Limu FUCOIDAN and Smokers

For quite some time I have been sharing with you the scientific
studies done on ingredients of LIMU MOUI. Especially limu,s main
ingredient FUCOIDAN
This time I have a new study that may hearten some of you that are
SMOKERS.

I wished no one smoked, but lets face it MORE THAN 20 million
people still smoke in this country.

Scientist say smoking contributes to the development of the
conditions that comes from Emphysema.
In a nutshell, Emphysema results from the expansion of LUNG CELLS
that loose their elasticity and tend to stay enlarged. A reaction
takes place in the body that cause other Macrophage cells to pile-up
in those areas.
The result is INCREDIBLE. Shortness of breath, Blood flow
restriction, Anemia ,Low oxygen intake and all that can mean for
your feel. Of course General health can deteriorate under those
circumstances.

Sometimes the condition is coming on for many years. The end of it
all is , lesser quality or shortened Life.

If anyone smokes or have a LOVE ONE or friend that does , should
LISTEN-UP.

The Study below helps me to understand why a FRIEND OF MINE no
longer have that HACKING cough that she had in the past. I got her
to drink LIMU MOUI.. After reading the New study below, do yourself,
OR a love one a favor. Make sure they take advantage of this
wonderful product.

To ORDER call (866-852-4832. You will need my new ID 1236501. Or
to Odrer online: http://thelimuman.originallimu.com.

After the study summary below I will show You how to get it
wholesale OR even FREE

Remember: No hype here, I let the scientists speak for themselves.
No one can abuse me of miss-characterizing their study. UNUSUAL
isn't it? As always, if you have any trouble with the scientific
speak, skip to their conclusion OR ask your doctor.

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THE STUDY




Free Radic Biol Med. 2003 Oct 1;35(7):697-710. Related Articles,
Links


Cigarette smoke triggers macrophage adhesion and activation: role of
lipid peroxidation products and scavenger receptor.

Kirkham PA, Spooner G, Ffoulkes-Jones C, Calvez R.

Novartis HRC, Horsham, West Sussex, England, UK.
paul.kirkham@...

Pulmonary emphysema in chronic obstructive pulmonary disease (COPD)
is characterized by the destruction of the alveolar walls leading to
permanent enlargement of distal respiratory air spaces. A major
causal factor is cigarette smoking, which produces conditions of
chronic oxidative stress within the lungs. At a cellular level,
increased macrophage accumulation and retention within the alveolar
interstitial spaces is pivotal to the development of emphysema. To
date it has been unclear as to the underlying mechanisms relating
chronic oxidative stress to macrophage accumulation and retention.
Our study was initiated to ascertain the role of modification of
extracellular matrix proteins with cigarette smoke and products of
lipid peroxidation on macrophage adhesion and activation. Increased
numbers of macrophages were seen adhering to cigarette smoke-
modified collagen IV as compared to unmodified collagen, where
little or no adherent macrophages were observed. Similar
observations were made when collagen was modified with either
acrolein or 4-hydroxy-2-nonenal. Adhesion could be blocked with
either fucoidan or a monoclonal antibody against the Type A
macrophage scavenger receptor. Also, modified collagen triggered
both oxidative burst and MCP-1 release in macrophages. These
results, therefore, highlight a potential mechanism by which
oxidative stress through the production of reactive carbonyls
promotes macrophage accumulation, retention, and activation,
independently of other proinflammatory stimuli. The implications of
this for the development of emphysema in COPD are discussed.

PMID: 14583334 [PubMed - in process]