Alveolar macrophage secretory products effect type 2 pneumocytes undergoing hypoxia-reoxygenation.

Background: Activation of the alveolar macrophage is centrally important to the development of lung ischemia reperfusion injury. Alveolar macrophages and type 2 pneumocytes secrete a variety of proinflammatory mediators in response to oxidative stress. The manner in which they interact and how the macrophage may influence pneumocyte responses in lung ischemia reperfusion injury is unknown.

Scratch collapse test for evaluation of carpal and cubital tunnel syndrome.

Purpose: The purpose of this study was to evaluate the clinical usefulness of a new test, the scratch collapse test, for the diagnosis of carpal tunnel syndrome and cubital tunnel syndrome.

Methods: The scratch collapse test was prospectively compared with Tinel's sign and flexion/nerve compression in 169 patients and 109 controls. One hundred nineteen patients were diagnosed with carpal tunnel syndrome and 70 patients were diagnosed with cubital tunnel syndrome based on history, examination, and positive electrodiagnostic test.

Interleukin-6 regulation of direct lung ischemia reperfusion injury.

Background: Lung ischemia reperfusion injury continues to adversely affect patient and graft survival after transplantation. While the role of interleukin-6 has been studied in ischemia-reperfusion models of intestine, liver, and heart, its participation in lung reperfusion injury has not been characterized.

Methods: We administered recombinant interleukin-6 to rat lungs through the intratracheal route before inducing left lung ischemia and reperfusion.

The effect of anti-inflammatory properties of mycophenolate mofetil on the development of lung reperfusion injury.

Background: Lung ischemia-reperfusion injury (LIRI) is associated with an increased incidence of both primary graft failure and obliterative bronchiolitis. The immunosuppressant mycophenolate mofetil (MMF) has recently been shown to attenuate inflammatory injury in acute ischemia-reperfusion models via a mechanism that is presently unclear. These experiments studied the effects of MMF in a warm, in situ LIRI model, focusing on transcriptional regulation of pro-inflammatory mediators.

Poly (ADP) ribose polymerase inhibition improves rat cardiac allograft survival.

Background: Heart transplantation is an accepted treatment modality for end-stage heart failure. However, acute cellular rejection (ACR) continues to be a morbid complication. Recently a novel mechanism of inflammatory allograft injury has been characterized which involves overactivation of the nuclear enzyme poly (ADP-ribose) polymerase (PARP).

Obliterative airway disease in rat tracheal allografts requires tumor necrosis factor alpha.

Obliterative bronchiolitis is the major complication affecting long-term lung transplant survivors. Tumor necrosis factor-alpha (TNF-alpha) promotes inflammation and fibrosis in chronic lung injury models. These experiments defined the role of TNF-alpha in an established model of obliterative airway disease (OAD).

The role of CC and CXC chemokines in cardiac allograft rejection in rats.

Acute cellular rejection is due in part to an upregulation of chemokine genes, resulting in eventual cell-mediated cytotoxicity. The role of chemokines in acute cardiac allograft rejection is not fully characterized presently. These studies compared the patterns of expression for multiple chemokines in rodent cardiac allograft rejection.

Cyclosporine modulates the response to hypoxia-reoxygenation in pulmonary artery endothelial cells.

Background: Depletion of macrophages, neutrophils, or lymphocytes confers only partial protection against experimental lung reperfusion injury, suggesting that inflammatory responses in other cell types contribute to tissue injury. Endothelial cell activation has previously been shown to be critical to the development of ischemia-reperfusion injury in other vascular beds. Furthermore, cyclosporine (CSA) reduces in vivo lung reperfusion injury through attenuated secretion of proinflammatory mediators.

FR167653 reduces obliterative airway disease in rats.

Background: Obliterative bronchiolitis (OB) is the main cause of late mortality among long-term survivors of lung transplantation. Although p38 kinase is functional in multiple acute inflammatory injury models, its role in chronic lung rejection is undefined. p38 regulates the expression of the cytokines tumor necrosis (TNF)-alpha and interleukin (IL)-1beta, 2 mediators involved in the development of OB in a tracheal transplant model.