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Article ; Online: Development of a human iPSC-derived placental barrier-on-chip model.

Lermant, Agathe / Rabussier, Gwenaëlle / Lanz, Henriëtte L / Davidson, Lindsay / Porter, Iain M / Murdoch, Colin E

iScience

2023 Volume 26, Issue 7, Page(s) 107240

Abstract: Although recently developed placenta-on-chip systems opened promising perspectives for placental barrier modeling, they still lack physiologically relevant trophoblasts and are poorly amenable to high-throughput studies. We aimed to implement human- ... ...

Abstract	Although recently developed placenta-on-chip systems opened promising perspectives for placental barrier modeling, they still lack physiologically relevant trophoblasts and are poorly amenable to high-throughput studies. We aimed to implement human-induced pluripotent stem cells (hiPSC)-derived trophoblasts into a multi-well microfluidic device to develop a physiologically relevant and scalable placental barrier model. When cultured in a perfused micro-channel against a collagen-based matrix, hiPSC-derived trophoblasts self-arranged into a 3D structure showing invasive behavior, fusogenic and endocrine activities, structural integrity, and expressing placental transporters. RNA-seq analysis revealed that the microfluidic 3D environment boosted expression of genes related to early placental structural development, mainly involved in mechanosensing and cell surface receptor signaling. These results demonstrated the feasibility of generating a differentiated primitive syncytium from hiPSC in a microfluidic platform. Besides expanding hiPSC-derived trophoblast scope of applications, this study constitutes an important resource to improve placental barrier models and boost research and therapeutics evaluation in pregnancy.
Language	English
Publishing date	2023-07-13
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.107240
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Article ; Online: The Ndc80 complex targets Bod1 to human mitotic kinetochores.

Schleicher, Katharina / Porter, Michael / Ten Have, Sara / Sundaramoorthy, Ramasubramanian / Porter, Iain M / Swedlow, Jason R

Open biology

2017 Volume 7, Issue 11

Abstract: Regulation of protein phosphatase activity by endogenous protein inhibitors is an important mechanism to control protein phosphorylation in cells. We recently identified Biorientation defective 1 (Bod1) as a small protein inhibitor of protein phosphatase ...

Abstract	Regulation of protein phosphatase activity by endogenous protein inhibitors is an important mechanism to control protein phosphorylation in cells. We recently identified Biorientation defective 1 (Bod1) as a small protein inhibitor of protein phosphatase 2A containing the B56 regulatory subunit (PP2A-B56). This phosphatase controls the amount of phosphorylation of several kinetochore proteins and thus the establishment of load-bearing chromosome-spindle attachments in time for accurate separation of sister chromatids in mitosis. Like PP2A-B56, Bod1 directly localizes to mitotic kinetochores and is required for correct segregation of mitotic chromosomes. In this report, we have probed the spatio-temporal regulation of Bod1 during mitotic progression. Kinetochore localization of Bod1 increases from nuclear envelope breakdown until metaphase. Phosphorylation of Bod1 at threonine 95 (T95), which increases Bod1's binding to and inhibition of PP2A-B56, peaks in prometaphase when PP2A-B56 localization to kinetochores is highest. We demonstrate here that kinetochore targeting of Bod1 depends on the outer kinetochore protein Ndc80 and not PP2A-B56. Crucially, Bod1 depletion functionally affects Ndc80 phosphorylation at the N-terminal serine 55 (S55), as well as a number of other phosphorylation sites within the outer kinetochore, including Knl1 at serine 24 and 60 (S24, S60), and threonine T943 and T1155 (T943, T1155). Therefore, Ndc80 recruits a phosphatase inhibitor to kinetochores which directly feeds forward to regulate Ndc80, and Knl1 phosphorylation, including sites that mediate the attachment of microtubules to kinetochores.
MeSH term(s)	Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Chromosome Segregation ; Cytoskeletal Proteins ; Feedback, Physiological ; HeLa Cells ; Humans ; Kinetochores/metabolism ; Microtubule-Associated Proteins/metabolism ; Mitosis ; Nuclear Envelope/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Binding ; Protein Processing, Post-Translational
Chemical Substances	Bod1 protein, human ; Cell Cycle Proteins ; Cytoskeletal Proteins ; Knl1 protein, human ; Microtubule-Associated Proteins ; NDC80 protein, human ; Nuclear Proteins
Language	English
Publishing date	2017-11-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2630944-0
ISSN	2046-2441 ; 2046-2441
ISSN (online)	2046-2441
ISSN	2046-2441
DOI	10.1098/rsob.170099
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Book ; Online: The Edinburgh companion to poststructuralism

Dillet, Benoît / Mackenzie, Iain M / Porter, Robert

2013

Abstract: Written by experts in their field, this Companion surveys the challenges and provocations raised by the major voices of poststructuralism: Foucault, Deleuze, Derrida, Cixous, Lyotard, Guattari, Kristeva, Irigaray, Barthes and Baudrillard. Thematically ... ...

Author's details	edited by Benoît Dillet, Iain Mackenzie and Robert Porter
Abstract	Written by experts in their field, this Companion surveys the challenges and provocations raised by the major voices of poststructuralism: Foucault, Deleuze, Derrida, Cixous, Lyotard, Guattari, Kristeva, Irigaray, Barthes and Baudrillard. Thematically organised and clearly written, it will guide students and researchers in philosophy, literature, art, geography, politics, sociology, law, film, and cultural studies around the nature and contemporary relevance of poststructuralism
Keywords	Poststructuralism
Language	English
Size	Online-Ressource
Publisher	Edinburgh University Press
Publishing place	Edinburgh
Document type	Book ; Online
Note	Description based upon print version of record
ISBN	074864122X ; 0748653694 ; 9780748641222 ; 9780748653690
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Mortality surrogates in combined pulmonary fibrosis and emphysema.

Zhao, An / Gudmundsson, Eyjolfur / Mogulkoc, Nesrin / van Moorsel, Coline / Corte, Tamera J / Vasudev, Pardeep / Romei, Chiara / Chapman, Robert / Wallis, Tim J M / Denneny, Emma / Goos, Tinne / Savas, Recep / Ahmed, Asia / Brereton, Christopher J / van Es, Hendrik W / Jo, Helen / De Liperi, Annalisa / Duncan, Mark / Pontoppidan, Katarina /

The European respiratory journal

2024 Volume 63, Issue 4

Abstract: Background: Idiopathic pulmonary fibrosis (IPF) with coexistent emphysema, termed combined pulmonary fibrosis and emphysema (CPFE) may associate with reduced forced vital capacity (FVC) declines compared to non-CPFE IPF patients. We examined ... ...

Abstract	Background: Idiopathic pulmonary fibrosis (IPF) with coexistent emphysema, termed combined pulmonary fibrosis and emphysema (CPFE) may associate with reduced forced vital capacity (FVC) declines compared to non-CPFE IPF patients. We examined associations between mortality and functional measures of disease progression in two IPF cohorts. Methods: Visual emphysema presence (>0% emphysema) scored on computed tomography identified CPFE patients (CPFE/non-CPFE: derivation cohort n=317/n=183, replication cohort n=358/n=152), who were subgrouped using 10% or 15% visual emphysema thresholds, and an unsupervised machine-learning model considering emphysema and interstitial lung disease extents. Baseline characteristics, 1-year relative FVC and diffusing capacity of the lung for carbon monoxide ( Results: In both IPF cohorts, CPFE patients with ≥10% emphysema had a greater smoking history and lower baseline Conclusion: When assessing disease progression in IPF,
MeSH term(s)	Humans ; Pulmonary Emphysema/complications ; Lung ; Fibrosis ; Idiopathic Pulmonary Fibrosis ; Emphysema/complications ; Disease Progression ; Retrospective Studies
Language	English
Publishing date	2024-04-04
Publishing country	England
Document type	Journal Article
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.00127-2023
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Article: Delineating associations of progressive pleuroparenchymal fibroelastosis in patients with pulmonary fibrosis.

Gudmundsson, Eyjolfur / Zhao, An / Mogulkoc, Nesrin / van Beek, Frouke / Goos, Tinne / Brereton, Christopher J / Veltkamp, Marcel / Chapman, Robert / van Es, Hendrik W / Garthwaite, Helen / Gholipour, Bahareh / Heightman, Melissa / Nair, Arjun / Pontoppidan, Katarina / Savas, Recep / Ahmed, Asia / Vermant, Marie / Unat, Omer / Procter, Alex /

De Sadeleer, Laurens / Denneny, Emma / Wallis, Timothy / Duncan, Mark / Taylor, Magali / Verleden, Stijn / Janes, Sam M / Alexander, Daniel C / Wells, Athol U / Porter, Joanna / Jones, Mark G / Stewart, Iain / van Moorsel, Coline H M / Wuyts, Wim / Jacob, Joseph

ERJ open research

2023 Volume 9, Issue 2

Abstract: Background: Computer quantification of baseline computed tomography (CT) radiological pleuroparenchymal fibroelastosis (PPFE) associates with mortality in idiopathic pulmonary fibrosis (IPF). We examined mortality associations of longitudinal change in ... ...

Abstract	Background: Computer quantification of baseline computed tomography (CT) radiological pleuroparenchymal fibroelastosis (PPFE) associates with mortality in idiopathic pulmonary fibrosis (IPF). We examined mortality associations of longitudinal change in computer-quantified PPFE-like lesions in IPF and fibrotic hypersensitivity pneumonitis (FHP). Methods: Two CT scans 6-36 months apart were retrospectively examined in one IPF (n=414) and one FHP population (n=98). Annualised change in computerised upper-zone pleural surface area comprising radiological PPFE-like lesions (Δ-PPFE) was calculated. Δ-PPFE >1.25% defined progressive PPFE above scan noise. Mixed-effects models evaluated Δ-PPFE against change in visual CT interstitial lung disease (ILD) extent and annualised forced vital capacity (FVC) decline. Multivariable models were adjusted for age, sex, smoking history, baseline emphysema presence, antifibrotic use and diffusion capacity of the lung for carbon monoxide. Mortality analyses further adjusted for baseline presence of clinically important PPFE-like lesions and ILD change. Results: Δ-PPFE associated weakly with ILD and FVC change. 22-26% of IPF and FHP cohorts demonstrated progressive PPFE-like lesions which independently associated with mortality in the IPF cohort (hazard ratio 1.25, 95% CI 1.16-1.34, p<0.0001) and the FHP cohort (hazard ratio 1.16, 95% CI 1.00-1.35, p=0.045). Interpretation: Progression of PPFE-like lesions independently associates with mortality in IPF and FHP but does not associate strongly with measures of fibrosis progression.
Language	English
Publishing date	2023-03-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2827830-6
ISSN	2312-0541
ISSN	2312-0541
DOI	10.1183/23120541.00637-2022
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Article ; Online: Bod1 regulates protein phosphatase 2A at mitotic kinetochores.

Porter, Iain M / Schleicher, Katharina / Porter, Michael / Swedlow, Jason R

Nature communications

2013 Volume 4, Page(s) 2677

Abstract: Mitotic entry and progression require the activation of several mitotic kinases and the proper regulation and localization of several phosphatases. The activity and localization of each of these enzymes is tightly controlled through a series of specific ... ...

Abstract	Mitotic entry and progression require the activation of several mitotic kinases and the proper regulation and localization of several phosphatases. The activity and localization of each of these enzymes is tightly controlled through a series of specific activators, inhibitors and regulatory subunits. Two proteins, Ensa and Arpp-19, were recently identified as specific inhibitors of PP2A-B55 and are critical for allowing full activity of Cdk1/cyclin B and entry into mitosis. Here we show that Bod1, a protein required for proper chromosome alignment at mitosis, shares sequence similarity with Ensa and Arpp-19 and specifically inhibits the kinetochore-associated PP2A-B56 holoenzyme. PP2A-B56 regulates the stability of kinetochore-microtubule attachments by dephosphorylating several kinetochore proteins. Loss of Bod1 changes the balance of phosphorylation at kinetochores, causing defects in kinetochore function. Bod1, Ensa and Arpp-19 define a family of specific PP2A inhibitors that regulate specific PP2A holoenzymes at distinct locations and points in the cell cycle.
MeSH term(s)	Amino Acid Sequence ; CDC2 Protein Kinase/genetics ; CDC2 Protein Kinase/metabolism ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Chromosomes, Human/metabolism ; Chromosomes, Human/ultrastructure ; Cyclin B/genetics ; Cyclin B/metabolism ; Gene Expression Regulation ; HeLa Cells ; Humans ; Kinetochores/metabolism ; Kinetochores/ultrastructure ; Microscopy, Fluorescence ; Microtubules/metabolism ; Microtubules/ultrastructure ; Mitosis ; Molecular Sequence Data ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Phosphatase 2/genetics ; Protein Phosphatase 2/metabolism ; Protein Subunits/genetics ; Protein Subunits/metabolism ; Sequence Alignment ; Sequence Homology, Amino Acid ; Signal Transduction ; Time-Lapse Imaging
Chemical Substances	Bod1 protein, human ; Cell Cycle Proteins ; Cyclin B ; Phosphoproteins ; Protein Subunits ; cyclic AMP-regulated phosphoprotein 19 ; CDC2 Protein Kinase (EC 2.7.11.22) ; Protein Phosphatase 2 (EC 3.1.3.16)
Language	English
Publishing date	2013-10-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/ncomms3677
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Therapeutic blockade of granulocyte macrophage colony-stimulating factor in COVID-19-associated hyperinflammation: challenges and opportunities.

Mehta, Puja / Porter, Joanna C / Manson, Jessica J / Isaacs, John D / Openshaw, Peter J M / McInnes, Iain B / Summers, Charlotte / Chambers, Rachel C

The Lancet. Respiratory medicine

2020 Volume 8, Issue 8, Page(s) 822–830

Abstract: The COVID-19 pandemic is a global public health crisis, with considerable mortality and morbidity exerting pressure on health-care resources, including critical care. An excessive host inflammatory response in a subgroup of patients with severe COVID-19 ... ...

Abstract	The COVID-19 pandemic is a global public health crisis, with considerable mortality and morbidity exerting pressure on health-care resources, including critical care. An excessive host inflammatory response in a subgroup of patients with severe COVID-19 might contribute to the development of acute respiratory distress syndrome (ARDS) and multiorgan failure. Timely therapeutic intervention with immunomodulation in patients with hyperinflammation could prevent disease progression to ARDS and obviate the need for invasive ventilation. Granulocyte macrophage colony-stimulating factor (GM-CSF) is an immunoregulatory cytokine with a pivotal role in initiation and perpetuation of inflammatory diseases. GM-CSF could link T-cell-driven acute pulmonary inflammation with an autocrine, self-amplifying cytokine loop leading to monocyte and macrophage activation. This axis has been targeted in cytokine storm syndromes and chronic inflammatory disorders. Here, we consider the scientific rationale for therapeutic targeting of GM-CSF in COVID-19-associated hyperinflammation. Since GM-CSF also has a key role in homoeostasis and host defence, we discuss potential risks associated with inhibition of GM-CSF in the context of viral infection and the challenges of doing clinical trials in this setting, highlighting in particular the need for a patient risk-stratification algorithm.
MeSH term(s)	Betacoronavirus/immunology ; COVID-19 ; Coronavirus Infections/complications ; Coronavirus Infections/drug therapy ; Coronavirus Infections/virology ; Disease Progression ; Granulocyte-Macrophage Colony-Stimulating Factor/antagonists & inhibitors ; Humans ; Immunologic Factors/therapeutic use ; Immunomodulation ; Pandemics ; Pneumonia, Viral/complications ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/virology ; Respiratory Distress Syndrome/prevention & control ; Respiratory Distress Syndrome/virology ; SARS-CoV-2 ; COVID-19 Drug Treatment
Chemical Substances	Immunologic Factors ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Keywords	covid19
Language	English
Publishing date	2020-06-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2686754-0
ISSN	2213-2619 ; 2213-2600
ISSN (online)	2213-2619
ISSN	2213-2600
DOI	10.1016/S2213-2600(20)30267-8
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Zs.A 7041: Show issues

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Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: L-DOPA functionalized, multi-branched gold nanoparticles as brain-targeted nano-vehicles.

Gonzalez-Carter, Daniel A / Ong, Zhan Yuin / McGilvery, Catriona M / Dunlop, Iain E / Dexter, David T / Porter, Alexandra E

Nanomedicine : nanotechnology, biology, and medicine

2018 Volume 15, Issue 1, Page(s) 1–11

Abstract: The blood-brain barrier (BBB) is a protective endothelial barrier lining the brain microvasculature which prevents brain delivery of therapies against brain diseases. Hence, there is an urgent need to develop vehicles which efficiently penetrate the BBB ... ...

Abstract	The blood-brain barrier (BBB) is a protective endothelial barrier lining the brain microvasculature which prevents brain delivery of therapies against brain diseases. Hence, there is an urgent need to develop vehicles which efficiently penetrate the BBB to deliver therapies into the brain. The drug L-DOPA efficiently and specifically crosses the BBB via the large neutral amino acid transporter (LAT)-1 protein to enter the brain. Thus, we synthesized L-DOPA-functionalized multi-branched nanoflower-like gold nanoparticles (L-DOPA-AuNFs) using a seed-mediated method involving catechols as a direct reducing-cum-capping agent, and examined their ability to cross the BBB to act as brain-penetrating nanovehicles. We show that L-DOPA-AuNFs efficiently penetrate the BBB compared to similarly sized and shaped AuNFs functionalized with a non-targeting ligand. Furthermore, we show that L-DOPA-AuNFs are efficiently internalized by brain macrophages without inducing inflammation. These results demonstrate the application of L-DOPA-AuNFs as a non-inflammatory BBB-penetrating nanovehicle to efficiently deliver therapies into the brain.
MeSH term(s)	Animals ; Blood-Brain Barrier/metabolism ; Brain/metabolism ; Cells, Cultured ; Dopamine Agents/administration & dosage ; Dopamine Agents/chemistry ; Drug Delivery Systems ; Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Gold/chemistry ; Humans ; Levodopa/administration & dosage ; Levodopa/chemistry ; Male ; Metal Nanoparticles/administration & dosage ; Metal Nanoparticles/chemistry ; Rats ; Rats, Wistar
Chemical Substances	Dopamine Agents ; Levodopa (46627O600J) ; Gold (7440-57-5)
Language	English
Publishing date	2018-09-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2183417-9
ISSN	1549-9642 ; 1549-9634
ISSN (online)	1549-9642
ISSN	1549-9634
DOI	10.1016/j.nano.2018.08.011
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book: Dramatizing the political

MacKenzie, Iain M / Porter, Robert

Deleuze and Guattari

2011

Author's details	Iain MacKenzie, Robert Porter
Keywords	Aesthetics/Political aspects ; Political science/Philosophy
Language	English
Size	VII, 153 S.
Publisher	Palgrave Macmillan
Publishing place	Houndmills, Basingstoke u.a.
Document type	Book
Note	Includes index
ISBN	9780230580718 ; 0230580718
Database	Former special subject collection: coastal and deep sea fishing

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Article ; Online: Delineating associations of progressive pleuroparenchymal fibroelastosis in patients with pulmonary fibrosis

Eyjolfur Gudmundsson / An Zhao / Nesrin Mogulkoc / Frouke van Beek / Tinne Goos / Christopher J. Brereton / Marcel Veltkamp / Robert Chapman / Hendrik W. van Es / Helen Garthwaite / Bahareh Gholipour / Melissa Heightman / Arjun Nair / Katarina Pontoppidan / Recep Savas / Asia Ahmed / Marie Vermant / Omer Unat / Alex Procter /

Laurens De Sadeleer / Emma Denneny / Timothy Wallis / Mark Duncan / Magali Taylor / Stijn Verleden / Sam M. Janes / Daniel C. Alexander / Athol U. Wells / Joanna Porter / Mark G. Jones / Iain Stewart / Coline H.M. van Moorsel / Wim Wuyts / Joseph Jacob

ERJ Open Research, Vol 9, Iss

2023 Volume 2

Abstract: Background Computer quantification of baseline computed tomography (CT) radiological pleuroparenchymal fibroelastosis (PPFE) associates with mortality in idiopathic pulmonary fibrosis (IPF). We examined mortality associations of longitudinal change in ... ...

Abstract	Background Computer quantification of baseline computed tomography (CT) radiological pleuroparenchymal fibroelastosis (PPFE) associates with mortality in idiopathic pulmonary fibrosis (IPF). We examined mortality associations of longitudinal change in computer-quantified PPFE-like lesions in IPF and fibrotic hypersensitivity pneumonitis (FHP). Methods Two CT scans 6–36 months apart were retrospectively examined in one IPF (n=414) and one FHP population (n=98). Annualised change in computerised upper-zone pleural surface area comprising radiological PPFE-like lesions (Δ-PPFE) was calculated. Δ-PPFE >1.25% defined progressive PPFE above scan noise. Mixed-effects models evaluated Δ-PPFE against change in visual CT interstitial lung disease (ILD) extent and annualised forced vital capacity (FVC) decline. Multivariable models were adjusted for age, sex, smoking history, baseline emphysema presence, antifibrotic use and diffusion capacity of the lung for carbon monoxide. Mortality analyses further adjusted for baseline presence of clinically important PPFE-like lesions and ILD change. Results Δ-PPFE associated weakly with ILD and FVC change. 22–26% of IPF and FHP cohorts demonstrated progressive PPFE-like lesions which independently associated with mortality in the IPF cohort (hazard ratio 1.25, 95% CI 1.16–1.34, p<0.0001) and the FHP cohort (hazard ratio 1.16, 95% CI 1.00–1.35, p=0.045). Interpretation Progression of PPFE-like lesions independently associates with mortality in IPF and FHP but does not associate strongly with measures of fibrosis progression.
Keywords	Medicine ; R
Subject code	310
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	European Respiratory Society
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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