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  1. Article ; Online: Gastric acid hypersecretory states: recent insights and advances.

    Osefo, Nauramy / Ito, Tetsuhide / Jensen, Robert T

    Current gastroenterology reports

    2009  Volume 11, Issue 6, Page(s) 433–441

    Abstract: Gastric acid hypersecretory states are characterized by basal hypersecretion of gastric acid and historically include disorders associated with hypergastrinemia, hyperhistaminemia, and those of unknown etiology. Although gastric acid secretion is ... ...

    Abstract Gastric acid hypersecretory states are characterized by basal hypersecretion of gastric acid and historically include disorders associated with hypergastrinemia, hyperhistaminemia, and those of unknown etiology. Although gastric acid secretion is infrequently measured, it is important to recognize the role of gastric hypersecretion in the symptoms of these disorders because they share several features of pathogenesis and treatment. In this article, recent important articles reporting insights into their diagnosis, pathogenesis, and treatment are reviewed. Particular attention is paid to Zollinger-Ellison syndrome, because it has the most extreme acid hypersecretion of this group of disorders and because numerous recent articles deal with various aspects of the diagnosis, molecular pathogenesis, and treatment of the gastrinoma itself or the acid hypersecretion. Two new hypersecretory disorders are reviewed: rebound acid hypersecretion after the use of proton pump inhibitors and acid hypersecretion with cysteamine treatment in children with cystinosis.
    MeSH term(s) Cystamine/adverse effects ; Cystamine/therapeutic use ; Cystinosis/drug therapy ; Enzyme Inhibitors/adverse effects ; Enzyme Inhibitors/therapeutic use ; Gastric Acid/metabolism ; Gastrins/metabolism ; Histamine/metabolism ; Humans ; Proton Pump Inhibitors/adverse effects ; Stomach Diseases/chemically induced ; Stomach Diseases/diagnosis ; Stomach Diseases/physiopathology ; Stomach Diseases/therapy ; Zollinger-Ellison Syndrome/physiopathology
    Chemical Substances Enzyme Inhibitors ; Gastrins ; Proton Pump Inhibitors ; Histamine (820484N8I3) ; Cystamine (R110LV8L02)
    Language English
    Publishing date 2009-11-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Review
    ZDB-ID 2041376-2
    ISSN 1534-312X ; 1522-8037
    ISSN (online) 1534-312X
    ISSN 1522-8037
    DOI 10.1007/s11894-009-0067-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5751: 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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  2. Article ; Online: Pituitary adenylate cyclase-activating polypeptide causes tyrosine phosphorylation of the epidermal growth factor receptor in lung cancer cells.

    Moody, Terry W / Osefo, Nauramy / Nuche-Berenguer, Bernardo / Ridnour, Lisa / Wink, David / Jensen, Robert T

    The Journal of pharmacology and experimental therapeutics

    2012  Volume 341, Issue 3, Page(s) 873–881

    Abstract: Pituitary adenylate cyclase-activating polypeptide (PACAP) is an autocrine growth factor for some lung cancer cells. The activated PACAP receptor (PAC1) causes phosphatidylinositol turnover, elevates cAMP, and increases the proliferation of lung cancer ... ...

    Abstract Pituitary adenylate cyclase-activating polypeptide (PACAP) is an autocrine growth factor for some lung cancer cells. The activated PACAP receptor (PAC1) causes phosphatidylinositol turnover, elevates cAMP, and increases the proliferation of lung cancer cells. PAC1 and epidermal growth factor receptor (EGFR) are present in non-small-cell lung cancer (NSCLC) cells, and the growth of NSCLC cells is inhibited by the PAC1 antagonist PACAP(6-38) and the EGFR tyrosine kinase inhibitor gefitinib. Here, the ability of PACAP to transactivate the EGFR was investigated. Western blot analysis indicated that the addition of PACAP but not the structurally related vasoactive intestinal peptide increased EGFR tyrosine phosphorylation in NCI-H838 or H345 cells. PACAP-27, in a concentration-dependent manner, increased EGFR transactivation 4-fold 2 min after addition to NCI-H838 cells. The ability of 100 nM PACAP-27 to increase EGFR or extracellular signal-regulated kinase tyrosine phosphorylation in NCI-H838 cells was inhibited by PACAP(6-38), gefitinib, 4-amino-5-(4-chlorophenyl)-7-(dimethylethyl)pyrazolo[3,4-d]pyrimidine (PP2; Src inhibitor), (R)-N4-hydroxy-N1-[(S)-2-(1H-indol-3-yl)-1-methylcarbamoyl-ethyl]-2-isobutyl-succinamide (GM6001; matrix metalloprotease inhibitor), or antibody to transforming growth factor α (TGFα). By enzyme-linked immunosorbent assay, PACAP addition to NCI-H838 cells increased TGFα secretion into conditioned media. EGFR transactivation caused by the addition of PACAP to NCI-H838 cells was inhibited by N-acetyl-cysteine (antioxidant), tiron (superoxide scavenger), diphenylene iodonium (NADPH oxidase inhibitor), or 1-[6-[[(17β)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U73122; phospholipase C inhibitor), but not N-[2-[[3-(4-bromophenyl)-2-propenyl]amino]ethyl]-5-isoquinolinesulfonamide (H89; protein kinase A inhibitor). PACAP addition to NCI-H838 cells significantly increased reactive oxygen species, and the increase was inhibited by tiron. The results indicate that PACAP causes transactivation of the EGFR in NSCLC cells in an oxygen-dependent manner that involves phospholipase C but not protein kinase A.
    MeSH term(s) Blotting, Western ; Enzyme-Linked Immunosorbent Assay ; ErbB Receptors/metabolism ; Humans ; Lung Neoplasms/metabolism ; Phosphorylation ; Pituitary Adenylate Cyclase-Activating Polypeptide/pharmacology ; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide/metabolism ; Tumor Cells, Cultured/metabolism ; Tyrosine/metabolism
    Chemical Substances Pituitary Adenylate Cyclase-Activating Polypeptide ; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide ; Tyrosine (42HK56048U) ; ErbB Receptors (EC 2.7.10.1)
    Language English
    Publishing date 2012-03-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 3106-9
    ISSN 1521-0103 ; 0022-3565
    ISSN (online) 1521-0103
    ISSN 0022-3565
    DOI 10.1124/jpet.111.190033
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uf I Zs.40: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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