.date.available","2018-11-07T11:21:38Z"],["dc.date.issued","2001"],["dc.description.abstract","Automatic atrial anti-tachy pacing (aATP) is a novel approach to treat paroxysmal/persistent atrial tachyarrhythmias in pacemaker patients. To evaluate the efficacy of aATP in terminating spontaneous atrial flutter/tachycardia episodes (AT), a dual-chamber stimulator with extensive diagnostic capabilities and programmable aATP therapies (AT500(TM), Medtronic Inc.) was implanted in 30 patients with conventional pacing indications. During a mean follow-up time of 5.5 (1-12) months, aATP was delivered for 10494 AT. According to automatic device analysis, 8289 AT were treated with success (success-rate 79.0%). On 468 AT stored with the corresponding atrial EGM, an additional manual analysis was performed. The success-rate based on automatic analysis of these AT episodes (73.1%) was comparable to that found for all treated AT (79.0%), but manual EGM analysis revealed that only 209 of the 468 treated AT episodes (44.7%) were actually terminated by aATP. The aATP success-rate in the slower (cycle length 360-270 ms) AT detection zone was significantly higher (73.8%, 62/84 eps) than in the overlapping, faster (cycle length 270-220 ms) AT zone (38.3%, 147/384 eps, P < 0.01). Conclusions: According to manual analysis, 1. aATP was safe and had a success-rate of 44.7%, 2. aATP success-rate was higher for AT in the slower than in the faster detection zone and 3. automatic analysis overestimated the efficacy of aATP."],["dc.identifier.doi","10.1023/A:1013262431932"],["dc.identifier.isi","000172805600013"],["dc.identifier.pmid","11752917"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55819"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Kluwer Academic Publ"],["dc.relation.issn","1383-875X"],["dc.title","Automatic atrial anti-tachy pacing for the termination of spontaneous atrial tachyarrhythmias: Clinical experience with a novel dual-chamber pacemaker"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","323"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","333"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Schneiderman, Jacob"],["dc.contributor.author","Schumann, Bettina"],["dc.contributor.author","Glueckermann, Roland"],["dc.contributor.author","Grimmas, Petros"],["dc.contributor.author","Buchwald, Arnd B."],["dc.contributor.author","Tirilomis, Theodor"],["dc.contributor.author","Schoendube, Friedrich Albert"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T10:58:06Z"],["dc.date.available","2018-11-07T10:58:06Z"],["dc.date.issued","2007"],["dc.description.abstract","Clinical and experimental evidence suggests that the adipokine leptin may be important for the development of cardiovascular complications associated with obesity, possibly through interaction with its receptor on vascular cells. In the present study, we systematically analysed expression of the leptin receptor in normal and diseased vascular specimens using immunohistochemistry, immunofluorescence and quantitative real time-PCR. In particular, human atherosclerotic plaques as well as experimental vascular lesions induced in hypercholesterolemic mice and minipigs, respectively, were examined. Our results demonstrate the presence of the leptin receptor in normal vessel wall segments as well as neointimal or atherosclerotic lesions. In the latter, ObR expressing cells were predominantly localised on the luminal border and within the subintima, and coexpression of von Willebrand factor, VEGF receptor-2 or VE cadherin identified them as endothelial cells. Moreover, CD14-positive monocytes/macrophages were strongly positive for the leptin receptor. In contrast, only few ObR-expressing smooth muscle cells could be detected in human atherosclerotic plaques. The findings of the present study thus support a possible action of leptin on the cardiovascular system by demonstrating expression of the leptin receptor in different types of vascular lesions."],["dc.identifier.doi","10.1007/s00418-007-0319-1"],["dc.identifier.isi","000249523100005"],["dc.identifier.pmid","17680264"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50402"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0948-6143"],["dc.title","Expression of the leptin receptor in different types of vascular lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","60"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Liver International"],["dc.bibliographiccitation.lastpage","65"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Nolte, Wilhelm"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Pahl, Karoline"],["dc.contributor.author","Unterberg, Knut"],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Schindler, Christian G."],["dc.contributor.author","Figulla, Hans Reiner"],["dc.contributor.author","Buchwald, Arnd B."],["dc.contributor.author","Hartmann, Heinz"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2017-09-07T11:44:24Z"],["dc.date.available","2017-09-07T11:44:24Z"],["dc.date.issued","2000"],["dc.description.abstract","Aims/Background: Endothelin-1 (ET-1) may be a mediator for portal hypertension in liver cirrhosis. The aim of the present study was to determine the concentrations of ET-1 in the systemic and splanchnic circulation before and after reduction of portal hypertension by transjugular intrahepatic portosystemic shunt implantation (TIPS). Methods: Plasma concentrations of immunoreactive ET-1 were measured in peripheral venous blood samples from 25 patients with liver cirrhosis before and at 1, 3, 9 and 15 months after TIPS. Furthermore, acute effects of TIPS on ET-1 were studied in plasma samples from the hepatic vein, the portal vein 30 minutes before and after TIPS and in the femoral artery (only after TIPS) in a subgroup of 15 patients. In addition, the portocaval pressure gradient was determined before and after TIPS. Results: Before TIPS peripheral venous plasma ET-1 concentrations (n=25; median 4.2 pg/ml; range 1.9–14.7) were significantly increased in patients with refractory ascites (n=7; median 7.8, range 3.5–14.7) compared to patients with repetitive bleeding (n=18; median 3.4; range 1.9–7.1) (p=0.003). Furthermore, peripheral ET-1 concentrations correlated with the degree of liver dysfunction according to the Child-Pugh classification (Spearman's r=0.46; p=0.02). Following TIPS, peripheral ET-1 concentrations remained unchanged during a follow-up of 15 months. Before TIPS, a positive gradient of ET-1 concentrations from portalvenous to hepatovenous and peripheral venous levels was found (p<0.03). Immediately after TIPS, arterial ET-1 concentrations reached markedly increased levels in individual patients (88, 92 and 103 pg/ml). Severe systemic reactions to these high levels were not observed. Peripheral venous, hepatovenous and portalvenous ET-1 concentrations did not correlate with portocaval pressure gradients. Conclusion: Cirrhotic patients demonstrated unchanged peripheral venous ET-1 concentrations up to 15 months after TIPS. Portal congestion was associated with increased ET-1 levels in the prehepatic splanchnic area. The effect of portal decompression on splanchnic and systemic ET-1 levels deserves further investigation."],["dc.identifier.doi","10.1034/j.1600-0676.2000.020001060.x"],["dc.identifier.gro","3151647"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8464"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","1478-3223"],["dc.title","Systemic and splanchnic endothelin-1 plasma levels in liver cirrhosis before and after transjugular intrahepatic portosystemic shunt (TIPS)"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","841"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","847"],["dc.bibliographiccitation.volume","95"],["dc.contributor.author","Cattaruzza, Marco"],["dc.contributor.author","Guzik, T. J."],["dc.contributor.author","Slodowski, W."],["dc.contributor.author","Pelvan, A."],["dc.contributor.author","Becker, J."],["dc.contributor.author","Halle, Martin"],["dc.contributor.author","Buchwald, Arnd B."],["dc.contributor.author","Channon, K. M."],["dc.contributor.author","Hecker, M."],["dc.date.accessioned","2018-11-07T10:44:48Z"],["dc.date.available","2018-11-07T10:44:48Z"],["dc.date.issued","2004"],["dc.description.abstract","Coronary heart disease (CHD) is based on the development of atherosclerosis in coronary arteries. Shear stress-induced endothelial nitric oxide (NO) release not only contributes to local blood pressure control but also effectively helps to retard atherosclerosis. Therefore, functionally relevant polymorphisms in the endothelial NO synthase (NOS-3) gene may contribute to the development of CHD. NOS-3 expression was analyzed in endothelial cells isolated from umbilical cords genotyped for the C-786/T single nucleotide polymorphism (SNP) of the human nos-3 gene. Moreover, NO-dependent relaxation was examined in segments of saphenous vein isolated from genotyped patients undergoing aortocoronary bypass surgery, and patients subjected to quantitative coronary angiography were genotyped to verify an association between this SNP and CHD. Shear stress-induced NOS-3 mRNA and protein expression was present in TT and CT genotype cells but absent in cells with CC genotype. Pretreatment of these cells with a decoy oligonucleotide comprising position -800 to -779 of the C-type nos-3 promoter reconstituted shear stress-induced NOS-3 expression. These results were confirmed by reporter gene analysis with the corresponding nos-3 promoter luciferase constructs. In addition, the NO-mediated relaxant response of vein grafts from CC genotype patients was significantly attenuated as compared with the CT or TT genotype, and in CHD-positive patients, the CC genotype was significantly more frequent (19.0%) than in CHD-negative patients (4.4%). The C-786/T SNP of the nos-3 gene thus constitutes a genetic risk factor for CHD, presumably due to binding of an inhibitory transcription factor to the C-type promoter blocking shear stress-dependent maintenance of NOS-3 expression."],["dc.identifier.doi","10.1161/01.RES.0000145359.47708.2f"],["dc.identifier.isi","000224466300013"],["dc.identifier.pmid","15375006"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47350"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0009-7330"],["dc.title","Shear stress insensitivity of endothelial nitric oxide synthase expression as a genetic risk factor for coronary heart disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1611"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Pacing and Clinical Electrophysiology"],["dc.bibliographiccitation.lastpage","1617"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Unterberg, Christina"],["dc.contributor.author","Stevens, J"],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Buchwald, Arnd B."],["dc.date.accessioned","2017-09-07T11:46:45Z"],["dc.date.available","2017-09-07T11:46:45Z"],["dc.date.issued","2000"],["dc.description.abstract","Inappropriate therapy by ICDs due to SVTs is an important problem. A third generation ICD with a new detection criterion (\"EGM width criterion\") for differentiation of SVTs and VTs by measuring the width of the intracardiac EGM was studied in 47 patients. A wide EGM was defined as the longest measured EGM plus 4-12 ms (programmed as EGM width threshold). EGM width detection function was programmed to the \"Passive\" mode so that no therapy was withheld. During a follow-up of 29.9 +/- 8.3 (12-45) months, 489 spontaneous episodes were analyzed. SVTs occurred in ten patients with 305 episodes; 301 were correctly classified by use of the new detection criterion. In four patients four episodes were incorrectly detected as wide QRS tachycardias. Thus specificity for SVT was 98.7% (on a per episode basis) and 60% on a per patient basis. Of 184 VTs in 23 patients, 118 episodes were correctly classified (19 patients), however, in 4 patients 66 VTs were falsely detected as SVTS, 62 (94%) of which occurred in I patient with complete left BBB and continuously increasing QRS width in 12-lead surface ECGs. Overall sensitivity (on a per episode basis) for VT detection was 64.1% and 96.7% in patients with stable width of the QRS complex in a 12-lead surface. ECG. These data show that this criterion is not superior to data on rate dependent detection criteria and furthermore not applicable in patients with complete BBB."],["dc.identifier.doi","10.1046/j.1460-9592.2000.01611.x"],["dc.identifier.gro","3144347"],["dc.identifier.isi","000165755700006"],["dc.identifier.pmid","11138297"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1961"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Futura Publ Co"],["dc.relation.issn","0147-8389"],["dc.title","Long-term clinical experience with the EGM width detection criterion for differentiation of supraventricular and ventricular tachycardia in patients with implantable cardioverter defibrillators"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","435"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Experimental and Clinical Endocrinology & Diabetes"],["dc.bibliographiccitation.lastpage","442"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Nolte, W."],["dc.contributor.author","Wirtz, M."],["dc.contributor.author","Rossbach, C."],["dc.contributor.author","Leonhardt, U."],["dc.contributor.author","Buchwald, A."],["dc.contributor.author","Scholz, K.-H."],["dc.contributor.author","Ramadori, G."],["dc.date.accessioned","2021-06-01T10:51:00Z"],["dc.date.available","2021-06-01T10:51:00Z"],["dc.date.issued","2003"],["dc.description.abstract","Increased leptin levels in patients with liver cirrhosis are postulated to result in malnutrition and increased energy expenditure. Since cirrhotic patients show improved nutritional status after a transjugular intrahepatic portosystemic stent shunt (TIPS), it was the aim of this study to evaluate plasma leptin levels and their influence on nutritional status prior to and after the TIPS procedure. We evaluated plasma leptin levels, body mass index (BMI), Child-Pugh score and pertinent biochemical parameters in 31 patients (19 men and 12 women) with severe complications of liver cirrhosis (74% ethyltoxic men, 50% ethyltoxic in women), prior to and after TIPS. Nineteen cirrhotic patients without TIPS served as controls. In women ascitic-free BMI significantly increased (from 22.8 +/- 4.6 kg/m(2) to 23.9 +/- 4.9; p = 0.004 three months after TIPS), whereas in men only a tendency toward higher values (26.1 +/- 4.7 vs. 26.7 +/- 4.4; p = 0.28) was found. Analysis of peripheral venous leptin concentrations before and three months after TIPS revealed a significant increase in women (11.9 +/- 8.8 ng/ml vs. 18.6 +/- 14.9; p = 0.009) and in men (7.7 +/- 6.2 ng/ml vs. 12.2 +/- 9.0; p = 0.005). In addition, the leptin-BMI ratio increase significantly in women and men three months after TIPS implantation (women 0.49 +/- 0.29 vs. 0.73 +/- 0.52; p = 0.017; men 0.28 +/- 0.22 vs. 0.43 +/- 0.28; p = 0.002). On the other hand, patients without TIPS implantation showed no significant alterations of BMI and peripheral venous leptin concentrations. After TIPS implantation in liver cirrhotic patients, leptin levels were increased and the nutritional status improved. Therefore, our analysis suggests that in patients with predominantly ethyltoxic liver cirrhosis, elevated leptin levels are not a major reason for poorer body composition."],["dc.identifier.doi","10.1055/s-2003-44291"],["dc.identifier.isi","000186805900005"],["dc.identifier.pmid","14614651"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86856"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Johann Ambrosius Barth Verlag Medizinverlage Heidelberg Gmbh"],["dc.relation.eissn","1439-3646"],["dc.relation.issn","0947-7349"],["dc.title","TIPS Implantation Raises Leptin Levels in Patients with Liver Cirrhosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]