Publications by authors named "Daniel von der Beck"

Article Synopsis
  • Type II alveolar epithelial cells (AEC2s) are injured in idiopathic pulmonary fibrosis (IPF), but they play a role in lung epithelial regeneration, which is influenced by Notch signaling.
  • The study used various methods to analyze how Notch signaling affects AEC2 proliferation, differentiation, and the development of lung fibrosis, highlighting defects in surfactant protein processing due to loss of Napsin A.
  • Notch1 signaling was found to activate early in IPF and inhibits AEC2 differentiation while promoting proliferation and fibrosis; however, inhibiting Notch signaling can improve surfactant processing and reduce fibrosis.
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Background: The overall incidence of interstitial lung disease and disease-associated mortality have been found on the rise. Hospitalizations for interstitial lung disease are typically caused by airway infection or the acute exacerbation of the underlying disease. Seasonal variance in ambient air pollution has recently been linked to exacerbation and mortality.

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Background: The aim of this study was to analyze the relative frequency, clinical characteristics, disease onset and progression in f-IPF vs. sporadic IPF (s-IPF).

Methods: Familial IPF index patients and their family members were recruited into the European IPF registry/biobank (eurIPFreg) at the Universities of Giessen and Marburg (UGMLC).

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Background: In this study, we retrospectively assessed the relationships among physiologic measurements, survival, and quantitative high-resolution CT (HRCT) scanning indexes in patients with idiopathic pulmonary fibrosis (IPF).

Methods: Seventy patients (48 male; mean [SD] age, 66.4 [9.

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Rationale: From June of 2009 to August of 2010 the influenza subtype H1N1pdm09 caused a worldwide pandemic. The impact on populations and health care systems around the globe evolved differently. Substantial data come from the German national surveillance network in an outpatient and private practice setting, while information on hospitalized patients in Germany is rather limited.

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Background: Activation and differentiation of fibroblasts into contractile protein-expressing myofibroblasts and their acquired apoptosis-resistant phenotype are critical factors towards the development of idiopathic pulmonary fibrosis (IPF), a fatal disease characterised by distorted pulmonary structure and excessive extracellular matrix (ECM) deposition. The molecular mechanisms underlying these processes in IPF remain incompletely understood. We investigated the possible implication of aberrant overexpression and activity of histone deacetylases (HDACs) in IPF.

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Unlabelled: Among the idiopathic interstitial pneumonias (IIP), the two entities IPF and NSIP seem to be clinically related, but NSIP has a better outcome. The proteomic signatures which distinguish NSIP from IPF remain still elusive. We therefore performed comparative proteomic analysis of peripheral lung tissue from patients with sporadic IPF (n=14) and fibrotic NSIP (fNSIP, n=8) and organ donors (Controls, n=10), by using the 2-dimensional DIGE technique and MALDI-TOF-MS.

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Idiopathic pulmonary fibrosis (IPF) is a life-threatening condition, with a median survival of <3 yrs. The pathophysiology is not fully understood, but chronic injury of alveolar epithelial type II cells (AECII) is considered key. In IPF, disturbed folding and processing of surfactant proteins and impaired DNA repair may represent underlying reasons for maladaptive endoplasmic reticulum stress responses, increased reactive oxygen species production and/or DNA damage.

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