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Journal articles on the topic 'Calcium-deficient'

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Published: 10 December 2022

Last updated: 29 January 2023

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1

Herminiati, Ainia. "The effectivity of Difructose Anhydride III to increase absorption of calcium in the femur bone of calcium deficient rats." Functional Foods in Health and Disease 10, no. 4 (April 30, 2020): 168. http://dx.doi.org/10.31989/ffhd.v10i4.701.

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Background: Dried yogurt enriched by Difructose Anhydride III when used as a functional food has been observed to increase calcium absorption, making it useful in osteoporosis prevention. The objective of this study was to analyze the effectiveness of Difructose Anhydride III in increasing the absorption of calcium in female rat models, strain Sprague Dawley, in the pre-menopausal age during which they’re calcium deficient.Methods: The effectiveness test of Difructose Anhydride III to increase absorption of calcium in pre-menopausal Sprague Dawley rats was performed in calcium-deficient conditions. A completely randomized experimental design was used with 4 treatments for 6 weeks and 4 replications: normal rats fed with purified diet (C), calcium-deficient rats fed with calcium-deficient diet (CD), calcium-deficient rats fed with calcium-deficient diet and DFA III (dahlia tubers) fortified in dry yogurt (CD+DFA III dahlia), and calcium-deficient rats fed with a calcium-deficient diet and DFA III (chicory roots) fortified in dry yogurt (CD+DFA III chicory). The parameters measured were serum calcium concentration, femur bone calcium concentration, femur bone matrix condition, and femur bone strength.Results: DFA III (dahlia tubers and chicory roots) fortified in dry yogurt contained 0.334% and 0.322% of calcium concentration. The provision of a calcium-deficient diet for 12 weeks was shown to reduce the serum calcium concentration of the deficient calcium rat to 7.72±1.08 mg dL-1 and the control rat to 11.60±0.85 mg dL-1. CD+DFA III chicory treatments also showed a high calcium concentration in the femur bone (34.94±3.21%), a relatively higher bone strength (9.34±3.61 kg cm-2), and a denser femur bone matrix condition than the control. The femur bone calcium level of rats treated with CD+DFA III dahlia and chicory tubers was 28.95±1.95% and 34.94±3.21%, respectively. These results were significantly different than the CD treatment (17.49±4.38%).Conclusion: The evidence from this study suggests that sufficient calcium intake could provide high calcium deposits in the bones. Diets containing 3.60% w/w DFA III fortified in dry yogurt have been shown to enhance calcium absorption in calcium-deficient rats. Additionally, the effectiveness of dried yogurt enriched by DFA III from chicory tubers was higher than that of the dried yogurt enriched by DFA III from dahlia tubers.Preclinical Trial Registration: Animal Ethics Committee at IPB University No. 12-2013Keywords: Bone femur; calcium deficiency; effectivity of Difructose Anhydride III

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2

Ipekoglu, M., and S. Altintas. "Silver substituted nanosized calcium deficient hydroxyapatite." Materials Technology 25, no. 5 (November 2010): 295–301. http://dx.doi.org/10.1179/175355510x12692596613648.

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3

Sakamoto, Kiyoko, Kazuno Mizuguchi, Takuya Nomoto, Shunro Yamaguchi, Junko Ichihara, Yoh Sasaki, and Koichi Niihara. "Thermoluminescence of Calcium-Deficient Fluoridated Hydroxyapatite." Phosphorus, Sulfur, and Silicon and the Related Elements 177, no. 8-9 (August 2002): 2261. http://dx.doi.org/10.1080/10426500213376.

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4

Dykman, A. S., O. Ye Batalin, V. M. Yevgrashin, and E. I. Rubinstein. "Catalytic Activity of Calcium-Deficient Hydroxylapatites." Phosphorus, Sulfur, and Silicon and the Related Elements 51, no. 1 (1990): 433. http://dx.doi.org/10.1080/10426509008544475.

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5

Sissons, H. A., G. J. Kelman, and G. Marotti. "Bone resorption in calcium-deficient rats." Bone 6, no. 5 (1985): 345–47. http://dx.doi.org/10.1016/8756-3282(85)90328-x.

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6

Park, Myoung-Gyu, Tae-Yul Ha, and Kwang-Soon Shin. "Bioavailability of Aspartic Acid Chelated Calcium in Calcium Deficient Rats." Korean Journal of Nutrition 44, no. 6 (2011): 474. http://dx.doi.org/10.4163/kjn.2011.44.6.474.

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7

Lausson, S., J. F. Staub, G. Milhaud, and A. M. Perault-Staub. "Circadian variations in plasma calcium and calcitonin: effect of calcium deficiency and fasting." Journal of Endocrinology 107, no. 3 (December 1985): 389–95. http://dx.doi.org/10.1677/joe.0.1070389.

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ABSTRACT Circadian fluctuations of plasma calcium and immunoassayable calcitonin levels were studied in normal and calcium-deficient 2-month-old rats. The relationship between these parameters was also studied in animals which had been fasted for short periods. The plasma calcium rhythm persisted and was even amplified in rats placed on a 4-week calcium-deficient diet. In these rats, as in normal rats, the plasma calcium concentration diminished during the dark period. Calcitonin levels increased at the onset of the feeding period in normal rats but, in calcium-deficient rats, the pattern changed completely, with a major peak at the end of the light period and remaining at a low level during the dark feeding period. This modification of calcitonin rhythmicity appeared to be dependent on the degree of calcium deficiency. Fasting had little effect on calcitonin rhythms in either normal or calcium-deficient rats. It is concluded that the calcitonin rhythm is relatively independent of feeding per se and that there appears to be no simple relationship between plasma calcium and calcitonin concentrations. It is suggested that the results may best be interpreted as reflecting the presence of rhythmic endogenous phenomena which are intrinsic to calcium metabolism and its regulation in the rat. J. Endocr. (1985) 107, 389–395

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8

KIKUNAGA, Shigeshi, Miwako ARIMORI, and Masayuki TAKAHASHI. "The bioavailability of calcium in spinach and calcium-oxalate to calcium-deficient rats." Journal of Nutritional Science and Vitaminology 34, no. 2 (1988): 195–207. http://dx.doi.org/10.3177/jnsv.34.195.

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9

De Flora, A., U. Benatti, L. Guida, G. Forteleoni, and T. Meloni. "Favism: disordered erythrocyte calcium homeostasis." Blood 66, no. 2 (August 1, 1985): 294–97. http://dx.doi.org/10.1182/blood.v66.2.294.294.

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Abstract The biochemical events that take place during acute hemolysis of G6PD- deficient subjects in favism are far from being elucidated. Evidence is here reported for a constantly and heavily disordered calcium homeostasis in the erythrocytes from seven favic patients. The abnormality, ie, a significantly impaired calcium ATPase activity and a parallel marked increase of intracellular calcium levels, was characteristic of the acute hemolytic crisis although unrelated to the attendant reticulocytosis. Concomitantly, a remarkable decrease of intracellular potassium was also observed. The mean +/- SD Ca2+-ATPase activity in the favic patients was 20.8 +/- 7.8 mumol Pi/g Hb/h compared with 37.2 +/- 8.5 in the matched controls represented by 12 healthy G6PD-deficient subjects (P less than .001). The mean +/- SD intraerythrocytic calcium content was 288 +/- 158 mumol/L of erythrocytes in the favic patients as compared with 22.0 +/- 8.2 in the G6PD-deficient controls (P less than .001). The intraerythrocytic potassium content was 76.6 +/- 19.3 mmol/L of erythrocytes in the favic patients and 106.6 +/- 8.2 in the G6PD-deficient controls (P less than .001). In vitro incubation of normal and G6PD-deficient erythrocytes with divicine, a pyrimidine aglycone present in fava beans and strongly implicated in the pathogenesis of favism, reproduces most of these events, including drop of calcium ATPase, increased intracellular calcium, and leakage of erythrocyte potassium.

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10

De Flora, A., U. Benatti, L. Guida, G. Forteleoni, and T. Meloni. "Favism: disordered erythrocyte calcium homeostasis." Blood 66, no. 2 (August 1, 1985): 294–97. http://dx.doi.org/10.1182/blood.v66.2.294.bloodjournal662294.

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The biochemical events that take place during acute hemolysis of G6PD- deficient subjects in favism are far from being elucidated. Evidence is here reported for a constantly and heavily disordered calcium homeostasis in the erythrocytes from seven favic patients. The abnormality, ie, a significantly impaired calcium ATPase activity and a parallel marked increase of intracellular calcium levels, was characteristic of the acute hemolytic crisis although unrelated to the attendant reticulocytosis. Concomitantly, a remarkable decrease of intracellular potassium was also observed. The mean +/- SD Ca2+-ATPase activity in the favic patients was 20.8 +/- 7.8 mumol Pi/g Hb/h compared with 37.2 +/- 8.5 in the matched controls represented by 12 healthy G6PD-deficient subjects (P less than .001). The mean +/- SD intraerythrocytic calcium content was 288 +/- 158 mumol/L of erythrocytes in the favic patients as compared with 22.0 +/- 8.2 in the G6PD-deficient controls (P less than .001). The intraerythrocytic potassium content was 76.6 +/- 19.3 mmol/L of erythrocytes in the favic patients and 106.6 +/- 8.2 in the G6PD-deficient controls (P less than .001). In vitro incubation of normal and G6PD-deficient erythrocytes with divicine, a pyrimidine aglycone present in fava beans and strongly implicated in the pathogenesis of favism, reproduces most of these events, including drop of calcium ATPase, increased intracellular calcium, and leakage of erythrocyte potassium.

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11

Tuan, R. S., and H. Q. Nguyen. "Cardiovascular changes in calcium-deficient chick embryos." Journal of Experimental Medicine 165, no. 5 (May 1, 1987): 1418–23. http://dx.doi.org/10.1084/jem.165.5.1418.

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We have developed an experimental system involving calcium-deficient chick embryos to examine the relationship between calcium homeostasis and cardiovascular activities. We have found that the calcium-deficient embryos, when compared with control animals, exhibit tachycardia and are significantly hypertensive. The effects are unlikely to be due to gross cardiac malformations or hypertrophy. The hypertensive condition appears to be a specific result of the systemic calcium deficiency since calcium supplementation to these embryos significantly restores the functions to normality.

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12

Koval, S. F., and R. G. E. Murray. "Effect of calcium on the in vivo assembly of the surface protein of Aquaspirillum serpens VHA." Canadian Journal of Microbiology 31, no. 3 (March 1, 1985): 261–67. http://dx.doi.org/10.1139/m85-049.

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Aquaspirillum serpens VHA grown in minimal medium supplemented with 0.5 mM calcium possesses the regularly structured (RS) superficial protein layer. Cells grown in calcium-deficient medium lack the RS layer, but secrete small amounts of RS protein into the culture supernatant. Thus calcium is not required for synthesis of this protein. Addition of 0.5 mM calcium to midexponential phase cells in calcium-deficient conditions results in the rapid (within 10 min) assembly of a stable RS layer on the outer membrane. The RS layer is assembled from secreted and newly synthesized protein. No periplasmic pool of RS protein was found in calcium-deficient conditions. It is suggested that calcium is required to establish the correct conformation of the protein to allow assembly.

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13

OKAMURA, Hisakazu, Morihiro YASUDA, and Masatoshi OHTA. "Synthesis of Calcium-deficient Hydroxyapatite-collagen Composite." Electrochemistry 68, no. 6 (June 5, 2000): 486–88. http://dx.doi.org/10.5796/electrochemistry.68.486.

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14

Dykman, A. S., O. Ye Batalin, V. M. Yevgrashin, and E. I. Rubinstein. "Catalytic Activity of Calcium-Deficient Hydroxyl-Apatites." Phosphorus, Sulfur, and Silicon and the Related Elements 51, no. 1-4 (September 1990): 433. http://dx.doi.org/10.1080/10426509008040957.

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15

Williams, Bernadette Manuel. "Older African Americans and Calcium-Deficient Diets." Topics in Geriatric Rehabilitation 21, no. 1 (January 2005): 88–92. http://dx.doi.org/10.1097/00013614-200501000-00010.

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16

VALLETREGI, M. "Synthesis and characterisation of calcium deficient apatite." Solid State Ionics 101-103 (November 1997): 1279–85. http://dx.doi.org/10.1016/s0167-2738(97)00213-0.

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17

Csernoch, Laszlo, Dora Bodnar, Olga Ruzsnavszky, Nikolett Geyer, Bence Hegyi, Beatrix Dienes, Monika Sztretye, and Peter Szentesi. "Myostatin Deficient Mice Display Altered Calcium Signaling." Biophysical Journal 104, no. 2 (January 2013): 289a. http://dx.doi.org/10.1016/j.bpj.2012.11.1616.

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18

Zafar, Tasleem A., Dorothy Teegarden, Curtis Ashendel, Michael A. Dunn, and Connie M. Weaver. "Aluminum negatively impacts calcium utilization and bone in calcium-deficient rats." Nutrition Research 24, no. 3 (March 2004): 243–59. http://dx.doi.org/10.1016/j.nutres.2003.12.002.

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19

Dijksma, F. J. J., J. F. Vente, E. Frikkee, and D. J. W. IJdo. "The structure of a calcium deficient hexagonal calcium iridium oxide compound." Materials Research Bulletin 28, no. 11 (November 1993): 1145–51. http://dx.doi.org/10.1016/0025-5408(93)90094-t.

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20

Walters, J. R., and M. M. Weiser. "Calcium transport by rat duodenal villus and crypt basolateral membranes." American Journal of Physiology-Gastrointestinal and Liver Physiology 252, no. 2 (February 1, 1987): G170—G177. http://dx.doi.org/10.1152/ajpgi.1987.252.2.g170.

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Rat duodenal cells were isolated sequentially to give fractions enriched for villus and crypt cells. From each of these fractions, basolateral-enriched membrane vesicles were prepared and ATP-dependent calcium uptake was studied. Calcium uptake was sensitive to temperature, was inhibited by vanadate and by A23187, and was lower in vitamin D-deficient animals. In normal animals, calcium transport was approximately twofold greater in villus-tip than in crypt cell-fraction basolateral membranes though the affinity of the uptake for calcium was similar (Km = 0.3 microM). In vitamin D-deficient animals, the crypt-to-villus gradient was reduced, and in all fractions, calcium transport was similar to or lower than that in the crypts of normal animals. Six hours after vitamin D-deficient animals were repleted with 1,25-dihydroxycholecalciferol, a significant increase in calcium transport by everted gut sacs was present; however, basolateral calcium transport was significantly increased in only the mid-villus fractions, and no change was seen in the villus-tip fractions. Thus vitamin D appears necessary for the development of increased basolateral membrane calcium pump activity in duodenal villus cells, but not all cells in vitamin D-deficient rats are able to respond to 1,25-dihydroxycholecalciferol.

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21

Żyła, K., M. Mika, S. Świątkiewicz, J. Koreleski, and J. Piironen. "Effects of phytase B on laying performance, eggshell quality and on phosphorus and calcium balance in laying hens fed phosphorus-deficient maize-soybean meal diets." Czech Journal of Animal Science 56, No. 9 (September 19, 2011): 406–13. http://dx.doi.org/10.17221/1290-cjas.

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A study was conducted to evaluate the effects of dietary supplementation of phytase B (product of the Aspergillus niger phyB gene expressed in Trichoderma reesei) on feed intake, laying performance, eggshell quality, and on phosphorus and calcium balance in laying hens. Seventy-two, 40 weeks old Hy Line Brown hens were fed for 14 weeks the following four phosphorus-deficient (0.12% nonphytate phosphorus, NPP), maize-soybean meal-based diets: (1) calcium-deficient (2.8% Ca) control diet; (2) diet 1 + phytase B at the activity of 2.5 acid phosphatase units (AcPU/kg); (3) control diet (3.8% Ca); (4) diet 3 + phytase B at the activity of 2.5 AcPU/ kg. Each dietary treatment was fed to 18 cages of hens, 1 hen/cage kept in individual cages. Hens fed the NPP- and Ca-deficient diets consumed more feed (P < 0.01) and excreted less calcium (P < 0.01) than those receiving P-deficient diets with the standard calcium level. There were no effects of calcium level on feed utilization, egg mass, egg weight, and eggshell breaking strength. Egg production, although numerically higher in hens fed low Ca diets with no enzyme added, failed to be significantly different due to the low number of hens investigated and therefore the measurement should be considered as preliminary and supplementary. Phytase B increased mean egg weight by about 7% in layers fed the NPP- and Ca-deficient diet (Ca × phytase B interaction, P < 0.05), increased shell breaking strength, particularly at the standard calcium level, significantly enhanced amounts of calcium retained by layers and amounts of  phosphorus retained by hens fed the Ca-deficient diets. Additionally, phytase B improved Ca retention at both dietary Ca levels and phosphorus retention in hens fed the Ca-deficient diets. Results of the study indicate that the efficacy of phytase B in NPP-deficient diets is strongly influenced by the dietary calcium level and the enzyme may modulate egg weight, eggshell quality, phosphorus and calcium retention in laying hens fed low-NPP, maize-soybean meal-based diets.

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22

Sun, Hong-Ye, Wei-Wei Zhang, Hai-Yong Qu, Sha-Sha Gou, Li-Xia Li, Hui-Hui Song, Hong-Qiang Yang, et al. "Transcriptomics Reveals the ERF2-bHLH2-CML5 Module Responses to H2S and ROS in Postharvest Calcium Deficiency Apples." International Journal of Molecular Sciences 22, no. 23 (December 1, 2021): 13013. http://dx.doi.org/10.3390/ijms222313013.

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Calcium deficiency usually causes accelerated quality deterioration in postharvest fruit, whereas the underlining mechanism is still unclear. Here, we report that calcium deficiency induced the development of bitter pit on the surface of apple peels compared with the healthy appearance in control apples during postharvest storage. Physiological analysis indicates that calcium-deficient peels contained higher levels of superoxide anion (O2•−), malondialdehyde (MDA), total phenol, flavonoid contents and polyphenol oxidase (PPO) activity, and reduced calcium, H2S production, anthocyanin, soluble protein content, and peroxidase (POD) activity compared with those in calcium-sufficient peels. The principal component analysis (PCA) results show that calcium content, ROS, and H2S production were the main factors between calcium-deficient and calcium-sufficient apple peels. Transcriptome data indicated that four calmodulin-like proteins (CMLs), seven AP2/ERFs, and three bHLHs transcripts were significantly differentially expressed in calcium-deficient apple peels. RT-qPCR and correlation analyses further revealed that CML5 expression was significantly positively correlated with the expression of ERF2/17, bHLH2, and H2S production related genes. In addition, transcriptional co-activation of CML5 by ERF2 and bHLH2 was demonstrated by apple transient expression assays and dual-luciferase reporter system experiments. Therefore, these findings provide a basis for studying the molecular mechanism of postharvest quality decline in calcium-deficient apples and the potential interaction between Ca2+ and endogenous H2S.

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23

Jayaraman, T., and A. R. Marks. "T cells deficient in inositol 1,4,5-trisphosphate receptor are resistant to apoptosis." Molecular and Cellular Biology 17, no. 6 (June 1997): 3005–12. http://dx.doi.org/10.1128/mcb.17.6.3005.

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The type 1 inositol 1,4,5-trisphosphate receptor (IP3R1) calcium release channel is present on the endoplasmic reticulum of most cell types. T lymphocytes which have been made deficient in IP3R1 lack detectable IP3-induced intracellular calcium release and exhibit defective signaling via the T-cell receptor (TCR) (T. Jayaraman, E. Ondriasova, K. Ondrias, D. Harnick, and A. R. Marks, Proc. Natl. Acad. Sci. USA 92:6007-6011, 1995). We now show that IP3R1-deficient T cells are resistant to apoptosis induced by dexamethasone, TCR stimulation, ionizing radiation, and Fas. Resistance to TCR-mediated apoptosis in IP3R1-deficient cells is reversed by pharmacologically raising cytoplasmic calcium levels. TCR-mediated apoptosis can be induced in calcium-free media, indicating that extracellular calcium influx is not required. These findings suggest that intracellular calcium release via the IP3R1 is a critical mediator of apoptosis.

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24

Finke, M. D. "Complete nutrient content of three species of wild caught insects, pallid-winged grasshopper, rhinoceros beetles and white-lined sphinx moth." Journal of Insects as Food and Feed 1, no. 4 (December 7, 2015): 281–92. http://dx.doi.org/10.3920/jiff2015.0033.

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Insects serve as a major source of nutrients for many animal species, but complete nutritional information of wild insects is lacking. Wild pallid-winged grasshoppers, rhinoceros beetles and white-lined sphinx moths were caught in Rio Verde, Arizona, in the summer of 2013 (grasshoppers and beetle) or the spring of 2015 (moths). Pallid-winged grasshoppers, rhinoceros beetles and white-lined sphinx moths were analysed for moisture, crude protein, fat, ash, acid detergent fibre, minerals, amino acids, fatty acids and vitamins and values compared the nutrient requirements for both rats and poultry as reported by the National Research Council (NRC). The acid detergent fibre was also analysed for nitrogen. When compared to the nutrient requirements as established by the NRC for growing rats, grasshoppers were deficient in calcium, vitamin A, vitamin D, thiamine and vitamin B12, beetles were deficient in calcium, vitamin A, vitamin E, thiamine, pyridoxine and linoleic acid and moths were deficient in calcium, sodium, vitamin A, vitamin D, pyridoxine and vitamin B12. In contrast when compared to the nutrient requirements as established by the NRC for growing broiler chickens, grasshoppers were only deficient in calcium, manganese, and vitamin A, beetles were deficient in calcium, manganese, vitamin A, vitamin E, thiamine and linoleic acid and moths were deficient in calcium, sodium, manganese, vitamin A, vitamin D, and linoleic acid. These data show that Pallid-winged grasshoppers, Rhinoceros beetles and White-lined sphinx moths were good sources of most known nutrients including all essential amino acids, most minerals and most vitamins.

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25

Mondin, Ludivine, Haouaria Balghi, Bruno Constantin, Christian Cognard, and Stéphane Sebille. "Negative modulation of inositol 1,4,5-trisphosphate type 1 receptor expression prevents dystrophin-deficient muscle cells death." American Journal of Physiology-Cell Physiology 297, no. 5 (November 2009): C1133—C1145. http://dx.doi.org/10.1152/ajpcell.00048.2009.

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Evidence for a modulatory effect of cyclosporin A (CsA) on calcium signaling and cell survival in dystrophin-deficient cells is presented. Our previous works strongly supported the hypothesis of an overactivation of Ca2+ release via inositol 1,4,5-trisphosphate (IP3) receptors (IP3R) in dystrophin-deficient cells, both during membrane depolarization and at rest, through spontaneous Ca2+ release events. Forced expression of mini-dystrophin in these cells contributed, during stimulation and in resting condition, to the recovery of a controlled calcium homeostasis. In the present work, we demonstrate that CsA exposure displayed a dual-modulator effect on calcium signaling in dystrophin-deficient cells. Short-time incubation induced a decrease of IP3-dependent calcium release, leading to patterns of release similar to those observed in myotubes expressing mini-dystrophin, whereas long-time incubation reduced the expression of the type I of IP3 receptors (IP3R-1) RNA levels. Moreover, both IP3R-1 knockdown and blockade through 2-aminoethoxydiphenyle borate or CsA induced improved survival of dystrophin-deficient myotubes, demonstrating the cell death dependence on the IP3-dependent calcium signaling as well as the protective effect of CsA. Inhibition of the IP3 pathway could be a very interesting approach for reducing the natural cell death of dystrophin-deficient cells in development.

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26

Kwiecinksi, G. G., G. I. Petrie, and H. F. DeLuca. "1,25-Dihydroxyvitamin D3 restores fertility of vitamin D-deficient female rats." American Journal of Physiology-Endocrinology and Metabolism 256, no. 4 (April 1, 1989): E483—E487. http://dx.doi.org/10.1152/ajpendo.1989.256.4.e483.

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Vitamin D deficiency reduces mating success and fertility in female rats, but it is not known if the reduction in reproductive performance is a direct action of vitamin D or the hypocalcemia associated with vitamin D deficiency. The effect of vitamin D deficiency with normocalcemia on fertility and reproductive capacity in female rats was investigated. Female weanling rats were maintained on vitamin D-deficient or vitamin D-replete diets until maturity and mated to age-matched, normal, vitamin D-replete males. Three groups of vitamin D-deficient females were maintained on diets varying in calcium and Pi concentrations to test the effect of vitamin D deficiency with different serum calcium and Pi concentrations on reproductive performance. Vitamin D-deficient females were capable of reproduction, but successful matings by all groups of vitamin D-deficient females were markedly reduced regardless of serum calcium concentration, when compared with matings with vitamin D-replete females. Fertility was also drastically reduced in litters from all groups of vitamin D-deficient females regardless of serum calcium concentration, when compared with litters from vitamin D-replete females. Vitamin D-deficient female rats that received vitamin D or 1,25-dihydroxyvitamin D3 were capable of successfully mating and giving rise to normal, healthy litters. These results indicate that vitamin D and not hypocalcemia is directly responsible for reduced reproductive capacity and fertility in vitamin D-deficient female rats.

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27

Miyahara, Takashi, and Rocky S. Tuan. "Abnormal calcium handling by ventricular myocytes of hypertensive, calcium-deficient chick embryos." Journal of the American College of Cardiology 17, no. 2 (February 1991): A202. http://dx.doi.org/10.1016/0735-1097(91)91773-8.

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28

Jia, Wei, and You-Wen He. "Autophagy is essential for ER homeostasis and calcium mobilization in T lymphocytes (35.13)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 35.13. http://dx.doi.org/10.4049/jimmunol.182.supp.35.13.

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Abstract The evolutionarily conserved intracellular bulk degradation pathway, macroautophagy, is involved in eliminating intracellular pathogens, endogenous antigen presentation in MHC-II pathway and T lymphocytes homeostasis. However, the underlying mechanisms by which autophagy regulates T lymphocyte function remain unknown. Here we used autophagy related protein 7 (Atg7) conditional knockout mice to investigate these mechanisms. Comparing to wild type T cells, Atg7-deficient T cells displayed impaired calcium influx upon TCR triggering or lower concentration of ionomycin stimulation. However, the proximal signaling of TCR in Atg7-deficient T cells was intact. The calcium influx defect in Atg7-deficient T cells may be related to an abnormal expansion of endoplasmic reticulum (ER) and higher intracellular calcium stores. We found that higher amount of ionomycin or the ER sarco/endoplasmic reticulum Ca2+ATPase (SERCA) pump inhibitor, thapsigargin, could rescue the calcium influx defect in Atg7-deficient T lymphocytes. Atg7-deficient T cells failed to efficiently proliferate and were blocked at S phase when stimulated by TCR or PMA plus ionomycin respectively. In contrast, Atg7-deficient T cells were fully activated and capable of secreting IL-2. Our results suggest that an important role for autophagy in T cells is to maintain ER homeostasis.

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29

Silva, Ian V., Carol J. Blaisdell, Sandra E. Guggino, and William B. Guggino. "PTH regulates expression of ClC-5 chloride channel in the kidney." American Journal of Physiology-Renal Physiology 278, no. 2 (February 1, 2000): F238—F245. http://dx.doi.org/10.1152/ajprenal.2000.278.2.f238.

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Mutations in the chloride channel, ClC-5, have been described in several inherited diseases that result in the formation of kidney stones. To determine whether ClC-5 is also involved in calcium homeostasis, we investigated whether ClC-5 mRNA and protein expression are modulated in rats deficient in 1α,25(OH)2 vitamin D3 with and without thyroparathyroidectomy. Parathyroid hormone (PTH) was replaced in some animals. Vitamin D-deficient, thyroparathyrodectomized rats had lower serum and higher urinary calcium concentrations compared with control animals as well as lower serum PTH and calcitonin concentrations. ClC-5 mRNA and protein levels in the cortex decrease in vitamin D-deficient, thyroparathyroidectomized rats compared with both control and vitamin D-deficient animals. ClC-5 mRNA and protein expression increase near to control levels in vitamin D-deficient, thyroparathyroidectomized rats injected with PTH. No significant changes in ClC-5 mRNA and protein expression in the medulla were detected in any experimental group. Our results suggest that PTH modulates the expression of ClC-5 in the kidney cortex and that neither 1α,25(OH)2 vitamin D3 nor PTH regulates ClC-5 expression in the medulla. The pattern of expression of ClC-5 varies with urinary calcium. Animals with higher urinary calcium concentrations have lower levels of ClC-5 mRNA and protein expression, suggesting that the ClC-5 chloride channel plays a role in calcium reabsorption.

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30

Zalite, Vita, Janis Lungevics, Jana Vecstaudza, Liga Stipniece, and Janis Locs. "Nanosized calcium deficient hydroxyapatites for tooth enamel protection." Journal of Biomedical Materials Research Part B: Applied Biomaterials 110, no. 6 (December 29, 2021): 1354–67. http://dx.doi.org/10.1002/jbm.b.35005.

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31

Griessen, M., B. Cochet, F. Infante, A. Jung, P. Bartholdi, A. Donath, E. Loizeau, and B. Courvoisier. "Calcium absorption from milk in lactase-deficient subjects." American Journal of Clinical Nutrition 49, no. 2 (February 1, 1989): 377–84. http://dx.doi.org/10.1093/ajcn/49.2.377.

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32

Nishikawa, Harumitsu, and Hideki Monma. "Oxidative Decomposition of Chlorobenzene over Calcium-Deficient Hydroxyapatite." Bulletin of the Chemical Society of Japan 67, no. 9 (September 1994): 2454–56. http://dx.doi.org/10.1246/bcsj.67.2454.

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33

Siddharthan, A., S. K. Seshadri, and T. S. Sampath Kumar. "Microwave accelerated synthesis of nanosized calcium deficient hydroxyapatite." Journal of Materials Science: Materials in Medicine 15, no. 12 (December 2004): 1279–84. http://dx.doi.org/10.1007/s10856-004-5735-3.

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34

Yamaguchi, Seiji, Phuc Thi Minh Le, Morihiro Ito, Seine A. Shintani, and Hiroaki Takadama. "Tri-Functional Calcium-Deficient Calcium Titanate Coating on Titanium Metal by Chemical and Heat Treatment." Coatings 9, no. 9 (September 3, 2019): 561. http://dx.doi.org/10.3390/coatings9090561.

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The main problem of orthopedic and dental titanium (Ti) implants has been poor bone-bonding to the metal. Various coatings to improve the bone-bonding, including the hydroxyapatite and titania, have been developed, and some of them have been to successfully applied clinical use. On the other hand, there are still challenges to provide antibacterial activity and promotion of bone growth on Ti. It was shown that a calcium-deficient calcium titanate coating on Ti and its alloys exhibits high bone-bonding owing to its apatite formation. In this study, Sr and Ag ions, known for their promotion of bone growth and antibacterial activity, were introduced into the calcium-deficient calcium titanate by a three-step aqueous solution treatment combined with heat. The treated metal formed apatite within 3 days in a simulated body fluid and exhibited antibacterial activity to Escherichia coli without showing any cytotoxicity in MC3T3-E1 preosteoblast cells. Furthermore, the metal slowly released 1.29 ppm of Sr ions. The Ti with calcium-deficient calcium titanate doped with Sr and Ag will be useful for orthopedic and dental implants, since it should bond to bone because of its apatite formation, promote bone growth due to Sr ion release, and prevent infection owing to its antibacterial activity.

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35

Turrini, F., A. Naitana, L. Mannuzzu, G. Pescarmona, and P. Arese. "Increased red cell calcium, decreased calcium adenosine triphosphatase, and altered membrane proteins during fava bean hemolysis in glucose-6- phosphate dehydrogenase-deficient (Mediterranean variant) individuals." Blood 66, no. 2 (August 1, 1985): 302–5. http://dx.doi.org/10.1182/blood.v66.2.302.302.

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Abstract RBCs from four glucose-6-phosphate dehydrogenase (G6PD)-deficient (Mediterranean variant) subjects were studied during fava bean hemolysis. In the density-fractionated RBC calcium level, Ca2+-ATPase activity, reduced glutathione level, and ghost protein pattern were studied. In the bottom fraction, containing most heavily damaged RBCs, calcium level ranged from 143 to 244 mumol/L RBCs (healthy G6PD- deficient controls: 17 +/- 5 mumol/L RBCs). The Ca2+-ATPase activity ranged from 0.87 to 1.84 mumol ATP consumed/g Hb/min (healthy G6PD- deficient controls: 2.27 +/- 0.4). Sodium dodecyl sulfate- polyacrylamide gel electrophoresis (SDS-PAGE) of ghosts showed: (1) the presence of high mol wt aggregates (in three cases they were reduced by dithioerythritol; in one case, only partial reduction was possible); (2) the presence of multiple, scattered new bands; and (3) the reduction of band 3. Oxidant-mediated damage to active calcium extrusion, hypothetically associated with increased calcium permeability, may explain the large increase in calcium levels. They, in turn, could activate calcium-dependent protease activity, giving rise to the profound changes in the ghost protein pattern.

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36

Turrini, F., A. Naitana, L. Mannuzzu, G. Pescarmona, and P. Arese. "Increased red cell calcium, decreased calcium adenosine triphosphatase, and altered membrane proteins during fava bean hemolysis in glucose-6- phosphate dehydrogenase-deficient (Mediterranean variant) individuals." Blood 66, no. 2 (August 1, 1985): 302–5. http://dx.doi.org/10.1182/blood.v66.2.302.bloodjournal662302.

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RBCs from four glucose-6-phosphate dehydrogenase (G6PD)-deficient (Mediterranean variant) subjects were studied during fava bean hemolysis. In the density-fractionated RBC calcium level, Ca2+-ATPase activity, reduced glutathione level, and ghost protein pattern were studied. In the bottom fraction, containing most heavily damaged RBCs, calcium level ranged from 143 to 244 mumol/L RBCs (healthy G6PD- deficient controls: 17 +/- 5 mumol/L RBCs). The Ca2+-ATPase activity ranged from 0.87 to 1.84 mumol ATP consumed/g Hb/min (healthy G6PD- deficient controls: 2.27 +/- 0.4). Sodium dodecyl sulfate- polyacrylamide gel electrophoresis (SDS-PAGE) of ghosts showed: (1) the presence of high mol wt aggregates (in three cases they were reduced by dithioerythritol; in one case, only partial reduction was possible); (2) the presence of multiple, scattered new bands; and (3) the reduction of band 3. Oxidant-mediated damage to active calcium extrusion, hypothetically associated with increased calcium permeability, may explain the large increase in calcium levels. They, in turn, could activate calcium-dependent protease activity, giving rise to the profound changes in the ghost protein pattern.

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37

Driver, John P., Deanna J. Lamont, Conny Gysemans, Chantal Mathieu, and David V. Serreze. "Calcium Insufficiency Accelerates Type 1 Diabetes in Vitamin D Receptor-Deficient Nonobese Diabetic (NOD) Mice." Endocrinology 152, no. 12 (September 27, 2011): 4620–29. http://dx.doi.org/10.1210/en.2011-1074.

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Vitamin D exerts important regulatory effects on the endocrine and immune systems. Autoimmune type 1 diabetes (T1D) development in the inbred NOD mouse strain can be accelerated by vitamin D insufficiency or suppressed by chronic treatment with high levels of 1α,25-dihydroxyvitamin D3. Consequently, a report that T1D development was unaffected in NOD mice genetically lacking the vitamin D receptor (VDR) was unexpected. To further assess this result, the mutant stock was imported to The Jackson Laboratory, backcrossed once to NOD/ShiLtJ, and progeny rederived through embryo transfer. VDR-deficient NOD mice of both sexes showed significant acceleration of T1D. This acceleration was not associated with alterations in immune cells targeting pancreatic β-cells. Rather, the capacity of β-cells to produce and/or secrete insulin was severely impaired by the hypocalcaemia developing in VDR-deficient NOD mice fed a standard rodent chow diet. Feeding a high-lactose calcium rescue diet that circumvents a VDR requirement for calcium absorption from the intestine normalized serum calcium levels, restored β-cell insulin secretion, corrected glucose intolerance, and eliminated accelerated T1D in VDR-deficient NOD mice. These findings suggest that calcium and/or vitamin D supplementation may improve disease outcomes in some T1D-prone individuals that are calcium deficient.

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38

Soni, Gunjan. "Beneficial Effect of Calcium Supplementation on Bone Mineral Density of Calcium Deficient Adolescents." International Journal of Food Science and Biotechnology 3, no. 3 (2018): 83. http://dx.doi.org/10.11648/j.ijfsb.20180303.12.

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39

Goodman, George, and Trent R. Jones. "The chiropractic profession, dietary calcium, and the diseases associated with calcium-deficient diets." Journal of Manipulative and Physiological Therapeutics 24, no. 4 (May 2001): 305–7. http://dx.doi.org/10.1067/mmt.2001.114358.

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40

Bae, Yun Jung, and Mi-Hyun Kim. "Calcium and Magnesium Supplementation Improves Serum OPG/RANKL in Calcium-Deficient Ovariectomized Rats." Calcified Tissue International 87, no. 4 (September 2, 2010): 365–72. http://dx.doi.org/10.1007/s00223-010-9410-z.

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41

Ohta, Yuki, Yoshikazu Nagao, Naojiro Minami, Satoshi Tsukamoto, and Seiji Kito. "Deficiencies in extrusion of the second polar body due to high calcium concentrations during in vitro fertilization in inbred C3H/He mice." Zygote 24, no. 4 (October 27, 2015): 603–16. http://dx.doi.org/10.1017/s096719941500060x.

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SummarySuccessful in vitro fertilization (IVF) of all inbred strains of laboratory mice has not yet been accomplished. We have previously shown that a high calcium concentration improved IVF in various inbred mice. However, we also found that in cumulus-free ova of C3H/He mice such IVF conditions significantly increased the deficiency of extrusion of the second polar body (PBII) in a dose-dependent manner (2% at 1.71 mM and 29% at 6.84 mM, P < 0.05) and that PBII extrusion was affected by high calcium levels at 2–3 h post-insemination. While developmental competence of ova without PBII extrusion to blastocysts after 96 h culture was not affected, a significant reduction in the nuclear number of the inner cell mass was observed in blastocyst fertilized under high calcium condition. We also examined how high calcium concentration during IVF affects PBII extrusion in C3H/He mice. Cumulus cells cultured under high calcium conditions showed a significantly alleviated deficient PBII extrusion. This phenomenon is likely to be specific to C3H/He ova because deficient PBII extrusion in reciprocal fertilization between C3H and BDF1 gametes was observed only in C3H/He ova. Sperm factor(s) was still involved in deficient PBII extrusion due to high calcium concentrations, as this phenomenon was not observed in ova activated by ethanol. The cytoskeletal organization of ova without PBII extrusion showed disturbed spindle rotation, incomplete formation of contractile ring and disturbed localization of actin, suggesting that high calcium levels affect the anchoring machinery of the meiotic spindle. These results indicate that in C3H/He mice high calcium levels induce abnormal fertilization, i.e. deficient PBII extrusion by affecting the cytoskeletal organization, resulting in disturbed cytokinesis during the second meiotic division. Thus, use of high calcium media for IVF should be avoided for this strain.

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42

Liu, Hou Cheng, Wen Peng Liu, Shi Wei Song, Guang Wen Sun, and Ri Yuan Chen. "Effect of Calcium Nutrient on Calcium Distribution and Ultrastructure of Cell and Chloroplast in Bunching Onion Leaf." Applied Mechanics and Materials 142 (November 2011): 111–15. http://dx.doi.org/10.4028/www.scientific.net/amm.142.111.

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Effect of calcium nutrient on calcium distribution and ultrastructure of cell and chloroplast in Bunching Onion (Allium fistulosum L. var. caespitosum Makino) leaf was studied in sands with 4 Ca2+ treatments (0, 40, 80 and 160 mg/L ), in which the solution was Hoagland's. Localization and distribution of calcSuperscript textium and the influence of calcium nutrition on cell ultrastructure were observed by transmission electron microscopy combined with in situ precipitation of calcium with potassium pyroantimonate technique. The results showed that Ca2+ were mainly located in cell membrane, vacuoles, envelope of chloroplast and intercellular space in normal cells of bunching onion, however, Ca2+ was found to compartment in cytosol in large quantity, and the release of membrane-associated Ca2+ to cytosol and wall-associated Ca2+ to the intercellular spaces was observed in Ca-deficient leaves. In serious Ca-deficient leaves, Ca2+ quantities in cell decreased. Under Ca-deficiency, chloroplast membranes, plasma membranes and nuclear membranes were damaged, and cell walls disassociated, an enlarged space could be found between cells. In serious Ca-deficient leaves, cell compartmentation was destroyed, chloroplast deformed, plasma separated from cell wall, then whole cell constricted.

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Grimes, Derayvia, Ryan Johnson, Madeline Pashos, Celeste Cummings, Chen Kang, Georgia R. Sampedro, Eric Tycksen, et al. "ORAI1 and ORAI2 modulate murine neutrophil calcium signaling, cellular activation, and host defense." Proceedings of the National Academy of Sciences 117, no. 39 (September 14, 2020): 24403–14. http://dx.doi.org/10.1073/pnas.2008032117.

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Calcium signals are initiated in immune cells by the process of store-operated calcium entry (SOCE), where receptor activation triggers transient calcium release from the endoplasmic reticulum, followed by opening of plasma-membrane calcium-release activated calcium (CRAC) channels. ORAI1, ORAI2, and ORAI3 are known to comprise the CRAC channel; however, the contributions of individual isoforms to neutrophil function are not well understood. Here, we show that loss of ORAI1 partially decreases calcium influx, while loss of both ORAI1 and ORAI2 completely abolishes SOCE. In other immune-cell types, loss of ORAI2 enhances SOCE. In contrast, we find that ORAI2-deficient neutrophils display decreased calcium influx, which is correlated with measurable differences in the regulation of neutrophil membrane potential via KCa3.1. Decreased SOCE in ORAI1-, ORAI2-, and ORAI1/2-deficient neutrophils impairs multiple neutrophil functions, including phagocytosis, degranulation, leukotriene, and reactive oxygen species (ROS) production, rendering ORAI1/2-deficient mice highly susceptible to staphylococcal infection. This study demonstrates that ORAI1 and ORAI2 are the primary components of the neutrophil CRAC channel and identifies subpopulations of neutrophils where cell-membrane potential functions as a rheostat to modulate the SOCE response. These findings have implications for mechanisms that modulate neutrophil function during infection, acute and chronic inflammatory conditions, and cancer.

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Zhou, Hong Hui, Hui Li, and Ling Hong Guo. "Molecular and Crystal Structure Characterization of Calcium-Deficient Apatite." Key Engineering Materials 330-332 (February 2007): 119–22. http://dx.doi.org/10.4028/www.scientific.net/kem.330-332.119.

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Calcium-deficient hydroxylapatite (CDHA) powders with Ca/P ratios from1.5 to 1.67 were synthesized by wet-chemical method. Rietveld structure refinement was performed on the X-ray diffraction data and Fourier transform infrared spectroscopy was used to characterize molecular and crystal structure of CDHA. With the decrease of Ca/P ratio, the crystallite size and crystallinity decreased, but the acid phosphate content and amount of vacancies in hydroxyapatite hexagonal structure increased. The disorder of CDHA structure increase indicated calcium-deficiency and HPO4 replacement resulted in disorder of crystal in apatite structure. The more calcium is deficient, the more disorder or imperfect in CDHA structure

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45

Manetz, Timothy Scott, Claudia Gonzalez-Espinosa, Ramachandran Arudchandran, Sandhya Xirasagar, Victor Tybulewicz, and Juan Rivera. "Vav1 Regulates Phospholipase Cγ Activation and Calcium Responses in Mast Cells." Molecular and Cellular Biology 21, no. 11 (June 1, 2001): 3763–74. http://dx.doi.org/10.1128/mcb.21.11.3763-3774.2001.

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ABSTRACT The hematopoietic cell-specific protein Vav1 is a substrate of tyrosine kinases activated following engagement of many receptors, including FcɛRI. Vav1-deficient mice contain normal numbers of mast cells but respond more weakly than their normal counterparts to a passive systemic anaphylaxis challenge. Vav1-deficient bone marrow-derived mast cells also exhibited reduced degranulation and cytokine production, although tyrosine phosphorylation of FcɛRI, Syk, and LAT (linker for activation of T cells) was normal. In contrast, tyrosine phosphorylation of phospholipase Cγ1 (PLCγ1) and PLCγ2 and calcium mobilization were markedly inhibited. Reconstitution of deficient mast cells with Vav1 restored normal tyrosine phosphorylation of PLCγ1 and PLCγ2 and calcium responses. Thus, Vav1 is essential to FcɛRI-mediated activation of PLCγ and calcium mobilization in mast cells. In addition to its known role as an activator of Rac1 GTPases, these findings demonstrate a novel function for Vav1 as a regulator of PLCγ-activated calcium signals.

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46

Hämäläinen, Mauri M. "Bone Repair in Calcium-Deficient Rats: Comparison of Xylitol + Calcium Carbonate with Calcium Carbonate, Calcium Lactate and Calcium Citrate on the Repletion of Calcium." Journal of Nutrition 124, no. 6 (June 1, 1994): 874–81. http://dx.doi.org/10.1093/jn/124.6.874.

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47

Hinkle, Karen L., Gina C. Bane, Ali Jazayeri, and Linda C. Samuelson. "Enhanced calcium signaling and acid secretion in parietal cells isolated from gastrin-deficient mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 1 (January 1, 2003): G145—G153. http://dx.doi.org/10.1152/ajpgi.00283.2002.

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Gastrin-deficient mice have impaired basal and agonist-stimulated gastric acid secretion. To analyze whether an intrinsic parietal cell defect contributed to the reduced acid secretion, we analyzed parietal cell calcium responses and acid secretory function in vitro. Parietal cells were purified by light-scatter cell sorting and calcium responses to gastrin, histamine, and carbachol were measured in gastrin-deficient and wild-type mice cell preparations. Surprisingly, basal and histamine-induced calcium concentrations were higher in the mutant cell preparations. [14C]aminopyrine uptake analysis in acutely isolated gastric glands revealed that basal acid accumulation was enhanced in gastrin-deficient cell preparations as well as on treatment with carbachol or histamine. These results suggested that an intrinsic parietal cell defect was not responsible for the reduced acid secretion in gastrin-deficient mice. Flow cytometric analysis of dispersed, H+-K+-ATPase-immunostained gastric mucosal preparations revealed a marked increase in parietal cell number in gastrin-deficient mice, which may have accounted for the enhanced in vitro acid secretion detected in this study. Parietal cells were found to be significantly smaller in the mutant cell preparations, suggesting that gastrin stimulation modulates parietal cell morphology.

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48

Ioku, Koji, Masanobu Kamitakahara, Noriaki Watanabe, Osamu Kawaguchi, Setsuaki Murakami, and Tohru Ikeda. "Calcium Phosphate Porous Materials with Unique Microstructures." Key Engineering Materials 396-398 (October 2008): 645–48. http://dx.doi.org/10.4028/www.scientific.net/kem.396-398.645.

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Three types of calcium phosphate porous materials were prepared by the applied hydrothermal method. One of them was non-stoichiometric hydroxyapatite (HA) with calcium deficient composition and the others were β-tricalcium phosphate (β-TCP) and HA/β-TCP bi-phase material. Granules with several millimeter in size of calcium deficient HA, β-TCP and HA/β-TCP could be prepared. These granules with porosity over 70 % were composed of rod-shaped particles with aspect ratio about 10. Rod-shaped particles were locked together to make sub-micro-sized pores of about 0.1 to 0.5 µm in size. These materials must be suitable for the bone graft materials and as the scaffolds of cultured bone.

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49

OKANO, T., T. KIMURA, N. TSUGAWA, M. FUJIWARA, M. YAMAMOTO, and T. KOBAYASHI. "Bioavailability of calcium from bovine-bone-marrow calcium (BBMCa) and calcium carbonate in vitamin D-deficient rats." Food Chemistry 51, no. 1 (1994): 61–67. http://dx.doi.org/10.1016/0308-8146(94)90048-5.

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50

Zamani Moghaddam, Abdol, Hossein Hassanpour, Sarang Soroori, Mehrdad Yadegari, and Ghodsieh Tajeri. "Effect of dietary calcium deficiency on the cardiac function of broiler chickens based on electro- and echocardiography." Acta Veterinaria Hungarica 58, no. 2 (June 1, 2010): 167–76. http://dx.doi.org/10.1556/avet.58.2010.2.3.

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To determine the effects of dietary calcium deficiency on the heart function of broiler chickens based on electro- and echocardiography, chicks were reared for 42 days and fed rations with different amounts of calcium. At 28 and 42 days of age, electrocardiographic and echocardiographic parameters were assessed. There were significant reductions of R wave amplitude (leads II and aVR) in the Ca-deficient group II at 42 day of age as compared to the control. S wave amplitudes were decreased in most leads but the decrease was significant (P < 0.05) only at 28 days (lead aVL, Ca-deficient group I) and 42 days (leads III, aVR, aVF, Ca-deficient groups I and II). T wave amplitudes were significantly (P < 0.05) decreased at 42 days (leads II, aVR and aVF) in the Ca-deficient group II compared to the control group. Variations in QT, ST and RR intervals were insignificant in the Ca-deficient groups compared with the control. There was a significant (P < 0.05) increase in left ventricular diameter at end-systole and a reduction of left ventricular fractional shortening in the Ca-deficient group II at 28 and 42 days as compared to the controls. Right ventricular fractional shortening was significantly (P < 0.05) decreased only in the Ca-deficient group II at 42 days of age. These results suggest that dose-dependent dietary calcium deficiency alters variations in electro- and echocardiographic parameters which could reflect decreased cardiac function in growing broiler chickens.

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