Calcium Movements Research Articles

Studying Drosophila Larval Behavior in Agarose Channels.

Larvae of the fruit fly Drosophila melanogaster are a popular and tractable model system for studying the development and function of sensorimotor circuits, thanks to the relative numerical simplicity of their nervous system and the wealth of available genetic tools to manipulate the anatomy, activity, and function of specific cell types. Researchers studying the role of a particular gene or cell type in sensorimotor circuit activity or function may wish to observe the effects of an experimental manipulation during behavior in the intact animal. Observing these effects, which may include changes in the intracellular calcium concentration or movement of small numbers of neurons, muscles, etc., typically requires high-spatial-resolution imaging, which poses several difficulties in the freely crawling larva. Freely crawling larvae can move quickly and with changeable heading, making manual or automatic tracking challenging; additionally, they may make three-dimensional movements, such as rearing, that can degrade imaging focus. These challenges are potentially solvable using advanced imaging and algorithmic tracking setups, but cost, space, or development time may be prohibitive. This protocol describes a simple and cost-effective method for placing larvae inside agarose channels, thereby restricting larval crawling to a single dimension and enabling higher-magnification time-series imaging of fluorescently labeled structures during many cycles of locomotion. By using larvae that express fluorescent calcium indicators in cells of interest, researchers can apply this method to study the effects of experimental manipulations on neural or muscular activity during behavior in the intact animal.

Role of Divalent Cations in Infections in Host-Pathogen Interaction.

With increasing numbers of patients worldwide diagnosed with diabetes mellitus, renal disease, and iatrogenic immune deficiencies, an increased understanding of the role of electrolyte interactions in mitigating pathogen virulence is necessary. The levels of divalent cations affect host susceptibility and pathogen survival in persons with relative immune insufficiency. For instance, when host cellular levels of calcium are high compared to magnesium, this relationship contributes to insulin resistance and triples the risk of clinical tuberculosis. The movement of divalent cations within intracellular spaces contributes to the host defense, causing apoptosis or autophagy of the pathogen. The control of divalent cation flow is dependent in part upon the mammalian natural resistance-associated macrophage protein (NRAMP) in the host. Survival of pathogens such as M tuberculosis within the bronchoalveolar macrophage is also dependent upon NRAMP. Pathogens evolve mutations to control the movement of calcium through external and internal channels. The host NRAMP as a metal transporter competes for divalent cations with the pathogen NRAMP in M tuberculosis (whether in latent, dormant, or active phase). This review paper summarizes mechanisms of pathogen offense and patient defense using inflow and efflux through divalent cation channels under the influence of parathyroid hormone vitamin D and calcitonin.

Leveraging Quantitative Systems Pharmacology and Artificial Intelligence to advance treatment of Chronic Kidney Disease Mineral Bone Disorder.

Chronic kidney disease mineral bone disorder (CKD-MBD) is a complex clinical syndrome responsible for the accelerated cardiovascular mortality seen in individuals afflicted with CKD. Current approaches to therapy have failed to improve clinical outcomes adequately, likely due to targeting surrogate biochemical parameters as articulated by the guideline developer, KDIGO (Kidney Disease: Improving Global Outcomes). We hypothesized that using a Systems Biology Approach combining machine learning with mathematical modeling, we could test a novel approach to therapy targeting the abnormal movement of mineral out of bone and into soft tissue that is characteristic of CKD-MBD. The mathematical model describes the movement of calcium and phosphate between body compartments in response to standard therapeutic agents. The machine learning technique we applied is Reinforcement Learning (RL). We compared calcium, phosphate, PTH, and mineral movement out of bone and into soft tissue under four scenarios: standard approach (KDIGO), achievement of KDIGO guidelines using RL (RLKDIGO), targeting abnormal mineral flux (RLFLUX), and combining achievement of KDIGO guidelines with minimization of abnormal mineral flux (RLKDIGOFLUX). We demonstrate through simulations that explicitly targeting abnormal mineral flux significantly decreases abnormal mineral movement compared to standard approach while achieving acceptable biochemical outcomes. These investigations highlight the limitations of current therapeutic targets, primarily secondary hyperparathyroidism, and emphasize the central role of deranged phosphate homeostasis in the genesis of the CKD-MBD syndrome.

Lipid Toxicity in the Cardiovascular-Kidney-Metabolic Syndrome (CKMS).

Recent studies of Cardiovascular-Kidney-Metabolic Syndrome (CKMS) indicate that elevated concentrations of derivatives of phospholipids (ceramide, sphingosine), oxidized LDL, and lipoproteins (a, b) are toxic to kidney and heart function. Energy production for renal proximal tubule resorption of critical fuels and electrolytes is required for homeostasis. Cardiac energy for ventricular contraction/relaxation is preferentially supplied by long chain fatty acids. Metabolism of long chain fatty acids is accomplished within the cardiomyocyte cytoplasm and mitochondria by means of the glycolytic, tricarboxylic acid, and electron transport cycles. Toxic lipids and excessive lipid concentrations may inhibit cardiac function. Cardiac contraction requires calcium movement from the sarcoplasmic reticulum from a high to a low concentration at relatively low energy cost. Cardiac relaxation involves calcium return to the sarcoplasmic reticulum from a lower to a higher concentration and requires more energy consumption. Diastolic cardiac dysfunction occurs when cardiomyocyte energy conversion is inadequate. Diastolic dysfunction from diminished ATP availability occurs in the presence of inadequate blood pressure, glycemia, or lipid control and may lead to heart failure. Similar disruption of renal proximal tubular resorption of fuels/electrolytes has been found to be associated with phospholipid (sphingolipid) accumulation. Elevated concentrations of tissue oxidized low-density lipoprotein cholesterols are associated with loss of filtration efficiency at the level of the renal glomerular podocyte. Macroscopically excessive deposits of epicardial and intra-nephric adipose are associated with vascular pathology, fibrosis, and inhibition of essential functions in both heart and kidney. Chronic triglyceride accumulation is associated with fibrosis of the liver, cardiac and renal structures. Successful liver, kidney, or cardiac allograft of these vital organs does not eliminate the risk of lipid toxicity. Lipid lowering therapy may assist in protecting vital organ function before and after allograft transplantation.

Prenatal and early life lead exposure induced neurotoxicity.

Lead (Pb) has become a major environmental contaminant. There are several ways in which lead can enter the human body and cause toxic effects on human health. This review focuses on the impact of lead toxicity at prenatal and early life stages and its effect on neurodevelopment. Lead exposure to the developing foetus targets foetal neural stem cells. Hence, it has detrimental effects on developing neural and glial cells, adversely influencing cognition and behaviour. Lead has a profound influence on the movement of calcium ions (Ca2+), which can be attributed to most of the mechanisms by which lead affects neurodevelopment. There is no known safe threshold of lead exposure for children. Lead can affect foetal neurodevelopment leading to various neurological disorders, and neurotoxic effects on behavioural and cognitive outcomes. In this review, we discuss prenatal and early-life lead exposure, its mechanism, and consequences for neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease in later stages of life. This review further highlights the importance of lead exposure during pregnancy and lactation periods as well as early development of the child in understanding the extent of lead-induced neurological damage to the foetus/children and the associated future risks.

Calcium’s Role and Signaling in Aging Muscle, Cellular Senescence, and Mineral Interactions

Calcium research, since its pivotal discovery in the early 1800s through the heating of limestone, has led to the identification of its multi-functional roles. These include its functions as a reducing agent in chemical processes, structural properties in shells and bones, and significant role in cells relating to this review: cellular signaling. Calcium signaling involves the movement of calcium ions within or between cells, which can affect the electrochemical gradients between intra- and extracellular membranes, ligand binding, enzyme activity, and other mechanisms that determine cell fate. Calcium signaling in muscle, as elucidated by the sliding filament model, plays a significant role in muscle contraction. However, as organisms age, alterations occur within muscle tissue. These changes include sarcopenia, loss of neuromuscular junctions, and changes in mineral concentration, all of which have implications for calcium’s role. Additionally, a field of study that has gained recent attention, cellular senescence, is associated with aging and disturbed calcium homeostasis, and is thought to affect sarcopenia progression. Changes seen in calcium upon aging may also be influenced by its crosstalk with other minerals such as iron and zinc. This review investigates the role of calcium signaling in aging muscle and cellular senescence. We also aim to elucidate the interactions among calcium, iron, and zinc across various cells and conditions, ultimately deepening our understanding of calcium signaling in muscle aging.

Tumor Suppressor Candidate 2 (TUSC2): Discovery, Functions, and Cancer Therapy.

Tumor Suppressor Candidate 2 (TUSC2) was first discovered as a potential tumor suppressor gene residing in the frequently deleted 3p21.3 chromosomal region. Since its discovery, TUSC2 has been found to play vital roles in normal immune function, and TUSC2 loss is associated with the development of autoimmune diseases as well as impaired responses within the innate immune system. TUSC2 also plays a vital role in regulating normal cellular mitochondrial calcium movement and homeostasis. Moreover, TUSC2 serves as an important factor in premature aging. In addition to TUSC2's normal cellular functions, TUSC2 has been studied as a tumor suppressor gene that is frequently deleted or lost in a multitude of cancers, including glioma, sarcoma, and cancers of the lung, breast, ovaries, and thyroid. TUSC2 is frequently lost in cancer due to somatic deletion within the 3p21.3 region, transcriptional inactivation via TUSC2 promoter methylation, post-transcriptional regulation via microRNAs, and post-translational regulation via polyubiquitination and proteasomal degradation. Additionally, restoration of TUSC2 expression promotes tumor suppression, eventuating in decreased cell proliferation, stemness, and tumor growth, as well as increased apoptosis. Consequently, TUSC2 gene therapy has been tested in patients with non-small cell lung cancer. This review will focus on the current understanding of TUSC2 functions in both normal and cancerous tissues, mechanisms of TUSC2 loss, TUSC2 cancer therapeutics, open questions, and future directions.

Digitalis Historical Background and Current Status

The earliest recorded treatment of digitalis is typically credited to William Witherings investigation on the foxglove, which was published in 1785. The rich background of digitalis is intriguing. Yet, there is evidence of some awareness of herbs used for remedies for heart failure with complications that have effects similar to those of digitalis dating back to roman times. In relation to this, the foxglove's natural components (Digitalis purpurea and Digitalis lanata) also include ouabain, a quick-acting glycoside typically derived from Strophanthus gratus. These substances are known as cardiotonic steroids. These medications are effective sodium-potassium adenosine triphosphatase antagonists. Digitalis as well as its metabolites, specifically digoxin, served as the gold standard of treatment for CHF during the duration of the 20th century. As the century came to a close, however, several concerns—particularly those related to ensuring enhanced safety—were raised regarding their usage as additional therapies for CHF, such as lowering the left ventricle's preload. An important medication used to treat cardiac arrhythmias and high blood pressure is still digitalis glycosides. The properties of the all cardioactive glycosides enhance the myocardial fibre contractile strength in a manner that is similar. Almost 100% of digoxin is absorbed, has a T½ life of 5 to 7 days, and is mainly excreted in the urine as cardioinactive metabolites with just 8% of it being converted to digoxin. The inhibition of membrane Na+/K+ ATPase and its resulting impacts on calcium movement are thought to be the reason behind this. Digitalis and certain medications can interact, most commonly with diuretics that cause hypokalaemia or hypomagnesaemia. The management of cardiac arrhythmias following digitalis toxicity is mainly possible by favourable interactions with antiarrhythmic pharmaceuticals (lignocaine, phenytoin), however the efficiency of other medications, such propranolol, is occasionally constrained by their adverse inotropic effects

Effects of parathyroid hormone on renal tubular calcium and phosphate handling.

Central to the maintenance of calcium homeostasis is the regulated reabsorption of calcium along the nephron. To this end, parathyroid hormone (PTH) is released from the parathyroid gland in response to lowered plasma calcium levels. This hormone acts through the PTH 1 receptor along the nephron to increase urinary phosphate excretion and decrease urinary calcium excretion. In the proximal tubule, PTH inhibits phosphate reabsorption by reducing the abundance of sodium phosphate cotransporters in the apical membrane. PTH likely decreases calcium reabsorption from the proximal tubule, by reducing the reabsorption of sodium, an event necessary for the paracellular movement of calcium across this segment. In the thick ascending limb (TAL), PTH increases calcium permeability and may increase the electrical driving force thereby increasing calcium reabsorption in the TAL. Finally, in the distal convolution, PTH acts to increase transcellular calcium reabsorption by increasing the activity and abundance of the apically expressed calcium channel TRPV5.

Whole genome DNA methylation and mutational profiles identify novel changes in proliferative verrucous leukoplakia

Proliferative verrucous leukoplakia (PVL) is a rare form of oral leukoplakia with a relatively high transformation rate resulting in oral squamous cell carcinoma (OSCC). Molecular analysis of PVL at the genome level is limited and has only identified molecular similarities between PVL and OSCC. However, the clinical profile of PVL suggests that molecular differences may be more important. Whole exome sequencing of 5 PVL-associated OSCC (PVL-OSCC) and paired blood samples was used to identify somatic mutations common to the tumors. Whole methylome analysis of samples from 4 PVL-associated OSCC and 3 OSCC of non-PVL origin samples was conducted to explore differential methylation. In contrast to conventional OSCC, PVL-associated OSCC showed infrequent TP53 mutation and altered spectra of PIK3CA and NOTCH1 mutations. Unsupervised hierarchical clustering identified 63 probes that discriminated between PVL-associated OSCC and OSCC of non-PVL origin. Differences in methylation were most significant for divalent metal ion transport, particularly calcium movement. Specific differences in mutation and methylation profiles between PVL-derived OSCC and OSCC of non-PVL origin suggest differences in their transformation pathways. Further studies of early PVL lesions may identify markers of transformation that are also applicable to more common oral premalignant disorders such as oral epithelial dysplasia.

Direct and in situ observations of plants under various light illumination conditions using electrochemical impedance spectroscopy

The possibility of using electrochemical impedance spectroscopy (EIS) for direct and real-time monitoring of plants was investigated. Since EIS is an in situ monitoring technique and the obtained signals tend to reflect the ions in plant cells and tissues, it can be used to observe the ion fluctuations that result from the changes in the lighting conditions. Changes in EIS signals and the fitted parameters were observed upon application of an external stimulation to a Marchantia polymorpha individual, which has been known to cause the movement of calcium ions in cellular tissues. In addition, the EIS signals and fitted parameters also changed by altering the lighting conditions. Although further investigation is required, these fundamental experiments indicate that EIS could be applied to monitor in situ ionic phenomena that occur in plants.

Muscle calcium stress cleaves junctophilin1, unleashing a gene regulatory program predicted to correct glucose dysregulation.

Calcium ion movements between cellular stores and the cytosol govern muscle contraction, the most energy-consuming function in mammals, which confers skeletal myofibers a pivotal role in glycemia regulation. Chronic myoplasmic calcium elevation ("calcium stress"), found in malignant hyperthermia-susceptible (MHS) patients and multiple myopathies, has been suggested to underlie the progression from hyperglycemia to insulin resistance. What drives such progression remains elusive. We find that muscle cells derived from MHS patients have increased content of an activated fragment of GSK3β - a specialized kinase that inhibits glycogen synthase, impairing glucose utilization and delineating a path to hyperglycemia. We also find decreased content of junctophilin1, an essential structural protein that colocalizes in the couplon with the voltage-sensing CaV1.1, the calcium channel RyR1 and calpain1, accompanied by an increase in a 44 kDa junctophilin1 fragment (JPh44) that moves into nuclei. We trace these changes to activated proteolysis by calpain1, secondary to increased myoplasmic calcium. We demonstrate that a JPh44-like construct induces transcriptional changes predictive of increased glucose utilization in myoblasts, including less transcription and translation of GSK3β and decreased transcription of proteins that reduce utilization of glucose. These effects reveal a stress-adaptive response, mediated by the novel regulator of transcription JPh44.

Three-dimensional reduced graphene reinforced cement with enhanced safety and durability for drinking water distribution applications: Long-term experimental and theoretical study

Cement mortar lining (CML) is commonly used for iron pipe internal corrosion inhibition in drinking water distribution system (DWDS), however, the corrosion of CML itself is still a problem, particularly under soft water conditions. In this study, both long-term experimental study and theoretical studies were conducted to evaluate the effects of graphene oxide (GO) and three-dimensional reduced graphene oxide (3D-rGO) as additives on the stability of CML and the corresponding water quality. Results showed that during a 182-day leaching experiment, the 3D-rGO modified cement had a higher ability to inhibit the cement constituent leaching than GO modified and original cements. Structural characterization indicated that the addition of 3D-rGO could slightly promote the degree of calcium hydroxide crystallization in CML. Molecular dynamics simulation demonstrated that the 3D-rGO nanosheets strengthened the tensile strain of the cement and restricted the movement of calcium ions by forming strong bonds with the calcium-silicate-hydrate gel network. In addition, compared with GO modified cement and original cement, the 3D-rGO modified cement could somewhat reduce the disinfection by-products formation and the microbial richness in drinking water. Thus, the reinforcement of cement by 3D-rGO could enhance the safety and durability of CML iron pipes in DWDS.

The effects of N-NO3: N-NH4 ratios and calcium concentration of the nutrient solution on the growth parameters and partitioning of nitrogen and calcium in tomato plants (Solanum lycopersicum L.)

Calcium (Ca) and nitrogen (N) are essential elements for plant growth; however, the N form ratio in the nutrient solution affects plant growth as well as the uptake and partitioning of other nutrient elements differently. This experiment was conducted to determine the effects of different N-NO3: N-NH4 ratios and calcium levels on calcium movement, partitioning, and N metabolism in tomato (Solanum lycopersicum) plants. Nitrogen was applied at four N-NO3: N-NH4 ratios (NR1 = 100:0, NR2 = 75:25, NR3 = 50:50, NR4 = 25:75) and Ca at three levels (80, 160, and 320 mg/l) using hydroponic culture. A factorial experiment was conducted in a greenhouse at the Isfahan University of Technology Research Center using a completely randomized design with four repetitions, three plants in each replication. The results showed that the Ca application decreased shoot length, but increased shoot diameter. Elevation of Ca concentration in the nutrient solution by 320 mg/l Ca treatment increased total amino acid, protein, yield, and Ca content of the fruit, but suppressed the nitrogen content of the shoot, root, and fruit. The highest nitrate and ammonium contents of tomato plants were in NR1 and NR2 treatments, respectively. With increasing the level of Ca, the concentration of Ca increased in the apoplast and xylem sap, but decreased in the symplast. The results showed that the NO3: NH4 ratio significantly affected the growth and calcium partitioning of tomato plants. The NO3: NH4 ratio of 75:25 corresponding to 320 mg/l of Ca improved yield and Ca movement to the distal of tomato fruit, resulting in preventing blossom-end rot and the best fruit quality.

A stochastic mathematical model for coupling the cytosolic and sarcoplasmic calcium movements in diseased cardiac myocytes

Several computational studies have been undertaken to explore the Ca2+-induced Ca2+ release (CICR) events in cardiac myocytes and along with experimental studies it has given us invaluable insight into the mechanism of CICR from spark/blink initiation to termination and regulation, and their interplay under normal and pathological conditions. The computational modelling of this mechanism has mainly been investigated using coupled differential equations (DEs). However, there is a lack of computational investigation into (1) how the different formulation of coupled DEs capture the Ca2+ movement in the cytosol and sarcoplasmic reticulum (SR), (2) the buffer and dye inclusion in both compartments, and (3) the effect of buffer and dye properties on the calcium behaviour. This work is set out to explore (1) the effect of different coupled formulation of DEs on spark/blink occurrence, (2) the inclusion of improved sarcoplasmic buffering properties, and (3) the effects of cytosolic and sarcoplasmic dye and buffer properties on Ca2+ movement. The simulation results show large discrepancies between different formulations of the governing equations. Additionally, extension of the model to include sarcoplasmic buffering properties show normalised fluorescent dye profiles to be in good agreement with experimental and amongst its one- and two-dimensional representations.

Calcium in peroxisomes: An essential messenger in an essential cell organelle.

Calcium is a central signal transduction element in biology. Peroxisomes are essential cellular organelles, yet calcium handling in peroxisomes has been contentious. Recent advances show that peroxisomes are part of calcium homeostasis in cardiac myocytes and therefore may contribute to or even shape their calcium-dependent functionality. However, the mechanisms of calcium movement between peroxisomes and other cellular sites and their mediators remain elusive. Here, we review calcium handling in peroxisomes in concert with other organelles and summarize the most recent knowledge on peroxisomal involvement in calcium dynamics with a focus on mammalian cells.

Assessment of Sub Lethal Toxicity of Hydrocortisone (C21H30O5): Physiological and Hematological Biomarker Reactions on Anabas Testudineus

Application of wide range of pharmaceuticals is a serious threat to the environment causing a significant deterioration of aquatic faunal health as well as its survival status. The widespread detection of various types of drugs (antibiotics, nonsteroidal anti-inflammatory drugs, beta-blockers, etc.) present in the aquatic ecosystem directly works on physiological parameters at different levels of aquatic organisms especially the bioindicators, fishes. The experiment was carried out to evaluate the exposure of sub lethal concentration of hydrocortisone on oxygen consumption, gill movement, haematological and percentage of bone calcium of the freshwater fish, Anabas testudineus . When compared to control, the exposed fishes exhibit significant alterations in their physiological activity. The rate of oxygen consumption is indirectly proportional to dosage concentration as well as exposure time. Both the rate of gill movement and oxygen consumption were decreased with increasing concentration of hydrocortisone. Under exposure, the marked decline was recorded in both RBCs and Hb count when compared to control (P < .05). The percentage of bone calcium level was significantly decreased by the toxicity of hydrocortisone. The current study stipulates that the exposure of sub lethal concentration of hydrocortisone on Anabas testudineus alters the physiological and hematological parameters. From the results, it is noteworthy that the steroid drug, hydrocortisone even at low concentrations causes deteriorative impacts on the health conditions of aquatic organism. KEYWORDS : Hydrocortisone, oxygen consumption, gill movement, haematology, bone calcium, Anabas testudineus.

Piezo1 regulates shear-dependent nitric oxide production in human erythrocytes.

Mature circulating red blood cells (RBCs) are classically viewed as passive participants in circulatory function, given erythroblasts eject their organelles during maturation. Endogenous production of nitric oxide (NO) and its effects are of particular significance; however, the integration between RBC sensation of the local environment and subsequent activation of mechano-sensitive signaling networks that generate NO remain poorly understood. The present study investigated endogenous NO production via the RBC-specific nitric oxide synthase isoform (RBC-NOS), connecting membrane strain with intracellular enzymatic processes. Isolated RBCs were obtained from apparently healthy humans. Intracellular NO was compared at rest and following shear (cellular deformation) using semiquantitative fluorescent imaging. Concurrently, RBC-NOS phosphorylation at its serine1177 (Ser1177) residue was measured. The contribution of cellular deformation to shear-induced NO production in RBCs was determined by rigidifying RBCs with the thiol-oxidizing agent diamide; rigid RBCs exhibited significantly impaired (up to 80%) capacity to generate NO via RBC-NOS during shear. Standardizing membrane strain of rigid RBCs by applying increased shear did not normalize NO production, or RBC-NOS activation. Calcium imaging with fluo-4 revealed that diamide-treated RBCs exhibited a 42% impairment in Piezo1-mediated calcium movement when compared with untreated RBCs. Pharmacological inhibition of Piezo1 with GsMTx4 during shear inhibited RBC-NOS activation in untreated RBCs, whereas Piezo1 activation with Yoda1 in the absence of shear stimulated RBC-NOS activation. Collectively, a novel, mechanically activated signaling pathway in mature RBCs is described. Opening of Piezo1 and subsequent influx of calcium appear to be required for endogenous production of NO in response to mechanical shear, which is accompanied by phosphorylation of RBC-NOS at Ser1177.NEW & NOTEWORTHY The mechano-sensitive ion channel Piezo1 is expressed in enucleated red blood cells and provides a mechanism of shear-induced red cell nitric oxide production via nitric oxide synthase phosphorylation. Thiol oxidation of red cells decreases Piezo1-dependent calcium movement and thus impairs nitric oxide generation in response to mechanical force. The emerging descriptions of exclusively posttranslational signaling networks in circulating red cells as acute regulators of cell function support that these cells play an important role in cardiovascular physiology that extends beyond passive oxygen transport.

Preventing c2c12 muscular cells damage combining magnesium and potassium with vitamin D3 and curcumin

Background and aimPhysical activity is defined as any bodily movement produced by skeletal muscles which causes energy consumption; moderate and constant physical activity is known to be beneficial and to slow the muscle loss process associated with aging. The aim of the present study was to test, in an in vitro exercise model, the biological effects of a new formulation composed of magnesium and potassium combined with vitamin D and curcumin created to support muscle activity and to prevent hypercontraction damage. Experimental procedureC2C12 cells were treated with vitamin D, buffered magnesium bisglycinate, curcumin, and potassium citrate. Cell viability, morpho-functional changes, calcium and magnesium movements, and the main kinases involved in glucose uptake were analyzed. The glycogen level and lactate were also evaluated. Results and conclusionImportant results about a positive effect on mitochondrial activity, ATP production, oxygen consumption and in the physiological differentiation of C2C12 cells were obtained. Further experiments were performed under conditions that mimic the biological aspects of strenuous exercise. The combination of magnesium, vitamin D3, curcumin, and potassium citrate revealed beneficial effects on skeletal muscle cells under physiological conditions as well as while mimicking intense activity. In particular, in an in vitro model, they were able to control the hypercontraction, restoring ion fluxes, reducing inflammation signaling and supporting the main mechanism involved on aerobic activity. Our results have indicated for the first time that this new combination could be considered as a new nutraceutical formulation to improve physical performance and muscle recovery.

Effect of Soil Compaction and Application of Lime and Gypsum on Soil Properties and Yield of Soybean

ABSTRACT Lime and gypsum application is one strategy for correcting soil acidity and improving soil fertility. However, soil compaction in no-till systems can influence these dynamics. This study aimed to assess the effect of lime and gypsum application under different soil compaction levels on soybean yield and soil chemical attributes. The application of lime and gypsum under artificial compaction levels and the movement of exchangeable calcium (Ca2+), magnesium (Mg2+), potassium (K+), and soil pH were monitored in the 0–0.05, 0.05–0.10, 0.10–0.20, and 0.20–0.40 m soil layer depths. Soybean grain yield was not influenced by the gypsum and lime applications and artificial compaction levels. In the 0.05–0.1, 0.1–0.2, and 0.2–0.4 m soil layers, the exclusive surface application of lime was effective in increasing the soil pH. Ca2+ and Mg2+ carbonates had low solubility and mobility in the soil; however, a rapid reaction to the surface over a relatively short period was observed. K+ concentration in the 0–0.05 m soil layer did not vary after the gypsum and lime applications. Therefore, the superficial application of lime is effective in acidity correction in no-till systems when the soil is not compacted.