"exposure to DE during an influenza infection polarizes the local immune responses to an IL-4 dominated profile in association with increased viral disease, and some aspects of this effect can be reversed with antioxidants."
Read abstract: CiteULike: Role of oxidative stress on diesel-enhanced influenza infection in mice:
Explores the mental, physical, cellular and biochemical aspects of environmental illnesses such as obesity, diabetes, chronic fatigue syndrome, PTSD, fibromyalgia, chemical sensitivities, neurological disorders and numerous others. We advocate for better access to medical care, healthier lifestyles, resource conservation and the use of assistance animals for the disabled to promote a better quality of life.
Showing posts with label influenza. Show all posts
Showing posts with label influenza. Show all posts
Friday, November 26, 2010
Friday, February 19, 2010
Flu-Induced Stress Response Necessary for Resistance to Secondary Illness
Flu-induced stress response is critical for resistance to secondary infection
ScienceDaily (2010-02-19) -- A new study reveals how infection with the influenza virus impacts the way that the immune system responds to subsequent infections. The research provides a new understanding of the physiological and pathological consequences of the flu. ... > read full article
Friday, December 25, 2009
Vaccinating Against Bacterial Infections May Reduce Flu-Related Pneumonia Deaths
Vaccinating Against Bacterial Infections May Reduce Flu-Related Pneumonia Deaths: "URL: Vaccinating Against Bacterial Infections May Reduce Flu-Related Pneumonia Deaths
"
HEIRS Health & Home
http://www.heirs-online.com/
heirshealth@gmail.com
Shop HEIRS Amazon or specialty items on HEIRS Store online.
HEIRS Health & Home
http://www.heirs-online.com/
heirshealth@gmail.com
Shop HEIRS Amazon or specialty items on HEIRS Store online.
Thursday, December 17, 2009
First immunological clue to why some H1N1 patients get very ill or die
First immunological clue to why some H1N1 patients get very ill or die: "URL: First immunological clue to why some H1N1 patients get very ill or die
"
Read and find out more...
HEIRS Health & Home
http://www.heirs-online.com/
heirshealth@gmail.com
Check out some of our cool, more eco-friendly, non-toxic or got-to-have items in the HEIRS Web Store at Amazon or specialty items on our store portal.
Read and find out more...
HEIRS Health & Home
http://www.heirs-online.com/
heirshealth@gmail.com
Check out some of our cool, more eco-friendly, non-toxic or got-to-have items in the HEIRS Web Store at Amazon or specialty items on our store portal.
Wednesday, November 4, 2009
Sunday, September 20, 2009
Wednesday, September 9, 2009
The AhR and Diseases of the Lung!
Nrf2 is a modulator of inflammatory mediators as well as, interacts with the aryl hydrocarbon (AhR). Neff-Layford suggests that activation of the AhR by pollutants dysregulates IFN-gamma through an iNOS pathway which may lead to a difference in the severity of infection. The author explains further that overproduction of IFN-gamma leads to hyperinflammation in lungs of humans and animals and the levels of IFN-gamma and iNOS correlates with severity of those with acute respiratory distress syndrome. She points out that both influenza and activation of the AhR have been implicated as increasing the severity of these diseases. She concludes that inappropriate activation of the AhR contributes to the severity and complexity of diseases of the lung.
Neff-LaFord, H., Teske, S., Bushnell, T. P., and Lawrence, B. P. (2007). Aryl hydrocarbon receptor activation during influenza virus infection unveils a novel pathway of ifn- production by phagocytic cells1. The Journal of Immunology, 179:247-255 http://www.citeulike.org/user/HEIRS/article/5759129
Neff-LaFord, H., Teske, S., Bushnell, T. P., and Lawrence, B. P. (2007). Aryl hydrocarbon receptor activation during influenza virus infection unveils a novel pathway of ifn- production by phagocytic cells1. The Journal of Immunology, 179:247-255 http://www.citeulike.org/user/HEIRS/article/5759129
Subscribe to:
Posts (Atom)