Changes In Calcium Research Articles

Calcium change of transported soils from 1995 to 2010 in acid rain areas in China

Acid rain, a significant environmental threat, negatively impacts soil health and ecosystems. It can leach calcium (Ca) from soils, affecting plant growth and other ecological processes. China has experienced widespread acid rain, particularly in the southern regions. Two national geochemical mapping projects: Environmental Geochemical Monitoring Networks (EGMON) and China Geochemical Baselines (CGB), were conducted to establish baselines for soil Ca. This study compares these baselines to quantify Ca changes in China's acid rain areas from 1995 to 2010 and identify key controlling factors. Our analysis revealed a significant decrease in Ca content in transported soils across these regions during this period. Notably, the median Ca concentration in the top soil (TS) decreased from 0.47 % to 0.36 %, and in the deep soil (DS) from 0.39 % to 0.31 %. Areas experiencing Ca depletion contents were roughly twice as those with increases. Estimated net Ca change rates were −0.07 Pg/a for TS and 0.04 Pg/a for DS, indicating a net Ca loss of 1.25 Pg from the study region's top 125 cm of soil. This translates to a loss rate of 0.083 Pg/a or 0.026 g Ca2+ kg−1 soil per year. Calcium contents in transported soils were influenced by the interplay of acid rain, rainfall, and parent rocks. Acid rain could dissolve Ca from carbonate-rich rocks, enriching nearby rivers with Ca2+. Upon deposition, clay minerals in the soils could adsorb Ca2+, potentially increasing soil Ca content. However, intense acid rain (pH <5.0) could leach Ca2+ from the soil and outweigh the positive influence of parent carbonate-rich rocks, leading to Ca depletion. Additionally, in regions with sufficient rainfall (>1600 mm/a), combined with the leaching effect of acid rain, Ca content could decrease due to overall mobilization and transport out of the soil.

Depolarization induces calcium-dependent BMP4 release from mouse embryonic palate mesenchymal cells

Bone Morphogenetic Protein (BMP) signaling is essential for craniofacial development, though little is known about the mechanisms that govern BMP secretion. We show that depolarization induces calcium-dependent BMP4 release from mouse embryonic palate mesenchyme. We show endogenous transient changes in intracellular calcium occur in cranial neural crest cells, the cells from which embryonic palate mesenchyme derives. Waves of transient changes in intracellular calcium suggest that these cells are electrically coupled and may temporally coordinate BMP release. These transient changes in intracellular calcium persist in palate mesenchyme cells from embryonic day 9.5 to 13.5 mice. Disruption of a potassium channel called Kcnj2 significantly decreases the amplitude of calcium transients and the ability of cells to secrete BMP. Kcnj2 knockout mice have cleft palate and reduced BMP signaling. Our data suggest that temporal control of developmental cues is regulated by ion channels, depolarization, and intracellular calcium for mammalian craniofacial morphogenesis.

Reorganization of the flagellum scaffolding induces a sperm standstill during fertilization.

Mammalian sperm delve into the female reproductive tract to fertilize the female gamete. The available information about how sperm regulate their motility during the final journey to the fertilization site is extremely limited. In this work, we investigated the structural and functional changes in the sperm flagellum after acrosomal exocytosis (AE) and during the interaction with the eggs. The evidence demonstrates that the double helix actin network surrounding the mitochondrial sheath of the midpiece undergoes structural changes prior to the motility cessation. This structural modification is accompanied by a decrease in diameter of the midpiece and is driven by intracellular calcium changes that occur concomitant with a reorganization of the actin helicoidal cortex. Midpiece contraction occurs in a subset of cells that undergo AE, and live-cell imaging during in vitro fertilization showed that the midpiece contraction is required for motility cessation after fusion is initiated. These findings provide the first evidence of the F-actin network's role in regulating sperm motility, adapting its function to meet specific cellular requirements during fertilization, and highlighting the broader significance of understanding sperm motility.

Reorganization of the flagellum scaffolding induces a sperm standstill during fertilization

Mammalian sperm delve into the female reproductive tract to fertilize the female gamete. The available information about how sperm regulate their motility during the final journey to the fertilization site is extremely limited. In this work, we investigated the structural and functional changes in the sperm flagellum after acrosomal exocytosis (AE) and during the interaction with the eggs. The evidence demonstrates that the double helix actin network surrounding the mitochondrial sheath of the midpiece undergoes structural changes prior to the motility cessation. This structural modification is accompanied by a decrease in diameter of the midpiece and is driven by intracellular calcium changes that occur concomitant with a reorganization of the actin helicoidal cortex. Midpiece contraction occurs in a subset of cells that undergo AE, and live-cell imaging during in vitro fertilization showed that the midpiece contraction is required for motility cessation after fusion is initiated. These findings provide the first evidence of the F-actin network’s role in regulating sperm motility, adapting its function to meet specific cellular requirements during fertilization, and highlighting the broader significance of understanding sperm motility.

Regulation of ADAM10 activity through microdomain-dependent intracellular calcium changes

A disintegrin and metalloproteinases (ADAMs) are transmembrane proteases that cleave other proteins close to the surface in a process called shedding. The prominent member ADAM10 has been linked to several pathologies such as Alzheimer’s disease, bacterial infection, cancer development and metastasis. Although the regulation of the ADAM10 activity by calcium influx and calmodulin inhibition has been reported, the spatiotemporal regulation of Ca2+-dependent ADAM10 activation and the required source of Ca2+ ions have not been thoroughly studied. In the present study, we observed the rapid Ca2+-dependent activation of ADAM10 in A549 lung carcinoma cells upon stimulation with ionomycin. The calmodulin-inhibitors trifluoperazine and ophiobolin A mediated delayed activation of ADAM10, which apparently did not depend on intracellular Ca2+ in the case of trifluoperazine. Furthermore, the surface translocation and release of ADAM10 in extracellular vesicles exhibited different kinetics and were only partially linked to catalytic activation. Finally, ADAM10 activation was observed after the entry of Ca2+ through certain channels, such as canonical members of transient receptor potential (TRP) channels. Therefore, the opening of particular channels for Ca2+ entry points and subsequent Ca2+ flux as well as the temporal aspects of the consequent increase in Ca2+ levels, must be considered for future therapeutic options involving the increasing or decreasing ADAM10 activity.

Diabetic Cardiomyopathy: An Update on Emerging Pathological Mechanisms.

Diabetic Cardiomyopathy (DCM) is a notable consequence of diabetes mellitus, distinguished by cardiac dysfunction that occurs separately from coronary artery disease or hypertension. A recent study has revealed an intricate interaction of pathogenic processes that contribute to DCM. Important aspects involve the dysregulation of glucose metabolism, resulting in heightened oxidative stress and impaired mitochondrial function. In addition, persistent high blood sugar levels stimulate inflammatory pathways, which contribute to the development of heart fibrosis and remodelling. Additionally, changes in the way calcium is managed and the presence of insulin resistance are crucial factors in the formation and advancement of DCM. This may be due to the involvement of many molecular mechanistic pathways such as NLRP3, NF- κB, PKC, and MAPK with their downstream associated signaling pathways. Gaining a comprehensive understanding of these newly identified pathogenic pathways is crucial in order to design precise therapy approaches that can enhance the results for individuals suffering from diabetes. In addition, this review offers an in-depth review of not just pathogenic pathways and molecular mechanistic pathways but also diagnostic methods, treatment options, and clinical trials.

Alterations in serum levels of calcium, vitamin D, phosphorus, and parathyroid hormone in patients with clinically confirmed familial hypercholesterolemia: a cross-sectional study.

Familial hypercholesterolemia (FH), an autosomal dominant disease, is associated with an increased risk of premature cardiovascular disease (CVD). This study aimed to examine the variations in serum levels of calcium, vitamin D, phosphorus, and parathyroid hormone (PTH) among FH patients, as these factors have been associated with an increased susceptibility to CVD. In this cross-sectional study, the authors used data from Isfahan FH registry. The Dutch Lipid Clinic Network (DLCN) criteria was used for diagnoses of FH patients. Control group included participants with hyperlipidemia and were unlikely FH according to DLCN criteria. All biochemical parameters were measured using standard methods. A total of 131 patients (mean age, 53.1 ± 12.2; male, 51.4%) were included in the analysis. Patients with FH had lower serum vitamin D levels compared with control groups in the unadjusted model (P= 0.028). The relationship between serum vitamin D and FH was not significant after adjustment for traditional risk factor (P= 0.184). No significant association was observed between FH and serum calcium (P= 0.886), phosphorus (P= 0.463), and PTH (P= 0.849). Besides, there was no significant association between LDL-C or total cholesterol and serum minerals in FH patients. This study found no significant changes in serum calcium, vitamin D, phosphorus, and PTH in patients with FH.

Characterization of the calmodulin-like protein family in Chara braunii and their conserved interaction with the calmodulin-binding transcription activator family.

Calcium sensor proteins play important roles by detecting changes in intracellular calcium and relaying that information onto downstream targets through protein-protein interaction. Very little is known about calcium sensors from plant species that predate land colonization and the evolution of embryophytes. Here, we examined the genome of the multicellular algae, Chara braunii, for orthologs to the evolutionarily-conserved calcium sensor calmodulin (CaM), and for CaM-like proteins (CMLs). We identified one CaM and eight CML isoforms which range in size from 16.4 to 21.3 kDa and are predicted to have between two to four calcium-binding (EF-hand) domains. Using recombinant protein, we tested whether CbCaM and CbCMLs1-7 possess biochemical properties of typical calcium sensors. CbCaM and the CbCMLs all displayed high-affinity calcium binding with estimated global KD,app values in the physiological µM range. In response to calcium binding, CbCaM and the CbCMLs exhibited varying degrees of increase in exposed hydrophobicity, suggesting different calcium-induced conformational changes occur among isoforms. We found many examples of putative CaM targets encoded in the C. braunii genome and explored the ability of CbCaM and CbCMLs to interact in planta with a representative putative target, a C. braunii CaM-binding transcription factor (CbCAMTA1). CbCaM, CbCML2, and CbCML4 associated with the C-terminal region of CbCAMTA1. Collectively, our data support the hypothesis that complex calcium signaling and sensing networks involving CaM and CMLs evolved early in the green lineage. Similarly, it seems likely that calcium-mediated regulation of transcription occurs in C. braunii via CAMTAs and is an ancient trait predating embryophytic emergence.

Effect of Hydroxyapatite Nanoparticle Crystallinity and Colloidal Stability on Cytotoxicity.

Hydroxyapatite nanoparticles (nHA) have gained attention as potential intracellular drug delivery vehicles due to their high binding affinity for various biomolecules and pH-dependent solubility. Yet, the dependence of nHA cytocompatibility on their physicochemical properties remains unclear since numerous studies have revealed starkly contrasting results. These discrepancies may be attributed to differences in size, shape, crystallinity, and aggregation state of nHA, which complicates fundamental understanding of the factors driving nHA cytotoxicity. Here, we hypothesize that nHA cytotoxicity is primarily driven by intracellular calcium levels following the internalization of nHA nanoparticles. By investigating the cytotoxicity of spherical nHA with different crystallinity and dispersity, we find that both lower crystallinity and increased agglomeration of nHA raise cytotoxicity, with nanoparticle agglomeration being the more dominant factor. We show that the internalization of nHA enhances intracellular calcium levels and increases the production of reactive oxygen species (ROS). However, only subtle changes in intracellular calcium are observed, and their physiological relevance remains to be confirmed. In conclusion, we show that nHA agglomeration enhances ROS production and the associated cytotoxicity. These findings provide important guidelines for the future design of nHA-containing formulations for biomedical applications, implying that nHA crystallinity and especially agglomeration should be carefully controlled to optimize biocompatibility and therapeutic efficacy.

Analysis of changes in serum calcium and magnesium levels during plateletpheresis on different apheresis machines in healthy donors: A cross-sectional study

Abstract: BACKGROUND: The most common observed complication of plateletpheresis procedure is hypocalcemia due to citrate’s chelation of free calcium. Magnesium is also affected by citrate infusion. We have evaluated the impact of plateletpheresis on the total serum calcium (Ca++) and magnesium (Mg++) levels of the donor. MATERIALS AND METHODS: One hundred and thirty-seven healthy plateletpheresis donors were included in the study. Samples were collected from the donor at 0 min (baseline), 30 min, and 60 min, at the end of the procedure and 30 min after completion of the procedure. The pattern of changes in serum Ca++ and serum Mg++ levels at different time points for different apheresis machines (Fenwal Amicus, Fresenius COM.TEC, Spectra Optia, and Hemonetics MCS+) was studied. RESULTS: A significant decline in serum Ca++ and serum Mg++ levels from baseline to the end of the procedure was observed. This decline was observed maximum for Hemonetics MCS+. The baseline values were regained 30 min after completion of the procedure. Difference from baseline values 30 min after the procedure was lowest in amicus in the case of serum Ca++ and COM.TEC in case of serum Mg++. Twenty donors (14.60%) experienced adverse donor reactions. CONCLUSION: Serum calcium and serum magnesium levels decreased transiently during the procedure and regained normal values after 30 min of the completion of the plateletpheresis procedure on all four apheresis machines (whether based on continuous or intermittent centrifugation). Hence, it is concluded from our study that plateletpheresis is a well-tolerated and safe procedure.

Chemical mapping of the surface interactome of PIEZO1 identifies CADM1 as a modulator of channel inactivation

The propeller-shaped blades of the PIEZO1 and PIEZO2 ion channels partition into the plasma membrane and respond to indentation or stretching of the lipid bilayer, thus converting mechanical forces into signals that can be interpreted by cells, in the form of calcium flux and changes in membrane potential. While PIEZO channels participate in diverse physiological processes, from sensing the shear stress of blood flow in the vasculature to detecting touch through mechanoreceptors in the skin, the molecular details that enable these mechanosensors to tune their responses over a vast dynamic range of forces remain largely uncharacterized. To survey the molecular landscape surrounding PIEZO channels at the cell surface, we employed a mass spectrometry-based proteomic approach to capture and identify extracellularly exposed proteins in the vicinity of PIEZO1. This PIEZO1-proximal interactome was enriched in surface proteins localized to cell junctions and signaling hubs within the plasma membrane. Functional screening of these interaction candidates by calcium imaging and electrophysiology in an overexpression system identified the adhesion molecule CADM1/SynCAM that slows the inactivation kinetics of PIEZO1 with little effect on PIEZO2. Conversely, we found that CADM1 knockdown accelerates inactivation of endogenous PIEZO1 in Neuro-2a cells. Systematic deletion of CADM1 domains indicates that the transmembrane region is critical for the observed effects on PIEZO1, suggesting that modulation of inactivation is mediated by interactions in or near the lipid bilayer.

Effects of active vitamin D analogs and calcimimetic agents on PTH and bone mineral biomarkers in hemodialysis patients with SHPT: a network meta-analysis.

Active vitamin D analogs and calcimimetic agents are primary drugs for patients with secondary hyperparathyroidism. Due to the different pharmacological mechanisms, they have different effects on the level of parathyroid hormone, serum calcium, phosphorus, and bone turnover biomarkers. This study aimed to evaluate the active vitamin D analogs and calcimimetic agents in hemodialysis patients with secondary hyperparathyroidism. We included randomized clinical trials of hemodialysis patients with secondary hyperparathyroidism, comparing active vitamin D analogs to calcimimetic agents or placebo/control. The primary outcome was the change of PTH level from baseline to end-up. The secondary outcome was the change in serum calcium, phosphorus, calcium-phosphorus product, and bone turnover biomarkers. A network meta-analysis method was applied to complete this study. The forest plots reflected statistical differences in the outcomes between active vitamin D analogs and calcimimetic agents. The SUCRA result presented the ranking of impact on the outcomes. Twenty-one randomized clinical trials with 4653 patients were included in this network meta-analysis. Global and splitting-node inconsistencies provided no evidence of inconsistency in this study. There was no statistical difference between two active vitamin D analogs and three calcimimetic agents in the PTH, and phosphorus levels changed. Considering serum calcium level, compared with placebo, calcitriol (9.73, 3.09 to 16.38) and paricalcitol (9.74, 3.87 to 15.60) increase serum calcium. However, cinacalcet (- 1.94, - 3.72 to - 0.15) and etelcalcetide (- 7.80, - 11.80 to - 3.80) reduced the serum calcium, even a joint use of cinacalcet with active vitamin D analogs (- 5.83, - 9.73 to - 1.93). Three calcimimetic agents decreased calcium levels much more than calcitriol and paricalcitol. The same type of drugs was not distinct, with each one affecting the change in calcium level. Cinacalcet reduced calcium-phosphorus product much more than paricalcitol (- 3.66, - 6.72 to - 0.60). Evocalcet decreased calcium-phosphorus product more than cinacalcet (- 5.64, - 8.91 to - 2.37), calcitriol (- 9.36, - 14.81 to - 3.92), and paricalcitol (- 9.30, - 13.78 to - 4.82). Compared with paricalcitol, cinacalcet significantly increases the level of ALP (24.50, 23.05 to 25.95) and bALP (0.67, 0.03 to 1.31). The incidence of gastrointestinal disorders in cinacacet (29.35, 1.71 to 504.98) and etelcalcetide (20.92, 1.20 to 365.68) was notably higher than in paricalcitol. Etelcalcetide (0.71, 0.53 to 0.96) and evocalcet (0.46, 0.33 to 0.64) presented a lower rate of gastrointestinal disorders than cinacalcet. Cinacalcet ranked first in adverse gastrointestinal, nervous, and respiratory reactions. The same kinds of agents perform similar efficacy on the level of PTH, serum calcium, phosphorus, and calcium-phosphorus product. Paricalcitol did not lead to more hypercalcemia than calcitriol. The calcium decrease induced by cinacalcet was not settled even by associating it with active vitamin D analogs. Cinacalcet and evocalcet were superior to calcitriol and paricacitol in reducing calcium-phosphorus product. Calcimimetics induced more gastrointestinal disorders than active vitamin D analogs, especially cinacalcet.

The role of anatomical and functional orientation in identification of parathyroid glands for patients with parathyroidectomy.

To investigate diagnostic approaches for preoperative localization of secondary hyperparathyroidism, as well as to give surgeons with precise parathyroid gland localization and imaging so that surgery can be performed safely. The clinical data of 710 patients with secondary hyperparathyroidism who underwent surgery in our center from October 2009 to October 2023 were retrospectively analyzed. The changes in calcium, phosphorus, and parathyroid hormone levels were observed to ascertain the anatomical location and number of parathyroid glands. Among the 710 patients, 55 underwent total parathyroidectomy, the others underwent total parathyroidectomy with autotransplantation. In total, 2,658 parathyroid glands were removed, with 43 glands being removed in 35 reoperation cases. The median parathyroid hormone level at 6 months postoperatively was 13.40 (interquartile range, 7.00-29.80) pg/mL. The detection rates of the parathyroid glands before first and repeat surgeries were higher using 99mTc-MIBI SPECT/CT fusion imaging than ultrasound (P<0.05). The sensitivity of combined preoperative 99mTc-MIBI SPECT/CT and ultrasound was 92.31%, higher than that of either 99mTc-MIBI SPECT/CT fusion imaging or ultrasound alone (P < 0.05). The incidence of ectopic parathyroid glands was 23.8%, and the incidence of ectopic left lower parathyroid glands was 13.2%. The left lower parathyroid gland was the most prone to ectopia. 99mTc-MIBI SPECT/CT fusion imaging, paired with high-frequency ultrasound, can be utilized to diagnose SHPT preoperatively. The most common ectopia site is the left lower parathyroid gland, which is located primarily in the thymus and superior mediastinum. Understanding the functional anatomical distribution of the parathyroid glands is critical for developing effective surgical methods for secondary hyperparathyroidism.

The Effect of a 12-week Plyometric Training on Growth Hormone, IGF-1 and Bone Health Indexes in Adolescent Boys

Background: During adolescence, physical activity influences bone mass, which is determined by both genetic and environmental factors. Objectives: This study examines the effect of plyometric exercises on serum markers in male adolescents, including growth hormone, vitamin D, parathyroid hormone, phosphate, and calcium. Methods: The study involved a sample of 30 male adolescents aged 15 years ± 6 months. The participants were divided into two groups: The first group, named the plyometric group (PG), included 15 adolescents who underwent plyometric training sessions three times a week for a duration of 12 weeks. The second group, called the control group (CG), consisted of 15 adolescents who only attended their normal school lessons without any physical training. Resting levels of GH, IGF-1, vitamin D, calcium, phosphate, and PTH were measured before and 48 hours after the last training session, along with bone mass density (BMD) measurements of the femoral neck, lumbar spine, and total body. To evaluate power, the vertical Sargent jump test was used. Results: The results indicate that the PG demonstrated significant improvements in BMD, explosive strength, GH, IGF-1, and vitamin D levels compared to the CG group (P &lt; 0.05). Changes in phosphate, calcium, and PTH were not significant in the PG compared to the CG after 12 weeks of plyometric training (P &gt; 0.05). Conclusions: The 12-week plyometric program resulted in notable enhancements in bone health, explosive strength, and anabolic hormones such as GH and IGF-1, as well as 25-hydroxyvitamin D serum levels.

Rapamycin Treatment Reduces Brain Pericyte Constriction in Ischemic Stroke.

The contraction and subsequent death of brain pericytes may play a role in microvascular no-reflow following the reopening of an occluded artery during ischemic stroke. Mammalian target of rapamycin (mTOR) inhibition has been shown to reduce motility/contractility of various cancer cell lines and reduce neuronal cell death in stroke. However, the effects of mTOR inhibition on brain pericyte contraction and death during ischemia have not yet been investigated. Cultured pericytes exposed to simulated ischemia for 12 h in vitro contracted after less than 1 h, which was about 7 h prior to cell death. Rapamycin significantly reduced the rate of pericyte contraction during ischemia; however, it did not have a significant effect on pericyte viability at any time point. Rapamycin appeared to reduce pericyte contraction through a mechanism that is independent of changes in intracellular calcium. Using a mouse model of middle cerebral artery occlusion, we showed that rapamycin significantly increased the diameter of capillaries underneath pericytes and increased the number of open capillaries 30 min following recanalisation. Our findings suggest that rapamycin may be a useful adjuvant therapeutic to reduce pericyte contraction and improve cerebral reperfusion post-stroke.

Responses to Herbal Compounds in Brain Cancer Cells: two Cell-Calcium Assays and a Molecular Docking Computation Study

Herbal plant secondary metabolites such as curcumin, resveratrol, and capsaicin are becoming increasingly popular as natural remedies. These herbal compounds are also known to act on the calcium signaling pathways, and therefore cell calcium assays can be used to study the relative interactions of these compounds with cellular receptors pertaining to natural remedies. To investigate this, Fluo-4, a fluorophore that specifically binds to Ca2+, was used to detect the increase in calcium signaling in human glioblastoma cells treated with curcumin, resveratrol, and capsaicin. The human cells used are U87 MG cells which expresses TRPV1, a pain receptor on the cell membrane. The increases of the fluorescence intensity in the cells treated with the three herbal compounds were measured using a bulk microplate assay, which generates data in a high throughput, and a microfluidic single-cell assay, which allows for the observation of the cell calcium changes in real-time. It was found that all three compounds would increase the intracellular Ca2+ concentrations on the two assays, with curcumin generating the highest increase, which confirms the greatest responses elicited by this herbal compound from the cell. Furthermore, the data obtained by a molecular docking computation study, which has been used to determine the binding affinities of the three compounds with the TRPV1 receptor, corroborate with the experimental finding of the highest cellular response due to curcumin.

Changes in 24-Hour Urine Chemistry in Patients with Nephrolithiasis during Weight Loss with Glucagon-Like Peptide 1-Based Therapies.

Key Points In obese kidney stone formers, weight loss with glucagon-like peptide-1 (GLP)-based therapy was associated with a significant decline in 24-hour urine oxalate and sulfate excretion rates.Weight loss through GLP-based therapies was associated with nonsignificant changes in urine saturation indices.In obese kidney stone formers, GLP-based therapy appears to be a safe option for weight loss on the basis of 24-hour urine studies. Background Obesity is an independent risk factor of incident and recurrent nephrolithiasis. The effect of weight loss through glucagon-like peptide 1 (GLP-1) receptor agonists and dual GLP-1/gastric inhibitory polypeptide receptor agonists (GLP-based therapies) on nephrolithiasis is not well understood. This study examined the changes in 24-hour urine chemistry assessing for stone risk during weight loss through GLP-based therapies. Methods This retrospective analysis identified adult stone formers followed at our academic institution's weight wellness clinic between September 2015 and August 2023 and included patients with at least two 24-hour urine collections for stone risk assessment. 24-hour urine parameters before and during weight loss in patients on GLP-based therapies were compared. Results Forty-four obese patients with nephrolithiasis experienced significant weight reduction (−6.6±7.3 kg, P &lt; 0.001) over a median 1.1 years of follow-up with GLP-based therapies. During this period, there was a significant decrease in 24-hour urine oxalate (40±16 to 32±11 mg/d, P = 0.002), sulfate (21±10 to 17±9 mmol/d, P = 0005), and ammonium (35±22 to 29±15 mEq/d, P = 0.01) excretion rates. There were nonsignificant changes in urine calcium, citrate, uric acid, pH, phosphorus, sodium, potassium, magnesium, chloride, creatinine, or total volume. In addition, there was no statistical difference in urine supersaturation indices with respect to calcium oxalate, calcium phosphate, and uric acid. Conclusions Our results indicate that weight loss through GLP-based therapies is not associated with prolithogenic changes in 24-hour urine chemistry in patients with nephrolithiasis, unlike what happens with other weight loss modalities.

Urinary Metal Levels and Coronary Artery Calcification: Longitudinal Evidence in the Multi-Ethnic Study of Atherosclerosis

BackgroundExposure to metals, a newly recognized risk factor for cardiovascular disease (CVD), could be related to atherosclerosis progression. ObjectivesThe authors hypothesized that higher urinary levels of nonessential (cadmium, tungsten, uranium) and essential (cobalt, copper, zinc) metals previously associated with CVD would be associated with baseline and rate of change of coronary artery calcium (CAC) progression, a subclinical marker of CVD in MESA (Multi-Ethnic Study of Atherosclerosis). MethodsWe analyzed data from 6,418 MESA participants with spot urinary metal levels at baseline (2000-2002) and 1 to 4 repeated, continuous measures of CAC over a 10-year period. We used linear mixed-effect models to assess the association of baseline urinary metal levels with baseline CAC and cumulative change in CAC over a 10-year period. Urinary metals (μg/g creatinine) and CAC were log transformed. Models were adjusted for baseline sociodemographic factors, estimated glomerular filtration rate, lifestyle factors, and clinical factors. ResultsAt baseline, the median CAC was 6.3 (Q1-Q3: 0.7-58.2). Comparing the highest to lowest quartile of urinary cadmium, CAC levels were 51% (95% CI: 32%, 74%) higher at baseline and 75% (95% CI: 47%, 107%) higher over the 10-year period. For urinary tungsten, uranium, and cobalt, the corresponding CAC levels over the 10-year period were 45% (95% CI: 23%, 71%), 39% (95% CI: 17%, 64%), and 47% (95% CI: 25%, 74%) higher, respectively, with no difference for models with and without adjustment for clinical factors. For copper and zinc, the corresponding estimates dropped from 55% to 33% and from 85% to 57%, respectively, after adjustment for clinical factors. The associations of metals with CAC were comparable in magnitude to those for classical CVD risk factors. ConclusionsExposure to metals was generally associated with extent of coronary calcification at baseline and follow-up. These findings support that metals are associated with the progression of atherosclerosis, potentially providing a novel strategy for the prevention and treatment of atherosclerosis progression.

Serum Electrolytes and Calcium Levels in Neonates Receiving Phototherapy for Neonatal Jaundice

Background: Neonatal Jaundice (NJ) is one of the most common causes of neonatal admission. Phototherapy is an important treatment modality for NJ. However, this treatment modality may itself result in changes of different biochemical parameters. The study aimed to evaluate the changes in serum electrolytes (Sodium, potassium and chloride) and calcium in neonates receiving phototherapy for NJ. Materials and methods: One hundred and two term neonates admitted to the Special Care Newborn Unit, Chattogram Medical College Hospital for the management of NJ by phototherapy were enrolled in this prospective observational study. Serum bilirubin, sodium, potassium, chloride and calcium were measured before and after 48 hours of phototherapy and compared. Results: The mean gestational age and mean age of admission of the neonates were 38.6±0.6 weeks and 6.42 ± .67 day respectively. The mean sodium, potassium and calcium level before therapy was respectively, 138.4±1.8 mmol/L, 4.1±0.3 mmol/L and 8.8±0.3 mg/dl. There was significant decrease in the level of mean sodium (136.4±1.6 mmol/L), potassium (3.8 ± 0.3 mmol/L) and calcium (8.4±0.4 mg/dL) after phototherapy. All neonates had normal level of serum calcium, sodium, potassium and chloride before phototherapy. After 48 hours of phototherapy, 46 (45.1%) of them had abnormal values with the incidence hypocalcaemia, hyponatraemia and hypokalemia respectively in 21.6%, 25.5% and 10.8% of the neonates. Conclusion: Neonates undergoing phototherapy are at risk of developing hyponatraemia, hypokalaemia and hypocalcaemia. Closed monitoring is essential to observe the changes in sodium, potassium and calcium and should be managed accordingly. IAHS Medical Journal Volume 6(2) December 2023; 83-86

Debulking surgery after muscular paraffin oil injections: Effects on calcium homeostasis and patient satisfaction.

Cosmetic paraffin oil injections can lead to granuloma formation causing hypercalcemia and kidney failure. This study explores whether debulking surgery is an effective treatment for improving calcium homeostasis, inflammation and clinical symptoms. In a retrospective study, we reviewed 33 patients undergoing debulking surgery. Changes in calcium, inflammatory markers, and renal function from baseline up to twelve months post-surgery were assessed. Patients were interviewed post-surgery. The patients were 34.6 years (SD 6.9) and had 1,104 grams (SD 591) of granuloma tissue removed following injection of 1,329 mL (SD 803) paraffin oil 7.9 years (SD 3.2) earlier. Seventeen patients had hypercalcemia and experienced a significant decline in ionized calcium from 1.48 mmol/L (SD 0.16) at baseline to 1.33 mmol/L (SD 0.03) at twelve months (p<0.002), although only four men (23.5%) became normocalcemic. Serum ferritin was reduced by 50% after twelve months (p=0.048). Sixteen patients were normocalcemic and had no change in calcium homeostasis but experienced a 20% drop in serum ferritin levels (p=0.025) after surgery. Fifteen patients completed all their planned surgeries within the study period and experienced a decline in serum ionized calcium (p=0.031), ferritin (p=0.011), and interleukin 2-receptor (p=0.037). A patient satisfaction survey showed that 55% of patients reported post-operative satisfaction scores of 10/10, and 59% of the patients reported reduced pain. Surgery improved calcium homeostasis in a fraction of patients, reduced inflammation and subjective symptoms such as pain and mental well-being in a patient group left with few treatment options except high-dose prednisolone.