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Peter König

Bio: Peter König is an academic researcher from University of Lübeck. The author has contributed to research in topics: T cell & Optical coherence tomography. The author has an hindex of 29, co-authored 73 publications receiving 2445 citations. Previous affiliations of Peter König include University of Osnabrück & University of Hamburg.


Papers
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Journal ArticleDOI
TL;DR: An important role for NOX4 in the vascular remodeling associated with development of pulmonary hypertension is supported by results supported by screening lung tissue for the expression of NADPH oxidase subunits.
Abstract: Nonphagocytic NADPH oxidases have recently been suggested to play a major role in the regulation of physiological and pathophysiological processes, in particular, hypertrophy, remodeling, and angiogenesis in the systemic circulation. Moreover, NADPH oxidases have been suggested to serve as oxygen sensors in the lung. Chronic hypoxia induces vascular remodeling with medial hypertrophy leading to the development of pulmonary hypertension. We screened lung tissue for the expression of NADPH oxidase subunits. NOX1, NOXA1, NOXO1, p22phox, p47phox, p40phox, p67phox, NOX2, and NOX4 were present in mouse lung tissue. Comparing mice maintained for 21 days under hypoxic (10% O 2 ) or normoxic (21% O 2 ) conditions, an upregulation exclusively of NOX4 mRNA was observed under hypoxia in homogenized lung tissue, concomitant with increased levels in microdissected pulmonary arterial vessels. In situ hybridization and immunohistological staining for NOX4 in mouse lungs revealed a localization of NOX4 mRNA and protein predominantly in the media of small pulmonary arteries, with increased labeling intensities after chronic exposure to hypoxia. In isolated pulmonary arterial smooth muscle cells (PASMCs), NOX4 was localized primarily to the perinuclear space and its expression levels were increased after exposure to hypoxia. Treatment of PASMCs with siRNA directed against NOX4 decreased NOX4 mRNA levels and reduced PASMC proliferation as well as generation of reactive oxygen species. In lungs from patients with idiopathic pulmonary arterial hypertension (IPAH), expression levels of NOX4, which was localized in the vessel media, were 2.5-fold upregulated. These results support an important role for NOX4 in the vascular remodeling associated with development of pulmonary hypertension.

314 citations

Journal ArticleDOI
TL;DR: TRPM5 is considered to be an intrinsic signaling component of mammalian chemosensory organs, and its expression in rat and mouse tissues is investigated to provide evidence for brush cells being an important cellular correlate in the periphery.
Abstract: A growing number of TRP channels have been identified as key players in the sensation of smell, temperature, mechanical forces and taste. TRPM5 is known to be abundantly expressed in taste receptor cells where it participates in sweet, amino acid and bitter perception. A role of TRPM5 in other sensory systems, however, has not been studied so far. Here, we systematically investigated the expression of TRPM5 in rat and mouse tissues. Apart from taste buds, where we found TRPM5 to be predominantly localized on the basolateral surface of taste receptor cells, TRPM5 immunoreactivity was seen in other chemosensory organs – the main olfactory epithelium and the vomeronasal organ. Most strikingly, we found solitary TRPM5-enriched epithelial cells in all parts of the respiratory and gastrointestinal tract. Based on their tissue distribution, the low cell density, morphological features and co-immunostaining with different epithelial markers, we identified these cells as brush cells (also known as tuft, fibrillovesicular, multivesicular or caveolated cells). In terms of morphological characteristics, brush cells resemble taste receptor cells, while their origin and biological role are still under intensive debate. We consider TRPM5 to be an intrinsic signaling component of mammalian chemosensory organs, and provide evidence for brush cells being an important cellular correlate in the periphery.

195 citations

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TL;DR: Prepubescent children treated with fluticasone propionate 50 microg and 100 microg administered twice daily for 1 year grew at rates similar to placebo-treated control subjects and at rates equal to expected growth velocity for age.

174 citations

Journal ArticleDOI
TL;DR: The early embryo is able to induce the formation of secretory cells, modify vascularization, and downregulate speed of transport, thus creating the prerequisite for the first embryo-maternal communication in the oviduct.
Abstract: Using a digital videomicroscopic analysis system in the bovine, we showed that the mechanisms of transport caused by ciliary beating are distinctly different in ampulla and isthmus of the oviduct. The average particle transport speed (PTS) in the oviduct (mean, 133 μm/sec) does not differ in the cycle (metestrus) and during pregnancy after implantation, but it is locally modulated at the site of the embryo. Using videomicroscopy, we were able to document that after entering the ampulla, the cumulus-oocyte complex (COC) is not transported by ciliary beating down the oviduct, but firmly attaches to the ampullar epithelium. This attachment is mediated by the cumulus cells. However, when a COC is degenerated, it is floating in the oviductal lumen. As soon as a vital COC is in the ampulla, the sperm bound in the sperm reservoir of the ampullar isthmic junction leave the reservoir and hurry to the oocyte. When a sperm has penetrated the zona pellucida, the COC detaches and continues its migration. Quantitative measurements showed that the early embryo is able to locally downregulate PTS during its migration down the oviduct. It locally changes the pattern of vascularization and induces the formation of secretory cells. Our studies imply that the oviductal epithelium is able to select vital oocytes. The early embryo is able to induce the formation of secretory cells, modify vascularization, and downregulate speed of transport, thus creating the prerequisite for the first embryo-maternal communication in the oviduct.

134 citations

Journal ArticleDOI
TL;DR: Peyton A. Eggleston, M.D., Richard R. Rosenthal, and Joseph J. Trautlein are the co-chairs of the Study Group on Exercise Challenge, Bronchoprovocation Committee.
Abstract: Peyton A. Eggleston, M.D., Richard R. Rosenthal, M.D., Chairmen, Sandra A. Anderson, Ph.D., Ross Anderton, M.D., C. Warren Bierman, M.D., Eugene R. Bleecker, M.D., Hyman Chai, M.D., Gerd J. A. Cropp, M.D., Ph.D., Jerry D. Johnson, Ph.D., Peter Konig, M.D., John Morse, M.D., Laurie J. Smith, M.D., Richard J. Summers, M.D., and Joseph J. Trautlein, M.D. Study Group on Exercise Challenge, Bronchoprovocation Committee. American Academy of Allergy

131 citations


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TL;DR: The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.
Abstract: Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.

2,813 citations

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TL;DR: This study presents a meta-analysis of the Methacholine Challenge Pretest Questionnaire results to assess the response of the participants and recommend further studies to investigate its application in clinical practice.
Abstract: I. Purpose and Scope II. Methacholine Challenge Testing A. Indications B. Contraindications C. Technician Training/Qualifications D. Safety E. Patient Preparation F. Choice and Preparation of Methacholine G. Dosing Protocols 1. Two-Minute Tidal Breathing Dosing Protocol 2. Five-Breath Dosimeter Protocol H. Nebulizers and Dosimeters I. Spirometry and Other End-point Measures J. Data Presentation K. Interpretation III. Exercise Challenge A. Indications B. Contraindications and Patient Preparation C. Exercise Challenge Testing D. Assessing the Response References Appendix A: Sample Methacholine Challenge Test Consent Form Appendix B: Sample Methacholine Challenge Pretest Questionnaire Appendix C: Sample Report Format Appendix D: Equipment Sources

2,395 citations