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Article ; Online: Comment on 'SARS-CoV-2 suppresses anticoagulant and fibrinolytic gene expression in the lung'.

FitzGerald, Ethan S / Jamieson, Amanda M

2022 Volume 11

Abstract: Mast et al. analyzed transcriptome data derived from RNA-sequencing (RNA-seq) of COVID-19 patient bronchoalveolar lavage fluid (BALF) samples, as compared to BALF RNA-seq samples from a study investigating microbiome and inflammatory interactions in ... ...

Abstract	Mast et al. analyzed transcriptome data derived from RNA-sequencing (RNA-seq) of COVID-19 patient bronchoalveolar lavage fluid (BALF) samples, as compared to BALF RNA-seq samples from a study investigating microbiome and inflammatory interactions in obese and asthmatic adults (Mast et al., 2021). Based on their analysis of these data, Mast et al. concluded that mRNA expression of key regulators of the extrinsic coagulation cascade and fibrinolysis were significantly reduced in COVID-19 patients. Notably, they reported that the expression of the extrinsic coagulation cascade master regulator Tissue Factor (F3) remained unchanged, while there was an 8-fold upregulation of its cognate inhibitor Tissue Factor Pathway Inhibitor (TFPI). From this they conclude that "pulmonary fibrin deposition does not stem from enhanced local [tissue factor] production and that counterintuitively, COVID-19 may dampen [tissue factor]-dependent mechanisms in the lungs". They also reported decreased Activated Protein C (aPC) mediated anticoagulant activity and major increases in fibrinogen expression and other key regulators of clot formation. Many of these results are contradictory to findings in most of the field, particularly the findings regarding extrinsic coagulation cascade mediated coagulopathies. Here, we present a complete re-analysis of the data sets analyzed by Mast et al. This re-analysis demonstrates that the two data sets utilized were not comparable between one another, and that the COVID-19 sample set was not suitable for the transcriptomic analysis Mast et al. performed. We also identified other significant flaws in the design of their retrospective analysis, such as poor-quality control and filtering standards. Given the issues with the datasets and analysis, their conclusions are not supported.
MeSH term(s)	Anticoagulants ; COVID-19 ; Humans ; Lung ; Retrospective Studies ; SARS-CoV-2 ; Transcriptome
Chemical Substances	Anticoagulants
Language	English
Publishing date	2022-01-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.74268
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Comment on ‘SARS-CoV-2 suppresses anticoagulant and fibrinolytic gene expression in the lung’

Ethan S FitzGerald / Amanda M Jamieson

eLife, Vol

2022 Volume 11

Abstract	Mast et al. analyzed transcriptome data derived from RNA-sequencing (RNA-seq) of COVID-19 patient bronchoalveolar lavage fluid (BALF) samples, as compared to BALF RNA-seq samples from a study investigating microbiome and inflammatory interactions in obese and asthmatic adults (Mast et al., 2021). Based on their analysis of these data, Mast et al. concluded that mRNA expression of key regulators of the extrinsic coagulation cascade and fibrinolysis were significantly reduced in COVID-19 patients. Notably, they reported that the expression of the extrinsic coagulation cascade master regulator Tissue Factor (F3) remained unchanged, while there was an 8-fold upregulation of its cognate inhibitor Tissue Factor Pathway Inhibitor (TFPI). From this they conclude that “pulmonary fibrin deposition does not stem from enhanced local [tissue factor] production and that counterintuitively, COVID-19 may dampen [tissue factor]-dependent mechanisms in the lungs”. They also reported decreased Activated Protein C (aPC) mediated anticoagulant activity and major increases in fibrinogen expression and other key regulators of clot formation. Many of these results are contradictory to findings in most of the field, particularly the findings regarding extrinsic coagulation cascade mediated coagulopathies. Here, we present a complete re-analysis of the data sets analyzed by Mast et al. This re-analysis demonstrates that the two data sets utilized were not comparable between one another, and that the COVID-19 sample set was not suitable for the transcriptomic analysis Mast et al. performed. We also identified other significant flaws in the design of their retrospective analysis, such as poor-quality control and filtering standards. Given the issues with the datasets and analysis, their conclusions are not supported.
Keywords	COVID-19 ; coagulation ; SARS-CoV-2 ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	306
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Unique transcriptional changes in coagulation cascade genes in SARS-CoV-2-infected lung epithelial cells: A potential factor in COVID-19 coagulopathies.

FitzGerald, Ethan S / Jamieson, Amanda M

bioRxiv : the preprint server for biology

2020

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly become a global pandemic. In addition to the acute pulmonary symptoms of COVID-19 (the disease associated with SARS-CoV-2 infection), pulmonary and distal coagulopathies have caused ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly become a global pandemic. In addition to the acute pulmonary symptoms of COVID-19 (the disease associated with SARS-CoV-2 infection), pulmonary and distal coagulopathies have caused morbidity and mortality in many patients. Currently, the molecular pathogenesis underlying COVID-19 associated coagulopathies are unknown. While there are many theories for the cause of this pathology, including hyper inflammation and excess tissue damage, the cellular and molecular underpinnings are not yet clear. By analyzing transcriptomic data sets from experimental and clinical research teams, we determined that changes in the gene expression of genes important in the extrinsic coagulation cascade in the lung epithelium may be important triggers for COVID-19 coagulopathy. This regulation of the extrinsic blood coagulation cascade is not seen with influenza A virus (IAV)-infected NHBEs suggesting that the lung epithelial derived coagulopathies are specific to SARS-Cov-2 infection. This study is the first to identify potential lung epithelial cell derived factors contributing to COVID-19 associated coagulopathy.
Keywords	covid19
Language	English
Publishing date	2020-07-07
Publishing country	United States
Document type	Preprint
DOI	10.1101/2020.07.06.182972
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Article ; Online: Lung Epithelial Cell Transcriptional Regulation as a Factor in COVID-19-associated Coagulopathies.

FitzGerald, Ethan S / Chen, Yongzhi / Fitzgerald, Katherine A / Jamieson, Amanda M

American journal of respiratory cell and molecular biology

2021 Volume 64, Issue 6, Page(s) 687–697

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly become a global pandemic. In addition to the acute pulmonary symptoms of coronavirus disease (COVID-19) (the disease associated with SARS-CoV-2 infection), pulmonary and distal ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly become a global pandemic. In addition to the acute pulmonary symptoms of coronavirus disease (COVID-19) (the disease associated with SARS-CoV-2 infection), pulmonary and distal coagulopathies have caused morbidity and mortality in many patients. Currently, the molecular pathogenesis underlying COVID-19-associated coagulopathies are unknown. Identifying the molecular basis of how SARS-CoV-2 drives coagulation is essential to mitigating short- and long-term thrombotic risks of sick and recovered patients with COVID-19. We aimed to perform coagulation-focused transcriptome analysis of
MeSH term(s)	Alveolar Epithelial Cells/metabolism ; Alveolar Epithelial Cells/pathology ; Alveolar Epithelial Cells/virology ; Blood Coagulation Disorders/etiology ; Blood Coagulation Disorders/metabolism ; Blood Coagulation Disorders/pathology ; COVID-19/complications ; COVID-19/metabolism ; COVID-19/pathology ; Cell Line ; Female ; Gene Expression Regulation ; Humans ; Influenza A virus/metabolism ; Influenza, Human/complications ; Influenza, Human/metabolism ; Influenza, Human/pathology ; Male ; SARS-CoV-2/metabolism ; Signal Transduction ; Transcription, Genetic
Language	English
Publishing date	2021-03-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2020-0453OC
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Repurposing the Homing Endonuclease I-SceI for Positive Selection and Development of Gene-Editing Technologies.

Lee, Kok Zhi / Mechikoff, Michael A / Parasa, Mrugesh Krishna / Rankin, Tyler J / Pandolfi, Paula / Fitzgerald, Kevin S / Hillman, Ethan T / Solomon, Kevin V

ACS synthetic biology

2022 Volume 11, Issue 1, Page(s) 53–60

Abstract: Prokaryote genomes encode diverse programmable DNA endonucleases with significant potential for biotechnology and gene editing. However, these endonucleases differ significantly in their properties, which must be screened and measured. While positive ... ...

Abstract	Prokaryote genomes encode diverse programmable DNA endonucleases with significant potential for biotechnology and gene editing. However, these endonucleases differ significantly in their properties, which must be screened and measured. While positive selection screens based on ccdB and barnase have been developed to evaluate such proteins, their high levels of toxicity make them challenging to use. Here, we develop and validate a more robust positive selection screen based on the homing endonuclease I-SceI. Candidate endonucleases target and cure the I-SceI expression plasmid preventing induction of I-SceI-mediated double strand DNA breaks that lead to cell death in
MeSH term(s)	Deoxyribonuclease I ; Deoxyribonucleases, Type II Site-Specific/genetics ; Escherichia coli/genetics ; Escherichia coli/metabolism ; Gene Editing ; Saccharomyces cerevisiae Proteins/genetics
Chemical Substances	Saccharomyces cerevisiae Proteins ; Deoxyribonuclease I (EC 3.1.21.1) ; Deoxyribonucleases, Type II Site-Specific (EC 3.1.21.4)
Language	English
Publishing date	2022-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	2161-5063
ISSN (online)	2161-5063
DOI	10.1021/acssynbio.1c00340
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Article ; Online: Competitive Cell Death Interactions in Pulmonary Infection: Host Modulation Versus Pathogen Manipulation.

FitzGerald, Ethan S / Luz, Nivea F / Jamieson, Amanda M

Frontiers in immunology

2020 Volume 11, Page(s) 814

Abstract: In the context of pulmonary infection, both hosts and pathogens have evolved a multitude of mechanisms to regulate the process of host cell death. The host aims to rapidly induce an inflammatory response at the site of infection, promote pathogen ... ...

Abstract	In the context of pulmonary infection, both hosts and pathogens have evolved a multitude of mechanisms to regulate the process of host cell death. The host aims to rapidly induce an inflammatory response at the site of infection, promote pathogen clearance, quickly resolve inflammation, and return to tissue homeostasis. The appropriate modulation of cell death in respiratory epithelial cells and pulmonary immune cells is central in the execution of all these processes. Cell death can be either inflammatory or anti-inflammatory depending on regulated cell death (RCD) modality triggered and the infection context. In addition, diverse bacterial pathogens have evolved many means to manipulate host cell death to increase bacterial survival and spread. The multitude of ways that hosts and bacteria engage in a molecular tug of war to modulate cell death dynamics during infection emphasizes its relevance in host responses and pathogen virulence at the host pathogen interface. This narrative review outlines several current lines of research characterizing bacterial pathogen manipulation of host cell death pathways in the lung. We postulate that understanding these interactions and the dynamics of intracellular and extracellular bacteria RCD manipulation, may lead to novel therapeutic approaches for the treatment of intractable respiratory infections.
MeSH term(s)	Animals ; Cell Communication/immunology ; Cell Death/immunology ; Gram-Negative Bacteria/pathogenicity ; Gram-Positive Bacteria/pathogenicity ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate ; Macrophages/immunology ; Neutrophils/immunology ; Pneumonia, Bacterial/immunology ; Pneumonia, Bacterial/microbiology ; Respiratory Mucosa/immunology ; Virulence
Language	English
Publishing date	2020-05-19
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.00814
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book ; Online: Education for a Future in Crisis

Lee, Ethan / Hart, Ariel Nicole / Searles, Thomas A. / Levis-Fitzgerald, Marc / Barthelemy, Ramón S. / Shaked, Shanna / Marks, Victoria / Carbajo, Sergio

Developing a Humanities-Informed STEM Curriculum

2023

Abstract: In the popular imagination, science and technology are often seen as fields of knowledge production critical to social progress and a cooperative future. This optimistic portrayal of technological advancement also features prominently in internal ... ...

Abstract	In the popular imagination, science and technology are often seen as fields of knowledge production critical to social progress and a cooperative future. This optimistic portrayal of technological advancement also features prominently in internal discourses amongst scientists, industry leaders, and STEM students alike. Yet, an overwhelming body of research, investigation, and first-person accounts highlight the varying ways modern science, technology, and engineering industries contribute to the degradation of our changing environments and exploit and harm global low-income and marginalized populations. By and large, siloed higher-education STEM curricula provide inadequate opportunities for undergraduate and graduate students to critically analyze the historical and epistemological foundations of scientific knowledge production and even fewer tools to engage with and respond to modern community-based cases. Here, we describe the development of a humanities- and social sciences-informed curriculum designed to address the theory, content, and skill-based needs of traditional STEM students considering technoscientific careers. In essence, this course is designed to foster behavior change, de-center dominant ways of knowing in the sciences, and bolster self-reflection and critical-thinking skills to equip the developing STEM workforce with a more nuanced and accurate understanding of the social, political, and economic role of science and technology. This curriculum has the potential to empower STEM-educated professionals to contribute to a more promising, inclusive future. Our framework foregrounds key insights from science and technology studies, Black and Native feminisms, queer theory, and disability studies, alongside real-world case studies using critical pedagogies. Comment: 25 pages, 1 figure, 4 tables
Keywords	Physics - Physics Education
Subject code	306
Publishing date	2023-11-11
Publishing country	us
Document type	Book ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Unique transcriptional changes in coagulation cascade genes in SARS-CoV-2-infected lung epithelial cells: A potential factor in COVID-19 coagulopathies

FitzGerald, Ethan S. / Jamieson, Amanda M.

bioRxiv

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly become a global pandemic. In addition to the acute pulmonary symptoms of COVID-19 (the disease associated with SARS-CoV-2 infection), pulmonary and distal coagulopathies have caused morbidity and mortality in many patients. Currently, the molecular pathogenesis underlying COVID-19 associated coagulopathies are unknown. While there are many theories for the cause of this pathology, including hyper inflammation and excess tissue damage, the cellular and molecular underpinnings are not yet clear. By analyzing transcriptomic data sets from experimental and clinical research teams, we determined that changes in the gene expression of genes important in the extrinsic coagulation cascade in the lung epithelium may be important triggers for COVID-19 coagulopathy. This regulation of the extrinsic blood coagulation cascade is not seen with influenza A virus (IAV)-infected NHBEs suggesting that the lung epithelial derived coagulopathies are specific to SARS-Cov-2 infection. This study is the first to identify transcriptional changes at the level of the lung epithelium that have the to drive the COVID-19 associated coagulopathy.
Keywords	covid19
Language	English
Publishing date	2020-07-07
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2020.07.06.182972
Database	COVID19

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Article: Unique transcriptional changes in coagulation cascade genes in SARS-CoV-2-infected lung epithelial cells: A potential factor in COVID-19 coagulopathies

FitzGerald, Ethan S. / Jamieson, Amanda M.

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly become a global pandemic In addition to the acute pulmonary symptoms of COVID-19 (the disease associated with SARS-CoV-2 infection), pulmonary and distal coagulopathies have caused ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly become a global pandemic In addition to the acute pulmonary symptoms of COVID-19 (the disease associated with SARS-CoV-2 infection), pulmonary and distal coagulopathies have caused morbidity and mortality in many patients Currently, the molecular pathogenesis underlying COVID-19 associated coagulopathies are unknown While there are many theories for the cause of this pathology, including hyper inflammation and excess tissue damage, the cellular and molecular underpinnings are not yet clear By analyzing transcriptomic data sets from experimental and clinical research teams, we determined that changes in the gene expression of genes important in the extrinsic coagulation cascade in the lung epithelium may be important triggers for COVID-19 coagulopathy This regulation of the extrinsic blood coagulation cascade is not seen with influenza A virus (IAV)-infected NHBEs suggesting that the lung epithelial derived coagulopathies are specific to SARS-Cov-2 infection This study is the first to identify potential lung epithelial cell derived factors contributing to COVID-19 associated coagulopathy GRAPHICAL ABSTRACT: AUTHOR SUMMARY: Why was this study done?: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly become a global pandemic In addition to the acute pulmonary symptoms of COVID-19 (the disease associated with SARS-CoV-2 infection), pulmonary and distal coagulopathies have caused morbidity and mortality in many patients Currently, the molecular pathogenesis underlying COVID-19 associated coagulopathies are unknown Understanding the molecular basis of dysregulated blood coagulation during SARS-CoV-2 infection may help promote new therapeutic strategies to mitigate these complications in COVID-19 patients What did the researchers do and find?: We analyzed three publicly available RNA sequencing datasets to identify possible molecular etiologies of COVID-19 associated coagulopathies These data sets include sequencing libraries from clinically isolated samples of bronchoalveolar lavage fluid (BALF) and peripheral blood mononuclear cells (PBMCs) from SARS-CoV-2 positive patients and healthy controls We also analyzed a publicly available RNA sequencing dataset derived from in vitro SARS-CoV-2 infected primary normal human bronchial epithelial (NHBE) cells and mock infected samples Pathway analysis of both NHBE and BALF differential gene expression gene sets We found that SARS-CoV-2 infection induces the activation of the extrinsic blood coagulation cascade and suppression of the plasminogen activation system in both NHBEs and cells isolated from the BALF PBMCs did not differentially express genes regulating blood coagulation Comparison with influenza A virus (IAV)-infected NHBEs revealed that the regulation of the extrinsic blood coagulation cascade is unique to SARS-CoV-2, and not seen with IAV infection What do these findings mean?: The hyper-activation of the extrinsic blood coagulation cascade and the suppression of the plasminogen activation system in SARS-CoV-2 infected epithelial cells may drive diverse coagulopathies in the lung and distal organ systems The gene transcription pattern in SARS-CoV-2 infected epithelial cells is distinct from IAV infected epithelial cells with regards to the regulation of blood coagulation
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #663598
Database	COVID19

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Article: Surviving Deadly Lung Infections: Innate Host Tolerance Mechanisms in the Pulmonary System.

Crane, Meredith J / Lee, Kayla M / FitzGerald, Ethan S / Jamieson, Amanda M

Frontiers in immunology

2018 Volume 9, Page(s) 1421

Abstract: Much research on infectious diseases focuses on clearing the pathogen through the use of antimicrobial drugs, the immune response, or a combination of both. Rapid clearance of pathogens allows for a quick return to a healthy state and increased survival. ...

Abstract	Much research on infectious diseases focuses on clearing the pathogen through the use of antimicrobial drugs, the immune response, or a combination of both. Rapid clearance of pathogens allows for a quick return to a healthy state and increased survival. Pathogen-targeted approaches to combating infection have inherent limitations, including their pathogen-specific nature, the potential for antimicrobial resistance, and poor vaccine efficacy, among others. Another way to survive an infection is to tolerate the alterations to homeostasis that occur during a disease state through a process called host tolerance or resilience, which is independent from pathogen burden. Alterations in homeostasis during infection are numerous and include tissue damage, increased inflammation, metabolic changes, temperature changes, and changes in respiration. Given its importance and sensitivity, the lung is a good system for understanding host tolerance to infectious disease. Pneumonia is the leading cause of death for children under five worldwide. One reason for this is because when the pulmonary system is altered dramatically it greatly impacts the overall health and survival of a patient. Targeting host pathways involved in maintenance of pulmonary host tolerance during infection could provide an alternative therapeutic avenue that may be broadly applicable across a variety of pathologies. In this review, we will summarize recent findings on tolerance to host lung infection. We will focus on the involvement of innate immune responses in tolerance and how an initial viral lung infection may alter tolerance mechanisms in leukocytic, epithelial, and endothelial compartments to a subsequent bacterial infection. By understanding tolerance mechanisms in the lung we can better address treatment options for deadly pulmonary infections.
Keywords	covid19
Language	English
Publishing date	2018-06-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.01421
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