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  1. Article ; Online: Screening asymptomatic

    Morrell, Nicholas W

    The European respiratory journal

    2021  Volume 58, Issue 1

    MeSH term(s) Bone Morphogenetic Protein Receptors, Type II/genetics ; Humans ; Hypertension, Pulmonary/diagnosis ; Hypertension, Pulmonary/genetics ; Mutation ; Physicians
    Chemical Substances BMPR2 protein, human (EC 2.7.11.30) ; Bone Morphogenetic Protein Receptors, Type II (EC 2.7.11.30)
    Language English
    Publishing date 2021-07-22
    Publishing country England
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.00286-2021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2322: Show issues Location:
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  2. Article: Understanding what drives genetic study participation: Perspectives of patients, carers, and relatives.

    Swietlik, Emilia M / Fay, Michaela / Morrell, Nicholas W

    Pulmonary circulation

    2024  Volume 14, Issue 1, Page(s) e12346

    Abstract: Genetic research's growing importance in understanding pulmonary arterial hypertension (PAH) and developing effective treatments prompted the RAPID-PAH study. This study sought feedback from stakeholders who participated in two genomic studies to enhance ...

    Abstract Genetic research's growing importance in understanding pulmonary arterial hypertension (PAH) and developing effective treatments prompted the RAPID-PAH study. This study sought feedback from stakeholders who participated in two genomic studies to enhance genetic study delivery and clinical integration. Stakeholders from nine UK PH centres, representing various roles, ages, genders, and mutation statuses, took part in 53 semi-structured interviews and focus groups. Transcripts were thematically coded using inductive analysis. Clustering analysis was conducted to identify patient groups that shared attitudes. In this paper, we focus on patients', carers', and relatives' perspectives. The key interview themes revealed insights into participants' attitudes toward genetic research and testing more generally, expertise and knowledge of the disease itself, motivations and barriers to participating in genetic research, awareness of and interest in consent procedures and the use of personal and genetic data, as well as the process of communicating individual genetic results. Factors influencing genetic research participation included altruistic motives, personal diagnostic experiences, and family-related hopes. Clustering analysis produced distinct clusters based on the presence of barriers and motivators for research participation; however, hardly any patients shared identical sets of attitudes, emphasising the need for personalised approaches to recruitment. Most patients reported poor engagement with study-related materials. Patients who received individual genetic results expressed satisfaction with the process, whereas those who did not were disappointed with the lack of feedback. Reflecting on patient perspectives, we offer recommendations to improve the genetic study delivery process. Enhancing genetic research integration into clinical practice requires tailored engagement, clear communication, and support from healthcare stakeholders.
    Language English
    Publishing date 2024-02-15
    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 10.1002/pul2.12346
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Unlocking the potential of genetic research in pulmonary arterial hypertension: Insights from clinicians, researchers, and study team.

    Swietlik, Emilia M / Fay, Michaela / Morrell, Nicholas W

    Pulmonary circulation

    2024  Volume 14, Issue 1, Page(s) e12353

    Abstract: Genetic research and testing are increasingly important for understanding and treating pulmonary arterial hypertension. We aimed to explore how attitudes toward genetic research among clinical and research teams impacted the engagement in genetic ... ...

    Abstract Genetic research and testing are increasingly important for understanding and treating pulmonary arterial hypertension. We aimed to explore how attitudes toward genetic research among clinical and research teams impacted the engagement in genetic research and the integration of genetic insights into clinical practice. We conducted 53 semistructured interviews and focus groups with patients, clinicians, and researchers from nine UK Pulmonary Hypertension centers, who had genetic research experience. Transcripts were thematically coded using inductive analysis. In this study, we focus on the researchers', clinicians', and study team's perspectives. From the interview data, several key themes emerged, ranging from study design, recruitment, and consent procedures to the return of individual genetic results. Additionally, participants reflected on both the successes of these studies and the future directions of genetic research. The analysis highlighted the critical importance of fostering collaborative networks firmly rooted in existing clinical and research infrastructure in rare disease study setups. Furthermore, the significance of trust-building, personalized communication, and transparency among stakeholders was underscored. The study offered valuable insights into the motivating and hindering factors to participant recruitment and consent procedures. Lastly, the findings gathered from processes surrounding the return of individual genetic results, genetic counselling, and the recruitment of relatives provided invaluable lessons regarding the integration of genetics into clinical practice. This in-depth analysis yields a crucial understanding of attitudes to genetic research among various stakeholders and sheds light on the complexities of genetic research and the evidence-practice gap.
    Language English
    Publishing date 2024-03-12
    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 10.1002/pul2.12353
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Finding the needle in the haystack: BMP9 and 10 emerge from the genome in pulmonary arterial hypertension.

    Morrell, Nicholas W

    The European respiratory journal

    2019  Volume 53, Issue 3

    MeSH term(s) Familial Primary Pulmonary Hypertension ; Germ Cells ; Germ-Line Mutation ; Humans ; Hypertension, Pulmonary ; Pulmonary Arterial Hypertension
    Language English
    Publishing date 2019-03-14
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.00078-2019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    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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  5. Article ; Online: BMPR2

    Cuthbertson, Iona / Morrell, Nicholas W / Caruso, Paola

    Circulation research

    2023  Volume 132, Issue 1, Page(s) 109–126

    Abstract: Pulmonary arterial hypertension forms the first and most severe of the 5 categories of pulmonary hypertension. Disease pathogenesis is driven by progressive remodeling of peripheral pulmonary arteries, caused by the excessive proliferation of vascular ... ...

    Abstract Pulmonary arterial hypertension forms the first and most severe of the 5 categories of pulmonary hypertension. Disease pathogenesis is driven by progressive remodeling of peripheral pulmonary arteries, caused by the excessive proliferation of vascular wall cells, including endothelial cells, smooth muscle cells and fibroblasts, and perivascular inflammation. Compelling evidence from animal models suggests endothelial cell dysfunction is a key initial trigger of pulmonary vascular remodeling, which is characterised by hyperproliferation and early apoptosis followed by enrichment of apoptosis-resistant populations. Dysfunctional pulmonary arterial endothelial cells lose their ability to produce vasodilatory mediators, together leading to augmented pulmonary arterial smooth muscle cell responses, increased pulmonary vascular pressures and right ventricular afterload, and progressive right ventricular hypertrophy and heart failure. It is recognized that a range of abnormal cellular molecular signatures underpin the pathophysiology of pulmonary arterial hypertension and are enhanced by loss-of-function mutations in the
    MeSH term(s) Animals ; Bone Morphogenetic Protein Receptors, Type II/genetics ; Bone Morphogenetic Protein Receptors, Type II/metabolism ; Endothelial Cells/metabolism ; Hypertension, Pulmonary/etiology ; Mutation ; Pulmonary Arterial Hypertension/metabolism ; Pulmonary Artery/metabolism ; Humans
    Chemical Substances Bone Morphogenetic Protein Receptors, Type II (EC 2.7.11.30)
    Language English
    Publishing date 2023-01-05
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.122.321554
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui IV Zs.70: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Ui IV Zs.60: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  6. Article ; Online: New Mutations and Pathogenesis of Pulmonary Hypertension: Progress and Puzzles in Disease Pathogenesis.

    Aldred, Micheala A / Morrell, Nicholas W / Guignabert, Christophe

    Circulation research

    2022  Volume 130, Issue 9, Page(s) 1365–1381

    Abstract: Pulmonary arterial hypertension (PAH) is a complex multifactorial disease with poor prognosis characterized by functional and structural alterations of the pulmonary circulation causing marked increase in pulmonary vascular resistance, ultimately leading ...

    Abstract Pulmonary arterial hypertension (PAH) is a complex multifactorial disease with poor prognosis characterized by functional and structural alterations of the pulmonary circulation causing marked increase in pulmonary vascular resistance, ultimately leading to right heart failure and death. Mutations in the gene encoding BMPRII-a receptor for the TGF-β (transforming growth factor-beta) superfamily-account for over 70% of families with PAH and ≈20% of sporadic cases. In recent years, however, less common or rare mutations in other genes have been identified. This review will consider how these newly discovered PAH genes could help to provide a better understanding of the molecular and cellular bases of the maintenance of the pulmonary vascular integrity, as well as their role in the PAH pathogenesis underlying occlusion of arterioles in the lung. We will also discuss how insights into the genetic contributions of these new PAH-related genes may open up new therapeutic targets for this, currently incurable, cardiopulmonary disorder.
    MeSH term(s) Humans ; Hypertension, Pulmonary/pathology ; Mutation ; Pulmonary Arterial Hypertension ; Transforming Growth Factor beta/genetics ; Vascular Resistance
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2022-04-28
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.122.320084
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui IV Zs.70: Show issues Location:
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    Ui IV Zs.60: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  7. Article ; Online: An emerging class of new therapeutics targeting TGF, Activin, and BMP ligands in pulmonary arterial hypertension.

    Upton, Paul D / Dunmore, Benjamin J / Li, Wei / Morrell, Nicholas W

    Developmental dynamics : an official publication of the American Association of Anatomists

    2022  Volume 252, Issue 3, Page(s) 327–342

    Abstract: Pulmonary arterial hypertension (PAH) is an often fatal condition, the primary pathology of which involves loss of pulmonary vascular perfusion due to progressive aberrant vessel remodeling. The reduced capacity of the pulmonary circulation places ... ...

    Abstract Pulmonary arterial hypertension (PAH) is an often fatal condition, the primary pathology of which involves loss of pulmonary vascular perfusion due to progressive aberrant vessel remodeling. The reduced capacity of the pulmonary circulation places increasing strain on the right ventricle of the heart, leading to death by heart failure. Currently, licensed therapies are primarily vasodilators, which have increased the median post-diagnosis life expectancy from 2.8 to 7 years. Although this represents a substantial improvement, the search continues for transformative therapeutics that reverse established disease. The genetics of human PAH heavily implicates reduced endothelial bone morphogenetic protein (BMP) signaling as a causal role for the disease pathobiology. Recent approaches have focused on directly enhancing BMP signaling or removing the inhibitory influence of pathways that repress BMP signaling. In this critical commentary, we review the evidence underpinning the development of two approaches: BMP-based agonists and inhibition of activin/GDF signaling. We also address the key considerations and questions that remain regarding these approaches.
    MeSH term(s) Humans ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/pathology ; Ligands ; Pulmonary Arterial Hypertension/complications ; Pulmonary Arterial Hypertension/metabolism ; Pulmonary Arterial Hypertension/pathology ; Pulmonary Artery/metabolism ; Pulmonary Artery/pathology ; Signal Transduction/physiology ; Activins/metabolism ; Bone Morphogenetic Proteins/metabolism ; Cytokines
    Chemical Substances Ligands ; Activins (104625-48-1) ; Bone Morphogenetic Proteins ; Cytokines
    Language English
    Publishing date 2022-04-27
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1102541-4
    ISSN 1097-0177 ; 1058-8388
    ISSN (online) 1097-0177
    ISSN 1058-8388
    DOI 10.1002/dvdy.478
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Future breakthroughs in the genetics of pulmonary arterial hypertension.

    Morrell, Nicholas W

    Pulmonary circulation

    2014  Volume 3, Issue 3, Page(s) 451–453

    Language English
    Publishing date 2014-03-10
    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 10.1086/674305
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: The role of genomics and genetics in pulmonary arterial hypertension.

    Swietlik, Emilia M / Gräf, Stefan / Morrell, Nicholas W

    Global cardiology science & practice

    2020  Volume 2020, Issue 1, Page(s) e202013

    Language English
    Publishing date 2020-04-30
    Publishing country Qatar
    Document type Journal Article ; Review
    ZDB-ID 2738381-7
    ISSN 2305-7823
    ISSN 2305-7823
    DOI 10.21542/gcsp.2020.13
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The

    Aman, Jurjan / Morrell, Nicholas W / Rhodes, Christopher J / Wilkins, Martin R / Bogaard, Harm Jan

    The European respiratory journal

    2022  Volume 60, Issue 6

    MeSH term(s) Humans ; Pulmonary Arterial Hypertension/therapy ; Familial Primary Pulmonary Hypertension ; SOXF Transcription Factors/genetics
    Chemical Substances SOX17 protein, human ; SOXF Transcription Factors
    Language English
    Publishing date 2022-12-08
    Publishing country England
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.01438-2022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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