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  1. Artikel: Advancements in Host-Based Interventions for Influenza Treatment.

    Yip, Tsz-Fung / Selim, Aisha Sami Mohammed / Lian, Ida / Lee, Suki Man-Yan

    Frontiers in immunology

    2018  Band 9, Seite(n) 1547

    Abstract: Influenza is a major acute respiratory infection that causes mortality and morbidity worldwide. Two classes of conventional antivirals, M2 ion channel blockers and neuraminidase inhibitors, are mainstays in managing influenza disease to lessen symptoms ... ...

    Abstract Influenza is a major acute respiratory infection that causes mortality and morbidity worldwide. Two classes of conventional antivirals, M2 ion channel blockers and neuraminidase inhibitors, are mainstays in managing influenza disease to lessen symptoms while minimizing hospitalization and death in patients with severe influenza. However, the development of viral resistance to both drug classes has become a major public health concern. Vaccines are prophylaxis mainstays but are limited in efficacy due to the difficulty in matching predicted dominant viral strains to circulating strains. As such, other potential interventions are being explored. Since viruses rely on host cellular functions to replicate, recent therapeutic developments focus on targeting host factors involved in virus replication. Besides controlling virus replication, potential targets for drug development include controlling virus-induced host immune responses such as the recently suggested involvement of innate lymphoid cells and NADPH oxidases in influenza virus pathogenesis and immune cell metabolism. In this review, we will discuss the advancements in novel host-based interventions for treating influenza disease.
    Schlagwörter covid19
    Sprache Englisch
    Erscheinungsdatum 2018
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2018.01547
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Recognition of Double-Stranded RNA and Regulation of Interferon Pathway by Toll-Like Receptor 10.

    Lee, Suki Man-Yan / Yip, Tsz-Fung / Yan, Sheng / Jin, Dong-Yan / Wei, Hong-Li / Guo, Rey-Ting / Peiris, Joseph Sriyal Malik

    Frontiers in immunology

    2018  Band 9, Seite(n) 516

    Abstract: Toll-like receptor (TLR)-10 remains an orphan receptor without well-characterized ligands or functions. Here, we reveal that TLR10 is predominantly localized to endosomes and binds ... ...

    Abstract Toll-like receptor (TLR)-10 remains an orphan receptor without well-characterized ligands or functions. Here, we reveal that TLR10 is predominantly localized to endosomes and binds dsRNA
    Mesh-Begriff(e) Endosomes/metabolism ; Humans ; Interferons/metabolism ; RNA, Double-Stranded/metabolism ; Signal Transduction ; THP-1 Cells ; Toll-Like Receptor 10/metabolism ; Toll-Like Receptor 3/metabolism
    Chemische Substanzen RNA, Double-Stranded ; TLR10 protein, human ; TLR3 protein, human ; Toll-Like Receptor 10 ; Toll-Like Receptor 3 ; Interferons (9008-11-1)
    Sprache Englisch
    Erscheinungsdatum 2018-03-16
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2018.00516
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  3. Artikel ; Online: Targeting the host or the virus: current and novel concepts for antiviral approaches against influenza virus infection.

    Lee, Suki Man-Yan / Yen, Hui-Ling

    Antiviral research

    2012  Band 96, Heft 3, Seite(n) 391–404

    Abstract: Influenza epidemics and pandemics are constant threats to human health. The application of antiviral drugs provides an immediate and direct control of influenza virus infection. At present, the major strategy for managing patients with influenza is ... ...

    Abstract Influenza epidemics and pandemics are constant threats to human health. The application of antiviral drugs provides an immediate and direct control of influenza virus infection. At present, the major strategy for managing patients with influenza is through targeting conserved viral proteins critical for viral replication. Two classes of conventional antiviral drugs, the M2 ion channel blockers and the neuraminidase inhibitors, are frequently used. In recent years, increasing levels of resistance to both drug classes has become a major public health concern, highlighting the urgent need for the development of alternative treatments. Novel classes of antiviral compounds or biomolecules targeting viral replication mechanism are under development, using approaches including high-throughput small-molecule screening platforms and structure-based designs. In response to influenza virus infection, host cellular mechanisms are triggered to defend against the invaders. At the same time, viruses as obligate intracellular pathogens have evolved to exploit cellular responses in support of their efficient replication, including antagonizing the host type I interferon response as well as activation of specific cellular pathways at different stages of the replication cycle. Numerous studies have highlighted the possibility of targeting virus-host interactions and host cellular mechanisms to develop new treatment regimens. This review aims to give an overview of current and novel concepts targeting the virus and the host for managing influenza.
    Mesh-Begriff(e) Amides/pharmacology ; Animals ; Antibodies, Viral/metabolism ; Antiviral Agents/pharmacology ; Cross Reactions ; Host-Pathogen Interactions ; Humans ; Immunomodulation ; Influenza A virus/drug effects ; Influenza A virus/pathogenicity ; Influenza A virus/physiology ; Orthomyxoviridae Infections/drug therapy ; Orthomyxoviridae Infections/virology ; Pyrazines/pharmacology ; Receptors, Cell Surface/antagonists & inhibitors ; Viral Matrix Proteins/antagonists & inhibitors ; Virus Attachment/drug effects ; Virus Internalization/drug effects ; Virus Replication
    Chemische Substanzen Amides ; Antibodies, Viral ; Antiviral Agents ; M2 protein, Influenza A virus ; Pyrazines ; Receptors, Cell Surface ; Viral Matrix Proteins ; sialic acid receptor ; favipiravir (EW5GL2X7E0)
    Schlagwörter covid19
    Sprache Englisch
    Erscheinungsdatum 2012-09-26
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 306628-9
    ISSN 1872-9096 ; 0166-3542
    ISSN (online) 1872-9096
    ISSN 0166-3542
    DOI 10.1016/j.antiviral.2012.09.013
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Whole transcriptome analysis reveals differential gene expression profile reflecting macrophage polarization in response to influenza A H5N1 virus infection

    Na Zhang / Yun-Juan Bao / Amy Hin-Yan Tong / Scott Zuyderduyn / Gary D. Bader / J. S. Malik Peiris / Si Lok / Suki Man-Yan Lee

    BMC Medical Genomics, Vol 11, Iss 1, Pp 1-

    2018  Band 14

    Abstract: Abstract Background Avian influenza A H5N1 virus can cause lethal disease in humans. The virus can trigger severe pneumonia and lead to acute respiratory distress syndrome. Data from clinical, in vitro and in vivo suggest that virus-induced cytokine ... ...

    Abstract Abstract Background Avian influenza A H5N1 virus can cause lethal disease in humans. The virus can trigger severe pneumonia and lead to acute respiratory distress syndrome. Data from clinical, in vitro and in vivo suggest that virus-induced cytokine dysregulation could be a contributory factor to the pathogenesis of human H5N1 disease. However, the precise mechanism of H5N1 infection eliciting the unique host response are still not well understood. Methods To obtain a better understanding of the molecular events at the earliest time points, we used RNA-Seq to quantify and compare the host mRNA and miRNA transcriptomes induced by the highly pathogenic influenza A H5N1 (A/Vietnam/3212/04) or low virulent H1N1 (A/Hong Kong/54/98) viruses in human monocyte-derived macrophages at 1-, 3-, and 6-h post infection. Results Our data reveals that two macrophage populations corresponding to M1 (classically activated) and M2 (alternatively activated) macrophage subtypes respond distinctly to H5N1 virus infection when compared to H1N1 virus or mock infection, a distinction that could not be made from previous microarray studies. When this confounding variable is considered in our statistical model, a clear set of dysregulated genes and pathways emerges specifically in H5N1 virus-infected macrophages at 6-h post infection, whilst was not found with H1N1 virus infection. Furthermore, altered expression of genes in these pathways, which have been previously implicated in viral host response, occurs specifically in the M1 subtype. We observe a significant up-regulation of genes in the RIG-I-like receptor signaling pathway. In particular, interferons, and interferon-stimulated genes are broadly affected. The negative regulators of interferon signaling, the suppressors of cytokine signaling, SOCS-1 and SOCS-3, were found to be markedly up-regulated in the initial round of H5N1 virus replication. Elevated levels of these suppressors could lead to the eventual suppression of cellular antiviral genes, contributing to pathophysiology ...
    Schlagwörter Influenza A virus ; H5N1 ; Macrophage polarization ; Transcriptomics ; RNA-Seq ; Internal medicine ; RC31-1245 ; Genetics ; QH426-470
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2018-02-01T00:00:00Z
    Verlag BMC
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Whole transcriptome analysis reveals differential gene expression profile reflecting macrophage polarization in response to influenza A H5N1 virus infection.

    Zhang, Na / Bao, Yun-Juan / Tong, Amy Hin-Yan / Zuyderduyn, Scott / Bader, Gary D / Malik Peiris, J S / Lok, Si / Lee, Suki Man-Yan

    BMC medical genomics

    2018  Band 11, Heft 1, Seite(n) 20

    Abstract: Background: Avian influenza A H5N1 virus can cause lethal disease in humans. The virus can trigger severe pneumonia and lead to acute respiratory distress syndrome. Data from clinical, in vitro and in vivo suggest that virus-induced cytokine ... ...

    Abstract Background: Avian influenza A H5N1 virus can cause lethal disease in humans. The virus can trigger severe pneumonia and lead to acute respiratory distress syndrome. Data from clinical, in vitro and in vivo suggest that virus-induced cytokine dysregulation could be a contributory factor to the pathogenesis of human H5N1 disease. However, the precise mechanism of H5N1 infection eliciting the unique host response are still not well understood.
    Methods: To obtain a better understanding of the molecular events at the earliest time points, we used RNA-Seq to quantify and compare the host mRNA and miRNA transcriptomes induced by the highly pathogenic influenza A H5N1 (A/Vietnam/3212/04) or low virulent H1N1 (A/Hong Kong/54/98) viruses in human monocyte-derived macrophages at 1-, 3-, and 6-h post infection.
    Results: Our data reveals that two macrophage populations corresponding to M1 (classically activated) and M2 (alternatively activated) macrophage subtypes respond distinctly to H5N1 virus infection when compared to H1N1 virus or mock infection, a distinction that could not be made from previous microarray studies. When this confounding variable is considered in our statistical model, a clear set of dysregulated genes and pathways emerges specifically in H5N1 virus-infected macrophages at 6-h post infection, whilst was not found with H1N1 virus infection. Furthermore, altered expression of genes in these pathways, which have been previously implicated in viral host response, occurs specifically in the M1 subtype. We observe a significant up-regulation of genes in the RIG-I-like receptor signaling pathway. In particular, interferons, and interferon-stimulated genes are broadly affected. The negative regulators of interferon signaling, the suppressors of cytokine signaling, SOCS-1 and SOCS-3, were found to be markedly up-regulated in the initial round of H5N1 virus replication. Elevated levels of these suppressors could lead to the eventual suppression of cellular antiviral genes, contributing to pathophysiology of H5N1 virus infection.
    Conclusions: Our study provides important mechanistic insights into the understanding of H5N1 viral pathogenesis and the multi-faceted host immune responses. The dysregulated genes could be potential candidates as therapeutic targets for treating H5N1 disease.
    Mesh-Begriff(e) Gene Expression Profiling ; Humans ; Immunity, Innate/genetics ; Influenza A Virus, H1N1 Subtype/physiology ; Influenza A Virus, H5N1 Subtype/physiology ; Macrophages/cytology ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/virology ; MicroRNAs/genetics
    Chemische Substanzen MicroRNAs
    Sprache Englisch
    Erscheinungsdatum 2018-02-23
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1755-8794
    ISSN (online) 1755-8794
    DOI 10.1186/s12920-018-0335-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: A novel biparatopic hybrid antibody-ACE2 fusion that blocks SARS-CoV-2 infection

    Miao, Xiaoniu / Luo, Yi / Huang, Xi / Lee, Suki M. Y. / Yuan, Zhijun / Tang, Yongzhou / Chen, Liandi / Wang, Chao / Wu, Fan / Xu, Yifeng / Jiang, Wenchao / Gao, Wei / Song, Xuedong / Yan, Yao / Pang, Tuling / Chen, Cheng / Zou, Yuefeng / Fu, Weihui / Wan, Liping /
    Gilbert-Jaramillo, Javier / Knight, Michael / Tan, Tiong Kit / Rijal, Pramila / Townsend, Alain / Sun, Joanne / Liu, Xiaolin / James, William / Tsun, Andy / Xu, Yingda

    mAbs

    implications for therapy

    2020  Band 12, Heft 1, Seite(n) 1804241

    Schlagwörter Immunology ; Immunology and Allergy ; covid19
    Sprache Englisch
    Verlag Informa UK Limited
    Erscheinungsland uk
    Dokumenttyp Artikel ; Online
    ZDB-ID 2537838-7
    ISSN 1942-0870 ; 1942-0862
    ISSN (online) 1942-0870
    ISSN 1942-0862
    DOI 10.1080/19420862.2020.1804241
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: A novel biparatopic hybrid antibody-ACE2 fusion that blocks SARS-CoV-2 infection: implications for therapy.

    Miao, Xiaoniu / Luo, Yi / Huang, Xi / Lee, Suki M Y / Yuan, Zhijun / Tang, Yongzhou / Chen, Liandi / Wang, Chao / Wu, Fan / Xu, Yifeng / Jiang, Wenchao / Gao, Wei / Song, Xuedong / Yan, Yao / Pang, Tuling / Chen, Cheng / Zou, Yuefeng / Fu, Weihui / Wan, Liping /
    Gilbert-Jaramillo, Javier / Knight, Michael / Tan, Tiong Kit / Rijal, Pramila / Townsend, Alain / Sun, Joanne / Liu, Xiaolin / James, William / Tsun, Andy / Xu, Yingda

    mAbs

    2020  Band 12, Heft 1, Seite(n) 1804241

    Abstract: In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provide a strong lead. We have developed a new class of ... ...

    Abstract In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provide a strong lead. We have developed a new class of tetravalent, biparatopic therapy, 89C8-ACE2. It combines the specificity of a monoclonal antibody (89C8) that recognizes the relatively conserved N-terminal domain of the viral Spike (S) glycoprotein, and the ectodomain of ACE2, which binds to the receptor-binding domain of S. This molecule shows exceptional performance
    Mesh-Begriff(e) Angiotensin-Converting Enzyme 2 ; Antibodies, Monoclonal/pharmacology ; Antibodies, Neutralizing/pharmacology ; Antibodies, Viral/pharmacology ; Betacoronavirus/drug effects ; COVID-19 ; Coronavirus Infections ; Drug Design ; Drug Discovery ; Humans ; Pandemics ; Peptidyl-Dipeptidase A/drug effects ; Pneumonia, Viral ; Recombinant Proteins ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus/drug effects
    Chemische Substanzen Antibodies, Monoclonal ; Antibodies, Neutralizing ; Antibodies, Viral ; Recombinant Proteins ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2 ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Schlagwörter covid19
    Sprache Englisch
    Erscheinungsdatum 2020-08-17
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2537838-7
    ISSN 1942-0870 ; 1942-0870
    ISSN (online) 1942-0870
    ISSN 1942-0870
    DOI 10.1080/19420862.2020.1804241
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: A novel biparatopic antibody-ACE2 fusion that blocks SARS-CoV-2 infection: implications for therapy

    Miao, Xiaoniu / Luo, Yi / Huang, Xi / Lee, Suki M. Y. / Yuan, Zhijun / Tang, Yongzhou / Chen, Liandi / Wang, Chao / Jiang, Wenchao / Gao, Wei / Song, Xuedong / Yan, Yao / Pang, Tuling / Zou, Yuefeng / Fu, Weihui / Wan, Liping / Gilbert-Jaramillo, Javier / Knight, Michael / Tan, Tiong Kit /
    Rijal, Pramila / Townsend, Alain / Sun, Joanne / Liu, Xiaolin / James, William / Tsun, Andy / Xu, Yingda

    bioRxiv

    Abstract: In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provides a strong lead. We have developed a new class of ... ...

    Abstract In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provides a strong lead. We have developed a new class of tetravalent, biparatopic therapy, 89C8-ACE2. It combines the specificity of a monoclonal antibody (89C8) that recognizes the relatively conserved N-terminal domain (NTD) of the viral S glycoprotein, and the ectodomain of ACE2, which binds to the receptor-binding domain (RBD) of S. This molecule shows exceptional performance in vitro, inhibiting the interaction of recombinant S1 to ACE2 and transduction of ACE2-overexpressing cells by S-pseudotyped lentivirus with IC50s substantially below 100 pM, and with potency approximately 100-fold greater than ACE2-Fc itself. Moreover, 89C8-ACE2 was able to neutralize authentic virus infection in a standard assay at low nanomolar concentrations, making this class of molecule a promising lead for therapeutic applications.
    Schlagwörter covid19
    Verlag BioRxiv; WHO
    Dokumenttyp Artikel ; Online
    DOI 10.1101/2020.06.14.147868
    Datenquelle COVID19

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  9. Artikel: A novel biparatopic hybrid antibody-ACE2 fusion that blocks SARS-CoV-2 infection: implications for therapy

    Miao, Xiaoniu / Luo, Yi / Huang, Xi / Lee, Suki M Y / Yuan, Zhijun / Tang, Yongzhou / Chen, Liandi / Wang, Chao / Wu, Fan / Xu, Yifeng / Jiang, Wenchao / Gao, Wei / Song, Xuedong / Yan, Yao / Pang, Tuling / Chen, Cheng / Zou, Yuefeng / Fu, Weihui / Wan, Liping /
    Gilbert-Jaramillo, Javier / Knight, Michael / Tan, Tiong Kit / Rijal, Pramila / Townsend, Alain / Sun, Joanne / Liu, Xiaolin / James, William / Tsun, Andy / Xu, Yingda

    MAbs

    Abstract: In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provide a strong lead. We have developed a new class of ... ...

    Abstract In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provide a strong lead. We have developed a new class of tetravalent, biparatopic therapy, 89C8-ACE2. It combines the specificity of a monoclonal antibody (89C8) that recognizes the relatively conserved N-terminal domain of the viral Spike (S) glycoprotein, and the ectodomain of ACE2, which binds to the receptor-binding domain of S. This molecule shows exceptional performance in vitro, inhibiting the interaction of recombinant S1 to ACE2 and transduction of ACE2-overexpressing cells by S-pseudotyped lentivirus with IC50s substantially below 100 pM, and with potency approximately 100-fold greater than ACE2-Fc itself. Moreover, 89C8-ACE2 was able to neutralize authentic viral infection in a standard 96-h co-incubation assay at low nanomolar concentrations, making this class of molecule a promising lead for therapeutic applications.
    Schlagwörter covid19
    Verlag WHO
    Dokumenttyp Artikel
    Anmerkung WHO #Covidence: #720912
    Datenquelle COVID19

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  10. Artikel ; Online: Toll-like receptor 10 is involved in induction of innate immune responses to influenza virus infection.

    Lee, Suki M Y / Kok, Kin-Hang / Jaume, Martial / Cheung, Timothy K W / Yip, Tsz-Fung / Lai, Jimmy C C / Guan, Yi / Webster, Robert G / Jin, Dong-Yan / Peiris, J S Malik

    Proceedings of the National Academy of Sciences of the United States of America

    2014  Band 111, Heft 10, Seite(n) 3793–3798

    Abstract: Toll-like receptors (TLRs) play key roles in innate immune recognition of pathogen-associated molecular patterns of invading microbes. Among the 10 TLR family members identified in humans, TLR10 remains an orphan receptor without known agonist or ... ...

    Abstract Toll-like receptors (TLRs) play key roles in innate immune recognition of pathogen-associated molecular patterns of invading microbes. Among the 10 TLR family members identified in humans, TLR10 remains an orphan receptor without known agonist or function. TLR10 is a pseudogene in mice and mouse models are noninformative in this regard. Using influenza virus infection in primary human peripheral blood monocyte-derived macrophages and a human monocytic cell line, we now provide previously unidentified evidence that TLR10 plays a role in innate immune responses following viral infection. Influenza virus infection increased TLR10 expression and TLR10 contributed to innate immune sensing of viral infection leading to cytokine induction, including proinflammatory cytokines and interferons. TLR10 induction is more pronounced following infection with highly pathogenic avian influenza H5N1 virus compared with a low pathogenic H1N1 virus. Induction of TLR10 by virus infection requires active virus replication and de novo protein synthesis. Culture supernatants of virus-infected cells modestly up-regulate TLR10 expression in nonvirus-infected cells. Signaling via TLR10 was activated by the functional RNA-protein complex of influenza virus leading to robust induction of cytokine expression. Taken together, our findings identify TLR10 as an important innate immune sensor of viral infection and its role in innate immune defense and immunopathology following viral and bacterial pathogens deserves attention.
    Mesh-Begriff(e) Animals ; Blotting, Western ; DNA Primers/genetics ; Dogs ; Enzyme-Linked Immunosorbent Assay ; Fluorescent Antibody Technique ; Humans ; Immunity, Innate/immunology ; Influenza A Virus, H1N1 Subtype/immunology ; Influenza A Virus, H5N1 Subtype/immunology ; Influenza, Human/immunology ; Macrophages ; Madin Darby Canine Kidney Cells ; Mice ; Organic Chemicals ; RNA, Small Interfering/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Toll-Like Receptor 10/immunology ; Toll-Like Receptor 10/metabolism
    Chemische Substanzen DNA Primers ; Organic Chemicals ; RNA, Small Interfering ; Toll-Like Receptor 10 ; SYBR Green I (163795-75-3)
    Sprache Englisch
    Erscheinungsdatum 2014-02-24
    Erscheinungsland United States
    Dokumenttyp Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1324266111
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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