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Article ; Online: Thiazolidinediones Decrease the Recurrence of Intracerebral Hemorrhage in Type 2 Diabetes Mellitus Patients: A Nested Case-Control Study.

Chiu, Cheng-Di / Chiu, You-Pen / Yip, Hei-Tung / Ji, Hui-Ru / Cho, Der-Yang / Cheng, Irene Han-Juo / Chen, Cho-Yi

2024

Abstract: Introduction: Preclinical evidence demonstrated the therapeutic potential of TZDs for the treatment of intracerebral hemorrhage (ICH). The present study conducted an investigation of cerebrovascular and cardiovascular outcomes following ICH in patients ... ...

Abstract	Introduction: Preclinical evidence demonstrated the therapeutic potential of TZDs for the treatment of intracerebral hemorrhage (ICH). The present study conducted an investigation of cerebrovascular and cardiovascular outcomes following ICH in patients with type 2 diabetes mellitus (T2DM) treated with or without TZDs. Methods: This retrospective nested case-control study used data from the Taiwan National Health Insurance Research Database. A total of 62,515 T2DM patients who were hospitalized with a diagnosis of ICH were enrolled, including 7,603 TZD users. Data for TZD non-users were extracted using propensity score matching. Primary outcomes included death and major adverse cardiovascular events (MACEs), which were defined as a composite of ischemic stroke, hemorrhagic stroke (HS), acute myocardial infarction (AMI), and congestive heart failure (CHF). Patients aged < 20 years with a history of traumatic brain injury or any prior history of MACEs were excluded. Results: TZD users had significantly lower MACE risks compared with TZD non-users following ICH (adjusted hazard ratio [aHR]: 0.90, 95% confidence interval [CI]: 0.85-0.94, p < 0.001). The most significant MACE difference reported for TZD users was HS, which possessed lower incidence than in TZD non-users, especially for the events that happened within 3 months following ICH (aHR: 0.74, 95% CI: 0.62-0.89 within one month, p < 0.01; aHR: 0.68, 95% CI: 0.54-0.85 between 1-3 month). Conclusion: The use of TZD in patients with T2DM was associated with a lower risk of subsequent HS and mortality following ICH.
Language	English
Publishing date	2024-05-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	603189-4
ISSN	1423-0208 ; 0251-5350
ISSN (online)	1423-0208
ISSN	0251-5350
DOI	10.1159/000539001
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Zs.A 1722: Show issues

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Article: CASK Mediates Oxidative Stress-Induced Microglial Apoptosis-Inducing Factor-Independent Parthanatos Cell Death via Promoting PARP-1 Hyperactivation and Mitochondrial Dysfunction.

Cheong, Keith Jun Hao / Huang, Duen-Yi / Sekar, Ponarulselvam / Chen, Rou Jhen / Cheng, Irene Han-Juo / Chan, Chi-Ming / Chen, Yuan-Shen / Lin, Wan-Wan

Antioxidants (Basel, Switzerland)

2024 Volume 13, Issue 3

Abstract: Calcium/calmodulin-dependent serine protein kinase (CASK) is a scaffold protein and plays critical roles in neuronal synaptic formation and brain development. Previously, CASK was shown to associate with EGFR to maintain the vulval cell differentiation ... ...

Abstract	Calcium/calmodulin-dependent serine protein kinase (CASK) is a scaffold protein and plays critical roles in neuronal synaptic formation and brain development. Previously, CASK was shown to associate with EGFR to maintain the vulval cell differentiation in
Language	English
Publishing date	2024-03-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox13030343
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Article ; Online: Altered nociception in Alzheimer disease is associated with striatal-enriched protein tyrosine phosphatase signaling.

Lee, Zhung-Fu / Huang, Tzu-Hsuan / Chen, Shih-Pin / Cheng, Irene Han-Juo

Pain

2021 Volume 162, Issue 6, Page(s) 1669–1680

Abstract: Abstract: Alzheimer disease (AD) is the most common form of dementia, accounting for approximately 60% of cases. In addition to memory loss, changes in pain sensitivity are found in a substantial proportion of patients with AD. However, the mechanism of ...

Abstract	Abstract: Alzheimer disease (AD) is the most common form of dementia, accounting for approximately 60% of cases. In addition to memory loss, changes in pain sensitivity are found in a substantial proportion of patients with AD. However, the mechanism of nociception deficits in AD is still unclear. Here, we hypothesize that the nociception abnormality in AD is due to the aberrant activation of striatal-enriched protein tyrosine phosphatase (STEP) signaling, which modulates proteins related to nociception transduction. Our results indicated that the transgenic mice carrying human amyloid precursor protein (APP) gene had lower sensitivity to mechanical and thermal stimulation than the wild-type group at the ages of 6, 9, and 12 months. These APP mice exhibited elevated STEP activity and decreased phosphorylation of proteins involved in nociception transduction in hippocampi. The pharmacological inhibition of STEP activity using TC-2153 further reversed nociception and cognitive deficits in the APP mice. Moreover, the phosphorylation of nociception-related proteins in the APP mice was also rescued after STEP inhibitor treatment, indicating the key role of STEP in nociception alteration. In summary, this study identifies a mechanism for the reduced nociceptive sensitivity in an AD mouse model that could serve as a therapeutic target to improve the quality of life for patients with AD.
MeSH term(s)	Alzheimer Disease/complications ; Alzheimer Disease/genetics ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor/genetics ; Animals ; Disease Models, Animal ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nociception ; Protein Tyrosine Phosphatases ; Quality of Life
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Protein Tyrosine Phosphatases (EC 3.1.3.48)
Language	English
Publishing date	2021-01-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	193153-2
ISSN	1872-6623 ; 0304-3959
ISSN (online)	1872-6623
ISSN	0304-3959
DOI	10.1097/j.pain.0000000000002180
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Zs.A 1158: Show issues

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Article ; Online: Connectivity and synaptic features of hilar mossy cells and their effects on granule cell activity along the hippocampal longitudinal axis.

Abdulmajeed, Wahab Imam / Wang, Kai-Yi / Wu, Jei-Wei / Ajibola, Musa Iyiola / Cheng, Irene Han-Juo / Lien, Cheng-Chang

The Journal of physiology

2022 Volume 600, Issue 14, Page(s) 3355–3381

Abstract: The hippocampus is an elongated brain structure which runs along a ventral-to-dorsal axis in rodents, corresponding to the anterior-to-posterior axis in humans. A glutamatergic cell type in the dentate gyrus (DG), the mossy cells (MCs), establishes ... ...

Abstract	The hippocampus is an elongated brain structure which runs along a ventral-to-dorsal axis in rodents, corresponding to the anterior-to-posterior axis in humans. A glutamatergic cell type in the dentate gyrus (DG), the mossy cells (MCs), establishes extensive excitatory collateral connections with the DG principal cells, the granule cells (GCs), and inhibitory interneurons in both hippocampal hemispheres along the longitudinal axis. Although coupling of two physically separated GC populations via long-axis projecting MCs is instrumental for information processing, the connectivity and synaptic features of MCs along the longitudinal axis are poorly defined. Here, using channelrhodopsin-2 assisted circuit mapping, we showed that MC excitation results in a low synaptic excitation-inhibition (E/I) balance in the intralamellar (local) GCs, but a high synaptic E/I balance in the translamellar (distant) ones. In agreement with the differential E/I balance along the ventrodorsal axis, activation of MCs either enhances or suppresses the local GC response to the cortical input, but primarily promotes the distant GC activation. Moreover, activation of MCs enhances the spike timing precision of the local GCs, but not that of the distant ones. Collectively, these findings suggest that MCs differentially regulate the local and distant GC activity through distinct synaptic mechanisms. KEY POINTS: Hippocampal mossy cell (MC) pathways differentially regulate granule cell (GC) activity along the longitudinal axis. MCs mediate a low excitation-inhibition balance in intralamellar (local) GCs, but a high excitation-inhibition balance in translamellar (distant) GCs. MCs enhance the spiking precision of local GCs, but not distant GCs. MCs either promote or suppress local GC activity, but primarily promote distant GC activation.
MeSH term(s)	Channelrhodopsins ; Dentate Gyrus/physiology ; Hippocampus/physiology ; Humans ; Interneurons ; Mossy Fibers, Hippocampal/physiology
Chemical Substances	Channelrhodopsins
Language	English
Publishing date	2022-06-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP282804
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Uc I Zs.65: Show issues

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Article ; Online: Endoplasmic reticulum stress induces Alzheimer disease-like phenotypes in the neuron derived from the induced pluripotent stem cell with D678H mutation on amyloid precursor protein.

Devina, Tania / Wong, Yu-Hui / Hsiao, Chiao-Wan / Li, Yu-Jui / Lien, Cheng-Chang / Cheng, Irene Han-Juo

Journal of neurochemistry

2022 Volume 163, Issue 1, Page(s) 26–39

Abstract: Alzheimer disease (AD), a progressive neurodegenerative disorder, is mainly caused by the interaction of genetic and environmental factors. The impact of environmental factors on the genetic mutation in the amyloid precursor protein (APP) is not well ... ...

Abstract	Alzheimer disease (AD), a progressive neurodegenerative disorder, is mainly caused by the interaction of genetic and environmental factors. The impact of environmental factors on the genetic mutation in the amyloid precursor protein (APP) is not well characterized. We hypothesized that endoplasmic reticulum (ER) stress would promote disease for the patient carrying the APP D678H mutation. Therefore, we analyzed the impact of a familial AD mutation on amyloid precursor protein (APP D678H) under ER stress. Induced pluripotent stem cells (iPSCs) from APP D678H mutant carrier was differentiated into neurons, which were then analyzed for AD-like changes. Immunocytochemistry and whole-cell patch-clamp recording revealed that the derived neurons on day 28 after differentiation showed neuronal markers and electrophysiological properties similar to those of mature neurons. However, the APP D678H mutant neurons did not have significant alterations in the levels of amyloid-β (Aβ) and phosphorylated tau (pTau) compared to its isogenic wild-type neurons. Only under ER stress, the neurons with the APP D678H mutation had more Aβ and pTau via immune detection assays. The higher level of Aβ in the APP D678H mutant neurons was probably due to the increased level of β-site APP cleaving enzyme (BACE1) and decreased level of Aβ-degrading enzymes under ER stress. Increased Aβ and pTau under ER stress reduced the N-methyl-D-aspartate receptor (NMDAR) in Western blot analysis and altered electrophysiological properties in the mutant neurons. Our study provides evidence that the interaction between genetic mutation and ER stress would induce AD-like changes. Cover Image for this issue: https://doi.org/10.1111/jnc.15420.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid Precursor Protein Secretases/genetics ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Aspartic Acid Endopeptidases/metabolism ; Endoplasmic Reticulum Stress/genetics ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Mutation/genetics ; Neurons/metabolism ; Phenotype ; Receptors, N-Methyl-D-Aspartate/metabolism
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Receptors, N-Methyl-D-Aspartate ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Aspartic Acid Endopeptidases (EC 3.4.23.-)
Language	English
Publishing date	2022-08-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15687
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Ui II Zs.170: Show issues

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Article: Differential expression of GABA

Huang, Tzu-Hsuan / Lin, Yi-Sian / Hsiao, Chiao-Wan / Wang, Liang-Yun / Ajibola, Musa Iyiola / Abdulmajeed, Wahab Imam / Lin, Yu-Ling / Li, Yu-Jui / Chen, Cho-Yi / Lien, Cheng-Chang / Chiu, Cheng-Di / Cheng, Irene Han-Juo

Frontiers in cellular neuroscience

2023 Volume 17, Page(s) 1146278

Abstract: Inhibitory γ-aminobutyric acid (GABA)-ergic interneurons mediate inhibition in neuronal circuitry and support normal brain function. Consequently, dysregulation of inhibition is implicated in various brain disorders. Parvalbumin (PV) and somatostatin ( ... ...

Abstract	Inhibitory γ-aminobutyric acid (GABA)-ergic interneurons mediate inhibition in neuronal circuitry and support normal brain function. Consequently, dysregulation of inhibition is implicated in various brain disorders. Parvalbumin (PV) and somatostatin (SST) interneurons, the two major types of GABAergic inhibitory interneurons in the hippocampus, exhibit distinct morpho-physiological properties and coordinate information processing and memory formation. However, the molecular mechanisms underlying the specialized properties of PV and SST interneurons remain unclear. This study aimed to compare the transcriptomic differences between these two classes of interneurons in the hippocampus using the ribosome tagging approach. The results revealed distinct expressions of genes such as voltage-gated ion channels and GABA
Language	English
Publishing date	2023-07-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2023.1146278
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Article ; Online: Behavioral alterations following blood-brain barrier disruption stimulated by focused ultrasound.

Yang, Feng-Yi / Huang, Sheng-Fang / Cheng, Irene Han-Juo

Oncotarget

2016 Volume 7, Issue 19, Page(s) 27916–27925

Abstract: The purpose of this study was to investigate the behavioral alterations and histological changes of the brain after FUS-induced BBB disruption (BBBD). Rats were behaviorally tested using the open field, hole-board, and grip strength tests from day 1 ... ...

Abstract	The purpose of this study was to investigate the behavioral alterations and histological changes of the brain after FUS-induced BBB disruption (BBBD). Rats were behaviorally tested using the open field, hole-board, and grip strength tests from day 1 through day 32 after undergoing BBBD induced by FUS with either a mild or heavy parameter. In the open field test, we found an increase in center entries on day 1 and day 9 following heavy FUS treatment and a decrease in center entries at day 18 following mild FUS treatment. With regard to memory-related alterations, rats subjected to heavy FUS treatment exhibited longer latency to start exploring and to find the first baited hole. However, rats subjected to mild FUS treatment exhibited no significant differences in terms of memory performance or grip force. The obtained data suggest that heavy FUS treatment might induce hyperactivity, spatial memory impairment, and forelimb gripping deficits. Furthermore, while mild FUS treatment may have an impact on anxiety-related behaviors, the data suggested it had no impact on locomotor activity, memory, or grip force. Thus, the behavioral alterations following FUS-induced BBBD require further investigation before clinical application.
Language	English
Publishing date	2016-05-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.8444
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Article: Graptopetalum paraguayense Extract Ameliorates Proteotoxicity in Aging and Age-Related Diseases in Model Systems

Chen, Yan-Xi / Le, Phuong Thu Nguyen / Tzeng, Tsai-Teng / Tran, Thu-Ha / Nguyen, Anh Thuc / Cheng, Irene Han-Juo / Huang, Chi-Ying F. / Shiao, Young-Ji / Ching, Tsui-Ting

Nutrients. 2021 Nov. 29, v. 13, no. 12

2021

Abstract: Declines in physiological functions are the predominant risk factors for age-related diseases, such as cancers and neurodegenerative diseases. Therefore, delaying the aging process is believed to be beneficial in preventing the onset of age-related ... ...

Abstract	Declines in physiological functions are the predominant risk factors for age-related diseases, such as cancers and neurodegenerative diseases. Therefore, delaying the aging process is believed to be beneficial in preventing the onset of age-related diseases. Previous studies have demonstrated that Graptopetalum paraguayense (GP) extract inhibits liver cancer cell growth and reduces the pathological phenotypes of Alzheimer’s disease (AD) in patient IPS-derived neurons. Here, we show that GP extract suppresses β-amyloid pathology in SH-SYS5Y-APP₆₉₅ cells and APP/PS1 mice. Moreover, AMP-activated protein kinase (AMPK) activity is enhanced by GP extract in U87 cells and APP/PS1 mice. Intriguingly, GP extract enhances autophagy in SH-SYS5Y-APP₆₉₅ cells, U87 cells, and the nematode Caenorhabditis elegans, suggesting a conserved molecular mechanism by which GP extract might regulate autophagy. In agreement with its role as an autophagy activator, GP extract markedly diminishes mobility decline in polyglutamine Q35 mutants and aged wild-type N2 animals in C. elegans. Furthermore, GP extract significantly extends lifespan in C. elegans.
Keywords	AMP-activated protein kinase ; Caenorhabditis elegans ; Graptopetalum paraguayense ; autophagy ; cell growth ; decline ; liver neoplasms ; longevity ; neoplasm cells ; patients
Language	English
Dates of publication	2021-1129
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu13124317
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Graptopetalum paraguayense

Chen, Yan-Xi / Le, Phuong Thu Nguyen / Tzeng, Tsai-Teng / Tran, Thu-Ha / Nguyen, Anh Thuc / Cheng, Irene Han-Juo / Huang, Chi-Ying F / Shiao, Young-Ji / Ching, Tsui-Ting

Nutrients

2021 Volume 13, Issue 12

Abstract	Declines in physiological functions are the predominant risk factors for age-related diseases, such as cancers and neurodegenerative diseases. Therefore, delaying the aging process is believed to be beneficial in preventing the onset of age-related diseases. Previous studies have demonstrated that
MeSH term(s)	AMP-Activated Protein Kinases/drug effects ; Aging/drug effects ; Amyloid beta-Peptides/drug effects ; Animals ; Autophagy/drug effects ; Caenorhabditis elegans/drug effects ; Cell Culture Techniques ; Crassulaceae/chemistry ; Disease Models, Animal ; Humans ; Longevity/drug effects ; Mice ; Mice, Transgenic ; Plant Extracts/pharmacology
Chemical Substances	Amyloid beta-Peptides ; Plant Extracts ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2021-11-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu13124317
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Article ; Online: Amelioration of amyloid-β-induced deficits by DcR3 in an Alzheimer's disease model.

Liu, Yi-Ling / Chen, Wei-Ting / Lin, Yu-Yi / Lu, Po-Hung / Hsieh, Shie-Liang / Cheng, Irene Han-Juo

Molecular neurodegeneration

2017 Volume 12, Issue 1, Page(s) 30

Abstract: Background: Microglia mediate amyloid-beta peptide (Aβ)-induced neuroinflammation, which is one of the key events in the pathogenesis of Alzheimer's disease (AD). Decoy receptor 3 (DcR3)/TNFRSF6B is a pleiotropic immunomodulator that promotes macrophage ...

Abstract	Background: Microglia mediate amyloid-beta peptide (Aβ)-induced neuroinflammation, which is one of the key events in the pathogenesis of Alzheimer's disease (AD). Decoy receptor 3 (DcR3)/TNFRSF6B is a pleiotropic immunomodulator that promotes macrophage differentiation toward the M2 anti-inflammatory phenotype. Based on its role as an immunosupressor, we examined whether DcR3 could alleviate neuroinflammation and AD-like deficits in the central nervous system. Method: We crossed human APP transgenic mice (line J20) with human DcR3 transgenic mice to generate wild-type, APP, DcR3, and APP/DcR3 mice for pathological analysis. The Morris water maze, fear conditioning test, open-field, and elevated-plus maze were used to access their cognitive behavioral changes. Furthermore, the pathological and immune profiles were examined by immunostaining, ELISA, Q-PCR, and IP. In vitro assays were designed to examine DcR3-mediated innate cytokine profile alteration and the potential protective mechanism. Results: We reported that DcR3 ameliorates hippocampus-dependent memory deficits and reduces amyloid plaque deposition in APP transgenic mouse. The protective mechanism of DcR3 mediates through interacting with heparan sulfate proteoglycans and activating IL-4 Conclusion: The neuroprotective effect of DcR3 is mediated via modulating microglia activation into anti-inflammatory M2a phenotype, and upregulating DcR3 expression in the brain may be a potential therapeutic approach for AD.
Language	English
Publishing date	2017--24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1750-1326
ISSN (online)	1750-1326
DOI	10.1186/s13024-017-0173-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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