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Naturopathic Doctor Uses Nutrition To Cure 8-Year Old of Brain Cancer After Surgery, Chemotherapy and Radiation Failed

Prevent Disease | Sep 21, 2014 |Dave Mihalovic

After surgery, chemotherapy and radiation, an eight year old was still fighting for her life with subsequent brain tumors and given weeks to live. Her parents frantic search for alternatives led them to a naturopathic doctor who cured her with nutrition.

Her parents searched the internet for anything that could help their daughter and found Dr Bernardo Majalca, a naturopath, who offered them hope as well as a natural cure for Josie Nunez who was eight years old at the time.

Dr Majalca found that Josie wasn’t dying of cancer but was dying from acidosis, and that only by addressing this issue would her body finally be able to heal. He prescribed an alkalizing diet which included drinking 4 freshly made juices per day, as well as various herbs to help detoxify and rebuild her immune system.

“As the pH goes up, the lactic acid goes down which means the cancer activity is going down. The body repairs itself once it is given the stuff that it needs. Most doctors have no idea that nutrition has anything to do with cancer.” said Dr Bernardo Majalca

After months of experiencing a variety of symptoms and illnesses, Josie Nunez was diagnosed with a Medulloblastoma of the brain and spine in February of 2008.

After having a 6 week post-operative recovery period, Josie began six weeks of radiation andchemotherapy which was followed by a one month break and then a second round of chemotherapy which her doctors said would last for an additional 6 months. It wasn’t long before the second round of treatments began taking a toll on her little body and her parents reported that she suffered from nausea, constipation, abdominal pain, severe anemia, leg paralysis, constant infections, fever, hair loss, burned skin and weight loss.

By the fourth month of treatments, the doctors said that her spinal tumor had disappeared, however she then relapsed with a second brain tumor. At this point, doctors recommended that her family make arrangements for hospice care and that they should make the best of their final days together. Upon hearing the devastating news, Josie’s parents began frantically searching the internet for anything that could help their daughter and through a mutual friend they found Bernardo Majalca, a naturopathic doctor practicing out of San Deigo, CA, who offered them hope as well as a natural cure for Josie. When Josie first met with Dr Majalca she weighed only 40 pounds and was very weak.

After assessing Josie he determined that she wasn’t dying from the cancer but was actually dying from acidosis, and that only by addressing this issue would her body finally be able to heal. He then prescribed an alkalizing diet which included drinking 4 freshly made juices per day which would help her body to detoxify and then rebuild her immune system. He describes more about his treatment plans in the video below.

Alkalizing Diet

She could not eat any conventionally raised meat or dairy products, as well as anything that was man-made. That meant no fast foods, soda, candy, fries, sugars,  regular pasta, regular bread, or processed foods of any kind.

1st juicing recipe (taken 2 x per day): 1/2 mashed avocado mixed together with 8 oz of freshly made carrot juice, both are mixed together with a wooden spoon because metal can destroy some of the beneficial enzymes. They show how to make this recipe in the video that is linked below.

2nd juicing recipe (taken 2 x per day):

1 granny smith apple
1 cup of raw broccoli
1/2 inch slice of fresh pineapple (not canned)
1/2 of a beet
handful of cilantro
1/4 inch slice of ginger
1/2 inch slice of Daikon radish
1 carrot
1/2 cucumber
5 asparagus spears
run all items through a juicer

TESTING pH

Measuring Josie’s saliva pH– Josie’s family started each day by measuring her pH before she ate or drank anything using Ph Test Strips. Test strips can be purchased online or from a health food store. The range for saliva pH is considered to be 5.6 to 7.9 according to the International Journal of Drug Testing. The first test of the day is taken immediately upon waking before eating or drinking anything, otherwise wait at least two hours after eating or drinking to ensure that the food consumed does not alter the test results. To test you should cleanse the mouth by filling it with saliva and then swallow or spit it out. Fill the mouth a second time with saliva and place the test strip on the tongue for 10 seconds.

The strip will change colors based on the results. Use the insert from the package to determine the corresponding pH and monitor this 4 times per day to get a clear picture of what is going on inside of your body. You will find that your pH will fluctuate throughout the day, this is normal. Also it takes time to raise the pH, sometimes up to 12 weeks to become alkaline.

Dr Majalca said that cancer thrives in a pH of 5.5 or lower. When Josie’s family first started testing her saliva it wasn’t even registering on the strip because the lowest mark was 5.5 and she was well below that. It took at least 3 weeks before Josie was able to register above the 5.5 mark and then she slowly moved her way upwards. Dr Majalca says that when your saliva pH reaches 6.8 the cancer will stop growing, anything above that and the cancer begins to die. Their goal was to lift Josie’s pH to at least 7.2 – 7.4. It took a total of 8 weeks of being on a strict alkaline diet before Josie actually reached the 7.2 mark, she then had to hold herself at the level until she was confirmed to be cancer free.

Fresh air and sunlight- Her family reports that she also had access to plenty of fresh air and sunlight everyday. This means that her body was producing vitamin D from the sun exposure. Spending a short time in the mid-day sun (20- 30 minutes) can produce the equivalent of 10,000 IU or more of vitamin D. People looking to use the sun for vitamin D manufacturing should have at least 20 minutes of high noon sun exposure, per day, without the use of sunscreens as they will reduce the bodies ability to produce vitamin D by 95%, and most contain harmful chemicals which are absorbed into the skin. The key here is sensible sun exposure, you don’t want to burn.

Fresh water and alkaline water- Josie drank about 30 ounces of spring water daily. For for an adult that would be equivalent to 10 glasses of water per day. Spring water does not contain added fluoride or chlorine compounds and it has the natural minerals in it which makes this water more alkaline that regular tap water. Check out Find A Spring which is a national database to locate public access springs near you, or you can purchase bottled spring water at your local store.

Another option would be to drink water that has been filtered with a reverse osmosis mechanism with the minerals added back into it. Reverse osmosis water is acidic unless it has a mineral filter stage. Regular maintenance is required on this type of filtration system as the filters needing to be changed regularly. If you are not a mechanically inclined individual, many companies offer to rent the system for a monthly fee and then they come to your home and do all of the maintenance for you.

Other ways to add minerals back into reverse osmosis water would be to slice up a organic lemon along with a tsp of Himalayan Sea Salt to one gallon of water, or by adding Minerals Drops into filtered water and storing this in the refrigerator. Additionally, water can be made alkaline by adding 1/2 tsp of baking soda to an 8 ounce glass of water. This should be taken away from mealtimes as it will disrupt digestion, or taken at bedtime when you don’t have to worry about food intake. This should be limited to 3 tsp per day.

Josie’s cancer is healed- Josie’s family reports that they had previously scheduled an MRI for Josie when she was released from care, and to everyone’s astonishment the results of the MRI showed that the tumor had shrunk by 75%. Josie continued on with the fresh vegetable juices and diet program until the results from a second MRI confirmed that the tumor was completely gone. Her family received the amazing news on February 3, 2009, approximately one year after her original diagnosis.

Dr Bernardo Majalca– Dr Bernardo passed away in 2010 and to this day his treatment plans are highly regarded by holistic health professionals worldwide.

According to Dr Bernardo you can eat as many organic green vegetables as possible (except for green peas), as well red skinned potatoes (eaten with the skins). Include juicing and blending of the fruits and vegetables because this is an easy way to get many servings into your diet, especially when working with sick children. Raw vegetables are better than cooked, and if you do cook them they should be lightly steamed only. 80% of your diet should be vegetables with only 20% meats, and that meat is only allowed if one needs to regain weight. Acceptable meats include wild caught fish, organic venison, buffalo, lamb, or small amounts of turkey. A drink that will also help a person to put weight on if this is an issue: organic whipping cream, coconut milk, almond milk and a little Stevia Extract, this will taste like a vanilla shake. If you bake anything you must use stevia in place of sugar and use a gluten free mix instead of wheat flour. For example: pancakes can be made with buckwheat flour. Ezekiel sprouted bread is the only one allowed by Dr Bernardo, or bread that is homemade without gluten or preservatives. Only organic eggs and organic butter are allowed and should be raw (unpasteurized) if possible. The only oil allowed is extra virgin olive oil. The only dressing you can have is olive oil and vinegar, or olive oil with a squeeze of fresh lemon on it. Drink lots of water with freshly squeezed lemon, with a little Stevia to sweeten if needed. Nothing can be packaged or processed.

Link to Dr. Majalca’s e-book on diet and other therapies prescribed to heal cancer

Sources:
cancercompassalternateroute.com

Cancer cells want high fat and an attack on the Pancreas

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High Fat is what cancer cell wants

One feature that distinguishes tumor cells from normal cells is their dysregulated metabolism. For example, tumor cells undergo glycolytic rather than oxidative metabolism, a change known as the Warburg effect, and they synthesize greater amounts of proteins and fatty acids than do normal cells (see the commentary by Yecies and Manning).

Connie’s notes: Cancer cells use MAGL and LIPE and Insulin inhibits LIPE.

Sci. Signal. 12 Jan 2010:
Vol. 3, Issue 104, pp. ec8
DOI: 10.1126/scisignal.3104ec8

The authors found that monoacylgycerol lipase (MAGL), a serine hydrolase that degrades the endogenous cannabinoid 2-arachidonylglycerol and other MAGs, was enriched in the aggressive cell lines. MAGL was also more abundant in high-grade, human ovarian tumors than in benign tumors. Knockdown of MAGL in aggressive cancer cell lines by short hairpin RNA (shRNA) resulted in decreased amounts of free fatty acids (FFAs) and inhibited the migration, survival, and invasiveness of the cells, as assessed in vitro; conversely, lentiviral-mediated overexpression of MAGL in nonaggressive cancer cell lines had opposing effects. Transfer of an aggressive melanoma cell line containing MAGL-specific shRNA into immune-deficient mice resulted in smaller tumors than occurred when control shRNA-treated cells were used; however, the effect of knockdown of MAGL on tumor growth was reversed when the mice were fed a high-fat diet. Lipidomic analysis revealed the increased abundance of protumorigenic lipids, such as lysophosphatidic acid and prostaglandin E₂, in aggressive cell lines, and blockade of the receptors for these lipids decreased the migration of these cell lines in vitro. Together, these data suggest that tumor cells use MAGL to generate a range of protumorigenic lipid signals that increase malignancy.

http://stke.sciencemag.org/content/3/104/ec8

Monoacylglycerol lipase functions together with hormone-sensitive lipase (LIPE)

Monoacylglycerol lipase functions together with hormone-sensitive lipase (LIPE) to hydrolyze intracellular triglyceride stores in adipocytes and other cells to fatty acids and glycerol. MGLL may also complement lipoprotein lipase (LPL) in completing hydrolysis of monoglycerides resulting from degradation of lipoprotein triglycerides.^[5]
Monoacylglycerol lipase is a key enzyme in the hydrolysis of the endocannabinoid 2-arachidonoylglycerol (2-AG).^[6][7] It converts monoacylglycerols to the free fatty acid and glycerol. The contribution of MAGL to total brain 2-AG hydrolysis activity has been estimated to be ~85% (ABHD6 and ABHD12 are responsible for ~4% and ~9%, respectively, of the remainder),^[8][9] and this in vitro estimate has been confirmed in vivo by the selective MAGL inhibitor JZL184.^[10] Chronic inactivation of MAGL results in massive (>10-fold) elevations of brain 2-AG in mice, along with marked compensatory downregulation of CB₁ receptors in selective brain areas.^[

Hormone-sensitive lipase mobilizes stored fats

The main function of hormone-sensitive lipase is to mobilize the stored fats. Mobilization and Cellular Uptake of Stored Fats (with Animation) HSL functions to hydrolyze the first fatty acid from a triacylglycerol molecule, freeing a fatty acid and diglyceride. It is also known as triglyceride lipase, while the enzyme that cleaves the second fatty acid in the triglyceride is known as diglyceride lipase, and the third enzyme that cleaves the final fatty acid is called monoglyceride lipase. Only the initial enzyme is affected by hormones, hence its hormone-sensitive lipase name. The diglyceride and monoglyceride enzymes are tens to hundreds of times faster, hence HSL is the rate-limiting step in cleaving fatty acids from the triglyceride molecule.^[8][9]
HSL is activated when the body needs to mobilize energy stores, and so responds positively to catecholamines, ACTH. It is inhibited by insulin. Previously, glucagon was thought to activate HSL, however the removal of insulin’s inhibitory effects (“cutting the brakes”) is the source of activation. The lipolytic effect of glucagon in adipose tissue is minimal in humans.^{[citation needed]}
Another important role is the release of cholesterol from cholesterol esters for use in the production of steroids.^[10

HCL is inhibited by insulin

Insulin (from the Latin, insula meaning island) is a peptide hormone produced by beta cells of the pancreatic islets, and by the Brockmann body in some teleost fish.^[3] It has important effects on the metabolism of carbohydrates, fats and protein by promoting the absorption of, especially, glucose from the blood into fat, liver and skeletal muscle^[4] In these tissues the absorbed glucose is converted into either glycogen or fats (triglycerides), or, in the case of the liver, into both.^[4] Glucose production (and excretion into the blood) by the liver is strongly inhibited by high concentrations of insulin in the blood.^[5] Circulating insulin also affects the synthesis of proteins in a wide variety of tissues. In high concentrations in the blood it is therefore an anabolic hormone, promoting the conversion of small molecules in the blood into large molecules inside the cells. Low insulin levels in the blood have the opposite effect by promoting widespread catabolism.
The pancreatic beta cells (β cells) are known to be sensitive to the glucose concentration in the blood. When the blood glucose levels are high they secrete insulin into the blood; when the levels are low they cease their secretion of this hormone into the general circulation.^[6] Their neighboring alpha cells, probably by taking their cues from the beta cells,^[6] secrete glucagon into the blood in the opposite manner: high secretion rates when the blood glucose concentrations are low, and low secretion rates when the glucose levels are high.^[4][6] High glucagon concentrations in the blood plasma powerfully stimulate the liver to release glucose into the blood by glycogenolysis and gluconeogenesis, thus having the opposite effect on the blood glucose level to that produced by high insulin concentrations.^[4][6] The secretion of insulin and glucagon into the blood in response to the blood glucose concentration is the primary mechanism responsible for keeping the glucose levels in the extracellular fluids within very narrow limits at rest, after meals, and during exercise and starvation.^[6]
When the pancreatic beta cells are destroyed by an autoimmune process, insulin can no longer be synthesized or be secreted into the blood. This results in type 1 diabetes mellitus, which is characterized by very high blood sugar levels, and generalized body wasting, which is fatal if not treated. This can only be corrected by injecting the hormone, either directly into the blood if the patient is very ill and confused or comatosed, or subcutaneously for routine maintenance therapy, which must be continued for the rest of the person’s life.^[7] The exact details of how much insulin needs to be injected, and when during the day, has to be adjusted according to the patient’s daily routine of meals and exercise, in order to mimic the physiological secretion of insulin as closely as is practically possible.

Summary of Cancer Metabolism

Reprogrammed metabolic pathways are essential for cancer cell survival and growth.
Frequently reprogrammed activities include those that allow tumor cells to take up abundant nutrients and use them to produce ATP, generate biosynthetic precursors and macromolecules, and tolerate stresses associated with malignancy (for example, redox stress and hypoxia).
An emerging class of reprogrammed pathways includes those allowing cancer cells to tolerate nutrient depletion by catabolizing macromolecules from inside or outside the cell (for example, autophagy, macropinocytosis, and lipid scavenging).
Reprogramming may be regulated intrinsically by tumorigenic mutations in cancer cells or extrinsically by influences of the microenvironment.
Oncometabolites (for example, 2HG) accumulate as a consequence of genetic changes within a tumor and contribute to the molecular process of malignant transformation.
Many metabolites exert their biological effects outside of the classical metabolic network, affecting signal transduction, epigenetics, and other functions.
New approaches to assess metabolism in living tumors in humans and mice may improve our ability to understand how metabolic reprogramming is regulated and which altered pathways hold opportunities to improve care of cancer patients.

First, metabolic reprogramming is essential for the biology of malignant cells, particularly their ability to survive and grow by using conventional metabolic pathways to produce energy, synthesize biosynthetic precursors, and maintain redox balance.
Second, metabolic reprogramming is the result of mutations in oncogenes and tumor suppressors, leading to activation of PI3K and mTORC1 signaling pathways and transcriptional networks involving HIFs, MYC, and SREBP-1.
Third, alterations in metabolite levels can affect cellular signaling, epigenetics, and gene expression through posttranslational modifications such as acetylation, methylation, and thiol oxidation.
Fourth, taken together, studies on cultured cells have demonstrated a remarkable diversity of anabolic and catabolic pathways in cancer, with induction of autophagy and utilization of extracellular lipids and proteins complementing the classical pathways like glycolysis and glutaminolysis.

Tumor-suppressive functions of p53

Another commonly deregulated pathway in cancer is gain of function of MYC by chromosomal translocations, gene amplification, and single-nucleotide polymorphisms. MYC increases the expression of many genes that support anabolic growth, including transporters and enzymes involved in glycolysis, fatty acid synthesis, glutaminolysis, serine metabolism, and mitochondrial metabolism (18). Oncogenes like Kras, which is frequently mutated in lung, colon, and pancreatic cancers, co-opt the physiological functions of PI3K and MYC pathways to promote tumorigenicity. Aside from oncogenes, tumor suppressors such as the p53 transcription factor can also regulate metabolism (19). The p53 protein–encoding gene TP53 (tumor protein p53) is mutated or deleted in 50% of all human cancers. The tumor-suppressive functions of p53 have been ascribed to execution of DNA repair, cell cycle arrest, senescence, and apoptosis. However, recent studies indicate that p53 tumor-suppressive actions might be independent of these canonical p53 activities but rather dependent on the regulation of metabolism and oxidative stress (20, 21). Loss of p53 increases glycolytic flux to promote anabolism and redox balance, two key processes that promote tumorigenesis.

Mitochondrial metabolism

Mitochondrial metabolism has also emerged as a key target for cancer therapy, in part, due to the revelation that the antidiabetic drug metformin is an anticancer agent (153). Numerous epidemiological studies first suggested that diabetic patients taking metformin, to control their blood glucose levels, were less likely to develop cancer and had an improved survival rate if cancer was already present (154). Laboratory-based studies have also provided evidence that metformin may serve as an anticancer agent (155–157). Biochemists recognized that metformin reversibly inhibits mitochondrial complex I (158–160). Recent studies indicate that metformin acts as an anticancer agent by inhibiting mitochondrial ETC complex I (161). Specifically, metformin inhibits mitochondrial ATP production, inducing cancer cell death when glycolytic ATP levels diminish as a result of limited glucose availability.

Metformin

Metformin also inhibits the biosynthetic capacity of the mitochondria to generate macromolecules (lipids, amino acids, and nucleotides) within cancer cells (162). The remarkable safety profile of metformin is due to its uptake by organic cation transporters (OCTs), which are only present in a few tissues, such as the liver and kidney (163). Certain tumor cells also express OCTs to allow the uptake of metformin (164). However, in the absence of OCTs, tumors would not accumulate metformin to inhibit mitochondrial complex I. Ongoing clinical trials using metformin as an anticancer agent should assess the expression levels of OCTs to identify the tumors with highest expression, which are likely to be susceptible to metformin.

Vitamin C

An interesting approach to depleting NADPH levels and increasing ROS is to administer high doses of vitamin C (ascorbate). Vitamin C is imported into cells through sodium-dependent vitamin C transporters, whereas the oxidized form of vitamin C, dehydroascorbate (DHA), is imported into cells through glucose transporters such as GLUT1 (179). When the cell takes up DHA, it is reduced back to vitamin C by glutathione (GSH), which consequently becomes GSSG. Subsequently, GSSG is converted back to GSH by NADPH-dependent GR. Because the blood is an oxidizing environment, vitamin C becomes oxidized to DHA before being taken up by the cell. Thus, high doses of vitamin C diminish the tumorigenesis of colorectal tumors that harbor oncogenic KRAS mutations and express high levels of GLUT1 by depleting the NADPH and GSH pools and consequently increasing ROS levels to induce cancer cell death (179, 180). Vitamin C administered at high doses intravenously is safe in humans and, in conjunction with conventional paclitaxel-carboplatin therapy, demonstrated a benefit in a small number of patients (181). Additional strategies to diminish GSH include the administration of buthionine sulfoximine, an irreversible inhibitor of γ-glutamylcysteine synthetase, which can be safely administered to humans and is efficacious in preclinical tumor models (182). Moreover, glutathione is a tripeptide consisting of cysteine, glutamate, and glycine. Thus, decreasing glutamate levels using glutaminase inhibitors or diminishing cysteine levels by preventing extracellular cysteine (two linked cysteine molecules) uptake can also raise ROS levels in cancer cells to induce cell death.

Scientists are finding way to target cancer cells using their metabolic pathways

Another potential therapeutic strategy to inhibit mitochondrial metabolism in certain tumors would be to use autophagy or glutaminase inhibitors. Autophagy provides amino acids, such as glutamine, that fuel the TCA cycle in NSCLC and pancreatic cancers, and short-term autophagy inhibition has been shown to decrease tumor progression without incurring systemic toxicity in mouse models of NSCLC (168, 169). Some tumors are addicted to using glutamine to support TCA cycle metabolism even in the absence of autophagy; thus, glutaminase inhibitors can reduce tumor burden in these models (4, 75,170). An alternative approach is to target acetate metabolism. Although a major function of the mitochondria is to provide acetyl-CoA to the cell, cancer cells can also use acetate to support cell growth and survival during metabolic stress (hypoxia or nutrient deprivation) (96, 171). The cytosolic enzyme acetyl-CoA synthase 2 (ACCS2), which converts acetate to acetyl-CoA, is dispensable for normal development; thus, ACCS2 is a promising target of acetate metabolism. ACCS2 knockout mice do not display overt pathologies, but genetic loss of ACCS2 reduces tumor burden in models of hepatocellular carcinoma (171). Human glioblastomas can oxidize acetate and may be sensitive to inhibitors of this process (172). Thus, targeting metabolism with inhibitors of autophagy, acetate metabolism, and other pathways that supply key metabolic intermediates may be efficacious in some contexts.

Blood Cancer Risk Factor Formula

Blood Cancer (BC) Risk Factor

1.0 = 0.2 + 0.2 + 0.1 + 0.2 + 0.1 + 0.1 + 0.1

©Connie Dello Buono 15Sept2016

Sex M=0.2 , F = 0.1
Age > 15 yrs = 0.2 , < 15 yrs =0.1
Race = 0.1 (South Asian, Caucasian)
Prenatal exposure to x-rays/chemicals/alcohol ; = 0.2
Environmental toxins, therapeutic radiation ; previous cancer treatment: Certain types of chemotherapy and radiation therapy for other cancers are considered leukemia risk factors ; smoking ; Diabetes 0.1
Specific genetic syndromes ; Down syndrome ; 0.1
Virus = 0.1

BC Risk Factor =1.0 (High) ; BC Risk Factor =

Please email your entries to motherhealth@gmail.com to create a database and get health data insights about Alzheimer’s disease

blood-cancer-risks

Modified Blood Risk Factor

Sex
Male = 0.2
Female =0.1

Age > 15yrs=0.2
15yrs <= 0.1

Race = 0.1 (south asian)

Prenatal exposure to x-rays, chemicals, medications/drugs, alcohol = 0.2

Environmental toxins, therapeutic radiation , non-ionizing radiation,; previous cancer treatment: Certain types of chemotherapy and radiation therapy for other

Metabolic and diet:
Diabetes 0.1

smoking = 0.1

Specific genetic syndromes ; Down syndrome = 0.1

Polymorphic alleles of the human leukocyte antigen (HLA) class II genes = 0.1

Weak immune and metabolic system:
Infection and allergy 0.1

Prenatal health of mother may contribute to childhood leukemia

Prenatal exposure to x-rays, and genetic syndromes chromosomal alterations and mutations that disrupt the normal process by which lymphoid or myeloid progenitor cells differentiate and senesce. The underlying triggers for molecular damage may be inherited during pregnancy and may develop during infancy and childhood. These translocations are a ‘‘hallmark’’ genetic event in leukemia. Many leukemia patients have a chromosomal translocation that is often the only observable cytogenetic aberration. These abnormalities help categorize leukemia for treatment strategy and prognosis and may also delineate specific causal pathways to malignancy.

Recently, genetic backtracking analyses, using archived newborn blood specimens and pretreatment bone marrow or peripheral blood specimens obtained at the time of diagnosis, have been applied to study the timing of various translocations. To date, a prenatal origin has been established for several chromosomal abnormalities.

This link points to environmental carcinogens as one of the causes of blood cancer – > http://superfund.berkeley.edu/pdf/28.pdf

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