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Winthrop K.L.,Oregon Health And Science University | Iseman M.,National Jewish Medical and Research Center
Nature Reviews Rheumatology | Year: 2013

In modern times a relationship between tuberculosis (TB) and rheumatoid arthritis (RA) has been firmly recognized, and is primarily attributable to the immunosuppressive therapies used to treat RA. Whereas TB can complicate the successful management of RA, nontuberculous mycobacteria have now perhaps become as important as (if not more so than) TB in the setting of RA, and can represent an even greater challenge to the rheumatologist wishing to use immunosuppressive therapies. This article reviews our most recent understanding of the epidemiological and clinical aspects of mycobacterial disease as it relates to RA, and the existing and emerging immunosuppressive therapies used to treat this disease. © 2013 Macmillan Publishers Limited. All rights reserved. Source


Kenn K.,Allergology Hospital | Balkissoon R.,National Jewish Medical and Research Center
European Respiratory Journal | Year: 2011

Vocal cord dysfunction (VCD) is a disorder caused by episodic unintentional paradoxical adduction of the vocal cords, which may induce acute severe dyspnoea attacks not responsive to conventional asthma therapy. The aetiology of VCD is complex and often multifactorial. The essential pathophysiology is that of a hyperfunctional laryngeal reflex to protect the lower airway as a result of any combination of post-nasal drip, gastro-oesophageal reflux, laryngopharyngeal reflux and/or psychological conditions. Laryngoscopic demonstration of the paradoxical motion while wheezing or stridorous is considered the diagnostic gold standard. Speech therapy, including the use of special relaxed-throat breathing patterns is effective for VCD that is purely of the functional nature. Knowledge of the clinical features of VCD and identifying factors that may be contributing to the development of VCD can provide adequate clues to the correct diagnosis and management. Copyright©ERS 2011. Source


Jaramillo M.C.,University of Arizona | Briehl M.M.,University of Arizona | Crapo J.D.,National Jewish Medical and Research Center | Batinic-Haberle I.,Duke University | Tome M.E.,University of Arizona
Free Radical Biology and Medicine | Year: 2012

Using current chemotherapy protocols, over 55% of lymphoma patients fail treatment. Novel agents are needed to improve lymphoma survival. The manganese porphyrin, MnTE-2-PyP 5 +, augments glucocorticoid-induced apoptosis in WEHI7.2 murine thymic lymphoma cells, suggesting that it may have potential as a lymphoma therapeutic. However, the mechanism by which MnTE-2-PyP 5 + potentiates glucocorticoid-induced apoptosis is unknown. Previously, we showed that glucocorticoid treatment increases the steady state levels of hydrogen peroxide ([H 2O 2] ss) and oxidizes the redox environment in WEHI7.2 cells. In the current study, we found that when MnTE-2-PyP 5 + is combined with glucocorticoids, it augments dexamethasone-induced oxidative stress however, it does not augment the [H 2O 2] ss levels. The combined treatment depletes GSH, oxidizes the 2GSH:GSSG ratio, and causes protein glutathionylation to a greater extent than glucocorticoid treatment alone. Removal of the glucocorticoid-generated H 2O 2 or depletion of glutathione by BSO prevents MnTE-2-PyP 5 + from augmenting glucocorticoid-induced apoptosis. In combination with glucocorticoids, MnTE-2-PyP 5 + glutathionylates p65 NF-κB and inhibits NF-κB activity. Inhibition of NF-κB with SN50, an NF- κB inhibitor, enhances glucocorticoid-induced apoptosis to the same extent as MnTE-2-PyP 5 +. Taken together, these findings indicate that: 1) H 2O 2 is important for MnTE-2-PyP 5 + activity; 2) Mn-TE-2-PyP 5 + cycles with GSH; and 3) MnTE-2-PyP 5 + potentiates glucocorticoid-induced apoptosis by glutathionylating and inhibiting critical survival proteins, including NF-κB. In the clinic, over-expression of NF-κB is associated with a poor prognosis in lymphoma. MnTE-2-PyP 5 + may therefore, synergize with glucocorticoids to inhibit NF-κB and improve current treatment. © 2012 Elsevier Inc. All rights reserved. Source


Patent
National Jewish Medical And Research Center | Date: 2014-02-13

Methods for therapy of cystic fibrosis and other conditions are provided. The methods comprise one or more agents capable of increasing thiol-containing compound transport via a transporter system (i.e. ABC transporters such as MDR-1 or MRP-2) in cells. Other embodiments include the use of agents to modulate transport of thiol-containing compounds within the cell. Therapeutic methods involve the administration of such agents to a patient afflicted with cystic fibrosis and/or another condition responsive to stimulation of thiol-containing compound transport.


Patent
Aeolus Inc., National Jewish Medical And Research Center and Health Science University | Date: 2010-11-08

The present invention relates, in one embodiment, to a method of preventing or treating diabetes using low molecular weight antioxidants. In a further embodiment, the invention relates to a method of protecting and/or enhancing viability of cells/tissues/organs during isolation (harvesting), preservation, expansion and/or transplantation. In yet another embodiment, the present invention relates to a method of inducing immune tolerance. The invention also relates to compounds and compositions suitable for use in such methods.

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