Grimm, Michael

[["dc.bibliographiccitation.firstpage","642"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","651"],["dc.bibliographiccitation.volume","79"],["dc.contributor.author","Kockskaemper, Jens"],["dc.contributor.author","Khafaga, Mounir"],["dc.contributor.author","Grimm, Michael"],["dc.contributor.author","Elgner, Andreas"],["dc.contributor.author","Walther, Stefanie"],["dc.contributor.author","Kockskaemper, Anke"],["dc.contributor.author","von Lewinski, Dirk"],["dc.contributor.author","Post, Heiner"],["dc.contributor.author","Grossmann, Marius"],["dc.contributor.author","Doerge, Hilmar"],["dc.contributor.author","Gottlieb, Philip A."],["dc.contributor.author","Sachs, Frederick"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Schoendube, Friedrich Albert"],["dc.contributor.author","Pieske, Burkert M."],["dc.date.accessioned","2018-11-07T11:11:08Z"],["dc.date.available","2018-11-07T11:11:08Z"],["dc.date.issued","2008"],["dc.description.abstract","Aims Stretch is an important regulator of atrial function. The functional effects of stretch on human atrium, however, are poorly understood. Thus, we characterized the stretch-induced force response in human atrium and evaluated the underlying cellular mechanisms. Methods and results Isometric twitch force of human atrial trabeculae (n = 252) was recorded (37 C, 1 Hz stimulation) following stretch from 88 (L88) to 98% (L98) of optimal length. [Na(+)](i) and pH(i) were measured using SBFI and BCECF epifluorescence, respectively. Stretch induced a biphasic force increase: an immediate increase [first-phase, Frank-Starting mechanism (FSM)] to similar to 190% of force at L88 followed by an additional slower increase [5-10 min; stow force response (SFR)] to similar to 120% of the FSM. FSM and SFR were unaffected by gender, age, ejection fraction, and pre-medication with major cardiovascular drugs. There was a positive correlation between the amplitude of the FSM and the SFR. [Na(+)](i) rose by similar to 1 mmol/L and pH(i) remained unchanged during the SFR. Inhibition of Na(+)/H(+)-exchange (3 mu M HOE642), Na(+)/Ca(2+)-exchange (5 mu M KB-R7943), or stretch-activated channels (0.5 mu M, GsMtx-4 and 80 mu M streptomycin) did not reduce the SFR. Inhibition of angiotensin-II (AngII) receptors (5 mu M saralasin and 0.5 mu M PD123319) or pre-application of 0.5 mu M AngII, however, reduced the SFR by similar to 40-60%. Moreover, stretch increased phosphorylation of myosin tight chain 2 (MLC2a) and inhibition of MLC kinase (10 mu M ML-7 and 5 mu M wortmannin) decreased the SFR by similar to 40-85%. Conclusion Stretch elicits a SFR in human atrium. The atrial SFR is mediated by stretch-induced release and autocrine/paracrine actions of AngII and increased myofilament Ca(2+) responsiveness via phosphorylation of MLC2a by MLC kinase."],["dc.identifier.doi","10.1093/cvr/cvn126"],["dc.identifier.isi","000259301600014"],["dc.identifier.pmid","18503051"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6310"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53362"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Angiotensin II and myosin light-chain phosphorylation contribute to the stretch-induced slow force response in human atrial myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1105"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","U46"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Boy, Oliver"],["dc.contributor.author","Christalla, Peter"],["dc.contributor.author","Doeker, Stephan"],["dc.contributor.author","Naito, Hiroshi"],["dc.contributor.author","Karikkineth, Bijoy Chandapillai"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Grimm, Michael"],["dc.contributor.author","Nose, Monika"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Katschinski, Dörthe M."],["dc.contributor.author","Hamdani, Nazha"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Yin, Xiaoke"],["dc.contributor.author","Mayr, Manuel"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2017-09-07T11:43:18Z"],["dc.date.available","2017-09-07T11:43:18Z"],["dc.date.issued","2011"],["dc.description.abstract","Rationale: Cardiac tissue engineering should provide \"realistic\" in vitro heart muscle models and surrogate tissue for myocardial repair. For either application, engineered myocardium should display features of native myocardium, including terminal differentiation, organotypic maturation, and hypertrophic growth. Objective: To test the hypothesis that 3D-engineered heart tissue (EHT) culture supports (1) terminal differentiation as well as (2) organotypic assembly and maturation of immature cardiomyocytes, and (3) constitutes a methodological platform to investigate mechanisms underlying hypertrophic growth. Methods and Results: We generated EHTs from neonatal rat cardiomyocytes and compared morphological and molecular properties of EHT and native myocardium from fetal, neonatal, and adult rats. We made the following key observations: cardiomyocytes in EHT (1) gained a high level of binucleation in the absence of notable cytokinesis, (2) regained a rod-shape and anisotropic sarcomere organization, (3) demonstrated a fetal-to-adult gene expression pattern, and (4) responded to distinct hypertrophic stimuli with concentric or eccentric hypertrophy and reexpression of fetal genes. The process of terminal differentiation and maturation (culture days 7-12) was preceded by a tissue consolidation phase (culture days 0-7) with substantial cardiomyocyte apoptosis and dynamic extracellular matrix restructuring. Conclusions: This study documents the propensity of immature cardiomyocytes to terminally differentiate and mature in EHT in a remarkably organotypic manner. It moreover provides the rationale for the utility of the EHT technology as a methodological bridge between 2D cell culture and animal models. (Circ Res. 2011;109:1105-1114.)"],["dc.identifier.doi","10.1161/CIRCRESAHA.111.251843"],["dc.identifier.gro","3142637"],["dc.identifier.isi","000296417200005"],["dc.identifier.pmid","21921264"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7826"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/63"],["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.relation.issn","0009-7330"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Terminal Differentiation, Advanced Organotypic Maturation, and Modeling of Hypertrophic Growth in Engineered Heart Tissue"],["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","191"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Social indicators research"],["dc.bibliographiccitation.lastpage","211"],["dc.bibliographiccitation.volume","97"],["dc.contributor.author","Grimm, Michael"],["dc.contributor.author","Harttgen, Kenneth"],["dc.contributor.author","Klasen, Stephan"],["dc.contributor.author","Misselhorn, Mark"],["dc.contributor.author","Munzi, Teresa"],["dc.contributor.author","Smeeding, Timothy"],["dc.date.accessioned","2018-06-05T08:28:05Z"],["dc.date.available","2018-06-05T08:28:05Z"],["dc.date.issued","2010-06"],["dc.description.abstract","One of the most frequent critiques of the HDI is that is does not take into account inequality within countries in its three dimensions. In this paper, we apply a simply approach to compute the three components and the overall HDI for quintiles of the income distribution. This allows a comparison of the level in human development of the poor with the level of the non-poor within countries, but also across countries. This is an application of the method presented in Grimm et al. (World Development 36(12):2527-2546, 2008) to a sample of 21 low and middle income countries and 11 industrialized countries. In particular the inclusion of the industrialized countries, which were not included in the previous work, implies to deal with a number of additional challenges, which we outline in this paper. Our results show that inequality in human development within countries is high, both in developed and industrialized countries. In fact, the HDI of the lowest quintiles in industrialized countries is often below the HDI of the richest quintile in many middle income countries. We also find, however, a strong overall negative correlation between the level of human development and inequality in human development."],["dc.identifier.doi","10.1007/s11205-009-9497-7"],["dc.identifier.pmid","20461123"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7650"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/14874"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.orgunit","Wirtschaftswissenschaftliche Fakultät"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Inequality in Human Development: An Empirical Assessment of 32 Countries"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e47916"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Biermann, Daniel"],["dc.contributor.author","Heilmann, Andreas"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Schlossarek, Saskia"],["dc.contributor.author","Wahab, Azadeh"],["dc.contributor.author","Grimm, Michael"],["dc.contributor.author","Roemer, Maria"],["dc.contributor.author","Reichenspurner, Hermann"],["dc.contributor.author","Sultan, Karim R."],["dc.contributor.author","Steenpass, Anna"],["dc.contributor.author","Erguen, Sueleyman"],["dc.contributor.author","Donzelli, Sonia"],["dc.contributor.author","Carrier, Lucie"],["dc.contributor.author","Ehmke, Heimo"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Hein, Lutz"],["dc.contributor.author","Böger, Rainer H."],["dc.contributor.author","Benndorf, Ralf A."],["dc.date.accessioned","2017-09-07T11:48:22Z"],["dc.date.available","2017-09-07T11:48:22Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: The angiotensin II receptor subtype 2 (AT2 receptor) is ubiquitously and highly expressed in early postnatal life. However, its role in postnatal cardiac development remained unclear. Methodology/Principal Findings: Hearts from 1, 7, 14 and 56 days old wild-type (WT) and AT2 receptor-deficient (KO) mice were extracted for histomorphometrical analysis as well as analysis of cardiac signaling and gene expression. Furthermore, heart and body weights of examined animals were recorded and echocardiographic analysis of cardiac function as well as telemetric blood pressure measurements were performed. Moreover, gene expression, sarcomere shortening and calcium transients were examined in ventricular cardiomyocytes isolated from both genotypes. KO mice exhibited an accelerated body weight gain and a reduced heart to body weight ratio as compared to WT mice in the postnatal period. However, in adult KO mice the heart to body weight ratio was significantly increased most likely due to elevated systemic blood pressure. At postnatal day 7 ventricular capillarization index and the density of alpha-smooth muscle cell actin-positive blood vessels were higher in KO mice as compared to WT mice but normalized during adolescence. Echocardiographic assessment of cardiac systolic function at postnatal day 7 revealed decreased contractility of KO hearts in response to beta-adrenergic stimulation. Moreover, cardiomyocytes from KO mice showed a decreased sarcomere shortening and an increased peak Ca2+ transient in response to isoprenaline when stimulated concomitantly with angiotensin II. Conclusion: The AT2 receptor affects postnatal cardiac growth possibly via reducing body weight gain and systemic blood pressure. Moreover, it moderately attenuates postnatal vascularization of the heart and modulates the beta adrenergic response of the neonatal heart. These AT2 receptor-mediated effects may be implicated in the physiological maturation process of the heart."],["dc.identifier.doi","10.1371/journal.pone.0047916"],["dc.identifier.gro","3142448"],["dc.identifier.isi","000310705300024"],["dc.identifier.pmid","23144713"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8323"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8396"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Impact of AT2 Receptor Deficiency on Postnatal Cardiovascular Development"],["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","1347"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Health Economics"],["dc.bibliographiccitation.lastpage","1367"],["dc.bibliographiccitation.volume","31"],["dc.contributor.affiliation","Grimm, Michael; 1\r\nUniversity of Passau, IZA and RWI Research Network\r\nPassau Germany"],["dc.contributor.author","Grimm, Michael"],["dc.contributor.author","Hartwig, Renate"],["dc.date.accessioned","2022-05-02T08:02:12Z"],["dc.date.available","2022-05-02T08:02:12Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:13:40Z"],["dc.description.abstract","Abstract\r\nVision impairment is the most common disability worldwide and it is untreated in large parts of the developing world. We assess the willingness‐to‐pay (WTP) for eyeglasses among adults in a resource‐poor rural setting. We elicit the WTP using the Becker‐DeGroot‐Marschak (BDM) method. We combine this approach with a layaway scheme and a video intervention to probe to what extent liquidity constraints and information influence the WTP. Our results show that the average WTP is close to the cost of production for corrective glasses. Nevertheless, we find evidence for information constraints. Our video intervention raises the WTP for corrective glasses by 16 percent. We do not find evidence of screening effects, that is after 6 months, use is unrelated to the initial WTP."],["dc.description.sponsorship","Fonds De La Recherche Scientifique ‐ FNRS http://dx.doi.org/10.13039/501100002661"],["dc.identifier.doi","10.1002/hec.4511"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107256"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","1099-1050"],["dc.relation.issn","1057-9230"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","All eyes on the price: An assessment of the willingness‐to‐pay for eyeglasses in rural Burkina Faso"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]