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Thursday, May 26, 2016

Most common Diseases Free and Longevity of 50 plus - Turmeric Part D By Foods to prevent and treat cancers

Kyle J. Norton(Scholar and Master of Nutrients, all right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

Over the years of research, 4 foods appeared mostly in medical studies in preventing and treating diseases, are Green Tea, Grape seed and skin, Turmeric and Organic Soy(Not for Western Women). All Right Reserved.


III. Turmeric
Turmeric, principal curcuminoid of the popular Indian spice, a rhizomatousherbaceous perennial plant of the ginger family, Zingiberaceae, native totropical South Asia, according to "Effects of different drying methods on the antioxidant properties of leaves and tea of ginger species" by E.W.C. Chan, Y.Y. Lim, S.K. Wong, K.K. Lim, S.P. Tan, F.S. Lianto and M.Y. Yong, posted in Science Direct. It has been used in traditional herbal medicine as an anti-inflammatory agent and to treat gastrointestinal symptoms associated with irritable bowel syndrome and other digestive disorders. Curcumin is a phytochemical found abundant in the plant. In acidic solutions (pH <7.4) it turns yellow, whereas in basic (pH > 8.6) solutions it turns bright red.

D. By Foods to prevent and treat cancers
1. Bone cancer (Osteosarcoma(35%))
Curcumin the main ingredient of turmeric has shown to induce cell apoptosis in human osteosarcoma. Dr. Li Y, and scientists at the Qilu Hospital, Shandong University indicated that curcumin caused marked inhibition of osteosarcoma cell growth and G2/M phase cell cycle arrest. This was associated with concomitant attenuation of Notch-1 and downregulation of its downstream genes, such as matrix metalloproteinases, resulting in the inhibition of osteosarcoma cell invasion through Matrigel. We also found that specific downregulation of Notch-1 via small-interfering RNA prior to curcumin treatment resulted in enhanced inhibition of cell growth and invasion(1).

2. Bone cancer (Chondrosarcoma(25%))
Turmeric, principal curcuminoid of the popular Indian spice, a rhizomatousherbaceous perennial plant of the ginger family, Zingiberaceae, native to tropicalSouth Asia, Curcumin the main ingredient of turmeric has shown to induce cell apoptosis in human chondrosarcoma. Dr. Lee HP, and scientists at the China Medical University Hospital, found that Curcumin induced upregulation of Fas, FasL, and DR5 expression in chondrosarcoma cells. Transfection of cells with Fas, FasL, or DR5 siRNA reduced curcumin-induced cell death. In addition, p53 involved in curcumin-mediated Fas, FasL, and DR5 expression and cell apoptosis in chondrosarcoma cells. Most importantly, animal studies revealed a dramatic 60% reduction in tumor volume after 21days of treatment(2).

3. Bone cancer (Ewing's sarcoma(16%))
Curcumin is a naturally occurring polyphenolic compound found in the turmeric.Under investigation as a chemotherapeutic and chemopreventive agent in adult cancer models at both pre-clinical and clinical levels. In this preliminary study, showed that curcumin is effective in causing cell cycle arrest, inducing apoptosis, and suppressing colony formation in the Ewing sarcoma cell line SK-NEP-1. Curcumin causes upregulation of cleaved caspase 3 and downregulation of phospho-Akt, producing apoptosis in Ewing sarcoma cells at an inhibitory concentration 50% (IC50) of approximately 4 μM. (3)

4. Cervical cancer
Epidemiological and preclinical evidence suggests that polyphenolicphytochemicals exemplified by epigallocatechin gallate from tea, curcumin from curry and soya isoflavones possess cancer chemopreventive properties. Dr. Thomasset SC and scientists at the University of Leicester, in the review of above showed that the available evidence for tea polyphenols tentatively supports their advancement into phase III clinical intervention trials aimed at the prevention of progression of prostate intraepithelial neoplasia, leukoplakia or premalignantcervical disease. In the case of curcumin and soya isoflavones more studies in premalignacies seem appropriate to optimise the nature and design of suitable phase III trials. The abundance of flavonoids and related polyphenols in the plant kingdom makes it possible that several hitherto uncharacterised agents with chemopreventive efficacy are still to be identified, which may constitute attractive alternatives to currently used chemopreventive drugs(4).

5. Hodgkin's lymphoma
Turmeric, a principal curcuminoid of the popular Indian spice, a rhizomatousherbaceous perennial plant of the ginger family, Zingiberaceae, native to tropicalSouth Asia, according to "Effects of different drying methods on the antioxidant properties of leaves and tea of ginger species" by E.W.C. Chan, Y.Y. Lim, S.K. Wong, K.K. Lim, S.P. Tan, F.S. Lianto and M.Y. Yong, posted in Science Direct. It has been used in traditional herbal medicine as an anti-inflammatory agent and to treat gastrointestinal symptoms associated with irritable bowel syndrome and other digestive disorders. Curcumin is a phytochemical found abundant in the plant. In acidic solutions (pH <7.4) it turns yellow, whereas in basic (pH > 8.6) solutions it turns bright red. In the study to to find new therapies that specifically target the deregulated signaling cascades, such as NF-kappaB and STAT3, which causeHodgkin and Reed-Sternberg (H-RS) cell proliferation and resistance of apoptosis, indicated that Curcumin is incorporated into H-RS cells and acts inhibiting both NF-kappaB and STAT3 activation, leading to a decreased expression of proteins involved in cell proliferation and apoptosis, e.g. Bcl-2, Bcl-xL, cFLIP, XIAP, c-IAP1, survivin, c-myc and cyclin D1. Interestingly, curcumin caused cell cycle arrest in G2-M and a significant reduction (80-97%) in H-RS cell viability. Furthermore, curcumin triggered cell death by apoptosis, as evidenced by the activation of caspase-3 and caspase-9, changes in nuclear morphology and phosphatidylserine translocation. The above findings provide a mechanistic rationale for the potential use of curcumin as a therapeutic agent for patients with HL(5).

6. Renal cell carcinoma (Kidney cancer/renal cells)
Curcumin (1,7-bis(4-hydroxy-3-methoxyphenyl)-1E,6E-heptadiene-3,5-dione or diferuloyl methane) is a polyphenol derived from the Curcuma longa plant, commonly known as turmeric.Dr. Kössler S and scientists at the Paracelsus Medical University, in the study of Curcumin affects cell survival and cell volume regulation in human renal and intestinal cells showed that Curcumin exposure induces apoptosis in human kidney cells, and at a concentration of 5.0-10 μM induces the appearance of a sub-population of cells with a dramatically increased volume. In these cells the regulation of the cell volume seems to be impaired, most likely as a consequence of the ICl(swell) blockade. Similarly, 50 μMcurcumin induced apoptosis, caused cell cycle arrest in G1-phase and increased the volume of human colorectal adenocarcinoma HT-29 cells. The cell cycle arrest in G1 phase may be the mechanism underlying the volume increase observed in this cell line after exposure to curcumin(6)

7. Ovarian cancer
a. In the study to analyze the impact of sphingosine kinase-1 (SphK-1) inhibition on ceramides production, and evaluated SphK1 inhibitor II (SKI-II) as a potentialcurcumin chemo-sensitizer in ovarian cancer cells, found that inhibition of SphK1 by SKI-II or by RNA interference (RNAi) knockdown dramatically enhancedcurcumin-induced apoptosis and growth inhibition in ovarian cancer cells. SKI-II facilitated curcumin-induced ceramides production, p38 activation and Akt inhibition. Inhibition of p38 by the pharmacological inhibitor (SB 203580), a dominant-negative expression vector, or by RNAi diminished curcumin and SKI-II co-administration-induced ovarian cancer cell apoptosis, and, to restore Akt activation by introducing a constitutively active Akt (CA-Akt), or to inhibit ceramides production by fumonisin B1 also inhibited curcumin plus SKI-II co-administration-induced in vitro anti-ovarian cancer effect(7).
b. Others found that curcumin exhibited time- and dose-dependent cytotoxicity against monolayer cultures of ovarian carcinoma cell lines with differing p53 status (wild-type p53: HEY, OVCA429; mutant p53: OCC1; null p53: SKOV3). In addition, p53 knockdown or p53 inhibition did not diminish curcumin killing of HEY cells, confirming p53-independent cytotoxicity. Curcumin also killed OVCA429, and SKOV3 cells grown as multicellular spheroids(7a).

8. Stomach Cancer/Gastric Cancer
Curcumin, a phytochemical compound found in Turmeric has exerted the inhibitory effect against Gastric Cancer. Dr. Sintara K and scientist at the Chulalongkorn University, indicated that curcumin treatments for 3 and 20 weeks reduced thecancer incidence resulting in a decrease of phospho-IκBα expression in benign tumor-bearing rats compared with MNU + s-NaCl. Curcumin treatment for 20 weeks also decreased 8-OHdG expression in benign tumor-bearing rats compared with MNU + s-NaCl. Curcumin can attenuate cancer via a reduction of phospho-IκBα and 8-OHdG expressions, which may play a promising role in gastriccarcinogenesis(8).

9. Skin cancer
In the study of curcumin loaded chitin nanogels (CCNGs) were developed using biocompatible and biodegradable chitin with an anticancer curcumin drug. Chitin, as well as curcumin, is insoluble in water,
indicated that The CCNGs showed a 4-fold increase in steady state transdermal flux of curcumin as compared to that of control curcumin solution. The histopathology studies of the porcine skin samples treated with the prepared materials showed loosening of the horny layer of the epidermis, facilitating penetration with no observed signs of inflammation. These results suggest that the formulated CCNGs offer specific advantage for the treatment of melanoma, the most common and serious type of skin cancer, by effective transdermal penetration(9).

10. Prostate cancer
In the study to examine of a prospective study with 225 incident cases of prostate cancer in 12,395 California Seventh-Day Adventist men who in 1976 stated how often they drank soy milk.
suggests that men with high consumption of soy milk are at reduced risk ofprostate cancer. Possible associations between soy bean products, isoflavones and prostate cancer risk should be further investigated(10).

11. Pancreatic cancer
the study of Impact of curcumin, raspberry extract, and neem leaf extract on rel protein-regulated cell death/radiosensitization in pancreatic cancer cells showed that CUR, NLE, and RSE may serve as effective "deliverables" to potentiate RT in PC cure and further throw light that these phytochemicals-induced cell killing may involve selective regulation of RT-induced NF-κB(11).

12. Pharynx Cancer or pharyngeal cancer
In the study to investigate the mechanism underlying the curcumin-induced apoptosis of nasopharyngeal carcinoma (NPC) cell line NCE cells, indicated that Several evidences of apoptosis were obtained from curcumin-treated NCE cells by acridine orange and ethidium bromide stains, ultrastructure identification, DNA fragmentation assay and TUNEL staining. And the mean TUNEL-positive rates increased significantly at the 3 different time points (12 h, 24 h and 48 h; 25.6%, 40.3% and 54.5%, respectively). In the curcumin-treated-groups, delta psi m altered significantly and the positive rates increased in a time-dependent manner. At the 3 different time points, the mean positive rates were 26.8%, 42.3% and 68.2%, respectively. When caspase-3 activity was detected, 80.5% cells presented proteases activities after 12 h incubation with curcumin. Western Blot analysis showed that cytoplasmic cytochrome C increased significantly after incubation with curcumin. Flow cytometry and RT-PCR analysis showed thatcurcumin could up-regulate the Fas expression in time-depended manner , the positive rates of Fas protein increased from 33.6% to 89.9%(12).

13. Multiple myeloma (Myeloma)
In the study of Curcumin (diferuloylmethane) down-regulates the constitutive activation of nuclear factor-kappa B and IkappaBalpha kinase in human multiple myeloma cells, leading to suppression of proliferation and induction of apoptosis, scientists at the The University of Texas MD Anderson Cancer Center, showed that Curcumin suppressed the constitutive IkappaBalpha phosphorylation through the inhibition of IKK activity. Curcumin also down-regulated the expression of NF-kappaB-regulated gene products, including IkappaBalpha, Bcl-2, Bcl-x(L), cyclin D1, and interleukin-6. This led to the suppression of proliferation and arrest of cells at the G(1)/S phase of the cell cycle. Suppression of NF-kappaB complex by IKKgamma/NF-kappaB essential modulator-binding domain peptide also suppressed the proliferation of MM cells. Curcumin also activated caspase-7 and caspase-9 and induced polyadenosine-5'-diphosphate-ribose polymerase (PARP) cleavage. Curcumin-induced down-regulation of NF-kappaB, a factor that has been implicated in chemoresistance, also induced chemosensitivity to vincristine and melphalan(13).

14. Oral cancer
Curcumin, a major active component and principal curcuminoid of the popular Indian spice of turmeric, ,has been shown to have inhibitory effects on cancers. Dr. Kim JY, and scientists in the study of Curcumin-induced autophagy contributes to the decreased survival of oral cancer cells. indicated that curcumin induced reactive oxygen species (ROS) production and autophagic vacuoles formation bycurcumin was almost completely blocked in the presence of N-acetylcystein (NAC), an antioxidant. Rescue experiments using an autophagy inhibitor suppressed curcumin-induced cell death in OSCC, confirming that autophagy acts as a pro-death signal. Furthermore, curcumin shows anticancer activity against OSCC via both autophagy and apoptosis (14).

15. Melanoma skin cancer
Curcumin is a phytochemical found abundant in the plant. In acidic solutions (pH <7.4) it turns yellow, whereas in basic (pH > 8.6) solutions it turns bright red. In the successfully incorporated curcumin into a bilayer of dodecanoic acid attached to magnetite nanoparticles in an effort to maximize solubility and delivery efficiency, found that fluorescent microscopy revealed that curcumin associated magnetite nanoparticles were internalized by the melanoma cells and remained in the cytoplasm. The curcumin/magnetic nanoparticles synthesized in this study possess magnetic and water solubility properties making this a novel curcuminformulation with therapeutic potential(15).

16. Non-Hodgkin's Lymphoma
In the study investigated a novel drug delivery nanovehicle enriched with the bioactive polyphenol, curcumin (curcumin nanodisks; curcumin-ND), showed that cells treated with curcumin-ND showed a dose-dependent increase in apoptosis. This was accompanied by enhanced generation of reactive oxygen species (ROS). The antioxidant, N-acetylcysteine, inhibited curcumin-ND induced apoptosis, suggesting that ROS generation plays a role in curcumin action on MCL cells.Curcumin-ND decreased cyclin D1, pAkt, pIκBα, and Bcl(2) protein. In addition, enhanced FoxO3a and p27 expression as well as caspase-9, -3, and poly(ADP-ribose) polymerase (PARP) cleavage were observed. Curcumin-ND treatment led to enhanced G(1) arrest in two cultured cell models of MCL(16).

17. Leukemia
Curcumin is a phytochemical found abundant in Turmeric. In acidic solutions (pH <7.4) it turns yellow, whereas in basic (pH > 8.6) solutions it turns bright red. In the study to investigate the anti-cancer effect and action of curcumin on THP-1 cells, showed that Curcumin induced cell apoptosis of THP-1 cells as shown by cell viability, cell cycle analysis and caspase activity. Curcumin significantly increased the phosphorylation of ERK, JNK and their downstream molecules (c-Jun and Jun B). Inhibitor of JNK and ERK reduced the pro-apoptotic effect of curcumin on THP-1 cells as evidenced by caspase activity and the activation of ERK/JNK/Jun cascades. On the contrary, the pro-apoptotic effect of curcumin was abolished in the differentiated THP-1 cells mediated by PMA(17).

18. Etc.

Side effects
1. Overdose may cause gastrointestinal discomfort such as nausea and diarrhea and liver damage.
2. Topical use may be allergic to skin such irritation to certain peoples
3. Do not use the herb in new born, children or if you are pregnant and breast feeding without approval from the related field specialist.
4. Etc.


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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/22521131
(2) http://www.ncbi.nlm.nih.gov/pubmed/22522053
(3) http://www.ncbi.nlm.nih.gov/pubmed/19859844
(4) http://www.ncbi.nlm.nih.gov/pubmed/17131309
(5) http://www.ncbi.nlm.nih.gov/pubmed/18386790
(6) http://www.ncbi.nlm.nih.gov/pubmed/22178266
(7) http://www.ncbi.nlm.nih.gov/pubmed/22594559
(7a) http://www.ncbi.nlm.nih.gov/pubmed?term=Curcumin%20also%20killed%20OVCA429%2C%20and%20SKOV3%20cells%20grown%20as%20multicellular%20spheroids
(8) http://www.ncbi.nlm.nih.gov/pubmed/22690125
(9) http://www.ncbi.nlm.nih.gov/pubmed/22080352
(10) http://www.ncbi.nlm.nih.gov/pubmed/10189040
(11) http://www.ncbi.nlm.nih.gov/pubmed/21697760
(12) http://www.ncbi.nlm.nih.gov/pubmed/17039805
(13) http://www.ncbi.nlm.nih.gov/pubmed/12393461
(14) http://www.ncbi.nlm.nih.gov/pubmed/22554995
(15) http://www.ncbi.nlm.nih.gov/pubmed/20974686
(16) http://www.ncbi.nlm.nih.gov/pubmed/21699455
(17) http://www.ncbi.nlm.nih.gov/pubmed/22443687

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