Flowchart: Preparation: Nadph
 

 


                  

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COPD

                                                

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Curr Pharm Biotechnol. 2006 May;7(2):81-6.

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Current Understanding of the Mechanism and Role of ROS in Angiotensin II Signal Transduction.

Suzuki H, Frank GD, Utsunomiya H, Higuchi S, Eguchi S.

Cardiovascular Research Center, Temple University School of Medicine, 3420 N. Broad Street, Philadelphia, PA 19140, USA. seguchi@temple.edu.

Reactive oxygen species (ROS) are proposed to induce cardiovascular diseases, such as atherosclerosis and hypertension, through several mechanisms. One such mechanism involves ROS acting as intracellular second messengers, which lead to induction of unique signal transductions. Angiotensin II (AngII), a potent cardiovascular pathogen, stimulates ROS production through vascular NADPH oxidases. The ROS production induced by AngII activates downstream ROS-sensitive kinases that are critical in mediating cardiovascular remodeling. Recent advances in gene transfer/knockout techniques have lead to numerous in vitro and in vivo studies that identify the potential components and mechanisms of ROS signal transduction by AngII which promote cardiovascular remodeling. In this review, we will focus our discussion on the signal transduction research elucidating ROS production and function induced by AngII using currently available molecular biotechnologies.

PMID: 16724941 [PubMed - in process]

 

Am J Physiol Heart Circ Physiol. 2006 May 19; [Epub ahead of print]

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Angiotensin II-Mediated Oxidative Stress and Pro-collagen-1 Expression in Cardiac Fibroblasts: Blockade by Pravastatin and Pioglitazone.

Chen J, Mehta JL.

Division of Cardiovascular Medicine,
University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States.

Angiotensin II (Ang II), a product of renin-angiotensin-system activation, enhances collagen synthesis which is a key event in cardiac remodeling following myocardial infarction. Inhibition of cardiac remodeling is now a target of multiple therapies, including HMG Coenzyme A reductase inhibitors, commonly known as statins, and peroxisome proliferator-activated receptor-gamma(PPAR-gamma) ligands. We examined the potential anti-fibrotic effect of the combination of a statin (pravastatin) and a PPAR-gamma ligand (pioglitazone) in Ang II-treated mouse cardiac fibroblasts. Ang II treatment induced pro-collagen-1 expression, which was inhibited by pravastatin and pioglitazone in a dose-dependent fashion. Pre-treatment of fibroblasts with low therapeutic concentrations of either pravastatin (0.1microM) or pioglitazone (5microM) only slightly decreased Ang II-induced NADPH oxidase expression, superoxide anion production and pro-collagen-1 expression; but the combination of pravastatin and pioglitazone markedly modulated these effects of Ang II. The combination also blocked Ang II-mediated p38MAPK and p44/42 MAPK activation. Electrophoretic mobility shift assay showed that Ang II activated transcription factors NF-kappa|B and AP-1. While pravastatin and pioglitazone alone had a variable effect on NF-kappaB and AP-1 activation, their combination exerted a potent inhibitory effect on the activation of both NF-kappaB and AP-1. The effects of pravastatin and pioglitazone combination on superoxide generation and pro-collagen-1 expression mimicked those of alpha-tocopherol and gamma-tocopherol, two potent antioxidants. Thus it appears that there is a positive interaction between pravastatin and pioglitazone in modulating Ang II-mediated oxidative stress, inhibiting MAPK activation and pro-collagen-1 expression.

PMID: 16714359 [PubMed - as supplied by publisher]

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

J Occup Med Toxicol. 2006 Feb 2;1(1):2.

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Work life of persons with asthma, rhinitis, and COPD: A study using a national, population-based sample.

Yelin E, Katz P, Balmes J, Trupin L, Earnest G, Eisner M, Blanc P.

Division of Rheumatology, Department of Medicine, University of California, San Francisco, San Francisco, CA 94143-0920, USA. ed.yelin@ucsf.edu.

ABSTRACT : OBJECTIVE : To estimate the duration of work life among persons reporting a physician's diagnosis of COPD, asthma, or rhinitis compared to those with select non-respiratory conditions or none and to delineate the factors associated with continuance of employment. METHODS : Persons ages 55 to 75 reporting a physician's diagnosis of COPD, asthma, or rhinitis as well as those without any of these conditions were identified by random-digit dialing (RDD) in the continental U.S and administered a structured survey. We used Kaplan-Meier life table analysis to estimate the duration of work life among persons with and without the three conditions and Cox proportional hazard regression to examine the role of demographic and work characteristics in the proportion leaving employment in each time interval. RESULTS : Persons with COPD, asthma, and rhinitis were no less likely than the remainder of the population to have ever worked, but those with COPD were less likely to be working when interviewed or as of age 65, whichever came first. As of age 55, only 62 percent of persons with COPD continued to work versus 72 and 78 percent of persons with asthma and rhinitis, respectively. Persons with COPD, asthma, and rhinitis all had an elevated risk of leaving work prior to age 65 relative to those without chronic conditions, with and without adjustment for demographic and work characteristics. CONCLUSION : COPD and to a lesser extent asthma and rhinitis were associated with a substantially shortened work life, an effect not due to demographic and work characteristics.

PMID: 16722563 [PubMed - in process]