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  1. Book: Murray and Nadel's textbook of respiratory medicine / 1 / V. Courtney Broaddus [und weitere]

    Mason, Robert J. / Murray, John F. / Nadel, Jay A. / Broaddus, V. Courtney

    2021  

    Author's details ed. Robert J. Mason
    Collection Murray and Nadel's textbook of respiratory medicine
    Language English
    Size xli, 1004, I-81 Seiten, Illustrationen
    Edition Seventh edition
    Publishing place 2021
    Publishing country United States
    Document type Book
    Note Zugang zu Online-Ausgabe über Code
    HBZ-ID HT020991186
    ISBN 978-0-323-79371-1 ; 0-323-79371-1
    Database Catalogue ZB MED Medicine, Health

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    2021 A 968 available for loan (reading room) Lesesaal EG
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  2. Book: Murray and Nadel's textbook of respiratory medicine / 2 / V. Courtney Broaddus [und weitere]

    Mason, Robert J. / Murray, John F. / Nadel, Jay A. / Broaddus, V. Courtney

    2021  

    Author's details ed. Robert J. Mason
    Collection Murray and Nadel's textbook of respiratory medicine
    Language English
    Size xli Seiten, Seite 1005 - 1993, I-81 Seiten, Illustrationen
    Edition Seventh edition
    Publishing place 2021
    Publishing country United States
    Document type Book
    HBZ-ID HT020991181
    ISBN 978-0-323-65587-3 ; 0-323-65587-4
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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  3. Article ; Online: Clearing the Air - A Conservative Option for Spontaneous Pneumothorax.

    Broaddus, V Courtney

    The New England journal of medicine

    2020  Volume 382, Issue 5, Page(s) 469–470

    MeSH term(s) Humans ; Pleurodesis ; Pneumothorax
    Language English
    Publishing date 2020-01-29
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMe1916844
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Autophagy in 3D In Vitro and Ex Vivo Cancer Models.

    Follo, Carlo / Barbone, Dario / Richards, William G / Bueno, Raphael / Courtney Broaddus, V

    Methods in molecular biology (Clifton, N.J.)

    2019  Volume 1880, Page(s) 491–510

    Abstract: Three-dimensional (3D) models are acquiring importance in cancer research due to their ability to mimic multiple features of the tumor microenvironment more accurately than standard monolayer two-dimensional (2D) cultures. Several groups, including our ... ...

    Abstract Three-dimensional (3D) models are acquiring importance in cancer research due to their ability to mimic multiple features of the tumor microenvironment more accurately than standard monolayer two-dimensional (2D) cultures. Several groups, including our laboratory, are now accumulating evidence that autophagy in solid tumors is also better represented in 3D than in 2D. Here we detail how we generate 3D models, both in vitro multicellular spheroids generated from cell lines and ex vivo tumor fragment spheroids generated from tumor samples, and how autophagy can be measured in 3D cultures.
    MeSH term(s) Adaptor Proteins, Signal Transducing/analysis ; Adaptor Proteins, Signal Transducing/metabolism ; Autophagy/physiology ; Autophagy-Related Proteins/analysis ; Autophagy-Related Proteins/metabolism ; Cell Culture Techniques/instrumentation ; Cell Culture Techniques/methods ; Cell Line, Tumor ; Humans ; Mesothelioma/pathology ; Microscopy, Fluorescence/instrumentation ; Microscopy, Fluorescence/methods ; Microtubule-Associated Proteins/analysis ; Microtubule-Associated Proteins/metabolism ; Spheroids, Cellular/pathology ; Tubulin/analysis ; Tubulin/metabolism
    Chemical Substances ATG13 protein, human ; Adaptor Proteins, Signal Transducing ; Autophagy-Related Proteins ; MAP1LC3B protein, human ; Microtubule-Associated Proteins ; Tubulin
    Language English
    Publishing date 2019-01-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-8873-0_31
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Medical Subspecialty Textbooks in the 21st Century. Essential or Headed for Extinction?

    Broaddus, V Courtney / Grippi, Michael A

    Annals of the American Thoracic Society

    2015  Volume 12, Issue 8, Page(s) 1113–1115

    Abstract: In recent years, the role of medical subspecialty textbooks as sources of information for students, trainees, and practicing clinicians has been challenged. Although the structure of textbooks continues to evolve from standard, printed versions to ... ...

    Abstract In recent years, the role of medical subspecialty textbooks as sources of information for students, trainees, and practicing clinicians has been challenged. Although the structure of textbooks continues to evolve from standard, printed versions to digital formats, including e-books and online texts, we maintain that the authoritative compilation of clinical and scientific material by experts in the field (i.e., a modern-day textbook) remains central to the education, training, and practice of subspecialists. Regardless of format, an effective medical subspecialty textbook is authoritative, comprehensive, and integrated in its coverage of the subject. Textbook content represents a unique synthesis of clinical and scientific material of real educational and clinical value. Incorporation of illustrations, including figures, tables, videos, and audios, bolsters the presentation and further solidifies the reader's understanding of the subject. The textbook, both printed and digital, reinforces the many widely available online resources and serves as a platform from which to evaluate other sources of information and to launch additional scientific and clinical inquiry.
    MeSH term(s) Education, Medical, Continuing/trends ; History, 21st Century ; Humans ; Medical Writing/standards ; Textbooks as Topic/history ; Topography, Medical/standards
    Language English
    Publishing date 2015-08
    Publishing country United States
    Document type Historical Article ; Journal Article ; Video-Audio Media
    ZDB-ID 2717461-X
    ISSN 2325-6621 ; 1943-5665 ; 2325-6621
    ISSN (online) 2325-6621 ; 1943-5665
    ISSN 2325-6621
    DOI 10.1513/AnnalsATS.201506-335OI
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5828: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  6. Book: Murray & Nadel's textbook of respiratory medicine

    Broaddus, V. Courtney / Mason, Robert J

    2016  

    Title variant Textbook of respiratory medicine
    Author's details editor-in-chief, V. Courtney Broaddus ; editors, Robert J. Mason, Joel D. Ernst, Talmadge E. King Jr., Stephen C. Lazarus, John F. Murray, Jay A. Nadel, Arthur S. Slutsky ; thoracic imaging editor, Michael B. Gotway
    MeSH term(s) Respiratory Tract Diseases
    Language English
    Size 2 v. (various pagings) :, illustrations.
    Edition 6th edition.
    Document type Book
    Note Preceded by Murray and Nadel's textbook of respiratory medicine. 5th ed. / editors, Robert J. Mason ... [et al.]. c2010.
    ISBN 9781455733835 ; 1455733830
    Database Catalogue of the US National Library of Medicine (NLM)

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  7. Book ; Collection: Murray and Nadel's textbook of respiratory medicine

    Mason, Robert J. / Murray, John F. / Nadel, Jay A. / Broaddus, V. Courtney

    2005  

    Title variant Textbook of respiratory medicine ; Murray & Nadel's textbook of respiratory medicine
    Author's details ed. Robert J. Mason
    Keywords Respiratory Tract Diseases ; Atemwegskrankheit ; Pulmonologie ; Atmungsorgan ; Krankheit
    Subject Atemwegekrankheit ; Atemwege ; Atemwegserkrankung ; Erkrankung ; Krankheitszustand ; Krankheiten ; Morbus ; Nosos ; Pathos ; Atemorgan ; Atmungsorgane ; Lungenheilkunde ; Pneumologie ; Pulmologie
    Language English
    Dates of publication 2005-9999
    Publisher Saunders Elsevier
    Publishing place Philadelphia, Pa
    Publishing country United States
    Document type Book ; Collection (display volumes)
    Note 4. Aufl. erschienen im Verl. Elsevier, Philadelphia, Pa.
    Accompanying material 5. Aufl. mit Zugang zur Internetausgabe über Code
    Old title Bis 3. Aufl. u.d.T. Textbook of respiratory medicine
    HBZ-ID HT014385685
    ISBN 978-1-4160-4710-0 ; 1-4160-4710-7
    Database Catalogue ZB MED Medicine, Health

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  8. Article ; Online: Erlotinib Activates Different Cell Death Pathways in EGFR-mutant Lung Cancer Cells Grown in 3D

    Lee, Hyun-Kyung / Noh, Min Hye / Hong, Seung-Woo / Kim, Seung-Mi / Kim, Sung Hyun / Kim, Yeong Seok / Broaddus, V Courtney / Hur, Dae Young

    Anticancer research

    2021  Volume 41, Issue 3, Page(s) 1261–1269

    Abstract: Background/aim: Non-small cell lung cancer patients with epidermal growth factor receptor (EGFR) mutation have been shown to have a good response to erlotinib, a receptor tyrosine kinase inhibitor of EGFR. In this study, we found that the cell death ... ...

    Abstract Background/aim: Non-small cell lung cancer patients with epidermal growth factor receptor (EGFR) mutation have been shown to have a good response to erlotinib, a receptor tyrosine kinase inhibitor of EGFR. In this study, we found that the cell death pathways activated by erlotinib in 2D and 3D culture systems are different.
    Materials and methods: The cell death pathways induced by erlotinib were evaluated by flow cytometry and immunoblotting in both 2D and 3D culture systems of EGFR mutant lung cancer cells.
    Results: Treatment with erlotinib induced caspase 8 activation and up-regulation of TNF-related apoptosis-inducing ligand (TRAIL) expression only in 3D cultures. Knockdown of TRAIL attenuated both erlotinib-induced activation of caspase-8 and apoptosis in 3D cultures. Erlotinib also increased LC3, an autophagy marker, expression and c-Jun N terminal kinase (JNK) activation. Both 3-MA as an autophagy inhibitor and SP600125 as a JNK inhibitor, significantly inhibited erlotinib-induced cell death.
    Conclusion: Erlotinib induces apoptotic cell death in 3D cultures through an autophagy-TRAIL-JNK pathway.
    MeSH term(s) Apoptosis/drug effects ; Autophagy/physiology ; Caspase 8/metabolism ; Cell Culture Techniques/methods ; Cell Death/drug effects ; Cell Line, Tumor ; ErbB Receptors/antagonists & inhibitors ; ErbB Receptors/genetics ; Erlotinib Hydrochloride/pharmacology ; Erlotinib Hydrochloride/therapeutic use ; Humans ; JNK Mitogen-Activated Protein Kinases/physiology ; Lung Neoplasms/drug therapy ; Lung Neoplasms/pathology ; Mutation ; TNF-Related Apoptosis-Inducing Ligand/physiology
    Chemical Substances TNF-Related Apoptosis-Inducing Ligand ; TNFSF10 protein, human ; Erlotinib Hydrochloride (DA87705X9K) ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; CASP8 protein, human (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-)
    Language English
    Publishing date 2021-03-31
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 604549-2
    ISSN 1791-7530 ; 0250-7005
    ISSN (online) 1791-7530
    ISSN 0250-7005
    DOI 10.21873/anticanres.14883
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1642: Show issues Location:
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  9. Article ; Online: Autophagy facilitates the release of immunogenic signals following chemotherapy in 3D models of mesothelioma.

    Follo, Carlo / Cheng, Yao / Richards, William G / Bueno, Raphael / Broaddus, V Courtney

    Molecular carcinogenesis

    2019  Volume 58, Issue 10, Page(s) 1754–1769

    Abstract: We have previously shown that nearly half of mesothelioma patients have tumors with low autophagy and that these patients have a significantly worse outcome than those with high autophagy. We hypothesized that autophagy may be beneficial by facilitating ... ...

    Abstract We have previously shown that nearly half of mesothelioma patients have tumors with low autophagy and that these patients have a significantly worse outcome than those with high autophagy. We hypothesized that autophagy may be beneficial by facilitating immunogenic cell death (ICD) of tumor cells following chemotherapy. An important hallmark of ICD is that death of tumor cells is preceded or accompanied by the release of damage-associated molecular pattern molecules (DAMPs), which then can stimulate an antitumor immune response. Therefore, we measured how autophagy affected the release of three major DAMPs: high mobility group box 1 (HMGB1), ATP, and calreticulin following chemotherapy. We found that autophagy in three-dimensional (3D) models with low autophagy at baseline could be upregulated with the cell-permeant Tat-BECN1 peptide and confirmed that autophagy in 3D models with high autophagy at baseline could be inhibited with MRT 68921 or ATG7 RNAi, as we have previously shown. In in vitro 3D spheroids, we found that, when autophagy was high or upregulated, DAMPs were released following chemotherapy; however, when autophagy was low or inhibited, DAMPs release was significantly impaired. Similarly, in ex vivo tumors, when autophagy was high or upregulated, HMGB1 was released following chemotherapy but, when autophagy was low, HMGB1 release was not seen. We conclude that autophagy can be upregulated in at least some tumors with low autophagy and that upregulation of autophagy can restore the release of DAMPs following chemotherapy. Autophagy may be necessary for ICD in this tumor.
    MeSH term(s) Adenosine Triphosphate/genetics ; Alarmins/genetics ; Antineoplastic Agents/pharmacology ; Autophagy/drug effects ; Autophagy/genetics ; Autophagy-Related Protein 7/antagonists & inhibitors ; Autophagy-Related Proteins/genetics ; Beclin-1/genetics ; Calreticulin/genetics ; Cell Culture Techniques ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic/drug effects ; HMGB1 Protein/genetics ; Humans ; Immunity, Cellular/genetics ; Immunogenic Cell Death/genetics ; Mesothelioma/drug therapy ; Mesothelioma/genetics ; Mesothelioma/pathology ; RNA Interference ; Spheroids, Cellular/drug effects ; Spheroids, Cellular/pathology
    Chemical Substances ATG13 protein, human ; Alarmins ; Antineoplastic Agents ; Autophagy-Related Proteins ; BECN1 protein, human ; Beclin-1 ; Calreticulin ; HMGB1 Protein ; HMGB1 protein, human ; Adenosine Triphosphate (8L70Q75FXE) ; Autophagy-Related Protein 7 (EC 6.2.1.45)
    Language English
    Publishing date 2019-06-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1004029-8
    ISSN 1098-2744 ; 0899-1987
    ISSN (online) 1098-2744
    ISSN 0899-1987
    DOI 10.1002/mc.23050
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2664: Show issues Location:
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  10. Article ; Online: Autophagy initiation correlates with the autophagic flux in 3D models of mesothelioma and with patient outcome.

    Follo, Carlo / Barbone, Dario / Richards, William G / Bueno, Raphael / Broaddus, V Courtney

    Autophagy

    2016  Volume 12, Issue 7, Page(s) 1180–1194

    Abstract: Understanding the role of autophagy in cancer has been limited by the inability to measure this dynamic process in formalin-fixed tissue. We considered that 3-dimensional models including ex vivo tumor, such as we have developed for studying mesothelioma, ...

    Abstract Understanding the role of autophagy in cancer has been limited by the inability to measure this dynamic process in formalin-fixed tissue. We considered that 3-dimensional models including ex vivo tumor, such as we have developed for studying mesothelioma, would provide valuable insights. Using these models, in which we could use lysosomal inhibitors to measure the autophagic flux, we sought a marker of autophagy that would be valid in formalin-fixed tumor and be used to assess the role of autophagy in patient outcome. Autophagy was studied in mesothelioma cell lines, as 2-dimensional (2D) monolayers and 3-dimensional (3D) multicellular spheroids (MCS), and in tumor from 25 chemonaive patients, both as ex vivo 3D tumor fragment spheroids (TFS) and as formalin-fixed tissue. Autophagy was evaluated as autophagic flux by detection of the accumulation of LC3 after lysosomal inhibition and as autophagy initiation by detection of ATG13 puncta. We found that autophagic flux in 3D, but not in 2D, correlated with ATG13 positivity. In each TFS, ATG13 positivity was similar to that of the original tumor. When tested in tissue microarrays of 109 chemonaive patients, higher ATG13 positivity correlated with better prognosis and provided information independent of known prognostic factors. Our results show that ATG13 is a static marker of the autophagic flux in 3D models of mesothelioma and may also reflect autophagy levels in formalin-fixed tumor. If confirmed, this marker would represent a novel prognostic factor for mesothelioma, supporting the notion that autophagy plays an important role in this cancer.
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Autophagy/physiology ; Autophagy-Related Proteins/metabolism ; Cell Culture Techniques ; Cell Line ; Formaldehyde ; Humans ; Mesothelioma/metabolism ; Mesothelioma/therapy ; Treatment Outcome
    Chemical Substances ATG13 protein, human ; Adaptor Proteins, Signal Transducing ; Autophagy-Related Proteins ; Formaldehyde (1HG84L3525)
    Language English
    Publishing date 2016-04-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2016.1173799
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