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Article: The Clock Takes Shape-24 h Dynamics in Genome Topology.

Tartour, Kévin / Padmanabhan, Kiran

Frontiers in cell and developmental biology

2022 Volume 9, Page(s) 799971

Abstract: Circadian rhythms orchestrate organismal physiology and behavior in order to anticipate daily changes in the environment. Virtually all cells have an internal rhythm that is synchronized every day by Zeitgebers (environmental cues). The synchrony between ...

Abstract	Circadian rhythms orchestrate organismal physiology and behavior in order to anticipate daily changes in the environment. Virtually all cells have an internal rhythm that is synchronized every day by Zeitgebers (environmental cues). The synchrony between clocks within the animal enables the fitness and the health of organisms. Conversely, disruption of rhythms is linked to a variety of disorders: aging, cancer, metabolic diseases, and psychological disorders among others. At the cellular level, mammalian circadian rhythms are built on several layers of complexity. The transcriptional-translational feedback loop (TTFL) was the first to be described in the 90s. Thereafter oscillations in epigenetic marks highlighted the role of chromatin state in organizing the TTFL. More recently, studies on the 3D organization of the genome suggest that genome topology could be yet another layer of control on cellular circadian rhythms. The dynamic nature of genome topology over a solar day implies that the 3D mammalian genome has to be considered in the fourth dimension-in time. Whether oscillations in genome topology are a consequence of 24 h gene-expression or a driver of transcriptional cycles remains an open question. All said and done, circadian clock-gated phenomena such as gene expression, DNA damage response, cell metabolism and animal behavior-go hand in hand with 24 h rhythms in genome topology.
Language	English
Publishing date	2022-01-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.799971
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Article ; Online: The Clock Takes Shape—24 h Dynamics in Genome Topology

Kévin Tartour / Kiran Padmanabhan

Frontiers in Cell and Developmental Biology, Vol

2022 Volume 9

Abstract	Circadian rhythms orchestrate organismal physiology and behavior in order to anticipate daily changes in the environment. Virtually all cells have an internal rhythm that is synchronized every day by Zeitgebers (environmental cues). The synchrony between clocks within the animal enables the fitness and the health of organisms. Conversely, disruption of rhythms is linked to a variety of disorders: aging, cancer, metabolic diseases, and psychological disorders among others. At the cellular level, mammalian circadian rhythms are built on several layers of complexity. The transcriptional-translational feedback loop (TTFL) was the first to be described in the 90s. Thereafter oscillations in epigenetic marks highlighted the role of chromatin state in organizing the TTFL. More recently, studies on the 3D organization of the genome suggest that genome topology could be yet another layer of control on cellular circadian rhythms. The dynamic nature of genome topology over a solar day implies that the 3D mammalian genome has to be considered in the fourth dimension-in time. Whether oscillations in genome topology are a consequence of 24 h gene-expression or a driver of transcriptional cycles remains an open question. All said and done, circadian clock-gated phenomena such as gene expression, DNA damage response, cell metabolism and animal behavior—go hand in hand with 24 h rhythms in genome topology.
Keywords	circadian rhythm ; clock ; genome topology ; 3D genome ; chromatin ; DNA damage ; Biology (General) ; QH301-705.5
Subject code	612
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Touch receptor end-organ innervation and function require sensory neuron expression of the transcription factor Meis2.

Desiderio, Simon / Schwaller, Frederick / Tartour, Kevin / Padmanabhan, Kiran / Lewin, Gary R / Carroll, Patrick / Marmigere, Frederic

eLife

2024 Volume 12

Abstract: Touch sensation is primarily encoded by mechanoreceptors, called low-threshold mechanoreceptors (LTMRs), with their cell bodies in the dorsal root ganglia. Because of their great diversity in terms of molecular signature, terminal endings morphology, and ...

Abstract	Touch sensation is primarily encoded by mechanoreceptors, called low-threshold mechanoreceptors (LTMRs), with their cell bodies in the dorsal root ganglia. Because of their great diversity in terms of molecular signature, terminal endings morphology, and electrophysiological properties, mirroring the complexity of tactile experience, LTMRs are a model of choice to study the molecular cues differentially controlling neuronal diversification. While the transcriptional codes that define different LTMR subtypes have been extensively studied, the molecular players that participate in their late maturation and in particular in the striking diversity of their end-organ morphological specialization are largely unknown. Here we identified the TALE homeodomain transcription factor Meis2 as a key regulator of LTMRs target-field innervation in mice.
MeSH term(s)	Animals ; Mice ; Gene Expression Regulation ; Mechanoreceptors ; Nervous System Physiological Phenomena ; Sensory Receptor Cells ; Transcription Factors/genetics ; Homeodomain Proteins/genetics
Chemical Substances	Transcription Factors ; Mrg1 protein, mouse ; Homeodomain Proteins
Language	English
Publishing date	2024-02-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.89287
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Article ; Online: Detecting abnormal cell behaviors from dry mass time series.

Bailly, Romain / Malfante, Marielle / Allier, Cédric / Paviolo, Chiara / Ghenim, Lamya / Padmanabhan, Kiran / Bardin, Sabine / Mars, Jérôme

Scientific reports

2024 Volume 14, Issue 1, Page(s) 7053

Abstract: The prediction of pathological changes on single cell behaviour is a challenging task for deep learning models. Indeed, in self-supervised learning methods, no prior labels are used for the training and all of the information for event predictions are ... ...

Abstract	The prediction of pathological changes on single cell behaviour is a challenging task for deep learning models. Indeed, in self-supervised learning methods, no prior labels are used for the training and all of the information for event predictions are extracted from the data themselves. We present here a novel self-supervised learning model for the detection of anomalies in a given cell population, StArDusTS. Cells are monitored over time, and analysed to extract time-series of dry mass values. We assessed its performances on different cell lines, showing a precision of 96% in the automatic detection of anomalies. Additionally, anomaly detection was also associated with cell measurement errors inherent to the acquisition or analysis pipelines, leading to an improvement of the upstream methods for feature extraction. Our results pave the way to novel architectures for the continuous monitoring of cell cultures in applied research or bioproduction applications, and for the prediction of pathological cellular changes.
MeSH term(s)	Humans ; Time Factors ; Problem Behavior ; Cell Culture Techniques ; Cell Line ; Self-Management
Language	English
Publishing date	2024-03-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-57684-w
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Article: Desynchronization of Circadian Clocks in Cancer: A Metabolic and Epigenetic Connection.

Padmanabhan, Kiran / Billaud, Marc

Frontiers in endocrinology

2017 Volume 8, Page(s) 136

Abstract: Circadian clocks are innate oscillators that drive daily rhythms in metabolism, physiology, and behavior. 24-h rhythms in gene expression, driven by core clock transcription factors, reflect the epigenetic state of the cell, which in turn is dictated by ... ...

Abstract	Circadian clocks are innate oscillators that drive daily rhythms in metabolism, physiology, and behavior. 24-h rhythms in gene expression, driven by core clock transcription factors, reflect the epigenetic state of the cell, which in turn is dictated by the metabolic environment. Cancer cells alter their metabolic state and gene expression and therefore are likely to tweak circadian clock function in their favor. Over the past decade, we have witnessed an extraordinary increase in systems-level studies that suggest intricate mechanistic links between the cellular metabolome and the circadian epigenome. In parallel, reprogramming of cellular clock function in cancers is increasingly evident and the role of clock genes in the development of hematological tumors, as well as their pathophysiological effects on tissues distal to the tumor, has been described. Furthermore, the interplay between components of the circadian clock, metabolic enzymes, and oncogenes is starting to be better understood, such as the close association between overexpression of the Myc oncogene and perturbation of circadian and metabolic rhythms, thus opening new avenues to treat cancers. This review article explores current knowledge on the circadian metabolome and the molecular pathways they control, with a focus on their involvement in the development of hematopoietic malignancies.
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2017.00136
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Article ; Online: Oppositional poly(A) tail length regulation by FMRP and CPEB1.

Shin, Jihae / Paek, Ki Young / Chikhaoui, Lies / Jung, Suna / Ponny, SitharaRaju / Suzuki, Yutaka / Padmanabhan, Kiran / Richter, Joel D

RNA (New York, N.Y.)

2022 Volume 28, Issue 5, Page(s) 756–765

Abstract: Poly(A) tail length is regulated in both the nucleus and cytoplasm. One factor that controls polyadenylation in the cytoplasm is CPEB1, an RNA binding protein that associates with specific mRNA 3'UTR sequences to tether enzymes that add and remove poly(A) ...

Abstract	Poly(A) tail length is regulated in both the nucleus and cytoplasm. One factor that controls polyadenylation in the cytoplasm is CPEB1, an RNA binding protein that associates with specific mRNA 3'UTR sequences to tether enzymes that add and remove poly(A). Two of these enzymes, the noncanonical poly(A) polymerases GLD2 (TENT2, PAPD4, Wispy) and GLD4 (TENT4B, PAPD5, TRF4, TUT3), interact with CPEB1 to extend poly(A). To identify additional RNA binding proteins that might anchor GLD4 to RNA, we expressed double tagged GLD4 in U87MG cells, which was used for sequential immunoprecipitation and elution followed by mass spectrometry. We identified several RNA binding proteins that coprecipitated with GLD4, among which was FMRP. To assess whether FMRP regulates polyadenylation, we performed TAIL-seq from WT and FMRP-deficient HEK293 cells. Surprisingly, loss of FMRP resulted in an overall increase in poly(A), which was also observed for several specific mRNAs. Conversely, loss of CPEB1 elicited an expected decrease in poly(A), which was examined in cultured neurons. We also examined polyadenylation in wild type (WT) and FMRP-deficient mouse brain cortex by direct RNA nanopore sequencing, which identified RNAs with both increased and decreased poly(A). Our data show that FMRP has a role in mediating poly(A) tail length, which adds to its repertoire of RNA regulation.
MeSH term(s)	Animals ; HEK293 Cells ; Humans ; Mice ; Poly A/genetics ; Poly A/metabolism ; Polyadenylation ; Polynucleotide Adenylyltransferase/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Transcription Factors/genetics ; mRNA Cleavage and Polyadenylation Factors/genetics ; mRNA Cleavage and Polyadenylation Factors/metabolism
Chemical Substances	CPEB1 protein, human ; RNA, Messenger ; RNA-Binding Proteins ; Transcription Factors ; mRNA Cleavage and Polyadenylation Factors ; Poly A (24937-83-5) ; Polynucleotide Adenylyltransferase (EC 2.7.7.19)
Language	English
Publishing date	2022-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1241540-6
ISSN	1469-9001 ; 1355-8382
ISSN (online)	1469-9001
ISSN	1355-8382
DOI	10.1261/rna.079050.121
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Article ; Online: Mammalian PERIOD2 regulates H2A.Z incorporation in chromatin to orchestrate circadian negative feedback.

Tartour, Kevin / Andriani, Francesca / Folco, Eric G / Letkova, Dominika / Schneider, Raphael / Saidi, Isahak / Sato, Tomoki / Welz, Patrick-Simon / Benitah, Salvador Aznar / Allier, Cédric / Padmanabhan, Kiran

Nature structural & molecular biology

2022 Volume 29, Issue 6, Page(s) 549–562

Abstract: Mammalian circadian oscillators are built on a feedback loop in which the activity of the transcription factor CLOCK-BMAL1 is repressed by the PER-CRY complex. Here, we show that murine ... ...

Abstract	Mammalian circadian oscillators are built on a feedback loop in which the activity of the transcription factor CLOCK-BMAL1 is repressed by the PER-CRY complex. Here, we show that murine Per
MeSH term(s)	ARNTL Transcription Factors/genetics ; ARNTL Transcription Factors/metabolism ; Animals ; Chromatin ; Circadian Rhythm/physiology ; Feedback ; Histones/metabolism ; Mammals/genetics ; Mice ; Nucleosomes ; Period Circadian Proteins/metabolism
Chemical Substances	ARNTL Transcription Factors ; Chromatin ; Histones ; Nucleosomes ; Per2 protein, mouse ; Period Circadian Proteins
Language	English
Publishing date	2022-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2126708-X
ISSN	1545-9985 ; 1545-9993
ISSN (online)	1545-9985
ISSN	1545-9993
DOI	10.1038/s41594-022-00777-9
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Article ; Online: Comparative Evaluation of Remineralizing Effect of Novamin and Tricalcium Phosphate on Artificial Caries: An in vitro Study.

Jagga, Umang / Paul, Uttam / Padmanabhan, Vivek / Kashyap, Arpita / Guram, Guneet / Keswani, Kiran

The journal of contemporary dental practice

2018 Volume 19, Issue 1, Page(s) 109–112

Abstract: Aim: The aim of the present study was to compare the remineralizing efficacy of novamin and tricalcium phosphate (TCP).: Materials and methods: Nail varnish was coated to a total of 30 sound human premolars except for 5 mm × 5 mm window. Baseline ... ...

Abstract	Aim: The aim of the present study was to compare the remineralizing efficacy of novamin and tricalcium phosphate (TCP). Materials and methods: Nail varnish was coated to a total of 30 sound human premolars except for 5 mm × 5 mm window. Baseline microhardness was measured for all test samples. Artificial carious lesions were created for all teeth by subjecting them to demineralization process. Then microhardness of demineralized lesion was measured. Later artificial caries teeth were equally divided into two groups to treat with remineralization solution for 10 days; group I: novamin and group II: TCP. After 10 days of pH cycling, microhardness was measured. The data were statistically analyzed using Statistical Package for the Social Sciences (SPSS) statistical software from Chicago SPSS Inc., version 21 and using analysis of variance (ANOVA) post hoc multiple comparisons test for intergroup and significant difference at p < 0.05. Results: In the present study, group I indicated a higher value for remineralization compared with group II (p < 0.05). Conclusion: The present study showed that both novamin and TCP were effective in remineralizing the carious lesions. Clinical significance: This study evaluates the remineralizing potential of novamin and TCP on initial carious lesions.
MeSH term(s)	Bicuspid ; Calcium Phosphates/pharmacology ; Cariostatic Agents/pharmacology ; Dental Caries/drug therapy ; Dental Enamel/drug effects ; Glass ; Hardness Tests ; Humans ; Hydrogen-Ion Concentration ; In Vitro Techniques ; Tooth Demineralization/drug therapy
Chemical Substances	Calcium Phosphates ; Cariostatic Agents ; NovaMin ; tricalcium phosphate (K4C08XP666)
Language	English
Publishing date	2018-01-01
Publishing country	India
Document type	Journal Article
ISSN	1526-3711
ISSN (online)	1526-3711
DOI	10.5005/jp-journals-10024-2221
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Article ; Online: A Dominant C150Y Mutation in FHL1 Induces Structural Alterations in LIM2 Domain Causing Protein Aggregation In Human and Drosophila Indirect Flight Muscles.

Santhoshkumar, Rashmi / Preethish-Kumar, Veeramani / Mangalaparthi, Kiran K / Unni, Sruthi / Padmanabhan, Balasundaram / T S, Keshava Prasad / Nongthomba, Upendra / Atchayaram, Nalini / Narayanappa, Gayathri

Journal of molecular neuroscience : MN

2021 Volume 71, Issue 11, Page(s) 2324–2335

Abstract: FHL1-related myopathies are rare X-linked dominant myopathies. Though clinically classified into several subgroups, spinal and scapuloperoneal muscle involvement are common to all. In this study, we identified c.449G > A, p.C150Y mutation by clinical ... ...

Abstract	FHL1-related myopathies are rare X-linked dominant myopathies. Though clinically classified into several subgroups, spinal and scapuloperoneal muscle involvement are common to all. In this study, we identified c.449G > A, p.C150Y mutation by clinical exome sequencing in two patients from same family (son and mother) of Indian origin who presented with multiple contractures. Muscle biopsy showed numerous intracytoplasmic aggregates intensely stained on HE and MGT. The strong reactions to M-NBT revealed aggregates to be reducing bodies and positively labeled to anti-FHL1 antibody. Ultrastructurally, Z-band streaming and granular and granulofilamentous material were seen. Further, the translational evidence of mutant peptide was confirmed using mass spectrometric analysis. To establish p.C150Y as the cause for protein aggregation, in vivo studies were carried out using transgenic Drosophila model which highlighted Z-band abnormalities and protein aggregates in indirect flight muscles with compromised physiological function. Thus, recapitulating the X-linked human disease phenotype. Additionally, the molecular dynamics simulation analysis unraveled the drastic change in α-helix of LIM2, the region immediately next to site of C150Y mutation that could be the plausible cause for protein aggregation. To the best of our knowledge, this is the first study of p.C150Y mutation in FHL1 identified in Indian patients with in vivo and in silico analysis to establish the cause for protein aggregation in muscle.
MeSH term(s)	Adult ; Animals ; Child ; Drosophila melanogaster ; Female ; Genes, Dominant ; Genetic Diseases, X-Linked/genetics ; Genetic Diseases, X-Linked/metabolism ; Genetic Diseases, X-Linked/pathology ; Humans ; Intracellular Signaling Peptides and Proteins/chemistry ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; LIM Domain Proteins/chemistry ; LIM Domain Proteins/genetics ; LIM Domain Proteins/metabolism ; Male ; Muscle Proteins/chemistry ; Muscle Proteins/genetics ; Muscle Proteins/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Diseases/congenital ; Muscular Diseases/genetics ; Muscular Diseases/metabolism ; Muscular Diseases/pathology ; Mutation, Missense ; Protein Conformation, alpha-Helical ; Protein Domains ; Protein Multimerization
Chemical Substances	FHL1 protein, human ; Intracellular Signaling Peptides and Proteins ; LIM Domain Proteins ; Muscle Proteins
Language	English
Publishing date	2021-01-30
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	1043392-2
ISSN	1559-1166 ; 0895-8696
ISSN (online)	1559-1166
ISSN	0895-8696
DOI	10.1007/s12031-020-01777-4
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Article ; Online: H2A.Z is dispensable for both basal and activated transcription in post-mitotic mouse muscles.

Belotti, Edwige / Lacoste, Nicolas / Simonet, Thomas / Papin, Christophe / Padmanabhan, Kiran / Scionti, Isabella / Gangloff, Yann-Gaël / Ramos, Lorrie / Dalkara, Defne / Hamiche, Ali / Dimitrov, Stefan / Schaeffer, Laurent

Nucleic acids research

2020 Volume 48, Issue 9, Page(s) 4601–4613

Abstract: While the histone variant H2A.Z is known to be required for mitosis, it is also enriched in nucleosomes surrounding the transcription start site of active promoters, implicating H2A.Z in transcription. However, evidence obtained so far mainly rely on ... ...

Abstract	While the histone variant H2A.Z is known to be required for mitosis, it is also enriched in nucleosomes surrounding the transcription start site of active promoters, implicating H2A.Z in transcription. However, evidence obtained so far mainly rely on correlational data generated in actively dividing cells. We have exploited a paradigm in which transcription is uncoupled from the cell cycle by developing an in vivo system to inactivate H2A.Z in terminally differentiated post-mitotic muscle cells. ChIP-seq, RNA-seq and ATAC-seq experiments performed on H2A.Z KO post-mitotic muscle cells show that this histone variant is neither required to maintain nor to activate transcription. Altogether, this study provides in vivo evidence that in the absence of mitosis H2A.Z is dispensable for transcription and that the enrichment of H2A.Z on active promoters is a marker but not an active driver of transcription.
MeSH term(s)	Animals ; Cell Differentiation ; Cells, Cultured ; Chromatin ; Chromatin Immunoprecipitation Sequencing ; Histones/genetics ; Histones/metabolism ; Histones/physiology ; Mice ; Muscle Fibers, Skeletal ; Muscle, Skeletal/cytology ; Muscle, Skeletal/metabolism ; RNA-Seq ; Repetitive Sequences, Nucleic Acid ; Transcription Initiation Site ; Transcription, Genetic ; Transcriptional Activation
Chemical Substances	Chromatin ; H2az1 protein, mouse ; Histones
Language	English
Publishing date	2020-03-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkaa157
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