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Calcium supplementation has been shown to be efficacious in mitigating the progression of senile osteoporosis (SOP) and reducing the incidence of osteoporotic fractures resulting from prolonged calcium shortage. In this study, Grifola frondosa (GF) peptides-calcium chelate were synthesized through the interaction between peptide from GF and CaCl 2 . The chelation reaction was shown to involve the participation of the amino and carboxyl groups in the peptide, as revealed by scanning electron microscope, Fourier-transform infrared, and ultraviolet spectrophotometry. Furthermore, a mouse model of (SOP) induced by d-galactose was established (SCXK-2018-0004). Results demonstrated that low dosage of low-molecular weight GF peptides-calcium chelates (LLgps-Ca) could significantly improve serum index and pathological features of bone tissue and reduce bone injury. Further research suggested that LLgps-Ca could ameliorate SOP by modulating the disrupted metabolic pathway, which includes focal adhesion, extracellular matrix receptor interaction, and PI3K-Akt signaling pathway. Using Western blot, the differentially expressed proteins were further confirmed. Thus, calciumchelating peptides from GF could serve as functional calcium agents to alleviate SOP., (© 2024 Institute of Food Technologists.)

Background and Objectives: The adverse effects of plasma donation on the body has lowered the odds of donation. The aim of this study was to investigate the prevalence of abnormal serum calcium and total serum protein related to plasma donation, identify the influencing factors, and come up with suggestions to make plasma donation safer., Methods: Donors from 10 plasmapheresis centers in five provinces of China participated in this study. Serum samples were collected before donation. Serum calcium was measured by arsenazo III colorimetry, and the biuret method was used for total serum protein assay. An automatic biochemical analyzer was used to conduct serum calcium and total serum protein tests., Results: The mean serum calcium was 2.3 ± 0.15 mmol/L and total serum protein was 67.75 ± 6.02 g/L. The proportions of plasma donors whose serum calcium and total serum protein were lower than normal were 20.55% (815/3,966) and 27.99% (1,111/3,969), respectively. There were significant differences in mean serum calcium and total serum protein of plasma donors with different plasma donation frequencies, gender, age, regions, and body mass index (BMI), (all p  < 0.05). Logistic regression analysis revealed that donation frequencies, age, BMI and regions were significantly associated with a higher risk of low serum calcium level, and donation frequencies, gender, age and regions were significant determinants factors of odds of abnormal total serum protein., Conclusions: Donation frequencies, gender, age, regions, and BMI showed different effects on serum calcium and total serum protein. More attention should be paid to the age, donation frequency and region of plasma donors to reduce the probability of low serum calcium and low total serum protein., Competing Interests: Demei Dong and Yang Gao are employees of Beijing Tiantan Biological Products Co., LTD. Ding Yu is an employee of Chengdu Rongsheng Pharmaceuticals Co., LTD. The authors declare there are no competing interests., (©2022 Liu et al.)

Klebsiella pneumoniae is a gram-negative bacterium that can cause many diseases in hospitals and communities. Intestinal K. pneumoniae infections are relatively rare. Most K. pneumoniae infections begin with the colonization of the gastrointestinal system. In this study, clinically isolated K. pneumoniae strains were used to infect intestinal epithelial Caco-2 cells to study the possible intestinal translocation mechanism of K. pneumoniae. We found that of the three K. pneumoniae strains tested, KP1821 exhibited the strongest adhesive and invasive abilities and that the adhesion to Caco-2 intestinal epithelial cells was affected by the acidic environment of the stomach. Transcriptome sequencing revealed the involvement of molecules associated with the extracellular matrix and cell adhesion, inflammatory response, calcium ion and transforming growth factor β (TGF-β) signaling pathways, and other abnormalities in biological processes and cell signaling pathways. Additionally, tolloid-like protein 1 (TLL1) was significantly upregulated. Knocking down TLL1 with shRNA significantly reduced KP1821's ability to invade and adhere to intestinal epithelial cells. TLL1 is involved in the activation of the TGF-β signaling pathway. Inhibition of this pathway using the inhibitor SB431542 induced significantly reduced adhesion and invasion capabilities of KP1821. Our findings demonstrate that TLL1 participates in K. pneumoniae adhesion and invasion of intestinal epithelial cells by activating the TGF-β signaling pathway., Competing Interests: Conflict of interest All authors have no conflicts of interest., (Copyright © 2022 The Authors. Published by Elsevier GmbH.. All rights reserved.)

Mitochondria are the "power plant" of the cell, providing a constant source of energy, and are involved in a variety of intracellular signaling pathways. Among these pathways, Ca 2+ homeostasis is closely related to the normal function of mitochondria. By destroying the Ca 2+ steady state of mitochondria and disrupting their multiple cellular activities, tumor cell killing can be achieved. In addition, the presence of an intracellular oxidative stress state triggers the closure of cellular calcium channels, which leads to intracellular Ca 2+ retention and enrichment. We designed a targeted and tumor microenvironment (TME)-responsive CaO 2 -based nanosystem that can selectively target cancer cells for pH-controlled degradation and drug release, alter cellular physiological mechanisms by disrupting Ca 2+ homeostasis in an artificial manner, and introduce mitochondrial Ca 2+ excess-mediated apoptosis. Meanwhile, the production of Ca(OH) 2 will raise the pH of the microenvironment and subsequently promote the oxidation process of glutathione by H 2 O 2 released from CaO 2 degradation, achieving the goal of remodeling TME. Moreover, calcium overload of tumor cells and calcification of tissues can both inhibit tumor growth and act as a contrast agent for computed tomography imaging.

Objective: The purpose of this study was to investigate parathyroid hormone (PTH), serum calcium, phosphorus, and 25-hydroxyvitamin D (25-OH-VD) changes before and after radioactive iodine (RAI) in differentiated thyroid carcinoma (DTC) patients at different time points., Methods: A total of 259 DTC patients who received RAI were prospectively enrolled. We evaluated PTH, serum calcium, phosphorus, and 25-OH-VD levels at baseline pre-RAI, five days, six weeks, and six months post-RAI, respectively. We analyzed the risk factors of hypocalcemia at five days post-RAI., Results: The mean PTH, serum calcium and phosphorus values decreased five days post-RAI compared with pre-RAI (PTH 4.18 ± 1.23 pmol/L vs . 3.95 ± 1.41 pmol/L; calcium 2.27 ± 0.09 mmol/L vs . 2.20 ± 0.11 mmol/L; phosphorus 1.25 ± 0.17 vs . 0.98 ± 0.20 mmol/L, P < 0.05), and the differences were statistically significant. The mean 25-OH-VD levels did not significantly decrease at five days post-RAI. 21.2% (55/259) of patients had hypocalcemia at five days post-RAI, and all of them were given oral calcium supplements. At six weeks post-RAI, all of the above parameters were higher than those at five days post-RAI. Multivariate regression analysis showed that baseline pre-RAI serum calcium < 2.27 mmol/L, PTH < 4.18 pmol/L and negative 99m TcO 4 - thyroid imaging were risk factors for hypocalcemia at five days post-RAI., Conclusion: For DTC patients with normal PTH and serum calcium levels at pre-RAI, their PTH, serum calcium, and phosphorus levels decreased at five days post-RAI. About one-fifth of patients could have hypocalcemia at five days post-RAI. Lower baseline pre-RAI serum calcium and PTH levels and negative 99m TcO 4 - thyroid imaging were risk factors for hypocalcemia five days post-RAI., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Xiao, Zhang, Zhu, Wang, Liu, Huang and Li.)

Background: Accumulating evidence has shown that serum calcium and vitamin D may be associated with or influence various cancer risks. However, no prospective studies have evaluated the independent and joint associations between prediagnostic levels of serum calcium and vitamin D and future risk of incident primary liver cancer., Methods: We used a nested case-control design to evaluate subjects over 22 years of follow-up. Serum calcium, 25-hydroxy vitamin D [25(OH)D], and three markers of hepatitis B virus and hepatitis C virus were measured in baseline serum from 226 incident primary liver cancer cases and 1,061 matched controls. We calculated ORs and 95% confidence intervals (CI) using logistic regression to estimate the associations between calcium, 25(OH)D, and primary liver cancer risk., Results: Multivariable adjusted models showed that subjects with both low (OR Low/Medium = 1.48, 95% CI = 1.01-2.17) or high (OR High/Medium = 1.92, 95% CI = 1.34-2.76) calcium had an increased primary liver cancer risk, while those with high 25(OH)D had a decreased risk of primary liver cancer (OR High/Medium = 0.54, 95% CI = 0.35-0.82). In joint analyses, when compared with subjects with medium calcium and 25(OH)D, subjects with high calcium and medium 25(OH)D had elevated odds of developing primary liver cancer (OR = 1.89, 95% CI = 1.17-3.05); those with medium calcium and high 25(OH)D had reduced odds of developing primary liver cancer (OR = 0.34, 95% CI = 0.17-0.67); and subjects in other classifications of calcium and serum 25(OH)D levels had no change in the odds of developing primary liver cancer (all P > 0.05)., Conclusions: In a nutrient-deficient population, we found that serum calcium and serum 25(OH)D could potentially be modifiable risk or protective factors., Impact: Our findings provide potential targets for primary liver cancer prevention and control., (©2020 American Association for Cancer Research.)

Radiation-induced lung injury (RILI) is a common and severe side effect of thoracic radiotherapy, which compromises patients' quality of life. Recent studies revealed that early vascular injury, especially microvascular damage, played a central role in the development of RILI. For this reason, early vascular protection is essential for RILI therapy. The ATP-sensitive K + (K ATP ) channel is an ATP-dependent K + channel with multiple subunits. The protective role of the K ATP channel in vascular injury has been demonstrated in some published studies. In this work, we investigated the effect of K ATP channel on RILI. Our findings confirmed that the K ATP channel blocker glibenclamide, rather than the K ATP channel opener pinacidil, remitted RILI, and in particular, provided protection against radiation-induced vascular injury. Cytology experiments verified that glibenclamide enhanced cell viability, increased the potential of proliferation after irradiation and attenuated radiation-induced apoptosis. Involved mechanisms included increased Ca 2+ influx and PKC activation, which were induced by glibenclamide pretreatment. In conclusion, the K ATP channel blocker glibenclamide remitted RILI and inhibited the radiation-induced apoptosis of vascular endothelial cells by increased Ca 2+ influx and subsequent PKC activation.

Repurposing cationic amphiphilic drugs (CAD) for cancer treatment is emerging as an attractive means to enhance the efficacy of chemotherapy. Many commonly used CADs, including several cation amphiphilic antihistamines and antidepressants, induce cancer-specific, lysosome-dependent cell death and sensitize cancer cells to chemotherapy. CAD-induced inhibition of lysosomal acid sphingomyelinase is necessary, but not sufficient, for the subsequent lysosomal membrane permeabilization and cell death, while other pathways regulating this cell death pathway are largely unknown. Prompted by significant changes in the expression of genes involved in Ca 2+ and cyclic AMP (cAMP) signaling pathways in CAD-resistant MCF7 breast cancer cells, we identified here an early lysosomal Ca 2+ release through P2X purinergic receptor 4 (P2RX4) and subsequent Ca 2+ - and adenylyl cyclase 1 (ADCY1)-dependent synthesis of cAMP as a signaling route mediating CAD-induced lysosomal membrane permeabilization and cell death. Importantly, pharmacologic and genetic means to increase cellular cAMP levels either by activating cAMP-inducing G-protein-coupled receptors (GPR3 or β 2 adrenergic receptor) or ADCY1, or by inhibiting cAMP-reducing guanine nucleotide-binding protein G(i) subunit α2, C-X-C motif chemokine receptor type 4, or cAMP phosphodiesterases, sensitized cancer cells to CADs. These data reveal a previously unrecognized lysosomal P2RX4- and ADCY1-dependent signaling cascade as a pathway essential for CAD-induced lysosome-dependent cell death and encourage further investigations to find the most potent combinations of CADs and cAMP-inducing drugs for cancer therapy., (©2019 American Association for Cancer Research.)

In our current investigation, we evaluated the effect of Chlorella pyrenoidosa protein hydrolysate (CPPH) and Chlorella pyrenoidosa protein hydrolysate-calcium chelate (CPPH-Ca) on calcium absorption and gut microbiota composition, as well as their in vivo regulatory mechanism in SD rats fed low-calcium diets. Potent major compounds in CPPH were characterized by HPLC-MS/MS, and the calcium-binding mechanism was investigated through ultraviolet and infrared spectroscopy. Using high-throughput next-generation 16S rRNA gene sequencing, we analyzed the composition of gut microbiota in rats. Our study showed that HCPPH-Ca increased the levels of body weight gain, serum Ca, bone activity, bone mineral density (BMD) and bone mineral content (BMC), while decreased serum alkaline phosphatase (ALP) and inhibited the morphological changes of bone. HCPPH-Ca up-regulated the gene expressions of transient receptor potential cation V5 (TRPV5), TRPV6, calcium-binding protein-D9k (CaBP-D9k) and a calcium pump (plasma membrane Ca-ATPase, PMCA1b). It also improved the abundances of Firmicutes and Lactobacillus . Bifidobacterium and Sutterella were both positively correlated with calcium absorption. Collectively, these findings illustrate the potential of HCPPH-Ca as an effective calcium supplement.

Nanosecond pulsed electric field (nsPEF) has the ability to induce a host of intracellular biochemical processes in living cells as a function of parameter setting. In vitro experiments proved that nsPEF stimulation could remarkably promote biomineralization processes and new bone formation. However, the impact of nsPEF parameter settings on the calcium flux of osteoblasts, as well as the intracellular mechanisms underlying those observations have yet to be elucidated. In this study, live osteoblast-like MG63 cells were loaded with fluorescence indicator dye fluo-4 AM. nsPEF stimulation could induce intracellular calcium mobilization in MG63 cells with no refractory period. We confirmed that moderate output voltage (4-8 KV) and large pulse number (25) were required for efficient nsPEF irritation of MG63 cells. Additionally, nsPEF stimulation-induced calcium flux in MG63 cells was dramatically reduced with the treatment by ethylene glycol tetraacetic acid (EGTA), proving that the intake of extracellular calcium ions is crucial for increasing intracellular calcium concentration of nsPEF-treated MG63 cells. Our preliminary study investigated the mechanisms underlying nsPEF stimulation-induced calcium mobilization in osteoblast-like cells, and it has the potential to accelerate the application of nsPEF stimulation in new bone formation., (Copyright © 2018. Published by Elsevier B.V.)

Perylenequinones (PQ) that notably produce reactive oxygen species upon exposure to visible light are a class of photoactivated polyketide mycotoxins produced by fungal plant pathogens such as Shiraia sp. The involvement of Ca 2+ /calmodulin (CaM) signalling in PQ biosynthesis was investigated by submerged culturing of Shiraia sp. Slf14, a species that produces hypocrellins HA and HB and elsinochromes EA, EB, and EC. Our results showed that the total content of PQ reached 1894.66 ± 21.93 mg/L under optimal conditions of Ca 2+ addition, which represents a 5.8-fold improvement over controls. The addition of pharmacological Ca 2+ sensor inhibitors strongly inhibited PQ production, which indicates that Ca 2+ /CaM signalling regulates PQ biosynthesis. The expression levels of Ca 2+ sensor and PQ biosynthetic genes were downregulated following addition of inhibitors but were upregulated upon addition of Ca 2+ . Inhibition was partially released by external Ca 2+ supplementation. Fluo-3/AM experiments revealed that similar cytosolic Ca 2+ variation occurred under these conditions. These results demonstrated that Ca 2+ signalling via the CaM transduction pathway plays a pivotal role in PQ biosynthesis.

Transient receptor potential A1 (TRPA1) is a nonselective cation channel implicated in thermosensation and inflammatory pain. In this study, we show that TRPA1 (activated by allyl isothiocyanate, acrolein, and 4-hydroxynonenal) elevates the intracellular Ca 2+ concentration ([Ca 2+ ] i ) in dorsal root ganglion (DRG) neurons in the presence and absence of extracellular Ca 2+ Pharmacological and immunocytochemical analyses revealed the presence of TRPA1 channels both on the plasma membrane and in endolysosomes. Confocal line-scan imaging demonstrated Ca 2+ signals elicited from individual endolysosomes ("lysosome Ca 2+ sparks") by TRPA1 activation. In physiological solutions, the TRPA1-mediated endolysosomal Ca 2+ release contributed to ∼40% of the overall [Ca 2+ ] i rise and directly triggered vesicle exocytosis and calcitonin gene-related peptide release, which greatly enhanced the excitability of DRG neurons. Thus, in addition to working via Ca 2+ influx, TRPA1 channels trigger vesicle release in sensory neurons by releasing Ca 2+ from lysosome-like organelles., (© 2016 Shang et al.)

Although the effects and the underlying mechanism of sympathetic stimulation on cardiac Ca handling are relatively well established both in health and disease, the modes of action and mechanisms of parasympathetic modulation are poorly defined. Here, we demonstrate that parasympathetic stimulation initiates a novel mode of excitation-contraction coupling that enhances the efficiency of cardiac sarcoplasmic reticulum Ca store utilization. This efficient mode of excitation-contraction coupling involves reciprocal changes in the phosphorylation of ryanodine receptor 2 at Ser-2808 and Ser-2814. Specifically, Ser-2808 phosphorylation was mediated by muscarinic receptor subtype 2 and activation of PKG (protein kinase G), whereas dephosphorylation of Ser-2814 involved activation of muscarinic receptor subtype 3 and decreased reactive oxygen species-dependent activation of CaMKII (Ca/calmodulin-dependent protein kinase II). The overall effect of these changes in phosphorylation of ryanodine receptor 2 is an increase in systolic Ca release at the low sarcoplasmic reticulum Ca content and a paradoxical reduction in aberrant Ca leak. Accordingly, cholinergic stimulation of cardiomyocytes isolated from failing hearts improved Ca cycling efficiency by restoring altered ryanodine receptor 2 phosphorylation balance., Competing Interests: Conflict(s) of Interest/Disclosure(s) None, (© 2016 American Heart Association, Inc.)

Aims/hypothesis: Insulin is a key metabolic regulator in health and diabetes. In pancreatic beta cells, insulin release is regulated by the major second messengers Ca(2+) and cAMP: exocytosis is triggered by Ca(2+) and mediated by the cAMP/protein kinase A (PKA) signalling pathway. However, the causal link between these two processes in primary beta cells remains undefined., Methods: Time-resolved confocal imaging of fluorescence resonance energy transfer signals was performed to visualise PKA activity, and combined membrane capacitance recordings were used to monitor insulin secretion from patch-clamped rat beta cells., Results: Membrane depolarisation-induced Ca(2+) influx caused an increase in cytosolic PKA activity via activating a Ca(2+)-sensitive adenylyl cyclase 8 (ADCY8) subpool. Glucose stimulation triggered coupled Ca(2+) oscillations and PKA activation. ADCY8 knockdown significantly reduced the level of depolarisation-evoked PKA activation and impaired replenishment of the readily releasable vesicle pool. Pharmacological inhibition of PKA by two inhibitors reduced depolarisation-induced PKA activation to a similar extent and reduced the capacity for sustained vesicle exocytosis and insulin release., Conclusions/interpretation: Our findings suggest that depolarisation-induced Ca(2+) influx plays dual roles in regulating exocytosis in rat pancreatic beta cells by triggering vesicle fusion and replenishing the vesicle pool to support sustained insulin release. Therefore, Ca(2+) influx may be important for glucose-stimulated insulin secretion.

Classic calcium hypothesis states that depolarization-induced increase in intracellular Ca(2+) concentration ([Ca(2+)]i) triggers vesicle exocytosis by increasing vesicle release probability in neurons and neuroendocrine cells. The extracellular Ca(2+), in this calcium hypothesis, serves as a reservoir of Ca(2+) source. Recently we find that extracellular Ca(2+)per se inhibits the [Ca(2+)]i dependent vesicle exocytosis, but it remains unclear whether quantal size is regulated by extracellular, or intracellular Ca(2+) or both. In this work we showed that, in physiological condition, extracellular Ca(2+) per se specifically inhibited the quantal size of single vesicle release in rat adrenal slice chromaffin cells. The extracellular Ca(2+) in physiological concentration (2.5 mM) directly regulated fusion pore kinetics of spontaneous quantal release of catecholamine. In addition, removal of extracellular Ca(2+) directly triggered vesicle exocytosis without eliciting intracellular Ca(2+). We propose that intracellular Ca(2+) and extracellular Ca(2+)per se cooperately regulate single vesicle exocytosis. The vesicle release probability was jointly modulated by both intracellular and extracellular Ca(2+), while the vesicle quantal size was mainly determined by extracellular Ca(2+) in chromaffin cells physiologically., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Phosphorylation of the cardiac ryanodine receptor (RyR2) by protein kinase A (PKA) at Ser-2808 is suggested to mediate the physiological 'fight or flight' response and contribute to heart failure by rendering the sarcoplasmic reticulum (SR) leaky for Ca(2+). In the present study, we examined the potential role of RyR2 phosphorylation at Ser-2808 in the progression of Ca(2+)-dependent cardiomyopathy (CCM) by using mice genetically modified to feature elevated SR Ca(2+) leak while expressing RyR2s that cannot be phosphorylated at this site (S2808A). Surprisingly, rather than alleviating the disease phenotype, constitutive dephosphorylation of Ser-2808 aggravated CCM as manifested by shortened survival, deteriorated in vivo cardiac function, exacerbated SR Ca(2+) leak and mitochondrial injury. Notably, the deteriorations of cardiac function, myocyte Ca(2+) handling, and mitochondria integrity were consistently worse in mice with heterozygous ablation of Ser-2808 than in mice with complete ablation. Wild-type (WT) and CCM myocytes expressing unmutated RyR2s exhibited a high level of baseline phosphorylation at Ser-2808. Exposure of these CCM cells to protein phosphatase 1 caused a transitory increase in Ca(2+) leak attributable to partial dephosphorylation of RyR2 tetramers at Ser-2808 from more fully phosphorylated state. Thus, exacerbated Ca(2+) leak through partially dephosphorylated RyR2s accounts for the prevalence of the disease phenotype in the heterozygous S2808A CCM mice. These results do not support the importance of RyR2 hyperphosphorylation in Ca(2+)-dependent heart disease, and rather suggest roles for the opposite process, the RyR2 dephosphorylation at this residue in physiological and pathophysiological Ca(2+) signalling.

Adrenergic stimulation modulates cardiac function by altering the phosphorylation status of several cardiac proteins. The Troponin complex, which is the Ca(2+) sensor for cardiac contraction, is a hot spot for adrenergic phosphorylation. While the effect of β-adrenergic related PKA phosphorylation of troponin I at Ser23/24 is well established, the effects of α-adrenergic induced PKC phosphorylation on multiple sites of TnI (Ser43/45, Thr144) and TnT (Thr194, Ser198, Thr203 and Thr284) are much less clear. By utilizing an IAANS labeled fluorescent troponin C, TnC(IAANS)(T53C), we systematically examined the site specific effects of PKC phosphomimetic mutants of TnI and TnT on TnC's Ca(2+) binding properties in the Tn complex and reconstituted thin filament. The majority of the phosphomemetics had little effect on the Ca(2+) binding properties of the isolated Tn complex. However, when incorporated into the thin filament, the phosphomimetics typically altered thin filament Ca(2+) sensitivity in a way consistent with their respective effects on Ca(2+) sensitivity of skinned muscle preparations. The altered Ca(2+) sensitivity could be generally explained by a change in Ca(2+) dissociation rates. Within TnI, phosphomimetic Asp and Glu did not always behave similar, nor were Ala mutations (used to mimic non-phosphorylatable states) benign to Ca(2+) binding. Our results suggest that Troponin may act as a hub on the thin filament, sensing physiological stimuli to modulate the contractile performance of the heart.

Objective: To examine the association between serum calcium levels and the risk of liver cirrhosis., Methods: A nested case-control study was performed based on the nutritional intervention trial of esophageal carcinoma in Linxian, Henan province. Serum samples of 281 liver cirrhosis cases and 562 controls were tested for calcium concentrations, surface antigen (HBsAg) and core antibody (anti-HBc) on Hepatitis virus B and antibody on Hepatitis virus C (anti-HCV), using automatic serum biochemical analysis system and enzyme-linked immunoassay. Data on baseline characteristics were collected via a questionnaire. Serum calcium value was divided into tertiles and logistic regression model was used to calculate odds ratios and 95% confidence intervals., Results: Individuals in the case group showed higher calcium levels (1.81 ± 0.84) mmol/L when compared to the controls (1.65 ± 0.79) mmol/L, with t = -2.640 and P = 0.008. The calcium levels were associated with the risk of liver cirrhosis (χ(2) = 6.888, P = 0.0319). Risks for the individuals in the highest tertile were doubled when compared to the lowest (adjusted OR = 2.261, 95%CI: 1.497 - 3.416, P = 0.002). A positive correlation was observed between serum calcium level and the risk of liver cirrhosis (χ(2) = 6.842, P = 0.0089)., Conclusion: from our study revealed that the elevated serum calcium level might be an independent risk factor for liver cirrhosis. However, further investigations are anticipated to explore its potential mechanisms.

Aberrant myofilament Ca(2+) sensitivity is commonly observed with multiple cardiac diseases, especially familial cardiomyopathies. Although the etiology of the cardiomyopathies remains unclear, improving cardiac muscle Ca(2+) sensitivity through either pharmacological or genetic approaches shows promise of alleviating the disease-related symptoms. Due to its central role as the Ca(2+) sensor for cardiac muscle contraction, troponin C (TnC) stands out as an obvious and versatile target to reset disease-associated myofilament Ca(2+) sensitivity back to normal. To test the hypothesis that aberrant myofilament Ca(2+) sensitivity and its related function can be corrected through rationally engineered TnC constructs, three thin filament protein modifications representing different proteins (troponin I or troponin T), modifications (missense mutation, deletion, or truncation), and disease subtypes (familial or acquired) were studied. A fluorescent TnC was utilized to measure Ca(2+) binding to TnC in the physiologically relevant biochemical model system of reconstituted thin filaments. Consistent with the pathophysiology, the restrictive cardiomyopathy mutation, troponin I R192H, and ischemia-induced truncation of troponin I (residues 1-192) increased the Ca(2+) sensitivity of TnC on the thin filament, whereas the dilated cardiomyopathy mutation, troponin T ΔK210, decreased the Ca(2+) sensitivity of TnC on the thin filament. Rationally engineered TnC constructs corrected the abnormal Ca(2+) sensitivities of the thin filament, reconstituted actomyosin ATPase activity, and force generation in skinned trabeculae. Thus, the present study provides a novel and versatile therapeutic strategy to restore diseased cardiac muscle Ca(2+) sensitivity.

The contractile response of the heart can be altered by disease-related protein modifications to numerous contractile proteins. By utilizing an IAANS labeled fluorescent troponin C, [Formula: see text], we examined the effects of ten disease-related troponin modifications on the Ca(2+) binding properties of the troponin complex and the reconstituted thin filament. The selected modifications are associated with a broad range of cardiac diseases: three subtypes of familial cardiomyopathies (dilated, hypertrophic and restrictive) and ischemia-reperfusion injury. Consistent with previous studies, the majority of the protein modifications had no effect on the Ca(2+) binding properties of the isolated troponin complex. However, when incorporated into the thin filament, dilated cardiomyopathy mutations desensitized (up to 3.3-fold), while hypertrophic and restrictive cardiomyopathy mutations, and ischemia-induced truncation of troponin I, sensitized the thin filament to Ca(2+) (up to 6.3-fold). Kinetically, the dilated cardiomyopathy mutations increased the rate of Ca(2+) dissociation from the thin filament (up to 2.5-fold), while the hypertrophic and restrictive cardiomyopathy mutations, and the ischemia-induced truncation of troponin I decreased the rate (up to 2-fold). The protein modifications also increased (up to 5.4-fold) or decreased (up to 2.5-fold) the apparent rate of Ca(2+) association to the thin filament. Thus, the disease-related protein modifications alter Ca(2+) binding by influencing both the association and dissociation rates of thin filament Ca(2+) exchange. These alterations in Ca(2+) exchange kinetics influenced the response of the thin filament to artificial Ca(2+) transients generated in a stopped-flow apparatus. Troponin C may act as a hub, sensing physiological and pathological stimuli to modulate the Ca(2+)-binding properties of the thin filament and influence the contractile performance of the heart.

Astrocytes release a variety of signaling molecules including glutamate, D-serine, and ATP in a regulated manner. Although the functions of these molecules, from regulating synaptic transmission to controlling specific behavior, are well documented, the identity of their cellular compartment(s) is still unclear. Here we set out to study vesicular exocytosis and glutamate release in mouse hippocampal astrocytes. We found that small vesicles and lysosomes coexisted in the same freshly isolated or cultured astrocytes. Both small vesicles and lysosome fused with the plasma membrane in the same astrocytes in a Ca(2+)-regulated manner, although small vesicles were exocytosed more efficiently than lysosomes. Blockade of the vesicle glutamate transporter or cleavage of synaptobrevin 2 and cellubrevin (both are vesicle-associated membrane proteins) with a clostridial toxin greatly inhibited glutamate release from astrocytes, while lysosome exocytosis remained intact. Thus, both small vesicles and lysosomes contribute to Ca(2+)-dependent vesicular exocytosis, and small vesicles support glutamate release from astrocytes.

The calcium-dependent interactions between troponin C (TnC) and other thin and thick filament proteins play a key role in the regulation of cardiac muscle contraction. Five hydrophobic residues (Phe(20), Val(44), Met(45), Leu(48), and Met(81)) in the regulatory domain of TnC were individually substituted with polar Gln, to examine the effect of these mutations that sensitized isolated TnC to calcium on (1) the calcium binding and exchange with TnC in increasingly complex biochemical systems and (2) the calcium sensitivity of actomyosin ATPase. The hydrophobic residue mutations drastically affected calcium binding and exchange with TnC in increasingly complex biochemical systems, indicating that side chain intra- and intermolecular interactions of these residues play a crucial role in determining how TnC responds to calcium. However, the mutations that sensitized isolated TnC to calcium did not necessarily increase the calcium sensitivity of the troponin (Tn) complex or reconstituted thin filaments with or without myosin S1. Furthermore, the calcium sensitivity of reconstituted thin filaments (in the absence of myosin S1) was a better predictor of the calcium dependence of actomyosin ATPase activity than that of TnC or the Tn complex. Thus, both the intrinsic properties of TnC and its interactions with the other contractile proteins play a crucial role in modulating the binding of calcium to TnC in increasingly complex biochemical systems.

Background: Esophageal cancer (EC) remains a leading cause of cancer-related deaths in Linzhou (formerly Linxian) and Huixian of Henan province, northern China, which has been well recognized as the highest incidence area for EC. The lack of useful chemoprevention agents and early detection methods is the key factors for stable EC incidence in these areas. Human esophageal carcinogensis has been considered as a multistep progressive process. The natural history for EC, however is not very clear., Methods: Follow-up studies with linear repeated biopsies and histopathological examination were performed on 778 subjects from Linzhou and Huixian. Of these subjects, 578 subjects were followed for 11 years (1989-2000), 400 subjects with different severity of esophageal precancerous lesions were randomly divided into 2 groups for intervention studies with calcium and decaffeinated green tea (DGT). Each group included 200 subjects (100 subjects for treatment, and 100 subjects for placebo). In calcium group, each subject received an oral supplementation of 1,200 mg of calcium daily for 11 months. In DGT group, each subject received 5 mg of DGT daily for 12 months. In placebo group, each subject received placebo pill for 11 months (calcium group) and 12 month (DGT group). At the entry and the end of the trial, esophageal biopsy specimens were taken at the middle and the lower thirds of the esophagus and from macroscopic lesions, if only, of each subject., Results: DGT trail did not show apparent difference between the treatment and placebo group in alleviating the esophageal precancerous lesions and abnormal cell proliferation. For the calcium intervention study, after 11 years' follow-up, 10 subjects had developed into cancers in the calcium group (10%, 8 EC and 2 GCA), and 8 subjects developed into EC in the placebo group (8%). All these patients were diagnosed at very early stage of cancer (symptom-free). Of the 578 subjects, 25 (18 males and 7 females) had developed into EC (n = 23, 4.3%) and gastric cardia cancer (GCA, n = 2, 0.3%), during the 11 years' follow-up. The mean time of cancer development (from entry of the follow-up study to the cancer detection) was 5.0 +/- 2.9 years (males) and 4.7 +/- 3.2 years (females). Of the 25 patients with EC and GCA, 11 were from the 387 followed subjects with "normal" histomorphology of biopsy at the entry of the follow-up study (3%, 11/387), 2 were from the subjects with basal cell hyperplasia, grade I (BCH I, 2%, 2/94), 7 from the subjects with BCH grade II (BCH II, 10%, 7/72), and 5 from BCH III and dysplasia (20%, 5/25)., Conclusions: DGT trail was not shown to have beneficial effects in alleviating esophageal precancerous lesions and abnormal cell proliferation patterns. Calcium supplementation did not produce apparent long-term effects on EC. BCH II could be considered as precancerous lesions of EC. The quantitative histopathological analysis in terms of number of proliferating basal cell layers is of importance in determining the high-risk subjects for EC and evaluating the intervention results. Follow-up studies with repeated endoscopic biopsies are the powerful strategy for early detection and mortality control of EC and GAC in the high incidence area.

Graphical abstract Highlights • ATP evoked Ca2+ release from the ER though the P2Y 2 R-PLC-IP3 pathway. • Lysosomal-stored Ca2+ triggered Ca2+ release from the ER via the IP3 receptor without depleting ER Ca2+ stores. • ATP evoked ATP release from lysosomes through lysosomal exocytosis in a Ca2+-dependent manner. Abstract Adenosine triphosphate (ATP) is stored as lysosomal vesicles in marginal cells of the stria vascular in neonatal rats, but the mechanisms of ATP release are unclear. Primary cultures of marginal cells from 1-day-old Sprague–Dawley rats were established. P2Y 2 receptor and inositol 1,4,5-trisphosphate (IP3) receptor were immunolabelled in marginal cells of the stria vascular. We found that 30 μM ATP and 30 μM uridine triphosphate (UTP) evoked comparable significant increases in the intracellular Ca2+ concentration ([Ca2+] i) in the absence of extracellular Ca2+, whereas the response was suppressed by 100 μM suramin, 10 μM 1-(6-(17β-3-methoxyester-1,3,5(10)-trien-17-yl)amino)-hexyl)-1H-pyrrole-2,5-dione(U-73122), 100 μM 2-aminoethoxydiphenyl borate (2-APB) and 5 μM thapsigargin (TG), thus indicating that ATP coupled with the P2Y 2 R-PLC-IP3 pathway to evoke Ca2+ release from the endoplasmic reticulum (ER). Incubation with 200 μM Gly-Phe-β-naphthylamide (GPN) selectively disrupted lysosomes and caused significant increases in [Ca2+] I ; this effect was partly inhibited by P2Y 2 R-PLC-IP3 pathway antagonists. After pre-treatment with 5 μM TG, [Ca2+] i was significantly lower than that after treatment with P2Y 2 R-PLC-IP3 pathway antagonists under the same conditions, thus indicating that lysosomal Ca2+ triggers Ca2+ release from ER Ca2+ stores. Baseline [Ca2+] i declined after treatment with the Ca2+ chelator 50 μM bis-(aminophenolxy) ethane- N , N , N ʹ, N ʹ-tetra-acetic acid acetoxyme-thyl ester (BAPTA-AM) and 4 IU/ml apyrase. 30 μM ATP decrease of the number of quinacrine-positive vesicles via lysosome exocytosis, whereas the number of lysosomes did not change. However, lysosome exocytosis was significantly suppressed by pre-treatment with 5 μM vacuolin-1. Release of ATP and β-hexosaminidase both increased after treatment with 200 μM GPN and 5 μM TG, but decreased after incubation with 50 μM BAPTA-AM, 4 IU/ml apyrase and 5 μM vacuolin-1. We suggest that ATP triggers Ca2+ release from the ER, thereby contributing to secretion of lysosomal ATP via lysosomal exocytosis. Lysosomal stored Ca2+ triggers Ca2+ release from the ER directly though the IP3 receptors, and lysosomal ATP evokes Ca2+ signals indirectly via the P2Y 2 R-PLC-IP3 pathway. [ABSTRACT FROM AUTHOR]

• Balance of N/Ca, K/Ca and Mg/Ca was disrupted in the flesh with spongy tissue. • The increase of Cell wall Ca and CaOx, and the decrease of soluble Ca had close relationship of mango spongy tissue. • The key genes were identified involved in spongy tissue development. Spongy tissue, as one of internal flesh breakdown in mango fruits, is correlated with calcium (Ca) deficiency, and adversely affects fruit quality and yield worldwide. However, the underlying mechanism causing spongy tissue remains unknown. Here, we explored the effects of Ca deficiency on spongy tissue in a susceptible cultivar, 'Keitt', at the physiological and molecular levels. Nutrient analysis showed that flesh with spongy tissue had lower Ca content and higher N/Ca, K/Ca and Mg/Ca rations than healthy fruit flesh. Ca accumulation in the cell wall, especially in chelator-soluble pectin, was elevated due to increased pectin content, lower levels of pectin methylesterification, and increased pectin methylesterase (PME) activity. During spongy tissue development, levels of Ca oxalate (CaOx) and oxalic acid both increased, whereas soluble Ca content decreased in the flesh. Transcriptomic analysis of healthy flesh and flesh with spongy tissue revealed 2054 up-regulated and 996 down-regulated genes. Gene ontology term analysis showed that the up-regulated genes were mainly enriched in functions related to the transmembrane transporter activity, calcium ion binding, and the cell wall. Importantly, up-regulated genes in spongy tissue included five glucuronate 4-epimerase (GAE) genes and two galactosyltransferase (GALT) genes, which involved in pectin synthesis; four PME genes which control pectin demethylesterification; and eight autoinhibited calcium-transporting ATPase (ACA) genes and two vacuole H+/Ca2+ exchanger (CAX) genes which contribute to Ca influx in the vacuole. Our findings illustrate a mechanism by which Ca deficiency leads to spongy tissue, which will contribute to efforts to control this physiological disorder. [ABSTRACT FROM AUTHOR]

The appropriate design of multifunctional nanocarriers for chloroperoxidase (CPO) delivery and the simultaneous improvement of the efficiency of enzyme dynamic therapy (EDT) remain significant challenges. Herein, we report a facile one-step route to obtain a multifunctional nanocarrier for the formation of sodium hyaluronate-modified hollow calcium peroxide spheres with encapsulated L-buthionine sulfoximine (BSO), followed by delivery of CPO for enhanced EDT. After effective accumulation at the tumor sites, the nanocomposite rapidly decomposes and releases Ca2+, BSO molecules, CPO, and concurrently generates a large volume of hydrogen peroxide (H 2 O 2) in the endogenous tumor microenvironment (TME). BSO molecules inhibit the biosynthesis of glutathione (GSH) by inactivating γ-glutamyl cysteine synthetase. Due to BSO-induced GSH depletion and self-supply of H 2 O 2 , the EDT efficiency of CPO was significantly enhanced to achieve high tumor therapy efficiency. Additionally, overloaded Ca2+ caused mitochondrial damage and amplified the oxidative stress. Moreover, calcification resulted from the unbalanced calcium transport channel caused by enhanced oxidative stress, accelerating tumor apoptosis and improving the efficacy of computed tomography (CT) imaging visual tumor therapy. This simple and efficient design for multifunctional nanocomposites will likely take an important place in the field of combined tumor therapeutics. [Display omitted] • One-step synthesis of multifunctional nanocarrier for CPO delivery. • The nanocomposite can rapidly decompose through acid and HAD-response in TME. • GSH depletion, self-supplying H 2 O 2 , overloaded Ca2+-induced mitochondria damage. • The efficacy of EDT could be triply improved. • Calcification accelerates tumor apoptosis and enhances CT imaging efficacy. [ABSTRACT FROM AUTHOR]

ABSTRACT Ischemic postconditioning (Post C), which involves administration of a brief ischemia after the initial ischemic event, has been demonstrated to be strongly neuroprotective against global cerebral ischemia (GCI) and to improve cognitive outcome. To enhance understanding of the underlying mechanisms, the current study examined the role of NMDA receptors in mediating the beneficial effects of Post C (3 min ischemia) administered 2 days after GCI in adult male rats. The results revealed that Post C was strongly neuroprotective against GCI, and that this effect was blocked by administration of the NMDA receptor antagonist MK-801. Further work revealed that the NR2A-type NMDA receptors mediate the Post C beneficial effects as administration of a NR2A-preferring antagonist (NVP-A) blocked Post C neuroprotection and cognitive enhancement, while administration of a NR2B-preferring antagonist (Ro25) was without effect. Post C significantly up-regulated NR2A levels and phosphorylation of NR2A in the hippocampal CA1 region after Post C. Post C also increased Ca2+ influx and activation/phosphorylation of CamKIIα at Thr286, effects that were NR2A mediated as they were blocked by NVP-A. Phosphorylation of ERK and CREB was also increased by Post C, as were two downstream CREB-dependent prosurvival factors, brain derived neurotropic factor (BDNF) and Bcl2, effects that were blocked by the NR2A antagonist, NVP-A. Taken as a whole, the current study provides evidence that NR2A-activation and downstream prosurvival signaling is a critical mediator of Post C-induced neuroprotection and cognitive enhancement following GCI. © 2014 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Chinese fir (Cunninghamia LanceolataLamb, Hook) is generally considered a superior timber in southern China and other areas in the world. In the past few decades, aluminum (Al) toxicity has become one of biggest stress factors in the production and growth of Chinese fir, although this species prefers an acidic environment. To date, the selection of indicator species for Al toxicity remains critical in the field, and Al toxicity has not been successfully treated by artificially controlling Chinese fir plantations. To assess the Al toxicity risk, the height of the dominant tree, the concentration of calcium (Ca2+)/Al3+in soil solution, and the concentration of Ca2+ / [Ca2++ iron (Fe3+) + Al3+] in litter leached organic acids were introduced. The results indicated that eight plots had suffered Al toxicity. The threshold of Al toxicity was 37.53 mg kg−1in soil or 1.39 mmol L−1in soil solution, a pH of 4.15, a Ca2+ / (Ca2++ Fe3++ Al3+) molar ratio of 0.487, and a Ca2+/Al3+molar ratio of 1.599. The positive effects of exogenous nutrition (Ca, phosphorus [P], and nitrogen [N]) on the growth ofCunninghamia lanceolataseedlings was also studied in pot experiments based on results in the field. The cation nutrition can lead to detoxification, and the exogenous nutrition thresholds were Ca2+/ Al3+≥ 2.8, phosphorus (P)/ Al3+≥ 4.4, ammonium (NH4−)–nitrogen (N) / Al3+≥ 4.5. The data presented in this study are very helpful for the understanding of the degree of Al toxicity and have notable significance for the management of Chinese fir plantations. [ABSTRACT FROM AUTHOR]

Aims Recent studies suggest that proarrhythmic effects of cardiac glycosides (CGs) on cardiomyocyte Ca2+ handling involve generation of reactive oxygen species (ROS). However, the specific pathway(s) of ROS production and the subsequent downstream molecular events that mediate CG-dependent arrhythmogenesis remain to be defined. Methods and results We examined the effects of digitoxin (DGT) on Ca2+ handling and ROS production in cardiomyocytes using a combination of pharmacological approaches and genetic mouse models. Myocytes isolated from mice deficient in NADPH oxidase type 2 (NOX2KO) and mice transgenically overexpressing mitochondrial superoxide dismutase displayed markedly increased tolerance to the proarrhythmic action of DGT as manifested by the inhibition of DGT-dependent ROS and spontaneous Ca2+ waves (SCW). Additionally, DGT-induced mitochondrial membrane potential depolarization was abolished in NOX2KO cells. DGT-dependent ROS was suppressed by the inhibition of PI3K, PKC, and the mitochondrial KATP channel, suggesting roles for these proteins, respectively, in activation of NOX2 and in mitochondrial ROS generation. Western blot analysis revealed increased levels of oxidized CaMKII in WT but not in NOX2KO hearts treated with DGT. The DGT-induced increase in SCW frequency was abolished in myocytes isolated from mice in which the Ser 2814 CaMKII phosphorylation site on RyR2 is constitutively inactivated. Conclusion These results suggest that the arrhythmogenic adverse effects of CGs on Ca2+ handling involve PI3K- and PKC-mediated stimulation of NOX2 and subsequent NOX2-dependent ROS release from the mitochondria; mitochondria-derived ROS then activate CaMKII with consequent phosphorylation of RyR2 at Ser 2814. [ABSTRACT FROM AUTHOR]

Abstract: Tropomyosin (Tm) is a central protein in the Ca2+ regulation of striated muscle. The αTm isoform undergoes phosphorylation at serine residue 283. While the biochemical and steady-state muscle function of muscle purified Tm phosphorylation have been explored, the effects of Tm phosphorylation on the dynamic properties of muscle contraction and relaxation are unknown. To investigate the kinetic regulatory role of αTm phosphorylation we expressed and purified native N-terminal acetylated Ser-283 wild-type, S283A phosphorylation null and S283D pseudo-phosphorylation Tm mutants in insect cells. Purified Tm’s regulate thin filaments similar to that reported for muscle purified Tm. Steady-state Ca2+ binding to troponin C (TnC) in reconstituted thin filaments did not differ between the 3 Tm’s, however disassociation of Ca2+ from filaments containing pseudo-phosphorylated Tm was slowed compared to wild-type Tm. Replacement of pseudo-phosphorylated Tm into myofibrils similarly prolonged the slow phase of relaxation and decreased the rate of the fast phase without altering activation kinetics. These data demonstrate that Tm pseudo-phosphorylation slows deactivation of the thin filament and muscle force relaxation dynamics in the absence of dynamic and steady-state effects on muscle activation. This supports a role for Tm as a key protein in the regulation of muscle relaxation dynamics. [Copyright &y& Elsevier]

[Display omitted] • Fe(VI)/CaSO 3 was first proposed to control algal-source membrane fouling. • The characteristic of the reactive intermediates was fully used. • The oxidation efficiency was improved and the algae cell integrity was maintained. • Fe(VI)/CaSO 3 could eliminate intracellular organic matter already existed in water. • The mutual activation between Fe(VI) and CaSO 3 was verified. To alleviate severe algal-source membrane fouling in the ultrafiltration (UF) process, calcium sulfite (CaSO 3) integrated with ferrate (Fe(VI)) was proposed. With the integrated pre-treatment, the maximum removal rate of algae cells was improved to 91.19 %, and numerous larger flocs with great settleability were generated. The fluorescent organic components were effectively eliminated, as well as the dissolved organic matter decreased by 38.20 %. During the Fe(VI)/CaSO 3 process, oxidation played a fateful role in fouling alleviation and promoted the in-situ coagulation efficiency. Compared with single Fe(VI) treatment, the oxidation capacity was strengthened through the formation of a series of reactive intermediates (involving Fe(V), Fe(IV), SO 3 •−, SO 5 •−, SO 4 •− and •OH), which were easy to be quenched by the cell-coated extracellular organic matter. Moreover, the consumption of all the oxidants was also remarkably accelerated, thereby the cell integrity was well-kept, and the intercellular organic matter (IOM) was not released. The IOM which already existed in water could also be eliminated, as well as the effluent safety was well guaranteed. During UF, the terminal J/J 0 was elevated to 0.87 at most from 0.10, and the fouling resistances were strikingly reduced. The algal foulants deposition was effectively decreased, and the contact angle of the fouled membrane was closer to the virgin membrane. The dominant fouling mechanism was also converted to intermediate and standard blocking without forming the cake layer. [ABSTRACT FROM AUTHOR]

Calcium–magnesium–alumina–silicate (CMAS) corrosion resistance is an important issue on the design of next-generation thermal battier coatings. As one of the promising thermal battier coatings, the lanthanum zirconate coating has attracted continuous attention. In this work, three lanthanum zirconate coatings with different La/Zr composition, i.e., La 1.8 Zr 2.2 O 7.1 , La 2 Zr 2 O 7 , and La 2.5 Zr 1.5 O 6.75 , are fabricated by laser-enhanced chemical vapour deposition, and their resistance to CMAS corrosion at 1250 °C is investigated. Among them, La 2.5 Zr 1.5 O 6.75 shows the best CMAS corrosion resistance because increased La content is beneficial to the formation of a dense and continuous apatite Ca 2 La 8 (SiO 4 ) 6 O 2 layer, which effectively slows down the subsequent molten CMAS penetration. This study clarifies the significant role of rare earth on CMAS corrosion resistance and is expected to guide the future design of rare-earth-based thermal battier coatings through composition tailoring. [ABSTRACT FROM AUTHOR]

Perovskite structured calcium titanate can be directly synthesized at room temperature. Other partial amorphous phase will have started to crystallize at 600 °C following the incorporation of Pr ion into the lattice. The doping mechanism is studied. The relationship between processing and point defects is found. The lattice cell expends with the annealing temperature until 900 °C, after that, contracts suddenly at 1000 °C and then tends to a constant at the temperature over 1100 °C. The mechanism of photoluminescence of Pr 3+ doped CaTiO 3 is set up. The powders have the red emission at 613 nm by the activation of UV light. The intensity of the emission increases with the annealing temperature till 1000 °C and then decreases, due to it has a correlation with the concentration of incorporated Pr ion. The decay time increases with the annealing temperature. The photoluminescence behavior is associated with the point defects which can be tailored by the processing of the powders, especially by the annealing temperatures. [ABSTRACT FROM AUTHOR]

Cr(VI)-contaminated soils could be remediated by using calcium polysulfide (CPS), while natural iron oxides as a main composition of soil would influence the pathways of the remediation. Through kinetic batch tests, the kinetics of Cr(VI) removal from soil, the effects of the contents of natural iron oxides, soil environmental conditions and mechanisms of Cr(VI) removal by using CPS with the presence of natural iron oxides were investigated. The results show that the removal of Cr(VI) by using CPS in soil fitted the pseudo-second-order model best, and the appearance of goethite increased the apparent rate constant from 0.0002 kg mg−1 h−1 to 0.0005 kg mg−1 h−1. The presence of iron oxides enhanced the removal of Cr(VI) by using CPS, and an extended reductive atmosphere of soil was created. The enhancement of Cr(VI) removal increased with the contents of iron oxides from 0 to 9 g kg−1, and declined from 9 to 12 g kg−1. Acidic environment favored the removal of Cr(VI) from soil by using CPS with or without the iron oxides compared to neutral soil and increased it from 87% to 100% because of proton-consuming reactions and electrostatic attraction. Twenty-nine percent of exchangeable and bound-to-carbonates species of chromium declined after the remediation, while 24% bound-to-iron-and-manganese-oxide species increased simultaneously. The findings of the study indicate that natural iron oxides in soils catalyze the reduction of Cr(VI) in soil and facilitate significantly the remediation of Cr(VI)-contaminated soil by using CPS. • Iron oxides in soil affect the removal efficiency of Cr(VI) significantly. • An extended reductive atmosphere is created in soil at presence of iron oxides. • Acidic soil favors the removal of Cr(VI) using calcium polysulfide (CPS) in soil. • Iron oxides in soil promote the immobilization of Cr(VI) by using CPS. [ABSTRACT FROM AUTHOR]

• Goethite and hematite may significantly enhance Cr(VI) sequestration using CPS. • Cr(VI) uptake by CPS with goethite or hematite was markedly influenced at basic pH. • Mechanisms of promoted Cr(VI) uptake by CPS with iron oxides were proposed. Calcium polysulfide (CPS) has been widely used for the remediation of hexavalent chromium (Cr(VI))-contaminated environments; however, the roles of natural iron oxides during the process of Cr(VI) sequestration are not well understood. In this study, we investigated the impact of natural iron oxides on the remediation of environments containing Cr(VI) using CPS and the mechanisms underlying such effects. Goethite and hematite markedly accelerated Cr(VI) sequestration by CPS, while Cr(VI) removal efficiency and apparent rate constant were increased at pH 7.0. Goethite increased the Cr(VI) removal efficiency of CPS from 80.6% to 98.6% at pH 7.0, while the apparent rate constant increased from 0.0074 to 0.028 L mol−1 min−1. Similarly, hematite increased the Cr(VI) removal efficiency of CPS to 98.4%, while the apparent rate constant increased to 0.024 L mol−1 min−1. pH had a negligible impact on the efficiency of Cr(VI) uptake by CPS with goethite or hematite under acidic conditions, whereas a pronounced effect on Cr(VI) removal efficiency was shown under basic conditions. Moreover, pH could significantly influence processes of promoted Cr(VI) sequestration using CPS with goethite or hematite. At acidic pH, increased Cr(VI) uptake was attributed mainly to the adsorption of Cr(VI) on goethite and hematite, which was accompanied by minor Cr(VI) reduction by electrons from the surface channel of >Fe(III)-O-Fe(II) ↔ >Fe(II)-O-Fe(III) and Fe(II) from CPS-reacted goethite and hematite. At neutral and basic pH, polysulfide-activated Fe(III) on the surface of goethite and hematite acted as a bridge between CPS and Cr(VI), which accelerated electron shuttling from polysulfides to Cr(VI), while Cr(VI) reduction was enhanced by the reactions of Cr(VI) with FeS 2 and compounds containing Fe(II)-S bonds. Our study demonstrates that natural iron minerals can enhance Cr(VI) sequestration using CPS during the remediation of Cr(VI)-contaminated environments rich in iron oxides. [ABSTRACT FROM AUTHOR]