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Article ; Online: A tribute to Sebastián Cerdán and his key contributions to brain metabolism.

Satrustegui, Jorgina / Larrubia, Pilar López / Rodrigues, Tiago B / Choi, In-Young / McKenna, Mary C

2023

Abstract: This is a tribute to Sebastián Cerdán, a brilliant and innovative NMR spectroscopist whose studies contributed greatly to the fundamental information to the understanding of brain metabolism, particularly in regard to multinuclear magnetic resonance ... ...

Abstract	This is a tribute to Sebastián Cerdán, a brilliant and innovative NMR spectroscopist whose studies contributed greatly to the fundamental information to the understanding of brain metabolism, particularly in regard to multinuclear magnetic resonance spectroscopy (MRS) techniques. Sebastián Cerdán sadly passed away in May 2022. He was a wonderful mentor and colleague who will be greatly missed.
Language	English
Publishing date	2023-05-11
Publishing country	England
Document type	Journal Article
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15828
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Article ; Online: Regulation of neuronal energy metabolism by calcium: Role of MCU and Aralar/malate-aspartate shuttle.

Del Arco, Araceli / González-Moreno, Luis / Pérez-Liébana, Irene / Juaristi, Inés / González-Sánchez, Paloma / Contreras, Laura / Pardo, Beatriz / Satrústegui, Jorgina

Biochimica et biophysica acta. Molecular cell research

2023 Volume 1870, Issue 5, Page(s) 119468

Abstract: Calcium is a major regulator of cellular metabolism. Calcium controls mitochondrial respiration, and calcium signaling is used to meet cellular energetic demands through energy production in the organelle. Although it has been widely assumed that ... ...

Abstract	Calcium is a major regulator of cellular metabolism. Calcium controls mitochondrial respiration, and calcium signaling is used to meet cellular energetic demands through energy production in the organelle. Although it has been widely assumed that Ca
MeSH term(s)	Calcium/metabolism ; Aspartic Acid/metabolism ; Malates/metabolism ; NAD/metabolism ; Calcium Signaling ; Energy Metabolism ; Pyruvic Acid/metabolism ; Neurons/metabolism ; Glucose/metabolism
Chemical Substances	mitochondrial calcium uniporter ; Calcium (SY7Q814VUP) ; Aspartic Acid (30KYC7MIAI) ; Malates ; NAD (0U46U6E8UK) ; Pyruvic Acid (8558G7RUTR) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-03-28
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2023.119468
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Article ; Online: AGC1 Deficiency: Pathology and Molecular and Cellular Mechanisms of the Disease.

Pardo, Beatriz / Herrada-Soler, Eduardo / Satrústegui, Jorgina / Contreras, Laura / Del Arco, Araceli

International journal of molecular sciences

2022 Volume 23, Issue 1

Abstract: AGC1/Aralar/Slc25a12 is the mitochondrial carrier of aspartate-glutamate, the regulatory component of the NADH malate-aspartate shuttle (MAS) that transfers cytosolic redox power to neuronal mitochondria. The deficiency in AGC1/Aralar leads to the human ... ...

Abstract	AGC1/Aralar/Slc25a12 is the mitochondrial carrier of aspartate-glutamate, the regulatory component of the NADH malate-aspartate shuttle (MAS) that transfers cytosolic redox power to neuronal mitochondria. The deficiency in AGC1/Aralar leads to the human rare disease named "early infantile epileptic encephalopathy 39" (EIEE 39, OMIM # 612949) characterized by epilepsy, hypotonia, arrested psychomotor neurodevelopment, hypo myelination and a drastic drop in brain aspartate (Asp) and
MeSH term(s)	Aggrecans/deficiency ; Aggrecans/genetics ; Aggrecans/metabolism ; Amino Acid Transport Systems, Acidic/deficiency ; Amino Acid Transport Systems, Acidic/metabolism ; Animals ; Antiporters/deficiency ; Antiporters/metabolism ; Biomarkers ; Brain/metabolism ; Combined Modality Therapy ; Disease Management ; Disease Models, Animal ; Dopaminergic Neurons/metabolism ; Dopaminergic Neurons/pathology ; Energy Metabolism ; Genetic Association Studies ; Genetic Predisposition to Disease ; Glutamic Acid/metabolism ; Hereditary Central Nervous System Demyelinating Diseases/diagnosis ; Hereditary Central Nervous System Demyelinating Diseases/etiology ; Hereditary Central Nervous System Demyelinating Diseases/metabolism ; Hereditary Central Nervous System Demyelinating Diseases/therapy ; Humans ; Malates/metabolism ; Mice ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Diseases/diagnosis ; Mitochondrial Diseases/etiology ; Mitochondrial Diseases/metabolism ; Mitochondrial Diseases/therapy ; Myelin Sheath/metabolism ; Oxidation-Reduction ; Phenotype ; Psychomotor Disorders/diagnosis ; Psychomotor Disorders/etiology ; Psychomotor Disorders/metabolism ; Psychomotor Disorders/therapy
Chemical Substances	ACAN protein, human ; Aggrecans ; Amino Acid Transport Systems, Acidic ; Antiporters ; Biomarkers ; Malates ; Glutamic Acid (3KX376GY7L) ; malic acid (817L1N4CKP)
Language	English
Publishing date	2022-01-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23010528
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Article ; Online: AGC1 Deficiency

Beatriz Pardo / Eduardo Herrada-Soler / Jorgina Satrústegui / Laura Contreras / Araceli del Arco

International Journal of Molecular Sciences, Vol 23, Iss 528, p

Pathology and Molecular and Cellular Mechanisms of the Disease

2022 Volume 528

Abstract	AGC1/Aralar/Slc25a12 is the mitochondrial carrier of aspartate-glutamate, the regulatory component of the NADH malate-aspartate shuttle (MAS) that transfers cytosolic redox power to neuronal mitochondria. The deficiency in AGC1/Aralar leads to the human rare disease named “early infantile epileptic encephalopathy 39” (EIEE 39, OMIM # 612949) characterized by epilepsy, hypotonia, arrested psychomotor neurodevelopment, hypo myelination and a drastic drop in brain aspartate (Asp) and N -acetylaspartate (NAA). Current evidence suggest that neurons are the main brain cell type expressing Aralar. However, paradoxically, glial functions such as myelin and Glutamine (Gln) synthesis are markedly impaired in AGC1 deficiency. Herein, we discuss the role of the AGC1/Aralar-MAS pathway in neuronal functions such as Asp and NAA synthesis, lactate use, respiration on glucose, glutamate (Glu) oxidation and other neurometabolic aspects. The possible mechanism triggering the pathophysiological findings in AGC1 deficiency, such as epilepsy and postnatal hypomyelination observed in humans and mice, are also included. Many of these mechanisms arise from findings in the aralar -KO mice model that extensively recapitulate the human disease including the astroglial failure to synthesize Gln and the dopamine (DA) mishandling in the nigrostriatal system. Epilepsy and DA mishandling are a direct consequence of the metabolic defect in neurons due to AGC1/Aralar deficiency. However, the deficits in myelin and Gln synthesis may be a consequence of neuronal affectation or a direct effect of AGC1/Aralar deficiency in glial cells. Further research is needed to clarify this question and delineate the transcellular metabolic fluxes that control brain functions. Finally, we discuss therapeutic approaches successfully used in AGC1-deficient patients and mice.
Keywords	malate-aspartate shuttle ; AGC1/Aralar deficiency ; mitochondrial disorders ; mitochondrial aspartate-glutamate carrier ; mitochondrial function ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Calcium Deregulation and Mitochondrial Bioenergetics in GDAP1-Related CMT Disease.

González-Sánchez, Paloma / Satrústegui, Jorgina / Palau, Francesc / Del Arco, Araceli

International journal of molecular sciences

2019 Volume 20, Issue 2

Abstract: The pathology of Charcot-Marie-Tooth (CMT), a disease arising from mutations in different genes, has been associated with an impairment of mitochondrial dynamics and axonal biology of mitochondria. Mutations ... ...

Abstract	The pathology of Charcot-Marie-Tooth (CMT), a disease arising from mutations in different genes, has been associated with an impairment of mitochondrial dynamics and axonal biology of mitochondria. Mutations in
MeSH term(s)	Animals ; Biological Transport ; Calcium/metabolism ; Charcot-Marie-Tooth Disease/etiology ; Charcot-Marie-Tooth Disease/metabolism ; Charcot-Marie-Tooth Disease/pathology ; Disease Susceptibility ; Gene Expression Regulation ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Dynamics ; Mutation ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neurons/metabolism ; Protein Transport ; Signal Transduction
Chemical Substances	GDAP protein ; Nerve Tissue Proteins ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-01-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20020403
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Article ; Online: Extracellular ATP and glutamate drive pyruvate production and energy demand to regulate mitochondrial respiration in astrocytes.

Juaristi, Inés / Llorente-Folch, Irene / Satrústegui, Jorgina / Del Arco, Araceli

Glia

2019 Volume 67, Issue 4, Page(s) 759–774

Abstract: Astrocytes respond to energetic demands by upregulating glycolysis, lactate production, and respiration. This study addresses the role of respiration and calcium regulation of respiration as part of the astrocyte response to the workloads caused by ... ...

Abstract	Astrocytes respond to energetic demands by upregulating glycolysis, lactate production, and respiration. This study addresses the role of respiration and calcium regulation of respiration as part of the astrocyte response to the workloads caused by extracellular ATP and glutamate. Extracellular ATP (100 μM to 1 mM) causes a Ca
MeSH term(s)	Adenosine Triphosphate/pharmacology ; Analysis of Variance ; Animals ; Animals, Newborn ; Arginine/analogs & derivatives ; Arginine/genetics ; Arginine/metabolism ; Astrocytes/drug effects ; Astrocytes/ultrastructure ; Calcium/metabolism ; Cell Respiration/drug effects ; Cells, Cultured ; Coumarins/metabolism ; Extracellular Fluid/drug effects ; Female ; Glucose/pharmacology ; Glutamic Acid/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondria/drug effects ; Mitochondria/physiology ; Mitochondrial Membrane Transport Proteins/genetics ; Mitochondrial Membrane Transport Proteins/metabolism ; Oxygen Consumption/drug effects ; Pyruvic Acid/metabolism ; Sodium/metabolism
Chemical Substances	Coumarins ; Mitochondrial Membrane Transport Proteins ; carbobenzoxyargininamide-7-yl-4-methylcoumarin ; Glutamic Acid (3KX376GY7L) ; Pyruvic Acid (8558G7RUTR) ; Adenosine Triphosphate (8L70Q75FXE) ; Arginine (94ZLA3W45F) ; Sodium (9NEZ333N27) ; Glucose (IY9XDZ35W2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.23574
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Zs.A 2345: Show issues

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Article ; Online: Fluctuations in Cytosolic Calcium Regulate the Neuronal Malate-Aspartate NADH Shuttle: Implications for Neuronal Energy Metabolism.

Satrústegui, Jorgina / Bak, Lasse K

Neurochemical research

2015 Volume 40, Issue 12, Page(s) 2425–2430

Abstract: The malate-aspartate NADH shuttle (MAS) operates in neurons and other cells to translocate reducing equivalents from the cytosol to the mitochondrial matrix, thus allowing a continued flux through the glycolytic pathway and metabolism of extracellular ... ...

Abstract	The malate-aspartate NADH shuttle (MAS) operates in neurons and other cells to translocate reducing equivalents from the cytosol to the mitochondrial matrix, thus allowing a continued flux through the glycolytic pathway and metabolism of extracellular lactate. Recent discoveries have taught us that MAS is regulated by fluctuations in cytosolic Ca(2+) levels, and that this regulation is required to maintain a tight coupling between neuronal activity and mitochondrial respiration and oxidative phosphorylation. At cytosolic Ca(2+) fluctuations below the threshold of the mitochondrial calcium uniporter, there is a positive correlation between Ca(2+) and MAS activity; however, if cytosolic Ca(2+) increases above the threshold, MAS activity is thought to be reduced by an intricate mechanism. The latter forces the neurons to partly rely on anaerobic glycolysis producing lactate that may be metabolized subsequently, by neurons or other cells. In this review, we will discuss the evidence for Ca(2+)-mediated regulation of MAS that have been uncovered over the last decade or so, together with the need for further verification, and examine the metabolic ramifications for neurons.
MeSH term(s)	Animals ; Aspartic Acid/metabolism ; Calcium Signaling/physiology ; Cytosol/metabolism ; Energy Metabolism/physiology ; Humans ; Lactic Acid/metabolism ; Malates/metabolism ; Mitochondria/metabolism ; NAD/metabolism ; Neurons/metabolism
Chemical Substances	Malates ; NAD (0U46U6E8UK) ; Aspartic Acid (30KYC7MIAI) ; Lactic Acid (33X04XA5AT)
Language	English
Publishing date	2015-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	199335-5
ISSN	1573-6903 ; 0364-3190
ISSN (online)	1573-6903
ISSN	0364-3190
DOI	10.1007/s11064-015-1652-8
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Article ; Online: Mitochondria and calcium defects correlate with axonal dysfunction in GDAP1-related Charcot-Marie-Tooth mouse model.

Civera-Tregón, Azahara / Domínguez, Laura / Martínez-Valero, Paula / Serrano, Clàudia / Vallmitjana, Alex / Benítez, Raúl / Hoenicka, Janet / Satrústegui, Jorgina / Palau, Francesc

Neurobiology of disease

2021 Volume 152, Page(s) 105300

Abstract: Ganglioside-induced differentiation associated protein 1 (GDAP1) gene encodes a protein of the mitochondrial outer membrane and of the mitochondrial membrane contacts with the endoplasmic reticulum (MAMs) and lysosomes. Since mutations in GDAP1 cause ... ...

Abstract	Ganglioside-induced differentiation associated protein 1 (GDAP1) gene encodes a protein of the mitochondrial outer membrane and of the mitochondrial membrane contacts with the endoplasmic reticulum (MAMs) and lysosomes. Since mutations in GDAP1 cause Charcot-Marie-Tooth, an inherited motor and sensory neuropathy, its function is essential for peripheral nerve physiology. Our previous studies showed structural and functional defects in mitochondria and their contacts when GDAP1 is depleted. Nevertheless, the underlying axonal pathophysiological events remain unclear. Here, we have used embryonic motor neurons (eMNs) cultures from Gdap1 knockout (Gdap1
MeSH term(s)	Animals ; Axonal Transport/physiology ; Axons/pathology ; Calcium/metabolism ; Charcot-Marie-Tooth Disease ; Disease Models, Animal ; Mice ; Mice, Knockout ; Mitochondria/pathology ; Motor Neurons/metabolism ; Motor Neurons/pathology ; Nerve Tissue Proteins/deficiency ; Nerve Tissue Proteins/genetics ; Neuromuscular Junction/metabolism ; Neuromuscular Junction/pathology
Chemical Substances	GDAP protein ; Nerve Tissue Proteins ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2021.105300
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Article: Exogenous aralar/slc25a12 can replace citrin/slc25a13 as malate aspartate shuttle component in liver.

González-Moreno, Luis / Santamaría-Cano, Andrea / Paradela, Alberto / Martínez-Chantar, María Luz / Martín, Miguel Á / Pérez-Carreras, Mercedes / García-Picazo, Alberto / Vázquez, Jesús / Calvo, Enrique / González-Aseguinolaza, Gloria / Saheki, Takeyori / Del Arco, Araceli / Satrústegui, Jorgina / Contreras, Laura

Molecular genetics and metabolism reports

2023 Volume 35, Page(s) 100967

Abstract: The deficiency of CITRIN, the liver mitochondrial aspartate-glutamate carrier (AGC), is the cause of four human clinical phenotypes, neonatal intrahepatic cholestasis caused by CITRIN deficiency (NICCD), silent period, failure to thrive and dyslipidemia ... ...

Abstract	The deficiency of CITRIN, the liver mitochondrial aspartate-glutamate carrier (AGC), is the cause of four human clinical phenotypes, neonatal intrahepatic cholestasis caused by CITRIN deficiency (NICCD), silent period, failure to thrive and dyslipidemia caused by CITRIN deficiency (FTTDCD), and citrullinemia type II (CTLN2). Clinical symptoms can be traced back to disruption of the malate-aspartate shuttle due to the lack of citrin. A potential therapy for this condition is the expression of aralar, the AGC present in brain, to replace citrin. To explore this possibility we have first verified that the NADH/NAD
Language	English
Publishing date	2023-03-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2821908-9
ISSN	2214-4269
ISSN	2214-4269
DOI	10.1016/j.ymgmr.2023.100967
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Article ; Online: Calcium Deregulation and Mitochondrial Bioenergetics in GDAP1-Related CMT Disease

Paloma González-Sánchez / Jorgina Satrústegui / Francesc Palau / Araceli del Arco

International Journal of Molecular Sciences, Vol 20, Iss 2, p

2019 Volume 403

Abstract	The pathology of Charcot-Marie-Tooth (CMT), a disease arising from mutations in different genes, has been associated with an impairment of mitochondrial dynamics and axonal biology of mitochondria. Mutations in ganglioside-induced differentiation-associated protein 1 (GDAP1) cause several forms of CMT neuropathy, but the pathogenic mechanisms involved remain unclear. GDAP1 is an outer mitochondrial membrane protein highly expressed in neurons. It has been proposed to play a role in different aspects of mitochondrial physiology, including mitochondrial dynamics, oxidative stress processes, and mitochondrial transport along the axons. Disruption of the mitochondrial network in a neuroblastoma model of GDAP1-related CMT has been shown to decrease Ca2+ entry through the store-operated calcium entry (SOCE), which caused a failure in stimulation of mitochondrial respiration. In this review, we summarize the different functions proposed for GDAP1 and focus on the consequences for Ca2+ homeostasis and mitochondrial energy production linked to CMT disease caused by different GDAP1 mutations.
Keywords	GDAP1 ; recessive mutations ; store operated calcium entry ; mitochondrial location ; calcium regulated cell respiration ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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