569 results on '"Calcium balance"'
Search Results
2. Calcium balance: considerations for the bone response to exercise.
- Author
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Wherry SJ
- Subjects
- Humans, Female, Bone and Bones, Calcium, Dietary, Calcium, Bone Density physiology
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- 2024
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3. Calcium isotope composition in serum and urine for the assessment of bone calcium balance (BCaB) – results from a post-market surveillance clinical follow-up study on 2409 participants
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Eisenhauer, Anton, additional, Heuser, Alexander, additional, Lutz, Michael, additional, Müller, Michael, additional, and Oehme, Julius, additional
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- 2024
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- View/download PDF
4. Tomato Fruit Yield, Quality, and Nutrient Status in Response to Potassium: Calcium Balance and Electrical Conductivity in the Nutrient Solution
- Author
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Hernández-Pérez, Obed I., Valdez-Aguilar, Luis A., Alia-Tejacal, Irán, Cartmill, Andrew D., and Cartmill, Donita L.
- Abstract
Tomato fruits of high quality and yield are of interest to greenhouse growers. As potassium (K) and calcium (Ca) have been associated with fruit quality, we studied the effect of the balance between such cations and the electrical conductivity (EC) on fruit yield and quality. Plants were fertigated with K (Kext) and Ca (Caext) balances in the nutrient solution varying from 0.54–1.22 and 0.69–1.44 at ECs of 2.3 ± 0.1 dS m−1and 2.7 ± 0.1 dS m−1, respectively. Optimum balance for fruit yield was 0.82–0.85, and it was associated with high fruit K internal (Kint) concentration (~ 200 mmol kg−1). Higher EC increased firmness when the balance was ≤ 1.00, with the optimum at 0.85; firmness was correlated with Caintwhen EC was 2.3 dS m−1; however, at 2.7 dS m−1, increasing Kextincreased firmness and intensified the effect of Caext. Increasing a* values were associated with high lycopene and uniform maturation when that balance was 0.82 and 1.00 at low and high EC, respectively. Highest a* values were observed when Kintin the fruit was ~ 200 mmol kg−1, while 91 to 130 mmol kg−1were associated with lower a* values. Fruits contained higher starch (+ 20%), total (+ 12%), and reducing sugars (+ 29%) at high EC. The optimum K and Ca balance, 0.82–0.85, is independent of their concentration and was associated with high yield and firmness, improved fruit color, and increased lycopene and sugar concentrations.
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- 2024
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5. Deciphering simplified regional anticoagulation with citrate in intermittent hemodialysis: a clinical and computational study.
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Aniort, Julien, Richard, Felix, Thouy, François, Le Guen, Louis, Philipponnet, Carole, Garrouste, Cyril, Heng, Anne Elisabeth, Dupuis, Claire, Adda, Mireille, Julie, Durif, Elodie, Lebredonchel, Chupin, Laurent, Bouvier, Damien, Souweine, Bertrand, and Cindea, Nicolae
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CITRATES ,RENAL replacement therapy ,HEMODIALYSIS ,ANTICOAGULANTS - Abstract
Regional citrate anticoagulation use in intermittent hemodialysis is limited by the increased risk of metabolic complications due to faster solute exchanges than with continuous renal replacement therapies. Several simplifications have been proposed. The objective of this study was to validate a mathematical model of hemodialysis anticoagulated with citrate that was then used to evaluate different prescription scenarios on anticoagulant effectiveness (free calcium concentration in dialysis filter) and calcium balance. A study was conducted in hemodialyzed patients with a citrate infusion into the arterial line and a 1.25 mmol/L calcium dialysate. Calcium and citrate concentrations were measured upstream and downstream of the citrate infusion site and in the venous line. The values measured in the venous lines were compared with those predicted by the model using Bland and Altman diagrams. The model was then used with 22 patients to make simulations. The model can predict the concentration of free calcium, bound to citrate or albumin, accurately. Irrespective of the prescription scenario a decrease in free calcium below 0.4 mmol/L was obtained only in a fraction of the dialysis filter. A zero or slightly negative calcium balance was observed, and should be taken into account in case of prolonged use. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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6. Research Findings from Leiden University Medical Center Update Understanding of Hemofiltration (Plasma Parathormone Levels during Citrate Anticoagulated Continuous Venovenous Hemofiltration in ICU Patients).
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ACADEMIC medical centers ,SURGICAL technology ,NEWSPAPER editors ,HEMODIALYSIS ,CRITICAL care medicine - Abstract
A study conducted at Leiden University Medical Center in the Netherlands examined the effects of continuous venovenous hemofiltration (CVVH) with citrate anticoagulation on calcium balance in ICU patients. The researchers aimed to determine if monitoring plasma parathormone (PTH) levels could identify patients with negative calcium balance during CVVH. The study found that increased plasma concentrations of PTH were frequently found in ICU patients treated with citrate CVVH, but no association was found between PTH and the CVVH calcium balance over the last 72 hours. This research provides valuable insights into the potential effects of CVVH on calcium balance in ICU patients. [Extracted from the article]
- Published
- 2024
7. Spatial and single-cell explorations uncover prognostic significance and immunological functions of mitochondrial calcium uniporter in breast cancer.
- Author
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Li, Chia-Jung, Tzeng, Yen-Dun Tony, Hsiao, Jui-Hu, Tseng, Ling-Ming, Hsu, Tzu-Sheng, and Chu, Pei-Yi
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BREAST cancer ,REGULATOR genes ,GENE expression ,BRCA genes ,GENETIC variation ,ONCOLOGY ,CANCER cell growth ,CALCIUM ions - Abstract
The mitochondrial calcium uniporter (MCU) is a transmembrane protein facilitating the entry of calcium ions into mitochondria from the cell cytosol. Maintaining calcium balance is crucial for enhancing cellular energy supply and regulating cell death. The interplay of calcium balance through MCU and the sodium-calcium exchanger is known, but its regulation in the breast cancer tumor microenvironment remains elusive. Further investigations are warranted to explore MCU's potential in BRCA clinical pathology, tumor immune microenvironment, and precision oncology. Our study, employing a multi-omics approach, identifies MCU as an independent diagnostic biomarker for breast cancer (BRCA), correlated with advanced clinical status and poor overall survival. Utilizing public datasets from GEO and TCGA, we discern differentially expressed genes in BRCA and examine their associations with immune gene expression, overall survival, tumor stage, gene mutation status, and infiltrating immune cells. Spatial transcriptomics is employed to investigate MCU gene expression in various regions of BRCA, while spatial transcriptomics and single-cell RNA-sequencing methods explore the correlation between MCUs and immune cells. Our findings are validated through the analysis of 59 BRCA patient samples, utilizing immunohistochemistry and bioinformatics to examine the relationship between MCU expression, clinicopathological features, and prognosis. The study uncovers the expression of key gene regulators in BRCA associated with genetic variations, deletions, and the tumor microenvironment. Mutations in these regulators positively correlate with different immune cells in six immune datasets, playing a pivotal role in immune cell infiltration in BRCA. Notably, high MCU performance is linked to CD8 + T cells infiltration in BRCA. Furthermore, pharmacogenomic analysis of BRCA cell lines indicates that MCU inactivation is associated with increased sensitivity to specific small molecule drugs. Our findings suggest that MCU alterations may be linked to BRCA progression, unveiling new diagnostic and prognostic implications for MCU in BRCA. The study underscores MCU's role in the tumor immune microenvironment and cell cycle progression, positioning it as a potential tool for BRCA precision medicine and drug screening. [ABSTRACT FROM AUTHOR]
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- 2024
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8. Stereocilia fusion pathology in the cochlear outer hair cells at the nanoscale level.
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Ikäheimo, Kuu, Leinonen, Saija, Lankinen, Tuuli, Lindahl, Maria, Saarma, Mart, and Pirvola, Ulla
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HAIR cells , *MECHANOTRANSDUCTION (Cytology) , *DEAFNESS , *LABORATORY mice , *ENDOPLASMIC reticulum - Abstract
The hair bundle of cochlear hair cells comprises specialized microvilli, the stereocilia, which fulfil the role of mechanotransduction. Genetic defects and environmental noise challenge the maintenance of hair bundle structure, critically contributing to age‐related hearing loss. Stereocilia fusion is a major component of the hair bundle pathology in mature hair cells, but its role in hearing loss and its molecular basis are poorly understood. Here, we utilized super‐resolution expansion microscopy to examine the molecular anatomy of outer hair cell stereocilia fusion in mouse models of age‐related hearing loss, heightened endoplasmic reticulum stress and prolonged noise exposure. Prominent stereocilia fusion in our model of heightened endoplasmic reticulum stress, Manf (Mesencephalic astrocyte‐derived neurotrophic factor)‐inactivated mice in a background with Cadherin 23 missense mutation, impaired mechanotransduction and calcium balance in stereocilia. This was indicated by reduced FM1‐43 dye uptake through the mechanotransduction channels, reduced neuroplastin/PMCA2 expression and increased expression of the calcium buffer oncomodulin inside stereocilia. Sparse BAIAP2L2 and myosin 7a expression was retained in the fused stereocilia but mislocalized away from their functional sites at the tips. These hair bundle abnormalities preceded cell soma degeneration, suggesting a sequela from stereociliary molecular perturbations to cell death signalling. In the age‐related hearing loss and noise‐exposure models, stereocilia fusion was more restricted within the bundles, yet both models exhibited oncomodulin upregulation at the fusion sites, implying perturbed calcium homeostasis. We conclude that stereocilia fusion is linked with the failure to maintain cellular proteostasis and with disturbances in stereociliary calcium balance. Key points: Stereocilia fusion is a hair cell pathology causing hearing loss.Inactivation of Manf, a component of the endoplasmic reticulum proteostasis machinery, has a cell‐intrinsic mode of action in triggering outer hair cell stereocilia fusion and the death of these cells.The genetic background with Cadherin 23 missense mutation contributes to the high susceptibility of outer hair cells to stereocilia fusion, evidenced in Manf‐inactivated mice and in the mouse models of early‐onset hearing loss and noise exposure.Endoplasmic reticulum stress feeds to outer hair cell stereocilia bundle pathology and impairs the molecular anatomy of calcium regulation.The maintenance of the outer hair cell stereocilia bundle cohesion is challenged by intrinsic and extrinsic stressors, and understanding the underlying mechanisms will probably benefit the development of interventions to promote hearing health. [ABSTRACT FROM AUTHOR]
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- 2024
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9. Astrocyte dysregulation as an epileptogenic factor: a systematic review.
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Sumadewi, Komang Trisna, de Liyis, Bryan Gervais, Linawati, Ni Made, Widyadharma, I Putu Eka, and Astawa, I Nyoman Mantik
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CALCIUM-binding proteins ,GABA transporters ,GTPASE-activating protein ,GLUTAMATE transporters ,INTRACELLULAR calcium - Abstract
Background: Epilepsy initiation involves multifactorial etiologies, including genetic susceptibility, structural anomalies, and glial cell dysregulations, particularly in astrocytes. Despite advancements in understanding various factors, the mechanisms of astrocyte dysregulation in epilepsy, critical for neural homeostasis, remain elusive, requiring comprehensive evaluation of molecular pathways and cellular interactions for future targeted interventions. Methods: A systematic search of PubMed, ScienceDirect, and the Cochrane databases up to January 1st 2024 identified relevant studies predominantly from experimental models, forming the basis for an in-depth analysis of astrocytic contributions to epileptic pathophysiology. The aims, subjects, epilepsy induction techniques, assessment methods, and findings of each studies were presented. Results: A total of 24 clinical trials met the inclusion criteria and were included in the systematic review. Altered potassium buffering compromises extracellular potassium regulation, fostering hyperexcitability. Aquaporin dysfunction disrupts water homeostasis, aggravating seizure susceptibility. Disturbances in glutamatergic transmission, marked by changes in glutamate transporter function, contribute to excitotoxicity, fueling epileptogenesis. Intricacies in calcium signaling and disruptions in calcium-binding proteins tip intracellular calcium balance towards hyperexcitability. Dysfunctional GABA transporters compromise inhibitory neurotransmission, upsetting excitatory–inhibitory balance. Gap junction protein dysregulation disrupts astroglial networks, impacting neuronal synchronization in epileptogenic circuitry. Compromised BBB allows entry of epileptogenic factors, exacerbating the epileptogenic milieu. Conclusions: Collectively, these astrocytic dysregulations unveil intricate contributors to epilepsy onset and progression. [ABSTRACT FROM AUTHOR]
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- 2024
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10. Significance of Duodenal Prolactin Receptor Modulation by Calcium and Vitamin D in Sulpiride-Induced Hyperprolactinemia.
- Author
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Radojkovic, Danijela Branislav, Pesic, Milica, Radojkovic, Milan, Vukelic Nikolic, Marija, Jevtovic Stoimenov, Tatjana, Radenkovic, Sasa, Ciric, Vojislav, Basic, Dijana, and Radjenovic Petkovic, Tatjana
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VITAMIN D ,BONE health ,HYPERPROLACTINEMIA ,CALCIUM ,BONE density - Abstract
Background and Objectives: Hyperprolactinemia, as a potential side-effect of some antipsychotic medications, is associated with decreased bone density and an increased risk of fractures. This study investigates whether calcium and vitamin D supplementation affects prolactin receptor (Prlr) gene expression in the duodenum, vertebrae, and kidneys of female rats with sulpiride-induced hyperprolactinemia. Materials and Methods: Twenty-one-week-old female Wistar rats were assigned to three groups: Group S consisted of ten rats who received sulpiride injections (10 mg/kg) twice daily for 6 weeks; Group D (10 rats) received daily supplementation of 50 mg calcium and 500 IU vitamin D along with sulpiride for the last 3 weeks; and Group C consisting of seven age-matched nulliparous rats serving as a control group. Real-time PCR was used to assess Prlr gene expression in the duodenum, vertebrae, and kidneys. Results: In Group S, Prlr gene expression was notably decreased in the duodenum (p < 0.01) but elevated in the vertebrae and kidneys compared to Group C. Conversely, Group D exhibited significantly increased Prlr expression in the duodenum (p < 0.01) alongside elevated expression in the vertebrae and kidneys. Conclusions: In sulpiride-induced hyperprolactinemia, decreased Prlr gene expression in the duodenum may lead to reduced intestinal calcium absorption. Consequently, prolactin may draw calcium from the skeletal system to maintain calcium balance, facilitated by increased Prlr gene expression in the vertebrae. However, vitamin D supplementation in sulpiride-induced hyperprolactinemia notably enhances Prlr gene expression in the duodenum, potentially ameliorating intestinal calcium absorption and mitigating adverse effects on bone health. [ABSTRACT FROM AUTHOR]
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- 2024
- Full Text
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11. Functional Analysis and Tissue-Specific Expression of Calcitonin and CGRP with RAMP-Modulated Receptors CTR and CLR in Chickens.
- Author
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Huang, Tianjiao, Su, Jiancheng, Wang, Xinglong, Shi, Ningkun, Zhang, Xiao, He, Jiliang, Li, Juan, Zhang, Jiannan, and Wang, Yajun
- Abstract
Simple Summary: Our study provides an insightful look into the molecular interaction mechanisms of calcitonin and calcitonin gene-related peptide in chickens. The study highlights distinct pathways activated by these receptors and demonstrates that the calcitonin receptor and calcitonin receptor-like receptors have unique sensitivities to their ligands, which can be influenced by receptor activity-modifying proteins. Furthermore, an extensive expression analysis across chicken tissue revealed diverse roles for calcitonin and calcitonin gene-related peptide in avian biology. Our findings provide a fresh perspective on the evolutionary variations in hormone signaling between chickens and mammals, broadening the scope of knowledge in vertebrate endocrine systems. Calcitonin (CT) and calcitonin gene-related peptide (CGRP) are critical regulators of calcium balance and have extensive implications for vertebrate physiological processes. This study explores the CT and CGRP signaling systems in chickens through cloning and characterization of the chicken calcitonin receptor (CTR) and calcitonin receptor-like receptor (CLR), together with three receptor activity-modifying proteins (RAMPs). We illuminated the functional roles for chickens between the receptors examined alone and in RAMP-associated complexes using luciferase reporter assays. Chicken CTRs and CLRs stimulated the cAMP/PKA and MAPK/ERK signaling pathways, signifying their functional receptor status, with CT showing appreciable ligand activity at nanomolar concentrations across receptor combinations. Notably, it is revealed that chicken CLR can act as a functional receptor for CT without or with RAMPs. Furthermore, we uncovered a tissue-specific expression profile for CT, CGRP, CTR, CLR, and RAMPs in chickens, indicating the different physiological roles across various tissues. In conclusion, our data establish a clear molecular basis to reveal information on CT, CGRP, CTR, CLR, and RAMPs in chickens and contribute to understanding the conserved or divergent functions of this family in vertebrates. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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12. Activating mutations in JAK2 and CALR differentially affect intracellular calcium flux in store operated calcium entry.
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Bhuria, Vikas, Franz, Tobias, Baldauf, Conny, Böttcher, Martin, Chatain, Nicolas, Koschmieder, Steffen, Brümmendorf, Tim H., Mougiakakos, Dimitrios, Schraven, Burkhart, Kahlfuß, Sascha, and Fischer, Thomas
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INTRACELLULAR calcium ,ERYTHROPOIETIN receptors ,CALCIUM ,PHYSIOLOGIC salines ,CELL physiology ,CELL migration ,CELL growth - Abstract
Background: Calcium (Ca
2+ ) signaling regulates various vital cellular functions, including integrin activation and cell migration. Store-operated calcium entry (SOCE) via calcium release-activated calcium (CRAC) channels represents a major pathway for Ca2+ influx from the extracellular space in multiple cell types. The impact of JAK2-V617F and CALR mutations which are disease initiating in myeloproliferative neoplasms (MPN) on SOCE, calcium flux from the endoplasmic reticulum (ER) to the cytosol, and related key signaling pathways in the presence or absence of erythropoietin (EPO) or thrombopoietin (TPO) is poorly understood. Thus, this study aimed to elucidate the effects of these mutations on the aforementioned calcium dynamics, in cellular models of MPN. Methods: Intracellular Ca2+ levels were measured over a time frame of 0–1080 s in Fura-2 AM labeled myeloid progenitor 32D cells expressing various mutations (JAK2-WT/EpoR, JAK2-V617F/EpoR; CALR-WT/MPL, CALR-ins5/MPL, and del52/MPL). Basal Ca2+ concentrations were assessed from 0–108 s. Subsequently, cells were stimulated with EPO/TPO in Ca2+ -free Ringer solution, measuring Ca2+ levels from 109–594 s (store depletion). Then, 2 mM of Ca2+ buffer resembling physiological concentrations was added to induce SOCE, and Ca2+ levels were measured from 595–1080 s. Fura-2 AM emission ratios (F340/380) were used to quantify the integrated Ca2+ signal. Statistical significance was assessed by unpaired Student's t-test or Mann–Whitney-U-test, one-way or two-way ANOVA followed by Tukey's multiple comparison test. Results: Following EPO stimulation, the area under the curve (AUC) representing SOCE significantly increased in 32D-JAK2-V617F cells compared to JAK2-WT cells. In TPO-stimulated CALR cells, we observed elevated Ca2+ levels during store depletion and SOCE in CALR-WT cells compared to CALR-ins5 and del52 cells. Notably, upon stimulation, key components of the Ca2+ signaling pathways, including PLCγ-1 and IP3R, were differentially affected in these cell lines. Hyper-activated PLCγ-1 and IP3R were observed in JAK2-V617F but not in CALR mutated cells. Inhibition of calcium regulatory mechanisms suppressed cellular growth and induced apoptosis in JAK2-V617F cells. Conclusions: This report highlights the impact of JAK2 and CALR mutations on Ca2+ flux (store depletion and SOCE) in response to stimulation with EPO and TPO. The study shows that the JAK2-V617F mutation strongly alters the regulatory mechanism of EpoR/JAK2-dependent intracellular calcium balance, affecting baseline calcium levels, EPO-induced calcium entry, and PLCγ-1 signaling pathways. Our results reveal an important role of calcium flux in the homeostasis of JAK2-V617F positive cells. [ABSTRACT FROM AUTHOR]- Published
- 2024
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13. The Most Important Metabolic Diseases in Dairy Cattle during the Transition Period.
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Tufarelli, Vincenzo, Puvača, Nikola, Glamočić, Dragan, Pugliese, Gianluca, and Colonna, Maria Antonietta
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DAIRY cattle ,METABOLIC disorders ,MASTITIS ,CATTLE diseases ,HEALTH of cattle ,CATTLE productivity ,LACTATION in cattle - Abstract
Simple Summary: This review delves into key metabolic diseases affecting dairy cattle such as subacute ruminal acidosis (SARA), ketosis, and hypocalcemia. The aim of this review was to examine each disease in terms of its etiology, pathophysiology, clinical manifestations, diagnostic approaches, and treatment and prevention strategies. This review emphasizes early diagnosis and proactive management, so it can serve as a valuable resource for veterinarians, researchers, and dairy farmers, offering insights into the prevention and treatment of these prevalent metabolic diseases in dairy cattle. This review paper provides an in-depth analysis of three critical metabolic diseases affecting dairy cattle such as subacute ruminal acidosis (SARA), ketosis, and hypocalcemia. SARA represents a disorder of ruminal fermentation that is characterized by extended periods of depressed ruminal pH below 5.5–5.6. In the long term, dairy herds experiencing SARA usually exhibit secondary signs of the disease, such as episodes of laminitis, weight loss and poor body condition despite adequate energy intake, and unexplained abscesses usually 3–6 months after an episode of SARA. Depressed milk-fat content is commonly used as a diagnostic tool for SARA. A normal milk-fat test in Holstein dairy cows is >4%, so a milk-fat test of <3% can indicate SARA. However, bulk tank testing of milk fat is inappropriate to diagnose SARA at the herd level, so when >4 cows out of 12 and <60 days in milk are suspected to have SARA it can be considered that the herd has a problem. The rapid or abrupt introduction of fresh cows to high-concentrate diets is the most common cause of SARA. Changes in ruminal bacterial populations when exposed to higher concentrate rations require at least about 3 weeks, and it is recommended that concentrate levels increase by no more than 400 g/day during this period to avoid SARA. Ketosis, a prevalent metabolic disorder in dairy cattle, is scrutinized with a focus on its etiological factors and the physiological changes leading to elevated ketone bodies. In total mix ration-fed herds, an increased risk of mastitis and reduced fertility are usually the first clinical signs of ketosis. All dairy cows in early lactation are at risk of ketosis, with most cases occurring in the first 2–4 weeks of lactation. Cows with a body condition score ≥3.75 on a 5-point scale at calving are at a greater risk of ketosis than those with lower body condition scores. The determination of serum or whole blood acetone, acetoacetate, beta-hydroxybutyrate (BHB) concentration, non-esterified fatty acids (NEFA), and liver biopsies is considered the best way to detect and monitor subclinical ketosis, while urine or milk cowside tests can also be used in on-farm monitoring programs. Concentrations >1.0 mmol/L or 1.4 mmol/L blood or serum BHB are considered diagnostic of subclinical ketosis. The standard threshold used for blood is 1.2 mmol/L, which corresponds to thresholds of 100 mcmol/L for milk and 15 mg/dL for urine. Oral administration of propylene glycol (250–400 g, every 24 h for 3–5 days) is the standard and most efficacious treatment, as well as additional therapy with bolus glucose treatment. Hypocalcemia is a disease of adult dairy cows in which acute hypocalcemia causes acute to peracute, afebrile, flaccid paralysis that occurs most commonly at or soon after parturition. Dairy cows are at considerable risk for hypocalcemia at the onset of lactation, when daily calcium excretion suddenly increases from about 10 g to 30 g per day. Cows with hypocalcemia have a more profound decrease in blood calcium concentration—typically below 5.5 mg/dL. The prevention of parturient paresis has been historically approached by feeding cows low-calcium diets during the dry period. Negative calcium balance triggers calcium mobilization before calving and better equips the cow to respond to the massive calcium needs at the onset of lactation. Calcium intake must be limited to <20 g per day for calcium restriction to be effective. The most practical and proven method for monitoring hypocalcemia is by feeding cows an acidogenic diet for ~3 weeks before calving. Throughout the review, emphasis is placed on the importance of early diagnosis and proactive management strategies to mitigate the impact of these metabolic diseases on dairy cattle health and productivity. The comprehensive nature of this paper aims to serve as a valuable resource for veterinarians, researchers, and dairy farmers seeking a deeper understanding of these prevalent metabolic disorders in dairy cattle. [ABSTRACT FROM AUTHOR]
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- 2024
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14. Recommended calcium intake in adults and children with chronic kidney disease—a European consensus statement.
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Evenepoel, Pieter, Jørgensen, Hanne Skou, Bover, Jordi, Davenport, Andrew, Bacchetta, Justine, Haarhaus, Mathias, Hansen, Ditte, Gracia-Iguacel, Carolina, Ketteler, Markus, McAlister, Louise, White, Emily, Mazzaferro, Sandro, Vervloet, Marc, and Shroff, Rukshana
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BONE fractures , *RENAL osteodystrophy , *PEDIATRIC nephrology , *CHRONIC kidney failure , *HYPERPHOSPHATEMIA , *BONE health , *CALCIUM - Abstract
Mineral and bone disorders (MBD) are common in patients with chronic kidney disease (CKD), contributing to significant morbidity and mortality. For several decades, the first-line approach to controlling hyperparathyroidism in CKD was by exogenous calcium loading. Since the turn of the millennium, however, a growing awareness of vascular calcification risk has led to a paradigm shift in management and a move away from calcium-based phosphate binders. As a consequence, contemporary CKD patients may be at risk of a negative calcium balance, which, in turn, may compromise bone health, contributing to renal bone disease and increased fracture risk. A calcium intake below a certain threshold may be as problematic as a high intake, worsening the MBD syndrome of CKD, but is not addressed in current clinical practice guidelines. The CKD-MBD and European Renal Nutrition working groups of the European Renal Association (ERA), together with the CKD-MBD and Dialysis working groups of the European Society for Pediatric Nephrology (ESPN), developed key evidence points and clinical practice points on calcium management in children and adults with CKD across stages of disease. These were reviewed by a Delphi panel consisting of ERA and ESPN working groups members. The main clinical practice points include a suggested total calcium intake from diet and medications of 800–1000 mg/day and not exceeding 1500 mg/day to maintain a neutral calcium balance in adults with CKD. In children with CKD, total calcium intake should be kept within the age-appropriate normal range. These statements provide information and may assist in decision-making, but in the absence of high-level evidence must be carefully considered and adapted to individual patient needs. [ABSTRACT FROM AUTHOR]
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- 2024
- Full Text
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15. Assessing the Impact of Contraceptives on Bone Health Using 41Ca
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Purdue University and Mary Jane DeSouza, Professor of Kinesiology and Physiology
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- 2024
16. Calcium mass balance in adults during single hemodialysis and hemodiafiltration treatments using lower calcium dialysate concentrations.
- Author
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Chhabra, Roohi and Davenport, Andrew
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CONFIDENCE intervals , *HEMODIAFILTRATION , *CALCIUM , *HEMODIALYSIS , *DIALYSIS (Chemistry) - Abstract
Background: Debate continues as to the optimum hemodialysis (HD) dialysate calcium concentration. Although current guidelines advocate 1.25–1.5 mmol/L, some investigators have suggested these may cause calcium gains. As such we investigated whether using dialysate calcium of 1.25 mmol/L risked calcium gains, and whether there were differences between hemodiafiltration and high flux HD. Methods: We continuously collect an aliquot of effluent dialysate during dialysis sessions, and calculated dialysis calcium mass balance by the difference between the amount of calcium delivered as fresh dialysate and that lost in effluent dialysate. Results: We studied 106 stable outpatients, 64% male, mean age 64.4 ± 16.2 years, median dialysis vintage 32 (22–60) months. Most sessions (69%) used a 1.0 mmol/L calcium dialysate, with a median sessional loss of 13.7 (11.5–17.1) mmol, whereas using 1.25 mmol/L the median loss was 7.4 (4.9–10.1) mmol, but with 6.9% had a positive balance (p = 0.031 vs dialysate calcium 1.0 mmol/L). Most patients (85.8%) were treated by hemodiafiltration, but there was no difference in sessional losses (11.7 (8.4–15.8) vs 13.5 (8.1–16.8)) with high flux HD. Dialysis sessional calcium balance was associated with the use of lower dialysate calcium concentration (β −19.5, 95% confidence limits (95%CL) −27.7 to −11.3, p < 0.001), and sessional duration (β 0.07 (95% CL) 0.03–012, p = 0.002). Conclusion: Ideally, the choice of dialysate calcium should be individualized, but clinicians should be aware, that even when using a dialysate calcium of 1.25 mmol/L, some patients are at risk of a calcium gain during hemodiafiltration and high‐flux hemodialysis. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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17. Calcium signalling and transport in the kidney.
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Staruschenko, Alexander, Alexander, R. Todd, Caplan, Michael J., and Ilatovskaya, Daria V.
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POLYCYSTIC kidney disease , *FOCAL segmental glomerulosclerosis , *CALCIUM , *CALCIUM-binding proteins , *KIDNEY tubules - Abstract
The kidney plays a pivotal role in regulating calcium levels within the body. Approximately 98% of the filtered calcium is reabsorbed in the nephron, and this process is tightly controlled to maintain calcium homeostasis, which is required to facilitate optimal bone mineralization, preserve serum calcium levels within a narrow range, and support intracellular signalling mechanisms. The maintenance of these functions is attributed to a delicate balance achieved by various calcium channels, transporters, and calcium-binding proteins in renal cells. Perturbation of this balance due to deficiency or dysfunction of calcium channels and calcium-binding proteins can lead to severe complications. For example, polycystic kidney disease is linked to aberrant calcium transport and signalling. Furthermore, dysregulation of calcium levels can promote the formation of kidney stones. This Review provides an updated description of the key aspects of calcium handling in the kidney, focusing on the function of various calcium channels and the physiological stimuli that control these channels or are communicated through them. A discussion of the role of calcium as an intracellular second messenger and the pathophysiology of renal calcium dysregulation, as well as a summary of gaps in knowledge and future prospects, are also included. Calcium reabsorption along the nephron is essential for calcium homeostasis and whole-body electrolyte balance. Here, Staruschenko et al. highlight signalling pathways and molecules involved in renal calcium handling in health and disease, and discuss progress in the integration of systems-level and molecular understanding of calcium transport and regulation. Key points: The kidney has an essential role in the maintenance of serum calcium levels owing to its careful regulation of reabsorption along the nephron, which contributes to whole-body calcium balance. Physiologically relevant mechanisms that control calcium channels in the kidney include endocrine and paracrine signals and physical factors such as fluid flow. Tight control of calcium influx and intracellular calcium levels maintains intracellular calcium concentrations within the physiological range, despite acute and chronic variation in calcium intake. Failure to reabsorb calcium from renal tubules results in hypercalciuria and an increased risk of kidney stones. Aberrant calcium signalling in particular renal cell types is a hallmark of renal diseases such as polycystic kidney disease and focal segmental glomerulosclerosis. [ABSTRACT FROM AUTHOR]
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- 2024
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18. Cardiomyopathy in Duchenne Muscular Dystrophy and the Potential for Mitochondrial Therapeutics to Improve Treatment Response.
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Gandhi, Shivam, Sweeney, H. Lee, Hart, Cora C., Han, Renzhi, and Perry, Christopher G. R.
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DUCHENNE muscular dystrophy , *MYOCARDIUM , *DYSTROPHIN genes , *REACTIVE oxygen species , *NEUROMUSCULAR diseases - Abstract
Duchenne muscular dystrophy (DMD) is a progressive neuromuscular disease caused by mutations to the dystrophin gene, resulting in deficiency of dystrophin protein, loss of myofiber integrity in skeletal and cardiac muscle, and eventual cell death and replacement with fibrotic tissue. Pathologic cardiac manifestations occur in nearly every DMD patient, with the development of cardiomyopathy—the leading cause of death—inevitable by adulthood. As early cardiac abnormalities are difficult to detect, timely diagnosis and appropriate treatment modalities remain a challenge. There is no cure for DMD; treatment is aimed at delaying disease progression and alleviating symptoms. A comprehensive understanding of the pathophysiological mechanisms is crucial to the development of targeted treatments. While established hypotheses of underlying mechanisms include sarcolemmal weakening, upregulation of pro-inflammatory cytokines, and perturbed ion homeostasis, mitochondrial dysfunction is thought to be a potential key contributor. Several experimental compounds targeting the skeletal muscle pathology of DMD are in development, but the effects of such agents on cardiac function remain unclear. The synergistic integration of small molecule- and gene-target-based drugs with metabolic-, immune-, or ion balance-enhancing compounds into a combinatorial therapy offers potential for treating dystrophin deficiency-induced cardiomyopathy, making it crucial to understand the underlying mechanisms driving the disorder. [ABSTRACT FROM AUTHOR]
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- 2024
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19. Deciphering simplified regional anticoagulation with citrate in intermittent hemodialysis: a clinical and computational study
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Julien Aniort, Felix Richard, François Thouy, Louis Le Guen, Carole Philipponnet, Cyril Garrouste, Anne Elisabeth Heng, Claire Dupuis, Mireille Adda, Durif Julie, Lebredonchel Elodie, Laurent Chupin, Damien Bouvier, Bertrand Souweine, and Nicolae Cindea
- Subjects
Hemodialysis ,Calcium ,Citrate ,Dialysate ,Modeling ,Anticoagulation ,Medicine ,Science - Abstract
Abstract Regional citrate anticoagulation use in intermittent hemodialysis is limited by the increased risk of metabolic complications due to faster solute exchanges than with continuous renal replacement therapies. Several simplifications have been proposed. The objective of this study was to validate a mathematical model of hemodialysis anticoagulated with citrate that was then used to evaluate different prescription scenarios on anticoagulant effectiveness (free calcium concentration in dialysis filter) and calcium balance. A study was conducted in hemodialyzed patients with a citrate infusion into the arterial line and a 1.25 mmol/L calcium dialysate. Calcium and citrate concentrations were measured upstream and downstream of the citrate infusion site and in the venous line. The values measured in the venous lines were compared with those predicted by the model using Bland and Altman diagrams. The model was then used with 22 patients to make simulations. The model can predict the concentration of free calcium, bound to citrate or albumin, accurately. Irrespective of the prescription scenario a decrease in free calcium below 0.4 mmol/L was obtained only in a fraction of the dialysis filter. A zero or slightly negative calcium balance was observed, and should be taken into account in case of prolonged use.
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- 2024
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20. The study of the joint effect of the probiotic and the sorbent in the growing of pigs.
- Author
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Pskhatsieva, Zemfira, Bulatseva, Svetlana, Yurin, Denis, Tletseruk, Irina, and Gneush, Anna
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- 2024
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21. Pathophysiology of Cardiac Amyloidosis
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Morfino, Paolo, Aimo, Alberto, Franzini, Maria, Vergaro, Giuseppe, Castiglione, Vincenzo, Panichella, Giorgia, Limongelli, Giuseppe, and Emdin, Michele
- Abstract
Amyloidosis refers to a heterogeneous group of disorders sharing common pathophysiological mechanisms characterized by the extracellular accumulation of fibrillar deposits consisting of the aggregation of misfolded proteins. Cardiac amyloidosis (CA), usually caused by deposition of misfolded transthyretin or immunoglobulin light chains, is an increasingly recognized cause of heart failure burdened by a poor prognosis. CA manifests with a restrictive cardiomyopathy which progressively leads to biventricular thickening, diastolic and then systolic dysfunction, arrhythmias, and valvular disease. The pathophysiology of CA is multifactorial and includes increased oxidative stress, mitochondrial damage, apoptosis, impaired metabolism, and modifications of intracellular calcium balance.
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- 2024
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22. Spatial and single-cell explorations uncover prognostic significance and immunological functions of mitochondrial calcium uniporter in breast cancer
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Chia-Jung Li, Yen-Dun Tony Tzeng, Jui-Hu Hsiao, Ling-Ming Tseng, Tzu-Sheng Hsu, and Pei-Yi Chu
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MCU ,Immune infiltration ,Breast cancer ,Single-cell RNA-sequencing ,Spatial transcriptomics ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 ,Cytology ,QH573-671 - Abstract
Abstract The mitochondrial calcium uniporter (MCU) is a transmembrane protein facilitating the entry of calcium ions into mitochondria from the cell cytosol. Maintaining calcium balance is crucial for enhancing cellular energy supply and regulating cell death. The interplay of calcium balance through MCU and the sodium-calcium exchanger is known, but its regulation in the breast cancer tumor microenvironment remains elusive. Further investigations are warranted to explore MCU’s potential in BRCA clinical pathology, tumor immune microenvironment, and precision oncology. Our study, employing a multi-omics approach, identifies MCU as an independent diagnostic biomarker for breast cancer (BRCA), correlated with advanced clinical status and poor overall survival. Utilizing public datasets from GEO and TCGA, we discern differentially expressed genes in BRCA and examine their associations with immune gene expression, overall survival, tumor stage, gene mutation status, and infiltrating immune cells. Spatial transcriptomics is employed to investigate MCU gene expression in various regions of BRCA, while spatial transcriptomics and single-cell RNA-sequencing methods explore the correlation between MCUs and immune cells. Our findings are validated through the analysis of 59 BRCA patient samples, utilizing immunohistochemistry and bioinformatics to examine the relationship between MCU expression, clinicopathological features, and prognosis. The study uncovers the expression of key gene regulators in BRCA associated with genetic variations, deletions, and the tumor microenvironment. Mutations in these regulators positively correlate with different immune cells in six immune datasets, playing a pivotal role in immune cell infiltration in BRCA. Notably, high MCU performance is linked to CD8 + T cells infiltration in BRCA. Furthermore, pharmacogenomic analysis of BRCA cell lines indicates that MCU inactivation is associated with increased sensitivity to specific small molecule drugs. Our findings suggest that MCU alterations may be linked to BRCA progression, unveiling new diagnostic and prognostic implications for MCU in BRCA. The study underscores MCU's role in the tumor immune microenvironment and cell cycle progression, positioning it as a potential tool for BRCA precision medicine and drug screening.
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- 2024
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23. 女贞子防治骨质疏松症药理机制的研究.
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吴爽, 赵悦彤, 路晓洁, 刑云泽, and 杨波
- Abstract
Osteoporosis (OP) is a common bone metabolic disease. With the increase of aging in China, OP is a public health problem that is widely concerned in China today. Fructus ligustri lucidi (FLL), as a kidney-tonifying traditional Chinese medicine, is widely used in clinical practice and has unique advantages in the prevention and treatment of OP. Research has shown that FLL extract has a bone protective effect and reduces bone loss. However, its mechanism of action is not completely clear. Hence, this article employs databases like CNKI and PubMed to conduct a comprehensive search for pertinent domestic and international literature published within the last 15 years, utilizing keywords such as OP, FLL, osteogenesis, among others. Drawing upon existing research, this article primarily examines the preventive and therapeutic mechanism of FLL in relation to OP, including calcium balance, oxidative stress, bone metabolism, and parahormone effect. The aim is to furnish a foundation for future investigation on the role of FLL in preventing and treating OP, while also offering insights into the potential of traditional Chinese medicine in addressing this condition. [ABSTRACT FROM AUTHOR]
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- 2024
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24. Cardiorenal Syndrome: An Evolutionary Appraisal.
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Young, James B. and Eknoyan, Garabed
- Abstract
A recent American Heart Association Scientific Statement and Presidential Advisory recognized a new syndrome, the cardiovascular-kidney-metabolic syndrome. This expands our understanding of what has been called cardiorenal syndrome by incorporating the pathophysiological interrelatedness of metabolic risk factors into the previous concept of cardiorenal syndrome. Importantly, perturbation of cardiac or renal physiology combines to produce significant detrimental outcomes. The cardiorenal syndrome is a significant part of the cardiovascular-kidney-metabolic syndrome and contributes to health care cost, disability, and mortality. It is a vexing malady that has generated considerable interest. To understand the syndrome evaluation of its teleological origins is important. In life's beginning, eukaryotes acquired exocytosis for excretion, formed tubular secretory systems for clearance, and a mesenchymal nucleic acid vasoform for nutritional distribution. Those structures progressed to cardiovascular and renal systems of evolving organisms, whose migration to rivers and land imposed complex, coordinated, homeostatic roles to maintain intravascular stability. Tissue mineralization of vertebrate endoskeleton added renal calcium balance regulation, which in kidney failure results in cardiovascular calcification. Insight into cardiorenal disease can be traced to ancient Egyptian and Chinese medicine, through the Scientific Revolution, and into current insights regarding human physiology and pathophysiology. The post-World War II epidemic of cardiovascular mortality generated considerable information on cardiovascular disease, which being higher in patients with kidney disease, drew increasing health concerns. The cardiorenal syndrome was formally introduced in this setting with a focus on ultrafiltration to manage volume overload. An evolutionary review of insight into cardiorenal syndrome will help us better understand the new cardiovascular-kidney-metabolic syndrome. [ABSTRACT FROM AUTHOR]
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- 2024
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25. Calcium and vitamin D homoeostasis in male fertility.
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Yahyavi, Sam Kafai, Boisen, Ida Marie, Cui, Zhihui, Jorsal, Mads Joon, Kooij, Ireen, Holt, Rune, Juul, Anders, and Blomberg Jensen, Martin
- Abstract
Calcium and vitamin D have well-established roles in maintaining calcium balance and bone health. Decades of research in human subjects and animals have revealed that calcium and vitamin D also have effects on many other organs including male reproductive organs. The presence of calcium-sensing receptor, vitamin D receptor, vitamin D activating and inactivating enzymes and calcium channels in the testes, male reproductive tract and human spermatozoa suggests that vitamin D and calcium may modify male reproductive function. Functional animal models have shown that vitamin D deficiency in male rodents leads to a decrease in successful mating and fewer pregnancies, often caused by impaired sperm motility and poor sperm morphology. Human studies have to a lesser extent validated these findings; however, newer studies suggest a positive effect of vitamin D supplementation on semen quality in cases with vitamin D deficiency, which highlights the need for initiatives to prevent vitamin D deficiency. Calcium channels in male reproductive organs and spermatozoa contribute to the regulation of sperm motility and capacitation, both essential for successful fertilisation, which supports a need to avoid calcium deficiency. Studies have demonstrated that vitamin D, as a regulator of calcium homoeostasis, influences calcium influx in the testis and spermatozoa. Emerging evidence suggests a potential link between vitamin D deficiency and male infertility, although further investigation is needed to establish a definitive causal relationship. Understanding the interplay between vitamin D, calcium and male reproductive health may open new avenues for improving fertility outcomes in men. [ABSTRACT FROM AUTHOR]
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- 2024
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26. 口蹄疫疫苗诱发奶牛瘫痪的诊疗分析案例.
- Author
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王少利
- Abstract
Copyright of China Dairy is the property of China Dairy Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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- 2024
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27. Factors contributing to vitamin D deficiency in Erbil, Iraq: A statistical investigation
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Blbas, Hazhar Talaat Abubaker, Kahwachi, Wasfi Taher Saalih, Ahmed, Sirwan Khalid, Aziz, Khanda Gharib, Faraj, Shahen Mohammed, and Mohammed, Mohammed Subhan
- Abstract
Scientific evidence supports vitamin D's ability to prevent and treat a wide range of diseases, and its physiological importance extends to calcium balance and bone health. This study aimed to find the factors associated with vitamin D deficiency in Erbil, Iraq.
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- 2024
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28. Involvement of nucleus accumbens SERCA2b in methamphetamine‐induced conditioned place preference.
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Wang, Yujing, Duan, Fan, Li, Junda, Li, Xiangyu, Xia, Lingling, Zhao, Wei, Wang, Ze, Song, Xun, Chen, Juan, Wang, Jingjing, Wang, Yue, Zhang, Jing, Zhang, Xiaochu, and Jiao, Dongliang
- Subjects
- *
METHAMPHETAMINE , *NUCLEUS accumbens , *CALCIUM ions , *REWARD (Psychology) , *ION transport (Biology) , *ENDOPLASMIC reticulum - Abstract
Methamphetamine (METH) is a highly addictive psycho‐stimulant that induces addictive behaviour by stimulating increased dopamine release in the nucleus accumbens (NAc). The sarco/endoplasmic reticulum calcium ion transport ATPases (SERCA or ATP2A) is a calcium ion (Ca2+) pump in the endoplasmic reticulum (ER) membrane. SERCA2b is a SERCA subtype mainly distributed in the central nervous system. This study used conditioned place preference (CPP), a translational drug reward model, to observe the effects of SERCA and SERCA2b on METH‐CPP in mice. Result suggested that the activity of SERCA was significantly decreased in NAc after METH‐CPP. Intraperitoneal SERCA agonist CDN1163 injection or bilateral CDN1163 microinjection in the NAc inhibited METH‐CPP formation. SERCA2b overexpression by the Adeno‐associated virus can reduce the DA release of NAc and inhibit METH‐CPP formation. Although microinjection of SERCA inhibitor thapsigargin in the bilateral NAc did not significantly aggravate METH‐CPP, interference with SERCA2b expression in NAc by adeno‐associated virus increased DA release and promoted METH‐CPP formation. METH reduced the SERCA ability to transport Ca2+ into the ER in SHSY5Y cells in vitro, which was reversed by CDN1163. This study revealed that METH dysregulates intracellular calcium balance by downregulating SERCA2b function, increasing DA release in NAc and inducing METH‐CPP formation. Drugs that target SERCA2b may have the potential to treat METH addiction. [ABSTRACT FROM AUTHOR]
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- 2024
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29. Chronic kidney disease mineral bone disorder in childhood and young adulthood: a 'growing' understanding.
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Lalayiannis, Alexander D., Soeiro, Emilia M. D., Moysés, Rosa M. A., and Shroff, Rukshana
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BONE growth ,OSTEOCLASTS ,OSTEOBLASTS ,RENAL osteodystrophy ,RISK assessment ,VITAMIN D ,BONE remodeling ,CALCINOSIS ,CONNECTIVE tissue cells ,DIETARY calcium ,PHOSPHATES ,DISEASE complications ,CHILDREN ,ADULTS - Abstract
Chronic kidney disease (CKD) mineral and bone disorder (MBD) comprises a triad of biochemical abnormalities (of calcium, phosphate, parathyroid hormone and vitamin D), bone abnormalities (turnover, mineralization and growth) and extra-skeletal calcification. Mineral dysregulation leads to bone demineralization causing bone pain and an increased fracture risk compared to healthy peers. Vascular calcification, with hydroxyapatite deposition in the vessel wall, is a part of the CKD-MBD spectrum and, in turn, leads to vascular stiffness, left ventricular hypertrophy and a very high cardiovascular mortality risk. While the growing bone requires calcium, excess calcium can deposit in the vessels, such that the intake of calcium, calcium- containing medications and high calcium dialysate need to be carefully regulated. Normal physiological bone mineralization continues into the third decade of life, many years beyond the rapid growth in childhood and adolescence, implying that skeletal calcium requirements are much higher in younger people compared to the elderly. Much of the research into the link between bone (de)mineralization and vascular calcification in CKD has been performed in older adults and these data must not be extrapolated to children or younger adults. In this article, we explore the physiological changes in bone turnover and mineralization in children and young adults, the pathophysiology of mineral bone disease in CKD and a potential link between bone demineralization and vascular calcification. [ABSTRACT FROM AUTHOR]
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- 2024
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30. Redox signaling and antioxidant defense in osteoclasts.
- Author
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Tao, Huaqiang, Li, Xuefeng, Wang, Qiufei, Yu, Lei, Yang, Peng, Chen, Wenlong, Yang, Xing, Zhou, Jun, and Geng, Dechun
- Subjects
- *
OSTEOCLASTS , *BONE resorption , *BONE remodeling , *BONE growth , *OXIDATION-reduction reaction - Abstract
Bone remodeling is essential for the repair and replacement of damaged or aging bones. Continuous remodeling is necessary to prevent the accumulation of bone damage and to maintain bone strength and calcium balance. As bones age, the coupling mechanism between bone formation and absorption becomes dysregulated, and bone loss becomes dominant. Bone development and repair rely on interaction and communication between osteoclasts and surrounding cells. Osteoclasts are specialized cells that are accountable for bone resorption and degradation, and any abnormalities in their activity can result in notable alterations in bone structure and worsen disease symptoms. Recent findings from transgenic mouse models and bone analysis have greatly enhanced our understanding of the origin, differentiation pathway, and activation stages of osteoclasts. In this review, we explore osteoclasts and discuss the cellular and molecular events that drive their generation, focusing on intracellular oxidative and antioxidant signaling. This knowledge can help develop targeted therapies for diseases associated with osteoclast activation. [Display omitted] • Osteoclastic activation is often associated with redox instability in various bone diseases. • The mitigation of osteoclast overactivation shows promise for treating various bone-related disorders. • The surge of ROS leads to the overactivation of osteoclasts through multiple signaling pathways. • The establishment of an antioxidant system seems to have a positive effect in inhibiting osteoclasts. [ABSTRACT FROM AUTHOR]
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- 2024
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31. 41Ca的AMS测量方法及在生物医学领域的应用.
- Author
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毕艳婷 and 付云翀
- Abstract
Copyright of Journal of Isotopes is the property of Journal of Isotopes Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Published
- 2024
- Full Text
- View/download PDF
32. Characterization of a novel Ca2+-Activated potassium channel in rat brain rough endoplasmic reticulum.
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Fahanik-babaei, Javad, Bagheri, Maryam, and Salari, Sajjad
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- *
BILAYER lipid membranes , *WESTERN immunoblotting , *ENDOPLASMIC reticulum , *CELL membranes , *POTASSIUM channels , *ALZHEIMER'S disease - Abstract
Potassium channels in the endoplasmic reticulum (ER) are crucial for maintaining calcium balance during calcium fluxes. Disruption in ER calcium balance leads to ER stress, implicated in diseases like diabetes and Alzheimer's disease (AD). However, limited data exists on ER potassium channels in excitable tissues such as the brain. To fill this gap, we aimed to evaluate potassium currents in rat brain rough endoplasmic reticulum (RER). Rats were euthanized under deep anesthesia and their brains were immediately removed. The brains were then homogenized in ice-cold sucrose buffer, followed by the extraction of RER microsomes through a series of centrifugation processes. Purity of sample was evaluated using western blotting technique. Single channel recordings were done in voltage steps from +50 to −60 mV following incorporation of rat brain RER vesicles into planar bilayers. We observed a voltage-dependent potassium channel with an approximate conductance of 188 pS. Channel open probability was low at negative voltages, increasing at positive voltages. The channel was blocked by Charybdotoxin but not by Iberiotoxin. Additionally, TRAM-34, a specific KCa3.1 channel blocker, suppressed channel current amplitude and open probability. Western blot analysis revealed specific bands for anti -KCa3.1 antibody, approximately 50 kDa in brain homogenate and RER fraction. Our study provides strong evidence for the presence of an KCa3.1 channel on the RER membrane in rat brain, exhibiting distinct electro-pharmacological profile compared to plasma membrane and other organelles. [Display omitted] • Identified a novel potassium channel in rat brain rough endoplasmic reticulum (RER) with a conductance of approximately 188 pS, where the channel's open probability increases at positive voltages and decreases at negative voltages. • Channel open probability increases at positive voltages and decreases at negative voltages. • Channel blocked by Charybdotoxin but not by Iberiotoxin. • ATP has no effect on channel gating behavior at physiological concentrations. • TRAM-34, a KCa3.1-specific blocker, reduces channel current amplitude and open probability. • Western blot analysis detected a ∼50 kDa band for KCa3.1 in both brain homogenate and RER fraction. [ABSTRACT FROM AUTHOR]
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- 2024
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33. Adaptation of the Skeletal System During Long-Duration Spaceflight
- Author
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Sibonga, Jean, Cavanagh, Peter, Lang, Thomas, LeBlanc, Adrian, Schneider, Victor, Shackelford, Linda, Smith, Scott, and Vico, Laurence
- Abstract
Abstract: This review will highlight evidence from crew members flown on space missions >90 days to suggest that the adaptations of the skeletal system to mechanical unloading may predispose crew members to an accelerated onset of osteoporosis after return to Earth. By definition, osteoporosis is a skeletal disorder—characterized by low bone mineral density (BMD) and structural deterioration—that reduces the ability of bones to resist fracture under the loading of normal daily activities. “Involutional” or age-related osteoporosis is readily recognized as a syndrome afflicting the elderly population because of the insipid and asymptomatic nature of bone loss that does not typically manifest as fractures until after age ∼60. It is not the thesis of this review to suggest that spaceflight-induced bone loss is similar to bone loss induced by metabolic bone disease; rather this review draws parallels between the rapid and earlier loss in females that occurs with menopause and the rapid bone loss in middle-aged crew members that occurs with spaceflight unloading and how the cumulative effects of spaceflight and ageing could be detrimental, particularly if skeletal effects are totally or partially irreversible. In brief, this report will provide detailed evidence that long-duration crew members, exposed to the weightlessness of space for the typical long-duration (4–6 months) mission on Mir or the International Space Station, (1) display bone resorption that is aggressive, that targets normally weight-bearing skeletal sites, that is uncoupled to bone formation, and that results in areal BMD deficits that can range between 6 and 20% of preflight BMD; (2) display compartment-specific declines in volumetric BMD in the proximal femur (a skeletal site of clinical interest) that significantly reduces its compressive and bending strength and may account for the loss in hip bone strength (i.e., force to failure); (3) recover BMD over a post-flight time period that exceeds spaceflight exposure but for which the restoration of whole bone strength remains an open issue and may involve structural alteration; and (4) display risk factors for bone loss—such as the negative calcium balance and down-regulated calcium-regulating hormones in response to bone atrophy—that can be compounded by the constraints of conducting mission operations (inability to provide essential nutrients and vitamins). The full characterization of the skeletal response to mechanical unloading in space is not complete. In particular, countermeasures used to date have been inadequate, and it is not yet known whether more appropriate countermeasures can prevent the changes in bone that have been found in previous flights. Knowledge gaps related to the effects of prolonged (≥6 months) space exposure and to partial gravity environments are substantial, and longitudinal measurements on crew members after spaceflight are required to assess the full impact on skeletal recovery.
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- 2024
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34. Same therapy, same calcium mobilization? Exploring calcium exchange across body compartments using a patient-specific predictive model.
- Author
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Balsamello C, Mas MM, Rombolà G, Floreani R, Costantino ML, and Casagrande G
- Abstract
Background: Comprehensive, patient-specific models are essential to study calcium deposition and mobilization during dialysis. We aim to develop tools to support clinical prescriptions with a more accurate approach for the prediction of calcium mobilization while also considering major electrolytes and catabolites., Methods: We modified a multi-solute model predicting patient-specific dialysis response by incorporating a calcium buffer to represent bone exchanges. Data from four centers, involving 127 patients with six sessions each, were utilized. For each patient, three sessions were allocated for model training (ID
123 ), while the remaining sessions were for validation (PRED456). The normalized root mean square error (nRMSE%) was used to evaluate both descriptive and predictive accuracy. Correlations between initial data and calcium exchanges were also assessed., Results: The overall nRMSE% for ID123 was 3.92%. For PRED456 , it was 3.46% (ranging from a minimum of 1.17% for [Na+ ] to a maximum of 6.62% for [urea]). The median nRMSE% for plasma calcium varied between 1.13 and 8.32 for SHD sessions, depending on whether Ca_dialysis fluid (Cad ) was ≥ or <1.50 mmol/L, respectively. For HDF sessions, the range was between 2.90 and 5.89. A significant and moderate correlation was found between overall calcium removal and the buffer balance. The most robust correlation observed was between the amount of calcium administered via post-dilution fluid and the overall calcium removal in the dialysis filter., Conclusions: Identical therapy settings do not uniformly affect calcium mobilization, and our approach offers insight into calcium distribution across body compartments. This understanding will enhance clinical prescription practices., (© 2024 International Center for Artificial Organ and Transplantation (ICAOT) and Wiley Periodicals LLC.)- Published
- 2024
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35. The impact of low and high dialysate calcium concentrations on cardiovascular disease and death in patients undergoing maintenance hemodialysis: a systematic review and meta-analysis.
- Author
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Kamei K, Yamada S, Hashimoto K, Konta T, Hamano T, and Fukagawa M
- Subjects
- Humans, Randomized Controlled Trials as Topic, Parathyroid Hormone blood, Middle Aged, Vascular Calcification diagnostic imaging, Vascular Calcification prevention & control, Treatment Outcome, Renal Dialysis adverse effects, Calcium blood, Cardiovascular Diseases mortality, Cardiovascular Diseases prevention & control, Hemodialysis Solutions adverse effects, Hemodialysis Solutions chemistry
- Abstract
Background: The optimal dialysate calcium (Ca) concentration for patients undergoing hemodialysis remains inconclusive, particularly concerning cardiovascular protection., Methods: We conducted a systematic review of 19 randomized controlled trials (RCTs) and a meta-analysis of eight RCTs to determine the optimal dialysate Ca concentration for cardiovascular protection. We compared outcomes in patients receiving maintenance hemodialysis treated with either a low-Ca dialysate (LCD) (1.125 or 1.25 mmol/L) or a high-Ca dialysate (HCD) (1.5 or 1.75 mmol/L). The outcomes were coronary artery calcification score (CACS), all-cause and cardiovascular death, cardiovascular function and structure, and serum biochemical parameters., Results: There was no significant difference between LCD and HCD concerning CACS (standardized mean difference [SMD] = -0.16, 95% confidence interval [CI]: [-0.38, 0.07]), the risk of all-cause death, and cardiovascular death in patients treated with chronic maintenance hemodialysis. Conversely, LCD was associated with a significantly lower intima-media thickness (SMD = -0.49, 95% CI [-0.94, -0.05]) and pulse wave velocity than HCD (SMD = -0.86, 95% CI [-1.21, -0.51]). Furthermore, LCD significantly decreased serum Ca levels (mean difference [MD] = 0.52 mg/dL, 95% CI [0.19, 0.85]) and increased serum parathyroid hormone levels (MD = 44.8 pg/mL, 95% CI [16.2, 73.3]) compared with HCD. Notably, most RCTs examined in our analysis did not include patients receiving calcimimetics., Conclusions: Our meta-analysis showed no significant differences in cardiovascular calcification and death between LCD and HCD and revealed a paucity of RCTs on dialysate Ca concentrations, including those involving patients on calcimimetics, indicating the urgent need for further studies., (© 2024. The Author(s), under exclusive licence to Japanese Society of Nephrology.)
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- 2024
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36. Managing Osteoporosis in Dialysis—A Medical Catch-22.
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Khairallah, Pascale and Nickolas, Thomas L.
- Subjects
BONE fractures ,HIP fractures ,RENAL osteodystrophy ,OSTEOPOROSIS - Abstract
The article focuses on the challenges of managing osteoporosis in patients undergoing dialysis due to chronic kidney disease, emphasizing the increased fracture risk and limited treatment options. Topics include the emergence of denosumab as a potential treatment, and the significant risk of hypocalcemia associated with its use in dialysis patients, prompting the need for careful monitoring and development of multifaceted approaches to fracture prevention in this population.
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- 2024
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37. Sichuan University Researchers Have Provided New Study Findings on Peptide Hormones (Functional Analysis and Tissue-Specific Expression of Calcitonin and CGRP with RAMP-Modulated Receptors CTR and CLR in Chickens).
- Subjects
PEPTIDE hormones ,CALCITONIN ,FUNCTIONAL analysis ,RESEARCH personnel ,CHICKENS ,NEUROPEPTIDES - Abstract
Researchers from Sichuan University have conducted a study on peptide hormones, specifically calcitonin (CT) and calcitonin gene-related peptide (CGRP), and their role in calcium balance and physiological processes in chickens. The study involved cloning and characterizing the chicken calcitonin receptor (CTR) and calcitonin receptor-like receptor (CLR), as well as three receptor activity-modifying proteins (RAMPs). The researchers found that chicken CTRs and CLRs stimulate signaling pathways and have functional receptor status. They also discovered tissue-specific expression profiles for CT, CGRP, CTR, CLR, and RAMPs in chickens, indicating different physiological roles across various tissues. The study contributes to understanding the functions of this hormone family in vertebrates. [Extracted from the article]
- Published
- 2024
38. Theories of Alzheimer's disease: Amyloid hypothesis, blood-brain barrier hypothesis and cholinergic hypothesis.
- Author
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Liu, JingMing, Yang, BoYi, and Zhang, XingShu
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- 2024
- Full Text
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39. Mechanistic insights into carvedilol's potential protection against doxorubicin-induced cardiotoxicity.
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Elmorsy, Elsayed A., Saber, Sameh, Hamad, Rabab S., Abdel-Reheim, Mustafa Ahmed, El-kott, Attalla F., AlShehri, Mohammed A., Morsy, Kareem, Negm, Sally, and Youssef, Mahmoud E.
- Subjects
- *
DOXORUBICIN , *CARVEDILOL , *CARDIOTOXICITY , *HEART cells , *BCL-2 proteins , *RENIN-angiotensin system - Abstract
Doxorubicin (DOX) is an anthracycline chemotherapy drug widely employed in the treatment of various cancers, known for its potent antineoplastic properties but often associated with dose-dependent cardiotoxicity, limiting its clinical use. This review explores the complex molecular details that determine the heart-protective effectiveness of carvedilol in relation to cardiotoxicity caused by DOX. The harmful effects of DOX on heart cells could include oxidative stress, DNA damage, iron imbalance, disruption of autophagy, calcium imbalance, apoptosis, dysregulation of topoisomerase 2-beta, arrhythmogenicity, and inflammatory responses. This review carefully reveals how carvedilol serves as a strong protective mechanism, strategically reducing each aspect of cardiac damage caused by DOX. Carvedilol's antioxidant capabilities involve neutralizing free radicals and adjusting crucial antioxidant enzymes. It skillfully manages iron balance, controls autophagy, and restores the calcium balance essential for cellular stability. Moreover, the anti-apoptotic effects of carvedilol are outlined through the adjustment of Bcl-2 family proteins and activation of the Akt signaling pathway. The medication also controls topoisomerase 2-beta and reduces the renin-angiotensin-aldosterone system, together offering a thorough defense against cardiotoxicity induced by DOX. These findings not only provide detailed understanding into the molecular mechanisms that coordinate heart protection by carvedilol but also offer considerable potential for the creation of targeted treatment strategies intended to relieve cardiotoxicity caused by chemotherapy. [Display omitted] [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
40. Crosstalk between kidney and bone: insights from CKD-MBD.
- Author
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Suzuki, Kodai, Soeda, Keisuke, and Komaba, Hirotaka
- Subjects
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RENAL osteodystrophy , *FIBROBLAST growth factors , *CHRONIC kidney failure , *ARTERIAL calcification , *KIDNEYS , *CHRONICALLY ill , *PARATHYROID glands - Abstract
The kidneys play an important role in the regulation of phosphate and calcium balance and serum concentrations, coordinated by fibroblast growth factor 23 (FGF23), parathyroid hormone (PTH), and 1,25-dihydroxyvitamin D (1,25D). In patients with chronic kidney disease (CKD), this regulation is impaired, leading to CKD-mineral and bone disorder (CKD-MBD), characterized by decreased 1,25D, elevated FGF23, secondary hyperparathyroidism, hyperphosphatemia, bone abnormalities, and vascular and soft-tissue calcification. While bone abnormalities associated with CKD-MBD, known as renal osteodystrophy, have been recognized as the most typical interaction between the kidney and bone, a number of other kidney–bone interactions have been identified, for which our knowledge of the pathogenesis of CKD-MBD has played an important role. This article summarizes recent findings on CKD-MBD and explores the crosstalk between the kidney and bone from the perspective of CKD-MBD. [ABSTRACT FROM AUTHOR]
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- 2024
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41. The beneficial roles and mechanisms of estrogens in immune health and infection disease.
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Chen, Lan, Xu, Ting, Lou, Jun, Zhang, Ting, Wu, Sheng, Xie, Rui, and Xu, Jingyu
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SEX hormones , *ESTROGEN , *SEX factors in disease , *ESTROGEN receptors , *CELL receptors - Abstract
[Display omitted] • Estrogen can regulate various physiological activities through immunity, anti-inflammatory, antioxidant, apoptosis, calcium balance, metabolism, and vasoconstriction. • Estrogen has different regulatory mechanisms in different immune cells to exert beneficial effects on immune cells. • E2 can activate ER through multiple signaling pathways α, ER β Regulate anti-inflammatory response with GPER. • Postmenopausal women have decreased levels of anti-inflammatory cytokines and increased levels of pro-inflammatory substances. • Estrogen can regulate vascular dilation and contraction by activating the cAMP pathway, producing substances such as NO and PGI2. Multiple epidemiologic studies have revealed that gender is considered one of the important factors in the frequency and severity of certain infectious diseases, in which estrogens may play a vital role. There is growing evidence that estrogens as female sex hormone can modulate multiple biological functions outside of the reproductive system, such as in brain and cardiovascular system. However, it is largely unknown about the roles and mechanisms of estrogens/estrogen receptors in immune health and infection disease. Thence, by reading a lot of literature, we summarized the regulatory mechanisms of estrogens/estrogen receptors in immune cells and their roles in certain infectious diseases with gender differences. Therefore, estrogens may have therapeutic potentials to prevent and treat these infectious diseases, which needs further clinical investigation. [ABSTRACT FROM AUTHOR]
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- 2024
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42. 齐墩果酸调节Wnt/β-catenin 信号通路减轻大鼠激素性股骨头坏死.
- Author
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龚高进 and 黄海汛
- Abstract
Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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- 2024
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43. Unlocking the potential of exercise: harnessing myokines to delay musculoskeletal aging and improve cognitive health.
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Xing Gao, Yiyan Chen, and Peng Cheng
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Objectives: This review aims to summarize the common physiological mechanisms associated with both mild cognitive impairment (MCI) and musculoskeletal aging while also examining the relevant literature on how exercise regulation influences the levels of shared myokines in these conditions. Methods: The literature search was conducted via databases such as PubMed (including MEDLINE), EMBASE, and the Cochrane Library of Systematic Reviews. The searches were limited to full-text articles published in English, with the most recent search conducted on 16 July 2024. The inclusion criteria for this review focused on the role of exercise and myokines in delaying musculoskeletal aging and enhancing cognitive health. The Newcastle--Ottawa Scale (NOS) was utilized to assess the quality of nonrandomized studies, and only those studies with moderate to high quality scores, as per these criteria, were included in the final analysis. Data analysis was performed through narrative synthesis. Results: The primary outcome of this study was the evaluation of myokine expression, which included IL-6, IGF-1, BDNF, CTSB, irisin, and LIF. A total of 16 studies involving 633 older adults met the inclusion criteria. The current exercise modalities utilized in these studies primarily consisted of resistance training and moderate-to high-intensity cardiovascular exercise. The types of interventions included treadmill training, elastic band training, aquatic training, and Nordic walking training. The results indicated that both cardiovascular exercise and resistance exercise could delay musculoskeletal aging and enhance the cognitive functions of the brain. Additionally, different types and intensities of exercise exhibited varying effects on myokine expression. Conclusion: Current evidence suggests that exercise mediates the secretion of specific myokines, including IL-6, IGF-1, BDNF, CTSB, irisin, and LIF, which establish self-regulatory circuits between the brain and muscle. This interaction enhances cognitive function in the brain and improves skeletal muscle function. Future research should focus on elucidating the exact mechanisms that govern the release of myokines, the correlation between the intensity of exercise and the secretion of these myokines, and the distinct processes by which myokines influence the interaction between muscle and the brain. [ABSTRACT FROM AUTHOR]
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- 2024
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44. The relationship between physical activity levels and serum vitamin D levels varies among children and adolescents in different age groups.
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Shengrong Ouyang, Qin Li, Zhuo Liu, and Yan Yin
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- 2024
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45. A comprehensive review on the role of strontium in biodegradable metals.
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Huafang Li and Luqing Ma
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Biodegradable metals, including magnesium, iron, and zinc alloys, have attracted extensive attention due to their good biodegradability and biocompatibility. However, the mechanical properties and corrosion rates of most biodegradable metallic materials have not yet reached the ideal level required for clinical applications. Strontium, as an element of Group IIA in the periodic table of elements, has similar chemical and biological properties to calcium. It can promote bone tissue development and increase bone strength. In addition, strontium can also promote angiogenesis and facilitate the repair of infarcted heart activity. Thus, strontium is commonly used as one of the most alloying elements to improve the in vitro and in vivo properties of biodegradable metals. Besides, strontium is also widely used in various bioactive coatings to improve the comprehensive properties of biodegradable metals. This paper outlines the role of strontium in the human body and summarizes recent research and applications of strontium-containing biodegradable metallic materials. Finally, this paper also provides an outlook on the challenges faced in applying and researching strontium in biodegradable metals. [ABSTRACT FROM AUTHOR]
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- 2024
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46. A nomogram for individualized prediction of new-onset postoperative atrial fibrillation in acute type A aortic dissection patients: a retrospective study.
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Zhihao Yang, Chunxiao Liu, Chao Fu, and Xin Zhao
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- 2024
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47. Identifying the Pathogenic Variants in Heart Genes in Vietnamese Sudden Unexplained Death Victims by Next-Generation Sequencing.
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Nguyen Tat, Tho, Lien, Nguyen Thi Kim, Luu Sy, Hung, Ta Van, To, Dang Viet, Duc, Nguyen Thi, Hoa, Tung, Nguyen Van, Thanh, Le Tat, Xuan, Nguyen Thi, and Hoang, Nguyen Huy
- Subjects
SUDDEN death ,NUCLEOTIDE sequencing ,GENETIC variation ,GENETIC disorders ,DATABASES - Abstract
In forensics, one-third of sudden deaths remain unexplained after a forensic autopsy. A majority of these sudden unexplained deaths (SUDs) are considered to be caused by inherited cardiovascular diseases. In this study, we investigated 40 young SUD cases (<40 years), with non-diagnostic structural cardiac abnormalities, using Targeted NGS (next-generation sequencing) for 167 genes previously associated with inherited cardiomyopathies and channelopathies. Fifteen cases identified 17 variants on related genes including the following: AKAP9, CSRP3, GSN, HTRA1, KCNA5, LAMA4, MYBPC3, MYH6, MYLK, RYR2, SCN5A, SCN10A, SLC4A3, TNNI3, TNNI3K, and TNNT2. Of these, eight variants were novel, and nine variants were reported in the ClinVar database. Five were determined to be pathogenic and four were not evaluated. The novel and unevaluated variants were predicted by using in silico tools, which revealed that four novel variants (c.5187_5188dup, p.Arg1730llefsTer4 in the AKAP9 gene; c.1454A>T, p.Lys485Met in the MYH6 gene; c.2535+1G>A in the SLC4A3 gene; and c.10498G>T, p.Asp3500Tyr in the RYR2 gene) were pathogenic and three variants (c.292C>G, p.Arg98Gly in the TNNI3 gene; c.683C>A, p.Pro228His in the KCN5A gene; and c.2275G>A, p.Glu759Lys in the MYBPC3 gene) still need to be further verified experimentally. The results of our study contributed to the general understanding of the causes of SUDs. They provided a scientific basis for screening the risk of sudden death in family members of victims. They also suggested that the Targeted NGS method may be used to identify the pathogenic variants in SUD victims. [ABSTRACT FROM AUTHOR]
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- 2024
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48. Intrinsic and Extrinsic Factors Associated with Hair Graying (Canities) and Therapeutic Potential of Plant Extracts and Phytochemicals.
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Boo, Yong Chool
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NUCLEAR factor E2 related factor ,MICROPHTHALMIA-associated transcription factor ,TRANSCRIPTION factors ,MITOGEN-activated protein kinases ,ADRENERGIC receptors ,PHYTOCHEMICALS ,EMODIN - Abstract
This review aims to gain insight into the major causes of hair graying (canities) and how plant-derived extracts and phytochemicals could alleviate this symptom. Research articles on human hair graying were searched and selected using the PubMed, Web of Science, and Google Scholar databases. We first examined the intrinsic and extrinsic factors associated with hair graying, such as the reduced capacity of melanin synthesis and transfer, exhaustion of melanocyte stem cells (MSCs) and melanocytes, genetics and epigenetics, race, gender, family history, aging, oxidative stress, stress hormones, systematic disorders, nutrition, smoking, alcohol consumption, lifestyle, medications, and environmental factors. We also examined various plants and phytochemicals that have shown a potential to interfere with the onset or progression of human hair graying at different levels from in vitro studies to clinical studies: the extract of Polygonum multiflorum and its major components, 2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside and emodin; the extract of Eriodictyon angustifolium and its major flavonoid compounds, hydroxygenkwanin, sterubin, and luteolin; the extracts of Adzuki beans (Vigna angularis), Fuzhuan brick tea (Camellia sinensis), and Gynostemma pentaphyllum; bixin, a carotenoid compound found in Bixa orellana; and rhynchophylline, an alkaloid compound found in certain Uncaria species. Experimental evidence supports the notion that certain plant extracts and phytochemicals could alleviate hair graying by enhancing MSC maintenance or melanocyte function, reducing oxidative stress due to physiological and environmental influences, and managing the secretion and action of stress hormones to an appropriate level. It is suggested that hair graying may be reversible through the following tactical approaches: selective targeting of the p38 mitogen-activated protein kinase (MAPK)–microphthalmia-associated transcription factor (MITF) axis, nuclear factor erythroid 2-related factor 2 (NRF2), or the norepinephrine–β2 adrenergic receptor (β2AR)–protein kinase A (PKA) signaling pathway. [ABSTRACT FROM AUTHOR]
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- 2024
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49. A Novel Rare PSEN2 Val226Ala in PSEN2 in a Korean Patient with Atypical Alzheimer's Disease, and the Importance of PSEN2 5th Transmembrane Domain (TM5) in AD Pathogenesis.
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Yang, YoungSoon, Bagyinszky, Eva, and An, Seong Soo A.
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TRANSMEMBRANE domains ,DISEASE risk factors ,MEMORY disorders ,POSITRON emission tomography ,MAGNETIC resonance imaging - Abstract
In this manuscript, a novel presenilin-2 (PSEN2) mutation, Val226Ala, was found in a 59-year-old Korean patient who exhibited rapid progressive memory dysfunction and hallucinations six months prior to her first visit to the hospital. Her Magnetic Resonance Imaging (MRI) showed brain atrophy, and both amyloid positron emission tomography (PET) and multimer detection system-oligomeric amyloid-beta (Aβ) results were positive. The patient was diagnosed with early onset Alzheimer's disease. The whole-exome analysis revealed a new PSEN2 Val226Ala mutation with heterozygosity in the 5th transmembrane domain of the PSEN2 protein near the lumen region. Analyses of the structural prediction suggested structural changes in the helix, specifically a loss of a hydrogen bond between Val226 and Gln229, which may lead to elevated helix motion. Multiple PSEN2 mutations were reported in PSEN2 transmembrane-5 (TM5), such as Tyr231Cys, Ile235Phe, Ala237Val, Leu238Phe, Leu238Pro, and Met239Thr, highlighting the dynamic importance of the 5th transmembrane domain of PSEN2. Mutations in TM5 may alter the access tunnel of the Aβ substrate in the membrane to the gamma-secretase active site, indicating a possible influence on enzyme function that increases Aβ production. Interestingly, the current patient with the Val226Ala mutation presented with a combination of hallucinations and memory dysfunction. Although the causal mechanisms of hallucinations in AD remain unclear, it is possible that PSEN2 interacts with other disease risk factors, including Notch Receptor 3 (NOTCH3) or Glucosylceramidase Beta-1 (GBA) variants, enhancing the occurrence of hallucinations. In conclusion, the direct or indirect role of PSEN2 Val226Ala in AD onset cannot be ruled out. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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50. Navigating the Neuroimmunomodulation Frontier: Pioneering Approaches and Promising Horizons—A Comprehensive Review.
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Krsek, Antea, Ostojic, Leona, Zivalj, Dorotea, and Baticic, Lara
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VAGUS nerve stimulation ,NEUROIMMUNOLOGY ,IMMUNE system ,AFFECTIVE disorders ,IMMUNE response ,NEURAL stimulation ,TRANSCRANIAL magnetic stimulation ,TRANSCRANIAL direct current stimulation - Abstract
The research in neuroimmunomodulation aims to shed light on the complex relationships that exist between the immune and neurological systems and how they affect the human body. This multidisciplinary field focuses on the way immune responses are influenced by brain activity and how neural function is impacted by immunological signaling. This provides important insights into a range of medical disorders. Targeting both brain and immunological pathways, neuroimmunomodulatory approaches are used in clinical pain management to address chronic pain. Pharmacological therapies aim to modulate neuroimmune interactions and reduce inflammation. Furthermore, bioelectronic techniques like vagus nerve stimulation offer non-invasive control of these systems, while neuromodulation techniques like transcranial magnetic stimulation modify immunological and neuronal responses to reduce pain. Within the context of aging, neuroimmunomodulation analyzes the ways in which immunological and neurological alterations brought on by aging contribute to cognitive decline and neurodegenerative illnesses. Restoring neuroimmune homeostasis through strategies shows promise in reducing age-related cognitive decline. Research into mood disorders focuses on how immunological dysregulation relates to illnesses including anxiety and depression. Immune system fluctuations are increasingly recognized for their impact on brain function, leading to novel treatments that target these interactions. This review emphasizes how interdisciplinary cooperation and continuous research are necessary to better understand the complex relationship between the neurological and immune systems. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
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