6 results on '"Günther, Andreas"'
Search Results
2. Interstitial Lung Disease: Seasonality of Hospitalizations and In-Hospital Mortality 2005–2015.
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von der Beck, Daniel, Grimminger, Friedrich, Seeger, Werner, Günther, Andreas, and Löh, Benjamin
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AIR pollution , *DATABASES , *CONFIDENCE intervals , *INTERSTITIAL lung diseases , *HOSPITAL mortality , *SEASONS , *ARTIFICIAL respiration , *HOSPITAL care , *TIME series analysis , *DESCRIPTIVE statistics , *DATA analysis software , *ODDS ratio , *PULMONARY fibrosis , *COMORBIDITY - Abstract
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. We sought to examine the seasonal pattern of hospitalizations in Germany, use of mechanical ventilation, and in-hospital mortality on a year-by-year basis to identify their overall trend and to characterize seasonal patterns. Methods: The national in-patient database of the federal statistical office of Germany was searched for cases of interstitial lung disease. Results: A total of 130,366 hospitalizations for ILD occurred from 2005 to 2015. Time series data were examined for seasonality using X-11 statistics. The incidence of hospitalizations, mechanical ventilation, and in-hospital mortality show clear seasonal peaks in the cold season. The observed seasonality cannot be attributed to the variance of selected comorbidities. Also, there is a significant overall upward trend regarding hospitalization counts, especially in the use of non-invasive ventilation. Conclusion: Time series analysis of in-hospital data shows an ILD-related rise of hospitalizations, in-hospital mortality, and non-invasive ventilation. This emphasizes a growing importance of interstitial lung diseases for health-care systems. Strong seasonality is seen in these variables. Data therefore support previous studies of ILD exacerbation. More research on infectious causes and environmental factors is warranted. [ABSTRACT FROM AUTHOR]
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- 2022
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3. WNT1-inducible signaling protein-1 mediates pulmonary fibrosis in mice and is upregulated in humans with idiopathic pulmonary fibrosis.
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Königshoff, Melanie, Kramer, Monika, Balsara, Nisha, Wilhelm, Jochen, Amarie, Oana Veronica, Jahn, Andreas, Rose, Frank, Fink, Ludger, Seeger, Werner, Schaefer, Liliana, Günther, Andreas, Eickelberg, Oliver, Königshoff, Melanie, and Günther, Andreas
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PULMONARY fibrosis , *LABORATORY mice , *CELL proliferation , *GENE expression , *COLLAGEN , *HYPERPLASIA , *ANIMAL experimentation , *BIOCHEMISTRY , *BIOLOGICAL models , *BLEOMYCIN , *CELL physiology , *COMPARATIVE studies , *CYTOSKELETAL proteins , *EPITHELIAL cells , *GLYCOPROTEINS , *PHENOMENOLOGY , *RESEARCH methodology , *MEDICAL cooperation , *MICE , *PROTEINS , *PULMONARY alveoli , *RECOMBINANT proteins , *RESEARCH , *EVALUATION research , *CCN intercellular signaling proteins , *IDIOPATHIC pulmonary fibrosis , *SIGNAL peptides - Abstract
Idiopathic pulmonary fibrosis (IPF) is characterized by distorted lung architecture and loss of respiratory function. Enhanced (myo)fibroblast activation, ECM deposition, and alveolar epithelial type II (ATII) cell dysfunction contribute to IPF pathogenesis. However, the molecular pathways linking ATII cell dysfunction with the development of fibrosis are poorly understood. Here, we demonstrate, in a mouse model of pulmonary fibrosis, increased proliferation and altered expression of components of the WNT/beta-catenin signaling pathway in ATII cells. Further analysis revealed that expression of WNT1-inducible signaling protein-1 (WISP1), which is encoded by a WNT target gene, was increased in ATII cells in both a mouse model of pulmonary fibrosis and patients with IPF. Treatment of mouse primary ATII cells with recombinant WISP1 led to increased proliferation and epithelial-mesenchymal transition (EMT), while treatment of mouse and human lung fibroblasts with recombinant WISP1 enhanced deposition of ECM components. In the mouse model of pulmonary fibrosis, neutralizing mAbs specific for WISP1 reduced the expression of genes characteristic of fibrosis and reversed the expression of genes associated with EMT. More importantly, these changes in gene expression were associated with marked attenuation of lung fibrosis, including decreased collagen deposition and improved lung function and survival. Our study thus identifies WISP1 as a key regulator of ATII cell hyperplasia and plasticity as well as a potential therapeutic target for attenuation of pulmonary fibrosis. [ABSTRACT FROM AUTHOR]
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- 2009
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4. Linking progression of fibrotic lung remodeling and ultrastructural alterations of alveolar epithelial type II cells in the amiodarone mouse model.
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Birkelbach, Bastian, Lutz, Dennis, Ruppert, Clemens, Henneke, Ingrid, Lopez-Rodriguez, Elena, Günther, Andreas, Ochs, Matthias, Mahavadi, Poornima, and Knudsen, Lars
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PULMONARY fibrosis , *TISSUE remodeling , *EPITHELIAL cells , *AMIODARONE , *LABORATORY mice , *HYPERTROPHY - Abstract
Chronic injury of alveolar epithelial type II cells (AE2 cells) represents a key event in the development of lung fibrosis in animal models and in humans, such as idiopathic pulmonary fibrosis (IPF). Intratracheal delivery of amiodarone to mice results in a profound injury and macroautophagydependent apoptosis of AE2 cells. Increased autophagy manifested in AE2 cells by disturbances of the intracellular surfactant. Hence, we hypothesized that ultrastructural alterations of the intracellular surfactant pool are signs of epithelial stress correlating with the severity of fibrotic remodeling. With the use of design-based stereology, the amiodarone model of pulmonary fibrosis in mice was characterized at the light and ultrastructural level during progression. Mean volume of AE2 cells, volume of lamellar bodies per AE2 cell, and mean size of lamellar bodies were correlated to structural parameters reflecting severity of fibrosis like collagen content. Within 2 wk amiodarone leads to an increase in septal wall thickness and a decrease in alveolar numbers due to irreversible alveolar collapse associated with alveolar surfactant dysfunction. Progressive hypertrophy of AE2 cells and increase in mean individual size and total volume of lamellar bodies per AE2 cell were observed. A high positive correlation of these AE2 cell-related ultrastructural changes and the deposition of collagen fibrils within septal walls were established. Qualitatively, similar alterations could be found in IPF samples with mild to moderate fibrosis. We conclude that ultrastructural alterations of AE2 cells including the surfactant system are tightly correlated with the progression of fibrotic remodeling. [ABSTRACT FROM AUTHOR]
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- 2015
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5. Potential Applications of Flat-Panel Volumetric CT in Morphologic and Functional Small Animal Imaging.
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Greschus, Susanne, Kiessling, Fabian, Lichy, Matthias P., Moll, Jens, Mueller, Margareta M., Savai, Rajkumar, Rose, Frank, Ruppert, Clemens, Günther, Andreas, Luecke, Marcus, Fusenig, Norbert E., Semmler, Wolfhard, and Traupe, Horst
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DIAGNOSTIC imaging , *LUNG cancer , *TOMOGRAPHY , *PULMONARY fibrosis , *PERFUSION , *NONINVASIVE diagnostic tests - Abstract
Noninvasive radiologic imaging has recently gained considerable interest in basic and preclinical research for monitoring disease progression and therapeutic efficacy. In this report, we introduce flat-panel volumetric computed tomography (fpVCT) as a powerful new tool for noninvasive imaging of different organ systems in preclinical research. The three-dimensional visualization that is achieved by isotropic high-resolution datasets is illustrated for the skeleton, chest, abdominal organs, and brain of mice. The high image quality of chest scans enables the visualization of small lung nodules in an orthotopic lung cancer model and the reliable imaging of therapy side effects such as lung fibrosis. Using contrast-enhanced scans, fpVCT displayed the vascular trees of the brain, liver, and kidney down to the subsegmental level. Functional application of fpVCT in dynamic contrast-enhanced scans of the rat brain delivered physiologically reliable data of perfusion and tissue blood volume. Beyond scanning of small animal models as demonstrated here, fpVCT provides the ability to image animals up to the size of primates. [ABSTRACT FROM AUTHOR]
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- 2005
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6. Changes in pulmonary surfactant function and composition in bleomycin-induced pneumonitis and fibrosis
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Schmidt, Reinhold, Ruppert, Clemens, Markart, Philipp, Lübke, Norbert, Ermert, Leander, Weissmann, Norbert, Breithecker, Andreas, Ermert, Monika, Seeger, Werner, and Günther, Andreas
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BLEOMYCIN , *SURFACE active agents , *PNEUMONIA , *PULMONARY fibrosis - Abstract
Bleomycin is a widely accepted cancer drug but may induce life-threatening interstitial lung disease in a subset of patients. We evaluated the effect of bleomycin administration on pulmonary surfactant function and composition in rabbit lungs. In order to obtain a uniform response to bleomycin, aerosol technology was employed for bronchoalveolar delivery of 1.8 U/kg b.w. bleomycin. On days 4, 8, 16, 24, 32, and 64 after challenge, bronchoalveolar lavages were performed. Sham-aerosolized rabbits served as controls. In the early acute respiratory distress syndrome (ARDS)-like post-bleomycin period (4–16 days), marked loss of surface activity of the large surfactant aggregate (LA) fraction of surfactant was noted. In parallel, reduced percentages of LA, but only minor changes in surfactant apoproteins (SP)-A, SP-B, and SP-C, were encountered. Analysis of the surfactant lipid profile showed impressively enhanced cholesterol and significantly decreased phosphatidylglycerol (PG) levels. The relative content of dipalmitoyl-PC (DPPC) was slightly increased, and a several-fold increase within the 1-O-alkyl-2-acyl subclass of PC was observed. During the prolonged fibroproliferative period, a highly significant downregulation of SP-B and SP-C levels was observed. This was paralleled by an upregulation of the total extracellular phospholipid pool, with a far-reaching normalization of the (phospho)-lipid profile. The biophysical surfactant function never fully normalized within the 64-day observation period. In conclusion, bleomycin caused marked abnormalities of pulmonary surfactant, with the profile of changes being different between the early ARDS and the late fibrotic phase. [Copyright &y& Elsevier]
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- 2004
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