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  1. Article ; Online: Review of the British Thoracic Society Winter Meeting 2016, 7-9 December, London, UK.

    Woodcock, Hannah V / José, Ricardo J / Jenkins, Gisli

    Thorax

    2017  Volume 72, Issue 7, Page(s) 600–665

    Abstract: This article reviews the British Thoracic Society Winter Meeting 2016 and highlights the new developments in scientific and clinical research across the breadth of respiratory medicine. ...

    Abstract This article reviews the British Thoracic Society Winter Meeting 2016 and highlights the new developments in scientific and clinical research across the breadth of respiratory medicine.
    MeSH term(s) Humans ; London ; Pulmonary Medicine ; Respiratory Tract Diseases ; Societies, Medical
    Language English
    Publishing date 2017-05-04
    Publishing country England
    Document type Congress
    ZDB-ID 204353-1
    ISSN 1468-3296 ; 0040-6376
    ISSN (online) 1468-3296
    ISSN 0040-6376
    DOI 10.1136/thoraxjnl-2017-210154
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    In stock of ZB MED Cologne/Königswinter

    Ui III Zs.83: Show issues Location:
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  2. Article ; Online: Review of the British Thoracic Society Winter Meeting 2017, 6-8 December 2017, London, UK.

    Singanayagam, Aran / Woodcock, Hannah V / Molyneaux, Philip L / Jenkins, Gisli

    Thorax

    2018  Volume 73, Issue 9, Page(s) 872–876

    Abstract: This article reviews the British Thoracic Society Winter Meeting 2017 and summarises the new developments in scientific and clinical research across the breadth of respiratory medicine. The article discusses a number of symposia and selected abstract ... ...

    Abstract This article reviews the British Thoracic Society Winter Meeting 2017 and summarises the new developments in scientific and clinical research across the breadth of respiratory medicine. The article discusses a number of symposia and selected abstract presentations from the meeting.
    MeSH term(s) Biomedical Research ; Humans ; Lung Diseases/diagnosis ; Lung Diseases/etiology ; Lung Diseases/therapy ; Pulmonary Medicine ; Smoking ; Societies, Medical
    Language English
    Publishing date 2018-06-14
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 204353-1
    ISSN 1468-3296 ; 0040-6376
    ISSN (online) 1468-3296
    ISSN 0040-6376
    DOI 10.1136/thoraxjnl-2018-212012
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    In stock of ZB MED Cologne/Königswinter

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  3. Article: The treatment of idiopathic pulmonary fibrosis.

    Woodcock, Hannah V / Maher, Toby M

    F1000prime reports

    2014  Volume 6, Page(s) 16

    Abstract: Idiopathic pulmonary fibrosis (IPF) is a progressive and invariably fatal disease with a median survival of less than three years from diagnosis. The last decade has seen an exponential increase in clinical trial activity in IPF and this in turn has led ... ...

    Abstract Idiopathic pulmonary fibrosis (IPF) is a progressive and invariably fatal disease with a median survival of less than three years from diagnosis. The last decade has seen an exponential increase in clinical trial activity in IPF and this in turn has led to important developments in the treatment of this terrible disease. Previous therapeutic approaches based around regimens including corticosteroids and azathioprine have, when tested in randomized clinical trials, been shown to be harmful in IPF. By contrast, compounds with anti-fibrotic actions have been shown to be beneficial. Subsequently, the novel anti-fibrotic agent pirfenidone has, in many parts of the world, become the first treatment ever to be licensed for use in IPF. This exciting development, coupled with ongoing clinical trials of a range of other novel compounds, is bringing hope to patients and their clinicians and raises the prospect that, in the future, it may become possible to successfully arrest the development of progressive scarring in IPF.
    Language English
    Publishing date 2014-03-03
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2709303-7
    ISSN 2051-7599
    ISSN 2051-7599
    DOI 10.12703/P6-16
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  4. Article ; Online: Reducing lung function decline in patients with idiopathic pulmonary fibrosis: potential of nintedanib.

    Woodcock, Hannah V / Molyneaux, Philip L / Maher, Toby M

    Drug design, development and therapy

    2013  Volume 7, Page(s) 503–510

    Abstract: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic lung disease with no clear etiology and a paucity of therapeutic options. Nintedanib (previously known as BIBF 1120) is a tyrosine kinase receptor antagonist which inhibits a number ... ...

    Abstract Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic lung disease with no clear etiology and a paucity of therapeutic options. Nintedanib (previously known as BIBF 1120) is a tyrosine kinase receptor antagonist which inhibits a number of key receptors, including those for platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and fibroblast growth factor (FGF). These growth factors are profibrotic and each has been investigated as a potential standalone therapeutic target in IPF. Simultaneous inhibition of these receptors, with an analog of nintedanib, has proved to be effective in experimental animal models of pulmonary fibrosis. This observation, together with extensive safety and pharmacokinetic data from studies of nintedanib in malignancy, paved the way for the clinical development of this drug in IPF. The Phase IIb TOMORROW trial demonstrated that treatment with nintedanib may potentially slow decline in lung function, decrease the frequency of acute exacerbations, and improve quality of life in patients with IPF. While these observations are drawn from a single clinical trial, taken together with the preclinical data they suggest that nintedanib may yet become an important therapeutic option for individuals with IPF. The results of ongoing parallel, international, multicenter Phase III clinical trials are therefore eagerly awaited.
    MeSH term(s) Clinical Trials, Phase II as Topic ; ErbB Receptors/antagonists & inhibitors ; Humans ; Idiopathic Pulmonary Fibrosis/drug therapy ; Idiopathic Pulmonary Fibrosis/physiopathology ; Indoles/adverse effects ; Indoles/pharmacokinetics ; Indoles/therapeutic use ; Lung/physiopathology ; Protein Kinase Inhibitors/therapeutic use ; Receptors, Platelet-Derived Growth Factor/antagonists & inhibitors ; Receptors, Vascular Endothelial Growth Factor/antagonists & inhibitors
    Chemical Substances Indoles ; Protein Kinase Inhibitors ; ErbB Receptors (EC 2.7.10.1) ; Receptors, Platelet-Derived Growth Factor (EC 2.7.10.1) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1) ; nintedanib (G6HRD2P839)
    Language English
    Publishing date 2013-06-19
    Publishing country New Zealand
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2451346-5
    ISSN 1177-8881 ; 1177-8881
    ISSN (online) 1177-8881
    ISSN 1177-8881
    DOI 10.2147/DDDT.S38833
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Author Correction: The mTORC1/4E-BP1 axis represents a critical signaling node during fibrogenesis.

    Woodcock, Hannah V / Eley, Jessica D / Guillotin, Delphine / Platé, Manuela / Nanthakumar, Carmel B / Martufi, Matteo / Peace, Simon / Joberty, Gerard / Poeckel, Daniel / Good, Robert B / Taylor, Adam R / Zinn, Nico / Redding, Matthew / Forty, Ellen J / Hynds, Robert E / Swanton, Charles / Karsdal, Morten / Maher, Toby M / Fisher, Andrew /
    Bergamini, Giovanna / Marshall, Richard P / Blanchard, Andy D / Mercer, Paul F / Chambers, Rachel C

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 4680

    Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

    Abstract An amendment to this paper has been published and can be accessed via a link at the top of the paper.
    Language English
    Publishing date 2020-09-11
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-18621-3
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  6. Article: Keep calm and carry on learning: using Microsoft Teams to deliver a medical education programme during the COVID-19 pandemic.

    Henderson, Daisy / Woodcock, Hannah / Mehta, Jay / Khan, Nuzhath / Shivji, Victoria / Richardson, Charlotte / Aya, Haleema / Ziser, Shier / Pollara, Gabriele / Burns, Aine

    Future healthcare journal

    2020  Volume 7, Issue 3, Page(s) e67–e70

    Abstract: The outbreak of COVID-19 in the UK in March 2020 required a radical remodelling of the medical workforce at Royal Free London NHS Foundation Trust to prepare for the anticipated surge of hospital admissions. The provision of relevant teaching and ... ...

    Abstract The outbreak of COVID-19 in the UK in March 2020 required a radical remodelling of the medical workforce at Royal Free London NHS Foundation Trust to prepare for the anticipated surge of hospital admissions. The provision of relevant teaching and training was immediately identified as a priority, particularly for staff due to work outside their regular medical specialty. Rather than deliver face-to-face teaching, doctors at the Trust utilised Microsoft Teams, an online communications and collaboration platform, to deliver a multi-disciplinary Trust-wide education programme responsive to the needs of surveyed medical staff. To date members of 18 departments across the Trust have delivered 51 virtual teaching sessions which have been viewed 3,814 times. During this pandemic the virtual education programme has facilitated rapid dissemination of new information and provided a platform for discussion and unity amongst colleagues with overwhelmingly positive feedback from both learners and teachers.
    Keywords covid19
    Language English
    Publishing date 2020-10-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 3016427-8
    ISSN 2514-6653 ; 2514-6645
    ISSN (online) 2514-6653
    ISSN 2514-6645
    DOI 10.7861/fhj.2020-0071
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  7. Article ; Online: mTORC1 amplifies the ATF4-dependent de novo serine-glycine pathway to supply glycine during TGF-β

    Selvarajah, Brintha / Azuelos, Ilan / Platé, Manuela / Guillotin, Delphine / Forty, Ellen J / Contento, Greg / Woodcock, Hannah V / Redding, Matthew / Taylor, Adam / Brunori, Gino / Durrenberger, Pascal F / Ronzoni, Riccardo / Blanchard, Andy D / Mercer, Paul F / Anastasiou, Dimitrios / Chambers, Rachel C

    Science signaling

    2019  Volume 12, Issue 582

    Abstract: The differentiation of fibroblasts into a transient population of highly activated, extracellular matrix (ECM)-producing myofibroblasts at sites of tissue injury is critical for normal tissue repair. Excessive myofibroblast accumulation and persistence, ... ...

    Abstract The differentiation of fibroblasts into a transient population of highly activated, extracellular matrix (ECM)-producing myofibroblasts at sites of tissue injury is critical for normal tissue repair. Excessive myofibroblast accumulation and persistence, often as a result of a failure to undergo apoptosis when tissue repair is complete, lead to pathological fibrosis and are also features of the stromal response in cancer. Myofibroblast differentiation is accompanied by changes in cellular metabolism, including increased glycolysis, to meet the biosynthetic demands of enhanced ECM production. Here, we showed that transforming growth factor-β
    MeSH term(s) Activating Transcription Factor 4/genetics ; Activating Transcription Factor 4/metabolism ; Biosynthetic Pathways/drug effects ; Biosynthetic Pathways/genetics ; Cell Differentiation/drug effects ; Cell Differentiation/genetics ; Cells, Cultured ; Collagen/biosynthesis ; Extracellular Matrix/metabolism ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Gene Expression Regulation/drug effects ; Glycine/biosynthesis ; Humans ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Myofibroblasts/cytology ; Myofibroblasts/drug effects ; Myofibroblasts/metabolism ; Serine/biosynthesis ; Signal Transduction/drug effects ; Transforming Growth Factor beta1/pharmacology
    Chemical Substances Transforming Growth Factor beta1 ; Activating Transcription Factor 4 (145891-90-3) ; Serine (452VLY9402) ; Collagen (9007-34-5) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Glycine (TE7660XO1C)
    Language English
    Publishing date 2019-05-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.aav3048
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  8. Article ; Online: The mTORC1/4E-BP1 axis represents a critical signaling node during fibrogenesis.

    Woodcock, Hannah V / Eley, Jessica D / Guillotin, Delphine / Platé, Manuela / Nanthakumar, Carmel B / Martufi, Matteo / Peace, Simon / Joberty, Gerard / Poeckel, Daniel / Good, Robert B / Taylor, Adam R / Zinn, Nico / Redding, Matthew / Forty, Ellen J / Hynds, Robert E / Swanton, Charles / Karsdal, Morten / Maher, Toby M / Fisher, Andrew /
    Bergamini, Giovanna / Marshall, Richard P / Blanchard, Andy D / Mercer, Paul F / Chambers, Rachel C

    Nature communications

    2019  Volume 10, Issue 1, Page(s) 6

    Abstract: Myofibroblasts are the key effector cells responsible for excessive extracellular matrix deposition in multiple fibrotic conditions, including idiopathic pulmonary fibrosis (IPF). The PI3K/Akt/mTOR axis has been implicated in fibrosis, with pan-PI3K/mTOR ...

    Abstract Myofibroblasts are the key effector cells responsible for excessive extracellular matrix deposition in multiple fibrotic conditions, including idiopathic pulmonary fibrosis (IPF). The PI3K/Akt/mTOR axis has been implicated in fibrosis, with pan-PI3K/mTOR inhibition currently under clinical evaluation in IPF. Here we demonstrate that rapamycin-insensitive mTORC1 signaling via 4E-BP1 is a critical pathway for TGF-β
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Cell Cycle Proteins ; Cell Line ; Collagen/biosynthesis ; Fibroblasts/metabolism ; Humans ; Idiopathic Pulmonary Fibrosis/etiology ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoproteins/metabolism ; Signal Transduction ; Sirolimus ; TOR Serine-Threonine Kinases/metabolism ; Transforming Growth Factor beta1/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; EIF4EBP1 protein, human ; Phosphoproteins ; TGFB1 protein, human ; Transforming Growth Factor beta1 ; Collagen (9007-34-5) ; MTOR protein, human (EC 2.7.1.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Sirolimus (W36ZG6FT64)
    Language English
    Publishing date 2019-01-02
    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/s41467-018-07858-8
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  9. Article ; Online: A randomised, placebo-controlled study of omipalisib (PI3K/mTOR) in idiopathic pulmonary fibrosis.

    Lukey, Pauline T / Harrison, Stephen A / Yang, Shuying / Man, Yim / Holman, Beverley F / Rashidnasab, Alaleh / Azzopardi, Gabrielle / Grayer, Michael / Simpson, Juliet K / Bareille, Philippe / Paul, Lyn / Woodcock, Hannah V / Toshner, Richard / Saunders, Peter / Molyneaux, Philip L / Thielemans, Kris / Wilson, Frederick J / Mercer, Paul F / Chambers, Rachel C /
    Groves, Ashley M / Fahy, William A / Marshall, Richard P / Maher, Toby M

    The European respiratory journal

    2019  Volume 53, Issue 3

    Abstract: Phosphatidylinositol 3-kinases (PI3Ks) and mammalian target of rapamycin (mTOR) play a role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). Omipalisib (GSK2126458) is a potent inhibitor of PI3K/mTOR.A randomised, placebo-controlled, double- ... ...

    Abstract Phosphatidylinositol 3-kinases (PI3Ks) and mammalian target of rapamycin (mTOR) play a role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). Omipalisib (GSK2126458) is a potent inhibitor of PI3K/mTOR.A randomised, placebo-controlled, double-blind, repeat dose escalation, experimental medicine study of omipalisib in subjects with IPF was conducted (NCT01725139) to test safety, tolerability, pharmacokinetics and pharmacodynamics. Omipalisib was dosed at 0.25 mg, 1 mg and 2 mg twice daily for 8 days in four cohorts of four subjects randomised 3:1 to receive omipalisib or placebo (two cohorts received 2 mg twice daily).17 subjects with IPF were enrolled. The most common adverse event was diarrhoea, which was reported by four participants. Dose-related increases in insulin and glucose were observed. Pharmacokinetic analysis demonstrated that exposure in the blood predicts lung exposure. Exposure-dependent inhibition of phosphatidylinositol 3,4,5 trisphosphate and pAKT confirmed target engagement in blood and lungs.
    MeSH term(s) Administration, Oral ; Aged ; Dose-Response Relationship, Drug ; Double-Blind Method ; Female ; Fluorodeoxyglucose F18 ; Humans ; Idiopathic Pulmonary Fibrosis/diagnostic imaging ; Idiopathic Pulmonary Fibrosis/drug therapy ; Lung/diagnostic imaging ; Lung/pathology ; Male ; Middle Aged ; Phosphatidylinositol 3-Kinases/metabolism ; Positron Emission Tomography Computed Tomography ; Pyridazines ; Quinolines/administration & dosage ; Sulfonamides/administration & dosage ; TOR Serine-Threonine Kinases/metabolism ; Treatment Outcome
    Chemical Substances Pyridazines ; Quinolines ; Sulfonamides ; Fluorodeoxyglucose F18 (0Z5B2CJX4D) ; omipalisib (1X8F5A3NA0) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2019-03-18
    Publishing country England
    Document type Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.01992-2018
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  10. Article ; Online: Author Correction

    Hannah V. Woodcock / Jessica D. Eley / Delphine Guillotin / Manuela Platé / Carmel B. Nanthakumar / Matteo Martufi / Simon Peace / Gerard Joberty / Daniel Poeckel / Robert B. Good / Adam R. Taylor / Nico Zinn / Matthew Redding / Ellen J. Forty / Robert E. Hynds / Charles Swanton / Morten Karsdal / Toby M. Maher / Andrew Fisher /
    Giovanna Bergamini / Richard P. Marshall / Andy D. Blanchard / Paul F. Mercer / Rachel C. Chambers

    Nature Communications, Vol 11, Iss 1, Pp 1-

    The mTORC1/4E-BP1 axis represents a critical signaling node during fibrogenesis

    2020  Volume 1

    Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

    Abstract An amendment to this paper has been published and can be accessed via a link at the top of the paper.
    Keywords Science ; Q
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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