COPD
Curr Pharm Biotechnol. 2006 May;7(2):81-6. Am
J Physiol Heart Circ Physiol.
2006 May 19; [Epub ahead of print] J
Occup Med Toxicol.
2006 Feb 2;1(1):2.
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]
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,
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]
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]