Publications by authors named "Philipp Rath"

There is currently much interest in understanding the mechanisms of normal and aberrant lung alveolarization, particularly in the context of bronchopulmonary dysplasia, a common complication of preterm birth where alveolarization is impeded. To this end, the parenteral administration of pharmacological agents that modulate biochemical pathways, or facilitate modulation of gene expression in transgenic animals, has facilitated the discovery and validation of mechanisms that direct lung development. Such studies include control interventions, where the solvent vehicle, perhaps containing an inactive form of the agent applied, is administered; thereby providing a well-controlled point of reference for the analysis of the partner experiment.

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The quantitative assessment of the lung architecture forms the foundation of many studies on lung development and lung diseases, where parameters such as alveoli number, alveolar size, and septal thickness are quantitatively influenced by developmental or pathological processes. Given the pressing need for robust data that describe the lung structure, there is currently much enthusiasm for the development and refinement of methodological approaches for the unbiased assessment of lung structure with improved precision. The advent of stereological methods highlights one such approach.

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Article Synopsis
  • Postnatal lung maturation leads to the formation of numerous small alveoli and thinner septal walls, which increases gas exchange efficiency.
  • Disorders like bronchopulmonary dysplasia (BPD) disrupt this process, resulting in larger alveoli and thicker walls, hindering effective gas exchange.
  • A study observed the changes in lung structure of C57BL/6J mice over 22 months, finding peaks and declines in alveolar density, progressive thinning of septal walls, and notable sex differences in alveoli numbers related to lung volume.
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Background: Caffeine is widely used to manage apnea of prematurity, and reduces the incidence of bronchopulmonary dysplasia (BPD). Deregulated transforming growth factor (TGF)-β signaling underlies arrested postnatal lung maturation in BPD. It is unclear whether caffeine impacts TGF-β signaling or postnatal lung development in affected lungs.

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