Patient perception of osteopathic manipulative treatment in a hospitalized setting: a survey-based study.

Context: Although many studies on the effects of osteopathic manipulative treatment (OMT) have been published, few examine its role in treating hospitalized patients.

Objective: To determine patient perception of receiving OMT while hospitalized.

Methods: Patients were referred to receive OMT through a consultation service and were separated into four groups: medical, musculoskeletal, obstetric, or postsurgical.

c-Jun N-terminal kinase 1 is required for the development of pulmonary fibrosis.

Collagen deposition is observed in a diverse set of pulmonary diseases, and the unraveling of the molecular signaling pathways that facilitate collagen deposition represents an ongoing area of investigation. The stress-activated protein kinase, c-Jun N-terminal kinase 1 (JNK1), is activated by a large variety of cellular stresses and environmental insults. Recent work from our laboratory demonstrated the critical role of JNK1 in epithelial to mesenchymal transition.

Jun N-terminal kinase 1 regulates epithelial-to-mesenchymal transition induced by TGF-beta1.

Transforming growth factor beta1 (TGF-beta1) is a cardinal cytokine in the pathogenesis of airway remodeling, and promotes epithelial-to-mesenchymal transition (EMT). As a molecular interaction between TGF-beta1 and Jun N-terminal kinase (JNK) has been demonstrated, the goal of this study was to elucidate whether JNK plays a role in TGF-beta1-induced EMT. Primary cultures of mouse tracheal epithelial cells (MTEC) from wild-type, JNK1-/- or JNK2-/- mice were comparatively evaluated for their ability to undergo EMT in response to TGF-beta1.

Reactive nitrogen species-induced cell death requires Fas-dependent activation of c-Jun N-terminal kinase.

Nitrogen dioxide is a highly toxic reactive nitrogen species (RNS) recently discovered as an inflammatory oxidant with great potential to damage tissues. We demonstrate here that cell death by RNS was caused by c-Jun N-terminal kinase (JNK). Activation of JNK by RNS was density dependent and caused mitochondrial depolarization and nuclear condensation.

Eosinophil peroxidase catalyzes JNK-mediated membrane blebbing in a Rho kinase-dependent manner.

Eosinophilic influx is characteristic of numerous inflammatory conditions. Eosinophil peroxidase (EPO) is a major enzyme present in eosinophils and upon degranulation, becomes released into the airways of asthmatics. As a result of its cationic nature and its ability to catalyze the formation of highly toxic oxidants, EPO has significant potential to induce cellular injury.

Hydrogen peroxide signaling through tumor necrosis factor receptor 1 leads to selective activation of c-Jun N-terminal kinase.

Binding of tumor necrosis factor-alpha (TNFalpha) to its receptor, TNF-R1, results in the activation of inhibitor of kappaB kinase (IKK) and c-Jun N-terminal kinase (JNK) pathways that are coordinately regulated and important in survival and death. We demonstrated previously that in response to hydrogen peroxide (H2O2), the ability of TNFalpha to activate IKK in mouse lung epithelial cells (C10) was inhibited and that H2O2 alone was sufficient to activate JNK and induce cell death. In the current study, we investigated the involvement of TNF-R1 in H2O2-induced JNK activation.

Reactive nitrogen species and cell signaling: implications for death or survival of lung epithelium.

Reactive nitrogen species such as nitric oxide, peroxynitrite, and nitrogen dioxide have been implicated in the pathophysiology of inflammatory lung diseases. Yet, the molecular mechanisms and cell signaling events responsible for cellular injury remain to be elucidated. Two major signaling pathways, co-ordinately regulated and responsible for cell survival and cell death, involve nuclear factor kappa B and c-Jun-N-terminal kinase, respectively.