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Article ; Online: Direct AKT activation in tumor-infiltrating lymphocytes markedly increases interferon-γ (IFN-γ) for the regression of tumors resistant to PD-1 checkpoint blockade.

Santinon, François / Ezzahra, Bennani Fatima / Bachais, Meriem / Sarabia Pacis, Alain / Rudd, Christopher E

2022 Volume 12, Issue 1, Page(s) 18509

Abstract: PD-1 immune checkpoint blockade against inhibitory receptors such as receptor programmed cell death-1 (PD-1), has revolutionized cancer treatment. Effective immune reactivity against tumour antigens requires the infiltration and activation of tumour- ... ...

Abstract	PD-1 immune checkpoint blockade against inhibitory receptors such as receptor programmed cell death-1 (PD-1), has revolutionized cancer treatment. Effective immune reactivity against tumour antigens requires the infiltration and activation of tumour-infiltrating T-cells (TILs). In this context, ligation of the antigen-receptor complex (TCR) in combination with the co-receptor CD28 activates the intracellular mediator AKT (or PKB, protein kinase B) and its downstream targets. PD-1 inhibits the activation of AKT/PKB. Given this, we assessed whether the direct activation of AKT might be effective in activating the immune system to limit the growth of tumors that are resistant to PD-1 checkpoint blockade. We found that the small molecule activator of AKT (SC79) limited growth of a B16 tumor and an EMT-6 syngeneic breast tumor model that are poorly responsive to PD-1 immunotherapy. In the case of B16 tumors, direct AKT activation induced (i) a reduction of suppressor regulatory (Treg) TILs and (ii) an increase in effector CD8+ TILs. SC79 in vivo therapy caused a major increase in the numbers of CD4+ and CD8+ TILs to express interferon-γ (IFN-γ). This effect on IFN-γ expression distinguished responsive from non-responsive anti-tumor responses and could be recapitulated ex vivo with human T-cells. In CD4+FoxP3+Treg TILs, AKT induced IFN-γ expression was accompanied by a loss of suppressor activity, the conversation to CD4
MeSH term(s)	Humans ; Lymphocytes, Tumor-Infiltrating ; Programmed Cell Death 1 Receptor/metabolism ; Interferon-gamma/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; CD8-Positive T-Lymphocytes ; Neoplasms/pathology
Chemical Substances	Programmed Cell Death 1 Receptor ; Interferon-gamma (82115-62-6) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2022-11-02
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/s41598-022-23016-z
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Article ; Online: Genome graphs detect human polymorphisms in active epigenomic state during influenza infection.

Groza, Cristian / Chen, Xun / Pacis, Alain / Simon, Marie-Michelle / Pramatarova, Albena / Aracena, Katherine A / Pastinen, Tomi / Barreiro, Luis B / Bourque, Guillaume

Cell genomics

2023 Volume 3, Issue 5, Page(s) 100294

Abstract: Genetic variants, including mobile element insertions (MEIs), are known to impact the epigenome. We hypothesized that genome graphs, which encapsulate genetic diversity, could reveal missing epigenomic signals. To test this, we sequenced the epigenome of ...

Abstract	Genetic variants, including mobile element insertions (MEIs), are known to impact the epigenome. We hypothesized that genome graphs, which encapsulate genetic diversity, could reveal missing epigenomic signals. To test this, we sequenced the epigenome of monocyte-derived macrophages from 35 ancestrally diverse individuals before and after influenza infection, allowing us to investigate the role of MEIs in immunity. We characterized genetic variants and MEIs using linked reads and built a genome graph. Mapping epigenetic data revealed 2.3%-3% novel peaks for H3K4me1, H3K27ac chromatin immunoprecipitation sequencing (ChIP-seq), and ATAC-seq. Additionally, the use of a genome graph modified some quantitative trait loci estimates and revealed 375 polymorphic MEIs in an active epigenomic state. Among these is an AluYh3 polymorphism whose chromatin state changed after infection and was associated with the expression of
Language	English
Publishing date	2023-04-07
Publishing country	United States
Document type	Journal Article
ISSN	2666-979X
ISSN (online)	2666-979X
DOI	10.1016/j.xgen.2023.100294
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Article ; Online: EpiVar Browser: advanced exploration of epigenomics data under controlled access.

Lougheed, David R / Liu, Hanshi / Aracena, Katherine A / Grégoire, Romain / Pacis, Alain / Pastinen, Tomi / Barreiro, Luis B / Joly, Yann / Bujold, David / Bourque, Guillaume

Bioinformatics (Oxford, England)

2024 Volume 40, Issue 3

Abstract: Motivation: Human epigenomic data has been generated by large consortia for thousands of cell types to be used as a reference map of normal and disease chromatin states. Since epigenetic data contains potentially identifiable information, similarly to ... ...

Abstract	Motivation: Human epigenomic data has been generated by large consortia for thousands of cell types to be used as a reference map of normal and disease chromatin states. Since epigenetic data contains potentially identifiable information, similarly to genetic data, most raw files generated by these consortia are stored in controlled-access databases. It is important to protect identifiable information, but this should not hinder secure sharing of these valuable datasets. Results: Guided by the Framework for responsible sharing of genomic and health-related data from the Global Alliance for Genomics and Health (GA4GH), we have developed an approach and a tool to facilitate the exploration of epigenomics datasets' aggregate results, while filtering out identifiable information. Specifically, the EpiVar Browser allows a user to navigate an epigenetic dataset from a cohort of individuals and enables direct exploration of genotype-chromatin phenotype relationships. Because individual genotypes and epigenetic signal tracks are not directly accessible, and rather aggregated in the portal output, no identifiable data is released, yet the interface allows for dynamic genotype-epigenome interrogation. This approach has the potential to accelerate analyses that would otherwise require a lengthy multi-step approval process and provides a generalizable strategy to facilitate responsible access to sensitive epigenomics data. Availability and implementation: Online portal: https://computationalgenomics.ca/tools/epivar; EpiVar Browser source code: https://github.com/c3g/epivar-browser; bw-merge-window tool source code: https://github.com/c3g/bw-merge-window.
MeSH term(s)	Humans ; Epigenomics/methods ; Software ; Genome ; Genomics ; Chromatin/genetics
Chemical Substances	Chromatin
Language	English
Publishing date	2024-03-06
Publishing country	England
Document type	Journal Article
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btae136
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Zs.A 2374: Show issues

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Article ; Online: Single-Cell RNA-Seq Analysis of Cells from Degenerating and Non-Degenerating Intervertebral Discs from the Same Individual Reveals New Biomarkers for Intervertebral Disc Degeneration.

Cherif, Hosni / Mannarino, Matthew / Pacis, Alain Sarabia / Ragoussis, Jiannis / Rabau, Oded / Ouellet, Jean A / Haglund, Lisbet

International journal of molecular sciences

2022 Volume 23, Issue 7

Abstract: In this study, we used single-cell transcriptomic analysis to identify new specific biomarkers for nucleus pulposus (NP) and inner annulus fibrosis (iAF) cells, and to define cell populations within non-degenerating (nD) and degenerating (D) human ... ...

Abstract	In this study, we used single-cell transcriptomic analysis to identify new specific biomarkers for nucleus pulposus (NP) and inner annulus fibrosis (iAF) cells, and to define cell populations within non-degenerating (nD) and degenerating (D) human intervertebral discs (IVD) of the same individual. Cluster analysis based on differential gene expression delineated 14 cell clusters. Gene expression profiles at single-cell resolution revealed the potential functional differences linked to degeneration, and among NP and iAF subpopulations. GO and KEGG analyses discovered molecular functions, biological processes, and transcription factors linked to cell type and degeneration state. We propose two lists of biomarkers, one as specific cell type, including
MeSH term(s)	Biomarkers/metabolism ; Cell Cycle Proteins/metabolism ; Chitinases/metabolism ; F-Box Proteins/genetics ; Humans ; Intervertebral Disc/metabolism ; Intervertebral Disc Degeneration/genetics ; Intervertebral Disc Degeneration/metabolism ; Lectins, C-Type/metabolism ; Nerve Tissue Proteins/metabolism ; Nucleus Pulposus/metabolism ; Sequence Analysis, RNA
Chemical Substances	Biomarkers ; CLEC3A protein, human ; Cell Cycle Proteins ; F-Box Proteins ; FBXO2 protein, human ; Lectins, C-Type ; Nerve Tissue Proteins ; CHI3L2 protein, human (EC 3.2.1.14) ; Chitinases (EC 3.2.1.14)
Language	English
Publishing date	2022-04-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23073993
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Article ; Online: Transposable elements are associated with the variable response to influenza infection.

Chen, Xun / Pacis, Alain / Aracena, Katherine A / Gona, Saideep / Kwan, Tony / Groza, Cristian / Lin, Yen Lung / Sindeaux, Renata / Yotova, Vania / Pramatarova, Albena / Simon, Marie-Michelle / Pastinen, Tomi / Barreiro, Luis B / Bourque, Guillaume

Cell genomics

2023 Volume 3, Issue 5, Page(s) 100292

Abstract: Influenza A virus (IAV) infections are frequent every year and result in a range of disease severity. Here, we wanted to explore the potential contribution of transposable elements (TEs) to the variable human immune response. Transcriptome profiling in ... ...

Abstract	Influenza A virus (IAV) infections are frequent every year and result in a range of disease severity. Here, we wanted to explore the potential contribution of transposable elements (TEs) to the variable human immune response. Transcriptome profiling in monocyte-derived macrophages from 39 individuals following IAV infection revealed significant inter-individual variation in viral load post-infection. Using transposase-accessible chromatin using sequencing (ATAC-seq), we identified a set of TE families with either enhanced or reduced accessibility upon infection. Of the enhanced families, 15 showed high variability between individuals and had distinct epigenetic profiles. Motif analysis showed an association with known immune regulators (e.g., BATFs, FOSs/JUNs, IRFs, STATs, NFkBs, NFYs, and RELs) in stably enriched families and with other factors in variable families, including KRAB-ZNFs. We showed that TEs and host factors regulating TEs were predictive of viral load post-infection. Our findings shed light on the role TEs and KRAB-ZNFs may play in inter-individual variation in immunity.
Language	English
Publishing date	2023-04-07
Publishing country	United States
Document type	Journal Article
ISSN	2666-979X
ISSN (online)	2666-979X
DOI	10.1016/j.xgen.2023.100292
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Article: EpiVar Browser: advanced exploration of epigenomics data under controlled access.

Lougheed, David R / Liu, Hanshi / Aracena, Katherine A / Grégoire, Romain / Pacis, Alain / Pastinen, Tomi / Barreiro, Luis B / Joly, Yann / Bujold, David / Bourque, Guillaume

bioRxiv : the preprint server for biology

2023

Abstract	Motivation: Human epigenomic data has been generated by large consortia for thousands of cell types to be used as a reference map of normal and disease chromatin states. Since epigenetic data contains potentially identifiable information, similarly to genetic data, most raw files generated by these consortia are stored in controlled-access databases. It is important to protect identifiable information, but this should not hinder secure sharing of these valuable datasets. Results: Guided by the Availability and implementation: Online portal instance: https://computationalgenomics.ca/tools/epivarSource code: https://github.com/c3g/epivar-browser.
Language	English
Publishing date	2023-08-05
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.08.03.551309
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Article ; Online: Folliculin impairs breast tumor growth by repressing TFE3-dependent induction of the Warburg effect and angiogenesis.

El-Houjeiri, Leeanna / Biondini, Marco / Paquette, Mathieu / Kuasne, Helen / Pacis, Alain / Park, Morag / Siegel, Peter M / Pause, Arnim

The Journal of clinical investigation

2021 Volume 131, Issue 22

Abstract: Growing tumors exist in metabolically compromised environments that require activation of multiple pathways to scavenge nutrients to support accelerated rates of growth. The folliculin (FLCN) tumor suppressor complex (FLCN, FNIP1, FNIP2) is implicated in ...

Abstract	Growing tumors exist in metabolically compromised environments that require activation of multiple pathways to scavenge nutrients to support accelerated rates of growth. The folliculin (FLCN) tumor suppressor complex (FLCN, FNIP1, FNIP2) is implicated in the regulation of energy homeostasis via 2 metabolic master kinases: AMPK and mTORC1. Loss-of-function mutations of the FLCN tumor suppressor complex have only been reported in renal tumors in patients with the rare Birt-Hogg-Dube syndrome. Here, we revealed that FLCN, FNIP1, and FNIP2 are downregulated in many human cancers, including poor-prognosis invasive basal-like breast carcinomas where AMPK and TFE3 targets are activated compared with the luminal, less aggressive subtypes. FLCN loss in luminal breast cancer promoted tumor growth through TFE3 activation and subsequent induction of several pathways, including autophagy, lysosomal biogenesis, aerobic glycolysis, and angiogenesis. Strikingly, induction of aerobic glycolysis and angiogenesis in FLCN-deficient cells was dictated by the activation of the PGC-1α/HIF-1α pathway, which we showed to be TFE3 dependent, directly linking TFE3 to Warburg metabolic reprogramming and angiogenesis. Conversely, FLCN overexpression in invasive basal-like breast cancer models attenuated TFE3 nuclear localization, TFE3-dependent transcriptional activity, and tumor growth. These findings support a general role of a deregulated FLCN/TFE3 tumor suppressor pathway in human cancers.
MeSH term(s)	AMP-Activated Protein Kinases/physiology ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/physiology ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Female ; Humans ; Neovascularization, Pathologic/prevention & control ; Oxidative Phosphorylation ; Proto-Oncogene Proteins/physiology ; Tumor Suppressor Proteins/physiology ; Warburg Effect, Oncologic
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; FLCN protein, human ; Proto-Oncogene Proteins ; TFE3 protein, human ; Tumor Suppressor Proteins ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2021-11-14
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/JCI144871
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Ua VI Zs.184: Show issues

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Article ; Online: A coordinated progression of progenitor cell states initiates urinary tract development.

Sanchez-Ferras, Oraly / Pacis, Alain / Sotiropoulou, Maria / Zhang, Yuhong / Wang, Yu Chang / Bourgey, Mathieu / Bourque, Guillaume / Ragoussis, Jiannis / Bouchard, Maxime

Nature communications

2021 Volume 12, Issue 1, Page(s) 2627

Abstract: The kidney and upper urinary tract develop through reciprocal interactions between the ureteric bud and the surrounding mesenchyme. Ureteric bud branching forms the arborized collecting duct system of the kidney, while ureteric tips promote nephron ... ...

Abstract	The kidney and upper urinary tract develop through reciprocal interactions between the ureteric bud and the surrounding mesenchyme. Ureteric bud branching forms the arborized collecting duct system of the kidney, while ureteric tips promote nephron formation from dedicated progenitor cells. While nephron progenitor cells are relatively well characterized, the origin of ureteric bud progenitors has received little attention so far. It is well established that the ureteric bud is induced from the nephric duct, an epithelial duct derived from the intermediate mesoderm of the embryo. However, the cell state transitions underlying the progression from intermediate mesoderm to nephric duct and ureteric bud remain unknown. Here we show that nephric duct morphogenesis results from the coordinated organization of four major progenitor cell populations. Using single cell RNA-seq and Cluster RNA-seq, we show that these progenitors emerge in time and space according to a stereotypical pattern. We identify the transcription factors Tfap2a/b and Gata3 as critical coordinators of this progenitor cell progression. This study provides a better understanding of the cellular origin of the renal collecting duct system and associated urinary tract developmental diseases, which may inform guided differentiation of functional kidney tissue.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Embryo, Mammalian ; Female ; GATA3 Transcription Factor/metabolism ; Gene Expression Regulation, Developmental ; Male ; Mice ; Mice, Transgenic ; Models, Animal ; Nephrons/embryology ; Organogenesis/genetics ; RNA-Seq ; Single-Cell Analysis ; Stem Cells/physiology ; Transcription Factor AP-2/metabolism
Chemical Substances	GATA3 Transcription Factor ; Gata3 protein, mouse ; Tfap2a protein, mouse ; Tfap2b protein, mouse ; Transcription Factor AP-2
Language	English
Publishing date	2021-05-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-22931-5
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Article ; Online: Pancreatic Cancer Progression in a Patient With Lynch Syndrome Receiving Immunotherapy: A Cautionary Tale.

Wang, Yifan / Cuggia, Adeline / Pacis, Alain / Boileau, Jean-Christian / Marcus, Victoria A / Gao, Zu-Hua / Chong, George / Foulkes, William D / Zogopoulos, George

Journal of the National Comprehensive Cancer Network : JNCCN

2021 Volume 19, Issue 8, Page(s) 883–887

Abstract: Pancreatic ductal adenocarcinomas (PDACs) with DNA mismatch repair deficiency (MMRd) respond preferentially to immune checkpoint inhibitors (ICIs). However, a subset of MMRd PDACs does not respond to these agents. This report describes a patient with ... ...

Abstract	Pancreatic ductal adenocarcinomas (PDACs) with DNA mismatch repair deficiency (MMRd) respond preferentially to immune checkpoint inhibitors (ICIs). However, a subset of MMRd PDACs does not respond to these agents. This report describes a patient with PDAC who experienced rapid disease progression suggestive of hyperprogressive disease. The case involved a 63-year-old man carrying a pathogenic germline PMS2 mutation who developed metastatic PDAC. His tumor showed isolated loss of PMS2 expression by immunohistochemistry (IHC). He was treated with pembrolizumab, but his disease rapidly progressed. Whole-genome and transcriptome sequencing of a liver metastasis biopsy, acquired at disease progression, showed a retained wild-type PMS2 allele and hallmarks of microsatellite stability, including low tumor mutational burden and low MSIsensor score. PCR-based microsatellite instability (MSI) testing of the treatment-naïve tumor showed microsatellite stability. The ICI-treated tumor had a lower density of CD8+ T-cell infiltration than the treatment-naïve tumor, which is contrary to the expected evolution with ICI responsiveness. Through this case and a review of the literature, we highlight the low penetrance of PMS2 germline mutations in PDAC and discuss pitfalls in ascertaining MMRd and MSI based on IHC testing alone. An orthogonal confirmatory assay is warranted in the presence of uncommon immunophenotypes, such as isolated PMS2 loss, to optimize selection of patients with PDAC for immunotherapy.
MeSH term(s)	Colorectal Neoplasms, Hereditary Nonpolyposis/diagnosis ; Colorectal Neoplasms, Hereditary Nonpolyposis/genetics ; Colorectal Neoplasms, Hereditary Nonpolyposis/therapy ; DNA Mismatch Repair/genetics ; Humans ; Immunotherapy ; Male ; Microsatellite Instability ; Middle Aged ; Pancreatic Neoplasms/diagnosis ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/therapy
Language	English
Publishing date	2021-08-01
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2250759-0
ISSN	1540-1413 ; 1540-1405
ISSN (online)	1540-1413
ISSN	1540-1405
DOI	10.6004/jnccn.2021.7049
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Zs.A 6365: Show issues

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Article ; Online: Epigenetic variation impacts individual differences in the transcriptional response to influenza infection.

Nature genetics

2024 Volume 56, Issue 3, Page(s) 408–419

Abstract: Humans display remarkable interindividual variation in their immune response to identical challenges. Yet, our understanding of the genetic and epigenetic factors contributing to such variation remains limited. Here we performed in-depth genetic, ... ...

Abstract	Humans display remarkable interindividual variation in their immune response to identical challenges. Yet, our understanding of the genetic and epigenetic factors contributing to such variation remains limited. Here we performed in-depth genetic, epigenetic and transcriptional profiling on primary macrophages derived from individuals of European and African ancestry before and after infection with influenza A virus. We show that baseline epigenetic profiles are strongly predictive of the transcriptional response to influenza A virus across individuals. Quantitative trait locus (QTL) mapping revealed highly coordinated genetic effects on gene regulation, with many cis-acting genetic variants impacting concomitantly gene expression and multiple epigenetic marks. These data reveal that ancestry-associated differences in the epigenetic landscape can be genetically controlled, even more than gene expression. Lastly, among QTL variants that colocalized with immune-disease loci, only 7% were gene expression QTL, while the remaining genetic variants impact epigenetic marks, stressing the importance of considering molecular phenotypes beyond gene expression in disease-focused studies.
MeSH term(s)	Humans ; Influenza, Human/genetics ; Individuality ; Quantitative Trait Loci/genetics ; Chromosome Mapping ; Epigenesis, Genetic
Language	English
Publishing date	2024-02-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-024-01668-z
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Zs.A 3613: 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 46: Show issues

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