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Deletion of phosphodiesterase 4D in mice shortens alpha(2)-adrenoceptor-mediated anesthesia, a behavioral correlate of emesis.
Findings strongly support the hypothesis that inhibition of PDE4D is pivotal to the anesthesia-reversing effect of PMNPQ and is likely responsible for emesis induced by PDE 4 inhibitors. Expand
Human airway smooth muscle cells express and release RANTES in response to T helper 1 cytokines: regulation by T helper 2 cytokines and corticosteroids.
Airway smooth muscle cells have synthetic and secretory potential with the release of RANTES, and may participate in chronic airway inflammation by interacting with both Th1- and Th2-derived cytokines to modulate chemoattractant activity for eosinophils, activated T lymphocytes, and monocytes/macrophages. Expand
PDE4 inhibitors induce emesis in ferrets via a noradrenergic pathway
The studies suggest that the ferret is an appropriate model to study emesis induced by PDE4 inhibitors and that these compounds trigger the emetic reflex via a noradrenergic pathway, mimicking the pharmacological actions of a pre-synaptic alpha(2)-adrenoceptor inhibition. Expand
Assessing the emetic potential of PDE4 inhibitors in rats
This model is functionally coupled to PDE4, specific to alpha2‐adrenoceptors and relevant to Pde4 inhibitor‐induced emesis and provides a novel way of evaluating the emetic potential of PDE 4 inhibitors in rats. Expand
Inhaled corticosteroids increase interleukin-10 but reduce macrophage inflammatory protein-1alpha, granulocyte-macrophage colony-stimulating factor, and interferon-gamma release from alveolar
In comparison to alveolar macrophages from normal nonasthmatic volunteers, those from asthmatic patients released more MIP-1alpha, IFN-gamma, and GM-CSF but lower amounts of IL-10 particularly at baseline and after IL-1beta stimulation. Expand
IL-9 governs allergen-induced mast cell numbers in the lung and chronic remodeling of the airways.
The data suggest an important role for an IL-9-MC axis in the pathology associated with chronic asthma and demonstrate that an impact on this axis could lead to a reduction in chronic inflammation and improved lung function in patients with asthma. Expand
SARS-CoV-2 infection of hACE2 transgenic mice causes severe lung inflammation and impaired function
The transgenic mice expressing the human angiotensin I-converting enzyme 2 (ACE2) receptor driven by the cytokeratin-18 (K18) gene promoter are evaluated as a model of SARS-CoV-2 infection to define the basis of lung disease and test immune and antiviral-based countermeasures. Expand
Publisher Correction: SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
Emesis induced by inhibitors of type IV cyclic nucleotide phosphodiesterase (PDE IV) in the ferret
The results suggest that the PDE IV inhibitors studied are mixed peripheral-central emetogens, and whether emesis is mediated via a specific isoform of PDEIV remains to be established. Expand
Forced expiration measurements in mouse models of obstructive and restrictive lung diseases
Respiratory mechanics parameters (airway resistance, tissue damping and tissue elastance) confirmed disease-specific phenotypes either at baseline or following methacholine challenge and lung function defects could be detected in each disease model by at least one FE-related parameter. Expand