LIVIVO - Search results -

Search results

Result 1 - 10 of total 30

Search options

Book: UEBER DIE HAEUFIGKEIT UND DEN THERAPEUTISCHEN EFFEKT DER BEI ENTZUENDLICHEN GELENK- UND WIRBELSAEULENERKRANKUNGEN DURCHGEFUEHRTEN HERDSANIERUNGEN

Zenz, Rainer

1977

Size	42 S.
Document type	Book
Note	MAINZ, UNIV., FACHBEREICH 05-10 - MEDIZIN, DISS., 1977
HBZ-ID	HT002590846
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

Shelf mark	Loan status	Location
77 D 1911	order for loan	Magazin

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article: Jun signalling in the epidermis: From developmental defects to psoriasis and skin tumors.

Zenz, Rainer / Wagner, Erwin F

The international journal of biochemistry & cell biology

2006 Volume 38, Issue 7, Page(s) 1043–1049

Abstract: The Jun proteins Jun, JunB and JunD are core members of activator protein-1 (AP-1), a dimeric transcription factor complex consisting of homo- and heterodimers of the Jun, Fos, activating transcription factor (ATF) and musculoaponeurotic fibrosarcoma ( ... ...

Abstract	The Jun proteins Jun, JunB and JunD are core members of activator protein-1 (AP-1), a dimeric transcription factor complex consisting of homo- and heterodimers of the Jun, Fos, activating transcription factor (ATF) and musculoaponeurotic fibrosarcoma (Maf) families. Growth factors, hormones and a variety of environmental stresses activate mitogen activated protein kinase (MAPK) cascades that enhance Jun/AP-1 activity, e.g. through phosphorylation thereby regulating cell proliferation, differentiation, transformation and/or apoptosis. Embryonic lethality of various AP-1 knock-outs, e.g. for Jun, JunB, Fra-1 and Fra-2 largely prevented functional studies in vivo. Therefore, conditional knock-out strategies, in particular for the epidermis, have become an important model to study the regulation and function of AP-1 subunits in physiological and pathological processes in vivo. Jun is regarded as a positive regulator of keratinocyte proliferation/differentiation during development and in skin cancer through its direct transcriptional effect on epidermal growth factor receptor (EGFR) expression. In contrast, JunB can antagonize proliferation of keratinocytes and hematopoietic stem cells. Furthermore, it has been demonstrated in patient's samples and an inducible mouse model that down-regulation of JunB/AP-1 in keratinocytes is one initiating event in the aetiology of psoriasis which is characterized by increased cell proliferation and deregulated cytokine expression.
MeSH term(s)	Activating Transcription Factors/metabolism ; Animals ; DNA-Binding Proteins/metabolism ; Developmental Biology ; Epidermis/metabolism ; Humans ; Keratinocytes/metabolism ; MAP Kinase Kinase 1/metabolism ; Mice ; Proto-Oncogene Proteins c-fos/metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Psoriasis/physiopathology ; Signal Transduction/physiology ; Skin Neoplasms/physiopathology ; Transcription Factor AP-1/metabolism ; Transcription Factors/metabolism
Chemical Substances	Activating Transcription Factors ; DNA-Binding Proteins ; Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins c-jun ; Transcription Factor AP-1 ; Transcription Factors ; MAP Kinase Kinase 1 (EC 2.7.12.2)
Language	English
Publishing date	2006
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2005.11.011
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 431: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: STAT3 promotes melanoma metastasis by CEBP-induced repression of the MITF pathway.

Swoboda, Alexander / Soukup, Robert / Eckel, Oliver / Kinslechner, Katharina / Wingelhofer, Bettina / Schörghofer, David / Sternberg, Christina / Pham, Ha T T / Vallianou, Maria / Horvath, Jaqueline / Stoiber, Dagmar / Kenner, Lukas / Larue, Lionel / Poli, Valeria / Beermann, Friedrich / Yokota, Takashi / Kubicek, Stefan / Krausgruber, Thomas / Rendeiro, André F /

Bock, Christoph / Zenz, Rainer / Kovacic, Boris / Aberger, Fritz / Hengstschläger, Markus / Petzelbauer, Peter / Mikula, Mario / Moriggl, Richard

Oncogene

2020 Volume 40, Issue 6, Page(s) 1091–1105

Abstract: Metastatic melanoma is hallmarked by its ability of phenotype switching to more slowly proliferating, but highly invasive cells. Here, we tested the impact of signal transducer and activator of transcription 3 (STAT3) on melanoma progression in ... ...

Abstract	Metastatic melanoma is hallmarked by its ability of phenotype switching to more slowly proliferating, but highly invasive cells. Here, we tested the impact of signal transducer and activator of transcription 3 (STAT3) on melanoma progression in association with melanocyte inducing transcription factor (MITF) expression levels. We established a mouse melanoma model for deleting Stat3 in melanocytes with specific expression of human hyperactive NRAS
MeSH term(s)	Animals ; CCAAT-Enhancer-Binding Protein-beta/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Melanocytes/drug effects ; Melanoma/genetics ; Melanoma/pathology ; Mice ; Microphthalmia-Associated Transcription Factor/genetics ; Neoplasm Metastasis ; STAT3 Transcription Factor/genetics ; Signal Transduction/drug effects
Chemical Substances	CCAAT-Enhancer-Binding Protein-beta ; Cebpb protein, mouse ; Microphthalmia-Associated Transcription Factor ; Mitf protein, mouse ; STAT3 Transcription Factor ; Stat3 protein, mouse
Language	English
Publishing date	2020-12-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-020-01584-6
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2218: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: PhiC31-mediated cassette exchange into a bacterial artificial chromosome.

Blaas, Leander / Musteanu, Monica / Zenz, Rainer / Eferl, Robert / Casanova, Emilio

BioTechniques

2007 Volume 43, Issue 5, Page(s) 659–60, 662, 664

Abstract: The use of bacterial artificial chromosomes (BACs) modified via homologous recombination in Escherichia coli has become a powerful tool in the transgenic field. Homologous recombination allows the manipulation of BACs in very different ways. However this ...

Abstract	The use of bacterial artificial chromosomes (BACs) modified via homologous recombination in Escherichia coli has become a powerful tool in the transgenic field. Homologous recombination allows the manipulation of BACs in very different ways. However this process can be cumbersome and problematic when using large targeting constructs containing several repeated elements. In order to address this problem, we have established a phiC31 integrase-mediated cassette exchange into a BAC. As an example of this technique, we have exchanged a cassette previously recombined into a BAC containing the Rosa 26 locus, by a 16.5-kb incoming construct containing several repeated elements. The combination of homologous recombination in E. coli and cassette exchange should expand the tools for manipulating BACs, thus facilitating the generation of constructs with higher complexity.
MeSH term(s)	Bacteriophages/enzymology ; Chromosomes, Artificial, Bacterial/genetics ; Integrases/metabolism ; Mutagenesis, Insertional/methods
Chemical Substances	Integrases (EC 2.7.7.-)
Language	English
Publishing date	2007-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	48453-2
ISSN	1940-9818 ; 0736-6205
ISSN (online)	1940-9818
ISSN	0736-6205
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2435: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Simultaneous generation of fra-2 conditional and fra-2 knock-out mice.

Eferl, Robert / Zenz, Rainer / Theussl, Hans-Christian / Wagner, Erwin F

Genesis (New York, N.Y. : 2000)

2007 Volume 45, Issue 7, Page(s) 447–451

Abstract: Loss of function mouse models comprise knock-out mice, where a gene is deleted in the germline, and conditional knock-out mice with somatic deletion of a floxed allele in defined tissues. Both types of mice are used for comprehensive studies of gene ... ...

Abstract	Loss of function mouse models comprise knock-out mice, where a gene is deleted in the germline, and conditional knock-out mice with somatic deletion of a floxed allele in defined tissues. Both types of mice are used for comprehensive studies of gene functions in vivo. Here, we describe a simple method for simultaneous generation of mice with conditional or knock-out alleles for the transcription factor fra-2 (Fos-related antigen 2) using a single embryonic stem (ES) cell clone. ES cells with a floxed fra-2 allele were transiently transfected with a Cre-recombinase expression plasmid and plated at low density. Most of the resulting ES cell colonies consisted of a mixture of cells that have either retained or lost the conditional allele. We demonstrate that these mixed ES cell clones can be directly used for generation of chimeras that give rise to offspring with conditional or knock-out alleles simultaneously. This strategy shortens the time and reduces the number of germline transmission events to generate genetically modified mice.
MeSH term(s)	Animals ; Fos-Related Antigen-2/deficiency ; Fos-Related Antigen-2/genetics ; Genes, Lethal ; Mice ; Mice, Knockout
Chemical Substances	Fos-Related Antigen-2 ; Fosl2 protein, mouse
Language	English
Publishing date	2007-07
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2004544-X
ISSN	1526-968X ; 1526-954X
ISSN (online)	1526-968X
ISSN	1526-954X
DOI	10.1002/dvg.20311
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2772: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Differentiation-induced skin cancer suppression by FOS, p53, and TACE/ADAM17.

Guinea-Viniegra, Juan / Zenz, Rainer / Scheuch, Harald / Jiménez, María / Bakiri, Latifa / Petzelbauer, Peter / Wagner, Erwin F

The Journal of clinical investigation

2012 Volume 122, Issue 8, Page(s) 2898–2910

Abstract: Squamous cell carcinomas (SCCs) are heterogeneous and aggressive skin tumors for which innovative, targeted therapies are needed. Here, we identify a p53/TACE pathway that is negatively regulated by FOS and show that the FOS/p53/TACE axis suppresses SCC ... ...

Abstract	Squamous cell carcinomas (SCCs) are heterogeneous and aggressive skin tumors for which innovative, targeted therapies are needed. Here, we identify a p53/TACE pathway that is negatively regulated by FOS and show that the FOS/p53/TACE axis suppresses SCC by inducing differentiation. We found that epidermal Fos deletion in mouse tumor models or pharmacological FOS/AP-1 inhibition in human SCC cell lines induced p53 expression. Epidermal cell differentiation and skin tumor suppression were caused by a p53-dependent transcriptional activation of the metalloprotease TACE/ADAM17 (TNF-α-converting enzyme), a previously unknown p53 target gene that was required for NOTCH1 activation. Although half of cutaneous human SCCs display p53-inactivating mutations, restoring p53/TACE activity in mouse and human skin SCCs induced tumor cell differentiation independently of the p53 status. We propose FOS/AP-1 inhibition or p53/TACE reactivating strategies as differentiation-inducing therapies for SCCs.
MeSH term(s)	ADAM Proteins/genetics ; ADAM Proteins/metabolism ; ADAM17 Protein ; Animals ; Base Sequence ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; Carcinoma, Squamous Cell/therapy ; Cell Differentiation ; Cell Line, Tumor ; DNA Primers/genetics ; Gene Expression ; Humans ; Keratinocytes/metabolism ; Keratinocytes/pathology ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Proto-Oncogene Proteins c-fos/antagonists & inhibitors ; Proto-Oncogene Proteins c-fos/deficiency ; Proto-Oncogene Proteins c-fos/genetics ; Proto-Oncogene Proteins c-fos/metabolism ; Signal Transduction ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology ; Skin Neoplasms/therapy ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	DNA Primers ; Proto-Oncogene Proteins c-fos ; Tumor Suppressor Protein p53 ; ADAM Proteins (EC 3.4.24.-) ; ADAM17 Protein (EC 3.4.24.86) ; ADAM17 protein, human (EC 3.4.24.86) ; Adam17 protein, mouse (EC 3.4.24.86)
Language	English
Publishing date	2012-07-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI63103
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ua VI Zs.184: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Epigenetic silencing of miR-708 enhances NF-κB signaling in chronic lymphocytic leukemia.

Baer, Constance / Oakes, Christopher C / Ruppert, Amy S / Claus, Rainer / Kim-Wanner, Soo-Zin / Mertens, Daniel / Zenz, Thorsten / Stilgenbauer, Stephan / Byrd, John C / Plass, Christoph

International journal of cancer

2015 Volume 137, Issue 6, Page(s) 1352–1361

Abstract: MicroRNAs (miRNAs) are post-transcriptional regulators of gene expression and their deregulation is involved in tumor development. Epigenetic gene silencing in cancer by DNA methylation contributes to the silencing of tumor-suppressor genes, including ... ...

Abstract	MicroRNAs (miRNAs) are post-transcriptional regulators of gene expression and their deregulation is involved in tumor development. Epigenetic gene silencing in cancer by DNA methylation contributes to the silencing of tumor-suppressor genes, including miRNAs. We have recently shown that the promoter of miR-708 is aberrantly methylated in chronic lymphocytic leukemia (CLL). To characterize the molecular signaling networks that are influenced by miR-708, we performed a luciferase-based screen evaluating the effects of ectopic miR-708 expression on leukemia-relevant signaling pathways. We found that miR-708 strongly repressed NF-κB signaling, a pathway known to be deregulated in CLL. Among the predicted miR-708 targets was IKKβ (inhibitor of kappa light polypeptide gene enhancer in B cells, kinase-β/IKBKB), a key kinase facilitating NF-κB signaling. We validated the interaction of miR-708 with the 3'-untranslated region of IKKβ and found that miR-708 overexpression represses endogenous IKKβ. Phosphorylation of the IKKβ target IκBα and expression of known NF-κB target genes were impaired by miR-708. Furthermore, we identified an enhancer region downstream of the miR-708 promoter that displays a distinct DNA methylation status in CLL. High enhancer methylation is significantly correlated with lower miR-708 expression and is predominantly found in patients with poor prognosis and shorter time to treatment. These results demonstrate that miR-708 regulates the NF-κB pathway by targeting IKKβ, and that methylation of a key enhancer region contributes to its suppression in CLL.
MeSH term(s)	3' Untranslated Regions/genetics ; Cell Line ; DNA Methylation/genetics ; Epigenesis, Genetic/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Gene Silencing/physiology ; HEK293 Cells ; Humans ; I-kappa B Kinase/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; MicroRNAs/genetics ; NF-kappa B/genetics ; Phosphorylation/genetics ; Promoter Regions, Genetic/genetics ; Signal Transduction/genetics
Chemical Substances	3' Untranslated Regions ; MIRN708 microRNA, human ; MicroRNAs ; NF-kappa B ; I-kappa B Kinase (EC 2.7.11.10)
Language	English
Publishing date	2015-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.29491
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 478: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 576: Show issues

Order via subito

Details ▾

Article ; Online: ΦC31-mediated cassette exchange into a bacterial artificial chromosome

Leander Blaas / Monica Musteanu / Rainer Zenz / Robert Eferl / Emilio Casanova

BioTechniques, Vol 43, Iss 5, Pp 659-

2007 Volume 664

Abstract	The use of bacterial artificial chromosomes (BACs) modified via homologous recombination in Escherichia coli has become a powerful tool in the transgenic field. Homologous recombination allows the manipulation of BACs in very different ways. However, this process can be cumbersome and problematic when using large targeting constructs containing several repeated elements. In order to address this problem, we have established a ΦC31 integrase-mediated cassette exchange into a BAC. As an example of this technique, we have exchanged a cassette previously recombined into a BAC containing the Rosa 26 locus, by a 16.5-kb incoming construct containing several repeated elements. The combination of homologous recombination in E. coli and cassette exchange should expand the tools for manipulating BACs, thus facilitating the generation of constructs with higher complexity.
Keywords	Biology (General) ; QH301-705.5
Language	English
Publishing date	2007-11-01T00:00:00Z
Publisher	Future Science Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: EGFR has a tumour-promoting role in liver macrophages during hepatocellular carcinoma formation.

Lanaya, Hanane / Natarajan, Anuradha / Komposch, Karin / Li, Liang / Amberg, Nicole / Chen, Lei / Wculek, Stefanie K / Hammer, Martina / Zenz, Rainer / Peck-Radosavljevic, Markus / Sieghart, Wolfgang / Trauner, Michael / Wang, Hongyang / Sibilia, Maria

Nature cell biology

2014 Volume 16, Issue 10, Page(s) 972–977

Abstract: Hepatocellular carcinoma (HCC) is a frequent cancer with limited treatment options and poor prognosis. Tumorigenesis has been linked with macrophage-mediated chronic inflammation and diverse signalling pathways, including the epidermal growth factor ... ...

Abstract	Hepatocellular carcinoma (HCC) is a frequent cancer with limited treatment options and poor prognosis. Tumorigenesis has been linked with macrophage-mediated chronic inflammation and diverse signalling pathways, including the epidermal growth factor receptor (EGFR) pathway. The precise role of EGFR in HCC is unknown, and EGFR inhibitors have shown disappointing clinical results. Here we discover that EGFR is expressed in liver macrophages in both human HCC and in a mouse HCC model. Mice lacking EGFR in macrophages show impaired hepatocarcinogenesis, whereas mice lacking EGFR in hepatocytes unexpectedly develop more HCC owing to increased hepatocyte damage and compensatory proliferation. Mechanistically, following interleukin-1 stimulation, EGFR is required in liver macrophages to transcriptionally induce interleukin-6, which triggers hepatocyte proliferation and HCC. Importantly, the presence of EGFR-positive liver macrophages in HCC patients is associated with poor survival. This study demonstrates a tumour-promoting mechanism for EGFR in non-tumour cells, which could lead to more effective precision medicine strategies.
MeSH term(s)	Animals ; Blotting, Western ; Carcinoma, Hepatocellular/chemically induced ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Cells, Cultured ; Diethylnitrosamine ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Hepatocytes/metabolism ; Humans ; Immunohistochemistry ; Interleukin-1beta/pharmacology ; Kupffer Cells/drug effects ; Kupffer Cells/metabolism ; Liver/metabolism ; Liver/pathology ; Liver Neoplasms/chemically induced ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Macrophages/metabolism ; Male ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Knockout ; Mice, Transgenic ; Phosphorylation/drug effects
Chemical Substances	Interleukin-1beta ; Diethylnitrosamine (3IQ78TTX1A) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2014-08-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/ncb3031
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5169: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 12: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Book ; Thesis: Über die Häufigkeit und den therapeutischen Effekt der bei entzündlichen Gelenk- und Wirbelsäulenerkrankungen durchgeführten Herdsanierungen

Zenz, Rainer

1977

Author's details	Rainer Zenz
Language	German
Size	42 S
Document type	Book ; Thesis
Thesis / German Habilitation thesis	@Mainz, Univ., Fachbereich 05-10 - Medizin, Diss. : 1977
Database	Former special subject collection: coastal and deep sea fishing

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

To top

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Inter-library loan at ZB MED