@book{MatchaQuastenRabighomi2010,
  author    = {Matcha, Heike and Quasten, Gero and Rabighomi, Hossein},
  title     = {Qualit{\"a}tssteigerung im verdichteten Wohnungsbau {\"u}ber Erzeugung gr{\"o}ßerer Vielfalt und Flexibilit{\"a}t durch individualisierte Massenfertigung am Beispiel gestapelter Reihenh{\"a}user},
  publisher = {Fraunhofer IRB Verlag},
  address   = {Stuttgart},
  isbn      = {978-3-8167-8216-2},
  pages     = {171 S. : graph. Darst.},
  year      = {2010},
  language  = {de}
}
@incollection{Matcha2010,
  author    = {Matcha, Heike},
  title     = {Regelbasierte Planung - Parametrik},
  series = {Digitale Prozesse: Planung, Gestaltung, Fertigung},
  booktitle = {Digitale Prozesse: Planung, Gestaltung, Fertigung},
  editor    = {Hauschild, Moritz and Karzel, R{\"u}diger},
  publisher = {Ed. Detail},
  address   = {M{\"u}nchen},
  isbn      = {978-3-920034-35-5},
  pages     = {24 -- 24},
  year      = {2010},
  language  = {de}
}
@incollection{Matcha2010,
  author    = {Matcha, Heike},
  title     = {Regelbasierte Planung - Parametrik},
  series = {Digitale Prozesse : Planung, Gestaltung, Fertigung},
  booktitle = {Digitale Prozesse : Planung, Gestaltung, Fertigung},
  editor    = {Hauschild, Moritz and Karzel, R{\"u}diger},
  publisher = {Detail},
  address   = {M{\"u}nchen},
  isbn      = {978-3-95553-022-8},
  doi       = {10.11129/detail.9783955530228},
  pages     = {24 -- 24},
  year      = {2010},
  language  = {de}
}
@book{Matcha2010,
  author    = {Matcha, Heike},
  title     = {Expo 15 : Experimental Parametric Object ; Realisierung des Messestandes "Digital Origami" f{\"u}r den Fachbereich Architektur der Technischen Universit{\"a}t Darmstadt},
  publisher = {Technische Universit{\"a}t Darmstadt},
  address   = {Darmstadt},
  pages     = {54 S. : Ill.},
  year      = {2010},
  language  = {de}
}
@inproceedings{MatchaLjubas2010,
  author    = {Matcha, Heike and Ljubas, Ante},
  title     = {Parametric Origami: Adaptable temporary buildings},
  series = {Future cities: 28th eCAADe Conference Proceedings. eCAADe: Conferences. Zurich, Switzerland},
  booktitle = {Future cities: 28th eCAADe Conference Proceedings. eCAADe: Conferences. Zurich, Switzerland},
  isbn      = {978-0-9541183-7-2},
  pages     = {243 -- 251},
  year      = {2010},
  language  = {en}
}
@techreport{Buedenbender2010,
  type      = {Working Paper},
  author    = {B{\"u}denbender, Martin},
  title     = {Entflechtung von Stromnetzen in Deutschland und Europa im Rahmen des dritten EU-Legislativpakets - Eine Problemdarstellung},
  series = {Arbeitspapiere des Instituts f{\"u}r Genossenschaftswesen der Westf{\"a}lischen Wilhelms-Universit{\"a}t M{\"u}nster, Nr. 91},
  journal   = {Arbeitspapiere des Instituts f{\"u}r Genossenschaftswesen der Westf{\"a}lischen Wilhelms-Universit{\"a}t M{\"u}nster, Nr. 91},
  pages     = {35},
  year      = {2010},
  language  = {de}
}
@inproceedings{GoemmelFrauenrathOttenetal.2010,
  author    = {G{\"o}mmel, Andreas and Frauenrath, Tobias and Otten, Mario and Niendorf, Thoralf and Butenweg, Christoph},
  title     = {In-vivo measurements of vocal fold geometry using Magnetic Resonance Imaging},
  series = {Fortschritte der Akustik - DAGA 2010 36. Jahrestagung f{\"u}r Akustik, 15. bis 18. M{\"a}rz 2010 in Berlin},
  booktitle = {Fortschritte der Akustik - DAGA 2010 36. Jahrestagung f{\"u}r Akustik, 15. bis 18. M{\"a}rz 2010 in Berlin},
  editor    = {M{\"o}ser, Michael and Schulte-Fortkamp, Brgitte and Ochmann, Martin},
  publisher = {Deutsche Gesellschaft f{\"u}r Akustik},
  address   = {Berlin},
  isbn      = {978-3-9808659-8-2},
  year      = {2010},
  language  = {de}
}
@article{BeckerFrauenrathHezeletal.2010,
  author    = {Becker, Meike and Frauenrath, Tobias and Hezel, Fabian and Krombach, Gabriele A. and Kremer, Ute and Koppers, Benedikt and Butenweg, Christoph and Goemmel, Andreas and Utting, Jane F. and Schulz-Menger, Jeanette and Niendorf, Thoralf},
  title     = {Comparison of left ventricular function assessment using phonocardiogram- and electrocardiogram-triggered 2D SSFP CINE MR imaging at 1.5 T and 3.0 T},
  series = {European Radiology},
  volume    = {20},
  journal   = {European Radiology},
  publisher = {Springer},
  address   = {Berlin},
  issn      = {1432-1084 (Onlineausgabe)},
  doi       = {10.1007/s00330-009-1676-z},
  pages     = {1344 -- 1355},
  year      = {2010},
  abstract  = {Objective: As high-field cardiac MRI (CMR) becomes more widespread the propensity of ECG to interference from electromagnetic fields (EMF) and to magneto-hydrodynamic (MHD) effects increases and with it the motivation for a CMR triggering alternative. This study explores the suitability of acoustic cardiac triggering (ACT) for left ventricular (LV) function assessment in healthy subjects (n=14). Methods: Quantitative analysis of 2D CINE steady-state free precession (SSFP) images was conducted to compare ACT's performance with vector ECG (VCG). Endocardial border sharpness (EBS) was examined paralleled by quantitative LV function assessment. Results: Unlike VCG, ACT provided signal traces free of interference from EMF or MHD effects. In the case of correct Rwave recognition, VCG-triggered 2D CINE SSFP was immune to cardiac motion effects—even at 3.0 T. However, VCG-triggered 2D SSFP CINE imaging was prone to cardiac motion and EBS degradation if R-wave misregistration occurred. ACT-triggered acquisitions yielded LV parameters (end-diastolic volume (EDV), endsystolic volume (ESV), stroke volume (SV), ejection fraction (EF) and left ventricular mass (LVM)) comparable with those derived fromVCG-triggered acquisitions (1.5 T: ESVVCG=(56± 17) ml, EDVVCG=(151±32)ml, LVMVCG=(97±27) g, SVVCG=(94± 19)ml, EFVCG=(63±5)\% cf. ESVACT= (56±18) ml, EDVACT=(147±36) ml, LVMACT=(102±29) g, SVACT=(91± 22) ml, EFACT=(62±6)\%; 3.0 T: ESVVCG=(55±21) ml, EDVVCG=(151±32) ml, LVMVCG=(101±27) g, SVVCG=(96±15) ml, EFVCG=(65±7)\% cf. ESVACT=(54±20) ml, EDVACT=(146±35) ml, LVMACT= (101±30) g, SVACT=(92±17) ml, EFACT=(64±6)\%). Conclusions: ACT's intrinsic insensitivity to interference from electromagnetic fields renders},
  language  = {en}
}
@article{RossPlummerRodeetal.2010,
  author    = {Ross, Jillian and Plummer, Simon M. and Rode, Anja and Scheer, Nico and Bower, Conrad C. and Vogel, Ortwin and Henderson, Colin J. and Wolf, C. Roland and Elcombe, Clifford R.},
  title     = {Human constitutive androstane receptor (CAR) and pregnane X receptor (PXR) support the hypertrophic but not the hyperplastic response to the murine nongenotoxic hepatocarcinogens phenobarbital and chlordane in vivo},
  series = {Toxicological Sciences},
  volume    = {116},
  journal   = {Toxicological Sciences},
  number    = {2},
  publisher = {Oxford University Press},
  address   = {Oxford},
  issn      = {1096-0929},
  doi       = {10.1093/toxsci/kfq118},
  pages     = {452 -- 466},
  year      = {2010},
  abstract  = {Mouse nongenotoxic hepatocarcinogens phenobarbital (PB) and chlordane induce hepatomegaly characterized by hypertrophy and hyperplasia. Increased cell proliferation is implicated in the mechanism of tumor induction. The relevance of these tumors to human health is unclear. The xenoreceptors, constitutive androstane receptors (CARs), and pregnane X receptor (PXR) play key roles in these processes. Novel "humanized" and knockout models for both receptors were developed to investigate potential species differences in hepatomegaly. The effects of PB (80 mg/kg/4 days) and chlordane (10 mg/kg/4 days) were investigated in double humanized PXR and CAR (huPXR/huCAR), double knockout PXR and CAR (PXRKO/CARKO), and wild-type (WT) C57BL/6J mice. In WT mice, both compounds caused increased liver weight, hepatocellular hypertrophy, and cell proliferation. Both compounds caused alterations to a number of cell cycle genes consistent with induction of cell proliferation in WT mice. However, these gene expression changes did not occur in PXRKO/CARKO or huPXR/huCAR mice. Liver hypertrophy without hyperplasia was demonstrated in the huPXR/huCAR animals in response to both compounds. Induction of the CAR and PXR target genes, Cyp2b10 and Cyp3a11, was observed in both WT and huPXR/huCAR mouse lines following treatment with PB or chlordane. In the PXRKO/CARKO mice, neither liver growth nor induction of Cyp2b10 and Cyp3a11 was seen following PB or chlordane treatment, indicating that these effects are CAR/PXR dependent. These data suggest that the human receptors are able to support the chemically induced hypertrophic responses but not the hyperplastic (cell proliferation) responses. At this time, we cannot be certain that hCAR and hPXR when expressed in the mouse can function exactly as the genes do when they are expressed in human cells. However, all parameters investigated to date suggest that much of their functionality is maintained.},
  language  = {en}
}
@article{ScheerRossKapelyukhetal.2010,
  author    = {Scheer, Nico and Ross, Jillian and Kapelyukh, Yury and Rode, Anja and Wolf, C. Roland},
  title     = {In vivo responses of the human and murine pregnane X receptor to dexamethasone in mice},
  series = {Drug Metabolism and Disposition},
  volume    = {38},
  journal   = {Drug Metabolism and Disposition},
  number    = {7},
  publisher = {ASPET},
  address   = {Bethesda},
  issn      = {1521-009X},
  doi       = {10.1124/dmd.109.031872},
  pages     = {1046 -- 1053},
  year      = {2010},
  abstract  = {Dexamethasone (DEX) is a potent and widely used anti-inflammatory and immunosuppressant glucocorticoid. It can bind and activate the pregnane X receptor (PXR), which plays a critical role as xenobiotic sensor in mammals to induce the expression of many enzymes, including cytochromes P450 in the CYP3A family. This induction results in its own metabolism. We have used a series of transgenic mouse lines, including a novel, improved humanized PXR line, to compare the induction profile of PXR-regulated drug-metabolizing enzymes after DEX administration, as well as looking at hepatic responses to rifampicin (RIF). The new humanized PXR model has uncovered further intriguing differences between the human and mouse receptors in that RIF only induced Cyp2b10 in the new humanized model. DEX was found to be a much more potent inducer of Cyp3a proteins in wild-type mice than in mice humanized for PXR. To assess whether PXR is involved in the detoxification of DEX in the liver, we analyzed the consequences of high doses of the glucocorticoid on hepatotoxicity on different PXR genetic backgrounds. We also studied these effects in an additional mouse model in which functional mouse Cyp3a genes have been deleted. These strains exhibited different sensitivities to DEX, indicating a protective role of the PXR and CYP3A proteins against the hepatotoxicity of this compound.},
  language  = {en}
}