Apparently cancer cure has been around for a while

If you look at Yamamoto's research on this.
It makes alot of sense.
When your own body's healthy cells grow in the wrong place, which is cancer.
eg: a toenail cell growing in the middle of your brain.
The body's normal reaction is to attack it and kill it because it knows its in the wrong place.
But what these cells do before they announce themselves as what kind of cell they are.
Is turn off this communication process.
The immune system thinks this is just a normal brain cell but its not, its mutated into a toenail cell.
But the immune system now can not tell this.
This yamamoto process is turning it back on.
Its like a communication stream between cells and the damaged cells turn this off.
This process of course does exist or human life would be mutated all over the place.
It is not dissimilar to a virus in a computer, which gets in as a harmless file or packet, turns "off" the anti virus, then creates itself as the actual harmful virus and starts growing, and there is nothing you can do about it because the fighting processes have been disabled.
People might have many damaged cells, that turn into the wrong kind of cell during there lifetime.
And the body's macrophage process kills them.
The problem is there is no way to make much money from this.
Yamamoto has patented the process, and has made nothing so far.
Because its just not attractive to investors because its quick and cheap.
This needs to be available for people to try.
When you are at deaths door you should be able to try everything and anything.
I cant believe this isn't available to people.Even if no one can make money from it.It should be available.

any way , does anybody knows why in hell , this people that say that they have the cure for cancer with the glyco-protein , and that they dont have apatent but they do or what ever. since they can not say with in usa terretory that they have a cure for cancer , because it will never be accepted by the fda , wich is understood. but if they do why in hell dont they go to many different country i can think of and they start saving people lives there , countrys in wich not only they will be welcome , but they will let them and permit them say what ever they want , and practice what ever they want , as long as they proofe and cure people from cancer . thats something that people from here or anywhere in the world will travel to get treat it . isnt that the same thing as do in it here, that pisses me of when i here ho yea we have the cure we have that but nobody is interesting , because the medicine capital in the usa will loose money , well forget about the usa if thats the problem , go to many places in where you will be welcome , and give the oportunity of people from here to travel there and get cure . i mean this places there would not be any buracracy , the only thing they want to see is the cure . so i hope to get some answers , not only from writers , but from the real people , thats if they are real people backing up their statements , like we got the cure for nthis we got the cure for that . lets cut the cheap talk and go to real places in where the real action and proofe counts ,,,, im listening thanks

An update on this :

www.thenhf.com...


Article says May 2009. Interesting nobody seems to give a crap about this.
And I mean the media and all the corporations out there.

Originally posted by coven
Nice to read this two months after my uncle just died from prostate cancer...

This not being in the public eye the day it was announced is disgusting...

I agree

Nice to read this 8 years after my dad died of pancreatic cancer.

Good news... we're getting closer:

This was a matter of time. I work with this people everyday and despite the fact I agree progress is too slow advances are being made.

It has been published a good finding that points to a direction pharmaceutical companies won't like... the answer might be really simple.

Check my latest post:
www.abovetopsecret.com...

A new approach for identifying drugs that specifically attack cancer stem cells, the cellular culprits that are thought to start and maintain tumour growth, could change the way that drug companies and scientists search for therapies in the war against cancer.

This is a very crucial information. Bumping this thread up.

The subtle difference here is that this treatment has been "Peer Reviewed".

This Japanese researcher, Nobuto Yamamoto, has published several peer reviewed studies and articles involving GcMAF(also called Vitamin D3-Binding Protein-Derived Macrophage Activating Factor).

This is exactly like DCA, another downplayed treatment.

In spite of being peer reviewed, this has been ignored by the mainstream oncology establishment.

I will bump this up also; the problem is, there is no money for all those blood sucking weasels at the pharma corps and the researchers in providing a cheap effective cure for cancer; take lots of vitamin d and pass the word to everyone; money is the root of all evil and they would rather have everyone suffer and die just so they can make a buck off of it.

WAKE UP,PEOPLE!!!!

seeker

Cancer is a war waged in our bodies on a submicroscopic molecular scale. Taking a keen interest in this war wouldn’t be a bad idea, as its outcome will eventually determine whether about a third of us will live or die. The advent of Nagalase testing and GcMAF therapy gives us reason to hope and expect that we can soon eradicate the specter of cancer.

GcMAF is a research-proven cancer therapy—a human protein that activates specific immune cells (macrophages) that attack and destroy cancer cells.

Nagalse is the equivalent of a cholesterol test for cancer. Just as the presence of high levels of cholesterol indicate a high risk for atherosclerotic plaque, a high Nagalse level indicates the presence of cancer.

Nagalase, made by all cancer cells, blocks the immune response by sabotaging the production of GcMAF. This enables cancer to grow and spread. Without Nagalase, cancer cells wouldn't have a chance: our immune system's macrophage cells would just gobble them up.

When, in cancer patients, Nagalase has crippled normal production of GcMAF, administering it via injection bypasses the Nagalase-induced paralysis of the immune response. GcMAF injections re-activate the immune cells which then aggressively destroy cancer cells. The result is tumor shrinkage, cancer remission, and lower Nagalase levels.

Nagalase testing and GcMAF therapy could save millions of lives that would otherwise be lost to cancer.


Dr Tim Smith, M.D

gcmaf.timsmithmd.com...

2nd Gen version www.saisei-mirai.or.jp... & www.gc-maf.de...

Case Report: A Breast Cancer Patient Treated with GcMAF, Sonodynamic Therapy and Hormone Therapy www.saisei-mirai.or.jp... GcMAF Therapy Case Reports www.saisei-mirai.or.jp... & www.gcmaf.eu...

Dr Yamamoto was the first but since then many other papers have been published on the subject of activating macrophages using Vitamin D. However Dr Yamamoto was the first to trial GcMAF in humans. In all papers he can be quoted

"Stepwise treatment of purified Gc protein with immobilized beta-galactosidase and sialidase generated the most potent macrophage-activating factor (GcMAF) ever discovered, but it produces no side effect in humans."

Dr. Yamamoto’s 2008 breast cancer paper entitled: “Immunotherapy of metastatic breast cancer patients with vitamin D-binding protein-derived macrophage activating factor (GcMAF).” www.ncbi.nlm.nih.gov...

Dr. Yamamoto’s 2008 prostate cancer paper entitled: “Immunotherapy for Prostate Cancer with Gc Protein-Derived Macrophage-Activating Factor, GcMAF.” www.ncbi.nlm.nih.gov...

Dr. Yamamoto’s 2008 colorectal cancer paper entitled: “Immunotherapy of metastatic colorectal cancer with vitamin D-binding protein-derived macrophage-activating factor, GcMAF.” www.ncbi.nlm.nih.gov...

Dr. Yamamoto’s 2008 HIV paper entitled: “Immunotherapy of HIV-Infected Patients With Gc Protein-Derived Macrophage Activating Factor (GcMAF).” onlinelibrary.wiley.com...

Yamamoto’s three cancer studies showed that incredibly small weekly doses (100 billionths of a gram—an amount that is invisible to the naked eye) of GcMAF had cured early metastatic breast, prostate, and colon cancers in 100% of (nonanemic) patients. In a fourth paper, he used the same treatment to cure 100% of nonanemic HIV-infected patients.

For the three cancer studies, Dr. Yamamoto had chosen patients who had recently received the standard mainstream triad of surgery, chemo, and radiation. Despite these treatments, every patient had evidence of metastatic disease, which means that despite the best efforts of conventional medicine, their cancers were out of control and still growing. Their prognoses were poor at best. Nevertheless, this patient group had one thing in common: their tumor mass (also known as tumor burden) had been drastically reduced by the therapies they had received, and this in turn dramatically increased the likelihood that GcMAF would remove the remaining cancer cells.

PubMed search gcmaf www.ncbi.nlm.nih.gov...

PubMed search gcmaf cancer www.ncbi.nlm.nih.gov...

1: Inhibitory effect of vitamin D-binding protein-derived macrophage activating factor on DMBA-induced hamster cheek pouch carcinogenesis and its derived carcinoma cell line.

Summary: A study on GcMAF in hamsters infected with squamous cell cancer. All 15 hamsters in the control group died within 20 weeks.

The other group were infected and administered GcMAF, although the doses, source and intervals are not stated. 2 of the 14 hamsters in this group did not develop any tumours. The other 12 showed a significant delay in developing tumours and none died within the 20 weeks that they were observed.

GcMAF was administered to the 5 hamsters in the control group at week 13, and tumour growth was slightly suppressed, with all dying from tumour burden.

However, the mean survival time was significantly extended. (A further study also shows GcMAF as ineffective on skin cancer, although when combined with photodynamic light therapy, curative rates are 100%.)

Ref: Toyohara Y, Ha#ani S, Kishimoto H, Noguchi K, Yamamoto N, Urade M. Inhibitory effect of vitamin D-binding protein-derived macrophage activating factor on DMBA-induced hamster cheek pouch carcinogenesis and its derived carcinoma cell line. Oncol Lett. 2011 Jul;2(4):685-691. Epub 2011 May 13. PubMed PMID: 22848250; PubMed Central PMCID: PMC3406437.

2: Vitamin D-binding protein-derived macrophage-activating factor, GcMAF, and prostate cancer.

Summary: GcMAF was lost or reduced in prostate cancer patients due to high levels of nagalase.

Macrophages activated by GcMAF develop a considerable variation of receptors that recognize malignant cell surfaces. 16 nonanemic prostate cancer patients received weekly administration of 100 nanograms of GcMAF, during which time their nagalase levels reduced.

After 14 to 25 weeks all 16 patients had low nagalase levels equivalent to those of healthy people, indicating the patients were cancer free.

No recurrence occurred for 7 years.

Bear in mind that these patients had already undergone normal treatment options, but still had evidence of disease in the form of high nagalase levels. No visible tumours were apparent.

Ref: Bellone M, Rigamonti N. Vitamin D-binding protein-derived macrophage-activating factor, GcMAF, and prostate cancer. Cancer Immunol Immunother. 2012 Dec;61(12):2377-8. doi: 10.1007/s00262-012-1310-9. Epub 2012 Jun 28. PubMed PMID: 22740161.

3: Effects of vitamin D-binding protein-derived macrophage-activating factor on human breast cancer cells.

Summary: An in-vitro study on the effects of GcMAF on human breast cancer cells. It proved that it inhibited breast cancer cell proliferation, migration and metastatic potential.

Ref: Pacini S, Punzi T, Morucci G, Gulisano M, Ruggiero M. Effects of vitamin D-binding protein-derived macrophage-activating factor on human breast cancer cells. Anticancer Res. 2012 Jan;32(1):45-52. PubMed PMID: 22213287.

4: Gc protein-derived macrophage-activating factor (GcMAF) stimulates cAMP formation in human mononuclear cells and inhibits angiogenesis in chick embryo chorionallantoic membrane assay.

Summary: The effects of GcMAF have been studied in cancer and other conditions where blood supply conditions are deregulated. This study demonstrates that the division of human blood mononuclear cells (immune system cells) when treated with GcMAF was associated with the formation of chemical messenger pathways.

The effect was dose dependant, but maximum stimulation was achieved at 0.1ng/ml. Heparin (commonly used as an anitcoagulent) inhibited the formation of these chemical messenger pathways.

In addition, GcMAF at that dose inhibited the formation of prostate and breast cancer cell blood pathways in laboratory tests. They tested different GcMAF preparations in this type of test (CAM test) and this test proved to be a reliable, reproducible and inexpensive method of determining the potencies of different preparations and their stability. Storage at room temperature for 15 days decreased GcMAF potency by about 50%

Ref: Pacini S, Morucci G, Punzi T, Gulisano M, Ruggiero M. Gc protein-derived macrophage-activating factor (GcMAF) stimulates cAMP formation in human mononuclear cells and inhibits angiogenesis in chick embryo chorionallantoic membrane assay. Cancer Immunol Immunother. 2011 Apr;60(4):479-85. doi: 10.1007/s00262-010-0953-7. Epub 2010 Dec 14. PubMed PMID: 21170647.

5: Vitamin D binding protein-macrophage activating factor directly inhibits proliferation, migration, and uPAR expression of prostate cancer cells.

Summary: GcMAF shows a direct and potent effect on prostate tumour cells in the absence of macrophages.

It demonstrates a reduction in proliferation as well as metastic clones of these cells. Studies show that this is not due to the death of the cancer cells, but due to the reduction of multiplication.

GcMAF also prevents the migration of prostate cancer cells in the lab. It stopped the prostate cancer cells from producing a receptor, and evidence shows that this receptor correlates with metastasis. It concludes that GcMAF has strong inhibitory activity even in the absence of macrophages.

Ref: Gregory KJ, Zhao B, Bielenberg DR, Dridi S, Wu J, Jiang W, Huang B, Pirie-Shepherd S, Fannon M. Vitamin D binding protein-macrophage activating factor directly inhibits proliferation, migration, and uPAR expression of prostate cancer cells. PLoS One. 2010 Oct 18;5(10):e13428. doi:

6: Glycosylation status of vitamin D binding protein in cancer patients

Summary: Based on earlier studies, it appears that vitamin D binding protein (DBP) is significantly or completely deglycosylated in cancer patients, thus destroying the molecular precursor of the immunologically important GcMAF. This investigation was to directly investigate the volume of the three sugar molecules of serum derived DBP in various cancers. This study showed that there was no significant depletion of the trisaccharide in the 56 patients relative to healthy controls. This suggests that the hypotheses regarding the structural or molecular origins of GcMAF being a trisaccharide should be reconsidered.

Ref: Rehder DS, Nelson RW, Borges CR. Glycosylation status of vitamin D binding protein in cancer patients. Protein Sci. 2009 Oct;18(10):2036-42. doi:10.1002/pro.214. PubMed PMID: 19642159; PubMed Central PMCID: PMC2786967.

7: Immunotherapy for Prostate Cancer with Gc Protein-Derived Macrophage-Activating Factor, GcMAF.

Summary: Prostate cancer patients cannot produce their own GcMAF. 16 nonanemic prostate cancer patients received weekly injections of 100ng of GcMAF. After a 16-24 weeks all 16 patients had a normal nagalase reading equivalent to that of healthy controls, indicating the patients were tumour free. No recurrence in 7 years.

Ref: Yamamoto N, Suyama H, Yamamoto N. Immunotherapy for Prostate Cancer with GcProtein-Derived Macrophage-Activating Factor, GcMAF. Transl Oncol. 2008 Jul;1(2):65-72. PubMed PMID: 18633461; PubMed Central PMCID: PMC2510818.

8: Immunotherapy of metastatic colorectal cancer with vitamin D-binding protein-derived macrophage-activating factor

Summary: 100 ng GcMAF was administered weekly to eight non-anemic colorectal cancer patients who previously had tumor resection but still carried significant amounts of metastatic tumour cells. After 32-50 weeks all colorectal patients exhibited healthy controls of nagalase indicating eradication of tumour cells with no recurrence in 7 years.

Ref: Yamamoto N, Suyama H, Nakazato H, Yamamoto N, Koga Y. Immunotherapy of metastatic colorectal cancer with vitamin D-binding protein-derived macrophage-activating factor, GcMAF. Cancer Immunol Immunother. 2008 Jul;57(7):1007-16. PubMed PMID: 18058096.

9: Immunotherapy of metastatic breast cancer patients with vitamin D-binding protein-derived macrophage activating factor

Summary: 100 ng of GcMAF was administered weekly to 16 non anemic patients for treatment of metastatic breast cancer. After 16-22 administrations of GcMAF, the patients had healthy nagalase levels equivalent to healthy controls, with no recurrence for more than 4 years.

Ref: Yamamoto N, Suyama H, Yamamoto N, Ushijima N. Immunotherapy of metastatic breast cancer patients with vitamin D-binding protein-derived macrophage activating factor (GcMAF). Int J Cancer. 2008 Jan 15;122(2):461-7. PubMed PMID:17935130.

10: Pancreatic carcinogenesis: apoptosis and angiogenesis

Summary: Cell death and the creation of blood supplies to the cells (angiogenesis) are processes that are changed with cancers. Several reports show that a tumor suppressor gene that is in pancreatic cancer and related to malignancy can induce cell death and reduce the blood supply. This study has discovered two new angiogenesis inhibitors - one of them being GcMAF, the other aaAT-III. These molecules were able to regress tumours in immunodeficient mice, and show potent inhibition of circulatory cell proliferation. The angiogenesis inhibitors induced tumour dormancy in the animal model.

Ref: Onizuka S, Kawakami S, Taniguchi K, Fujioka H, Miya#a K. Pancreatic carcinogenesis: apoptosis and angiogenesis. Pancreas. 2004 Apr;28(3):317-9. PubMed PMID: 15084979.

11: Effect of salivary gland adenocarcinoma cell-derived alpha-N-acetylgalactosaminidase on the bioactivity of macrophage activating factor

Summary: To study the effects of nagalase on the bioactivity of GcMAF. A cancer cell line with high levels of nagalase, produced by the human salivary gland (HSG), was studied. GcMAF prepared enzymatically was able to activate macrophages. However, GcMAF treated with nagalase did not do this. Thus, salivary gland cancer in this study was able to produce large quantities of nagalase, which inactivates GcMAF produced from GcProtein, resulting in reduced phagocytic activity. This study suggests that HSG nagalase acts as an immunodeficiency factor in cancer patients.

Ref: Matsuura T, Uematsu T, Yamaoka M, Furusawa K. Effect of salivary gland adenocarcinoma cell-derived alpha-N-acetylgalactosaminidase on the bioactivity of macrophage activating factor. Int J Oncol. 2004 Mar;24(3):521-8. PubMed PMID:14767536.

12: Vitamin D binding protein-macrophage activating factor (DBP-maf) inhibits angiogenesis and tumor growth in mice.

Summary: Daily administration of GcMAF is able to slow down solid tumour growth (4ng/kg/4 days). At higher doses, GcMAF causes tumour regression (4ng/kg/day). The injections were into the body cavity (similar to IV in humans). The data suggests that GcMAF prevents the growth of blood supplies to tumours, and stimulates the macrophages to attack both the outside and the tumour cell compartment of a cancer.

Ref: Kisker O, Onizuka S, Becker CM, Fannon M, Flynn E, D'Amato R, Zetter B,Folkman J, Ray R, Swamy N, Pirie-Shepherd S. Vitamin D binding protein-macrophage activating factor (DBP-maf) inhibits angiogenesis and tumor growth in mice. Neoplasia. 2003 Jan-Feb;5(1):32-40. PubMed PMID: 12659668; PubMed Central PMCID: PMC1502120.

13: Effects of vitamin D(3)-binding protein-derived macrophage activating factor (GcMAF) on angiogenesis

Summary: As with other results, GcMAF inhibits cancer cell proliferation, independent of tissue origin, so it is not cancer specific. The ability of GcMAF to prevent blood supply creation to cancers may be regulated by the CD36 receptor.

Ref: Kanda S, Mochizuki Y, Miyata Y, Kanetake H, Yamamoto N. Effects of vitamin D(3)-binding protein-derived macrophage activating factor (GcMAF) on angiogenesis. J Natl Cancer Inst. 2002 Sep 4;94(17):1311-9. PubMed PMID:12208896.

14: Antitumor effect of vitamin D-binding protein-derived macrophage activating factor on Ehrlich ascites tumor-bearing mice

Summary: Administration of GcMAF to cancer bearing mice, to ascertain doses and intervals, using survival time and nagalase levels to record the effects.

The control group survived around 13 days.

a) Administration of 100pg (picogram)/mouse was given to 8 mice at the same time as tumour transplantation, 7 survived around 21 days, 1 more than 60.

b) Administrations of GcMAF, at day 0 and at day 4 after transplantation, 6 survived about 31 days, 2 more than 60 days.

c) Administrations of GcMAF in 4 day intervals after transplantation, 6 of the eight survived more than 60 days, with a nagalase level as low as healthy control group during the survival period. No mention of the survival time of the other 2 mice.

Conclusion is that the administration of small amounts of GcMAF caused protracted macrophage activation.

Ref: Koga Y, Naraparaju VR, Yamamoto N. Antitumor effect of vitamin D-binding protein-derived macrophage activating factor on Ehrlich ascites tumor-bearing mice. Proc Soc Exp Biol Med. 1999 Jan;220(1):20-6. PubMed PMID: 9893164.

15: Immunotherapy of BALB/c mice bearing Ehrlich ascites tumor with vitamin D-binding protein-derived macrophage activating factor

Summary: Administration of GcMAF and cdMAF to cancer bearing mice, to ascertain doses and intervals, using survival time and nagalase levels to record the effects. The readings of nagalase increased as the tumours grew.

The control group survived around 16 days.

a) Administration of GcMAF 100pg/mouse gave a survival time of 35 days.

b) Administrations of GcMAF, at day 0 and at day 4 after transplantation, survival increased to more than 50 days.

c) Mice that received GcMAF at days 4 and 8 after transplantation survived up to 32 days.

d) Administrations of GcMAF or cdMAF in 4 day intervals after transplantation, showed an extended survival of 90 days, with a nagalase level as low as healthy control group during the survival period.

This seems to be a poorly reported study, as it gives no indication of the performances of the different MAFs in relation to each other.

Ref: Yamamoto N, Naraparaju VR. Immunotherapy of BALB/c mice bearing Ehrlich ascites tumor with vitamin D-binding protein-derived macrophage activatingfactor. Cancer Res. 1997 Jun 1;57(11):2187-92. PubMed PMID: 9187119.

16: Prognostic utility of serum alpha-N-acetylgalactosaminidase and immunosuppression resulted from deglycosylation of serum Gc protein in oral cancer patients

Summary: 46 oral cancer patients were tested for Gcprotein. 22% had greatly reduced gcprotein, 61% was moderately reduced, 17% were equivalent to healthy controls. Patients with low gcprotein had high nagalase. Those with high Gcprotein had low nagalase. Thus there is an inverse relationship. Surgical removal of tumours results in a subtle decrease in nagalase. Tests in mice show that nagalase is directly proportional to tumour burden. Hence it could be used as a diagnostic

Ref: Yamamoto N, Naraparaju VR, Urade M. Prognostic utility of serum alpha-N-acetylgalactosaminidase and immunosuppression resulted from deglycosylation of serum Gc protein in oral cancer patients. Cancer Res. 1997 Jan
15;57(2):295-9. PubMed PMID: 9000571.

17: Macrophage-directed immunotherapy as adjuvant to photodynamic therapy of cancer

Summary: DBPMAF was made using mice serum (as opposed to GcMAF from human serum, as can mice make antibodies to human GcMAF). This alone was ineffective against skin cancer. Used with a PDT treatment, which was curative to 25% of the tumours, when DBPMAF was used alongside PDT, the cure rate increased to 100%.

Ref: Korbelik M, Naraparaju VR, Yamamoto N. Macrophage-directed immunotherapy as adjuvant to photodynamic therapy of cancer. Br J Cancer. 1997;75(2):202-7. PubMed PMID: 9010027; PubMed Central PMCID: PMC2063270.

18: Deglycosylation of serum vitamin D3-binding protein leads to immunosuppression in cancer patients

Summary: Blood monocytes / macrophages of 52 cancer patients were incubated with 100pg/ml of GcMAF. The monocytes / macrophages were efficiently activated. Naturally occurring GcMAF was severely reduced in about 25% of the patients, and moderately reduced in 45%. This was found to be the result of higher than normal levels of nagalase. The source of the nagalase appeared to be the cancerous cells as radiation therapy to reduce the cancer also reduced the level of nagalase. Thus both the levels of GcMAF and the levels of nagalase in the blood can serve as diagnostic indices.

Ref: Yamamoto N, Naraparaju VR, Asbell SO. Deglycosylation of serum vitamin D3-binding protein leads to immunosuppression in cancer patients. Cancer Res.1996 Jun 15;56(12):2827-31. PubMed PMID: 8665521.

19: Tumor cell alpha-N-acetylgalactosaminidase activity and its involvement in GcMAF-related macrophage activation

Summary: Nagalase causes the suppression of GcMAF. This is a study of the types of nagalase from several tumor cell lines. It concludes that nagalase derived from tumours is different to that from normal Chang liver cells (a type of laboratory cell line). Tumour derived nagalase decreases the potency of GcMAF activation.

Ref: Tumor cell alpha-N-acetylgalactosaminidase activity and its involvement in GcMAF-related macrophage activation. Mohamad SB, Nagasawa H, Uto Y, Hori H.

20: Vitamin D binding protein-macrophage activating factor inhibits HCC in SCID mice

Summary: GcMAF works on liver cancer in two ways – by reducing the blood supply to the tumour and by activating tumour killing macrophages.

Ref: Nonaka K, Onizuka S, Ishibashi H, Uto Y, Hori H, Nakayama T, Matsuura N,Kanematsu T, Fujioka H. Vitamin D binding protein-macrophage activating factor inhibits HCC in SCID mice. J Surg Res. 2012 Jan;172(1):116-22. doi:10.1016/j.jss.2010.07.057. Epub 2010 Sep 17. PubMed PMID: 20855083.