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1

National Institutes of Health (U.S.), ed. Optimal calcium intake. Bethesda, MD: National Institutes of Health, Office of the Director, 1994.

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2

NIH Consensus Development Conference on Optimal Calcium Intake (1994 National Institutes of Health). NIH Consensus Development Conference on Optimal Calcium Intake: [program and abstracts]. [Bethesda, Md: National Institutes of Health, 1994.

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3

Ulincy, Loretta D. Optimal calcium intake: January 1990 through April 1994 plus selected earlier citations : 775 citations. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Library of Medicine, Reference Section, 1994.

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Ulincy, Loretta D. Optimal calcium intake: January 1990 through April 1994 plus selected earlier citations : 775 citations. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Library of Medicine, Reference Section, 1994.

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5

NIH Consensus Development Conference on Optimal Calcium Intake (1994 National Institutes of Health). NIH Consensus Development Conference on Optimal Calcium Intake: NIH Consensus Development Conference, June 6-8, 1994, Masur Auditorium, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland. Bethesda, Md: The Institutes, 1994.

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6

NIH Consensus Development Conference on Optimal Calcium Intake (1994 National Institutes of Health). NIH Consensus Development Conference on Optimal Calcium Intake: NIH Consensus Development Conference, June 6-8, 1994, Masur Auditorium, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland. Bethesda, Md: The Institutes, 1994.

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7

NIH Consensus Development Conference on Optimal Calcium Intake (1994 National Institutes of Health). NIH Consensus Development Conference on Optimal Calcium Intake: NIH Consensus Development Conference, June 6-8, 1994, Masur Auditorium, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland. Bethesda, Md: The Institutes, 1994.

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8

Institute of Medicine (U. S.). Committee to Review Dietary Reference Intakes for Vitamin D and Calcium, ed. Dietary reference intakes for calcium and vitamin D. Washington, DC: National Academies Press, 2011.

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9

Institute of Medicine (U.S.). Standing Committee on the Scientific Evaluation of Dietary Reference Intakes., ed. Dietary reference intakes: For calcium, phosphorus, magnesium, vitamin D, and fluoride. Washington, D.C: National Academy Press, 1997.

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10

Faraut, Jacques. Calcul inte gral. Les Ulis, France: EDP Sciences, 2006.

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11

Hairer, E. L'analyse au fil de l'histoire. Berlin: Springer, 2001.

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12

Ikeda, Nobuyuki. Stochastic differential equations and diffusion processes. 2nd ed. Amsterdam: North-Holland Pub. Co., 1989.

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13

Calcium Channel Blockers: The Comprehensive Guide to Managing Calcium Intake and Ensuring Sufficient Calcium Intake for Optimal Health and Performance. Independently Published, 2022.

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14

Alder, Robert John. Calcium intake and the risk of colorectal cancer. 1989.

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15

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Calcium in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0018.

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Most calcium in the body is present in the skeleton, where it serves a structural role and also as a reservoir for use in other tissues. During pregnancy, calcium is accumulated in the fetal skeleton, mostly during the third trimester when bone growth is at its peak. Although this increases the demand on maternal bone stores, the calcium transfer to the fetus is balanced by increased intestinal calcium absorption in the mother, mediated by compensatory changes in vitamin D synthesis and endogenous hormone levels. Bone loss is minimized if calcium intake is maintained at 1,000#amp;#x2013;1,200 mg/day during pregnancy. This intake level builds up calcium stores in early pregnancy for increased fetal transfer in the third trimester. Additional dietary calcium is usually not required if pre-pregnancy intake is adequate, although pregnant adolescents and women carrying multiple fetuses may require supplementation.
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16

Turney, Ben, and John Reynard. Prevention of idiopathic calcium stones. Edited by John Reynard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0015.

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The main principles of idiopathic calcium oxalate stone prevention are to maintain dilute urine through increasing fluid intake and to reduce calcium and oxalate excretion. The influence of various urinary factors on the risk of stone formation has been quantified mathematically. Urine volume and urinary oxalate concentration are most influential on the risk of stone formation, while magnesium concentration contributes a small amount to risk. It is estimated that around 50% of stone formers will form another stone within five years. Some stone formers have frequent recurrences. Most stone formers ask how they can prevent future episodes. Advice can be generic or personalized, and treatment may include changes to diet, fluid intake, and addition of drugs to alter urine biochemistry.
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17

Bilezikian, John P. Optimal Calcium Intake: National Institutes of Health Development Conference: Proceedings, 1994. Diane Pub Co, 1994.

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18

Parent, Marie-Elise *. Effect of caffeine and calcium intake on the bone mass of postmenopausal women. 1988.

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19

Physical activity, calcium intake, body composition and stature as predictors of bone indices in college-aged men. 1988.

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20

Physical activity, calcium intake, body composition and stature as predictors of bone indices in college-aged men. 1990.

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21

Physical activity, calcium intake, body composition and stature as predictors of bone indices in college-aged men. 1990.

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22

Physical activity, calcium intake, body composition and stature as predictors of bone indices in college-aged men. 1990.

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23

Proudfoot, Morwenna. Forearm bone mineral density and its relation to calcium intake and grip strength: Measurements of young normal women. 1996.

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24

Chazminare, Allex Sun. Home Remedies for Kidney Stones: Drink Lots of Water, Lemons, Increase Magnesium Intake, Calcium Intake, Apple Cider Vinegar, Pomegranate Juice, Reduce Vitamin C Intake, Cut Back on Oxalate-Rich Foods, Reduce Animal Protein, Reduce Sodium. Independently Published, 2021.

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25

The Effects of Calcium Intake and Physical Activity on the Bone Mineral Content and Bone Mineral Density of the United States Naval Academy Midshipmen. Storming Media, 1997.

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26

Shepherd, Angela J., and Juliet M. Mckee. Osteoporosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190466268.003.0015.

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Osteoporotic fractures are major causes of suffering and death. Dual-energy x-ray absorptiometry (DEXA) is the standard of care for diagnosis (T-score ≤ –2.5) of osteoporosis. Prevention of fractures requires addressing bone and muscle strength and balance. Physical exercise, good nutrition (fruits, vegetables, adequate calcium), adequate vitamin intake (C, D, and K), tobacco cessation, and no more than moderate alcohol intake enhance bone health and decrease fracture risk. Long-term treatment with glucocorticoids, certain drugs used in breast or prostate cancer treatment, and proton pump inhibitors used for gastroesophageal reflux disease may increase the risk for osteoporosis. Pharmacologically, bisphosphonates are the mainstay of osteoporosis treatment.
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27

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin D in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0015.

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Vitamin D, which is synthesized in skin exposed to UV light, or is consumed in the diet, plays a key role in maintaining bone integrity via the regulation of calcium and phosphorus homeostasis. It also influences a number of extra-skeletal processes, including immune function and blood glucose homeostasis. Maternal vitamin D deficiency in pregnancy leads to poor fetal skeletal mineralization in utero that can manifest as rickets in newborns. In addition to skeletal effects, women with very low vitamin D status face increased risks of other adverse pregnancy outcomes and possible long-term effects on their own health and that of their offspring. However, controversy remains over definitions of vitamin D sufficiency and deficiency, complicating recommendations on maternal intakes. At a minimum, all pregnant women should take a supplement of 400 IU/day, in addition to sensible sun exposure and increasing their intake of food sources.
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28

Bardin, Thomas, and Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.

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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.
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29

Turney, Ben, and John Reynard. Kidney stones. Edited by John Reynard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0013.

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The composition of kidney stones is variable and the predisposing factors multifactorial. Consequently, a detailed evaluation of the patient’s lifestyle, diet, fluid intake, medical history, drug history, urinary tract anatomy, blood, and urine biochemistry and stone composition is required determine predisposing factors for stone formation in an individual patient. Combinatorial subtle variants in biochemistry may act synergistically to increase risk of stone formation/recurrence. Many medications may alter blood and/or urine biochemistry and predispose to stone formation. Corticosteroids increase absorption of calcium from the gut and cause hypercalciuria. Topirimate (for seizures or migraines), sulphasalazine (for rheumatoid arthritis), diuretics containing triamterene, acetazolamide (for myotonia), antacids containing trisilicate, calcium supplements, vitamin D supplements, vitamin C in high doses, indinavir (for HIV), and some herbal medicines (containing ephedrine) all increase stone risk.
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30

Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0146.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly those that result in phosphate deficiency, hypophosphatasia, and vitamin D receptor or metabolizing enzyme mutations. Additionally, the pathogenesis of tumour-induced osteomalacia is becoming better understood. Osteomalacia may present as bone pain and tenderness, muscle pain and weakness, and skeletal deformity or fracture. Key investigations include biochemical assessment and plain radiographs. Radioisotope bone scans and bone biopsy may be considered in selected cases. Differential diagnoses include osteoporosis, seronegative arthritides, and localized soft tissue disorders. Treatment, guided by the underlying aetiology, aims to reduce symptoms, fracture risk, bone deformity and sequelae. Vitamin D deficient patients require vitamin D and calcium replacement.
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31

Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0146_update_001.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly those that result in phosphate deficiency, hypophosphatasia, and vitamin D receptor or metabolizing enzyme mutations. Additionally, the pathogenesis of tumour-induced osteomalacia is becoming better understood. Osteomalacia may present as bone pain and tenderness, muscle pain and weakness, and skeletal deformity or fracture. Key investigations include biochemical assessment and plain radiographs. Radioisotope bone scans and bone biopsy may be considered in selected cases. Differential diagnoses include osteoporosis, seronegative arthritides, and localized soft tissue disorders. Treatment, guided by the underlying aetiology, aims to reduce symptoms, fracture risk, bone deformity and sequelae. Vitamin D deficient patients require vitamin D and calcium replacement.
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32

Taylor, Eric N., and Gary C. Curhan. Epidemiology of nephrolithiasis. Edited by Mark E. De Broe. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0199.

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Nephrolithiasis is common, costly, and painful. The prevalence of nephrolithiasis, defined as a history of stone disease, varies by age, sex, race, and geography while the incidence of nephrolithiasis, defined as the first stone event, varies by age, sex, and race. Epidemiologic studies have quantified the burden of kidney stone disease and expand our understanding of risk factors. A variety of dietary, non-dietary, and urinary risk factors contribute to the risk of stone formation and the importance of these varies by age, sex, and body mass index.Low fluid intake, high urinary oxalate or calcium or uric acid, and low urinary citrate are all associated with nephrolithiasis. These results from epidemiologic studies can be considered in the clinical setting when devising treatment plans to reduce stone recurrence.
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33

Dietary Reference Intakes for Calcium and Vitamin D. Washington, D.C.: National Academies Press, 2011. http://dx.doi.org/10.17226/13050.

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34

Committee to Review Dietary Reference Intakes for Vitamin D and Calcium, Heather B. Del, Ann L. Yaktine, Christine L. Taylor, and A. Catharine Ross. Dietary Reference Intakes for Calcium and Vitamin D. National Academies Press, 2011.

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35

Committee to Review Dietary Reference Intakes for Vitamin D and Calcium, Heather B. Del Valle, Food and Nutrition Board, Institute of Medicine, and Ann L. Yaktine. Dietary Reference Intakes for Calcium and Vitamin D. National Academies Press, 2011.

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36

Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, and Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride (Dietary Reference Intakes). National Academies Press, 1999.

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37

Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington, D.C.: National Academies Press, 1997. http://dx.doi.org/10.17226/5776.

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38

Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, and Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin d, and Fluoride. National Academies Press, 1999.

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39

Intakes, Standing Committee on the Scientific Evaluation of Dietary Reference, Food and Nutrition Board, and Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride (Dietary Reference Series). National Academies Press, 1999.

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40

The influence of glucose on calcium transport by isolated rat enterocytes and intact intestinal preparations. 1987.

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41

Benoist, Joël, and Alain Salinier. Exercices calcul intégral : Avec rappels de cours. Dunod, 2001.

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42

Voinescu, Alexandra, Nadia Wasi Iqbal, and Kevin J. Martin. Management of chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0118_update_001.

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In all patients with chronic kidney disease (CKD) stages 3–5, regular monitoring of serum markers of CKD-mineral and bone disorder, including calcium (Ca), phosphorus (P), parathyroid hormone (PTH), 25-hydroxyvitamin D, and alkaline phosphatase, is recommended. Target ranges for these markers are endorsed by guidelines. The principles of therapy for secondary hyperparathyroidism include control of hyperphosphataemia, correction of hypocalcaemia, use of vitamin D sterols, use of calcimimetics, and parathyroidectomy. of hyperphosphataemia is crucial and may be achieved by means of dietary P restriction, use of P binders, and P removal by dialysis. Dietary P restriction requires caution, as it may be associated with protein malnutrition. Aluminium salts are effective P binders, but they are not recommended for long-term use, as Aluminium toxicity (though from contaminated dialysis water rather than oral intake) may cause cognitive impairment, osteomalacia, refractory microcytic anaemia, and myopathy. Ca-based P binders are also quite effective, but should be avoided in patients with hypercalcaemia, vascular calcifications, or persistently low PTH levels. Non-aluminium, non-Ca binders, like sevelamer and lanthanum carbonate, may be more adequate for such patients; however, they are expensive and may have several side effects. Furthermore, comparative trials have failed so far to provide conclusive evidence on the superiority of these newer P binders over Ca-based binders in terms of preventing vascular calcifications, bone abnormalities, and mortality. P removal is about 1800–2700 mg per week with conventional thrice-weekly haemodialysis, but may be increased by using haemodiafiltration or intensified regimens, such as short daily, extended daily or three times weekly nocturnal haemodialysis. Several vitamin D derivatives are currently used for the treatment of secondary hyperparathyroidism. In comparison with the natural form calcitriol, the vitamin D analogue paricalcitol seems to be more fast-acting and less prone to induce hypercalcaemia and hyperphosphataemia, but whether these advantages translate into better clinical outcomes is unknown. Calcimimetics such as cinacalcet can significantly reduce PTH, Ca, and P levels, but they have failed to definitively prove any benefits in terms of mortality and cardiovascular events in dialysis patients. Parathyroidectomy is often indicated in CKD patients with severe persistent hyperparathyroidism, refractory to aggressive medical treatment with vitamin D analogues and/or calcimimetics. This procedure usually leads to rapid improvements in biochemical markers (i.e. significant lowering of serum Ca, P, and PTH) and clinical manifestations (such as pruritus and bone pain); however, the long-term benefits are still unclear.
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43

Clarke, Andrew. Water. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199551668.003.0005.

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Liquid water is essential for life, and a metabolically active cell is ~70% water. The physical properties of liquid water, and their temperature dependence, are dictated to a significant extent by the properties of hydrogen bonds. From an ecological perspective, the important properties of liquid water include its high latent heats of fusion and vapourisation, its high specific heat, the ionisation, low dynamic viscosity and high surface tension. The solubility in water of oxygen, carbon dioxide and the calcium carbonate used to build skeletons in many invertebrates groups all increase with decreasing temperature. The hydrophobic interaction is important in the formation of cellular membranes and the folding of proteins; its strength increases with temperature, which may be a factor in the cold-denaturation of cellular macromolecules. The cell is extremely crowded with macromolecules. Coupled with the highly structured water close to membranes or protein surfaces and the hydration shells around ions, this means that the behaviour of water in cells is different from that of bulk water. The thermal behaviour of isolated cellular components studied in dilute aqueous buffers many not reflect accurately their behaviour in the intact cell or tissue.
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44

Stochastic differential equations and diffusion processes. kodansha, 1997.

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45

Hamilton, Scott. An Analog Electronics Companion: Basic Circuit Design for Engineers and Scientists. Cambridge University Press, 2007.

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46

An Analog Electronics Companion. Cambridge University Press, 2003.

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47

An Analog Electronics Companion: Basic Circuit Design for Engineers and Scientists. Cambridge University Press, 2003.

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48

Skiba, Grzegorz. Fizjologiczne, żywieniowe i genetyczne uwarunkowania właściwości kości rosnących świń. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_gs_2020.

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Bones are multifunctional passive organs of movement that supports soft tissue and directly attached muscles. They also protect internal organs and are a reserve of calcium, phosphorus and magnesium. Each bone is covered with periosteum, and the adjacent bone surfaces are covered by articular cartilage. Histologically, the bone is an organ composed of many different tissues. The main component is bone tissue (cortical and spongy) composed of a set of bone cells and intercellular substance (mineral and organic), it also contains fat, hematopoietic (bone marrow) and cartilaginous tissue. Bones are a tissue that even in adult life retains the ability to change shape and structure depending on changes in their mechanical and hormonal environment, as well as self-renewal and repair capabilities. This process is called bone turnover. The basic processes of bone turnover are: • bone modeling (incessantly changes in bone shape during individual growth) following resorption and tissue formation at various locations (e.g. bone marrow formation) to increase mass and skeletal morphology. This process occurs in the bones of growing individuals and stops after reaching puberty • bone remodeling (processes involve in maintaining bone tissue by resorbing and replacing old bone tissue with new tissue in the same place, e.g. repairing micro fractures). It is a process involving the removal and internal remodeling of existing bone and is responsible for maintaining tissue mass and architecture of mature bones. Bone turnover is regulated by two types of transformation: • osteoclastogenesis, i.e. formation of cells responsible for bone resorption • osteoblastogenesis, i.e. formation of cells responsible for bone formation (bone matrix synthesis and mineralization) Bone maturity can be defined as the completion of basic structural development and mineralization leading to maximum mass and optimal mechanical strength. The highest rate of increase in pig bone mass is observed in the first twelve weeks after birth. This period of growth is considered crucial for optimizing the growth of the skeleton of pigs, because the degree of bone mineralization in later life stages (adulthood) depends largely on the amount of bone minerals accumulated in the early stages of their growth. The development of the technique allows to determine the condition of the skeletal system (or individual bones) in living animals by methods used in human medicine, or after their slaughter. For in vivo determination of bone properties, Abstract 10 double energy X-ray absorptiometry or computed tomography scanning techniques are used. Both methods allow the quantification of mineral content and bone mineral density. The most important property from a practical point of view is the bone’s bending strength, which is directly determined by the maximum bending force. The most important factors affecting bone strength are: • age (growth period), • gender and the associated hormonal balance, • genotype and modification of genes responsible for bone growth • chemical composition of the body (protein and fat content, and the proportion between these components), • physical activity and related bone load, • nutritional factors: – protein intake influencing synthesis of organic matrix of bone, – content of minerals in the feed (CA, P, Zn, Ca/P, Mg, Mn, Na, Cl, K, Cu ratio) influencing synthesis of the inorganic matrix of bone, – mineral/protein ratio in the diet (Ca/protein, P/protein, Zn/protein) – feed energy concentration, – energy source (content of saturated fatty acids - SFA, content of polyun saturated fatty acids - PUFA, in particular ALA, EPA, DPA, DHA), – feed additives, in particular: enzymes (e.g. phytase releasing of minerals bounded in phytin complexes), probiotics and prebiotics (e.g. inulin improving the function of the digestive tract by increasing absorption of nutrients), – vitamin content that regulate metabolism and biochemical changes occurring in bone tissue (e.g. vitamin D3, B6, C and K). This study was based on the results of research experiments from available literature, and studies on growing pigs carried out at the Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences. The tests were performed in total on 300 pigs of Duroc, Pietrain, Puławska breeds, line 990 and hybrids (Great White × Duroc, Great White × Landrace), PIC pigs, slaughtered at different body weight during the growth period from 15 to 130 kg. Bones for biomechanical tests were collected after slaughter from each pig. Their length, mass and volume were determined. Based on these measurements, the specific weight (density, g/cm3) was calculated. Then each bone was cut in the middle of the shaft and the outer and inner diameters were measured both horizontally and vertically. Based on these measurements, the following indicators were calculated: • cortical thickness, • cortical surface, • cortical index. Abstract 11 Bone strength was tested by a three-point bending test. The obtained data enabled the determination of: • bending force (the magnitude of the maximum force at which disintegration and disruption of bone structure occurs), • strength (the amount of maximum force needed to break/crack of bone), • stiffness (quotient of the force acting on the bone and the amount of displacement occurring under the influence of this force). Investigation of changes in physical and biomechanical features of bones during growth was performed on pigs of the synthetic 990 line growing from 15 to 130 kg body weight. The animals were slaughtered successively at a body weight of 15, 30, 40, 50, 70, 90, 110 and 130 kg. After slaughter, the following bones were separated from the right half-carcass: humerus, 3rd and 4th metatarsal bone, femur, tibia and fibula as well as 3rd and 4th metatarsal bone. The features of bones were determined using methods described in the methodology. Describing bone growth with the Gompertz equation, it was found that the earliest slowdown of bone growth curve was observed for metacarpal and metatarsal bones. This means that these bones matured the most quickly. The established data also indicate that the rib is the slowest maturing bone. The femur, humerus, tibia and fibula were between the values of these features for the metatarsal, metacarpal and rib bones. The rate of increase in bone mass and length differed significantly between the examined bones, but in all cases it was lower (coefficient b <1) than the growth rate of the whole body of the animal. The fastest growth rate was estimated for the rib mass (coefficient b = 0.93). Among the long bones, the humerus (coefficient b = 0.81) was characterized by the fastest rate of weight gain, however femur the smallest (coefficient b = 0.71). The lowest rate of bone mass increase was observed in the foot bones, with the metacarpal bones having a slightly higher value of coefficient b than the metatarsal bones (0.67 vs 0.62). The third bone had a lower growth rate than the fourth bone, regardless of whether they were metatarsal or metacarpal. The value of the bending force increased as the animals grew. Regardless of the growth point tested, the highest values were observed for the humerus, tibia and femur, smaller for the metatarsal and metacarpal bone, and the lowest for the fibula and rib. The rate of change in the value of this indicator increased at a similar rate as the body weight changes of the animals in the case of the fibula and the fourth metacarpal bone (b value = 0.98), and more slowly in the case of the metatarsal bone, the third metacarpal bone, and the tibia bone (values of the b ratio 0.81–0.85), and the slowest femur, humerus and rib (value of b = 0.60–0.66). Bone stiffness increased as animals grew. Regardless of the growth point tested, the highest values were observed for the humerus, tibia and femur, smaller for the metatarsal and metacarpal bone, and the lowest for the fibula and rib. Abstract 12 The rate of change in the value of this indicator changed at a faster rate than the increase in weight of pigs in the case of metacarpal and metatarsal bones (coefficient b = 1.01–1.22), slightly slower in the case of fibula (coefficient b = 0.92), definitely slower in the case of the tibia (b = 0.73), ribs (b = 0.66), femur (b = 0.59) and humerus (b = 0.50). Bone strength increased as animals grew. Regardless of the growth point tested, bone strength was as follows femur > tibia > humerus > 4 metacarpal> 3 metacarpal> 3 metatarsal > 4 metatarsal > rib> fibula. The rate of increase in strength of all examined bones was greater than the rate of weight gain of pigs (value of the coefficient b = 2.04–3.26). As the animals grew, the bone density increased. However, the growth rate of this indicator for the majority of bones was slower than the rate of weight gain (the value of the coefficient b ranged from 0.37 – humerus to 0.84 – fibula). The exception was the rib, whose density increased at a similar pace increasing the body weight of animals (value of the coefficient b = 0.97). The study on the influence of the breed and the feeding intensity on bone characteristics (physical and biomechanical) was performed on pigs of the breeds Duroc, Pietrain, and synthetic 990 during a growth period of 15 to 70 kg body weight. Animals were fed ad libitum or dosed system. After slaughter at a body weight of 70 kg, three bones were taken from the right half-carcass: femur, three metatarsal, and three metacarpal and subjected to the determinations described in the methodology. The weight of bones of animals fed aa libitum was significantly lower than in pigs fed restrictively All bones of Duroc breed were significantly heavier and longer than Pietrain and 990 pig bones. The average values of bending force for the examined bones took the following order: III metatarsal bone (63.5 kg) <III metacarpal bone (77.9 kg) <femur (271.5 kg). The feeding system and breed of pigs had no significant effect on the value of this indicator. The average values of the bones strength took the following order: III metatarsal bone (92.6 kg) <III metacarpal (107.2 kg) <femur (353.1 kg). Feeding intensity and breed of animals had no significant effect on the value of this feature of the bones tested. The average bone density took the following order: femur (1.23 g/cm3) <III metatarsal bone (1.26 g/cm3) <III metacarpal bone (1.34 g / cm3). The density of bones of animals fed aa libitum was higher (P<0.01) than in animals fed with a dosing system. The density of examined bones within the breeds took the following order: Pietrain race> line 990> Duroc race. The differences between the “extreme” breeds were: 7.2% (III metatarsal bone), 8.3% (III metacarpal bone), 8.4% (femur). Abstract 13 The average bone stiffness took the following order: III metatarsal bone (35.1 kg/mm) <III metacarpus (41.5 kg/mm) <femur (60.5 kg/mm). This indicator did not differ between the groups of pigs fed at different intensity, except for the metacarpal bone, which was more stiffer in pigs fed aa libitum (P<0.05). The femur of animals fed ad libitum showed a tendency (P<0.09) to be more stiffer and a force of 4.5 kg required for its displacement by 1 mm. Breed differences in stiffness were found for the femur (P <0.05) and III metacarpal bone (P <0.05). For femur, the highest value of this indicator was found in Pietrain pigs (64.5 kg/mm), lower in pigs of 990 line (61.6 kg/mm) and the lowest in Duroc pigs (55.3 kg/mm). In turn, the 3rd metacarpal bone of Duroc and Pietrain pigs had similar stiffness (39.0 and 40.0 kg/mm respectively) and was smaller than that of line 990 pigs (45.4 kg/mm). The thickness of the cortical bone layer took the following order: III metatarsal bone (2.25 mm) <III metacarpal bone (2.41 mm) <femur (5.12 mm). The feeding system did not affect this indicator. Breed differences (P <0.05) for this trait were found only for the femur bone: Duroc (5.42 mm)> line 990 (5.13 mm)> Pietrain (4.81 mm). The cross sectional area of the examined bones was arranged in the following order: III metatarsal bone (84 mm2) <III metacarpal bone (90 mm2) <femur (286 mm2). The feeding system had no effect on the value of this bone trait, with the exception of the femur, which in animals fed the dosing system was 4.7% higher (P<0.05) than in pigs fed ad libitum. Breed differences (P<0.01) in the coross sectional area were found only in femur and III metatarsal bone. The value of this indicator was the highest in Duroc pigs, lower in 990 animals and the lowest in Pietrain pigs. The cortical index of individual bones was in the following order: III metatarsal bone (31.86) <III metacarpal bone (33.86) <femur (44.75). However, its value did not significantly depend on the intensity of feeding or the breed of pigs.
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