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Article: Decreased MicroRNA-150 Exacerbates Neuronal Apoptosis in the Diabetic Retina.

Yu, Fei / Ko, Michael L / Ko, Gladys Y-P

2021 Volume 9, Issue 9

Abstract: Diabetic retinopathy (DR) is a chronic complication associated with diabetes and the number one cause of blindness in working adults in the US. More than 90% of diabetic patients have obesity-associated type 2 diabetes (T2D), and 60% of T2D patients will ...

Abstract	Diabetic retinopathy (DR) is a chronic complication associated with diabetes and the number one cause of blindness in working adults in the US. More than 90% of diabetic patients have obesity-associated type 2 diabetes (T2D), and 60% of T2D patients will develop DR. Photoreceptors undergo apoptosis shortly after the onset of diabetes, which contributes to the retinal dysfunction and microvascular complications leading to vision impairment. However, how diabetic insults cause photoreceptor apoptosis remains unclear. In this study, obesity-associated T2D mice and cultured photoreceptors were used to investigate how decreased microRNA-150 (miR-150) and its downstream target were involved in photoreceptor apoptosis. In the T2D retina, miR-150 was decreased with its target ETS-domain transcription factor (ELK1) and phosphorylated ELK1 at threonine 417 (pELK1
Language	English
Publishing date	2021-09-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines9091135
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Article ; Online: Circadian regulation in the retina: From molecules to network.

Ko, Gladys Y-P

The European journal of neuroscience

2018 Volume 51, Issue 1, Page(s) 194–216

Abstract: The mammalian retina is the most unique tissue among those that display robust circadian/diurnal oscillations. The retina is not only a light sensing tissue that relays light information to the brain, it has its own circadian "system" independent from ... ...

Abstract	The mammalian retina is the most unique tissue among those that display robust circadian/diurnal oscillations. The retina is not only a light sensing tissue that relays light information to the brain, it has its own circadian "system" independent from any influence from other circadian oscillators. While all retinal cells and retinal pigment epithelium (RPE) possess circadian oscillators, these oscillators integrate by means of neural synapses, electrical coupling (gap junctions), and released neurochemicals (such as dopamine, melatonin, adenosine, and ATP), so the whole retina functions as an integrated circadian system. Dysregulation of retinal clocks not only causes retinal or ocular diseases, it also impacts the circadian rhythm of the whole body, as the light information transmitted from the retina entrains the brain clock that governs the body circadian rhythms. In this review, how circadian oscillations in various retinal cells are integrated, and how retinal diseases affect daily rhythms.
MeSH term(s)	Animals ; Circadian Clocks ; Circadian Rhythm ; Dopamine ; Melatonin ; Retina ; Vision, Ocular
Chemical Substances	Melatonin (JL5DK93RCL) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2018-10-24
Publishing country	France
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/ejn.14185
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Article ; Online: MicroRNA-150 (miR-150) and Diabetic Retinopathy: Is miR-150 Only a Biomarker or Does It Contribute to Disease Progression?

Ko, Gladys Y-P / Yu, Fei / Bayless, Kayla J / Ko, Michael L

International journal of molecular sciences

2022 Volume 23, Issue 20

Abstract: Diabetic retinopathy (DR) is a chronic disease associated with diabetes mellitus and is a leading cause of visual impairment among the working population in the US. Clinically, DR has been diagnosed and treated as a vascular complication, but it ... ...

Abstract	Diabetic retinopathy (DR) is a chronic disease associated with diabetes mellitus and is a leading cause of visual impairment among the working population in the US. Clinically, DR has been diagnosed and treated as a vascular complication, but it adversely impacts both neural retina and retinal vasculature. Degeneration of retinal neurons and microvasculature manifests in the diabetic retina and early stages of DR. Retinal photoreceptors undergo apoptosis shortly after the onset of diabetes, which contributes to the retinal dysfunction and microvascular complications leading to vision impairment. Chronic inflammation is a hallmark of diabetes and a contributor to cell apoptosis, and retinal photoreceptors are a major source of intraocular inflammation that contributes to vascular abnormalities in diabetes. As the levels of microRNAs (miRs) are changed in the plasma and vitreous of diabetic patients, miRs have been suggested as biomarkers to determine the progression of diabetic ocular diseases, including DR. However, few miRs have been thoroughly investigated as contributors to the pathogenesis of DR. Among these miRs, miR-150 is downregulated in diabetic patients and is an endogenous suppressor of inflammation, apoptosis, and pathological angiogenesis. In this review, how miR-150 and its downstream targets contribute to diabetes-associated retinal degeneration and pathological angiogenesis in DR are discussed. Currently, there is no effective treatment to stop or reverse diabetes-caused neural and vascular degeneration in the retina. Understanding the molecular mechanism of the pathogenesis of DR may shed light for the future development of more effective treatments for DR and other diabetes-associated ocular diseases.
MeSH term(s)	Humans ; Diabetic Retinopathy/genetics ; Diabetic Retinopathy/pathology ; MicroRNAs/genetics ; Retina/pathology ; Inflammation/genetics ; Inflammation/pathology ; Neovascularization, Pathologic/pathology ; Biomarkers ; Disease Progression ; Diabetes Mellitus/pathology
Chemical Substances	MicroRNAs ; Biomarkers ; MIRN150 microRNA, human
Language	English
Publishing date	2022-10-11
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/ijms232012099
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Article ; Online: MicroRNA-150 and its target ETS-domain transcription factor 1 contribute to inflammation in diabetic photoreceptors.

Yu, Fei / Ko, Michael L / Ko, Gladys Y-P

Journal of cellular and molecular medicine

2021 Volume 25, Issue 22, Page(s) 10724–10735

Abstract: Obesity-associated type 2 diabetes (T2D) is on the rise in the United States due to the obesity epidemic, and 60% of T2D patients develop diabetic retinopathy (DR) in their lifetime. Chronic inflammation is a hallmark of obesity and T2D and a well- ... ...

Abstract	Obesity-associated type 2 diabetes (T2D) is on the rise in the United States due to the obesity epidemic, and 60% of T2D patients develop diabetic retinopathy (DR) in their lifetime. Chronic inflammation is a hallmark of obesity and T2D and a well-accepted major contributor to DR, and retinal photoreceptors are a major source of intraocular inflammation and directly contribute to vascular abnormalities in diabetes. However, how diabetic insults cause photoreceptor inflammation is not well known. In this study, we used a high-fat diet (HFD)-induced T2D mouse model and cultured photoreceptors treated with palmitic acid (PA) to decipher major players that mediate high-fat-induced photoreceptor inflammation. We found that PA-elicited microRNA-150 (miR-150) decreases with a consistent upregulation of ETS-domain transcription factor 1 (Elk1), a downstream target of miR-150, in PA-elicited photoreceptor inflammation. We compared wild-type (WT) and miR-150 null (miR-150
MeSH term(s)	Animals ; Biomarkers ; Cell Line ; Diabetes Mellitus, Type 2 ; Diabetic Retinopathy/etiology ; Diabetic Retinopathy/metabolism ; Diabetic Retinopathy/pathology ; Disease Models, Animal ; Disease Susceptibility ; Gene Expression Regulation ; Male ; Mice ; Mice, Knockout ; MicroRNAs/genetics ; Obesity ; Photoreceptor Cells/metabolism ; Photoreceptor Cells/pathology ; RNA Interference ; ets-Domain Protein Elk-1/genetics
Chemical Substances	Biomarkers ; Elk1 protein, mouse ; MicroRNAs ; Mirn150 microRNA, mouse ; ets-Domain Protein Elk-1
Language	English
Publishing date	2021-10-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.17012
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 5752: 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)

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Article ; Online: Decreased MicroRNA-150 Exacerbates Neuronal Apoptosis in the Diabetic Retina

Fei Yu / Michael L. Ko / Gladys Y.-P. Ko

Biomedicines, Vol 9, Iss 1135, p

2021 Volume 1135

Abstract	Diabetic retinopathy (DR) is a chronic complication associated with diabetes and the number one cause of blindness in working adults in the US. More than 90% of diabetic patients have obesity-associated type 2 diabetes (T2D), and 60% of T2D patients will develop DR. Photoreceptors undergo apoptosis shortly after the onset of diabetes, which contributes to the retinal dysfunction and microvascular complications leading to vision impairment. However, how diabetic insults cause photoreceptor apoptosis remains unclear. In this study, obesity-associated T2D mice and cultured photoreceptors were used to investigate how decreased microRNA-150 (miR-150) and its downstream target were involved in photoreceptor apoptosis. In the T2D retina, miR-150 was decreased with its target ETS-domain transcription factor (ELK1) and phosphorylated ELK1 at threonine 417 (pELK1 T417 ) upregulated. In cultured photoreceptors, treatments with palmitic acid (PA), to mimic a high-fat environment, decreased miR-150 but upregulated ELK1, pELK1 T417 , and the translocation of pELK1 T417 from the cytoplasm to the cell nucleus. Deletion of miR-150 (miR-150 −/− ) exacerbates T2D- or PA-induced photoreceptor apoptosis. Blocking the expression of ELK1 with small interfering RNA (siRNA) for Elk1 did not rescue PA-induced photoreceptor apoptosis. Translocation of pELK1 T417 from cytoplasm-to-nucleus appears to be the key step of diabetic insult-elicited photoreceptor apoptosis.
Keywords	diabetes ; diabetic retinopathy ; retina ; photoreceptor ; apoptosis ; microRNA ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Peptide Lv Promotes Trafficking and Membrane Insertion of K

Pham, Dylan L / Niemi, Autumn / Blank, Ria / Lomenzo, Gabriella / Tham, Jenivi / Ko, Michael L / Ko, Gladys Y-P

Cells

2023 Volume 12, Issue 12

Abstract: Peptide Lv is a small endogenous secretory peptide that is proangiogenic through hyperpolarizing vascular endothelial cells (ECs) by enhancing the current densities of ... ...

Abstract	Peptide Lv is a small endogenous secretory peptide that is proangiogenic through hyperpolarizing vascular endothelial cells (ECs) by enhancing the current densities of K
MeSH term(s)	Endothelial Cells/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; MAP Kinase Kinase 1/metabolism ; Peptides ; Phosphatidylinositol 3-Kinase/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction
Chemical Substances	Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Lv peptide, human ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; Peptides ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2023-06-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12121651
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Article ; Online: Peptide Lv Promotes Trafficking and Membrane Insertion of K Ca 3.1 through the MEK1–ERK and PI3K–Akt Signaling Pathways

Dylan L. Pham / Autumn Niemi / Ria Blank / Gabriella Lomenzo / Jenivi Tham / Michael L. Ko / Gladys Y.-P. Ko

Cells, Vol 12, Iss 1651, p

2023 Volume 1651

Abstract: Peptide Lv is a small endogenous secretory peptide that is proangiogenic through hyperpolarizing vascular endothelial cells (ECs) by enhancing the current densities of K Ca 3.1 channels. However, it is unclear how peptide Lv enhances these currents. One ... ...

Abstract	Peptide Lv is a small endogenous secretory peptide that is proangiogenic through hyperpolarizing vascular endothelial cells (ECs) by enhancing the current densities of K Ca 3.1 channels. However, it is unclear how peptide Lv enhances these currents. One way to enhance the current densities of ion channels is to promote its trafficking and insertion into the plasma membrane. We hypothesized that peptide Lv-elicited K Ca 3.1 augmentation occurs through activating the mitogen-activated protein kinase kinase 1 (MEK1)-extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K)–protein kinase B (Akt) signaling pathways, which are known to mediate ion channel trafficking and membrane insertion in neurons. To test this hypothesis, we employed patch-clamp electrophysiological recordings and cell-surface biotinylation assays on ECs treated with peptide Lv and pharmaceutical inhibitors of ERK and Akt. Blocking ERK or Akt activation diminished peptide Lv-elicited EC hyperpolarization and increase in K Ca 3.1 current densities. Blocking PI3K or Akt activation decreased the level of plasma membrane-bound, but not the total amount of K Ca 3.1 protein in ECs. Therefore, the peptide Lv-elicited EC hyperpolarization and K Ca 3.1 augmentation occurred in part through channel trafficking and insertion mediated by MEK1–ERK and PI3K–Akt activation. These results demonstrate the molecular mechanisms of how peptide Lv promotes EC-mediated angiogenesis.
Keywords	angiogenesis ; potassium channel ; endothelial cell ; peptide Lv ; protein trafficking ; signaling pathway ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Decreased miR-150 in obesity-associated type 2 diabetic mice increases intraocular inflammation and exacerbates retinal dysfunction.

Yu, Fei / Chapman, Samantha / Pham, Dylan Luc / Ko, Michael Lee / Zhou, Beiyan / Ko, Gladys Y-P

BMJ open diabetes research & care

2021 Volume 8, Issue 1

Abstract: Introduction: Diabetic retinopathy (DR) is the leading cause of blindness among the working population in the USA. Current therapies, including anti-vascular endothelial growth factor treatments, cannot completely reverse the visual defects induced by ... ...

Abstract	Introduction: Diabetic retinopathy (DR) is the leading cause of blindness among the working population in the USA. Current therapies, including anti-vascular endothelial growth factor treatments, cannot completely reverse the visual defects induced by DR. MicroRNA-150 (miR-150) is a regulator that suppresses inflammation and pathological angiogenesis. In patients with diabetes, miR-150 is downregulated. As chronic inflammation is a major contributor to the pathogenesis of DR, whether diabetes-associated decrease of miR-150 is merely associated with the disease progression or decreased miR-150 causes retinal inflammation and pathological angiogenesis is still unknown. Research design and methods: We used high-fat diet (HFD)-induced type 2 diabetes (T2D) in wild type (WT) and miR-150 knockout (miR-150 Results: We found that WT mice fed with an HFD for only 1 month had a significant decrease of miR-150 in the blood and retina, and retinal light sensitivity also decreased. The miR-150 Conclusion: These data suggest that decreased miR-150 caused by obesity or diabetic insults is not merely correlated to the disease progression, but it contributes to the retinal dysfunction and inflammation, as well as the development of DR.
MeSH term(s)	Animals ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/genetics ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/genetics ; Inflammation/genetics ; Mice ; Mice, Obese ; MicroRNAs/genetics ; Obesity/complications ; Obesity/genetics
Chemical Substances	MicroRNAs ; Mirn150 microRNA, mouse
Language	English
Publishing date	2021-03-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2732918-5
ISSN	2052-4897 ; 2052-4897
ISSN (online)	2052-4897
ISSN	2052-4897
DOI	10.1136/bmjdrc-2020-001446
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Article ; Online: Peptide Lv augments intermediate-conductance calcium-dependent potassium channels (KCa3.1) in endothelial cells to promote angiogenesis.

Pham, Dylan L / Niemi, Autumn / Ko, Michael L / Ko, Gladys Y P

PloS one

2022 Volume 17, Issue 10, Page(s) e0276744

Abstract: Peptide Lv is a small endogenous secretory peptide that is expressed in various tissues and conserved across different species. Patients with diabetic retinopathy, an ocular disease with pathological angiogenesis, have upregulated peptide Lv in their ... ...

Abstract	Peptide Lv is a small endogenous secretory peptide that is expressed in various tissues and conserved across different species. Patients with diabetic retinopathy, an ocular disease with pathological angiogenesis, have upregulated peptide Lv in their retinas. The pro-angiogenic activity of peptide Lv is in part through promoting vascular endothelial cell (EC) proliferation, migration, and sprouting, but its molecular mechanism is not completely understood. This study aimed to decipher how peptide Lv promotes EC-dependent angiogenesis by using patch-clamp electrophysiological recordings, Western immunoblotting, quantitative PCR, and cell proliferation assays in cultured ECs. Endothelial cells treated with peptide Lv became significantly hyperpolarized, an essential step for EC activation. Treatment with peptide Lv augmented the expression and current densities of the intermediate-conductance calcium-dependent potassium (KCa3.1) channels that contribute to EC hyperpolarization but did not augment other potassium channels. Blocking KCa3.1 attenuated peptide Lv-elicited EC proliferation. These results indicate that peptide Lv-stimulated increases of functional KCa3.1 in ECs contributes to EC activation and EC-dependent angiogenesis.
MeSH term(s)	Humans ; Endothelial Cells/metabolism ; Intermediate-Conductance Calcium-Activated Potassium Channels/genetics ; Intermediate-Conductance Calcium-Activated Potassium Channels/metabolism ; Calcium/metabolism ; Neovascularization, Pathologic/metabolism ; Peptides/metabolism ; Potassium/metabolism
Chemical Substances	Intermediate-Conductance Calcium-Activated Potassium Channels ; Calcium (SY7Q814VUP) ; Peptides ; Potassium (RWP5GA015D)
Language	English
Publishing date	2022-10-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0276744
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Article: Retinoschisin Facilitates the Function of L-Type Voltage-Gated Calcium Channels.

Shi, Liheng / Ko, Michael L / Ko, Gladys Y-P

Frontiers in cellular neuroscience

2017 Volume 11, Page(s) 232

Abstract: Modulation of ion channels by extracellular proteins plays critical roles in shaping synaptic plasticity. Retinoschisin (RS1) is an extracellular adhesive protein secreted from photoreceptors and bipolar cells, and it plays an important role during ... ...

Abstract	Modulation of ion channels by extracellular proteins plays critical roles in shaping synaptic plasticity. Retinoschisin (RS1) is an extracellular adhesive protein secreted from photoreceptors and bipolar cells, and it plays an important role during retinal development, as well as in maintaining the stability of retinal layers. RS1 is known to form homologous octamers and interact with molecules on the plasma membrane including phosphatidylserine, sodium-potassium exchanger complex, and L-type voltage-gated calcium channels (LTCCs). However, how this physical interaction between RS1 and ion channels might affect the channel gating properties is unclear. In retinal photoreceptors, two major LTCCs are Cav1.3 (α1D) and Cav1.4 (α1F) with distinct biophysical properties, functions and distributions. Cav1.3 is distributed from the inner segment (IS) to the synaptic terminal and is responsible for calcium influx to the photoreceptors and overall calcium homeostasis. Cav1.4 is only expressed at the synaptic terminal and is responsible for neurotransmitter release. Mutations of the gene encoding Cav1.4 cause X-linked incomplete congenital stationary night blindness type 2 (CSNB2), while null mutations of Cav1.3 cause a mild decrease of retinal light responses in mice. Even though RS1 is known to maintain retinal architecture, in this study, we present that RS1 interacts with both Cav1.3 and Cav1.4 and regulates their activations. RS1 was able to co-immunoprecipitate with Cav1.3 and Cav1.4 from porcine retinas, and it increased the LTCC currents and facilitated voltage-dependent activation in HEK cells co-transfected with RS1 and Cav1.3 or Cav1.4, thus providing evidence of a functional interaction between RS1 and LTCCs. The interaction between RS1 and Cav1.3 did not change the calcium-dependent inactivation of Cav1.3. In mice lacking RS1, the expression of Cav1.3 and Cav1.4 in the retina decreased, while in mice with Cav1.4 deletion, the retinal level of RS1 decreased. These results provide important evidence that RS1 is not only an adhesive protein promoting cell-cell adhesion, it is essential for anchoring other membrane proteins including ion channels and enhancing their function in the retina.
Language	English
Publishing date	2017-08-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2017.00232
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