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Article ; Online: Pharmacology and Rationale for Seralutinib in the Treatment of Pulmonary Arterial Hypertension.

Pullamsetti, Soni Savai / Sitapara, Ravikumar / Osterhout, Robin / Weiss, Astrid / Carter, Laura L / Zisman, Lawrence S / Schermuly, Ralph Theo

International journal of molecular sciences

2023 Volume 24, Issue 16

Abstract: Pulmonary arterial hypertension (PAH) is a complex disorder characterized by vascular remodeling and a consequent increase in pulmonary vascular resistance. The histologic hallmarks of PAH include plexiform and neointimal lesions of the pulmonary ... ...

Abstract	Pulmonary arterial hypertension (PAH) is a complex disorder characterized by vascular remodeling and a consequent increase in pulmonary vascular resistance. The histologic hallmarks of PAH include plexiform and neointimal lesions of the pulmonary arterioles, which are composed of dysregulated, apoptosis-resistant endothelial cells and myofibroblasts. Platelet-derived growth factor receptors (PDGFR) α and β, colony stimulating factor 1 receptor (CSF1R), and mast/stem cell growth factor receptor kit (c-KIT) are closely related kinases that have been implicated in PAH progression. In addition, emerging data indicate significant crosstalk between PDGF signaling and the bone morphogenetic protein receptor type 2 (BMPR2)/transforming growth factor β (TGFβ) receptor axis. This review will discuss the importance of the PDGFR-CSF1R-c-KIT signaling network in PAH pathogenesis, present evidence that the inhibition of all three nodes in this kinase network is a potential therapeutic approach for PAH, and highlight the therapeutic potential of seralutinib, currently in development for PAH, which targets these pathways.
MeSH term(s)	Humans ; Pulmonary Arterial Hypertension ; Endothelial Cells ; Familial Primary Pulmonary Hypertension ; Protein Kinase Inhibitors ; Receptor Protein-Tyrosine Kinases ; Proto-Oncogene Proteins c-kit
Chemical Substances	Protein Kinase Inhibitors ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1)
Language	English
Publishing date	2023-08-10
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/ijms241612653
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Phosphoproteomic analysis of lung tissue from patients with pulmonary arterial hypertension.

Sitapara, Ravikumar / Lam, TuKiet T / Gandjeva, Aneta / Tuder, Rubin M / Zisman, Lawrence S

Pulmonary circulation

2021 Volume 11, Issue 3, Page(s) 20458940211031109

Abstract: Pulmonary arterial hypertension (PAH) is a rare disorder associated with high morbidity and mortality despite currently available treatments. We compared the phosphoproteome of lung tissue from subjects with idiopathic PAH (iPAH) obtained at the time of ... ...

Abstract	Pulmonary arterial hypertension (PAH) is a rare disorder associated with high morbidity and mortality despite currently available treatments. We compared the phosphoproteome of lung tissue from subjects with idiopathic PAH (iPAH) obtained at the time of lung transplant with control lung tissue. The mass spectrometry-based analysis found 60,428 phosphopeptide features from which 6622 proteins were identified. Within the subset of identified proteins there were 1234 phosphopeptides with
Language	English
Publishing date	2021-08-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2638089-4
ISSN	2045-8940 ; 2045-8932
ISSN (online)	2045-8940
ISSN	2045-8932
DOI	10.1177/20458940211031109
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Article ; Online: Correction to: GTS-21, an α7nAChR agonist, increases pulmonary bacterial clearance in mice by restoring hyperoxia-compromised macrophage function.

Sitapara, Ravikumar A / Gauthier, Alex G / Patel, Vivek S / Lin, Mosi / Zur, Michelle / Ashby, Charles R / Mantell, Lin L

Molecular medicine (Cambridge, Mass.)

2021 Volume 27, Issue 1, Page(s) 93

Language	English
Publishing date	2021-08-23
Publishing country	England
Document type	Published Erratum
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.1186/s10020-021-00357-5
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Article: The Positive Allosteric Modulation of alpha7-Nicotinic Cholinergic Receptors by GAT107 Increases Bacterial Lung Clearance in Hyperoxic Mice by Decreasing Oxidative Stress in Macrophages.

Gauthier, Alex G / Wu, Jiaqi / Lin, Mosi / Sitapara, Ravikumar / Kulkarni, Abhijit / Thakur, Ganesh A / Schmidt, Edward E / Perron, Jeanette C / Ashby, Charles R / Mantell, Lin L

Antioxidants (Basel, Switzerland)

2021 Volume 10, Issue 1

Abstract: Supplemental oxygen therapy with supraphysiological concentrations of oxygen (hyperoxia; >21% ... ...

Abstract	Supplemental oxygen therapy with supraphysiological concentrations of oxygen (hyperoxia; >21% O
Language	English
Publishing date	2021-01-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10010135
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Article ; Online: Inhaled seralutinib exhibits potent efficacy in models of pulmonary arterial hypertension.

Galkin, Anna / Sitapara, Ravikumar / Clemons, Bryan / Garcia, Eduardo / Kennedy, Michael / Guimond, David / Carter, Laura L / Douthitt, Ashley / Osterhout, Robin / Gandjeva, Aneta / Slee, Deborah / Salter-Cid, Luisa / Tuder, Rubin M / Zisman, Lawrence S

The European respiratory journal

2022 Volume 60, Issue 6

Abstract: Background: Signalling through platelet-derived growth factor receptor (PDGFR), colony-stimulating factor 1 receptor (CSF1R) and mast/stem cell growth factor receptor kit (c-KIT) plays a critical role in pulmonary arterial hypertension (PAH). We ... ...

Abstract	Background: Signalling through platelet-derived growth factor receptor (PDGFR), colony-stimulating factor 1 receptor (CSF1R) and mast/stem cell growth factor receptor kit (c-KIT) plays a critical role in pulmonary arterial hypertension (PAH). We examined the preclinical efficacy of inhaled seralutinib, a unique small-molecule PDGFR/CSF1R/c-KIT kinase inhibitor in clinical development for PAH, in comparison to a proof-of-concept kinase inhibitor, imatinib. Methods: Seralutinib and imatinib potency and selectivity were compared. Inhaled seralutinib pharmacokinetics/pharmacodynamics were studied in healthy rats. Efficacy was evaluated in two rat models of PAH: SU5416/Hypoxia (SU5416/H) and monocrotaline pneumonectomy (MCTPN). Effects on inflammatory/cytokine signalling were examined. PDGFR, CSF1R and c-KIT immunohistochemistry in rat and human PAH lung samples and microRNA (miRNA) analysis in the SU5416/H model were performed. Results: Seralutinib potently inhibited PDGFRα/β, CSF1R and c-KIT. Inhaled seralutinib demonstrated dose-dependent inhibition of lung PDGFR and c-KIT signalling and increased bone morphogenetic protein receptor type 2 (BMPR2). Seralutinib improved cardiopulmonary haemodynamic parameters and reduced small pulmonary artery muscularisation and right ventricle hypertrophy in both models. In the SU5416/H model, seralutinib improved cardiopulmonary haemodynamic parameters, restored lung BMPR2 protein levels and decreased N-terminal pro-brain natriuretic peptide (NT-proBNP), more than imatinib. Quantitative immunohistochemistry in human lung PAH samples demonstrated increased PDGFR, CSF1R and c-KIT. miRNA analysis revealed candidates that could mediate seralutinib effects on BMPR2. Conclusions: Inhaled seralutinib was an effective treatment of severe PAH in two animal models, with improved cardiopulmonary haemodynamic parameters, a reduction in NT-proBNP, reverse remodelling of pulmonary vascular pathology and improvement in inflammatory biomarkers. Seralutinib showed greater efficacy compared to imatinib in a preclinical study.
MeSH term(s)	Rats ; Humans ; Animals ; Pulmonary Arterial Hypertension ; Imatinib Mesylate/pharmacology ; Imatinib Mesylate/metabolism ; Imatinib Mesylate/therapeutic use ; Monocrotaline ; Hypertension, Pulmonary ; Familial Primary Pulmonary Hypertension ; Pulmonary Artery ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Hypoxia ; MicroRNAs/metabolism ; Disease Models, Animal
Chemical Substances	Imatinib Mesylate (8A1O1M485B) ; Monocrotaline (73077K8HYV) ; Protein Kinase Inhibitors ; MicroRNAs
Language	English
Publishing date	2022-12-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.02356-2021
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Zs.A 2322: 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)
Zs.MO 292: Show issues

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Article ; Online: The α7 nicotinic acetylcholine receptor agonist GTS-21 improves bacterial clearance in mice by restoring hyperoxia-compromised macrophage function.

Sitapara, Ravikumar A / Gauthier, Alex G / Patel, Vivek S / Lin, Mosi / Zur, Michelle / Ashby, Charles R / Mantell, Lin L

Molecular medicine (Cambridge, Mass.)

2020 Volume 26, Issue 1, Page(s) 98

Abstract: Background: Mechanical ventilation, in combination with supraphysiological concentrations of oxygen (i.e., hyperoxia), is routinely used to treat patients with respiratory distress, such as COVID-19. However, prolonged exposure to hyperoxia compromises ... ...

Abstract	Background: Mechanical ventilation, in combination with supraphysiological concentrations of oxygen (i.e., hyperoxia), is routinely used to treat patients with respiratory distress, such as COVID-19. However, prolonged exposure to hyperoxia compromises the clearance of invading pathogens by impairing macrophage phagocytosis. Previously, we have shown that the exposure of mice to hyperoxia induces the release of the nuclear protein high mobility group box-1 (HMGB1) into the pulmonary airways. Furthermore, extracellular HMGB1 impairs macrophage phagocytosis and increases the mortality of mice infected with Pseudomonas aeruginosa (PA). The aim of this study was to determine whether GTS-21 (3-(2,4-dimethoxybenzylidene) anabaseine), an α7 nicotinic acetylcholine receptor (α7nAChR) agonist, could (1) inhibit hyperoxia-induced HMGB1 release into the airways; (2) enhance macrophage phagocytosis and (3) increase bacterial clearance from the lungs in a mouse model of ventilator-associated pneumonia. Method: GTS-21 (0.04, 0.4, and 4 mg/kg) or saline were administered by intraperitoneal injection to mice that were exposed to hyperoxia (≥ 99% O Results: The systemic administration of 4 mg/kg i.p. of GTS-21 significantly increased bacterial clearance, decreased acute lung injury and decreased accumulation of airway HMGB1 compared to the saline control. To determine the mechanism of action of GTS-21, RAW 264.7 cells, a macrophage-like cell line, were incubated with different concentrations of GTS-21 in the presence of 95% O Conclusions: Our results indicate that GTS-21 is efficacious in improving bacterial clearance and reducing acute lung injury via enhancing macrophage function by inhibiting the release of nuclear HMGB1. Therefore, the α7nAChR represents a possible pharmacological target to improve the clinical outcome of patients on ventilators by augmenting host defense against bacterial infections.
MeSH term(s)	Animals ; Benzylidene Compounds/pharmacology ; Disease Models, Animal ; HMGB1 Protein/metabolism ; Hyperoxia/diet therapy ; Hyperoxia/immunology ; Macrophages, Alveolar/drug effects ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phagocytosis/drug effects ; Pseudomonas Infections/drug therapy ; Pseudomonas aeruginosa ; Pyridines/pharmacology ; RAW 264.7 Cells ; Ventilator-Induced Lung Injury/drug therapy ; alpha7 Nicotinic Acetylcholine Receptor/antagonists & inhibitors
Chemical Substances	Benzylidene Compounds ; HMGB1 Protein ; HMGB1 protein, mouse ; Pyridines ; alpha7 Nicotinic Acetylcholine Receptor ; 3-(2,4-dimethoxybenzylidene)anabaseine (8S399XDN2K)
Keywords	covid19
Language	English
Publishing date	2020-10-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.1186/s10020-020-00224-9
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Article: SU5416 plus hypoxia but not selective VEGFR2 inhibition with cabozantinib plus hypoxia induces pulmonary hypertension in rats: potential role of BMPR2 signaling.

Sitapara, Ravikumar / Sugarragchaa, Chuluunbaatar / Zisman, Lawrence S

Pulmonary circulation

2021 Volume 11, Issue 3, Page(s) 20458940211021528

Abstract: SU5416 plus chronic hypoxia causes pulmonary arterial hypertension in rats and is assumed to occur through VEGFR2 inhibition. Cabozantinib is a far more potent VEGFR2 inhibitor than SU5416. Therefore, we hypothesized that cabozantinib plus hypoxia would ... ...

Abstract	SU5416 plus chronic hypoxia causes pulmonary arterial hypertension in rats and is assumed to occur through VEGFR2 inhibition. Cabozantinib is a far more potent VEGFR2 inhibitor than SU5416. Therefore, we hypothesized that cabozantinib plus hypoxia would induce severe pulmonary arterial hypertension in rats. Cell proliferation and pharmacokinetic studies were performed. Rats were given SU5416 or cabozantinib subcutaneously or via osmotic pump and kept hypoxic for three weeks. Right ventricular systolic pressure and hypertrophy were evaluated at days 14 and 28 following removal from hypoxia. Right ventricular fibrosis was evaluated with Picro-Sirius Red staining. Kinome inhibition profiles of SU5416 and cabozantinib were performed. Inhibitor binding constants of SU5416 and cabozantinib for BMPR2 were determined and Nanostring analyses of lung mRNA were performed. Cabozantinib was a more potent VEGFR inhibitor than SU5416 and had a longer half-life in rats. Cabozantinib subcutaneous plus hypoxia did not induce severe pulmonary arterial hypertension. Right ventricular systolic pressure at 14 and 28 days post-hypoxia was 36.8 ± 2.3 mmHg and 36.2 ± 3.4 mmHg, respectively, versus 27.5 ± 1.5 mmHg in normal controls. For cabozantinib given by osmotic pump during hypoxia, right ventricular systolic pressure was 40.0 ± 3.1 mmHg at 14 days and 27.9 ± 1.9 mmHg at 28 days post-hypoxia. SU5416 plus hypoxia induced severe pulmonary arterial hypertension (right ventricular systolic pressure 61.9 ± 6.1 mmHg and 64.9 ± 8.4 mmHg at 14 and 28 days post-hypoxia, respectively). Cabozantinib induced less right ventricular hypertrophy (right ventricular free wall weight/(left ventricular free wall weight + interventricular septum weight) at 14 days post-hypoxia compared to SU5416. Right ventricular fibrosis was more extensive in the SU5416 groups compared to the cabozantinib groups. SU5416 (but not cabozantinib) inhibited BMPR2. Nanostring analyses showed effects on pulmonary gene expression of BMP10 and VEGFR1 in the SU5416 28 days post-hypoxia group. In conclusion, selective VEGFR2 inhibition using cabozantinib plus hypoxia did not induce severe pulmonary arterial hypertension. Severe pulmonary arterial hypertension due to SU5416 plus hypoxia may be due to combined VEGFR2 and BMPR2 inhibition.
Language	English
Publishing date	2021-06-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2638089-4
ISSN	2045-8940 ; 2045-8932
ISSN (online)	2045-8940
ISSN	2045-8932
DOI	10.1177/20458940211021528
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Article ; Online: Retraction Note: The α7 nicotinic acetylcholine receptor agonist GTS-21 improves bacterial clearance in mice by restoring hyperoxia-compromised macrophage function.

Sitapara, Ravikumar A / Antoine, Daniel J / Sharma, Lokesh / Patel, Vivek S / Ashby, Charles R / Gorasiya, Samir / Yang, Huan / Zur, Michelle / Mantell, Lin L

Molecular medicine (Cambridge, Mass.)

2020 Volume 26, Issue 1, Page(s) 132

Language	English
Publishing date	2020-12-30
Publishing country	England
Document type	Retraction of Publication
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.1186/s10020-020-00265-0
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Article ; Online: Expression of Concern to: The α7 nicotine acetylcholine receptor agonist GTS-21 improves bacterial clearance in mice by restoring hyperoxia-compromised macrophage function.

Sitapara, Ravikumar A / Antoine, Daniel J / Sharma, Lokesh / Patel, Vivek S / Ashby, Charles R / Gorasiya, Samir / Yang, Huan / Zur, Michelle / Mantell, Lin L

Molecular medicine (Cambridge, Mass.)

2020 Volume 26, Issue 1, Page(s) 16

Abstract: The Editors-in-Chief would like to alert readers that this article (Sitapara et al. 2014) is part ...

Abstract	The Editors-in-Chief would like to alert readers that this article (Sitapara et al. 2014) is part of an investigation being conducted by the journal following the conclusions of an institutional enquiry at the University of Liverpool with respect to the quantitative mass spectrometry-generated results regarding acetylated and redox-modified HMGB1.
Language	English
Publishing date	2020-02-03
Publishing country	England
Document type	Editorial ; Expression of Concern
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.1186/s10020-020-0143-9
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Article ; Online: The α7 nicotinic acetylcholine receptor agonist GTS-21 improves bacterial clearance in mice by restoring hyperoxia-compromised macrophage function

Ravikumar A. Sitapara / Alex G. Gauthier / Vivek S. Patel / Mosi Lin / Michelle Zur / Charles R. Ashby / Lin L. Mantell

Molecular Medicine, Vol 26, Iss 1, Pp 1-

2020 Volume 13

Abstract: Abstract Background Mechanical ventilation, in combination with supraphysiological concentrations of oxygen (i.e., hyperoxia), is routinely used to treat patients with respiratory distress, such as COVID-19. However, prolonged exposure to hyperoxia ... ...

Abstract	Abstract Background Mechanical ventilation, in combination with supraphysiological concentrations of oxygen (i.e., hyperoxia), is routinely used to treat patients with respiratory distress, such as COVID-19. However, prolonged exposure to hyperoxia compromises the clearance of invading pathogens by impairing macrophage phagocytosis. Previously, we have shown that the exposure of mice to hyperoxia induces the release of the nuclear protein high mobility group box-1 (HMGB1) into the pulmonary airways. Furthermore, extracellular HMGB1 impairs macrophage phagocytosis and increases the mortality of mice infected with Pseudomonas aeruginosa (PA). The aim of this study was to determine whether GTS-21 (3-(2,4-dimethoxybenzylidene) anabaseine), an α7 nicotinic acetylcholine receptor (α7nAChR) agonist, could (1) inhibit hyperoxia-induced HMGB1 release into the airways; (2) enhance macrophage phagocytosis and (3) increase bacterial clearance from the lungs in a mouse model of ventilator-associated pneumonia. Method GTS-21 (0.04, 0.4, and 4 mg/kg) or saline were administered by intraperitoneal injection to mice that were exposed to hyperoxia (≥ 99% O2) and subsequently challenged with PA. Results The systemic administration of 4 mg/kg i.p. of GTS-21 significantly increased bacterial clearance, decreased acute lung injury and decreased accumulation of airway HMGB1 compared to the saline control. To determine the mechanism of action of GTS-21, RAW 264.7 cells, a macrophage-like cell line, were incubated with different concentrations of GTS-21 in the presence of 95% O2. The phagocytic activity of macrophages was significantly increased by GTS-21 in a dose-dependent manner. In addition, GTS-21 significantly inhibited the cytoplasmic translocation and release of HMGB1 from RAW 264.7 cells and attenuated hyperoxia-induced NF-κB activation in macrophages and mouse lungs exposed to hyperoxia and infected with PA. Conclusions Our results indicate that GTS-21 is efficacious in improving bacterial clearance and reducing acute lung injury via enhancing macrophage function by inhibiting the release of nuclear HMGB1. Therefore, the α7nAChR represents a possible pharmacological target to improve the clinical outcome of patients on ventilators by augmenting host defense against bacterial infections.
Keywords	α7nAChR ; Hyperoxia ; Macrophage function ; HMGB1 ; NF-κB ; Acute lung injury ; Therapeutics. Pharmacology ; RM1-950 ; Biochemistry ; QD415-436 ; covid19
Subject code	630
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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