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Article ; Online: Interference-Aware Two-Level Differentiated Transmission for Improving Downlink Spatial Reuse in Dense WLANs.

Kwon, Lam / Park, Eun-Chan

2022 Volume 22, Issue 12

Abstract: In this study, we address the problem of downlink throughput degradation in dense wireless local area networks (WLANs) based on the IEEE 802.11ax standard. We demonstrate that this problem essentially results from the asymmetric characteristic of carrier ...

Abstract	In this study, we address the problem of downlink throughput degradation in dense wireless local area networks (WLANs) based on the IEEE 802.11ax standard. We demonstrate that this problem essentially results from the asymmetric characteristic of carrier sense multiple access between downlink and uplink transmissions in infrastructure WLANs, and it is exacerbated by a dynamic sensitivity control algorithm that aims to improve spatial reuse (SR) in IEEE 802.11ax. To solve this problem, we propose the
Language	English
Publishing date	2022-06-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2052857-7
ISSN	1424-8220 ; 1424-8220
ISSN (online)	1424-8220
ISSN	1424-8220
DOI	10.3390/s22124429
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Article ; Online: An Efficient Relayed Broadcasting based on the Duplication Estimation Model for IoT Applications.

Kim, Youngboo / Park, Eun-Chan

Sensors (Basel, Switzerland)

2019 Volume 19, Issue 9

Abstract: In this paper, we consider relay-based broadcasting in wireless ad hoc networks, which can enable various emerging services in the Internet of Things (IoT). In this kind of traffic dissemination scheme, also known as flooding, all the nodes not only ... ...

Abstract	In this paper, we consider relay-based broadcasting in wireless ad hoc networks, which can enable various emerging services in the Internet of Things (IoT). In this kind of traffic dissemination scheme, also known as flooding, all the nodes not only receive frames but also rebroadcast them. However, without an appropriate relay suppression, a broadcast storm problem arises, i.e., the transmission may fail due to severe collisions and/or interference, many duplicate frames are unnecessarily transmitted, and the traffic dissemination time increases. To mitigate the broadcast storm problem, we propose a reasonable criterion to restrict the rebroadcasting named the duplication ratio. Based on this, we propose an efficient mechanism consisting of duplication suppression and re-queuing schemes. The former discards duplicate frames proactively in a probabilistic manner to decrease the redundancy whereas the latter provides a secondary transmission opportunity reactively to compensate for the delivery failure. Moreover, to apply the duplication ratio practically, we propose a simple method to approximate it based on the number of adjacent nodes. The simulation study confirms that the proposed mechanism tightly ensured the reliability and decreased the traffic dissemination time by up to 6-fold compared to conventional mechanisms.
Language	English
Publishing date	2019-04-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2052857-7
ISSN	1424-8220 ; 1424-8220
ISSN (online)	1424-8220
ISSN	1424-8220
DOI	10.3390/s19092038
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Article ; Online: OFDMA Backoff Control Scheme for Improving Channel Efficiency in the Dynamic Network Environment of IEEE 802.11ax WLANs.

Kim, Youngboo / Kwon, Lam / Park, Eun-Chan

Sensors (Basel, Switzerland)

2021 Volume 21, Issue 15

Abstract: IEEE 802.11ax uplink orthogonal frequency division multiple access (OFDMA)-based random access (UORA) is a new feature for random channel access in wireless local area networks (WLANs). Similar to the legacy random access scheme in WLANs, UORA performs ... ...

Abstract	IEEE 802.11ax uplink orthogonal frequency division multiple access (OFDMA)-based random access (UORA) is a new feature for random channel access in wireless local area networks (WLANs). Similar to the legacy random access scheme in WLANs, UORA performs the OFDMA backoff (OBO) procedure to access the channel and decides on a random OBO counter within the OFDMA contention window (OCW) value. An access point (AP) can determine the OCW range and inform each station (STA) of it. However, how to determine a reasonable OCW range is beyond the scope of the IEEE 802.11ax standard. The OCW range is crucial to the UORA performance, and it primarily depends on the number of contending STAs, but it is challenging for the AP to accurately and quickly estimate or keep track of the number of contending STAs without the aid of a specific signaling mechanism. In addition, the one for this purpose incurs an additional delay and overhead in the channel access procedure. Therefore, the performance of a UORA scheme can be degraded by an improper OCW range, especially when the number of contending STAs changes dynamically. We first observed the effect of OCW values on channel efficiency and derived its optimal value from an analytical model. Next, we proposed a simple yet effective OBO control scheme where each STA determines its own OBO counter in a distributed manner rather than adjusting the OCW value globally. In the proposed scheme, each STA determines an appropriate OBO counter depending on whether the previous transmission was successful or not so that collisions can be mitigated without leaving OFDMA resource units unnecessarily idle. The results of a simulation study confirm that the throughput of the proposed scheme is comparable to the optimal OCW-based scheme and is improved by up to 15 times compared to the standard UORA scheme.
Language	English
Publishing date	2021-07-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2052857-7
ISSN	1424-8220 ; 1424-8220
ISSN (online)	1424-8220
ISSN	1424-8220
DOI	10.3390/s21155111
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Article ; Online: RPM-1 and DLK-1 regulate pioneer axon outgrowth by controlling Wnt signaling.

Park, Eun Chan / Rongo, Christopher

Development (Cambridge, England)

2018 Volume 145, Issue 18

Abstract: Axons must correctly reach their targets for proper nervous system function, although we do not fully understand the underlying mechanism, particularly for the first 'pioneer' axons. ... ...

Abstract	Axons must correctly reach their targets for proper nervous system function, although we do not fully understand the underlying mechanism, particularly for the first 'pioneer' axons. In
MeSH term(s)	Animals ; Axons/metabolism ; CCAAT-Enhancer-Binding Proteins/metabolism ; Caenorhabditis elegans/embryology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Cell Differentiation/genetics ; Cell Proliferation/genetics ; Glycoproteins/metabolism ; Guanine Nucleotide Exchange Factors/genetics ; Guanine Nucleotide Exchange Factors/metabolism ; MAP Kinase Kinase Kinases/genetics ; MAP Kinase Kinase Kinases/metabolism ; Neurons/metabolism ; Wnt Proteins/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	CCAAT-Enhancer-Binding Proteins ; Caenorhabditis elegans Proteins ; Cebp-1 protein, C elegans ; Egl-20 protein, C elegans ; Glycoproteins ; Guanine Nucleotide Exchange Factors ; RPM-1 protein, C elegans ; Wnt Proteins ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; DLK-1 protein, C elegans (EC 2.7.11.25) ; MAP Kinase Kinase Kinases (EC 2.7.11.25)
Language	English
Publishing date	2018-09-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.164897
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Article ; Online: The p38 MAP kinase pathway modulates the hypoxia response and glutamate receptor trafficking in aging neurons.

Park, Eun Chan / Rongo, Christopher

eLife

2016 Volume 5

Abstract: Neurons are sensitive to low oxygen (hypoxia) and employ a conserved pathway to combat its effects. Here, we show that p38 MAP Kinase (MAPK) modulates this hypoxia response pathway in C. elegans. Mutants lacking p38 MAPK components pmk-1 or sek-1 ... ...

Abstract	Neurons are sensitive to low oxygen (hypoxia) and employ a conserved pathway to combat its effects. Here, we show that p38 MAP Kinase (MAPK) modulates this hypoxia response pathway in C. elegans. Mutants lacking p38 MAPK components pmk-1 or sek-1 resemble mutants lacking the hypoxia response component and prolyl hydroxylase egl-9, with impaired subcellular localization of Mint orthologue LIN-10, internalization of glutamate receptor GLR-1, and depression of GLR-1-mediated behaviors. Loss of p38 MAPK impairs EGL-9 protein localization in neurons and activates the hypoxia-inducible transcription factor HIF-1, suggesting that p38 MAPK inhibits the hypoxia response pathway through EGL-9. As animals age, p38 MAPK levels decrease, resulting in GLR-1 internalization; this age-dependent downregulation can be prevented through either p38 MAPK overexpression or removal of CDK-5, an antagonizing kinase. Our findings demonstrate that p38 MAPK inhibits the hypoxia response pathway and determines how aging neurons respond to hypoxia through a novel mechanism.
MeSH term(s)	Animals ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/metabolism ; Cell Hypoxia ; MAP Kinase Signaling System ; Neurons/physiology ; Receptors, Glutamate/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; Receptors, Glutamate ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2016-01-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.12010
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Article ; Online: FNDC-1-mediated mitophagy and ATFS-1 coordinate to protect against hypoxia-reoxygenation.

Lim, Yunki / Berry, Brandon / Viteri, Stephanie / McCall, Matthew / Park, Eun Chan / Rongo, Christopher / Brookes, Paul S / Nehrke, Keith

Autophagy

2021 Volume 17, Issue 11, Page(s) 3389–3401

Abstract: Mitochondrial quality control (MQC) balances organelle adaptation and elimination, and mechanistic crosstalk between the underlying molecular processes affects subsequent stress outcomes. FUNDC1 (FUN14 domain containing 1) is a mammalian mitophagy ... ...

Abstract	Mitochondrial quality control (MQC) balances organelle adaptation and elimination, and mechanistic crosstalk between the underlying molecular processes affects subsequent stress outcomes. FUNDC1 (FUN14 domain containing 1) is a mammalian mitophagy receptor that responds to hypoxia-reoxygenation (HR) stress. Here, we provide evidence that FNDC-1 is the
MeSH term(s)	Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/physiology ; Genes, Helminth ; Hypoxia/genetics ; Hypoxia/physiopathology ; Loss of Function Mutation ; Membrane Proteins/genetics ; Membrane Proteins/physiology ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/physiology ; Mitophagy/genetics ; Mitophagy/physiology ; Reperfusion Injury/genetics ; Reperfusion Injury/physiopathology ; Transcription Factors/genetics ; Transcription Factors/physiology
Chemical Substances	ATFS-1 protein, C elegans ; Caenorhabditis elegans Proteins ; Membrane Proteins ; Mitochondrial Proteins ; Transcription Factors
Language	English
Publishing date	2021-01-19
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	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2021.1872885
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Article ; Online: Medical-Grade Channel Access and Admission Control in 802.11e EDCA for Healthcare Applications.

Son, Sunghwa / Park, Kyung-Joon / Park, Eun-Chan

PloS one

2016 Volume 11, Issue 8, Page(s) e0160052

Abstract: In this paper, we deal with the problem of assuring medical-grade quality of service (QoS) for real-time medical applications in wireless healthcare systems based on IEEE 802.11e. Firstly, we show that the differentiated channel access of IEEE 802.11e ... ...

Abstract	In this paper, we deal with the problem of assuring medical-grade quality of service (QoS) for real-time medical applications in wireless healthcare systems based on IEEE 802.11e. Firstly, we show that the differentiated channel access of IEEE 802.11e cannot effectively assure medical-grade QoS because of priority inversion. To resolve this problem, we propose an efficient channel access algorithm. The proposed algorithm adjusts arbitrary inter-frame space (AIFS) in the IEEE 802.11e protocol depending on the QoS measurement of medical traffic, to provide differentiated near-absolute priority for medical traffic. In addition, based on rigorous capacity analysis, we propose an admission control scheme that can avoid performance degradation due to network overload. Via extensive simulations, we show that the proposed mechanism strictly assures the medical-grade QoS and improves the throughput of low-priority traffic by more than several times compared to the conventional IEEE 802.11e.
MeSH term(s)	Algorithms ; Clinical Alarms ; Computer Communication Networks ; Delivery of Health Care ; Electrocardiography ; Heart Rate/physiology ; Humans ; Wireless Technology
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0160052
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The ubiquitin ligase RPM-1 and the p38 MAPK PMK-3 regulate AMPA receptor trafficking.

Park, Eun Chan / Glodowski, Doreen R / Rongo, Christopher

PloS one

2009 Volume 4, Issue 1, Page(s) e4284

Abstract: Ubiquitination occurs at synapses, yet its role remains unclear. Previous studies demonstrated that the RPM-1 ubiquitin ligase organizes presynaptic boutons at neuromuscular junctions in C. elegans motorneurons. Here we find that RPM-1 has a novel ... ...

Abstract	Ubiquitination occurs at synapses, yet its role remains unclear. Previous studies demonstrated that the RPM-1 ubiquitin ligase organizes presynaptic boutons at neuromuscular junctions in C. elegans motorneurons. Here we find that RPM-1 has a novel postsynaptic role in interneurons, where it regulates the trafficking of the AMPA-type glutamate receptor GLR-1 from synapses into endosomes. Mutations in rpm-1 cause the aberrant accumulation of GLR-1 in neurites. Moreover, rpm-1 mutations enhance the endosomal accumulation of GLR-1 observed in mutants for lin-10, a Mint2 ortholog that promotes GLR-1 recycling from Syntaxin-13 containing endosomes. As in motorneurons, RPM-1 negatively regulates the pmk-3/p38 MAPK pathway in interneurons by repressing the protein levels of the MAPKKK DLK-1. This regulation of PMK-3 signaling is critical for RPM-1 function with respect to GLR-1 trafficking, as pmk-3 mutations suppress both lin-10 and rpm-1 mutations. Positive or negative changes in endocytosis mimic the effects of rpm-1 or pmk-3 mutations, respectively, on GLR-1 trafficking. Specifically, RAB-5(GDP), an inactive mutant of RAB-5 that reduces endocytosis, mimics the effect of pmk-3 mutations when introduced into wild-type animals, and occludes the effect of pmk-3 mutations when introduced into pmk-3 mutants. By contrast, RAB-5(GTP), which increases endocytosis, suppresses the effect of pmk-3 mutations, mimics the effect of rpm-1 mutations, and occludes the effect of rpm-1 mutations. Our findings indicate a novel specialized role for RPM-1 and PMK-3/p38 MAPK in regulating the endosomal trafficking of AMPARs at central synapses.
MeSH term(s)	Amino Acid Sequence ; Animals ; Caenorhabditis elegans ; Caenorhabditis elegans Proteins/metabolism ; Endocytosis ; Endosomes/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Models, Biological ; Models, Genetic ; Molecular Sequence Data ; Neuromuscular Junction ; Qa-SNARE Proteins/metabolism ; Receptors, AMPA/metabolism ; Sequence Homology, Amino Acid ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; Qa-SNARE Proteins ; Receptors, AMPA ; glr-1 protein, C elegans ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; pmk-3 protein, C elegans (EC 2.7.11.24)
Language	English
Publishing date	2009-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0004284
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Article ; Online: Anoxia-reoxygenation regulates mitochondrial dynamics through the hypoxia response pathway, SKN-1/Nrf, and stomatin-like protein STL-1/SLP-2.

Ghose, Piya / Park, Eun Chan / Tabakin, Alexandra / Salazar-Vasquez, Nathaly / Rongo, Christopher

PLoS genetics

2013 Volume 9, Issue 12, Page(s) e1004063

Abstract: Many aerobic organisms encounter oxygen-deprived environments and thus must have adaptive mechanisms to survive such stress. It is important to understand how mitochondria respond to oxygen deprivation given the critical role they play in using oxygen to ...

Abstract	Many aerobic organisms encounter oxygen-deprived environments and thus must have adaptive mechanisms to survive such stress. It is important to understand how mitochondria respond to oxygen deprivation given the critical role they play in using oxygen to generate cellular energy. Here we examine mitochondrial stress response in C. elegans, which adapt to extreme oxygen deprivation (anoxia, less than 0.1% oxygen) by entering into a reversible suspended animation state of locomotory arrest. We show that neuronal mitochondria undergo DRP-1-dependent fission in response to anoxia and undergo refusion upon reoxygenation. The hypoxia response pathway, including EGL-9 and HIF-1, is not required for anoxia-induced fission, but does regulate mitochondrial reconstitution during reoxygenation. Mutants for egl-9 exhibit a rapid refusion of mitochondria and a rapid behavioral recovery from suspended animation during reoxygenation; both phenotypes require HIF-1. Mitochondria are significantly larger in egl-9 mutants after reoxygenation, a phenotype similar to stress-induced mitochondria hyperfusion (SIMH). Anoxia results in mitochondrial oxidative stress, and the oxidative response factor SKN-1/Nrf is required for both rapid mitochondrial refusion and rapid behavioral recovery during reoxygenation. In response to anoxia, SKN-1 promotes the expression of the mitochondrial resident protein Stomatin-like 1 (STL-1), which helps facilitate mitochondrial dynamics following anoxia. Our results suggest the existence of a conserved anoxic stress response involving changes in mitochondrial fission and fusion.
MeSH term(s)	Aerobiosis/genetics ; Aerobiosis/physiology ; Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Cell Hypoxia/genetics ; Cell Hypoxia/physiology ; Dynamins/metabolism ; Hypoxia/genetics ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/physiology ; Mitochondrial Dynamics/genetics ; Mitochondrial Proteins/genetics ; NF-E2-Related Factor 1/genetics ; NF-E2-Related Factor 1/metabolism ; Neurons/cytology ; Neurons/metabolism ; Neurons/physiology ; Oxidation-Reduction ; Oxidative Stress/genetics ; Transcription Factors/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; Egl-9 protein, C elegans ; HIF-1 protein, C elegans ; Mitochondrial Proteins ; NF-E2-Related Factor 1 ; STL-1 protein, C elegans ; Transcription Factors ; Dynamins (EC 3.6.5.5) ; dynamin-related protein 1, C elegans (EC 3.6.5.5)
Language	English
Publishing date	2013-12-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1004063
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Article: Fast performance assessment of IEEE 802.11-based wireless networks

Kim, Hwangnam / Park, Eun-Chan / Lee, Suk Kyu / Hu, Chunyu

Mathematical and computer modelling. 2011 June, v. 53, no. 11-12

2011

Abstract: In this paper, we introduce a brand new analytical perspective for analyzing and evaluating the IEEE 802.11-based networks. We identify a tightly-coupled relationship between the number of contending nodes and their contention window sizes in the ... ...

Abstract	In this paper, we introduce a brand new analytical perspective for analyzing and evaluating the IEEE 802.11-based networks. We identify a tightly-coupled relationship between the number of contending nodes and their contention window sizes in the networks. Based on the relationship, we propose a downsizing model for reducing the computational complexity and for improving the simulation performance in the evaluation of the IEEE 802.11-based networks. We first formally prove that the proposed model preserves the operational characteristics of the original networks in their downsized networks through well-known analytical frameworks, such as the models proposed by Bianchi (2000) [7], Calí et al. (2000) [2], and Hu et al. (2006) [8]. We then demonstrate that the proposed model speeds up the simulation by maximally two orders of magnitude. Even though the simulation shows some difference between the results from an original network and those in its corresponding downsized networks in a wide range of network sizes and traffic patterns, the difference is acceptable since it has minimal values of 1% in most cases and maximum values of 10% in a very few cases. We also present the effectiveness of both the downsizing model and the downsizing-model-based simulation in comparison with other performance models and simulation techniques. As the size and complexity of wireless networks are increasing nowadays, we vision that the new proposed model will be of great advantage in conducting fast and accurate packet-level wireless simulations, as well as being a helpful tool for performing the numerically tractable theoretical studies for extensive performance evaluations, such as determining the network-wide throughput or end-to-end delays.
Keywords	computer techniques ; decision making ; mathematical models ; simulation models ; traffic
Language	English
Dates of publication	2011-06
Size	p. 2173-2191.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	2002543-9
ISSN	0895-7177
ISSN	0895-7177
DOI	10.1016/j.mcm.2010.08.024
Database	NAL-Catalogue (AGRICOLA)

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