Electrophysiological Properties of Endogenous Single Ca2+ Activated Cl− Channels Induced by Local Ca2+ Entry in HEK293

Microdomains formed by proteins of endoplasmic reticulum and plasma membrane play a key role in store-operated Ca²⁺ entry (SOCE). Ca²⁺ release through inositol 1,4,5-trisphosphate receptor (IP₃R) and subsequent Ca²⁺ store depletion activate STIM (stromal interaction molecules) proteins, sensors of intraluminal Ca²⁺, which, in turn, open the Orai channels in plasma membrane. Downstream to this process could be activated TRPC (transient receptor potential-canonical) calcium permeable channels. Using single channel patch-clamp technique we found that a local Ca²⁺ entry through TRPC1 channels activated endogenous Ca²⁺-activated chloride channels (CaCCs) with properties similar to Anoctamin6 (TMEM16F). Our data suggest that their outward rectification is based on the dependence from membrane potential of both the channel conductance and the channel activity: (1) The conductance of active CaCCs highly depends on the transmembrane potential (from 3 pS at negative potentials till 60 pS at positive potentials); (2) their activity (NPo) is enhanced with increasing Ca²⁺ concentration and/or transmembrane potential, conversely lowering of intracellular Ca²⁺ concentration reduced the open state dwell time; (3) CaCC amplitude is only slightly increased by intracellular Ca²⁺ concentration. Experiments with Ca²⁺ buffering by EGTA or BAPTA suggest close local arrangement of functional CaCCs and TRPC1 channels. It is supposed that Ca²⁺-activated chloride channels are involved in Ca²⁺ entry microdomains.     

Fibroblast Growth Factor 23 Stimulates Cardiac Fibroblast Activity through Phospholipase C-Mediated Calcium Signaling

Fibroblast growth factor (FGF)-23 induces hypertrophy and calcium (Ca²⁺) dysregulation in cardiomyocytes, leading to cardiac arrhythmia and heart failure. However, knowledge regarding the effects of FGF-23 on cardiac fibrogenesis remains limited. This study investigated whether FGF-23 modulates cardiac fibroblast activity and explored its underlying mechanisms. We performed MTS analysis, 5-ethynyl-2′-deoxyuridine assay, and wound-healing assay in cultured human atrial fibroblasts without and with FGF-23 (1, 5 and 25 ng/mL for 48 h) to analyze cell proliferation and migration. We found that FGF-23 (25 ng/mL, but not 1 or 5 ng/mL) increased proliferative and migratory abilities of human atrial fibroblasts. Compared to control cells, FGF-23 (25 ng/mL)-treated fibroblasts had a significantly higher Ca²⁺ entry and intracellular inositol 1,4,5-trisphosphate (IP₃) level (assessed by fura-2 ratiometric Ca²⁺ imaging and enzyme-linked immunosorbent assay). Western blot analysis showed that FGF-23 (25 ng/mL)-treated cardiac fibroblasts had higher expression levels of calcium release-activated calcium channel protein 1 (Orai1) and transient receptor potential canonical (TRPC) 1 channel, but similar expression levels of α-smooth muscle actin, collagen type IA1, collagen type Ⅲ, stromal interaction molecule 1, TRPC 3, TRPC6 and phosphorylated-calcium/calmodulin-dependent protein kinase II when compared with control fibroblasts. In the presence of ethylene glycol tetra-acetic acid (a free Ca²⁺ chelator, 1 mM) or U73122 (an inhibitor of phospholipase C, 1 μM), control and FGF-23-treated fibroblasts exhibited similar proliferative and migratory abilities. Moreover, polymerase chain reaction analysis revealed that atrial fibroblasts abundantly expressed FGF receptor 1 but lacked expressions of FGF receptors 2-4. FGF-23 significantly increased the phosphorylation of FGF receptor 1. Treatment with PD166866 (an antagonist of FGF receptor 1, 1 μM) attenuated the effects of FGF-23 on cardiac fibroblast activity. In conclusion, FGF-23 may activate FGF receptor 1 and subsequently phospholipase C/IP₃ signaling pathway, leading to an upregulation of Orai1 and/or TRPC1-mediated Ca²⁺ entry and thus enhancing human atrial fibroblast activity.     

Doxorubicin-Induced Fetal Mesangial Cell Death Occurs Independently of TRPC6 Channel Upregulation but Involves Mitochondrial Generation of Reactive Oxygen Species

Doxorubicin (DOX), a category D pregnancy drug, is a chemotherapeutic agent that has been shown in animal studies to induce fetal toxicity, including renal abnormalities. Upregulation of the transient receptor potential cation (TRPC) 6 channel is involved in DOX-induced podocyte apoptosis. We have previously reported that TRPC6-mediated Ca²⁺ signaling promotes neonatal glomerular mesangial cell (GMC) death. However, it is unknown whether DOX alters mesangial TRPC expression or viability in the fetus. In this study, cell growth was tracked in control and DOX-treated primary GMCs derived from fetal pigs. Live-cell imaging demonstrated that exposure to DOX inhibited the proliferation of fetal pig GMCs and induced cell death. DOX did not alter the TRPC3 expression levels. By contrast, TRPC6 protein expression in the cells was markedly reduced by DOX. DOX treatment also attenuated the TRPC6-mediated intracellular Ca²⁺ elevation. DOX stimulated mitochondrial reactive oxygen species (mtROS) generation and mitophagy by the GMCs. The DOX-induced mtROS generation and apoptosis were reversed by the mitochondria-targeted antioxidant mitoquinone. These data suggest that DOX-induced fetal pig GMC apoptosis is independent of TRPC6 channel upregulation but requires mtROS production. The mtROS-dependent GMC death may contribute to DOX-induced fetal nephrotoxicity when administered prenatally.     

Cerium-doped calcium phosphates precipitated on bacterial cellulose platform by mineralization

Bacterial cellulose (BC) membranes biosynthesized by Komagataeibacter rhaeticus AF1 strain were used as a platform for precipitating cerium-doped calcium phosphates (Ce:CaP), which were synthetized by successive soaking of BC membranes in solutions containing Ca²⁺, PO₄³⁻ and Ce³⁺ precursor ions. After obtaining the as-prepared composites, BC-Ce:CaP was submitted to a thermal treatment at 600 °C for 3 h, and Ce:CaP was characterized by scanning electronic microscopy (SEM), energy dispersive X-ray spectrometry (EDX), thermogravimetric analysis (TG), derivative thermogravimetric analysis (DTG) and X-ray diffraction (XRD). Ce:CaP presented hydroxyapatite, chlorapatite and buchwaldite (sodium calcium phosphate) phases and revealed a trabecular structure composed per nanowires with interconnected pores. Furthermore, BC-Ce:CaP and Ce:CaP show cell viability and has been suggested for use as a mineral scaffold.     

Transformation of Brushite (CaHPO4·2H2O) to Whitlockite (Ca9Mg(HPO4)(PO4)6) or Other CaPs in Physiologically Relevant Solutions

Brushite (dicalcium phosphate dihydrate, DCPD, CaHPO₄·2H₂O) and whitlockite [WH, Ca₉Mg(HPO₄)(PO₄)₆] are usually found in the mammalian metabolism in the form of diverse pathological calcifications, dental calculi, urinary tract stones, salivary gland deposits, cardiovascular or pulmonary calcified deposits, and even as prostate or cartilage calcifications. The hydrothermal transformation of synthetic brushite crystals into single‐phase whitlockite, octacalcium phosphate, or apatitic calcium phosphate was observed over the time period of 1 to 21 d and at 37°C, 70°C, and 115°C in nonstirred physiologically relevant solutions developed for this work. The strong influence of the physiologically relevant ions such as Mg²⁺ and HCO₃^? on hydrothermal transformations is exposed. The formation of the nanoglobules and nanofibrils of X‐ray amorphous calcium phosphate or Mg‐doped calcium phosphate on the surfaces of brushite crystals are observed for the first time in biomimetic solutions containing 10 mm Mg²⁺ and/or 27 mm HCO₃^?. The experimental conditions leading to the formation of such nanofibrils on brushite crystal surfaces are also found to stop the further transformation of brushite into any other calcium phosphate (CaP) phases even at high solution temperatures. Samples were characterized by scanning electron microscopy and powder X‐ray diffraction.     

When Isolated at Full Receptivity,in Vitro Fertilized Wheat (Triticum aestivum,L.) Egg Cells Reveal [Ca2+]cyt Oscillation of Intracellular Origin

During in vitro fertilization of wheat (Triticum aestivum, L.) in egg cells isolated at various developmental stages, changes in cytosolic free calcium ([Ca²⁺]_cyt) were observed. The dynamics of [Ca²⁺]_cyt elevation varied, reflecting the difference in the developmental stage of the eggs used. [Ca²⁺]_cyt oscillation was exclusively observed in fertile, mature egg cells fused with the sperm cell. To determine how [Ca²⁺]_cyt oscillation in mature egg cells is generated, egg cells were incubated in thapsigargin, which proved to be a specific inhibitor of the endoplasmic reticulum (ER) Ca²⁺-ATPase in wheat egg cells. In unfertilized egg cells, the addition of thapsigargin caused an abrupt transient increase in [Ca²⁺]_cyt in the absence of extracellular Ca²⁺, suggesting that an influx pathway for Ca²⁺ is activated by thapsigargin. The [Ca²⁺]_cyt oscillation seemed to require the filling of an intracellular calcium store for the onset of which, calcium influx through the plasma membrane appeared essential. This was demonstrated by omitting extracellular calcium from (or adding GdCl₃ to) the fusion medium, which prevented [Ca²⁺]_cyt oscillation in mature egg cells fused with the sperm. Combined, these data permit the hypothesis that the first sperm-induced transient increase in [Ca²⁺]_cyt depletes an intracellular Ca²⁺ store, triggering an increase in plasma membrane Ca²⁺ permeability, and this enhanced Ca²⁺ influx results in [Ca²⁺]_cyt oscillation.     

Synthesis and characterisation of nanophase hydroxyapatite co-substituted with strontium and zinc

In order to develop new bioactive calcium phosphate (CaP) materials to repair bone defects, it is important to ensure these materials more closely mimic the non-stoichiometric nature of biological hydroxyapatite (HA). Typically, biological HA combines various CaP phases with different impurity ions, which substitute within the HA lattice, including strontium (Sr²⁺), zinc (Zn²⁺), magnesium (Mg²⁺), carbonate (CO₃^2-) and fluoride (F^-), but to name a few. In addition to this biological HA have dimensions in the nanometre (nm) range, usually 60?nm in length by 5–20?nm wide. Both the effects of ion substitution and the nano-size crystals are seen as important factors for enhancing their potential biofunctionality. The driving hypothesis was to successfully synthesise nanoscale hydroxyapatite (nHA), co-substituted with strontium (Sr²⁺) and zinc (Zn²⁺) ions in varying concentrations using an aqueous precipitation method and to understand their chemical and physical properties. The materials were characterised using Fourier Transform Infrared Spectroscopy (FTIR), X-Ray Diffraction (XRD), X-Ray Photoelectron Spectroscopy (XPS) and Transmission Electron Microscopy (TEM) techniques. The FTIR, XRD and XPS results confirmed that the nHA was successfully co-substituted with Sr²⁺ and Zn²⁺, replacing Ca²⁺ within the nHA lattice at varying concentrations. The FTIR results confirmed that all of the samples were carbonated, with a significant loss of hydroxylation as a consequence of the incorporation of Sr²⁺ and Zn²⁺ into the nHA lattice. The TEM results showed that each sample produced was nano-sized, with the Sr/Zn-10%nHA having the smallest sized crystals approximately 17.6 ± 3.3?nm long and 10.2 ± 1.4?nm wide. None of the materials synthesised here in this study contained any other impurity CaP phases. Therefore, this study has shown that co-substituted nHA can be prepared, and that the degree of substitution (and the substituting ion) can have a profound effect on the attendant materials’ properties.     

Crosstalk among Calcium ATPases: PMCA,SERCA and SPCA in Mental Diseases

Calcium in mammalian neurons is essential for developmental processes, neurotransmitter release, apoptosis, and signal transduction. Incorrectly processed Ca²⁺ signal is well-known to trigger a cascade of events leading to altered response to variety of stimuli and persistent accumulation of pathological changes at the molecular level. To counterbalance potentially detrimental consequences of Ca²⁺, neurons are equipped with sophisticated mechanisms that function to keep its concentration in a tightly regulated range. Calcium pumps belonging to the P-type family of ATPases: plasma membrane Ca²⁺-ATPase (PMCA), sarco/endoplasmic Ca²⁺-ATPase (SERCA) and secretory pathway Ca²⁺-ATPase (SPCA) are considered efficient line of defense against abnormal Ca²⁺ rises. However, their role is not limited only to Ca²⁺ transport, as they present tissue-specific functionality and unique sensitive to the regulation by the main calcium signal decoding protein—calmodulin (CaM). Based on the available literature, in this review we analyze the contribution of these three types of Ca²⁺-ATPases to neuropathology, with a special emphasis on mental diseases.     

Na+/H+ Exchangers Involve in Regulating the pH-Sensitive Ion Channels in Mouse Sperm

Sperm-specific K⁺ ion channel (KSper) and Ca²⁺ ion channel (CatSper), whose elimination causes male infertility in mice, determine the membrane potential and Ca²⁺ influx, respectively. KSper and CatSper can be activated by cytosolic alkalization, which occurs during sperm going through the alkaline environment of the female reproductive tract. However, which intracellular pH (pH_i) regulator functionally couples to the activation of KSper/CatSper remains obscure. Although Na⁺/H⁺ exchangers (NHEs) have been implicated to mediate pH_i in sperm, there is a lack of direct evidence confirming the functional coupling between NHEs and KSper/CatSper. Here, 5-(N,N-dimethyl)-amiloride (DMA), an NHEs inhibitor that firstly proved not to affect KSper/CatSper directly, was chosen to examine NHEs function on KSper/CatSper in mouse sperm. The results of patch clamping recordings showed that, when extracellular pH was at the physiological level of 7.4, DMA application caused KSper inhibition and the depolarization of membrane potential when pipette solutions were not pH-buffered. In contrast, these effects were minimized when pipette solutions were pH-buffered, indicating that they solely resulted from pH_i acidification caused by NHEs inhibition. Similarly, DMA treatment reduced CatSper current and intracellular Ca²⁺, effects also dependent on the buffer capacity of pH in pipette solutions. The impairment of sperm motility was also observed after DMA incubation. These results manifested that NHEs activity is coupled to the activation of KSper/CatSper under physiological conditions.     

More Than Just Simple Interaction between STIM and Orai Proteins: CRAC Channel Function Enabled by a Network of Interactions with Regulatory Proteins

The calcium-release-activated calcium (CRAC) channel, activated by the release of Ca²⁺ from the endoplasmic reticulum (ER), is critical for Ca²⁺ homeostasis and active signal transduction in a plethora of cell types. Spurred by the long-sought decryption of the molecular nature of the CRAC channel, considerable scientific effort has been devoted to gaining insights into functional and structural mechanisms underlying this signalling cascade. Key players in CRAC channel function are the Stromal interaction molecule 1 (STIM1) and Orai1. STIM1 proteins span through the membrane of the ER, are competent in sensing luminal Ca²⁺ concentration, and in turn, are responsible for relaying the signal of Ca²⁺ store-depletion to pore-forming Orai1 proteins in the plasma membrane. A direct interaction of STIM1 and Orai1 allows for the re-entry of Ca²⁺ from the extracellular space. Although much is already known about the structure, function, and interaction of STIM1 and Orai1, there is growing evidence that CRAC under physiological conditions is dependent on additional proteins to function properly. Several auxiliary proteins have been shown to regulate CRAC channel activity by means of direct interactions with STIM1 and/or Orai1, promoting or hindering Ca²⁺ influx in a mechanistically diverse manner. Various proteins have also been identified to exert a modulatory role on the CRAC signalling cascade although inherently lacking an affinity for both STIM1 and Orai1. Apart from ubiquitously expressed representatives, a subset of such regulatory mechanisms seems to allow for a cell-type-specific control of CRAC channel function, considering the rather restricted expression patterns of the specific proteins. Given the high functional and clinical relevance of both generic and cell-type-specific interacting networks, the following review shall provide a comprehensive summary of regulators of the multilayered CRAC channel signalling cascade. It also includes proteins expressed in a narrow spectrum of cells and tissues that are often disregarded in other reviews of similar topics.     

Systematic Review of Calcium Channels and Intracellular Calcium Signaling: Relevance to Pesticide Neurotoxicity

Pesticides of different chemical classes exert their toxic effects on the nervous system by acting on the different regulatory mechanisms of calcium (Ca²⁺) homeostasis. Pesticides have been shown to alter Ca²⁺ homeostasis, mainly by increasing its intracellular concentration above physiological levels. The pesticide-induced Ca²⁺ overload occurs through two main mechanisms: the entry of Ca²⁺ from the extracellular medium through the different types of Ca²⁺ channels present in the plasma membrane or its release into the cytoplasm from intracellular stocks, mainly from the endoplasmic reticulum. It has also been observed that intracellular increases in the Ca²⁺ concentrations are maintained over time, because pesticides inhibit the enzymes involved in reducing its levels. Thus, the alteration of Ca²⁺ levels can lead to the activation of various signaling pathways that generate oxidative stress, neuroinflammation and, finally, neuronal death. In this review, we also discuss some proposed strategies to counteract the detrimental effects of pesticides on Ca²⁺ homeostasis.     

Abnormal Ca2+ Signals in Reactive Astrocytes as a Common Cause of Brain Diseases

In pathological brain conditions, glial cells become reactive and show a variety of responses. We examined Ca²⁺ signals in pathological brains and found that reactive astrocytes share abnormal Ca²⁺ signals, even in different types of diseases. In a neuropathic pain model, astrocytes in the primary sensory cortex became reactive and showed frequent Ca²⁺ signals, resulting in the production of synaptogenic molecules, which led to misconnections of tactile and pain networks in the sensory cortex, thus causing neuropathic pain. In an epileptogenic model, hippocampal astrocytes also became reactive and showed frequent Ca²⁺ signals. In an Alexander disease (AxD) model, hGFAP-R239H knock-in mice showed accumulation of Rosenthal fibers, a typical pathological marker of AxD, and excessively large Ca²⁺ signals. Because the abnormal astrocytic Ca²⁺ signals observed in the above three disease models are dependent on type II inositol 1,4,5-trisphosphate receptors (IP₃RII), we reanalyzed these pathological events using IP₃RII-deficient mice and found that all abnormal Ca²⁺ signals and pathologies were markedly reduced. These findings indicate that abnormal Ca²⁺ signaling is not only a consequence but may also be greatly involved in the cause of these diseases. Abnormal Ca²⁺ signals in reactive astrocytes may represent an underlying pathology common to multiple diseases.     

Activation of Cx43 Hemichannels Induces the Generation of Ca2+ Oscillations in White Adipocytes and Stimulates Lipolysis

The aim of the study was to investigate the mechanisms of Ca²⁺ oscillation generation upon activation of connexin-43 and regulation of the lipolysis/lipogenesis balance in white adipocytes through vesicular ATP release. With fluorescence microscopy it was revealed that a decrease in the concentration of extracellular calcium ([Ca²⁺]_ex) results in two types of Ca²⁺ responses in white adipocytes: Ca²⁺ oscillations and transient Ca²⁺ signals. It was found that activation of the connexin half-channels is involved in the generation of Ca²⁺ oscillations, since the blockers of the connexin hemichannels—carbenoxolone, octanol, proadifen and Gap26—as well as Cx43 gene knockdown led to complete suppression of these signals. The activation of Cx43 in response to the reduction of [Ca²⁺]_ex was confirmed by TIRF microscopy. It was shown that in response to the activation of Cx43, ATP-containing vesicles were released from the adipocytes. This process was suppressed by knockdown of the Cx43 gene and by bafilomycin A1, an inhibitor of vacuolar ATPase. At the level of intracellular signaling, the generation of Ca²⁺ oscillations in white adipocytes in response to a decrease in [Ca²⁺]_ex occurred due to the mobilization of the Ca²⁺ ions from the thapsigargin-sensitive Ca²⁺ pool of IP₃R as a result of activation of the purinergic P2Y1 receptors and phosphoinositide signaling pathway. After activation of Cx43 and generation of the Ca²⁺ oscillations, changes in the expression levels of key genes and their encoding proteins involved in the regulation of lipolysis were observed in white adipocytes. This effect was accompanied by a decrease in the number of adipocytes containing lipid droplets, while inhibition or knockdown of Cx43 led to inhibition of lipolysis and accumulation of lipid droplets. In this study, we investigated the mechanism of Ca²⁺ oscillation generation in white adipocytes in response to a decrease in the concentration of Ca²⁺ ions in the external environment and established an interplay between periodic Ca²⁺ modes and the regulation of the lipolysis/lipogenesis balance.     

Macrophage Polarization Related to Crystal Phases of Calcium Phosphate Biomaterials

Calcium phosphate (CaP) materials influence macrophage polarization during bone healing. However, the effect of the crystal phase of CaP materials on the immune response of bone remains unclear. In this study, the effect of the crystal phases of CaP materials on the regulation of macrophage polarization was investigated. Human THP-1 cells and mouse RAW 264 cells were cultured with octacalcium phosphate (OCP) and its hydrolyzed form Ca-deficient hydroxyapatite to assess the expression of pro-inflammatory M1 and anti-inflammatory M2 macrophage-related genes. OCP inhibited the excessive inflammatory response and switched macrophages to the anti-inflammatory M2 phenotype, which promoted the expression of the interleukin 10 (IL10) gene. In contrast, HL stimulated an excessive inflammatory response by promoting the expression of pro-inflammatory M1 macrophage-related genes. To observe changes in the microenvironment induced by OCP and HL, inorganic phosphate (Pi) and calcium ion (Ca²⁺) concentrations and pH value in the medium were measured. The expression of the pro-inflammatory M1 macrophage-related genes (tumor necrosis factor alpha (TNFα) and interlukin 1beta (IL1β)) was closely related to the increase in ion concentration caused by the increase in the CaP dose. Together, these results suggest that the microenvironment caused by the crystal phase of CaP materials may be involved in the immune-regulation capacity of CaP materials.     

Synthesis and Characterization of a Specific Iodine-125-Labeled TRPC5 Radioligand

The nonselective Ca²⁺-permeable transient receptor potential channel subfamily member 5 (TRPC5) belongs to the transient receptor potential canonical (TRPC) superfamily and is widely expressed in the brain. Compelling evidence reveals that TRPC5 plays crucial roles in depression and other psychiatric disorders. To develop a TRPC5 radioligand, following up on our previous effort, we synthesized the iodine compound TZ66127 and its iodine-125-labeled counterpart [¹²⁵I]TZ66127. The synthesis of TZ66127 was achieved by replacing chloride with iodide in the structure of HC608, and the [¹²⁵I]TZ66127 was radiosynthesized using its corresponding tributylstannylated precursor. We established a stable human TRPC5-overexpressed HEK293-hTRPC5 cell line and performed Ca²⁺ imaging and a cell-binding assay study of TZ66127; these indicated that TZ66127 had good inhibition activity for TRPC5, and the inhibitory efficiency of TZ66127 toward TRPC5 presented in a dose-dependent manner. An in vitro autoradiography and immunohistochemistry study of rat brain sections suggested that [¹²⁵I]TZ66127 had binding specificity toward TRPC5. Altogether, [¹²⁵I]TZ66127 has high potential to serve as a radioligand for screening the binding activity of other new compounds toward TRPC5. The availability of [¹²⁵I]TZ66127 might facilitate the development of therapeutic drugs and PET imaging agents that target TRPC5.     

Strontium and zinc co-substituted nanophase hydroxyapatite

It is well documented that biological hydroxyapatite (HA) differs from pure and synthetically produced HA, and contains of a mixture of calcium phosphate (CaP) phases in addition to a range of impurity ions, such as strontium (Sr²⁺), zinc (Zn²⁺), magnesium (Mg²⁺), fluoride (F^-) and carbonate(CO₃^2-), but to name a few. Further to this, biological apatite is generally in the form of rod (or needle-like) crystals in the nanometre (nm) size range, typically 60 nm in length by 5–20 nm wide. In this study, a range of nano-hydroxyapatite (nHA), substituted nHA materials and co-substituted nHA (based on Sr²⁺ and Zn²⁺) were manufactured using an aqueous precipitation method. Sr²⁺ and Zn²⁺ were chosen due to the significant performance enhancements that these substitutions can deliver. The materials were then characterised using Fourier Transform Infrared Spectroscopy (FTIR), X-Ray Diffraction (XRD), X-Ray Photoelectron Spectroscopy (XPS) and Transmission Electron Microscopy (TEM) techniques. The TEM results show that all of the samples produced were nano-sized, with Zn-substituted nHA being the smallest crystals around 27 nm long and 8 nm wide. The FTIR, XRD and XPS results all confirm that the materials had undergone substitution with either Sr²⁺ and Zn²⁺, for Ca²⁺ within the HA lattice (or both in the case of the co-substituted materials). The FTIR results confirmed that all of the samples were carbonated, with a significant loss of hydroxylation as a consequence of the incorporation of Sr²⁺ and Zn²⁺ into the HA lattice. None of the materials synthesised here in this study contained any other impurity CaP phases. Therefore this study has shown that substituted and co-substituted nanoscale apatites can be prepared, and that the degree of substitution (and the substituting ion) can have a profound effect of the attendant materials’ properties.     

Calcium oxalate crystallization in silica and sugar solutions-characterization of crystal phases and habits

The effects of silica (SiO₂) and sugar on the crystallographic and morphological properties of calcium oxalate (CaOx) have been investigated using instrumental techniques including X-ray powder diffraction (XRD) and scanning electron microscopy (SEM). Addition of SiO₂ or sugar in a CaOx crystallization system promoted the formation of COT (calcium oxalate trihydrate) and COD (calcium oxalate dihydrate), respectively, and modified the crystal size and habit of COM (calcium oxalate monohydrate) crystals, the extent of which was dependent on the concentrations of SiO₂ and sugar. A variety of mechanisms including electrostatic effects, geometrical matching and stereochemical compatibility between CaOx crystallites and polymeric SiO₂/sucrose molecules have been proposed.