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Calcium Supplements and Fracture Prevention

Calcium Supplements and Fracture Prevention
Calcium Supplements and Fracture Prevention

T h e ne w engl a nd jour na l o f medicine

n engl j med 369;16 https://www.wendangku.net/doc/cf12909094.html, october 17, 2013

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This Journal feature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review of formal guidelines,

when they exist. The article ends with the author’s clinical recommendations.

An audio version of this article is available at https://www.wendangku.net/doc/cf12909094.html,

Caren G. Solomon, M.D., M.P.H., Editor

Calcium Supplements and Fracture Prevention

Douglas C. Bauer, M.D.

From the Departments of Medicine and Epidemiology and B iostatistics, Univer-sity of California, San Francisco, San Francisco. Address reprint requests to Dr. Bauer at the University of California, San Francisco, 185 Berry St., Suite 5700, San Francisco, CA 94105, or at dbauer@https://www.wendangku.net/doc/cf12909094.html,.

This article was updated on January 9, 2014, at https://www.wendangku.net/doc/cf12909094.html,.

N Engl J Med 2013;369:1537-43.DOI: 10.1056/NEJMcp1210380

Copyright ? 2013 Massachusetts Medical Society.

A 62-year-old healthy woman presents for routine care. She has no history of frac-ture, but she is worried about osteoporosis because her mother had a hip fracture at 72 years of age. She exercises regularly and has taken over-the-counter calcium car-bonate at a dose of 1000 mg three times a day since her menopause at 54 years of age. This regimen provides 1200 mg of elemental calcium per day. She eats a healthy diet with multiple servings of fruits and vegetables and consumes one 8-oz serving of low-fat yogurt and one glass of low-fat milk almost every day. She recently heard that calcium supplements could increase her risk of cardiovascular disease and wants your opinion about whether or not she should receive them. What would you advise?

The Clinical Problem

Both clinicians and patients are likely to be confused by the inconsistent and some-times conflicting advice about the amount of calcium intake required to reduce the risk of fracture and, in particular, whether calcium supplements are necessary. Long-term calcium deficiency can clearly confer a predisposition to osteoporosis,1 but many persons mistakenly believe that postmenopausal and age-related bone loss and the associated increase in susceptibility to fracture can largely be avoided with the use of calcium supplementation. Although some persons remain at risk for calcium deficiency, other persons, particularly those receiving calcium supplements, may receive more than the recommended daily intake.

The complex and incompletely understood interaction between calcium and vitamin D intake complicates our understanding of the benefits and risks associ-ated with either one alone.2,3 For example, a recent randomized trial showed that even high doses of vitamin D 3 (4800 IU per day) had modest beneficial effects on calcium absorption (a 6% increase) among postmenopausal women with low se-rum levels of 25-hydroxyvitamin D.4 Furthermore, a number of clinical trials have studied the combination of calcium plus vitamin D in various doses, but fewer trials have examined the effects of calcium alone on the skeleton.

This review summarizes our current understanding of calcium intake as it re-lates to fracture risk and discusses concerns about the safety of calcium supple-ments. Other reviews have addressed the physiology of calcium metabolism and the ongoing controversies about vitamin D.2,5

Strategies and Evidence

Calcium Requirements

More than 98% of all calcium in the body is contained within the skeleton. Bone serves as a reservoir for calcium, which can be stored and released when needed. Calcium has at least two key physiological functions in adults: it is an intracellular

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messenger and it is a key component of hydroxy-apatite, which is present in great quantities in the organic matrix of bone and provides strength and rigidity to the skeleton. Because of obligate losses in urine, sweat, and stool, insufficient cal-cium intake over a prolonged period may eventu-ally affect important physiological processes.Primarily on the basis of studies of calcium balance in persons younger than 50 years of age and the known acceleration of bone loss that occurs with menopause and advanced aging, the Institute of Medicine (IOM) has issued guide-lines regarding the dietary intake of calcium according to sex and age 5 (Table 1). The recom-mended calcium intake and the calcium content

of various foods and supplements are quantified in milligrams of elemental calcium. Different supplement formulations provide different amounts of elemental calcium. The recommend-ed dietary allowances are based on requirements for healthy populations. The recommended up-per intake levels are based primarily on the risk of nephrolithiasis observed in studies of calcium supplementation in postmenopausal women. Calcium absorption is increased in pregnant and lactating women, but the recommended calcium intake for these women does not differ from that for other women in the same age group.In a population-based study involving adults in the United States, the dietary intake of ele-mental calcium varied according to age group but averaged 900 to 1200 mg in men and 750 to 850 mg in women; the lowest intake was observed among men and women older than 70 years of age.6 More than 70% of dietary calcium comes from dairy products.5 To estimate a person’s daily dietary calcium intake, clinicians can as-sume that most adults consume about 300 mg of calcium per day from nondairy sources (e.g., various vegetables and grains) and then estimate the total daily intake by calculating the addi-tional daily intake of dairy products (Table 2). The use of calcium supplements is common; cross-sectional surveys have shown that 43% of U.S. adults (and almost 70% of postmenopausal women) regularly take calcium supplements.8 De-spite frequent use of calcium supplements, many adults in the United States, particularly postmeno-pausal women, do not consume the recommended

* The recommended dietary allowance (RDA) is the level of dietary intake that is likely to meet the needs of 97% of the population. The upper intake level is the level above which the potential for harm increases. Data are from the Institute of Medicine.5

? This category includes women older than 19 years of age who are pregnant or lactating.

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1000 to 1200 mg of elemental calcium per day, and few consume more than the recommended upper intake level of 2000 to 2500 mg per day.Dietary Calcium versus Calcium Supplements In general, calcium-rich foods and beverages, particularly dairy products, are the preferred sources of calcium because they are widely avail-able, and with the exception of lactose intoler-ance, they are associated with few adverse ef-fects. Some evidence suggests that a greater proportion of ingested calcium is absorbed from certain dietary sources such as broccoli and kale than from calcium supplements.5 Although data involving clinical outcomes (fractures) are lack-ing, physiological studies suggest no material differences in the metabolic actions of dietary calcium as compared with calcium obtained from supplements.9,10 Therefore, the decision about whether or not to receive supplements depends on the adequacy of dietary calcium intake and the balance between the potential benefits and harms of supplements. The safety and side-effect profile of calcium supplements are described

below.

Calcium supplements are available over the counter; labels commonly include both the total milligrams of calcium salt and the milligrams of elemental calcium in each tablet. Determination of the dose required to meet daily calcium re-quirements is based on the amount of elemental calcium. Commonly used preparations include purified calcium carbonate, calcium citrate, and, to a lesser extent, calcium lactate and calcium gluconate; preparations differ in the amount of elemental calcium provided (Table 3). Calcium carbonate provides relatively high elemental cal-cium content (40%) and is inexpensive and widely available. As compared with other calcium sup-plements, calcium carbonate is more likely to cause constipation and bloating 11 and should be

taken with meals, since gastric acidity is required

* These foods contain low levels of oxalic and phytic acid. Data are from the National Nutrient Database for Standard Reference of the U.S. Department of Agriculture.7

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for sufficient absorption. As compared with cal-cium carbonate, calcium citrate provides less elemental calcium (21%), but it is a reasonable alternative in patients with bothersome gastro-intestinal symptoms; it may be taken with or without meals, since absorption is not depen-dent on gastric acidity. If daily supplementation with more than 500 mg of elemental calcium is required, divided doses are recommended to improve absorption and minimize gastrointesti-nal side effects.Potential Benefits of Calcium Intake Perimenopausal and age-related bone loss, and the accompanying increased risk of fracture, oc-cur when there is a net loss of calcium in the skeleton due to an imbalance between bone re-sorption and bone formation. Although peri-menopausal bone loss is primarily related to the loss of estrogen, age-related bone loss in both men and women is determined by genetic, hor-monal, and other factors. Observational studies suggest that bone loss and fracture risk increase when calcium intake is below 700 to 800 mg per day.1,12 Conversely, the effect of additional calci-um intake on bone loss among persons who do not have a calcium deficiency is less clear and is probably modest.13Many trials have assessed the antifracture benefits of calcium supplements, but most, such as the Women’s Health Initiative (WHI) Calcium/Vitamin D Supplementation trial, included vita-min D as part of the intervention and did not preferentially recruit persons with low dietary calcium intake.14 The WHI trial did not show a significant reduction in hip fractures or other fractures in women randomly assigned to 1000 mg of elemental calcium plus 400 IU of vitamin D per day as compared with women assigned to placebo, perhaps because the mean calcium in-take in the placebo group was 1154 mg per day.15 However, pooled analyses of the combination of calcium plus vitamin D have suggested a modest protective effect on fractures, particularly among

frail and elderly persons.16,17 For example, a meta-analysis of 16 placebo-controlled trials of calcium and vitamin D supplements (including the WHI trial) recently performed for the U.S. Preventive Services Task Force showed an overall 12% re-duction in the risk of any fracture.16 In this analysis, the benefits of calcium and vitamin D with respect to fracture risk were significant among institutionalized persons (relative risk, 0.71; 95% confidence interval [CI], 0.57 to 0.89) but not among community-dwelling persons (relative risk, 0.89; 95% CI, 0.76 to 1.04) (P = 0.07 for interaction). Fewer trials have specifically examined the skeletal effects of calcium supple-ments alone, but a meta-analysis that pooled the results of 9 randomized trials of calcium supple-ments alone (involving a total of 6517 persons) showed that the overall reduction in fractures was 10%.17 Conversely, a pooled analysis of 3 tri-als of calcium alone showed an unexpected 50% increase in the risk of hip fracture.18 Thus,

current evidence suggests that supplementation

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with calcium and vitamin D or with calcium alone has a modest overall effect on the risk of fracture, and whether or not routine use of sup-plements is beneficial for community-dwelling persons remains uncertain.

Potential Harms of Calcium Intake

Although calcium supplements have few side ef-fects, minor constipation and dyspepsia are com-mon. The risk of nephrolithiasis is increased with the use of calcium supplements (the relative risk was 1.17 in the WHI trial),19 and the risk appears to be dose-dependent.20 Conversely, in observa-tional studies, a higher dietary intake of calcium has been associated with a lower risk of nephro-lithiasis, perhaps because of a reduction in the intestinal absorption of oxylate.21 Early studies suggested that the use of calcium supplements might increase the risk of prostate cancer among men, but a recent meta-analysis that included more than 4000 cases of prostate cancer showed no association with the use of calcium supple-ments.16

Several studies have raised concerns about a possible increase in cardiovascular risk associ-ated with calcium supplementation. A meta-analysis of published results of 11 placebo-con-trolled trials of calcium supplements without vitamin D showed an increased risk of myocar-dial infarction among persons randomly assigned to calcium (odds ratio, 1.27; 95% CI, 1.01 to 1.59).22 The authors speculated that transient supplement-related increases in serum calcium levels 18 might precipitate arrhythmias or perhaps promote vascular calcification. This meta-analy-sis received considerable attention but was criti-cized because of inconsistent adjudication of events, marginal statistical significance, and ex-clusion of trials assessing calcium plus vitamin D. Among the trials not included in this meta-analysis was the WHI trial,14 which involved more than 36,000 women and showed no sig-nificant increase in adjudicated cardiovascular events 23 or overall mortality 24 among women who received calcium plus vitamin D. In a sub-sequent meta-analysis, the same investigators included data from trials of calcium plus vita-min D, including some of the WHI trial data,25 but they still excluded WHI participants who were receiving calcium supplements at baseline (approximately 54%14,23); the pooled summary estimate of the risk of myocardial infarction as-

sociated with supplementation in this updated analysis yielded similar results (odds ratio, 1.24; 95% CI, 1.07 to 1.45). The exclusion was based on the argument that a risk associated with sup-plements might be obscured among these women if it was attributable to abrupt changes in plasma calcium concentrations after the consumption of supplements. This approach has been subject to criticism and to considerable debate.26-30 A 2010 meta-analysis 31 that included all participants in the WHI trial showed no significant relationship between supplementation and cardiovascular events in pooled analyses of 2 trials of calcium plus vitamin D (relative risk, 1.04; 95% CI, 0.92 to 1.18) or in 3 trials of calcium supplements alone (relative risk, 1.14; 95% CI, 0.92 to 1.41). In another placebo-controlled trial of supple-mentation with calcium carbonate (1200 mg of elemental calcium per day) involving 1460 older women (mean age, 75 years),32 calcium supple-mentation did not result in an increase in the risk of death or atherosclerotic events requiring hospitalization (identified through a validated registry) over a follow-up period of 5 years.Observational studies have also yielded con-flicting results.33-41 For example, whereas two large, prospective cohort studies showed that the use of calcium supplements was associated with an increased risk of cardiovascular events or death,33,34 a large Canadian prospective cohort study 35 and the extended follow-up of the WHI trial 36 showed no significant association between the use of calcium supplements and cardiovascu-lar events. Several studies have shown no rela-tionship between higher dietary intake of calcium and adverse cardiovascular outcomes.33-35,37-39 In contrast, a recent study involving a Swedish cohort showed that, as compared with women with intakes between 600 and 999 mg per day, rates of death from cardiovascular causes and death from any cause were higher among women with a dietary or total calcium intake of 1400 mg per day or more but there was no increased risk with intakes of 1000 to 1399 mg per day.40 Nei-ther the prospective Framingham Heart Study 41 nor the WHI trial 42 showed a relationship be-tween the use of calcium supplements and the coronary calcium score.

In summary, the evidence suggesting adverse cardiovascular effects of calcium supplementa-tion is inconsistent, and an accepted biologic ex-planation is lacking; the clinical significance of

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transient supplement-related increases in serum calcium levels is unknown. However, pending further data, a reasonable approach is to prefer-entially encourage dietary calcium intake and dis-courage the routine use of calcium supplements.

Patient Education

Patients who can consume dairy products with-out adverse effects should be encouraged to reg-ularly consume them along with other foods that have a high calcium content (Table 2). Since cal-cium fortification of processed food and bever-ages is variable, labels must be checked carefully to determine the calcium (and caloric) content per serving and the serving size. For persons who are unable to meet recommended daily calcium requirements with dietary intake alone, calcium supplementation should be discussed; the side-effect profile (Table 3) and cost should be consid-ered in choosing a supplement.11 Supplement

dosing combined with dietary intake should be sufficient to approximate but not exceed the IOM daily guidelines.Areas of Uncertainty Further research is needed to determine whether clinically important differences exist between formulations of calcium supplements with respect to skeletal benefits and potential side effects and to establish calcium requirements for premeno-pausal women, men, and nonwhite populations.43 In addition, data from randomized trials that in-clude systematic collection and adjudication of cardiovascular events are needed to clarify whether calcium supplementation increases car-diovascular risk.Guidelines The IOM has issued guidelines for daily dietary calcium intake in children and adults (Table 1).An expert panel convened in 2011 by the American Society for Bone and Mineral Research found that the evidence was insufficient to con-clude that calcium supplements cause cardiovas-cular events.44

In a 2013 update,45 the U.S. Preventive Ser-vices Task Force found insufficient evidence to assess the benefits and harms of daily supple-mentation with more than 1000 mg of calcium (or more than 400 IU of vitamin D) for the pri-mary prevention of fractures in noninstitutional-ized postmenopausal women. However, the task force cited the negative results of the WHI trial and recommended against routine daily supple-mentation with 1000 mg or less of calcium or 400 IU or less of vitamin D. They found insuffi-cient evidence to recommend for or against the use of calcium supplements in men and premeno-pausal women. Although the authors of the rec-ommendation statement acknowledged the im-portance of adequate calcium intake for skeletal health, they did not address supplementation spe-cifically in persons with inadequate dietary intake.

Conclusions and

R ecommendations

The healthy postmenopausal woman described in the vignette reports a current total daily intake of 2240 mg of elemental calcium: a dietary intake of

about 1040 mg (approximately 300 mg from non-dairy sources and 740 mg from dairy products) and supplements that provide 1200 mg of calcium. Since her calcium intake is substantially greater than the IOM recommendation of 1200 mg per day for postmenopausal women, I would recommend that she increase her dietary calcium intake by 200 mg per day and discontinue her calcium sup-plements. If increasing her dietary intake is not feasible, she can reduce her calcium carbonate supplementation to one 500-mg tablet each day. She should be informed that supplement use, but not increased dietary intake, modestly increases

the risk of nephrolithiasis, and she should be ad-vised about a potential increased risk of cardiovas-cular events, although the evidence of the latter is currently inconsistent and inconclusive. If she continues to supplement her dietary calcium in-take, she should be advised to take calcium car-bonate with meals to optimize absorption.Dr. Bauer reports receiving grant support through his institu-tion from Amgen and Novartis. No other potential conflict of interest relevant to this article was reported.

Disclosure forms provided by the author are available with the

full text of this article at https://www.wendangku.net/doc/cf12909094.html,.

References

1. Dawson-Hughes B. Calcium insuffi-ciency and fracture risk. Osteoporos Int 1996;6:Suppl 3:37-41.

2. Rosen CJ. Vitamin D insufficiency. N Engl J Med 2011;364:248-54.

3. Hunt CD, Johnson LK. Calcium re-quirements: new estimations for men and women by cross-sectional statistical analy-ses of calcium balance data from metabolic studies. Am J Clin Nutr 2007;86:1054-63.

4. Gallagher JC, Yalamanchili V, Smith

LM. The effect of vitamin D on calcium absorption in older women. J Clin Endo-crinol Metab 2012;97:3550-6.

5. Institute of Medicine. Dietary refer-

clinical practice

n engl j med 369;16 https://www.wendangku.net/doc/cf12909094.html, october 17, 2013

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ence intakes for calcium and vitamin D. Washington, DC: National Academies Press, 2011.6. Bailey RL, Dodd KW, Goldman JA, et al. Estimation of total usual calcium and vitamin D intakes in the United States. J Nutr 2010;140:817-22.7. USDA National Nutrient Database for Standard Reference, release 26. B eltsville, MD: U.S. Department of Agriculture Agri-cultural Research Service, 2013 (https://www.wendangku.net/doc/cf12909094.html,/Services/docs.htm?docid =8964).8. Gahche J, Bailey R, Burt V, et al. Dietary supplement use among U.S. adults has increased since NHANES III (1988-1994). NCHS Data Brief 2011;61:1-8.9. Rafferty K, Walters G, Heaney RP. Calcium fortificants: overview and strate-gies for improving calcium nutriture of the U.S. population. J Food Sci 2007;72: R152-R158.10. Prince R, Devine A, Dick I, et al. The effects of calcium supplementation (milk powder or tablets) and exercise on bone density in postmenopausal women. J Bone Miner Res 1995;10:1068-75.11. Straub DA. Calcium supplementation in clinical practice: a review of forms, doses, and indications. Nutr Clin Pract 2007;22:286-96.12. Warensj? E, Byberg L, Melhus H, et al. Dietary calcium intake and risk of frac-ture and osteoporosis: prospective lon-gitudinal cohort study. B MJ 2011;342: d1473.13. Shea B , Wells G, Cranney A, et al. Meta-analyses of therapies for postmeno-pausal osteoporosis. VII. Meta-analysis of calcium supplementation for the pre-vention of postmenopausal osteoporosis. Endocr Rev 2002;23:552-9.14. Jackson RD, LaCroix AZ, Gass M, et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med 2006;354:669-83. [Erratum, N Engl J Med 2006;354:1102.]15. Lappe JM, Heaney RP. Why random-ized controlled trials of calcium and vita-min D sometimes fail. Dermatoendocri-nol 2012;4:95-100.16. Chung M, Lee J, Terasawa T, Lau J, Trikalinos TA. Vitamin D with or without calcium supplementation for prevention of cancer and fractures: an updated meta-analysis for the U.S. Preventive Services Task Force. Ann Intern Med 2011;155:827-38.17. Tang B M, Eslick GD, Nowson C, Smith C, Bensoussan A. Use of calcium or calcium in combination with vitamin D supplementation to prevent fractures and bone loss in people aged 50 years and older: a meta-analysis. Lancet 2007;370: 657-66. [Erratum, Lancet 2012;380:806.]18. Reid IR, Bolland MJ, Grey A. Effect of calcium supplementation on hip fractures. Osteoporos Int 2008;19:1119-23.19. Wallace R , Wactawski-Wende J, O’Sullivan MJ, et al. Urinary tract stone occurrence in the Women’s Health Initia-tive (WHI) randomized clinical trial of calcium and vitamin D supplements. Am J Clin Nutr 2011;94:270-7.

20. Curhan GC, Willett WC, Speizer FE, Spiegelman D, Stampfer MJ. Comparison of dietary calcium with supplemental cal-cium and other nutrients as factors affect-ing the risk for kidney stones in women. Ann Intern Med 1997;126:497-504.

21. Taylor EN, Curhan GC. Dietary calci-um from dairy and nondairy sources, and risk of symptomatic kidney stones. J Urol 2013 March 25 (Epub ahead of print).22. Bolland MJ, Avenell A, Baron JA, et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. B MJ 2010;341:c3691.23. Hsia J, Heiss G, Ren H, et al. Calcium/vitamin D supplementation and cardiovas-cular events. Circulation 2007;115:846-54.24. LaCroix AZ, Kotchen J, Anderson G, et al. Calcium plus vitamin D supplementa-tion and mortality in postmenopausal women: the Women’s Health Initiative calcium-vitamin D randomized controlled trial. J Gerontol A Biol Sci Med Sci 2009; 64:559-67.

25. Bolland MJ, Grey A, Avenell A, Gam-ble GD, Reid IR. Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women’s Health Initiative limited access dataset and meta-analysis. BMJ 2011;342: d2040.26. Bolland MJ, Grey A, Reid IR. Authors’ response to editorial. B MJ 2011;342:d3520.27. Abrahamsen B, Sahota O. Do calcium plus vitamin D supplements increase car-diovascular risk? BMJ 2011;342:d2080.28. Nordin BE, Lewis JR, Daly RM, et al. The calcium scare — what would Austin B radford Hill have thought? Osteoporos Int 2011;22:3073-7.

29. Hennekens CH, B arice EJ. Calcium supplements and risk of myocardial in-farction: a hypothesis formulated but not yet adequately tested. Am J Med 2011;124: 1097-8.

30. Reid IR, Bolland MJ, Grey A. Calcium supplements and risk of myocardial in-farction: an hypothesis twice tested. Am J Med 2012;125(4):e15.

31. Wang L, Manson JE, Song Y, Sesso HD. Systematic review: vitamin D and cal-cium supplementation in prevention of cardiovascular events. Ann Intern Med 2010;152:315-23.

32. Lewis JR, Calver J, Zhu K, Flicker L, Prince RL. Calcium supplementation and the risks of atherosclerotic vascular dis-ease in older women: results of a 5-year RCT and a 4.5-year follow-up. J Bone Miner Res 2011;26:35-41.33. Li K, Kaaks R, Linseisen J, Rohrmann S. Associations of dietary calcium intake and calcium supplementation with myo-cardial infarction and stroke risk and overall cardiovascular mortality in the Heidelberg cohort of the European Pro-spective Investigation into Cancer and Nutrition study (EPIC-Heidelberg). Heart 2012;98:920-5.

34. Xiao Q, Murphy RA, Houston DK, Harris TB, Chow WH, Park Y. Dietary and supplemental calcium intake and cardio-vascular disease mortality: the National Institutes of Health–AARP diet and health study. JAMA Intern Med 2013;173:639-46.35. Langsetmo L, Berger C, Kreiger N, et al. Calcium and vitamin D intake and mor-tality: results from the Canadian Multi-centre Osteoporosis Study (CaMos). J Clin Endocrinol Metab 2013;98:3010-8.

36. Cauley J, Wactawski-Wende J, Robbins J, et al. The Women’s Health Initiative (WHI) calcium plus vitamin D supple-mentation trial: health outcomes 5 years after trial completion. J Womens Health (Larchmt) (in press).

37. Kaluza J, Orsini N, Levitan EB ,

B rzozowska A, Roszkowski W, Wolk A. Dietary calcium and magnesium intake and mortality: a prospective study of men. Am J Epidemiol 2010;171:801-7.

38. Al-Delaimy WK, Rimm E, Willett WC, Stampfer MJ, Hu FB. A prospective study of calcium intake from diet and supple-ments and risk of ischemic heart disease among men. Am J Clin Nutr 2003;77: 814-8.

39. Bostick RM, Kushi LH, Wu Y, Meyer KA, Sellers TA, Folsom AR. Relation of calcium, vitamin D, and dairy food intake to ischemic heart disease mortality among postmenopausal women. Am J Epidemiol 1999;149:151-61.

40. Micha?lsson K, Melhus H, Warensj? Lemming E, Wolk A, Byberg L. Long term calcium intake and rates of all cause and cardiovascular mortality: community based prospective longitudinal cohort study. BMJ 2013;346:f228.

41. Samelson EJ, Booth SL, Fox CS, et al. Calcium intake is not associated with in-creased coronary artery calcification: the Framingham Study. Am J Clin Nutr 2012; 96:1274-80.

42. Manson JE, Allison MA, Carr JJ, et al. Calcium/vitamin D supplementation and coronary artery calcification in the Wom-en’s Health Initiative. Menopause 2010;17: 683-91.

43. Vitamin D and calcium supplementa-tion to prevent cancer and osteoporotic fractures in adults: draft recommenda-tion statement. Rockville, MD: U.S. Pre-ventive Services Task Force, 2012 (https://www.wendangku.net/doc/cf12909094.html,/uspstf12/vitamind/draftrecvitd.htm).

44. Bockman RS, Zapalowski C, Kiel DP, Adler RA. Commentary on calcium sup-plements and cardiovascular events. J Clin Densitom 2012;15:130-4.

45. Moyer VA. Vitamin D and calcium supplementation to prevent fractures in adults: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2013;158:691-6.

Copyright ? 2013 Massachusetts Medical Society.

中国白癜风诊疗共识(2014版)

白癜风诊疗共识(2014版) 中国中西医结合学会皮肤性病专业委员会色素病学组 本指南以中国中西医结合学会皮肤性病专业委员会色素病学组制订的白癜风治疗共识(2009版)为基础,经色素病学组、中华医学会皮肤科分会白癜风研究中心部分专家及国内相关专家讨论制定。参加起草及讨 论的成员(按姓氏汉语拼音排序):傅雯雯、高天文、何黎、贾虹、李恒进、李铁男、李珊山、卢忠、鲁严、 李春英、李强、刘清、马东来、乔树芳、秦万章、宋智琦、孙越、宋秀祖、涂彩霞、温海、王玮蓁、许爱娥、项蕾红、张学军、张建中、郑志忠、赵广、朱光斗。 白癜风治疗目的是控制皮损发展,促进白斑复色。 一、选择治疗方法时主要考虑因素: 1.病期:分进展期和稳定期。进展期判定参考白癜风疾病活动度评分(VIDA)积分、同形反应、Wood灯。①VIDA积分:近6周内出现新皮损或原皮损扩大(+4分),近3个月出现新皮损或原皮损扩大(+3分),近6个月出现新皮损或原皮损扩大(+2分);近1年出现新皮损或原皮损扩大(+1分);至少稳定1年(0分);至少稳定1年且有自发色素再生(-1分)。总分>1分即为进展期,≥4分为快速进展期;②同形反应:皮肤损伤1年内局部出现白斑。损伤包括物理性(创伤、切割伤、抓伤)、机械性摩擦、化学性/热灼伤、过敏性(接触性皮炎)或刺激性反应(接种疫苗、纹身等)、慢性压力、炎症性皮肤病、治疗性(放射治疗、光疗)。白斑发生于持续的压力或摩擦部位,或者是衣物,饰品的慢性摩擦部位,形状特殊,明显由损伤诱发;③Wood灯:皮损颜色呈灰白色,边界欠清,wood灯下皮损面积大于目测面积,提示是进展期。皮损颜色是白色,边界清,wood灯下皮损面积≤目测面积,提示是稳定期。以上3条符合任何一条即可考虑病情进展;④可同时参考激光共聚焦扫描显微镜(简称皮肤CT)和皮肤镜的图像改变,辅以诊断。 2.白斑面积(手掌面积约为体表面积1%):1级为轻度,<l%;2级为中度,l%~5%; 3级为中重度,6%~50%;4级为重度,>50%。白斑面积也可按白癜风面积评分指数(vitiligo area scoring index,VASI)来判定。VASI=∑(身体各部占手掌单元数)×该区域色素脱失所占百分比,VASI值为0~100。 3.型别:根据2012年白癜风全球问题共识大会(VGICC)及专家讨论,分为节段型、非节段型、混合型及未定类型白癜风。①节段型白癜风:沿某一皮神经节段分布(完全或部分匹配皮肤节段),单侧的不对称的白癜风。少数可双侧多节段分布;②非节段型白癜风:包括散发型、泛发型、面肢端型和黏膜型。散发型指白斑≥2片,面积为1~3级;泛发型为白斑面积4级(>50%);面肢端型指白斑主要局限于头面、手足,尤其好发于指趾远端及面部腔口周围,可发展为散发型、泛发型;黏膜型指白斑分布于2个及以上黏膜部位,可发展为散发型、泛发型;③混合型白癜风:节段型和非节段型并存;④未定类型白癜风:指非节段型分布的单片皮损,面积为1级。 4.疗效:面部复色疗效好,口唇、手足部位复色疗效差。病程越短,疗效越好。儿童疗效优于成人。 二、治疗原则 (一)进展期白癜风: 1.未定类型(原称局限型):可外用糖皮质激素(简称激素)或钙调神经磷酸酶抑制剂(他克莫司软膏、吡美莫司乳膏)等,也可外用低浓度的光敏药,如浓度<0.1%的8-甲氧沙林(8-MOP);维生素D3衍生物;局部光疗可选窄谱中波紫外线(NB-UVB)、308nm准分子激光及准分子光。

新型类钙钛矿电极材料的设计和性能研究

新型类钙钛矿电极材料的设计和性能研究固体氧化物燃料电池(SOFC)是一种转换效率高且环境友好的能源转换设备,能够将燃料中的化学能高效的转换为电能,而其电化学逆过程(即固体氧化物电解电池,SOEC)则可以将电能转换为化学能储存在燃料中。SOFC-SOEC联用可以有效地解决风能、太阳能、潮汐能等清洁发电设备的输出波动问题,实现并网。 但是目前SOFC的商业化应用仍遇到很多困难,最重要的就是高性能电极材料的开发,包括可用于碳氢燃料的阳极材料以及高催化活性和稳定性的阴极材料等。为进一步发展高性能、稳定的电极材料,以提高电池的电化学性能和运行稳定性,本文主要进行以下几下研究:(1)新型质子型固体氧化物燃料电池(P-SOFC)的阴极材料-Sr3Fe207-δ的制备、性能和应用电化学性能研究;(2)Co和La掺杂对Sr3Fe2O7-δ性能的影响及其作为P-SOEC空气极的可行性研究; (3)Sr2Fe1.5Mo0.5O6-δ(SFM)单相陶瓷电极在可逆固体氧化物电池中的离子浸渍法制备及应用性能研究;(4)基于NiTiO3阳极重整层和Co2TiO4新阳极材料的单电池在碳氢燃料中的电化学行为研究。 论文的结果如下:第一章:简单介绍了SOFC的研究背景、运行原理和各组件的发展现状。重点阐述了SOFC中电极材料的发展现状和未来商业化要求对于电极材料的要求,提出本论文的研究方向和内容。 第二章:针对P-SOFC的阴极电化学反应过程,设计并研究了具有类钙钛矿R-P结构的Sr3Fe207-δ单相阴极材料。结果表明:(1) Sr3Fe207-δ (SFO)具有良好的电子电导率和氧离子电导率,800℃下氧渗透率为6.06*10-8molcm-2s-1,电子电导率最高可达60Scm-1。 (2)DFT理论计算表明其特殊的R-P层状结构使SFO具有很低的质子形成能

Sr-Ce-Fe-Mo-O-N双钙钛矿系列化合物的结构及其性质的研究

目录 第1章绪论 (1) 1.1 磁电阻效应 (1) 1.2 巨磁电阻材料的应用及研究进展 (2) 1.2.1 巨磁电阻材料的应用 (2) 1.2.2 巨磁电阻材料的现状与展望 (2) 1.3 双钙钛矿型氧化物介绍 (3) 1.3.1 双钙钛矿型氧化物的结构 (3) 1.3.2 双钙钛矿型氧化物的电磁性质 (4) 1.3.3 A位和B位取代对双钙钛矿型氧化物电磁性质的影响 (9) 1.3.4 双钙钛矿型氧化物的制备方法 (10) 1.4 本论文的研究动机以及研究内容 (12) 第2章实验理论、样品制备、表征手段 (13) 2.1 实验理论 (13) 2.1.1 Jahn-Teller效应 (13) 2.1.2 极化子 (13) 2.1.3 容忍因子 (14) 2.1.4 超交换作用 (14) 2.1.5 双交换作用 (16) 2.1.6 电输运性质 (17) 2.2 样品的固相反应制备法 (18) 2.3 样品的表征手段 (20) 2.3.1 样品的晶体结构的XRD表征 (20) 2.3.2 样品磁性能的表征 (22) 2.3.3 样品电性能的表征 (23) 2.3.4 样品氮含量的测定 (24)

第3章Sr2FeMoO6-x N x系列样品的结构和性质的研究 (26) 3.1 概述 (26) 3.2 氮含量的测定 (26) 3.3 晶体结构的分析 (26) 3.4 样品磁性能的分析 (31) 3.5 样品电性能的分析 (34) 3.6小结 (37) 第4章Sr2-x Ce x FeMoO6-x N x系列样品的结构和性质的研究 (38) 4.1 概述 (38) 4.2 晶体结构的分析 (38) 4.3 样品磁性能的分析 (43) 4.4 样品电性能的分析 (46) 4.5 小结 (48) 第5章Sr2FeMoO6-x N x和Sr2-x Ce x FeMoO6-x N x样品结构性质对比 (49) 5.1 概述 (49) 5.2 晶体结构的比较 (49) 5.3 样品磁性能的比较 (51) 5.4 样品电性能的比较 (52) 第6章结论 (54) 参考文献 (55) 致谢 (60) 攻读学位期间取得的科研成果 (61)

石膏检测 石膏成分检测

石膏检测石膏成分检测 一:石膏(003) 石膏是单斜晶系矿物,主要化学成分是硫酸钙(CaSO4)。石膏是一种用途广泛的工业材料和建筑材料。可用于水泥缓凝剂、石膏建筑制品、模型制作、医用食品添加剂、硫酸生产、纸张填料、油漆填料等。 二:石膏的主要化学成分 CaO 32.5,SO3 46.6,H2O+ 20.9。成分变化不大。常有粘土、有机质等机械混入物。有时含SiO2、Al2O3、Fe2O3、MgO、Na2O、CO2、Cl等杂质。 三:主要检测产品 石膏粉:磷石膏粉、脱硫石膏粉、柠檬酸石膏粉和氟石膏粉 石膏板:纸面石膏板、装饰石膏板、石膏空心条板、纤维石膏板、石膏吸音板、定位点石膏板 其他:生石膏,石膏纤维,石膏线,石膏砌块等。 四:主要检测项目 含量分析:含固体含量、硫酸钙含量、不挥发物含量、其他杂质含量 成分配比 物理性质:硬度、灰分、粘度、细度、粒度、挥发分、比重、比表面积、熔点、回粘性、光泽、吸水率、凝结时间、尺寸偏差和表面质量等; 力学性能:抗拉强度、脆性、弯曲试验、拉伸试验、耐冲击性等 化学性能:耐水性、耐久性、耐酸碱性、耐腐蚀性、耐候性、耐热性等。 防火性能:耐燃烧时间、火焰传播比值、质量损失、炭化体积 其他参数:隔音性能等。 五:部分检测标准 JC/T 517-2004 粉刷石膏 GB/T 9776-2008建筑石膏 GB/T 5483-2008 天然石膏 GB/T 5484-2012 石膏化学分析方法 GB/T 9775-2008 纸面石膏板 GB/T 9776-2008 建筑石膏 GB/T 5463.3-2013 非金属矿产品词汇第3部分:石膏

科标无机检测中心可提供专业石膏检测,可依据依照ASTM、ISO、EN、JIS等国际标准和GB国家标准对石膏产品进行相关的分析测试服务。

钙钛矿型催化剂催化氧化NO讲解

钙钛矿型催化剂La1-x Ce x CoO3对一氧化氮的氧化催化研究 摘要 本文介绍了在钙钛矿氧化物中的NO的氧化性能的研究La1-x Ce x CoO3 (x = 0, 0.05, 0.1, 0.2, 0.3, 0.4)通过柠檬酸盐法合成钙钛矿型氧化物并以XRD, BETand XPS为特征。当使用铈替代催化剂时催化活性显著增强,并取得了当x=0.2时活性最大,但X越大活性会降低。分析表明,表面上吸附的氧对NO氧化成NO2起着重要的作用。在室温下,NO和O2共吸附层之下的表面化合物,通过红外光谱和TPD实验进行了研究。有三个品种形成在表明上分别是:桥接硝酸盐,次硝酸和单齿硝酸盐。热稳定性的顺序为:单齿硝酸盐> 次硝酸>桥接硝酸盐。其中,仅单齿硝酸盐在300摄氏度以上会分解,解除吸附变为NO2进入气相。当Ce的加入,单齿硝酸盐解脱吸附的温度变低,另外两个品种的吸附减少。这可能与表面上的钴的氧化状态有关。通过对表征结果和催化活性的数据的结合分析显示,大量吸附的氧,表面上少量的非活性化合物和较低的NO2接触吸附温度会有利于NO的氧化。 #2007爱思唯尔B.V.保留所有权利。 1 介绍 对NO x催化消除的广泛研究已进行了多年。然而,除去柴油发动机和过量氧气贫燃条件下的汽油发动机中的NO x仍然是一个挑战。在研制的几个NO X氧化环境转化的过程中NO2总是比NO更加受宠,例如NO x的储存和还原技术(NSR)[1],为去除氮氧化物和烟尘的连续再生陷阱技术(CRT)[2],选择性催化还原氮氧化物(SCR),尤其是某些N-所含物种如氨或尿素。[3-5]我们还发现,形成二氧化氮是在NO的SCR的碳氢化合物机制的重要一步[6.7]。一些研究人员也开发了几种更复杂的系统,例如'VHRO系统'(V= 对NO到NO2的氧化催化剂,H =水解催化剂,R = SCR催化剂,O =对NH3的氧化催化剂)[5]和IAR法(在氧化和还原剂的还原催化剂之间加入)[8]。在这些系统中,它们都在NO的氧化添加还原剂之前设置一个预催化剂,使还原剂的效率得到显著改善。总之,在一氧化氮氧化为二氧化碳的过程中放置催化剂是使人非常感兴趣的。 铂基催化剂是现在最常用于NO氧化的催化剂。Despre′s Joe¨l等,观察到铂/二氧化硅(2.5重量%)可在300摄氏度时转换约80%的NO为NO2[9]。并且当铂

免疫抑制剂

免疫抑制剂的用药护理 免疫抑制剂定义 是一类通过抑制细胞及体液免疫反应,而使组织损伤得以减轻的化学或生物物质。其具有免疫抑制作用,可抑制机体异常的免疫反应,目前广泛应用于器官移植抗排斥反应和自身免疫性疾病的治疗。 免疫抑制剂的分类 1、钙调素抑制剂类:环孢菌素CsA类、他克莫司(FK506) 2、抗代谢类:硫唑嘌呤、霉酚酸脂(MMF) 3、激素类:甲强龙、醋酸泼尼松 4、生物制剂:抗T细胞球蛋白(ATG)、抗淋巴细胞球蛋白(ALG) 免疫抑制剂用药原则 1、预防性用药:环孢素A、FK506、霉酚酸脂(MMF)等。 2、治疗/逆转急性排斥反应(救治用药):MP(甲基强的松龙)、ALG或ATG、霉酚酸脂(MMF)、FK506等。 3、诱导性用药(因急性肾小管坏死而出现延迟肾功能、高危病人、二次移植、环孢素肾毒性病人):ATG、ALG等。 4、二联:激素(醋酸泼尼松)+抗代谢类(骁悉) 三联:激素(醋酸泼尼松)+抗代谢类(骁悉)+环孢素A(新山地明) 激素(醋酸泼尼松)+抗代谢类(骁悉)+FK506(他克莫司) 常用免疫抑制剂 1、环孢素(CsA):新山地明(进口)田可、赛斯平(国产) 作用机理

属于钙神经蛋白抑制剂,可以选择性抑制免疫应答,通过破坏使T细胞活化的细胞因子的表达,阻断参与排斥反应的体液和细胞效应机制,防止排斥反应的发生。 药物的吸收和代谢 新山地明受进食和昼夜节律的影响较山地明小,所以服药时间不必将用餐考虑在内。 环孢素A依靠胆汁排泄,肝功能障碍,胆汁淤积症或严重胃肠功能障碍都会影响环保素A的吸收和代谢。只有极少部分药物经肾脏排出,且不能经透析去除,所以对于肾脏功能不全者和需透析治疗的患者,均不需调整药物浓度。 副作用 (1)肾毒性:血清肌酐、尿素氮增高;肾功能损害。个体差异大,临床表现不典型,与其他原因引起的移植肾损害很难鉴别。且发生肾损害时,血药浓度可能正常,甚至偏低。 (2)接近半数的患者会出现肝脏毒性,其发生率与用药量密切相关。 (3)神经毒性:表现为肢体震颤、失眠、烦躁等。 (4)胃肠道反应:恶心、呕吐。 (5)其他并发证:高血压、高胆固醇血症、高钾血症、牙龈增生、糖尿病、多毛症。 用量 联合用药时:初始剂量为6~8mg/kg/d,Q12h,以后根据血药浓度调整。 注意事项 (1)严格按医嘱服药,定时服药,禁忌自行调整用药剂量。

硫酸钙的测定

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钙调磷酸酶抑制剂

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钙钛矿型复合氧化物材料

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新型双钙钛矿基对称固体氧化物燃料电池的制备及性能

第45卷第11期2017年11月 硅酸盐学报Vol. 45,No. 11 November,2017 JOURNAL OF THE CHINESE CERAMIC SOCIETY https://www.wendangku.net/doc/cf12909094.html, DOI:10.14062/j.issn.0454-5648.2017.11.16 新型双钙钛矿基对称固体氧化物燃料电池的制备及性能 陈永红1,杨洋1,2,杨雪1,田冬1,卢肖永1,丁岩芝1,林彬1,2 (1. 低温共烧材料安徽省重点实验室,淮南燃料电池材料工程技术研究中心,淮南师范学院,安徽淮南 232001; 2. 电子科技大学能源科学与工程学院,成都 611731) 摘要:采用柠檬酸-硝酸盐燃烧法制备PrBaFe2O5+δ(PBFO)和PrBaFe1.6Ni0.4O5+δ(PBFNO)电极材料,用高温固相法制备La0.9Sr0.1Ga0.8Mg0.2O3–δ(LSGM)电解质。以LSGM为电解质,PBFNO及PBFNO-SDC分别为对称电极制备单电池。利用X射线衍射法研究材料的物相结构,交流阻抗法记录界面极化行为,扫描电子显微镜观察电池的断面微结构,用自组装的测试系统评价电池输出性能。结果表明:合成的PBFO和PBFNO粉体呈现单一的钙钛矿结构;Ni掺杂能够明显改善空气气氛下的界面极化行为,800℃时电极–电解质的界面极化阻抗由1.94 ?·cm2降低到0.39?·cm2。通过PBFNO与SDC复合能够明显增大电极的三相反应界面,提高电池输出性能,单电池在800℃时的最大功率输出密度从332mW/cm2增大到372mW/cm2。PBFNO-SDC复合电极是潜在的对称固体氧化物燃料电池电极材料。 关键词:对称固体氧化物燃料电池;双钙钛矿;复合电极 中图分类号:TM911.47 文献标志码:A 文章编号:0454–5648(2017)11–1673–06 网络出版时间:2017–10–09 13:56:00 网络出版地址:https://www.wendangku.net/doc/cf12909094.html,/kcms/detail/11.2310.TQ.20171009.1356.008.html Preparation and Properties of Novel Symmetrical Solid Oxide Fuel Cells with Double Perovskite Electrodes CHEN Yonghong1, YANG Yang1,2, YANG Xue1, TIAN Dong1, LU Xiaoyong1, DING Yanzhi1, LIN Bin1,2 (1. Anhui Province Key Laboratory of Low Temperature Co-fired materials, Huainan Engineering Research Center for Fuel Cells, Huainan Normal University, Huainan 232001, China; 2. School of Energy Science and Engineering, University of Electronic Science and Technology of China, Chengdu 611731, China) Abstract: PrBaFe2O5+δ (PBFO) and PrBaFe1.6Ni0.4O5+δ(PBFNO) electrode materials were synthesized by a citric acid-nitrates self-propagating combustion method, and La0.9Sr0.1Ga0.8Mg0.2O3–δ (LSGM) electrolyte was prepared by a conventional solid-state reaction method. The LSGM-supported symmetrical solid oxide fuel cells using PBFNO and PBFNO-SDC as electrodes were prepared. The phase structure, polarization resistance, cross-section microstructure and the cell performance were investigated by X-ray diffraction, electrochemical impedance spectroscopy, scanning electron microscopy and self-assembly SOFC test system, respectively. The results indicate that PBFO and PBFNO powders calcined at 1 000 for 3 h both exhibit a single perovskite ℃ structure with cubic symmetry. The polarization performance is enhanced dramatically by Ni doping in air, which decreases from 1.94 ?·cm2 to 0.39 ?·cm2 at 800 . The maximum power density of cells increases from 3 ℃32 mW/cm2 to 372 mW/cm2 due to the enlarged triple-phase boundary by the introduction of SDC, indicating that PBFNO-SDC is a promising electrode material for symmetrical solid oxide fuel cells. Keywords: symmetrical solid oxide fuel cells; double perovskite; composite electrode 固体氧化物燃料电池(SOFCs)是一种能够将燃料的化学能直接转化为电能的电化学装置。由于其具有转换效率高、污染低、燃料适应性强等特点从而引起了人们的广泛关注[1–3]。传统的SOFCs是一 收稿日期:2017–06–30。修订日期:2017–08–12。 基金项目:国家自然科学基金(51102107),安徽高校自然科学研究(KJ2017A459)资助项目。 第一作者:陈永红(1962—),男,教授。 通信作者:林彬(1984—),男,博士,教授。Received date: 2017–06–30. Revised date: 2017–08–12. First author: CHEN Yonghong (1962–), male, Professor. E-mail: chenyh@https://www.wendangku.net/doc/cf12909094.html, Correspondent author: LIN Bin (1984–), male, Ph.D., Professor. E-mail:bin@https://www.wendangku.net/doc/cf12909094.html,

(完整版)钙钛矿结构示意图

一、钙钛矿结构示意图 钙钛矿型复合氧化物是结构与钙钛矿CaTiO3相同的一大类化合物,钙钛矿结构可以用ABO3表示(见上图),A位为稀土元素,阳离子呈12配位结构,位于由八面体构成的空穴内;B位为过渡金属元素,阳离子与六个氧离子形成八面体配位。钙钛矿型催化剂在中高温活性高,热稳定性好,成本低。研究发现,表面吸附氧和晶格氧同时影响钙钛矿催化活性。较低温度时,表面吸附氧起主要的氧化作用,这类吸附氧能力由B位置金属决定;温度较高时,晶格氧起作用,不仅改变A、B 位置的金属元素可以调节晶格氧数量和活性,用+2或+4价的原子部分替代晶格中+3价的A、B原子也能产生晶格缺陷或晶格氧,进而提高催化活性。 二、双钙钛矿结构示意图 近年来,双钙钛矿型氧化物得到了越来越广泛的关注,双钙钛矿的通式可表示为A2B’B’’O6,标准的A2B’B’’O6型氧化物可以看作是由不同的BO6八面体规则的相间排列而成。一般情况下B′和B″是不同的过渡金属离子,其晶体结构如图2所示。A2B’B’’O6结构双层钙钛矿型复合氧化物呈NaCl型结构相见排列。多数情况下双层钙钛矿氧化物结构也将发生畸变,它的结构一般由离子

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