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  1. Article: Evaluating tofacitinib citrate in the treatment of moderate-to-severe active ulcerative colitis: design, development and positioning of therapy.

    Tran, Vivy / Shammas, Rania M / Sauk, Jenny S / Padua, David

    Clinical and experimental gastroenterology

    2019  Volume 12, Page(s) 179–191

    Abstract: The etiology of ulcerative colitis (UC) is complex and involves a host of genetic, epigenetic and environmental factors. Over the last thirty years, signaling pathways like the Janus kinase (JAK) signaling pathway have been implicated in its pathogenesis. ...

    Abstract The etiology of ulcerative colitis (UC) is complex and involves a host of genetic, epigenetic and environmental factors. Over the last thirty years, signaling pathways like the Janus kinase (JAK) signaling pathway have been implicated in its pathogenesis. Pharmacologic blockade of this pathway is available through several small molecule inhibitors, including tofacitinib. Tofacitinib is an orally administered pan-JAK inhibitor that was first approved by the Food and Drug Administration (FDA) for use in rheumatologic disorders such as rheumatoid arthritis and psoriatic arthritis. The FDA approved its use in moderate-to-severe active ulcerative colitis in 2018. The aim of this review will be to discuss the role of tofacitinib in ulcerative colitis. We will discuss the role of JAK-STAT signaling, clinical data available for tofacitinib, and the safety profile for this therapy. Tofacitinib's place in the UC management algorithm is currently being debated. This effective oral therapy is poised to be a mainstay of UC therapeutics. This review will highlight the key clinical features and detail the UC experience to date.
    Language English
    Publishing date 2019-05-02
    Publishing country New Zealand
    Document type Journal Article ; Review
    ZDB-ID 2520690-4
    ISSN 1178-7023
    ISSN 1178-7023
    DOI 10.2147/CEG.S150908
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Remission in rheumatoid arthritis.

    Shammas, Rania M / Ranganath, Veena K / Paulus, Harold E

    Current rheumatology reports

    2010  Volume 12, Issue 5, Page(s) 355–362

    Abstract: With advancing therapeutic options, achieving a state of remission has become the treatment goal in rheumatoid arthritis. Agreeing on what constitutes remission and what measures should be used to assess disease activity has remained a challenge. ... ...

    Abstract With advancing therapeutic options, achieving a state of remission has become the treatment goal in rheumatoid arthritis. Agreeing on what constitutes remission and what measures should be used to assess disease activity has remained a challenge. Multiple remission criteria have been devised and modified, all with different strengths and limitations. A consensus definition of remission will need to be achieved if we are to be able to evaluate outcomes of clinical trials and establish treatment targets for practice. Remission defined as the complete absence of disease currently may not be a realistic therapeutic goal.
    MeSH term(s) Arthritis, Rheumatoid/physiopathology ; Arthritis, Rheumatoid/therapy ; Humans ; Remission Induction ; Terminology as Topic
    Language English
    Publishing date 2010-08-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2057357-1
    ISSN 1534-6307 ; 1523-3774
    ISSN (online) 1534-6307
    ISSN 1523-3774
    DOI 10.1007/s11926-010-0121-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5531: 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)

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  3. Article: Cardiomyocytes undergo apoptosis in human immunodeficiency virus cardiomyopathy through mitochondrion- and death receptor-controlled pathways.

    Twu, Cheryl / Liu, Nancy Q / Popik, Waldemar / Bukrinsky, Michael / Sayre, James / Roberts, Jaclyn / Rania, Shammas / Bramhandam, Vishnu / Roos, Kenneth P / MacLellan, W Robb / Fiala, Milan

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

    2002  Volume 99, Issue 22, Page(s) 14386–14391

    Abstract: We investigated 18 AIDS hearts (5 with and 13 without cardiomyopathy) by using immunocytochemistry and computerized image analysis regarding the roles of HIV-1 proteins and tumor necrosis factor ligands in HIV cardiomyopathy (HIVCM). HIVCM and ... ...

    Abstract We investigated 18 AIDS hearts (5 with and 13 without cardiomyopathy) by using immunocytochemistry and computerized image analysis regarding the roles of HIV-1 proteins and tumor necrosis factor ligands in HIV cardiomyopathy (HIVCM). HIVCM and cardiomyocyte apoptosis were significantly related to each other and to the expression by inflammatory cells of gp120 and tumor necrosis factor-alpha. In HIVCM heart, active caspase 9, a component of the mitochondrion-controlled apoptotic pathway, and the elements of the death receptor-mediated pathway, tumor necrosis factor-alpha and Fas ligand, were expressed strongly on macrophages and weakly on cardiomyocytes. HIVCM showed significantly greater macrophage infiltration and cardiomyocyte apoptosis rate compared with non-HIVCM. HIV-1 entered cultured neonatal rat ventricular myocytes by macropinocytosis but did not replicate. HIV-1- or gp120-induced apoptosis of rat myocytes through a mitochondrion-controlled pathway, which was inhibited by heparin, AOP-RANTES, or pertussis toxin, suggesting that cardiomyocyte apoptosis is induced by signaling through chemokine receptors. In conclusion, in patients with HIVCM, cardiomyocytes die through both mitochondrion- and death receptor-controlled apoptotic pathways.
    MeSH term(s) Acquired Immunodeficiency Syndrome/complications ; Acquired Immunodeficiency Syndrome/metabolism ; Acquired Immunodeficiency Syndrome/pathology ; Animals ; Apoptosis ; Cardiomyopathies/complications ; Cardiomyopathies/metabolism ; Cardiomyopathies/pathology ; Cells, Cultured ; Chemokine CCL5/analogs & derivatives ; Chemokine CCL5/metabolism ; Cholesterol/metabolism ; Fas Ligand Protein ; G(M1) Ganglioside/metabolism ; HIV Envelope Protein gp120/metabolism ; HIV-1/metabolism ; Heparin/metabolism ; Humans ; Macrophages ; Membrane Glycoproteins/metabolism ; Mitochondria/metabolism ; Myocardium/cytology ; Pinocytosis ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Chemokine CCL5 ; FASLG protein, human ; Fas Ligand Protein ; Faslg protein, rat ; HIV Envelope Protein gp120 ; Membrane Glycoproteins ; Tumor Necrosis Factor-alpha ; aminooxypentane-RANTES ; G(M1) Ganglioside (37758-47-7) ; Heparin (9005-49-6) ; Cholesterol (97C5T2UQ7J)
    Keywords covid19
    Language English
    Publishing date 2002-10-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.212327899
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

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