Sossalla, Samuel Tobias

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Tirilomis, Petros"],["dc.contributor.author","Stehle, Thea"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Knierim, Maria"],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Bengel, Philipp"],["dc.contributor.author","Holzamer, Andreas"],["dc.contributor.author","Hilker, Michael"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2020-12-10T14:10:25Z"],["dc.date.available","2020-12-10T14:10:25Z"],["dc.date.issued","2020"],["dc.description.abstract","Pharmacologic approaches for the treatment of atrial arrhythmias are limited due to side effects and low efficacy. Thus, the identification of new antiarrhythmic targets is of clinical interest. Recent genome studies suggested an involvement of SCN10A sodium channels (NaV1.8) in atrial electrophysiology. This study investigated the role and involvement of NaV1.8 (SCN10A) in arrhythmia generation in the human atria and in mice lacking NaV1.8. NaV1.8 mRNA and protein were detected in human atrial myocardium at a significant higher level compared to ventricular myocardium. Expression of NaV1.8 and NaV1.5 did not differ between myocardium from patients with atrial fibrillation and sinus rhythm. To determine the electrophysiological role of NaV1.8, we investigated isolated human atrial cardiomyocytes from patients with sinus rhythm stimulated with isoproterenol. Inhibition of NaV1.8 by A-803467 or PF-01247324 showed no effects on the human atrial action potential. However, we found that NaV1.8 significantly contributes to late Na+ current and consequently to an increased proarrhythmogenic diastolic sarcoplasmic reticulum Ca2+ leak in human atrial cardiomyocytes. Selective pharmacological inhibition of NaV1.8 potently reduced late Na+ current, proarrhythmic diastolic Ca2+ release, delayed afterdepolarizations as well as spontaneous action potentials. These findings could be confirmed in murine atrial cardiomyocytes from wild-type mice and also compared to SCN10A−/− mice (genetic ablation of NaV1.8). Pharmacological NaV1.8 inhibition showed no effects in SCN10A−/− mice. Importantly, in vivo experiments in SCN10A−/− mice showed that genetic ablation of NaV1.8 protects against atrial fibrillation induction. This study demonstrates that NaV1.8 is expressed in the murine and human atria and contributes to late Na+ current generation and cellular arrhythmogenesis. Blocking NaV1.8 selectively counteracts this pathomechanism and protects against atrial arrhythmias. Thus, our translational study reveals a new selective therapeutic target for treating atrial arrhythmias."],["dc.identifier.doi","10.1007/s00395-020-0780-8"],["dc.identifier.pmid","32078054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70756"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/349"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.rights","CC BY 4.0"],["dc.title","Inhibition of NaV1.8 prevents atrial arrhythmogenesis in human and mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","994"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","1010"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Knierim, Maria"],["dc.contributor.author","Stehle, Thea"],["dc.contributor.author","Alebrand, Felix"],["dc.contributor.author","Paulus, Michael"],["dc.contributor.author","Sieme, Marcel"],["dc.contributor.author","Herwig, Melissa"],["dc.contributor.author","Barsch, Friedrich"],["dc.contributor.author","Körtl, Thomas"],["dc.contributor.author","Pöppl, Arnold"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2022-04-01T10:03:03Z"],["dc.date.available","2022-04-01T10:03:03Z"],["dc.date.issued","2022"],["dc.description.abstract","Rationale: Atrial fibrillation (AF) and heart failure often coexist, but their interaction is poorly understood. Clinical data indicate that the arrhythmic component of AF may contribute to left ventricular (LV) dysfunction. Objective: This study investigates the effects and molecular mechanisms of AF on the human LV. Methods and Results: Ventricular myocardium from patients with aortic stenosis and preserved LV function with sinus rhythm or rate-controlled AF was studied. LV myocardium from patients with sinus rhythm and patients with AF showed no differences in fibrosis. In functional studies, systolic Ca 2+ transient amplitude of LV cardiomyocytes was reduced in patients with AF, while diastolic Ca 2+ levels and Ca 2+ transient kinetics were not statistically different. These results were confirmed in LV cardiomyocytes from nonfailing donors with sinus rhythm or AF. Moreover, normofrequent AF was simulated in vitro using arrhythmic or rhythmic pacing (both at 60 bpm). After 24 hours of AF-simulation, human LV cardiomyocytes from nonfailing donors showed an impaired Ca 2+ transient amplitude. For a standardized investigation of AF-simulation, human iPSC-cardiomyocytes were tested. Seven days of AF-simulation caused reduced systolic Ca 2+ transient amplitude and sarcoplasmic reticulum Ca 2+ load likely because of an increased diastolic sarcoplasmic reticulum Ca 2+ leak. Moreover, cytosolic Na + concentration was elevated and action potential duration was prolonged after AF-simulation. We detected an increased late Na + current as a potential trigger for the detrimentally altered Ca 2+ /Na + -interplay. Mechanistically, reactive oxygen species were higher in the LV of patients with AF. CaMKII (Ca 2+ /calmodulin-dependent protein kinase IIδc) was found to be more oxidized at Met281/282 in the LV of patients with AF leading to an increased CaMKII activity and consequent increased RyR2 phosphorylation. CaMKII inhibition and ROS scavenging ameliorated impaired systolic Ca 2+ handling after AF-simulation. Conclusions: AF causes distinct functional and molecular remodeling of the human LV. This translational study provides the first mechanistic characterization and the potential negative impact of AF in the absence of tachycardia on the human ventricle."],["dc.identifier.doi","10.1161/CIRCRESAHA.121.319718"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/106071"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/438"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation.eissn","1524-4571"],["dc.relation.issn","0009-7330"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Effects of Atrial Fibrillation on the Human Ventricle"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","102"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","107"],["dc.bibliographiccitation.volume","272"],["dc.contributor.author","Bergau, Leonard"],["dc.contributor.author","Willems, Rik"],["dc.contributor.author","Sprenkeler, David J."],["dc.contributor.author","Fischer, Thomas H."],["dc.contributor.author","Flevari, Panayota"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Katsaras, Dimitrios"],["dc.contributor.author","Kirova, Aleksandra"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Lüthje, Lars"],["dc.contributor.author","Röver, Christian"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Dunnink, Albert"],["dc.contributor.author","Sritharan, Rajevaa"],["dc.contributor.author","Tuinenburg, Anton E."],["dc.contributor.author","Vandenberk, Bert"],["dc.contributor.author","Vos, Marc A."],["dc.contributor.author","Wijers, Sofieke C."],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zabel, Markus"],["dc.date.accessioned","2019-07-09T11:50:23Z"],["dc.date.available","2019-07-09T11:50:23Z"],["dc.date.issued","2018"],["dc.description.abstract","BACKGROUND AND OBJECTIVE: We prospectively investigated combinations of risk stratifiers including multiple EP diagnostics in a cohort study of ICD patients. METHODS: For 672 enrolled patients, we collected history, LVEF, EP study and T-wave alternans testing, 24-h Holter, NT-proBNP, and the eGFR. All-cause mortality and first appropriate ICD shock were predefined endpoints. RESULTS: The 635 patients included in the final analyses were 63 ± 13 years old, 81% were male, LVEF averaged 40 ± 14%, 20% were inducible at EP study, 63% had a primary prophylactic ICD. During follow-up over 4.3 ± 1.5 years, 108 patients died (4.0% per year), and appropriate shock therapy occurred in n = 96 (3.9% per year). In multivariate regression, age (p < 0.001), LVEF (p < 0.001), NYHA functional class (p = 0.007), eGFR (p = 0.024), a history of atrial fibrillation (p = 0.011), and NT-pro-BNP (p = 0.002) were predictors of mortality. LVEF (p = 0.002), inducibility at EP study (p = 0.007), and secondary prophylaxis (p = 0.002) were identified as independent predictors of appropriate shocks. A high annualized risk of shocks of about 10% per year was prevalent in the upper quintile of the shock score. In contrast, a low annual risk of shocks (1.8% per year) was found in the lower two quintiles of the shock score. The lower two quintiles of the mortality score featured an annual mortality <0.6%. CONCLUSIONS: In a prospective ICD patient cohort, a very good approximation of mortality versus arrhythmic risk was possible using a multivariable diagnostic strategy. EP stimulation is the best test to assess risk of arrhythmias resulting in ICD shocks."],["dc.identifier.doi","10.1016/j.ijcard.2018.06.103"],["dc.identifier.pmid","29983251"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15929"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59764"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/15360 but duplicate"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/241526/EU//EUTRIGTREAT"],["dc.relation.issn","1874-1754"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.access","openAccess"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.subject.mesh","Aged"],["dc.subject.mesh","Aged, 80 and over"],["dc.subject.mesh","Arrhythmias, Cardiac"],["dc.subject.mesh","Cohort Studies"],["dc.subject.mesh","Death, Sudden, Cardiac"],["dc.subject.mesh","Defibrillators"],["dc.subject.mesh","Defibrillators, Implantable"],["dc.subject.mesh","Female"],["dc.subject.mesh","Follow-Up Studies"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Male"],["dc.subject.mesh","Middle Aged"],["dc.subject.mesh","Mortality"],["dc.subject.mesh","Multivariate Analysis"],["dc.subject.mesh","Natriuretic Peptide, Brain"],["dc.subject.mesh","Peptide Fragments"],["dc.subject.mesh","Prospective Studies"],["dc.subject.mesh","Risk Factors"],["dc.title","Differential multivariable risk prediction of appropriate shock versus competing mortality - A prospective cohort study to estimate benefits from ICD therapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","347"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Annals of Thoracic and Cardiovascular Surgery"],["dc.bibliographiccitation.lastpage","351"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Mirzaie, Masoud"],["dc.contributor.author","Fatehpur, Sheila"],["dc.contributor.author","Friedrich, Martin"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Schoendube, Friedrich Albert"],["dc.contributor.author","Schmitto, Jan Dieter"],["dc.date.accessioned","2018-11-07T08:53:26Z"],["dc.date.available","2018-11-07T08:53:26Z"],["dc.date.issued","2011"],["dc.description.abstract","Objective: The present paper exemplary describes several severe stenoses of supraaortic branches with its symptoms and operative treatments. Methods: Eight patients, two female (68 +/- 5 y), six male (73 +/- 4 y), were retrospectively evaluated. Patients showed neurological signs as followed: recurring attacks of vertigo (80%), temporary paresis of extremity (20%), speech disorders (20%) and subclavian and/or carotic-steel-syndrome (15%). Seven patients have already been previously treated with revascularization of the supraaortic branches in the past. The surgical techniques used were thrombendarterectomy of the internal carotid artery, carotid-subclavian bypass and complex aortotruncal, aorto-carotid and aorto-subclavian-bypass. Results: One patient died nine days postoperatively due to myocardial infarction. Mean duration of stay on intensive care unit was 1.5 days. Mean duration of postoperative ventilation was six hours. Average duration of stay on normal ward was nine days. Conclusion: This study presents several complex reconstructions of supraaortic branches, which were indicated in cases with severe stenoses of supraaortic branches. Even though treatment strategies were complex the peri- and postoperative complication rates are quite low. These therapeutic strategies were necessary to avoid severe neurological complications in these patients."],["dc.identifier.doi","10.5761/atcs.oa.09.01432"],["dc.identifier.isi","000294510200005"],["dc.identifier.pmid","21881320"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22408"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Medical Tribune Inc"],["dc.relation.issn","1341-1098"],["dc.title","Complex Reconstruction of Supraaortic Branches"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","975"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","991"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Borchert, Thomas"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Guessoum, Celina I."],["dc.contributor.author","Lam, Tuan-Dinh D."],["dc.contributor.author","Ghadri, Jelena R."],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Liaw, Norman Y."],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Huber, Mia A."],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Lüscher, Thomas F."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Templin, Christian"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2018-04-23T11:48:11Z"],["dc.date.available","2018-04-23T11:48:11Z"],["dc.date.issued","2017"],["dc.description.abstract","Background Takotsubo syndrome (TTS) is characterized by an acute left ventricular dysfunction and is associated with life-threating complications in the acute phase. The underlying disease mechanism in TTS is still unknown. A genetic basis has been suggested to be involved in the pathogenesis. Objectives The aims of the study were to establish an in vitro induced pluripotent stem cell (iPSC) model of TTS, to test the hypothesis of altered β-adrenergic signaling in TTS iPSC-cardiomyocytes (CMs), and to explore whether genetic susceptibility underlies the pathophysiology of TTS. Methods Somatic cells of patients with TTS and control subjects were reprogrammed to iPSCs and differentiated into CMs. Three-month-old CMs were subjected to catecholamine stimulation to simulate neurohumoral overstimulation. We investigated β-adrenergic signaling and TTS cardiomyocyte function. Results Enhanced β-adrenergic signaling in TTS-iPSC-CMs under catecholamine-induced stress increased expression of the cardiac stress marker NR4A1; cyclic adenosine monophosphate levels; and cyclic adenosine monophosphate–dependent protein kinase A–mediated hyperphosphorylation of RYR2-S2808, PLN-S16, TNI-S23/24, and Cav1.2-S1928, and leads to a reduced calcium time to transient 50% decay. These cellular catecholamine-dependent responses were mainly mediated by β1-adrenoceptor signaling in TTS. Engineered heart muscles from TTS-iPSC-CMs showed an impaired force of contraction and a higher sensitivity to isoprenaline-stimulated inotropy compared with control subjects. In addition, altered electrical activity and increased lipid accumulation were detected in catecholamine-treated TTS-iPSC-CMs, and were confirmed by differentially expressed lipid transporters CD36 and CPT1C. Furthermore, we uncovered genetic variants in different key regulators of cardiac function. Conclusions Enhanced β-adrenergic signaling and higher sensitivity to catecholamine-induced toxicity were identified as mechanisms associated with the TTS phenotype."],["dc.identifier.doi","10.1016/j.jacc.2017.06.061"],["dc.identifier.gro","3142333"],["dc.identifier.pmid","28818208"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13468"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/204"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | D02: Neue Mechanismen der genomischen Instabilität bei Herzinsuffizienz"],["dc.relation.issn","0735-1097"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Wollnik"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Catecholamine-Dependent β-Adrenergic Signaling in a Pluripotent Stem Cell Model of Takotsubo Cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Hamdani, Nazha"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2021-04-14T08:29:26Z"],["dc.date.available","2021-04-14T08:29:26Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1002/ejhf.2091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82903"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.title","A mechanistic rationale for the investigation of sodium–glucose co‐transporter 2 inhibitors in heart failure with preserved ejection fraction. Letter regarding the article ‘Baseline characteristics of patients with heart failure with preserved ejection fraction in the EMPEROR‐Preserved trial’"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","335"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Clinical Imaging"],["dc.bibliographiccitation.lastpage","341"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Amarteifio, Erick"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Heuser, Markus"],["dc.contributor.author","Obenauer, Silvia"],["dc.date.accessioned","2018-11-07T11:11:09Z"],["dc.date.available","2018-11-07T11:11:09Z"],["dc.date.issued","2008"],["dc.description.abstract","Aim: In this retrospective study, we assess the current role and future potential of computed tomography (CT) in the diagnostic algorithm of acute pulmonary embolism (PE). Materials and methods: Two hundred patients underwent 64-multidetector-row spiral CT of the chest, pelvis, and thigh for suspected PE. CT scans were reviewed, and the degree of contrast enhancement and the presence of PE and/or (deep) venous thrombosis were recorded. In the case of PE, the level of thrombus was noted as central, main, or lobar. If the scan yielded a positive result for thrombosis, intravenous localization was also determined. Patient age, length of admission, clinical course, clinical indication, and incidental findings were registered as well. Results: PE was detected in 60 of the 200 patients with a high clinical probability of having PE (30%). Thirty-four patients had a positive CT scan result for venous thrombosis (17%). Twenty-four of the 60 patients had proximal deep venous thrombosis (40%), and 2 patients had ann venous thrombosis (3%). Thirty-four of the 60 patients had without venous thrombosis (57%). Eight of the 200 patients had deep venous thrombosis without suspicion of PE (4%). The distribution of the proximal thrombi showed 15 in a central artery (25%), 13 in a main pulmonary artery (22%), and 32 in a lobar segmental artery (53%). There was diffuse allocation of the thrombus in all lobes. Furthermore, CT scan noted a total of 120 incidental findings. Conclusion: Our study indicates the potential clinical use of a diagnostic strategy for ruling out PE based on D-dimer testing and multidetector-row CT. A larger outcome study is needed before this approach can be adopted. (C) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.clinimag.2008.01.028"],["dc.identifier.isi","000259211600001"],["dc.identifier.pmid","18760719"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53366"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1873-4499"],["dc.relation.issn","0899-7071"],["dc.title","64-multidetector-row spiral CT in pulmonary embolism with emphasis on incidental findings"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","179"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Current Heart Failure Reports"],["dc.bibliographiccitation.lastpage","186"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Bengel, Philipp"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2019-01-30T13:29:01Z"],["dc.date.available","2019-01-30T13:29:01Z"],["dc.date.issued","2017"],["dc.description.abstract","Over the last years, evidence is accumulating that enhanced late sodium current (INaL) in cardiac pathologies has fundamental consequences for cellular electrophysiology. This review discusses the underlying mechanisms of INaL-induced arrhythmias and the significance of INaL-inhibition as a possible therapeutic approach."],["dc.identifier.doi","10.1007/s11897-017-0333-0"],["dc.identifier.pmid","28455610"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57422"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1546-9549"],["dc.title","Inhibition of Late Sodium Current as an Innovative Antiarrhythmic Strategy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","642"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","648"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Wagemann, Olivia"],["dc.contributor.author","Lücht, Charlotte M."],["dc.contributor.author","Trum, Maximilian"],["dc.contributor.author","Hammer, Karin P."],["dc.contributor.author","Sag, Can Martin"],["dc.contributor.author","Lebek, Simon"],["dc.contributor.author","Tarnowski, Daniel"],["dc.contributor.author","Reinders, Jörg"],["dc.contributor.author","Perbellini, Filippo"],["dc.contributor.author","Terracciano, Cesare"],["dc.contributor.author","Schmid, Christof"],["dc.contributor.author","Schopka, Simon"],["dc.contributor.author","Hilker, Michael"],["dc.contributor.author","Zausig, York"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Schweda, Frank"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Wagner, Stefan"],["dc.date.accessioned","2020-12-10T14:06:09Z"],["dc.date.available","2020-12-10T14:06:09Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1002/ehf2.12336"],["dc.identifier.issn","2055-5822"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69797"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Empagliflozin reduces Ca/calmodulin-dependent kinase II activity in isolated ventricular cardiomyocytes"],["dc.title.alternative","Empagliflozin reduces CaMKII activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","280"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical Imaging"],["dc.bibliographiccitation.lastpage","286"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Heuser, Markus"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Wolff, Hendrik"],["dc.contributor.author","Obenauer, Silvia"],["dc.date.accessioned","2018-11-07T11:13:19Z"],["dc.date.available","2018-11-07T11:13:19Z"],["dc.date.issued","2008"],["dc.description.abstract","Aim: In this retrospective study, we assess the current role and future potential of computed tomographic (CT) colonography as a viable alternative imaging tool for colorectal polyp detection and colon cancer screening. Materials and methods: Twenty patients have undergone virtual colonographic examinations with 64-multidetector-row spiral CT (MDCT), and three-dimensional images were created on a separate workstation that had the appropriate software for image processing. Images were reviewed by a radiologist, and anatomic division of the entire colon was used to locate the suspected lesions. Characteristics of bowel preparation, intracolonic, extracolonic, and incidental findings were noted, too. Results: Ten of the 20 patients (50%) had a positive CT colonography for polypoid lesions. Those lesions were distributed into the cecum (4 cases), colon ascendens (2 cases), colon descendens (2 cases), and sigma (2 cases). In 80%, bowel preparation was good, in 15% moderate, and in 5% inadequate. Furthermore, CT scan noted in total 20 incidental findings. Conclusion: CT colonography is currently a viable alternative imaging tool for colorectal polyp detection. There are several clinical situations where CT colonography may play an important role in patient care. These include for example evaluation of the colon after an incomplete conventional colonoscopic examination or evaluation in patients who are clinically unfit to undergo conventional colonoscopy. At centers where there is expertise in data acquisition and interpretation, CT colonography is being offered as a routine imaging examination. With continued improvements in bowel preparation, colonic distention, and CT colonography interpretation by sufficient numbers of radiologists this technology might have a substantial influence on colon cancer screening. (c) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.clinimag.2008.01.001"],["dc.identifier.isi","000257908300006"],["dc.identifier.pmid","18603183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53863"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0899-7071"],["dc.title","Current role and future potential of computed tomographic colonography for colorectal polyp detection and colon cancer screening - incidental findings"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]