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  • 1
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    Krüppel-like factor 15 expression dynamics with CRISPR-based gene activation controls cardiomyocyte remodeling in the failing heart
    Elsevier BV ; 2022
    In:  Journal of Molecular and Cellular Cardiology Vol. 173 ( 2022-12), p. S165-
    Details
    In: Journal of Molecular and Cellular Cardiology, Elsevier BV, Vol. 173 ( 2022-12), p. S165-
    Type of Medium: Online Resource
    ISSN: 0022-2828
    URL: Article
    DOI: 10.1016/j.yjmcc.2022.08.325
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1469767-1
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  • 2
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    Single-cell transcriptomics reveal extracellular vesicles secretion with a cardiomyocyte proteostasis signature during pathological remodeling
    Springer Science and Business Media LLC ; 2023
    In:  Communications Biology Vol. 6, No. 1 ( 2023-01-21)
    Details
    In: Communications Biology, Springer Science and Business Media LLC, Vol. 6, No. 1 ( 2023-01-21)
    Abstract: Aberrant Wnt activation has been reported in failing cardiomyocytes. Here we present single cell transcriptome profiling of hearts with inducible cardiomyocyte-specific Wnt activation (β-cat Δex3 ) as well as with compensatory and failing hypertrophic remodeling. We show that functional enrichment analysis points to an involvement of extracellular vesicles (EVs) related processes in hearts of β-cat Δex3 mice. A proteomic analysis of in vivo cardiac derived EVs from β-cat Δex3 hearts has identified differentially enriched proteins involving 20 S proteasome constitutes, protein quality control (PQC), chaperones and associated cardiac proteins including α-Crystallin B (CRYAB) and sarcomeric components. The hypertrophic model confirms that cardiomyocytes reacted with an acute early transcriptional upregulation of exosome biogenesis processes and chaperones transcripts including CRYAB, which is ameliorated in advanced remodeling. Finally, human induced pluripotent stem cells (iPSC)-derived cardiomyocytes subjected to pharmacological Wnt activation recapitulated the increased expression of exosomal markers, CRYAB accumulation and increased PQC signaling. These findings reveal that secretion of EVs with a proteostasis signature contributes to early patho-physiological adaptation of cardiomyocytes, which may serve as a read-out of disease progression and can be used for monitoring cellular remodeling in vivo with a possible diagnostic and prognostic role in the future.
    Type of Medium: Online Resource
    ISSN: 2399-3642
    URL: Article
    DOI: 10.1038/s42003-022-04402-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2919698-X
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  • 3
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    Abstract 238: Role of Erythropoietin Signaling in the Biology of Mouse Cardiac Progenitor Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Research Vol. 111, No. suppl_1 ( 2012-08-03)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 111, No. suppl_1 ( 2012-08-03)
    Abstract: Erythropoietin (Epo) was shown to improve cardiac function following ischemia reperfusion mainly via neo-angiogenesis and anti-apoptotic mechanisms. We found EpoR expression to be particularly high in adult cardiac progenitor cells (CPCs). Thus, we reasoned that Epo may play a role in the biology of these cells. We isolated CPCs from adult C57BL/6 hearts by enzymatic digestion and filtration (pore size: 30 µm). By means of immunofluorescence microscopy (IF) and flow cytometry (FC) we analyzed EpoR expression in the CPCs. 24±3% of the investigated cardiac cells were positive for EpoR with 3±2% of these being c-kit+ and 28%±2% Sca-1+. 52% of the EpoR+ cells expressed endothelial cell markers (40±2% CD34+, 9±2% FLK1+). 42±4% expressed myocyte markers (αMHC+, cTNT+). IF revealed a progenitor-like population with immature cell morphology and proliferation potential (ki67+). Cell cycle analysis showed an enrichment of αMHC+ EpoR+ cells in S and G2 phase (49±7%, n=3) as compared to the αMHC- EpoR- population (13±3%, n=3). Moreover, we tested the effect of Epo in the biology of these CPCs in vitro. At d14 we observed a two-fold increase of GATA4+ and cTnT+ cardiac cells in the co-cultures treated with Epo (n=3). CPC cycle arrest abrogated the aforementioned effects, suggesting that Epo influences mainly CPC proliferation. Finally, we tested the potential of Epo to protect against ischemia by inducing the proliferation of these αMHC+ CPCs in vivo in a myocardial infarction (MI) model. 4 weeks post MI, echocardiography did not reveal a significant functional improvement of the Epo receiving mice (2x, 2U/g Epo i.p). Nevertheless, FC analysis of the progenitor pool showed a significant augmentation of αMHC+ and cTnT+ cells (Sham: 19±3% vs Epo 35±3%, n=5; MI: 10.6±2.3%, n=6 vs Epo 20.3±1.9%, n=8). These data suggest an activation of myogenic progenitors by Epo, despite the lack of apparent regeneration under the investigated conditions. In conclusion, we found that EpoR is expressed in a putative cardiomyogenic progenitor cell pool in the adult heart. Epo drives their proliferation in vitro and in vivo even upon acute cardiac injury. We are currently investigating the long-term consequences of the observed progenitor cell activation in models of chronic ischemic injury.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.111.suppl_1.A238
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1467838-X
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  • 4
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    Abstract 36: Administration of 17β-Estradiol in C57Bl/6N Female Mice Leads to Cardiac Atrophy and Dysfunction via a β-Catenin Mechanism
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Circulation Research Vol. 117, No. suppl_1 ( 2015-07-17)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 117, No. suppl_1 ( 2015-07-17)
    Abstract: The steroid hormone 17β-estradiol (E2) regulates several biological processes. In contrast to its anti-hypertrophic effects under pressure overload, we recently found that E2 induced physiological hypertrophic growth in healthy C57Bl/6J mice but not C57Bl/6N mice. Here, we aimed at the characterization of the effects of E2 in C57Bl/6N mice and tested the hypothesis that β-catenin mediates these E2 effects. Following ovariectomy, 2-month-old C57Bl/6N wild-type and cardiac-specific β-catenin-deleted (β-cat Δex2-6 ) mice were randomized to an E2-containing or soy-free (control, CON) diet ( n = 7-13/group). Cardiac function was examined by echocardiography following established procedures. The 3-month physiological dose of E2 led to a higher relative uterus weight compared with CON ( P 〈 0.001) in both WT and β-cat Δex2-6 mice. The relative heart weight was significantly reduced by E2 compared with CON in WT mice ( P 〈 0.001), while there was no significant effect in β-cat Δex2-6 mice. Cardiomyocyte cross-sectional area was also significantly decreased by E2 ( n = 5-7/group; P 〈 0.001) compared with CON in WT mice, while there was no significant effect in β-cat Δex2-6 mice. Echocardiography revealed a significant decrease in septum width ( P 〈 0.001) and posterior wall thickness ( P 〈 0.01) in E2 treated WT mice compared with CON, while there was no significant effect in β-cat Δex2-6 mice ( n = 8/group). These E2-induced structural changes in WT mice were accompanied by a significant decrease in cardiac function, namely a 23% decrease in fractional shortening compared with CON ( P 〈 0.05), while there was no significant effect in β-cat Δex2-6 mice. Immunoblotting revealed a significant increase in the levels of the ubiquitin ligase and key regulator of proteasome-dependent protein degradation muscle-specific RING finger protein 1 (MuRF1) by E2 compared with CON in WT mice ( P 〈 0.05), while there was no significant effect in β-cat Δex2-6 mice. Although we hypothesized increased autophagic activity, we found no effect on the autophagy-related protein LC3 in WT or β-cat Δex2-6 mice. In conclusion, our surprising findings show that E2 leads to cardiac atrophy and dysfunction in C57Bl/6N mice via a β-catenin mechanism seemingly in an autophagy-independent manner.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.117.suppl_1.36
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1467838-X
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  • 5
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    Abstract MP217: Nuclease-deficient Cas9 Transcription Factors Restore Krueppel-like Factor 15 Expression In Stressed Mouse And Human Cardiomyocytes
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Research Vol. 129, No. Suppl_1 ( 2021-09-03)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 129, No. Suppl_1 ( 2021-09-03)
    Abstract: Transcriptional changes in cardiomyocytes drive heart failure progression, however, precise control over endogenous gene expression remains challenging. The expression of Krueppel-like factor 15 ( KLF15 ), an evolutionary conserved nuclear and cardiomyocyte specific inhibitor of WNT/CTNNB1 signalling in the heart, is lost upon cardiac remodelling, and accompanied by aberrantly active WNT/CTNNB1 resulting in heart failure progression. We investigated KLF15 expression dynamics employing CRISPR/Cas9-based tools in mouse cardiomyocytes in vivo and in human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CM) under the hypothesis that re-establishment of KLF15 levels in myocardial stress conditions prevents heart failure progression. Using a mouse model expressing enzymatically inactive Cas9 (dCas9) fused to transcriptional activators (VPR) under Myh6 -promoter control, we activated Klf15 in a murine pressure overload model by transverse aortic constriction. Delivery of Klf15 gRNAs targeted to the Klf15 promoter region via AAV9 induced Klf15 expression sufficiently to re-normalize Klf15 expression to transcript levels comparable to sham surgery hearts. This was accompanied by reduced decrease of fractional shortening as well as reduced cardiomyocyte hypertrophy in stressed Klf15 re-activated hearts compared to non-trageted (NT) gRNA hearts (n=3-8 per group, echo data from 4 and 8 weeks post-surgery). We achieved titratable KLF15 activation in dCas9VPR transgenic hiPSC-CM by selection of single and multiple gRNAs (n=3-4 replicates) and used these cells to generate human engineered myocardium by combining hiPSC-CM and fibroblasts which we subjected to isometric contractions in order to induce mechanical stress, which resulted in KLF15 expressional decrease in line with our in vivo data. This transcriptional loss was rescued in CRISPR/dCas9VPR hiPSC-CM targeted to the KLF15 locus compared to controls (n=6-9/2/4 tissues per group/casting sessions/differentiations). Additionally, TGFB1 induced cardiomyocyte stress resulted in decreased KLF15 expression levels in 2D hiPSC-CM cultures which were rescued by dCas9VPR- KLF15 targeting (n=3 experiments). In conclusion, we report controllable gene activity by CRISPR/dCas9VPR to restore the loss of KLF15 in stressed mouse and human cardiomyocytes. We furthermore evaluate the potential to gain full control over gene dose titratability with these models to validate and define novel therapeutic targets for the prevention of heart failure progression.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.129.suppl_1.MP217
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1467838-X
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  • 6
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    Abstract 400: Role of the 17beta-Estradiol/beta-Catenin Axis in Heart Failure
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Circulation Research Vol. 119, No. suppl_1 ( 2016-07-22)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 119, No. suppl_1 ( 2016-07-22)
    Abstract: The role of β-catenin and the actions of 17β-estradiol (E2) in cardiovascular (patho)physiology remain unclear. In the diseased heart, E2 is expected to be cardioprotective. However, in the absence of prior disease, complications in pregnancy or transgender individuals indicate that E2 might lead to cardiovascular disease. We aimed at the characterization of the effects of the E2/β-catenin axis in the healthy C57Bl/6N heart. Two-month-old female C57Bl/6N wild-type (WT) and cardiac-specific β-catenin-deleted (β-cat Δex2-6 ) mice were ovariectomized and randomized to an E2-containing or soy-free (control, CON) diet ( n = 7-13/group). The 3-month physiological dose of E2 led to a significant repression of nuclear β-catenin levels vs. CON ( P 〈 0.001) in WT mice. This was underlain by a significant decrease in the heart weight to tibia length ratio and cardiomyocyte cross-sectional area (E2 vs. CON WT mice P 〈 0.001). Echocardiography revealed a significant decrease in septum width ( P 〈 0.001), posterior wall thickness ( P 〈 0.01) and fractional shortening ( P 〈 0.05) in E2 vs. CON WT mice. Deletion of β-catenin abrogated these E2-mediated deleterious effects on cardiac structure and function. Mechanistically, we found a significant increase in the levels of the ubiquitin ligase and key regulator of proteasome-dependent protein degradation muscle-specific RING finger protein 1 (MuRF1) in E2 vs. CON WT mice ( P 〈 0.05), while there was no effect in β-cat Δex2-6 mice. Although we also hypothesized increased autophagic activity, we found no effect on the autophagy-related protein LC3 in WT or β-cat Δex2-6 mice. In a translational approach, we profiled the left ventricular transcriptome of female patients ( n = 5) with end-stage non-ischemic dilated cardiomyopathy (DCM) vs. healthy controls ( n = 8). We found a significant induction in the expression of the genes coding for SFRP5 , a negative regulator of Wnt signaling, DACT2 , an antagonist of β-catenin, and APC2 , which is required for targeted degradation of β-catenin ( P 〈 0.01), in DCM samples. Our mouse data indicate that repression but not deletion of β-catenin leads to heart failure and our human data suggest that targeting Wnt/β-catenin signaling in heart failure may be of therapeutic value.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.119.suppl_1.400
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1467838-X
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  • 7
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    Reversible reprogramming of cardiomyocytes to a fetal state drives heart regeneration in mice
    American Association for the Advancement of Science (AAAS) ; 2021
    In:  Science Vol. 373, No. 6562 ( 2021-09-24), p. 1537-1540
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 373, No. 6562 ( 2021-09-24), p. 1537-1540
    Abstract: Cardiomyocyte (CM) replacement is very slow in adult mammalian hearts, preventing regeneration of damaged myocardium. By contrast, fetal hearts display considerable regenerative potential owing to the presence of less mature CMs that still have the ability to proliferate. In this study, we demonstrate that heart-specific expression of Oct4, Sox2, Klf4, and c-Myc (OSKM) induces adult CMs to dedifferentiate, conferring regenerative capacity to adult hearts. Transient, CM-specific expression of OSKM extends the regenerative window for postnatal mouse hearts and induces a gene expression program in adult CMs that resembles that of fetal CMs. Extended expression of OSKM in CMs leads to cellular reprogramming and heart tumor formation. Short-term OSKM expression before and during myocardial infarction ameliorates myocardial damage and improves cardiac function, demonstrating that temporally controlled dedifferentiation and reprogramming enable cell cycle reentry of mammalian CMs and facilitate heart regeneration.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.abg5159
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2021
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 8
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    Preclinical evidence for the therapeutic value of TBX5 normalization in arrhythmia control
    Oxford University Press (OUP) ; 2021
    In:  Cardiovascular Research Vol. 117, No. 8 ( 2021-07-07), p. 1908-1922
    Details
    In: Cardiovascular Research, Oxford University Press (OUP), Vol. 117, No. 8 ( 2021-07-07), p. 1908-1922
    Abstract: Arrhythmias and sudden cardiac death (SCD) occur commonly in patients with heart failure. We found T-box 5 (TBX5) dysregulated in ventricular myocardium from heart failure patients and thus we hypothesized that TBX5 reduction contributes to arrhythmia development in these patients. To understand the underlying mechanisms, we aimed to reveal the ventricular TBX5-dependent transcriptional network and further test the therapeutic potential of TBX5 level normalization in mice with documented arrhythmias. Methods and results  We used a mouse model of TBX5 conditional deletion in ventricular cardiomyocytes. Ventricular (v) TBX5 loss in mice resulted in mild cardiac dysfunction and arrhythmias and was associated with a high mortality rate (60%) due to SCD. Upon angiotensin stimulation, vTbx5KO mice showed exacerbated cardiac remodelling and dysfunction suggesting a cardioprotective role of TBX5. RNA-sequencing of a ventricular-specific TBX5KO mouse and TBX5 chromatin immunoprecipitation was used to dissect TBX5 transcriptional network in cardiac ventricular tissue. Overall, we identified 47 transcripts expressed under the control of TBX5, which may have contributed to the fatal arrhythmias in vTbx5KO mice. These included transcripts encoding for proteins implicated in cardiac conduction and contraction (Gja1, Kcnj5, Kcng2, Cacna1g, Chrm2), in cytoskeleton organization (Fstl4, Pdlim4, Emilin2, Cmya5), and cardiac protection upon stress (Fhl2, Gpr22, Fgf16). Interestingly, after TBX5 loss and arrhythmia development in vTbx5KO mice, TBX5 protein-level normalization by systemic adeno-associated-virus (AAV) 9 application, re-established TBX5-dependent transcriptome. Consequently, cardiac dysfunction was ameliorated and the propensity of arrhythmia occurrence was reduced. Conclusions  This study uncovers a novel cardioprotective role of TBX5 in the adult heart and provides preclinical evidence for the therapeutic value of TBX5 protein normalization in the control of arrhythmia.
    Type of Medium: Online Resource
    ISSN: 0008-6363 , 1755-3245
    URL: Article
    DOI: 10.1093/cvr/cvaa239
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 1499917-1
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  • 9
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    Abstract 377: KLF15-TCF7L2-dependent Cardiac Transcriptional Reprogramming Induces Cardiomyocyte and Vascular Cell Remodeling in the Mammalian Heart
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Circulation Research Vol. 125, No. Suppl_1 ( 2019-08-02)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. Suppl_1 ( 2019-08-02)
    Abstract: Integrative biochemical and omic-based approaches have refined our understanding of how cells integrate the Wnt signal at the chromatin level to yield specific cellular responses. However, this aspect remains unexplored in the heart. Since Wnt/β-catenin signaling activation is a hallmark in pathological cardiac remodeling, we aimed to characterize the specific Wnt cardiac transcriptional network regulation, amenable to therapeutic intervention in the adult heart. In the adult heart, we found the transcription factor KLF15 occupying regulatory regions of tissue remodeling genes containing Wnt transcriptional activator, TCF7L2, binding sites, which are silenced in the healthy myocardium but are active during pathological remodeling. Supporting KLF15 repressive roles, its loss resulted in cardiac TCF7L2 activation, maladaptive reprograming and failure in vivo . We demonstrated that KLF15 possess transcriptional age-specific repressive functions controlling Wnt signaling, cardiomyocyte de-differentiation and vascular cell (VC) remodeling. Employing different transgenic mouse models we further identified a cooperative program inducing aberrant VC remodeling, caused by a reduction of KLF15 with a concomitant TCF7L2 activation in cardiomyocytes. Furthermore, we characterized a cardiac specific Wnt transcriptional inhibitory complex consisting of KLF15 directly interacting with β-catenin and TCF7L2 and identified the amino acids critical for these interactions. Next, using a CRISPR/Cas9-mediated approach we generated KLF15 knockout (KO) hESC lines differentiated into functional cardiomyocytes and used for engineering human myocardium (EHM) generation. KLF15 KO EHMs showed activation of TCF7L2-dependent transcription as well as impaired function in comparison to control lines, recapitulating the Klf15 KO mouse phenotype. Altogether, we uncover an exquisite evolutionary conserved cardiac specific regulation mediated by KLF15 on Wnt signaling in myocardium offering a basis for designing highly specific pharmacological intervention for controlling Wnt cardiac-specific gene activation to prevent irreversible heart failure. We also underscore the significance of KLF15-Wnt dynamics in VC remodeling of the adult heart.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.125.suppl_1.377
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 1467838-X
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  • 10
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    Wnt Signaling Molecules in Left Ventricular Remodeling : Focus on Dishevelled 1
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Hypertension Vol. 55, No. 4 ( 2010-04), p. 852-854
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 55, No. 4 ( 2010-04), p. 852-854
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.109.143297
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 2094210-2
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