Function Of Ca2 Research Articles

Structure-properties correlations in low-methylated pectin hydrogels and aerogels crosslinked by divalent ions

In this paper, structure-properties relationship between ionically crosslinked pectin hydrogels and aerogels is drawn, by focusing the study on the small amount of added cationic crosslinkers. Through this strategy and by coupling results from rheology and nanostructure of the gels provided by small-angle X-ray scattering, the early stages of the formation of ionic crosslinking junction zones are observed. Furthermore, as a major predictor of the samples' ability to resist linear shrinkage upon solvent exchange and supercritical drying processes, the gel-state (and thus rheological properties) emerges as a key element. Interestingly, after reaching a high enough crosslinking Ca2+-concentration to result in gelation, the average number of monomer segments between crosslinking points saturates as a function of Ca2+-concentration, while the size of the individual crosslinking junction zones continues to increase. When comparing the final characteristics of the supercritically-dried aerogels to these structural features of the cation-crosslinked hydrogels, crosslinking density of the hydrogels is observed to play a critical role.

Ca2+ Signaling in Cardiovascular Fibroblasts.

Fibrogenesis is a physiological process required for wound healing and tissue repair. It is induced by activation of quiescent fibroblasts, which first proliferate and then change their phenotype into migratory, contractile myofibroblasts. Myofibroblasts secrete extracellular matrix proteins, such as collagen, to form a scar. Once the healing process is terminated, most myofibroblasts undergo apoptosis. However, in some tissues, such as the heart, myofibroblasts remain active and sensitive to neurohumoral factors and inflammatory mediators, which lead eventually to excessive organ fibrosis. Many cellular processes involved in fibroblast activation, including cell proliferation, protein secretion and cell contraction, are highly regulated by intracellular Ca2+ signals. This review summarizes current research on Ca2+ signaling pathways underlying fibroblast activation. We present receptor- and ion channel-mediated Ca2+ signaling pathways, discuss how localized Ca2+ signals of the cell nucleus may be involved in fibroblast activation and present Ca2+-sensitive transcription pathways relevant for fibroblast biology. When investigated, we highlight how the function of Ca2+-handling proteins changes during cardiac and pulmonary fibrosis. Many aspects of Ca2+ signaling remain unexplored in different types of cardiovascular fibroblasts in relation to pathologies, and a better understanding of Ca2+ signaling in fibroblasts will help to design targeted therapies against fibrosis.

Optimizing a machine learning design of dielectric properties in lead-free piezoelectric ceramics

Designing lead-free piezoelectric ceramics with tailored electrical properties remains a critical challenge for various applications. In this paper we present a novel methodology integrating Machine Learning (ML) and optimization procedures to fine-tune electrical properties in lead-free (1-x) Na0.5 Bi0.5 TiO3 - x CaTiO3 piezoelectric ceramics. A comprehensive dataset of dielectric measurements serves as the foundation for training ML models that accurately predict the permittivity (ε′) and dielectric loss (tan δ) as functions of Ca2+ concentration (x % Ca), temperature and frequency. Two ML techniques are evaluated: random forest regression, and Multi-Layer Perceptron neural network Regression (MLPR). The MLPR model exhibited a superior regression performance, achieving a correlation coefficient of 0.931 and a root mean squared error of 0.029. The MLPR was then optimized by the Non-dominated Sorting Genetic Algorithm II (NSGA-II) to maximizes ε′ while minimizes tan δ. Within the NSGA-II framework, the optimal values were found at the Pareto curve knee, corresponding to a frequency, temperature, and x % Ca of 609.739 kHz, 398.15 K, and 6.10, respectively, resulting in ε′ equal to 857.87 and tan δ equal to 0.0120. This approach demonstrates the effectiveness of combining ML and optimization for designing the electrical properties of piezoelectric ceramics, paving the way for more efficient and targeted material development.

Calcium Influx Pathways in Breast Cancer: Opportunities for Pharmacological Intervention

Numerous cellular processes, including the release of neurotransmitters and the contraction of muscles, are largely triggered and regulated by Ca2+ inflow via Ca2+ permeable ion channels. In addition, Ca2+ influx regulates cellular migration and proliferation, two mechanisms linked to cancer. This study focuses on calcium influx in breast cancer cells and discusses how future drugs for breast cancer therapy may be pharmacological modulators of particular Ca2+ influx channels. Certain breast tumors have altered expression of particular calcium permeable ion channels. Such alterations may occasionally be connected to the prognosis and subtype of breast cancer. These days, models both in vivo and in vitro have assisted in identifying particular Ca2+ channels that are crucial for the growth and invasiveness of of cancerous breast cells. Nonetheless, additional research is still needed to fully understand several features of Ca2+ influx in breast cancer. These include figuring out the processes behind the changed expression and the best treatment plan to target breast cancer cells via particular Ca2+ channels. In the upcoming ten years, research should concentrate on the function of Ca2+ influx in mechanisms other than the migration and proliferation of breast cancer cells.

Pharmacological Therapeutic Potential in Breast Cancer through Calcium Influx Pathways

Numerous cellular processes, including the release of neurotransmitters and the contraction of muscles, are largely triggered and regulated by Ca2+ inflow via Ca2+ permeable ion channels. In addition, Ca2+ influx regulates cellular migration and proliferation, two mechanisms linked to cancer. This study focuses on calcium influx in breast cancer cells and discusses how future drugs for breast cancer therapy may be pharmacological modulators of particular Ca2+ influx channels. Certain breast tumors have altered expression of particular calcium permeable ion channels. Such alterations may occasionally be connected to the prognosis and subtype of breast cancer. These days, models both in vivo and in vitro have assisted in identifying particular Ca2+ channels that are crucial for the growth and invasiveness of cancerous breast cells. Nonetheless, additional research is still needed to fully understand several features of Ca2+ influx in breast cancer. These include figuring out the processes behind the changed expression and the best treatment plan to target breast cancer cells via particular Ca2+ channels. In the upcoming ten years, research should concentrate on the function of Ca2+ influx in mechanisms other than the migration and proliferation of breast cancer cells

Near-Infrared Laser Irradiation-Modulated High-Temperature Solid-Contact Ion-Selective Electrodes: Potentiometric Detection of Ca2+ in Seawater.

The high-temperature potentiometry operated by nonisothermal heating is a promising way to break through the traditional potentiometric responses of ion-selective electrodes (ISEs) at room temperature. Herein, a locally heated strategy through near-infrared region (NIR) laser irradiation upon the photothermal mesoporous carbon material placed between the ion-selective membrane and the glassy carbon substrate is introduced to obtain the high-temperature potentiometric performance of a solid-contact Ca2+-ISE for detection of Ca2+ in seawater. Based on the light-to-heat conversion of the mesoporous carbon-based solid contact, the temperature of the solid-contact Ca2+-ISE upon continuous NIR laser irradiation can be increased from room temperature to 60-70 °C, and the slope of the electrode is promoted up to about 30% according to the thermodynamic steady-state potentiometric response. The pulsed potentiometric response of the solid-contact Ca2+-ISE upon a pulsed NIR laser irradiation of 5 s also shows a linear change as a function of Ca2+ activities, and the improved slope from 27.1 ± 0.6 to 38.1 ± 0.9 mV/dec can be obtained under dual control of the temperature of the electrode and the transient current induced by the pulsed NIR laser irradiation. As compared to the traditional potentiometric measurement under zero-current conditions at room temperature, the NIR laser-modulated high-temperature potentiometric response provides an alternative way for measurement of the solid-contact ISEs.

Genome-Wide Identification of BrCAX Genes and Functional Analysis of BrCAX1 Involved in Ca2+ Transport and Ca2+ Deficiency-Induced Tip-Burn in Chinese Cabbage (Brassica rapa L. ssp. pekinensis).

Calcium (Ca2+) plays essential roles in plant growth and development. Ca2+ deficiency causes a physiological disorder of tip-burn in Brassiceae crops and is involved in the regulation of cellular Ca2+ homeostasis. Although the functions of Ca2+/H+ exchanger antiporters (CAXs) in mediating transmembrane transport of Ca2+ have been extensively characterized in multiple plant species, the potential roles of BrCAX genes remain unclear in Chinese cabbage. In this study, eight genes of the BrCAX family were genome-widely identified in Chinese cabbage. These BrCAX proteins contained conserved Na_Ca_ex domain and belonged to five members of the CAX family. Molecular evolutionary analysis and sequence alignment revealed the evolutionary conservation of BrCAX family genes. Expression profiling demonstrated that eight BrCAX genes exhibited differential expression in different tissues and under heat stress. Furthermore, Ca2+ deficiency treatment induced the typical symptoms of tip-burn in Chinese cabbage seedlings and a significant decrease in total Ca2+ content in both roots and leaves. The expression changes in BrCAX genes were related to the response to Ca2+ deficiency-induced tip-burn of Chinese cabbage. Specially, BrCAX1-1 and BrCAX1-2 genes were highly expressed gene members of the BrCAX family in the leaves and were significantly differentially expressed under Ca2+ deficiency stress. Moreover, overexpression of BrCAX1-1 and BrCAX1-2 genes in yeast and Chinese cabbage cotyledons exhibited a higher Ca2+ tolerance, indicating the Ca2+ transport capacity of BrCAX1-1 and BrCAX1-2. In addition, suppression expression of BrCAX1-1 and BrCAX1-2 genes reduced cytosolic Ca2+ levels in the root tips of Chinese cabbage. These results provide references for functional studies of BrCAX genes and to investigate the regulatory mechanisms underlying Ca2+ deficiency disorder in Brassiceae vegetables.

Cysteine-rich receptor-like protein kinases: emerging regulators of plant stress responses.

Cysteine-rich receptor-like kinases (CRKs) belong to a large DUF26-containing receptor-like kinase (RLK) family. They play key roles in immunity, abiotic stress response, and growth and development. How CRKs regulate diverse processes is a long-standing question. Recent studies have advanced our understanding of the molecular mechanisms underlying CRK functions in Ca2+ influx, reactive oxygen species (ROS) production, mitogen-activated protein kinase (MAPK) cascade activation, callose deposition, stomatal immunity, and programmed cell death (PCD). We review the CRK structure-function relationship with a focus on the roles of CRKs in immunity, the abiotic stress response, and the growth-stress tolerance tradeoff. We provide a critical analysis and synthesis of how CRKs control sophisticated regulatory networks that determine diverse plant phenotypic outputs.

Age-Dependent Changes in Calcium Regulation after Myocardial Ischemia–Reperfusion Injury

During aging, heart structure and function gradually deteriorate, which subsequently increases susceptibility to ischemia–reperfusion (IR). Maintenance of Ca2+ homeostasis is critical for cardiac contractility. We used Langendorff’s model to monitor the susceptibility of aging (6-, 15-, and 24-month-old) hearts to IR, with a specific focus on Ca2+-handling proteins. IR, but not aging itself, triggered left ventricular changes when the maximum rate of pressure development decreased in 24-month-olds, and the maximum rate of relaxation was most affected in 6-month-old hearts. Aging caused a deprivation of Ca2+-ATPase (SERCA2a), Na+/Ca2+ exchanger, mitochondrial Ca2+ uniporter, and ryanodine receptor contents. IR-induced damage to ryanodine receptor stimulates Ca2+ leakage in 6-month-old hearts and elevated phospholamban (PLN)-to-SERCA2a ratio can slow down Ca2+ reuptake seen at 2–5 μM Ca2+. Total and monomeric PLN mirrored the response of overexpressed SERCA2a after IR in 24-month-old hearts, resulting in stable Ca2+-ATPase activity. Upregulated PLN accelerated inhibition of Ca2+-ATPase activity at low free Ca2+ in 15-month-old after IR, and reduced SERCA2a content subsequently impairs the Ca2+-sequestering capacity. In conclusion, our study suggests that aging is associated with a significant decrease in the abundance and function of Ca2+-handling proteins. However, the IR-induced damage was not increased during aging.

Severe acute respiratory syndrome coronavirus-2 accessory proteins ORF3a and ORF7a modulate autophagic flux and Ca2+ homeostasis in yeast.

Virus infection involves the manipulation of key host cell functions by specialized virulence proteins. The Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) small accessory proteins ORF3a and ORF7a have been implicated in favoring virus replication and spreading by inhibiting the autophagic flux within the host cell. Here, we apply yeast models to gain insights into the physiological functions of both SARS-CoV-2 small open reading frames (ORFs). ORF3a and ORF7a can be stably overexpressed in yeast cells, producing a decrease in cellular fitness. Both proteins show a distinguishable intracellular localization. ORF3a localizes to the vacuolar membrane, whereas ORF7a targets the endoplasmic reticulum. Overexpression of ORF3a and ORF7a leads to the accumulation of Atg8 specific autophagosomes. However, the underlying mechanism is different for each viral protein as assessed by the quantification of the autophagic degradation of Atg8-GFP fusion proteins, which is inhibited by ORF3a and stimulated by ORF7a. Overexpression of both SARS-CoV-2 ORFs decreases cellular fitness upon starvation conditions, where autophagic processes become essential. These data confirm previous findings on SARS-CoV-2 ORF3a and ORF7a manipulating autophagic flux in mammalian cell models and are in agreement with a model where both small ORFs have synergistic functions in stimulating intracellular autophagosome accumulation, ORF3a by inhibiting autophagosome processing at the vacuole and ORF7a by promoting autophagosome formation at the ER. ORF3a has an additional function in Ca2+ homeostasis. The overexpression of ORF3a confers calcineurin-dependent Ca2+ tolerance and activates a Ca2+ sensitive FKS2-luciferase reporter, suggesting a possible ORF3a-mediated Ca2+ efflux from the vacuole. Taken together, we show that viral accessory proteins can be functionally investigated in yeast cells and that SARS-CoV-2 ORF3a and ORF7a proteins interfere with autophagosome formation and processing as well as with Ca2+ homeostasis from distinct cellular targets.

The C2 and PH domains of CAPS constitute an effective PI(4,5)P2-binding unit essential for Ca2+-regulated exocytosis

Ca2+-dependent activator proteins for secretion (CAPSs) are required for Ca2+-regulated exocytosis in neurons and neuroendocrine cells. CAPSs contain a pleckstrin homology (PH) domain that binds PI(4,5)P2-membrane. There is also a C2 domain residing adjacent to the PH domain, but its function remains unclear. In this study, we solved the crystal structure of the CAPS-1 C2PH module. The structure showed that the C2 and PH tandem packs against one another mainly via hydrophobic residues. With this interaction, the C2PH module exhibited enhanced binding to PI(4,5)P2-membrane compared with the isolated PH domain. In addition, we identified a new PI(4,5)P2-binding site on the C2 domain. Disruption of either the tight interaction between the C2 and PH domains or the PI(4,5)P2-binding sites on both domains significantly impairs CAPS-1 function in Ca2+-regulated exocytosis at the Caenorhabditis elegans neuromuscular junction (NMJ). These results suggest that the C2 and PH domains constitute an effective unit to promote Ca2+-regulated exocytosis.

Localization and expression of CRSH transcript, level of calcium ions, and cell cycle activity during Brassica napus L. seed development

Seeds are used as human food and animal feed, but the seed is also the onset of a new life. Therefore, seeds are a crucial agricultural product for global food security. Among several mechanisms involved in seed formation and maturation, the stringent response seems to be of great but rather overlooked significance. Plant homologs of bacterial RelA/SpoT proteins, called RSH, metabolize hyperphosphorylated regulatory nucleotides guanosine tetra- and pentaphosphate ((p)ppGpp, alarmones) which are involved in varied aspects of plant growth and development. The role of plant RSHs and alarmones in seed development remains elusive. In this study, the possible function of Ca2+-dependent RSH (CRSH) proteins during seed formation and maturation was verified. In silico analysis of plant CRSH proteins showed that EF-hand calcium-binding motif was highly conserved in monocotyledonous and dicotyledonous plants. Remarkably, this motif is present only in plant CRSH and has not been found in bacterial homologs. In developing Brassica napus (canola) seeds we analyzed the level and the localization of BnCRSH mRNAs by RT-qPCR and in situ localization, respectively. Further, we examined the cell cycle activity via flow cytometry, and the level of calcium ions using scanning electron microscopy. Our results showed that DNA replication intensity was at the highest level in seeds at the early stages of development, and then constantly decreased to the minimal level reached 70 days after flowering. In contrast, the level of calcium ions and BnCRSH transcript increased during canola seed maturation. The results of this study strongly suggest that calcium-dependent stringent response plays a significant role during canola seed development.

Comprehensive Sequence Analysis of Parvalbumins in Fish and Their Comparison with Parvalbumins in Tetrapod Species.

Parvalbumins are small molecules with important functions in Ca2+ signaling, but their sequence comparisons to date, especially in fish, have been relatively poor. We here, characterize sequence motifs that distinguish parvalbumin subfamilies across vertebrate species, as well as those that distinguish individual parvalbumins (orthologues) in fish, and map them to known parvalbumin structures. As already observed by others, all classes of jawed vertebrates possess parvalbumins of both the α-parvalbumin and oncomodulin subfamilies. However, we could not find convincing phylogenetic support for the common habit of classifying all non-α-parvalbumins together as "β-parvalbumins." In teleost (modern bony) fish, we here distinguish parvalbumins 1-to-10, of which the gene copy number can differ between species. The genes for α-parvalbumins (pvalb6 and pvalb7) and oncomodulins (pvalb8 and pvalb9) are well conserved between teleost species, but considerable variation is observed in their copy numbers of the non-α/non-oncomodulin genes pvalb1-to-5 and pvalb10. Teleost parvalbumins 1-to-4 are hardly distinguishable from each other and are highly expressed in muscle, and described allergens belong to this subfamily. However, in some fish species α-parvalbumin expression is also high in muscle. Pvalb5 and pvalb10 molecules form distinct lineages, the latter even predating the origin of teleosts, but have been lost in some teleost species. The present study aspires to be a frame of reference for future studies trying to compare different parvalbumins.

Phosphatase-independent role of phosphatase of regenerating liver in cancer progression.

Phosphatase of regenerating liver (PRL) is a family of protein tyrosine phosphatases (PTPs) that are anchored to the plasma membrane by prenylation. They are frequently overexpressed in various types of malignant cancers and their roles in cancer progression have received considerable attention. Mutational analyses of PRLs have shown that their intrinsic phosphatase activity is dispensable for tumor formation induced by PRL overexpression in a lung metastasis model using melanoma cells. Instead, PRLs directly bind to cyclin M (CNNM) Mg2+ exporters in the plasma membrane and potently inhibit their Mg2+ export activity, resulting in an increase in intracellular Mg2+ levels. Experiments using mammalian culture cells, mice, and C. elegans have collectively revealed that dysregulation of Mg2+ levels severely affects ATP and reactive oxygen species (ROS) levels as well as the function of Ca2+ -permeable channels. Moreover, PRL overexpression altered the optimal pH for cell proliferation from normal 7.5 to acidic 6.5, which is typically observed in malignant tumors. Here, we review the phosphatase-independent biological functions of PRLs, focusing on their interactions with CNNM Mg2+ exporters in cancer progression.

Ca(ClO)2 pretreatment enhancing suspended solids removal through flocculation from digested dairy wastewater and its mechanisms

Intensive animal farming produces large volume of digested liquid, and overdose application often causes the pollution of surface water and groundwater. Therefore, post-treatment is very necessary for the discharging of surplus digested liquid, but the removal of high concentrations of suspended solids (SS) in the digested liquid is a challenge. In this study, the effect of Ca(ClO)2 pretreatment on SS flocculation removal of digested dairy wastewater was investigated. The results showed that, without Ca(ClO)2 pretreatment, the flocculation by polyacrylamide (PAM), polyferric sulfate (PFS) or polymeric aluminum chloride (PAC) only removed 42.6 %–50.4 % SS from anaerobic digested liquid. With the combination of Ca(ClO)2 pretreatment and PAC flocculation together, the SS removal efficiency can reach 80 %. The total chemical oxygen demand (TCOD) removal had a similar trend with SS removal, but soluble chemical oxygen demand (SCOD) removal was less affected by the pretreatment and flocculation. More than 75 % of orthophosphate (SRP) and total soluble phosphorus (TSP) was removed after Ca(ClO)2 pretreatment and flocculation with PFS or PAC. Ca(ClO)2 pretreatment also effectively inactivated fecal bacteria. The mechanisms of Ca(ClO)2 pretreatment enhancing SS flocculation removal were further elucidated. The SS removal was the action of ClO− and Ca2+ together. The function of ClO− was to break down suspended particles, change the surface, and decrease the absolute Zeta potential, while the function of Ca2+ was to form precipitation. This result indicates that Ca(ClO)2 pretreatment can effectively enhance the SS flocculation removal of anaerobic digested liquid.

The functions of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in diabetes progression.

The increase in blood glucose causes a myriad of pathways and molecular components to malfunction, leading to diabetes. Diabetes affects each organ differently by activating distinct pathways. It has an impact on the liver, pancreas, kidney (nephropathy), eyes (retinopathy), and nervous system (neuropathy). Understanding the effects of diabetes on each organ is the first step in developing a sustained treatment for the disease. Among the many cellular molecules impacted by diabetes is Ca2+/calmodulin-dependent protein kinase II (CaMKII), a complex Ca2+/calmodulin-activated serine/threonine-protein kinase. When intracellular [Ca2+] rises, it binds to calmodulin (CaM) to produce Ca2+/CaM, which activates CaMKIIs. This factor is involved in the pancreas, liver, heart, muscles, and various organs. Thus, Understanding CaMKII action in each organ is critical for gaining a complete picture of diabetic complications. Therefore, this review covers CaMKII's functions in many organs and how it affects and has been affected by diabetes.

The C2 domains of dysferlin: roles in membrane localization, Ca2+ signalling and sarcolemmal repair.

Dysferlin is an integral membrane protein of the transverse tubules of skeletal muscle that is mutated or absent in limb girdle muscular dystrophy 2B and Miyoshi myopathy. Here we examine the role of dysferlin's seven C2 domains, C2A through C2G, in membrane repair and Ca2+ release, as well as in targeting dysferlin to the transverse tubules of skeletal muscle. We report that deletion of either domain C2A or C2B inhibits membrane repair completely, whereas deletion of C2C, C2D, C2E, C2F or C2G causes partial loss of membrane repair that is exacerbated in the absence of extracellular Ca2+ . Deletion of C2C, C2D, C2E, C2F or C2G also causes significant changes in Ca2+ release, measured as the amplitude of the Ca2+ transient before or after hypo-osmotic shock and the appearance of Ca2+ waves. Most deletants accumulate in endoplasmic reticulum. Only the C2A domain can be deleted without affecting dysferlin trafficking to transverse tubules, but Dysf-ΔC2A fails to support normal Ca2+ signalling after hypo-osmotic shock. Our data suggest that (i) every C2 domain contributes to repair; (ii) all C2 domains except C2B regulate Ca2+ signalling; (iii) transverse tubule localization is insufficient for normal Ca2+ signalling; and (iv) Ca2+ dependence of repair is mediated by C2C through C2G. Thus, dysferlin's C2 domains have distinct functions in Ca2+ signalling and sarcolemmal membrane repair and may play distinct roles in skeletal muscle. KEY POINTS: Dysferlin, a transmembrane protein containing seven C2 domains, C2A through C2G, concentrates in transverse tubules of skeletal muscle, where it stabilizes voltage-induced Ca2+ transients and participates in sarcolemmal membrane repair. Each of dysferlin's C2 domains except C2B regulate Ca2+ signalling. Localization of dysferlin variants to the transverse tubules is not sufficient to support normal Ca2+ signalling or membrane repair. Each of dysferlin's C2 domains contributes to sarcolemmal membrane repair. The Ca2+ dependence of membrane repair is mediated by C2C through C2G. Dysferlin's C2 domains therefore have distinct functions in Ca2+ signalling and sarcolemmal membrane repair.

Gravity induces asymmetric Ca2+ spikes in the root cap in the early stage of gravitropism

ABSTRACT Gravitropism is an important strategy for the adaptation of plants to the changing environment. Previous reports indicated that Ca2+ participated in plant gravity response. However, present information on the functions of Ca2+ in plant gravitropism was obtained mainly on coleoptiles, hypocotyls, and petioles, little is known about the dynamic changes of Ca2+ during root gravitropism. In the present study, the transgenic Arabidopsis thaliana R-GECO1 was placed horizontally and subsequently vertically on a refitted Leica SP8 laser scanning confocal microscopy with a vertical stage. Real-time observations indicated that gravistimulation induced not only an increase in the Ca2+ concentration, but also an accelerated occurrence of Ca2+ sparks in the root cap, especially in the lower side of the lateral root cap, indicating a strong tie between Ca2+ dynamics and gravistimulation during the early stage of root gravity response.

Nonmonotonic Coupled Dissolution‐Precipitation Reactions at the Mineral–Water Interface

AbstractDissolution is inherent to fluid‐mineral systems. Yet its impact on minerals reacting with electrolytes is overlooked. Here, a novel nonmonotonic behavior for the surface interactions of carbonates (calcite and Mg‐calcite) with organic acids is reported. Applying a bioinspired approach, Mg‐calcite sensors via amorphous precursors, avoiding any preconditioning with functional groups are synthesized. A quartz crystal microbalance is used to study the mass changes of the mineral on contact with organic acids under varying ionic conditions, temperatures, and flow velocities. Supported by confocal Raman microscopy and potentiometric titrations, nonmonotonous mass developments are found as a function of Ca2+concentration and flowrate, and attributed to three coupled chemical reactions: i) carbonate dissolution via Ca2+ion complexation with organic molecules, and the formation of organo‐calcium compounds as ii) a surface phase at the mineral–water interface, and iii) particles in the bulk fluid. These processes depend on local ion contents and the precipitation onset (i.e., saturation index) of organo‐calcium salts, both of which substantially differ in the bulk fluid and in the fluid boundary layer at mineral interfaces. This continuum between dissolution and precipitation provides a conceptual framework to address reactions at mineral interfacial across disciplines including biomineralization, ocean acidification and reservoir geochemistry.

L5-6 Spinal Nerve Ligation-induced Neuropathy Changes the Location and Function of Ca2+ Channels and Cdk5 and Affects the Compound Action Potential in Adjacent Intact L4 Afferent Fibers

Voltage-gated Ca2+ (CaV) channels regulate multiple cell processes, including neurotransmitter release, and have been associated with several pathological conditions, such as neuropathic pain. Cdk5, a neuron-specific kinase, may phosphorylate CaV channels, altering their functional expression. During peripheral nerve injury, upregulation of CaV channels and Cdk5 in the dorsal root ganglia (DRG) and the spinal cord, has been correlated with allodynia. We recently reported an increase in the amplitude of the C component of the compound action potential (cAP) of afferent fibers in animals with allodynia induced by L5-6 spinal nerve ligation (SNL), recorded in the corresponding dorsal roots. This was related to an increase in T-type (CaV3.2) channels generated by Cdk5-mediated phosphorylation. Here, we show that CaV channel functional expression is also altered in the L4 adjacent intact afferent fibers in rats with allodynia induced by L5-6 SNL. Western blot analysis showed that both Cdk5 and CaV3.2 total levels are not increased in the DRG L3-4, but their subcellular distribution changes by concentrating on the neuronal soma. Likewise, the Cdk5 inhibitor olomoucine affected the rapid and the slow C components of the cAP recorded in the dorsal roots. Patch-clamp recordings revealed an increase in T- and N-type currents recorded in the soma of acute isolated L3-4 sensory neurons after L5-6 SNL, which was prevented by olomoucine. These findings suggest changes in CaV channels location and function in L3-4 afferent fibers associated with Cdk5-mediated phosphorylation after L5-6 SNL, which may contribute to nerve injury-induced allodynia.