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Effects of Sigma Anti-bonding Molecule Calcium Carbonate on bone turnover and calcium balance in ovariectomized rats Copy

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Effects of Sigma Anti-bonding Molecule Calcium Carbonate on bone turnover and calcium balance in ovariectomized rats

So-Young Choi , Dongsun Park , Goeun Yang , Sun Hee Lee , Dae Kwon Bae , Seock-Yeon Hwang , Paul K Lee , Yun-Bae Kim , Ill-Hwa Kim , Hyun-Gu Kang:

This study was conducted to evaluate the effect of Sigma Anti-bonding Molecule Calcium Carbonate (SAC) as therapy for ovariectomy-induced osteoporosis in rats. Three weeks after surgery, fifteen ovariectomized Sprague-Dawley rats were divided randomly into 3 groups: sham-operated group (sham), ovariectomized group (OVX) and SAC-treatment group (OVX+SAC). The OVX+SAC group was given drinking water containing 0.0012% SAC for 12 weeks. Bone breaking force and mineralization as well as blood parameters related to the bone metabolism were analyzed. In OVX animals, blood concentration of 17β- estradiol decreased significantly, while osteocalcin and type I collagen C-terminal telopeptides (CTx) increased. Breaking force, bone mineral density (BMD), calcium and phosphorus in femurs, as well as uterine and vaginal weights, decreased significantly following OVX. However, SAC treatment (0.0012% in drinking water) not only remarkably restored the decreased 17β-estradiol and increased osteocalcin and CTx concentrations, but also recovered decreased femoral breaking force, BMD, calcium and phosphorus, although it did not reversed reproductive organ weights. It is suggested that SAC effectively improve bone density by preventing bone turnover mediated osteocalcin, CTx and minerals, and that it could be a potential candidate for therapy or prevention of menopausal osteoporosis.

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The Contribution of Cytotoxic Chemotherapy to 5-year Survival in Adult Malignancies

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The Contribution of Cytotoxic Chemotherapy to 5-year Survival in Adult Malignancies

Graeme Morgan*, Robyn Wardy, Michael Bartonz

ABSTRACT:

Aims: The debate on the funding and availability of cytotoxic drugs raises questions about the contribution of curative or adjuvant cytotoxic chemotherapy to survival in adult cancer patients.

Materials and methods: We undertook a literature search for randomised clinical trials reporting a 5-year survival benefit attributable solely to cytotoxic chemotherapy in adult malignancies. The total number of newly diagnosed cancer patients for 22 major adult malignancies was determined from cancer registry data in Australia and from the Surveillance Epidemiology and End Results data in the USA for 1998. For each malignancy, the absolute number to benefit was the product of (a) the total number of persons with that malignancy; (b) the proportion or subgroup(s) of that malignancy showing a benefit; and (c) the percentage increase in 5-year survival due solely to cytotoxic chemotherapy. The overall contribution was the sum total of the absolute numbers showing a 5-year survival benefit expressed as a percentage of the total number for the 22 malignancies.

Results: The overall contribution of curative and adjuvant cytotoxic chemotherapy to 5-year survival in adults was estimated to be 2.3% in Australia and 2.1% in the USA.

Conclusion: As the 5-year relative survival rate for cancer in Australia is now over 60%, it is clear that cytotoxic chemotherapy only makes a minor contribution to cancer survival. To justify the continued funding and availability of drugs used in cytotoxic chemotherapy, a rigorous evaluation of the cost-effectiveness and impact on quality of life is urgently required. Morgan, G. et al. (2004). Clinical Oncology 16, 549e560

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SAC Bone Dental

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The Contribution of Cytotoxic Chemotherapy to 5-year Survival in Adult Malignancies

Graeme Morgan*, Robyn Wardy, Michael Bartonz

ABSTRACT:

Aims: The debate on the funding and availability of cytotoxic drugs raises questions about the contribution of curative or adjuvant cytotoxic chemotherapy to survival in adult cancer patients.

Materials and methods: We undertook a literature search for randomised clinical trials reporting a 5-year survival benefit attributable solely to cytotoxic chemotherapy in adult malignancies. The total number of newly diagnosed cancer patients for 22 major adult malignancies was determined from cancer registry data in Australia and from the Surveillance Epidemiology and End Results data in the USA for 1998. For each malignancy, the absolute number to benefit was the product of (a) the total number of persons with that malignancy; (b) the proportion or subgroup(s) of that malignancy showing a benefit; and (c) the percentage increase in 5-year survival due solely to cytotoxic chemotherapy. The overall contribution was the sum total of the absolute numbers showing a 5-year survival benefit expressed as a percentage of the total number for the 22 malignancies.

Results: The overall contribution of curative and adjuvant cytotoxic chemotherapy to 5-year survival in adults was estimated to be 2.3% in Australia and 2.1% in the USA.

Conclusion: As the 5-year relative survival rate for cancer in Australia is now over 60%, it is clear that cytotoxic chemotherapy only makes a minor contribution to cancer survival. To justify the continued funding and availability of drugs used in cytotoxic chemotherapy, a rigorous evaluation of the cost-effectiveness and impact on quality of life is urgently required. Morgan, G. et al. (2004). Clinical Oncology 16, 549e560

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The molecular era of the mitochondrial calcium uniporter

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The molecular era of the mitochondrial calcium uniporter

Kimberli J. Kamer1,2 and Vamsi K. Mootha2–4

Abstract | The mitochondrial calcium uniporter is an evolutionarily conserved calcium channel, and its biophysical properties and relevance to cell death, bioenergetics and signalling have been investigated for decades. However, the genes encoding this channel have only recently been discovered, opening up a new ‘molecular era’ in the study of its biology. We now know that the uniporter is not a single protein but rather a macromolecular complex consisting of pore-forming and regulatory subunits. We review recent studies that harnessed the power of molecular biology and genetics to characterize the mechanism of action of the uniporter, its evolution and its contribution to physiology and human disease.

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Dairy products, calcium, and prostate cancer risk in the Physicians’ Health Study

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Dairy products, calcium, and prostate cancer risk in the Physicians’ Health Study

June M Chan, Meir J Stampfer, Jing Ma, Peter H Gann, J Michael Gaziano, and Edward L Giovannucci

Background: A high calcium intake, mainly from dairy products, may increase prostate cancer risk by lowering concentrations of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], a hormone thought to protect against prostate cancer. The results of epidemiologic studies of this hypothesis are inconclusive.

Objective: We investigated the association between dairy product and calcium intakes and prostate cancer risk in the Physicians’ Health Study, a cohort of male US physicians.

Design: At baseline, the men answered abbreviated dietary questionnaires. During 11 y of follow-up, we documented 1012 incident cases of prostate cancer among 20885 men. We estimated dairy calcium intake on the basis of consumption of 5 major dairy products and used logistic regression to estimate relative risk.

Results: At baseline, men who consumed >600 mg Ca/d from skim milk had lower plasma 1,25(OH)2D3 concentrations than did those consuming ≤150 mg Ca/d [71 compared with 85 pmol/L (30.06 compared with 35.64 pg/mL); P = 0.005]. Compared with men consuming ≤ 0.5 daily servings of dairy products, those consuming >2.5 servings had a multivariate relative risk of prostate cancer of 1.34 (95% CI: 1.04, 1.71) after adjustment for baseline age, body mass index, smoking, exercise, and randomized treatment assignment in the original placebo-controlled trial. Com- pared with men consuming ≤150 mg Ca/d from dairy products, men consuming >600 mg/d had a 32% higher risk of prostate cancer (95% CI: 1.08, 1.63).
Conclusions: These results support the hypothesis that dairy products and calcium are associated with a greater risk of prostate cancer.

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Vitamin D, calcium, and retinol intake, and pancreatic cancer

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Vitamin D, calcium, and retinol intake, and pancreatic cancer

Lydia B. Zablotska • Zhihong Gong • Furong Wang • Elizabeth A. Holly • Paige M. Bracci

Objective: The aim of this study was to evaluate a com- plex association among intake of dietary vitamin D, cal- cium, and retinol, and pancreatic cancer risk.
Methods Pancreatic cancer cases (n = 532) diagnosed in 1995–1999 were identified using rapid case ascertainment methods and were frequency matched to population-based controls (n = 1,701) in the San Francisco Bay Area. Detailed dietary data were collected during in-person interviews using a validated semi-quantitative food- frequency questionnaire. Adjusted unconditional logistic regression was used to estimate odds ratios (ORs) and confidence intervals.

Results: In men, increased pancreatic cancer risk was associated with currently recommended dietary vitamin D intake levels (highest (C450 IU/day) vs. lowest (\150 IU/ day) intake, OR = 2.6, trend-p = 0.009) and total vitamin D intake from diet and supplements (for \800 IU/day). ORs for dietary vitamin D intake remained increased after adjustment for intake of retinol and calcium, although confidence intervals included unity. Stratified analyses showed that ORs were higher among men with lower intake of retinol and lower physical activity but there was no evidence of statistical interaction. No associations with vitamin D intake were observed among women, although ORs typically were elevated. ORs increased with increased dietary calcium intake among men (trend-p = 0.008) and not women.

Conclusions: Our results among men showing an increased risk of pancreatic cancer associated with dietary intake of vitamin D and of calcium require confirmation in further studies. Continued investigation is needed to clarify the complex role of vitamin D and calcium in pancreatic cancer risk and to determine their optimal intake level and preventive effects for pancreatic cancer.

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Calcium, Magnesium, and Colorectal Cancer

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Calcium, Magnesium, and Colorectal Cancer

Qi Dai1, Robert S. Sandler2, Elizabeth L. Barry3, Robert W. Summers4, Maria V. Grau5, and
John A. Baron2,5,6

High calcium consumption may confer a reduced risk of colorectal cancer.1,2 Dai and colleagues3 recently reported in a case-control study that intake of calcium may be associated with a decreased risk of colorectal adenoma only when the dietary calcium:magnesium intake ratio is low. This finding provides one possible interpretation for inconsistencies in previous studies of the association of calcium intake with risk of colorectal neoplasia.4

Belonging to the same family in the periodic table, calcium (Ca2+) and magnesium (Mg2+) share the same homeostatic control system and have the potential to antagonize each other physiologically.5 A high calcium intake reduces absorption of both magnesium and calcium,6 whereas moderate magnesium deprivation results in negative magnesium balance but increased calcium retention7. Due to the potential competition between magnesium and calcium, we hypothesized that the dietary calcium:magnesium ratio may modify the effects of calcium supplementation on colorectal carcinogenesis.

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Calcium, cancer and killing

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Calcium, cancer and killing: The role of calcium in killing cancer cells by cytotoxic T lymphocytes and natural killer cells

Eva C. Schwarz, Bin Qu, Markus Hoth:

Killing cancer cells by cytotoxic T lymphocytes (CTL) and by natural killer (NK) cells is of vital importance. Cancer cell proliferation and apoptosis depend on the intracellular Ca2+ concentration, and the expression of numerous ion channels with the ability to control intracellular Ca2+ concentrations has been correlated with cancer. A rise of intracellular Ca2+ concentrations is also required for efficient CTL and NK cell function and thus for killing their targets, in this case cancer cells. Here, we review the data on Ca2+-dependent killing of cancer cells by CTL and NK cells. In addition, we discuss emerging ideas and present a model how Ca2+ may be used by CTL and NK cells to optimize their cancer cell killing efficiency. This article is part of a Special Issue entitled: 12th European Symposium on Calcium.

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Where cancer meets calcium — p53 crosstalk with EF-hands

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Where cancer meets calcium — p53 crosstalk with EF-hands

Mitsuhiko Ikura and Kyoko L. Yap:

S100B, an EF-hand Ca2+-binding protein, grasps the C-terminus of the tumor suppressor p53 and inhibits protein kinase C-dependent phosphorylation and acetylation of p53 in a Ca2+-dependent manner. The mode of interaction between S100B and p53 is different from the interactions seen in S100A–annexin complex structures.

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Switching p53 states by Calcium: Dynamics and Interaction of Stress Systems

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Effects of Sigma Anti-bonding Molecule Calcium Carbonate on bone turnover and calcium balance in ovariectomized rats

Md. Jahoor Alam,a Gurumayum Reenaroy Devi,a Ravins,a Romana Ishrat,a Subhash M. Agarwalb and R. K. Brojen Singh*a

The integration of calcium and a p53–Mdm2 oscillator model is studied using a deterministic as well as a stochastic approach, to investigate the impact of a calcium wave on single cell dynamics and on the inter-oscillator interaction. The high dose of calcium in the system activates the nitric oxide synthase, synthesizing nitric oxide which then downregulates Mdm2 and influences drastically the p53–Mdm2 network regulation, lifting the system from a normal to a stressed state. The increase in calcium level switches the system to different states, as identified by the different behaviours of the p53 temporal dynamics, i.e. oscillation death to sustain the oscillation state via a mixed state of dampened and oscillation death states. Further increase of the calcium dose in the system switches the system from sustained to oscillation death state again, while an excess of calcium shifts the cell to an apoptotic state. Another important property of the calcium ion is its ability to behave as a synchronizing agent among the interacting systems. The time evolution of the p53 dynamics of the two diffusively coupled systems at stress condition via Ca2+ shows synchronization between the two systems. The noise contained in the system interestingly helps the system to maintain its stabilized state (normal condition). However, noise has the tendency to destruct the synchronization effect, which means that it tries to restrict the system from external signals to maintain its normal condition. However, at the stress condition, the synchronization rate is found to be faster.

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