Hello friends,
Some are saying that they didn't get the cancer STUDIES.

Here they are again. If you get them twice I am sorry.

Almost one out of every two people is expected to get cancer during
their lifetime.

Just about all of us have a LOVE ONE that has suffered from it.

I am sharing SEVEN, that's right SEVEN SCIENTIFIC STUDIES from
various Countries. About LIMU MOUI,S FUCOIDAN and Cancer.

Tou will want to save this letter. Print it out. Show it to your
Doctor. You will find that Many Doctors haven't heard about them.
They are FASCINATING!

You will begin to understand ,maybe, why it is that we get GLOWING
testimonies from cancer patients.

LOOK THESE OVER. Then Get Some Limu Moui NOW!

I HATE HYPE. You know how I always let the Scientists speak for
themselves. The scientific minded will have little problem
understanding the studies.



REMEMBER, you can always SKIP to the scientists CONCLUSION. It,s
always fairly clear. You also can print this out , or email it to
your DOCTOR.



Once you see and understand the studies, you may want to get LIMU
MOUI AS SOON AS POSSIBLE. I will show you 2 ways right now.



TO GET LIMU do EITHER one below:



1. CALL (407)804-1931 and use ID 7649701

OR
2.http://ginasgift.originallimu.com/

OR

3. To hear more about Limu with FUCOIDAN go here and hear what it has
done for others: http://www.angelfire.com/ar/maybe4u2/limu.html

NOW THE AMAZING STUDIES


Antitumor activity and immunological properties of marine algal
polysaccharides, especially fucoidan, prepared from Sargassum
thunbergii of Phaeophyceae.



Itoh H, Noda H, Amano H, Zhuaug C, Mizuno T, Ito H.



Laboratory of Marine Biochemistry, Faculty of Bioresources, Mie
University, Japan.



Marine algal polysaccharide, GIV-A from Sargassum thunbergii markedly
inhibited the growth of Ehrlich ascites carcinoma at the dose of 20
mg/kg per day X10 with no sign of toxicity in mice. GIV-A is
suggested to be a hexouronic acid containing L-fucan sulfate,
fucoidan by the analyses of physicochemical properties and IR- and
NMR-spectra. The results of carbon clearance activity with fucoidan
demonstrated that it is acting as a so-called activator of the
reticuloendothelial system. Fucoidan enhanced the phagocytosis and
chemiluminescence of macrophages. By the immunofluorescent method,
binding of the third component of complement (C3) cleavage product to
macrophages and the proportion of C3 positive cells were increased.
In crossed immunoelectrophoresis, human serum C3 was converted by
fucoidan and appeared as the 3rd peak (converted C3). The height of
the 3rd peak was directly proportional to the doses of fucoidan. The
residual CH50 units of human serum decreased dose-dependently. These
results suggest that the antitumor activity of fucoidan is related to
the enhancement of immune responses. The present results indicate
that fucoidan may open new perspectives in cancer chemotherapy.



PMID: 8297113 [PubMed - indexed for MEDLINE]












Polysulfated heparinoids selectively inactivate heparin-binding
angiogenesis factors.



Zugmaier G, Favoni R, Jaeger R, Rosen N, Knabbe C.



Department of Hematology/Oncology, Philipps-University, Marburg,
Germany.



Angiogenesis is a prerequisite for tumor expansion and metastasis.
The angiogenic potential of the heparin-binding growth factors acidic
fibroblast growth factor (FGF) and basic FGF has been demonstrated in
various publications. We studied the inhibitory effects of suramin
and the polysulfated heparinoids pentosan polysulfate, dextran
sulfate, and fucoidan on the action of FGF. As an experimental model,
we used the adrenal cancer cell line SW 13, whose anchorage-
independent growth depends on the presence of FGF. The polysulfated
heparinoids inhibited FGF-induced growth and binding to the receptor
at an IC50 of 0.5-3 micrograms/ml. Suramin inhibited FGF at an IC50
of 100 micrograms/ml. The polysulfated heparinoids exerted no effect
on IGF-1 or TGF alpha-related growth. Suramin inhibited the anchorage-
independent growth induced by IGF-1 or TGF alpha only at an IC50 of
100 micrograms/ml. Our results indicate that suramin inhibits growth
factors in a nonselective way. By contrast, polysulfated heparinoids
exert a selective inhibitory effect on heparin binding angiogenesis
factors at an IC50, which is 100 times below the IC50 of suramin.
Therefore, the administration of polysulfated heparinoids might
become a novel approach to tumor therapy based on blocking
angiogenesis.



PMID: 10667230 [PubMed - indexed for MEDLINE]








Antitumor and antiproliferative effects of a fucan extracted from
ascophyllum nodosum against a non-small-cell bronchopulmonary
carcinoma line.



Riou D, Colliec-Jouault S, Pinczon du Sel D, Bosch S, Siavoshian S,
Le Bert V, Tomasoni C, Sinquin C, Durand P, Roussakis C.



ISOMer (Institut des Substances et Organismes de la Mer), SMAB,
Laboratoire de Pharmacologie Marine, Faculte de Pharmacie, Nantes,
France.



Fucans, sulfated polysaccharides extracted from brown seaweeds, have
been shown to be endowed with inhibitory effects cell growth in
various experimental models. We studied both the antiproliferative
and antitumor properties of a fucoidan extract (HF) obtained from the
brown seaweed Ascophyllum nodosum on a cell line derived from a non-
small-cell human bronchopulmonary carcinoma (NSCLC-N6), this type of
carcinoma is particularly chemo-resistant. HF exerts in vitro a
reversible antiproliferative activity with a block observed in the G1
phase the cell cycle. Studies performed with the NSCLC-bearing nude
mice show antitumor activity at subtoxic doses. These preliminary
results indicate that HF exhibits inhibitory effect both in vitro and
in vivo and is very potent antitumor agent in cancer therapy.



PMID: 8702239 [PubMed - indexed for MEDLINE]







Immunological analysis of inhibition of lung metastases by fucoidan
(GIV-A) prepared from brown seaweed Sargassum thunbergii.



Itoh H, Noda H, Amano H, Ito H.



Laboratory of Marine Biochemistry, Faculty of Bioresources, Mie
University, Tsu, Japan.



The antimetastatic effect of GIV-A (fucoidan) and/or 5-FU was
examined in an experimental model of lung metastases induced by Lewis
lung carcinoma in mice. Injection of GIV-A i.p. after removal of the
implanted primary tumor inhibited the development of lung metastases.
Combination treatment with GIV-A and 5-FU inhibited significantly the
lung metastases. The number of peritoneal macrophages, total cells
and macrophages in the lung increased in mice treated with GIV-A.
Binding of the third component of complement (C3) cleavage products
(C3b) to the C3 receptor on peritoneal macrophages after i.v.
injection of GIV-A was enhanced, as shown by the fluorescent antibody
technique. Lung metastases were inhibited by i.v. injection of
peritoneal macrophages activated with GIV-A. GIV-A depressed aniline
hydroxylase and aminopyrine demethylase activities of the hepatic
microsomal drug-metabolizing system in tumor-bearing mice. Moreover,
the concentration of 5-FU in the tissues (lung, liver, kidney, spleen
and blood) was increased significantly by coadministration of GIV-A.
The picryl chloride-induced delayed type hypersensitivity (PC-DTH)
response in mice was depressed after the implantation of tumor and
treatment with 5-FU. GIV-A restored the suppression of PC-DTH by 5-
FU, but did not increase the PC-DTH of normal mice. GIV-A not only
enhanced the degree of spleen cell-mediated sheep red blood cell
(SRBC) hemolysis (quantitative hemolysis of SRBC), the indexes of the
spleen and thymus and the number of spleen cells, but also restored
the suppressive effect of 5-FU. In the group receiving GIV-A, the
percentages of splenic Thy1.2-, L3T4- and asialo GM1-positive cells
were significantly increased as compared with the tumor-bearing mice
treated with saline. Furthermore, the L3T4+/Lyt2+ ratio showed a
tendency to increase, and the Lyt2+/Thy1.2+ ratio was decreased.
These results suggest that the antitumor effect of GIV-A may be
correlated with the changing pattern of the Thy1.2-, L3T4- and asialo
GM1-positive cells, C3 activation, macrophage activation and
depression of the hepatic microsomal drug-metabolizing system. These
findings raise the possibility that GIV-A may have clinical value in
the prevention of cancer metastasis.



PMID: 8572581 [PubMed - indexed for MEDLINE]








Antitumor active fucoidan from the brown seaweed, umitoranoo
(Sargassum thunbergii).



Zhuang C, Itoh H, Mizuno T, Ito H.



United Graduate School of Agricultural Sciences, Gifu University
(Shizuoka University), Japan.



Neutral and acidic polysaccharides and their protein complexes were
fractionated and purified from the brown seaweed umitoranoo
(Sargassum thunbergii) by fractional extraction, iron-exchange
chromatography, and gel filtration. Thirty-one polysaccharide
fractions were obtained and tested for antitumor activity in mice
with Ehrlich carcinoma transplanted i.p. Two of the fractions, GIV-A
([alpha]25D -127 degrees and mol. wt., 19,000) and GIV-B ([alpha]25D -
110 degrees and mol. wt., 13,500) had such activity. On the basis of
chemical and spectral analyses, these compounds were found to be a
fucoidan or L-fucan containing approx. 30% sulfate ester groups per
fucose residue, about 10% uronic acid, and less than 2% protein.



PMID: 7772818 [PubMed - indexed for MEDLINE]








Inhibitory effect of oversulfated fucoidan on invasion through
reconstituted basement membrane by murine Lewis lung carcinoma.



Soeda S, Ishida S, Shimeno H, Nagamatsu A.



Department of Biochemistry, Faculty of Pharmaceutical Sciences,
Fukuoka University.



We investigated the effects of native, oversulfated, and desulfated
fucoidans and heparin on the invasion of 3 LL cells through Matrigel.
Of the four polysaccharides tested, oversulfated fucoidan was the
most potent inhibitor of tumor cell invasion and inhibited most
potently and specifically the tumor cell adhesion to laminin. Sodium
dodecyl sulfate-polyacrylamide gel electrophoretic analysis of the
binding of elastase-cleaved laminin to fucoidan- and heparin-
Sepharoses showed that both polysaccharides bound to the 62 and 56
kDa fragments. Pretreatment of 3LL cells with native or oversulfated
fucoidan reduced their adhesive potency to laminin. The two fucoidans
inhibited further the laminin binding of 3 LL cells which had been
pretreated with a laminin-based pentapeptide, YIGSR. These results
suggest that fucoidan specifically binds to not only the heparin
binding domain(s) of laminin but also site(s) other than the cell
surface laminin receptor. 3 LL cells secreted a 50 kDa form of
urokinase-type plasminogen activator (u-PA). The extracellular level
of u-PA activity was increased 1.7 times by addition of laminin but
not type IV collagen. Oversulfated fucoidan most potently reduced the
increased u-PA levels. Therefore, the reduction in in vitro
invasiveness of 3 LL cells in response to either fucoidan or its
oversulfated derivative may result from an inhibition of physical
interaction between the tumor cells and the Matrigel (laminin),
followed by a suppression of the laminin-induced increase in
extracellular u-PA.



PMID: 7829400 [PubMed - indexed for MEDLINE]







Blocking of lectin-like adhesion molecules on pulmonary cells
inhibits lung sarcoma L-1 colonization in BALB/c-mice.



Roszkowski W, Beuth J, Ko HL, Uhlenbruck G, Pulverer G.



National Institute of Lung Diseases and Tuberculosis, Warsaw, Poland.



Adhesion and inhibition experiments with pulmonary cells of BALB/c-
mouse origin and syngeneic sarcoma L-1 cells indicated that L-fucose
specific lectin-like adhesion molecules, presumably situated on
pulmonary cell surfaces are (at least partly) responsible for the
specificity of this cell-cell interaction. Addition of specific
sugars and glycoconjugates (L-fucose and fucoidan, respectively) to
the incubation medium evidently inhibited the adhesion process as
quantified using radiolabelled tumor cells. Unspecific carbohydrates
(e.g. D-galactose) did not affect the cellular interaction. In vivo,
repeated administration of fucoidan (but not of unspecific
glycoconjugates) significantly inhibited the settling of metastatic
sarcoma L-1 cells in the lungs of BALB/c-mice. Therefore, when lectin-
like adhesion molecules on pulmonary cells were blocked with
competitive glycoconjugates, tumor cell colonization of the lung
could be significantly inhibited.



PMID: 2737266 [PubMed - indexed for MEDLINE]



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go here: http://www.angelfire.com/ar/maybe4u2/limu.html or email me
at gina1906@...
_______________________________________________________



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