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  1. Article ; Online: Obesity and its effects on the esophageal mucosal barrier.

    Paris, Shere / Ekeanyanwu, Rebecca / Jiang, Yuwei / Davis, Daniel / Spechler, Stuart Jon / Souza, Rhonda F

    American journal of physiology. Gastrointestinal and liver physiology

    2021  Volume 321, Issue 3, Page(s) G335–G343

    Abstract: Obesity is associated with gastroesophageal reflux disease (GERD) and its complications including reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma. Traditionally, these associations have been attributed to the mechanical effect of ... ...

    Abstract Obesity is associated with gastroesophageal reflux disease (GERD) and its complications including reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma. Traditionally, these associations have been attributed to the mechanical effect of abdominal fat in increasing intra-abdominal pressure, thereby promoting gastroesophageal reflux and causing disruption of antireflux mechanisms at the esophagogastric junction. However, recent studies suggest that visceral adipose tissue (VAT) produces numerous cytokines that can cause esophageal inflammation and impair esophageal mucosal barrier integrity through reflux-independent mechanisms that render the esophageal mucosa especially susceptible to GERD-induced injury. In this report, we review mechanisms of esophageal mucosal defense, the genesis and remodeling of visceral adipose tissue during obesity, and the potential role of substances produced by VAT, especially the VAT that encircles the esophagogastric junction, in the impairment of esophageal mucosal barrier integrity that leads to the development of GERD complications.
    MeSH term(s) Barrett Esophagus/metabolism ; Barrett Esophagus/pathology ; Esophageal Mucosa/metabolism ; Esophageal Mucosa/pathology ; Esophagitis, Peptic/metabolism ; Esophagitis, Peptic/pathology ; Esophagus/pathology ; Gastroesophageal Reflux/metabolism ; Gastroesophageal Reflux/pathology ; Humans ; Obesity/metabolism ; Obesity/pathology
    Language English
    Publishing date 2021-08-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 603840-2
    ISSN 1522-1547 ; 0193-1857
    ISSN (online) 1522-1547
    ISSN 0193-1857
    DOI 10.1152/ajpgi.00199.2021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.89: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Lower esophageal sphincter muscle of patients with achalasia exhibits profound mast cell degranulation.

    Nelson, Melissa / Zhang, Xi / Genta, Robert M / Turner, Kevin / Podgaetz, Eitan / Paris, Shere / Cardenas, Jacob / Gu, Jinghua / Leeds, Steven / Ward, Marc / Nguyen, Anh / Konda, Vani / Furuta, Glenn T / Pan, Zui / Souza, Rhonda F / Spechler, Stuart Jon

    Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society

    2020  Volume 33, Issue 5, Page(s) e14055

    Abstract: Background: Eosinophils and mast cells are key effectors of allergy. When they accumulate in the esophagus, their myoactive, pro-inflammatory, and cytotoxic products potentially could cause achalasia-like motility abnormalities and neuronal degeneration. ...

    Abstract Background: Eosinophils and mast cells are key effectors of allergy. When they accumulate in the esophagus, their myoactive, pro-inflammatory, and cytotoxic products potentially could cause achalasia-like motility abnormalities and neuronal degeneration. We hypothesized that there is an allergy-mediated form of achalasia.
    Methods: LES muscle samples obtained during Heller myotomy from patients with achalasia or EGJ outflow obstruction (EGJOO) and from organ donor controls were immunostained for tryptase. Eosinophil and mast cell density, and mast cell degranulation were assessed. LES muscle was evaluated by qPCR for genes mediating smooth muscle Ca
    Key results: There were 13 patients (7 men, median age 59; 10 achalasia, 3 EGJOO) and 7 controls (4 men, median age 42). Eosinophils were infrequent in LES muscle, but mast cells were plentiful. Patients and controls did not differ significantly in LES mast cell density. However, 12 of 13 patients exhibited profound LES mast cell degranulation involving perimysium and myenteric plexus nerves, while only mild degranulation was seen in 2 of 7 controls. Hierarchical clustering analysis of qPCR data revealed two "mototype" LES gene expression patterns, with all type II patients in one mototype, and type I and III patients in the other.
    Conclusions & inferences: LES muscle of patients with achalasia or EGJOO exhibits striking mast cell degranulation, and patients with different achalasia manometric phenotypes exhibit different LES patterns of expression for genes mediating Ca
    MeSH term(s) Adult ; Aged ; Case-Control Studies ; Cell Degranulation/immunology ; Cluster Analysis ; Eosinophils/immunology ; Eosinophils/pathology ; Esophageal Achalasia/immunology ; Esophageal Achalasia/pathology ; Esophageal Sphincter, Lower/immunology ; Esophageal Sphincter, Lower/metabolism ; Esophageal Sphincter, Lower/pathology ; Esophagogastric Junction/immunology ; Esophagogastric Junction/metabolism ; Esophagogastric Junction/pathology ; Female ; Gene Expression ; Humans ; Male ; Mast Cells/immunology ; Mast Cells/metabolism ; Mast Cells/pathology ; Middle Aged ; Myenteric Plexus/immunology ; Myenteric Plexus/pathology ; Young Adult
    Language English
    Publishing date 2020-12-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1186328-6
    ISSN 1365-2982 ; 1350-1925
    ISSN (online) 1365-2982
    ISSN 1350-1925
    DOI 10.1111/nmo.14055
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2979: 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 ; Online: NPM1 directs PIDDosome-dependent caspase-2 activation in the nucleolus.

    Ando, Kiyohiro / Parsons, Melissa J / Shah, Richa B / Charendoff, Chloé I / Paris, Sheré L / Liu, Peter H / Fassio, Sara R / Rohrman, Brittany A / Thompson, Ruth / Oberst, Andrew / Sidi, Samuel / Bouchier-Hayes, Lisa

    The Journal of cell biology

    2017  Volume 216, Issue 6, Page(s) 1795–1810

    Abstract: The PIDDosome (PIDD-RAIDD-caspase-2 complex) is considered to be the primary signaling platform for caspase-2 activation in response to genotoxic stress. Yet studies of PIDD-deficient mice show that caspase-2 activation can proceed in the absence of PIDD. ...

    Abstract The PIDDosome (PIDD-RAIDD-caspase-2 complex) is considered to be the primary signaling platform for caspase-2 activation in response to genotoxic stress. Yet studies of PIDD-deficient mice show that caspase-2 activation can proceed in the absence of PIDD. Here we show that DNA damage induces the assembly of at least two distinct activation platforms for caspase-2: a cytoplasmic platform that is RAIDD dependent but PIDD independent, and a nucleolar platform that requires both PIDD and RAIDD. Furthermore, the nucleolar phosphoprotein nucleophosmin (NPM1) acts as a scaffold for PIDD and is essential for PIDDosome assembly in the nucleolus after DNA damage. Inhibition of NPM1 impairs caspase-2 processing, apoptosis, and caspase-2-dependent inhibition of cell growth, demonstrating that the NPM1-dependent nucleolar PIDDosome is a key initiator of the caspase-2 activation cascade. Thus we have identified the nucleolus as a novel site for caspase-2 activation and function.
    MeSH term(s) Animals ; Apoptosis ; CRADD Signaling Adaptor Protein/metabolism ; Caspase 2/genetics ; Caspase 2/metabolism ; Cell Nucleolus/enzymology ; Cysteine Endopeptidases/genetics ; Cysteine Endopeptidases/metabolism ; DNA Damage ; Death Domain Receptor Signaling Adaptor Proteins/genetics ; Death Domain Receptor Signaling Adaptor Proteins/metabolism ; Enzyme Activation ; Genotype ; HEK293 Cells ; HeLa Cells ; Humans ; Mice, Knockout ; Microscopy, Confocal ; Microscopy, Fluorescence ; Microscopy, Video ; Multiprotein Complexes ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Phenotype ; Protein Binding ; RNA Interference ; Signal Transduction ; Transfection ; Zebrafish/genetics ; Zebrafish/metabolism ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
    Chemical Substances CRADD Signaling Adaptor Protein ; CRADD protein, human ; Death Domain Receptor Signaling Adaptor Proteins ; Multiprotein Complexes ; Nuclear Proteins ; PIDD1 protein, human ; Pidd1 protein, mouse ; Zebrafish Proteins ; nucleophosmin (117896-08-9) ; CASP2 protein, human (EC 3.4.22.-) ; Casp2 protein, mouse (EC 3.4.22.-) ; Caspase 2 (EC 3.4.22.-) ; Cysteine Endopeptidases (EC 3.4.22.-)
    Language English
    Publishing date 2017-04-21
    Publishing country United States
    Document type Journal Article ; Video-Audio Media
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.201608095
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ub I Zs.190: Show issues Location:
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