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Article: Tyro3 promotes the maturation of glutamatergic synapses.

Miao, Sheng / Fourgeaud, Lawrence / Burrola, Patrick G / Stern, Shani / Zhang, Yuhan / Happonen, Kaisa E / Novak, Sammy Weiser / Gage, Fred H / Lemke, Greg

Frontiers in neuroscience

2024 Volume 18, Page(s) 1327423

Abstract: The receptor tyrosine kinase Tyro3 is abundantly expressed in neurons of the neocortex, hippocampus, and striatum, but its role in these cells is unknown. We found that neuronal expression of this receptor was markedly up-regulated in the postnatal mouse ...

Abstract	The receptor tyrosine kinase Tyro3 is abundantly expressed in neurons of the neocortex, hippocampus, and striatum, but its role in these cells is unknown. We found that neuronal expression of this receptor was markedly up-regulated in the postnatal mouse neocortex immediately prior to the final development of glutamatergic synapses. In the absence of Tyro3, cortical and hippocampal synapses never completed end-stage differentiation and remained electrophysiologically and ultrastructurally immature.
Language	English
Publishing date	2024-02-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2024.1327423
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Article ; Online: New insights into tuft cell formation: Implications for structure-function relationships.

O'Leary, Claire E / Ma, Zhibo / Culpepper, Taylor / Novak, Sammy Weiser / DelGiorno, Kathleen E

Current opinion in cell biology

2022 Volume 76, Page(s) 102082

Abstract: Tuft cells are sentinel chemosensory cells that monitor the lumen of hollow organs for noxious or infectious stimuli and respond with disease- and tissue-specific effectors. The discovery of critical tuft cell functions in intestinal type 2 immune ... ...

Abstract	Tuft cells are sentinel chemosensory cells that monitor the lumen of hollow organs for noxious or infectious stimuli and respond with disease- and tissue-specific effectors. The discovery of critical tuft cell functions in intestinal type 2 immune responses and airway defense has sparked interest in the formation and function of this architecturally unique cell type. Recent advances in single-cell transcriptomics and computational biology allow for new insights into the genetics and environmental cues underlying tuft cell formation and maturation. Here, we summarize the most recent research on tuft cell development and function in various disease states and organ systems.
MeSH term(s)	Cell Differentiation ; Intestinal Mucosa/metabolism ; Structure-Activity Relationship
Language	English
Publishing date	2022-04-22
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1026381-0
ISSN	1879-0410 ; 0955-0674
ISSN (online)	1879-0410
ISSN	0955-0674
DOI	10.1016/j.ceb.2022.102082
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Article: Mutant Prion Protein Endoggresomes are Hubs for Local Axonal Organelle-Cytoskeletal Remodeling.

Chaiamarit, Tai / Verhelle, Adriaan / Chassefeyre, Romain / Shukla, Nandini / Novak, Sammy Weiser / Andrade, Leonardo R / Manor, Uri / Encalada, Sandra E

bioRxiv : the preprint server for biology

2023

Abstract: Dystrophic axons comprising misfolded mutant prion protein (PrP) aggregates are a characteristic pathological feature in the prionopathies. These aggregates form inside endolysosomes -called endoggresomes-, within swellings that line up the length of ... ...

Abstract	Dystrophic axons comprising misfolded mutant prion protein (PrP) aggregates are a characteristic pathological feature in the prionopathies. These aggregates form inside endolysosomes -called endoggresomes-, within swellings that line up the length of axons of degenerating neurons. The pathways impaired by endoggresomes that result in failed axonal and consequently neuronal health, remain undefined. Here, we dissect the local subcellular impairments that occur within individual mutant PrP endoggresome swelling sites in axons. Quantitative high-resolution light and electron microscopy revealed the selective impairment of the acetylated vs tyrosinated microtubule cytoskeleton, while micro-domain image analysis of live organelle dynamics within swelling sites revealed deficits uniquely to the MT-based active transport system that translocates mitochondria and endosomes toward the synapse. Cytoskeletal and defective transport results in the retention of mitochondria, endosomes, and molecular motors at swelling sites, enhancing mitochondria-Rab7 late endosome contacts that induce mitochondrial fission via the activity of Rab7, and render mitochondria dysfunctional. Our findings point to mutant Pr Pendoggresome swelling sites as selective hubs of cytoskeletal deficits and organelle retention that drive the remodeling of organelles along axons. We propose that the dysfunction imparted locally within these axonal micro-domains spreads throughout the axon over time, leading to axonal dysfunction in prionopathies.
Language	English
Publishing date	2023-03-21
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.03.19.533383
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Article ; Online: Oligodendrocyte calcium signaling promotes actin-dependent myelin sheath extension.

Iyer, Manasi / Kantarci, Husniye / Cooper, Madeline H / Ambiel, Nicholas / Novak, Sammy Weiser / Andrade, Leonardo R / Lam, Mable / Jones, Graham / Münch, Alexandra E / Yu, Xinzhu / Khakh, Baljit S / Manor, Uri / Zuchero, J Bradley

Nature communications

2024 Volume 15, Issue 1, Page(s) 265

Abstract: Myelin is essential for rapid nerve signaling and is increasingly found to play important roles in learning and in diverse diseases of the CNS. Morphological parameters of myelin such as sheath length are thought to precisely tune conduction velocity, ... ...

Abstract	Myelin is essential for rapid nerve signaling and is increasingly found to play important roles in learning and in diverse diseases of the CNS. Morphological parameters of myelin such as sheath length are thought to precisely tune conduction velocity, but the mechanisms controlling sheath morphology are poorly understood. Local calcium signaling has been observed in nascent myelin sheaths and can be modulated by neuronal activity. However, the role of calcium signaling in sheath formation remains incompletely understood. Here, we use genetic tools to attenuate oligodendrocyte calcium signaling during myelination in the developing mouse CNS. Surprisingly, genetic calcium attenuation does not grossly affect the number of myelinated axons or myelin thickness. Instead, calcium attenuation causes myelination defects resulting in shorter, dysmorphic sheaths. Mechanistically, calcium attenuation reduces actin filaments in oligodendrocytes, and an intact actin cytoskeleton is necessary and sufficient to achieve accurate myelin morphology. Together, our work reveals a cellular mechanism required for accurate CNS myelin formation and may provide mechanistic insight into how oligodendrocytes respond to neuronal activity to sculpt and refine myelin sheaths.
MeSH term(s)	Animals ; Mice ; Myelin Sheath/metabolism ; Actins/metabolism ; Calcium/metabolism ; Calcium Signaling ; Oligodendroglia ; Axons/physiology
Chemical Substances	Actins ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2024-01-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-44238-3
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Article ; Online: Morphological diversification and functional maturation of human astrocytes in glia-enriched cortical organoid transplanted in mouse brain.

Wang, Meiyan / Zhang, Lei / Novak, Sammy Weiser / Yu, Jingting / Gallina, Iryna S / Xu, Lynne L / Lim, Christina K / Fernandes, Sarah / Shokhirev, Maxim N / Williams, April E / Saxena, Monisha D / Coorapati, Shashank / Parylak, Sarah L / Quintero, Cristian / Molina, Elsa / Andrade, Leonardo R / Manor, Uri / Gage, Fred H

Nature biotechnology

2024

Abstract: Astrocytes, the most abundant glial cell type in the brain, are underrepresented in traditional cortical organoid models due to the delayed onset of cortical gliogenesis. Here we introduce a new glia-enriched cortical organoid model that exhibits ... ...

Abstract	Astrocytes, the most abundant glial cell type in the brain, are underrepresented in traditional cortical organoid models due to the delayed onset of cortical gliogenesis. Here we introduce a new glia-enriched cortical organoid model that exhibits accelerated astrogliogenesis. We demonstrated that induction of a gliogenic switch in a subset of progenitors enabled the rapid derivation of astroglial cells, which account for 25-31% of the cell population within 8-10 weeks of differentiation. Intracerebral transplantation of these organoids reliably generated a diverse repertoire of cortical neurons and anatomical subclasses of human astrocytes. Spatial transcriptome profiling identified layer-specific expression patterns among distinct subclasses of astrocytes within organoid transplants. Using an in vivo acute neuroinflammation model, we identified a subpopulation of astrocytes that rapidly activates pro-inflammatory pathways upon cytokine stimulation. Additionally, we demonstrated that CD38 signaling has a crucial role in mediating metabolic and mitochondrial stress in reactive astrocytes. This model provides a robust platform for investigating human astrocyte function.
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	1311932-1
ISSN	1546-1696 ; 1087-0156
ISSN (online)	1546-1696
ISSN	1087-0156
DOI	10.1038/s41587-024-02157-8
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Zs.A 2167: 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 137: Show issues
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Article ; Online: Endosomal sorting drives the formation of axonal prion protein endoggresomes.

Chassefeyre, Romain / Chaiamarit, Tai / Verhelle, Adriaan / Novak, Sammy Weiser / Andrade, Leonardo R / Leitão, André D G / Manor, Uri / Encalada, Sandra E

Science advances

2021 Volume 7, Issue 52, Page(s) eabg3693

Abstract: The pathogenic aggregation of misfolded prion protein (PrP) in axons underlies prion disease pathologies. The molecular mechanisms driving axonal misfolded PrP aggregate formation leading to neurotoxicity are unknown. We found that the small ... ...

Abstract	The pathogenic aggregation of misfolded prion protein (PrP) in axons underlies prion disease pathologies. The molecular mechanisms driving axonal misfolded PrP aggregate formation leading to neurotoxicity are unknown. We found that the small endolysosomal guanosine triphosphatase (GTPase) Arl8b recruits kinesin-1 and Vps41 (HOPS) onto endosomes carrying misfolded mutant PrP to promote their axonal entry and homotypic fusion toward aggregation inside enlarged endomembranes that we call endoggresomes. This axonal rapid endosomal sorting and transport-dependent aggregation (ARESTA) mechanism forms pathologic PrP endoggresomes that impair calcium dynamics and reduce neuronal viability. Inhibiting ARESTA diminishes endoggresome formation, rescues calcium influx, and prevents neuronal death. Our results identify ARESTA as a key pathway for the regulation of endoggresome formation and a new actionable antiaggregation target to ameliorate neuronal dysfunction in the prionopathies.
Language	English
Publishing date	2021-12-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abg3693
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Article ; Online: Microglial physiological properties and interactions with synapses are altered at presymptomatic stages in a mouse model of Huntington's disease pathology.

Savage, Julie C / St-Pierre, Marie-Kim / Carrier, Micaël / El Hajj, Hassan / Novak, Sammy Weiser / Sanchez, Maria Gabriela / Cicchetti, Francesca / Tremblay, Marie-Ève

Journal of neuroinflammation

2020 Volume 17, Issue 1, Page(s) 98

Abstract: Background: Huntington's disease (HD) is a dominantly inherited neurodegenerative disorder that affects cognitive and motor abilities by primarily targeting the striatum and cerebral cortex. HD is caused by a mutation elongating the CAG repeats within ... ...

Abstract	Background: Huntington's disease (HD) is a dominantly inherited neurodegenerative disorder that affects cognitive and motor abilities by primarily targeting the striatum and cerebral cortex. HD is caused by a mutation elongating the CAG repeats within the Huntingtin gene, resulting in HTT protein misfolding. Although the genetic cause of HD has been established, the specific susceptibility of neurons within various brain structures has remained elusive. Microglia, which are the brain's resident macrophages, have emerged as important players in neurodegeneration. Nevertheless, few studies have examined their implication in HD. Methods: To provide novel insights, we investigated the maturation and dysfunction of striatal microglia using the R6/2 mouse model of HD. This transgenic model, which presents with 120+/-5 CAG repeats, displays progressive motor deficits beginning at 6 weeks of age, with full incapacitation by 13 weeks. We studied microglial morphology, phagocytic capacity, and synaptic contacts in the striatum of R6/2 versus wild-type (WT) littermates at 3, 10, and 13 weeks of age, using a combination of light and transmission electron microscopy. We also reconstructed dendrites and determined synaptic density within the striatum of R6/2 and WT littermates, at nanoscale resolution using focused ion beam scanning electron microscopy. Results: At 3 weeks of age, prior to any known motor deficits, microglia in R6/2 animals displayed a more mature morphological phenotype than WT animals. Microglia from R6/2 mice across all ages also demonstrated increased phagocytosis, as revealed by light microscopy and transmission electron microscopy. Furthermore, microglial processes from 10-week-old R6/2 mice made fewer contacts with synaptic structures than microglial processes in 3-week-old R6/2 mice and age-matched WT littermates. Synaptic density was not affected by genotype at 3 weeks of age but increased with maturation in WT mice. The location of synapses was lastly modified in R6/2 mice compared with WT controls, from targeting dendritic spines to dendritic trunks at both 3 and 10 weeks of age. Conclusions: These findings suggest that microglia may play an intimate role in synaptic alteration and loss during HD pathogenesis.
MeSH term(s)	Animals ; Cell Shape/physiology ; Disease Models, Animal ; Female ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Huntington Disease/pathology ; Male ; Mice ; Mice, Transgenic ; Microglia/metabolism ; Microglia/pathology ; Neurons/metabolism ; Neurons/pathology ; Synapses/metabolism ; Synapses/pathology
Chemical Substances	Huntingtin Protein
Language	English
Publishing date	2020-04-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-020-01782-9
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Article ; Online: Deep learning-based point-scanning super-resolution imaging.

Fang, Linjing / Monroe, Fred / Novak, Sammy Weiser / Kirk, Lyndsey / Schiavon, Cara R / Yu, Seungyoon B / Zhang, Tong / Wu, Melissa / Kastner, Kyle / Latif, Alaa Abdel / Lin, Zijun / Shaw, Andrew / Kubota, Yoshiyuki / Mendenhall, John / Zhang, Zhao / Pekkurnaz, Gulcin / Harris, Kristen / Howard, Jeremy / Manor, Uri

Nature methods

2021 Volume 18, Issue 4, Page(s) 406–416

Abstract: Point-scanning imaging systems are among the most widely used tools for high-resolution cellular and tissue imaging, benefiting from arbitrarily defined pixel sizes. The resolution, speed, sample preservation and signal-to-noise ratio (SNR) of point- ... ...

Abstract	Point-scanning imaging systems are among the most widely used tools for high-resolution cellular and tissue imaging, benefiting from arbitrarily defined pixel sizes. The resolution, speed, sample preservation and signal-to-noise ratio (SNR) of point-scanning systems are difficult to optimize simultaneously. We show these limitations can be mitigated via the use of deep learning-based supersampling of undersampled images acquired on a point-scanning system, which we term point-scanning super-resolution (PSSR) imaging. We designed a 'crappifier' that computationally degrades high SNR, high-pixel resolution ground truth images to simulate low SNR, low-resolution counterparts for training PSSR models that can restore real-world undersampled images. For high spatiotemporal resolution fluorescence time-lapse data, we developed a 'multi-frame' PSSR approach that uses information in adjacent frames to improve model predictions. PSSR facilitates point-scanning image acquisition with otherwise unattainable resolution, speed and sensitivity. All the training data, models and code for PSSR are publicly available at 3DEM.org.
MeSH term(s)	Algorithms ; Deep Learning ; Microscopy, Electron/methods ; Signal-To-Noise Ratio
Language	English
Publishing date	2021-03-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2169522-2
ISSN	1548-7105 ; 1548-7091
ISSN (online)	1548-7105
ISSN	1548-7091
DOI	10.1038/s41592-021-01080-z
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Article ; Online: Regulation of the ER stress response by a mitochondrial microprotein.

Chu, Qian / Martinez, Thomas F / Novak, Sammy Weiser / Donaldson, Cynthia J / Tan, Dan / Vaughan, Joan M / Chang, Tina / Diedrich, Jolene K / Andrade, Leo / Kim, Andrew / Zhang, Tong / Manor, Uri / Saghatelian, Alan

Nature communications

2019 Volume 10, Issue 1, Page(s) 4883

Abstract: Cellular homeostasis relies on having dedicated and coordinated responses to a variety of stresses. The accumulation of unfolded proteins in the endoplasmic reticulum (ER) is a common stress that triggers a conserved pathway called the unfolded protein ... ...

Abstract	Cellular homeostasis relies on having dedicated and coordinated responses to a variety of stresses. The accumulation of unfolded proteins in the endoplasmic reticulum (ER) is a common stress that triggers a conserved pathway called the unfolded protein response (UPR) that mitigates damage, and dysregulation of UPR underlies several debilitating diseases. Here, we discover that a previously uncharacterized 54-amino acid microprotein PIGBOS regulates UPR. PIGBOS localizes to the mitochondrial outer membrane where it interacts with the ER protein CLCC1 at ER-mitochondria contact sites. Functional studies reveal that the loss of PIGBOS leads to heightened UPR and increased cell death. The characterization of PIGBOS reveals an undiscovered role for a mitochondrial protein, in this case a microprotein, in the regulation of UPR originating in the ER. This study demonstrates microproteins to be an unappreciated class of genes that are critical for inter-organelle communication, homeostasis, and cell survival.
MeSH term(s)	Animals ; COS Cells ; Cell Death ; Cell Line, Tumor ; Chloride Channels/metabolism ; Chlorocebus aethiops ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress ; HEK293 Cells ; HeLa Cells ; Humans ; Mitochondrial Membranes/metabolism ; Mitochondrial Proteins/metabolism ; Protein Interaction Maps ; Rabbits ; Rats ; Unfolded Protein Response
Chemical Substances	CLCC1 protein, human ; Chloride Channels ; Mitochondrial Proteins ; PIGBOS1 protein, human
Language	English
Publishing date	2019-10-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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/s41467-019-12816-z
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Article ; Online: Single-Cell Transcriptomics Reveals a Conserved Metaplasia Program in Pancreatic Injury.

Ma, Zhibo / Lytle, Nikki K / Chen, Bob / Jyotsana, Nidhi / Novak, Sammy Weiser / Cho, Charles J / Caplan, Leah / Ben-Levy, Olivia / Neininger, Abigail C / Burnette, Dylan T / Trinh, Vincent Q / Tan, Marcus C B / Patterson, Emilee A / Arrojo E Drigo, Rafael / Giraddi, Rajshekhar R / Ramos, Cynthia / Means, Anna L / Matsumoto, Ichiro / Manor, Uri /

Mills, Jason C / Goldenring, James R / Lau, Ken S / Wahl, Geoffrey M / DelGiorno, Kathleen E

Gastroenterology

2021 Volume 162, Issue 2, Page(s) 604–620.e20

Abstract: Background & aims: Acinar to ductal metaplasia (ADM) occurs in the pancreas in response to tissue injury and is a potential precursor for adenocarcinoma. The goal of these studies was to define the populations arising from ADM, the associated ... ...

Abstract	Background & aims: Acinar to ductal metaplasia (ADM) occurs in the pancreas in response to tissue injury and is a potential precursor for adenocarcinoma. The goal of these studies was to define the populations arising from ADM, the associated transcriptional changes, and markers of disease progression. Methods: Acinar cells were lineage-traced with enhanced yellow fluorescent protein (EYFP) to follow their fate post-injury. Transcripts of more than 13,000 EYFP+ cells were determined using single-cell RNA sequencing (scRNA-seq). Developmental trajectories were generated. Data were compared with gastric metaplasia, Kras Results: scRNA-seq of ADM revealed emergence of a mucin/ductal population resembling gastric pyloric metaplasia. Lineage trajectories suggest that some pyloric metaplasia cells can generate tuft and enteroendocrine cells (EECs). Comparison with Kras Conclusions: Under conditions of chronic injury, acinar cells undergo a pyloric-type metaplasia to mucinous progenitor-like populations, which seed disparate tuft cell and EEC lineages. ADM-derived EEC subtypes are diverse. Kras
MeSH term(s)	Acinar Cells/cytology ; Acinar Cells/metabolism ; Carcinoma, Pancreatic Ductal/genetics ; Cell Plasticity/genetics ; Enteroendocrine Cells/cytology ; Enteroendocrine Cells/metabolism ; Gene Expression Profiling ; Humans ; Metaplasia/genetics ; Metaplasia/metabolism ; Mucin 5AC/genetics ; Pancreas/cytology ; Pancreas/metabolism ; Pancreatic Ducts/cytology ; Pancreatic Ducts/metabolism ; Pancreatic Neoplasms/genetics ; Pancreatitis/genetics ; Pancreatitis/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Single-Cell Analysis
Chemical Substances	KRAS protein, human ; MUC5AC protein, human ; Mucin 5AC ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2021-10-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2021.10.027
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Zs.MO 572: Show issues

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