• Journal of Nutrition and Health
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• v.33 no.2
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• pp.147-157
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• 2000

This study examined the effects of excess intake of calcium (Ca) and iron (Fe) supplement on bone loss, nephrocalcinosis and renal function in osteoporotic model rats. Seven-week-old female rats were first fed a Ca-deficient diet for four weeks after ovariectomy operation, and then one of nine experimental diets for additional eight weeks, containing three levels of Ca, normal (0.5%) or high (1.5%) or excess (2.5%) and three levels of Fe, normal (35ppm) or high (210ppm) or excess (350ppm). The osteoporotic model rats showed a remarkable increase in body weight, serum alkaline phosphatase (ALP) and decrease in breaking force, Ca, P, Mg contents of femur. Serum Ca concentration was not significantly affected by dietary Ca and Fe levles. Liver Ca content increased in rats fed a high-and excess-Ca diet. Kidney Ca content and microscopic Ca deposition remarkably increased in osteoporotic model rats compared to control group, and showed a tendency to decrease in rats fed a excess-Ca diet. Breaking force of femur increased with increasing dietary Ca levels, but Ca, P contents of femur and serum ALP were not significantly affected by dietary Ca and Fe levels. Serum total protein decreased in rats fed a excess-Ca diet, BUN increased in rats fed a excess-Ca diet, while serum uric acid and creatinine were not significantly affected by dietary Ca levels. Urinary creatinine, GFR increased in rats fed a high-and excess-Ca, diet, and GFR was highest in rats fed a excess-Ca/excess-Fe diet. These results suggest that excess intake of Ca may increase breaking force of femur, but not increase mineral contents of femur, and decrease kidney function. Furthermore, excess intake of Fe and Ca concurrently may aggravate kidney function leading to potential health problems in ovariectomized osteoporotic model rats.

• Korean Journal of Community Nutrition
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• v.5 no.2
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• pp.243-252
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• 2000

This study examined the effects of excess intake of calcium(Ca) and iron(Fe) supplements on iron bioavailability, liver and kidney functions in anemic model rats. Seven-week-old female rats were first fed and Fe-deficient diet for ten weeks, and then fed one of nine experimental diets for an additional eight weeks, containing three levels of Ca, normal (0.5%) or high(1.5%) or excess (2.5%) and three levels of Fe, normal(35ppm) or high(210 ppm) or excess(350ppm). In anemic model rats, serum Fe, total iron binding capacity(TIBC), hemogolin(Hb), hematocrit(Hct) and liver Fe contents were significantly decreased. Apparent Fe absorption significantly increased with increasing dietary Fe levels, and decreased with increasing dietary Ca levels. serum Fe concentration significantly increased in rats fed a high- and excess-Fe diet, and decreased in rats fed a excess-Ca diet. TIBC was decreawed in rats fed a excess-Ca diet, and transferrin saturation(%) increased in rats fed ahigh- and excess-Fe diet. Hb and Hct were decreased in rats fed an excess-Ca diet regardless of dietary Fe levels. Fe and thiobarbituric acid reactin gsubstance(TBARS) Contents of liver significantly increased in rats fed a high- and excess0-Fe diet, and decreased in rats fed a high- and excess-Ca diet. Fe content of the spleen showed similar results. Urinary creatinine and GFR increased in rats fed an excess-Ca diet regardless of dietary Fe levels. GOT, GPT and LDH were not significantly affected by dietary Ca and Fe levels. These results suggest that excess intake of Fe may increase liver Fe deposits and TBARS, and excess intake of Ca may decrease Fe bioavailability and kidney function leading to potential health problems in anemic model rats.

• Asian-Australasian Journal of Animal Sciences
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• v.12 no.1
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• pp.49-55
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• 1999

The effect of fat supplementation of high calcium (Ca) diets on the performance, intestinal pH, body composition and size and weight of organs in growing chickens were investigated in two experiments. Growing chickens tolerated a high dietary level of Ca (22.5 vs 12.1 g/kg) in the presence of 6.3 g/kg of available phosphorus without any significant effect on performance. Intestinal pH was significantly increased by the addition of excess Ca and fat which probably created the right pH for the formation of insoluble Ca soaps. Excess dietary Ca increased carcass linoleic acid concentration at the expense of palmitic and stearic acid contents, whilst the addition of sunflower oil (80 g/kg diet) to the diet increased carcass linoleic acid concentration at the expense of palmitic acid content of the carcass. Intestinal and visceral organ size and weight were not influenced by excess Ca or fat. However, there was a non significant increase in the intestinal dry weight per unit of length caused by excess dietary Ca. It was concluded that excess dietary Ca of 22.5 g/kg did not significantly influence the performance of meat chickens. However, excess Ca increased intestinal pH and altered carcass fatty acid composition. Fat supplementation did not alter intestinal pH with high Ca diets. Excess dietary fat altered carcass fatty acid composition and reduced protein content. Intestinal and visceral organ size and weights were not influenced by excess dietary levels of Ca of fat.

• Journal of Nutrition and Health
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• v.37 no.8
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• pp.645-654
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• 2004

This study examined the effect of excess calcium (Ca) on the iron (Fe) bioavailability and bone growth of marginally Fe deficient animals. Two groups of weanling female SD rats were fed either normal Fe (35 ppm) or Fe deficient diet (8 ppm) for 3 weeks. Then each group of animals were assigned randomly to one of three groups and were fed one of six experimental diets additionally for 4 weeks, containing normal (35 ppm) or low (15 ppm) Fe and one of three levels of Ca as normal (0.5%), high (1.0%), or excess (1.5%). Feces and urine were collected during the last 3 days of treatment. After sacrifice blood, organs, and femur bone were collected for analysis. Final body weight and average food intake were not affected by either the levels of dietary Ca or Fe. Low Fe diet significantly reduced the level of serum ferritin, however, for Hb, Hct, and TIBC no difference was shown than those in the normal Fe group. TIBC increased slightly by high and excess Ca intake in low Fe groups. For both normal and low Fe groups, high and excess Ca intakes reduced the apparent absorption of Fe and Fe contents of liver significantly (p < 0.05). Calcium contents in kidney and Femur of rats that were fed high and excess levels of Ca were significantly greater than those of normal Ca groups. However, weight, length, and breaking force of the bone were not affected by increased Ca intakes. Both in control and low Fe groups, high and excess intakes of Ca decreased the apparent absorption of Ca. These results indicate that the excess intakes of calcium than the normal needs would be undesirable for Fe bioavailability and that the adverse effects be more serious in marginally iron deficient growing animals. In addition bone growth and strength would not be favorably affected by high Ca intakes, though, the long term effect of increased Ca contents in bone requires further examination.

• The Korean Journal of Pharmacology
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• v.27 no.2
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• pp.167-181
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• 1991

The present study was an attempt to investigate the effect of forskolin on secretion of catecholamines (CA) evoked by Ach, excess $K^+$, DMPP, McN-A-343 and caffeine from the isolated perfused rat adrenal glands and to elucidate its mechanism of action. The perfusion with forskolin (1.0 uM) for 1 min into the adrenal vein enhanced markedly the secreation of CA evoked by Ach (50 ug), excess $K^+$ (56 mM) DMPP (100 uM) and by caffeine (0.3 mM) but did not that by McN-A-343. Forskolin alone did not potentiate the CA secretion. Moreover, forskolin augmented the CA release evoked by the above same stimulation even in the absence of extracellular calcium. The 1 min perfusion of 300 uM-dibutyryl cyclic AMP (DBcAMP), which is known to increase cyclic AMP levels, led to enhancement of Ca secretion evoked by Ach, excess $K^+$ and DMPP but did not that by McN-A-343 and caffeine. DBcAMP by itself also did not augment the CA secretion. In the calcium-free medium DBcAMP significantly enhanced the CA secretion by the same stimulation, except for the case of McN-A-343. These experimental results suggest that forskolin activates adenylate cyclase, resulting the elevation of cyclic AMP which may potentiate cholinergic nicotinic receptor-mediated and also depolarization-dependent CA secretion and that it may alter the intracellular calcium homeostasis in the rat adrenal glands.

• Korean Journal of Materials Research
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• v.2 no.3
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• pp.207-212
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• 1992

The defect structure of calcium titanates with CaO excess or $TiO_2$ excess was studied by measuring electrical conductivities as a funcition of oxygen partial pressure at $85O^{\circ}C$ to $1050^{\circ}C$. Execess CaO may divide itself equally between A and B sites, resulting in $Ca_{Ti}$" and Vo", while excess $TiO_2$ form $V_{Ca}$" and Vo". The equilibrium electrical conductivity data indicate that the solubilities of CaO and $TiO_2$ in $CaTiO_3$ are 5000ppm and 2000ppm, respectively. Oxygen vacancies contributed to the ionic conduction which flatten the conductivity minima and did not make any defect association with oppositely charged defects.ely charged defects.

• Korean Journal of Materials Research
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• v.16 no.2
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• pp.92-98
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• 2006

Molecular dynamics simulations were performed to study interface structures between an $Al_2O_3$ crystalline phase and a interface phase of $CaAl_2Si_2O_8$. We calculated atomic structures and excess interface energies in systems with different thicknesses of the interface film. It was found that excess interface energies at first readily decreased with increasing film thickness, but increased for larger thicknesses of more than 2 nm. The excess energies of $Al_2O_3/CaAl_2Si_2O_8$ interfaces exhibit a minimum at a thickness around 1 nm. In this range of film thicknesses, the atoms in the interface film show a short-range ordered structure and slow diffusion rather than the random structure and rapid diffusion expected to an observation of an equilibrium thickness for interface films in ceramics.

• Journal of the Korean Ceramic Society
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• v.30 no.7
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• pp.527-534
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• 1993

The phenomena that excess sulfate hindred the C3S formation in the presence of clinker liquid phase were investigated. In the case of (NH4)2SO4, assuming SO3 atmospheric condition, sulfate stabilized C2S and was enriched at the surface of C2S grains, so C2S was prevented from being dissolved into clinker melt. CaSO4 showed the similar aspect with (NH4)2SO4, however, the prevention of C3S formation by CaSO4 took more influence that C2AS and C4A3 were formed below 100$0^{\circ}C$, and remained upto clinkering temperature, 145$0^{\circ}C$, thus these intermediate phases caught CaO which would participate the C3S formation.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.2
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• pp.173-184
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• 1998

The present study was undertaken to examine the influence of glucocorticoids on the secretory responses of catecholamines (CA) evoked by acetylcholine (ACh), DMPP, McN-A-343, excess K^+$ and Bay-K-8644 from the isolated perfused rat adrenal gland and to clarify the mechanism of its action. The perfusion of the synthetic glucocorticoid dexamethasone (10-100\;{\mu}M$) into an adrenal vein for 20 min produced a dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM), excess K^+$ (a membrane-depolarizor 56 mM), DMPP (a selective nicotinic receptor agonist, 100\;{\mu}M$ for 2 min), McN-A-343 (a muscarinic receptor agonist, 100\;{\mu}M$ for 4 min), Bay-K-8644 (a calcium channel activator, 10\;{\mu}M$ for 4 min) and cyclopiazonic acid (a releaser of intracellular $Ca^{2+}$, 10\;{\mu}M$ for 4 min). Similarly, the preperfusion of hydrocortisone (30\;{\mu}M$) for 20 min also attenuated significantly the secretory responses of CA evoked by nicotinic and muscarinic receptor stimulation as well as membrane-depolarization, $Ca^{2+}$ channel activation and the release of intracellular $Ca^{2+}$. Furthermore, even in the presence of betamethasone (30{\mu}M$), CA secretion evoked by ACh, excess K^+$, DMPP and McN-A-343 was also markedly inhibited. Taken together, the present results suggest that glucocorticoids cause the marked inhibition of CA secretion evoked by both cholinergic nicotinic and muscarinic receptor stimulation from the isolated perfused rat adrenal gland, indicating strongly that this inhibitory effect may be mediated by inhibiting influx of extracellular calcium as well as the release of intracellular calcium in the rat adrenomedullary chromaffin cells.

• The Korean Journal of Pharmacology
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• v.30 no.1
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• pp.87-100
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• 1994

It has been known for some time that dopamine-containing cells are existed in sympathetic ganglia, i.e., small, intensely fluorescent cells. However, its role and mechanism of action as a peripheral neurotransmitter are poorly understood so far. In the present study, an attempt was made to examine the effect of apomorphine, which is known to be a selective agonist of dopaminergic $D_2$. receptor on secretion of catecholamines (CA) from the isolated perfused rat adrenal gland. The perfusion of a low concentration of 10uM apomorphine into an adrenal vein for 20 min produced significant reduction in CA secretion induced by 5.32 mM ACh, 56 mM KCl, 100 uM DMPP and 100 uM McN-A-343. Increasing apomorphine concentration to 30 uM led to more markedly decreased CA secretion as compared to the case of 10 uM apomorphine and also did inhibit clearly CA release by $10^{-5}M$ Bay-K-8644. Furthermore, in adrenal glands preloaded with a higher dose of 100 uM apomorphine, CA releases evoked by ACh, excess $K^+$, DMPP and McN-A-343 were almost abolished by the drug. The perfusion of $3.3{\pm}10^{-5}M$ metoclopramide, which is well-known as a selective dopaminergic $D_2$ antagonist, produced significantly inhibitory effect of CA release by ACh, DMPP and McN-A-343 but did not affect that by excess $K^+$. However, preloading of 30uM apomorphine in the presence of metoclopramide did not modify the CA secretory effect of excess $K+$ and DMPP. These experimental results demonstrate that apomorphine causes dose-dependent inhibition of CA secretion by cholinergic receptor stimulation and also by membrane depolarization from the isolated perfused rat adrenal gland, suggesting that these effects appear to be exerted by inhibiting influx of extracellular calcium into the rat adrenal medullary chromaffin cells through activation of inhibitory dopaminergic receptors.