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Re: WOW read this. compares cu:zn in Alzheimer's and MS.

Post by 1eye » Mon Feb 13, 2017 7:39 am

Note well the increased venticle sizes. This is entirely traceable to increased internal pressure due to bad venous drainage.

If further commentary is of any use to those who don't want to have anything to do with the main purpose of this particlar forum, which is discussion of CCSVI, those comments are better aimed at the General forum. Many in this forum believe CCSVI is related to MS. Comments which have nothing to do with CCSVI may be useful to others (non-believers, as it were).
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Re: WOW read this. compares cu:zn in Alzheimer's and MS.

Post by David1949 » Mon Feb 13, 2017 12:09 pm

Jimmylegs do you have a link to the source for this data ?

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Re: WOW read this. compares cu:zn in Alzheimer's and MS.

Post by jimmylegs » Mon Feb 13, 2017 12:59 pm

For any newbies nonplussed by the above: yes you are reading in the Multiple Sclerosis area, under General Discussion. (edit: later moved to natural approach)
You are absolutely welcome to continue discussing the spectrum of copper zinc imbalance as it pertains to various neurological conditions including MS, here.
While 1eye's comment is misplaced, there is certainly a dedicated CCSVI forum for those interested in such topics.
You can find it under Treatments: http://www.thisisms.com/forum/chronic-c ... ccsvi-f40/
As always, i reject the notion that solutions in MS are either-or propositions. My related comments about blind men and elephants span over a decade here on the forum http://www.thisisms.com/forum/search.ph ... mit=Search
I'll look forward to the day when everyone's copper zinc balance, and status for all other essential nutrients, is right on the money, giving us a crystal clear picture of ms without nutritional impacts :) So far, we do not seem to be there.

Easter, R. N., Chan, Q., Lai, B., Ritman, E. L., Caruso, J. A., & Qin, Z. (2010). Vascular metallomics: copper in the vasculature. Vascular Medicine, 15(1), 61-69.
http://journals.sagepub.com/doi/abs/10. ... 3X09346656
"Owing to recent progress in analytical techniques, metallomics are evolving from detecting distinct trace metals in a defined state to monitor the dynamic changes in the abundance and location of trace metals in vitro and in vivo. Vascular metallomics is an emerging field that studies the role of trace metals in vasculature. This review will introduce common metallomics techniques including atomic absorption spectrometry, inductively coupled plasma-atomic emission spectrometry, inductively coupled plasma-mass spectrometry and X-ray fluorescence spectrometry with a summary table to compare these techniques. Moreover, we will summarize recent research findings that have applied these techniques to human population studies in cardiovascular diseases, with a particular emphasis on the role of copper in these diseases. In order to address the issue of interdisciplinary studies between metallomics and vascular biology, we will review the progress of efforts to understand the role of copper in neovascularization. This recent advance in the metallomics field may be a powerful tool to elucidate the signaling pathways and specific biological functions of these trace metals. Finally, we summarize the evidence to support the notion that copper is a dynamic signaling molecule. As a future direction, vascular metallomics studies may lead to the identification of targets for diagnosis and therapy in cardiovascular disease."

also

Bergomi, M., Rovesti, S., Vinceti, M., Vivoli, R., Caselgrandi, E., & Vivoli, G. (1997). Zinc and copper status and blood pressure. Journal of Trace Elements in Medicine and Biology, 11(3), 166-169.

in that ^ one, serum cu:zn is higher in hypertensives than in normotensives.
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Re: WOW read this. compares cu:zn in Alzheimer's and MS.

Post by jimmylegs » Mon Feb 13, 2017 2:41 pm

@david, certainly:
zinc tox study info already linked previously:
small AD study (n=7) posted dec 24 http://www.thisisms.com/forum/natural-a ... ml#p245062
larger AD study (n=308) also posted previously:
ms study posted feb 11 http://www.thisisms.com/forum/natural-a ... ml#p245866

one more from the 80s, posted in 2008 http://www.thisisms.com/forum/natural-a ... tml#p39241
another small one, differences are more subtle but still, cu:zn ratio is consistently higher in patients and lower in controls
in table 5, you can see the cu:zn ratio increasing in patients as degree of disability worsens. eg in the most disabled group, for men 1.4 in patients vs 1.0 in controls. and for the ladies 1.37 vs 1.29 in controls.

OMG the post right after LMAO i forgot about Keats, 1978 :lol: check him out

i see some language out there to the effect that autoimmune disease affects copper zinc ratio. i have to wonder to what extent immune system function is hampered in decreased dietary zinc intake and increased dietary copper intake. we already know excessive zinc can affect copper and vice versa.

related
Brewer, G. J. (2012). Copper excess, zinc deficiency, and cognition loss in Alzheimer's disease. Biofactors, 38(2), 107-113.
http://onlinelibrary.wiley.com/doi/10.1 ... .1005/full
"A nonblinded study about 20 years ago showed considerable improvement in AD with zinc therapy, and a mouse AD model study also showed significant cognitive benefit from zinc supplementation. In a small blinded study we carried out, post hoc analysis revealed that 6 months of zinc therapy resulted in significant benefit relative to placebo controls in two cognitive measuring systems. These two factors may be linked in that zinc therapy significantly reduced free copper levels. Thus, zinc may act by lowering copper toxicity or by direct benefit on neuronal health, or both."

i must say that for me personally, figuring out and fixing zinc deficiency made a HUGE difference in my cognitive functioning. i had severely impaired short term memory. if a minute went by, i wouldn't necessarily have details of whatever went on the minute before. i had to stand and concentrate hard for some time, before walking away from car or house, to firmly dial in that yes i locked it, yes i have my wallet, etc. if i was watching TV, when the ads were on i would have a hard time figuring out what show i was watching. fixing zinc was like turning the lights back on.

one other memory - i used to be able to physically feel my brain struggling, in a region behind my left eye. especially in highway traffic, because it was so hard to process spatial changes at speed. since fixing zinc i have no problems driving and have never since felt that weird *effort* going on behind my eye.
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Re: WOW read this. compares cu:zn in Alzheimer's and MS.

Post by jimmylegs » Mon Feb 13, 2017 5:41 pm

contrast: in this healthy control study, serum cu:zn is 1.06 for males, 1.3 for females.

Ghayour-Mobarhan, M., Taylor, A., New, S. A., Lamb, D. J., & Ferns, G. A. A. (2005). Determinants of serum copper, zinc and selenium in healthy subjects. Annals of clinical biochemistry, 42(5), 364-375.
http://journals.sagepub.com/doi/pdf/10. ... 3054889990

interesting that this study's healthy control group includes 20% obese individuals and 6 with metabolic syndrome. wonder what else is kicking around in there... if i had run across any of these folks independently, depending on any complaints i might have suggested aiming for higher zinc levels. if they then targeted the mid 18s (as i have seen several times in lit on healthy controls, as distinct from sort of healthy controls, or controls not evidencing condition under study), then if copper levels happened to stay the same, then on average this group would end up with serum cu:zn within that 0.7-1.0 range.
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Re: WOW read this. compares cu:zn in Alzheimer's and MS.

Post by jimmylegs » Tue Feb 14, 2017 9:14 am

@ david full disclosure: having a time finding the source of that optimal cu:zn or zn:cu ratio. related - have found a study showing taste disorder evident at cu:zn 1:1. more pending.
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Re: WOW read this. compares cu:zn in Alzheimer's and MS.

Post by jimmylegs » Tue Feb 14, 2017 6:55 pm

have not put a bunch of cu:zn research in one place before. i will probably move this south at some point.
in the meantime, table one from this study is good. the control group is CZr is 1.3 which you wouldn't think was that awesome, but it's much better than the numbers for those hospitalized. interesting that the gap is more narrow for those with mental/neuro issues in this study. zinc for the hospitalized crew is still low across the board however.

Belbraouet, S., Biaudet, H., Tébi, A., Chau, N., Gray-Donald, K., & Debry, G. (2007). Serum zinc and copper status in hospitalized vs. healthy elderly subjects. Journal of the American College of Nutrition, 26(6), 650-654.
https://www.researchgate.net/profile/Sl ... bjects.pdf
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Re: WOW read this. compares cu:zn in Alzheimer's and MS.

Post by jimmylegs » Tue Feb 14, 2017 7:09 pm

Crăciun, E. C., Bjørklund, G., Tinkov, A. A., Urbina, M. A., Skalny, A. V., Rad, F., & Dronca, E. (2016). Evaluation of whole blood zinc and copper levels in children with autism spectrum disorder. Metabolic brain disease, 31(4), 887-890.
http://link.springer.com/article/10.100 ... 016-9823-0
"The results indicate that the ASD children were characterized by ~10 % (p = 0.005) and ~12 % (p = 0.015) lower levels of whole blood Zn and Zn/Cu ratio, respectively, in comparison to controls. No significant difference in whole blood Cu was observed. However, Cu/Zn ratio was ~15 % (p = 0.008) higher in ASD children than that in the control ones. The results of the present study may be indicative of Zn deficiency in ASD children. Taking into account Zn-mediated up-regulation of metallothionein (MT) gene expression, these findings suggest a possible alteration in the functioning of the neuroprotective MT system. However, further investigations are required to test this hypothesis."

re zinc and upregulation of MT gene expression, tres interessant..

Expression and regulation of brain metallothionein
https://www.ncbi.nlm.nih.gov/pubmed/7655341
"The concentration of zinc has been shown to be altered in an extensive number of disorders of the central nervous system, including alcoholism. Alzheimer-type dementia, amyotrophic lateral sclerosis, Down's syndrome, epilepsy, Friedreich's ataxia, Guillaine-Barré syndrome, hepatic encephalopathy, multiple sclerosis, Parkinson's disease, Pick's disease, retinitis pigmentosa, retinal dystrophy, schizophrenia, and Wernicke-Korsakoff syndrome. The status of MT isoforms and other low molecular weight zinc-binding proteins in these conditions, diseases, disorders, or syndromes is being delineated at this time. Since several of these disorders, such as amyotrophic lateral sclerosis, are associated with oxidative stress, and since MT is able to prevent the formation of free radicals, it is believed that cytokine-induced induction of MT provides a long-lasting protection to avert oxidative damage."

Effect of dietary zinc deficiency on brain metallothionein-I and -III mRNA levels during stress and inflammation
http://www.sciencedirect.com/science/ar ... 8699001552
"Zinc is an essential heavy metal for the normal function of the central nervous system (CNS), but the knowledge of its metabolism and functions is scarce. In this report we have studied the effect of a zinc deficient diet on the regulation of brain metallothioneins (MTs). In situ hybridization analysis revealed that brain MT-I induction by restraint stress was significantly blunted in some but not all brain areas in the mice fed the zinc deficient diet compared to normally fed mice. In contrast, brain MT-I induction by the administration of bacterial lipopolysaccharide (LPS) was not significantly lower in the mice fed the zinc deficient diet. In contrast to MT-I, MT-III mRNA levels were minimally affected by either stress or LPS. Yet, significant decreasing effects of the zinc deficient diet were observed in areas such as the neocortex, CA1–CA3 neuronal layer and dentate gyrus of the hippocampus, and the Purkinje neuronal layer of the cerebellum. These results demonstrate that dietary zinc deficiency impairs the response of brain MTs during both stress and LPS-elicited inflammatory response in a highly specific manner."
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Re: WOW read this. compares cu:zn in Alzheimer's and MS.

Post by lyndacarol » Thu Feb 16, 2017 8:47 am

Zinc is a cofactor of vitamin D, which may also be involved in Alzheimer's disease:

News release: New Canadian study provides strong evidence that low vitamin D levels cause Alzheimer's disease
http://www.vitamindsociety.org/press_release.php?id=52

The Vitamin D Society
http://www.vitamindsociety.org/

About Us:
The Vitamin D Society is a Canadian nonprofit group organized to:

Increase awareness of the many health conditions strongly linked to vitamin D deficiency.
Encourage all Canadians to be proactive in protecting their health and have their vitamin D blood levels tested annually.
Fund valuable vitamin D research.

97% of Canadians are vitamin D deficient at some point in the year, according to University of Calgary research. Worldwide, an estimated 1 billion people don't get enough of "the sunshine vitamin".

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Re: WOW read this. compares cu:zn in Alzheimer's and MS.

Post by jimmylegs » Thu Feb 16, 2017 9:57 am

there are many secondary implications of low zinc in relation to copper
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drug nutrient interactions. study: PPIs deplete zinc

Post by jimmylegs » Thu Feb 16, 2017 10:42 am

Farrell, C. P., Morgan, M., Rudolph, D. S., Hwang, A., Albert, N. E., Valenzano, M. C., ... & Mullin, J. M. (2011). Proton pump inhibitors interfere with zinc absorption and zinc body stores. Gastroenterology Research, 4(6), 243.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5139861/

Background
Proton pump inhibitors (PPIs) cause a sharp elevation of gastro-duodenal luminal pH which in turn has resulted in reports of reduced absorption of magnesium and certain other nutrients.
Methods
Gastroesophageal reflux disease (GERD) patients on long-term PPI therapy (> 6 months) or healthy test subjects (not on any acid preventive or neutralizing medication) were administered oral doses of zinc gluconate (26.2 mg zinc, twice daily) for 14 days followed by 5 cc venous blood samples. Plasma was analyzed for total zinc content by atomic absorption spectrophotometry. Baseline plasma and red blood cell zinc levels were also measured in these two groups when not taking any zinc supplementation.
Results
Plasma zinc levels of healthy controls increased by 126% during the period of zinc supplementation compared to only a 37% increase for individuals on long-term PPI therapy. On their normal diet (with no zinc supplementation), PPI-users had a 28% lower plasma zinc level than healthy controls (P < 0.005).
Conclusions
PPI use dramatically reduces supplemental zinc uptake and can result in decreased zinc body stores. Certain individuals on long-term PPI therapy, such as infants being treated for colic, may be at risk for decreased systemic levels of trace metals needed for developmental, regenerative and immunological requirements.
Heidelbaugh, J. J., Kim, A. H., Chang, R., & Walker, P. C. (2012). Overutilization of proton-pump inhibitors: what the clinician needs to know. Therapeutic advances in gastroenterology, 5(4), 219-232.
http://journals.sagepub.com/doi/abs/10. ... 3X12437358

Proton-pump inhibitors (PPIs) remain the leading evidence-based therapy for upper gastrointestinal disorders, including gastroesophageal reflux disease, dyspepsia, and peptic ulcer disease. The effectiveness of PPIs has led to overutilization in multiple treatment arenas, exposing patients to an increasing number of potential risks. The overutilization of PPIs in ambulatory care settings is often a result of failure to re-evaluate the need for continuation of therapy, or insufficient use of on-demand and step-down therapy. PPI overutilization in the inpatient setting is often a result of inappropriate stress ulcer prophylaxis (SUP) in nonintensive care unit patients, and failure to discontinue SUP prior to hospital discharge. Potential consequences of prolonged PPI therapy include hypergastrinemia, enterochromaffin-like cell hyperplasia, and parietal cell hypertrophy, leading to rebound acid hypersecretion. PPIs have been linked via retrospective studies to increased risk of enteric infections including Clostridium difficile-associated diarrhea, community-acquired pneumonia, bone fracture, nutritional deficiencies, and interference with metabolism of antiplatelet agents.Reducing inappropriate prescribing of PPIs in the inpatient and outpatient settings can minimize potential for adverse events, and foster controllable cost expenditure.
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MS nutrient intakes below RDI

Post by jimmylegs » Thu Feb 16, 2017 12:57 pm

Bitarafan, S., Harirchian, M. H., Nafissi, S., Sahraian, M. A., Togha, M., Siassi, F., ... & Honarvar, N. M. (2014). Dietary intake of nutrients and its correlation with fatigue in multiple sclerosis patients. Iranian journal of neurology, 13(1), 28.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3968354/

Code: Select all

Table 2
Mean daily nutrient intake in MS patients and their significant differences with DRI values

Nutrients             Intake of males (Mean ± SD)	DRI for males     Intake of females (Mean ± SD)	DRI for females	P
Vitamin D (µg)	      2.77 ± 10.77                       15                    2.14 ± 12.59                  15	
Folate (µg)	       268.41 ± 66.93                      400                  284.15 ± 81.17                  400	
Iron (mg)             12.33 ± 3.47                         8                   11.79 ± 3.54                    18	
Zinc (mg)              8.22 ± 2.50                        11                    7.66 ± 1.90                     8	0.134
Calcium (mg)         631.36 ± 232.29                    1000                  583.99 ± 305.50                1000	
Magnesium (mg)       242.24 ± 63.97                      420                  240.25 ± 57.90                  320	
Fiber (g)             14.17 ± 3.71                        38                   14.69 ± 4.59                    25
p<0.001 throughout, except where noted for zinc.*
We did not measure the serum levels of the studied nutrients. Furthermore, we did not compare dietary intake of MS patients with a healthy control group ... The results of nutritional status analysis of 101 RRMS patients showed that dietary intakes of vitamin D, folate, calcium, and magnesium were lower than DRI. Lower magnesium and folate diets were correlated with higher fatigue scores in these patients. To our knowledge, there is no nutritional recommendation as complementary therapy in treatment of fatigue related to multiple sclerosis. Therefore, as a preliminary study this result can be helpful. We suggest recognizing and correcting the low dietary intake of nutrients in MS patients, according to DRI values, with specific consideration to folate and magnesium. This may improve fatigue syndrome in MS patients.
* DRI notes

for zinc, the DRI has been called into question (phew)
Hambidge, K. M., Miller, L. V., & Krebs, N. F. (2011). Physiological requirements for zinc. International Journal for Vitamin and Nutrition Research, 81(1), 72.
http://econtent.hogrefe.com/doi/abs/10. ... alCode=vit

In the Institute of Medicine's (IOM)3 2001 report (1) that included the Dietary Reference Intakes (DRI) for zinc (Zn), these estimates of the DRI were based on data derived from low-phytate or phytate-free meals. ... it is now widely accepted that the underlying estimates of physiologic requirements, although painstakingly and otherwise laudably determined, appear to be flawed, resulting in remarkably low and what are now considered erroneous estimates of physiologic requirements (1,2). Moreover, the phytate effect was based on multiple single meal studies which, for the same dietary intakes of phytate and Zn, give a distinctly lower figure for absorbed Zn than do total diet studies... This would now be an excellent, indeed urgent, time for the IOM to review the DRIs for zinc and extend these to include the inhibitory effect of dietary phytate. It would also be beneficial to see the IOM less reluctant to recognize the importance of the DRIs beyond North America and be willing to assume some broader, overt international responsibility as is likely to occur with the guidelines currently being developed by EURRECA (European Micronutrient Recommendations Aligned)
dri for magnesium also is not so good. see http://ajcn.nutrition.org/content/14/6/342.short
contrast: http://bit.ly/2lQxZyv
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2013 review: Oral contraceptives and changes in nutritional requirements

Post by jimmylegs » Wed Mar 08, 2017 2:53 pm

Oral contraceptives and changes in nutritional requirements
https://www.ncbi.nlm.nih.gov/pubmed/23852908%20
Oral contraceptives (OCs) are a major class of prescription drug, used by a large proportion of women starting from early adolescence. Much research has been conducted to investigate the physiological changes that occur in women who take OCs. These include changes in general health as well as in nutritional needs. In terms of nutrition, several studies investigated whether women on OCs need different amounts of some vitamins and minerals. In particular, a report from the World Health Organization (WHO) points out that the influence of OCs on nutrient requirements is a topic of high clinical relevance and should, therefore, receive great attention. It has been shown that the key nutrient depletions concern folic acid, vitamins B2, B6, B12, vitamin C and E and the minerals magnesium, selenium and zinc. Most research has focused on the levels of these vitamins and minerals in the blood of women who take OCs compared to women who do not. Since women who take OCs not always have adequate diet, may have unhealthy life style or may suffer from pathologies of malabsorption, the possibility to prevent vitamin and mineral deficiencies by taking appropriate dietary supplements should be considered a first-line approach by clinicians.
hmm quite a few 'usual suspects' in there... nutrition as a first line approach wouldn't that be something :D
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review: Vitamin D, micronutrients & metabolic syndrome

Post by jimmylegs » Thu Mar 16, 2017 3:04 pm

Is the Association between Vitamin D and Metabolic Syndrome Independent of Other Micronutrients
http://econtent.hogrefe.com/doi/abs/10. ... alCode=vit
Abstract. The incidence of metabolic syndrome (MetS) has been increasing globally and it is recognized as a major public health problem because MetS is associated with increased risk of diabetes, stroke, cancer, and other chronic diseases. Recently, MetS has been linked to vitamin D deficiency. However, the evidence on the association between vitamin D deficiency and the risk of MetS remains inconclusive. This review therefore aims to depict the existing evidence related to MetS and vitamin D deficiency, and examined some of the possible confounders which may affect the association between vitamin D status and risk of MetS. Earlier studies on the association between vitamin D deficiency and MetS have adjusted for the effect of some confounders including, age, sex, body mass index, race, physical activity, smoking, alcohol consumption, and energy intake. However, these studies failed to consider other potential confounders. There is evidence that vitamin A, zinc (Zn), and magnesium (Mg) play important roles in the activation and function of vitamin D and interact with gene expression. Furthermore, these micronutrients are also related to several components of the MetS including glucose intolerance, dyslipidemia, and obesity. Thus, there could be an interaction between these micronutrients, vitamin D, and MetS. This review highlights the possible interactions of vitamin A, Zn, Mg, and vitamin D with MetS and its components. The findings reinforce the need for further well-designed studies that take into account all potential confounders, including other micronutrients such as vitamin A, Zn, and Mg status, to investigate the independent association of vitamin D status with MetS and its components, and also to scrutinize for possible interactions among other nutrients which may have similar confounding effects.
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study: Serum Mg in the Cdn Population, assoc w diabetes

Post by jimmylegs » Sat Mar 25, 2017 11:14 am

Serum Magnesium Concentrations in the Canadian Population and Associations with Diabetes, Glycemic Regulation, and Insulin Resistance (2017)
http://www.mdpi.com/2072-6643/9/3/296/htm
Abstract: Total serum magnesium (Mg) concentration (SMC) is commonly used to assess Mg status. This study reports current SMCs of Canadians and their associations with demographic factors, diabetes, and measures of glycemic control and insulin resistance using results from the Canadian Health Measures Survey cycle 3 (2012–2013). Associations were examined in adults aged 20–79 years using linear mixed models. Mean SMCs and percentile distributions for 11 sex-age groups between 3 and 79 years (n = 5561) are reported. SMCs were normally distributed and differences (p < 0.05) among sex and age groups were small. Between 9.5% and 16.6% of adult sex-age groups had a SMC below the lower cut-off of a population-based reference interval (0.75–0.955 mmol·L−1) established in the United States population as part of the NHANES I conducted in 1971–1974. Having diabetes was associated with 0.04 to 0.07 mmol·L−1 lower SMC compared to not having diabetes in the various models. Body mass index, glycated hemoglobin, serum glucose and insulin concentrations, and homeostatic model assessment of insulin resistance were negatively associated with SMC. This is the first study to report SMCs in a nationally representative sample of the Canadian population. A substantial proportion of Canadians are hypomagnesaemic in relation to a population-based reference interval, and SMC was negatively associated with diabetes and indices of glycemic control and insulin resistance.

hmm wonder how many would have been hypomagnesemic if they used 0.95 mmol/L as the lower cutoff....
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