scholarly journals Effect of magnesium supplementation on circulating biomarkers of cardiovascular disease

2020 ◽  
Author(s):  
Alvaro Alonso ◽  
Lin Y. Chen ◽  
Kyle D. Rudser ◽  
Faye L. Norby ◽  
Mary R. Rooney ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Serum Magnesium ◽  
Interleukin 1 ◽  
Multiple Comparisons ◽  
Tartrate Resistant Acid Phosphatase ◽  
Magnesium Supplementation ◽  
Baseline Serum ◽  
Protein Levels ◽  
Link Type ◽  
Oral Magnesium

ABSTRACTBackgroundMagnesium supplementation may be effective for the prevention of cardiometabolic diseases, but mechanisms are unclear. Proteomic approaches can assist in identifying underlying mechanisms.MethodsWe collected repeated blood samples in 52 individuals enrolled in a double-blind trial which randomized participants 1:1 to oral magnesium supplementation (400 mg magnesium / day in the form of magnesium oxide) or matching placebo for 10 weeks. Plasma levels of 91 proteins were measured in baseline and follow-up samples using the Olink Cardiovascular Disease III proximity extension assay panel, and modeled as arbitrary units in log2 scale. We evaluated the effect of oral magnesium supplementation on changes in protein levels and the baseline association between serum magnesium and protein levels. The Holm procedure was used to adjust for multiple comparisons.ResultsParticipants were 73% women, 94% white, and had a mean age of 62. Changes in proteins did not significantly differ between the two intervention groups after correction for multiple comparisons. The most statistically significant effects were on myoglobin [difference −0.319 log2 units, 95% confidence interval (CI) (−0.550, −0.088), p = 0.008], tartrate-resistant acid phosphatase type 5 [−0.187, (−0.328, −0.045), p = 0.011], tumor necrosis factor ligand superfamily member 13B [−0.181, (−0.332, −0.031), p = 0.019], ST2 protein [−0.198, (−0.363, −0.032), p =0.020], and interleukin-1 receptor type 1 [−0.144, (−0.273, −0.015), p = 0.029]. Similarly, none of the associations of baseline serum magnesium with protein levels were significant after correction for multiple comparisons.ConclusionThough we did not identify statistically significant effects of oral magnesium supplementation in this relatively small study, this study demonstrates the value of proteomic approaches for the investigation of mechanisms underlying the beneficial effects of magnesium supplementation.Clinical Trials RegistrationClinicalTrials.govNCT02837328

scholarly journals Effect of Magnesium Supplementation on Circulating Biomarkers of Cardiovascular Disease

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1697
Author(s):  
Alvaro Alonso ◽  
Lin Y. Chen ◽  
Kyle D. Rudser ◽  
Faye L. Norby ◽  
Mary R. Rooney ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Serum Magnesium ◽  
Interleukin 1 ◽  
Multiple Comparisons ◽  
Tartrate Resistant Acid Phosphatase ◽  
Magnesium Supplementation ◽  
Double Blind ◽  
Baseline Serum ◽  
Protein Levels ◽  
Oral Magnesium

(1) Background: Magnesium supplementation may be effective for the prevention of cardiometabolic diseases, but the mechanisms are unclear. Proteomic approaches can assist in identifying the underlying mechanisms. (2) Methods: We collected repeated blood samples from 52 individuals enrolled in a double-blind trial which randomized participants 1:1 to oral magnesium supplementation (400 mg magnesium/day in the form of magnesium oxide) or a matching placebo for 10 weeks. Plasma levels of 91 proteins were measured at baseline with follow-up samples using the Olink Cardiovascular Disease III proximity extension assay panel and were modeled as arbitrary units in a log2 scale. We evaluated the effect of oral magnesium supplementation for changes in protein levels and the baseline association between serum magnesium and protein levels. The Holm procedure was used to adjust for multiple comparisons. (3) Results: Participants were 73% women, 94% white, and had a mean age of 62. Changes in proteins did not significantly differ between the two intervention groups after correction for multiple comparisons. The most statistically significant effects were on myoglobin [difference −0.319 log2 units, 95% confidence interval (CI) (−0.550, −0.088), p = 0.008], tartrate-resistant acid phosphatase type 5 (−0.187, (−0.328, −0.045), p = 0.011), tumor necrosis factor ligand superfamily member 13B (−0.181, (−0.332, −0.031), p = 0.019), ST2 protein (−0.198, (−0.363, −0.032), p = 0.020), and interleukin-1 receptor type 1 (−0.144, (−0.273, −0.015), p = 0.029). Similarly, none of the associations of baseline serum magnesium with protein levels were significant after correction for multiple comparisons. (4) Conclusions: Although we did not identify statistically significant effects of oral magnesium supplementation in this relatively small study, this study demonstrates the value of proteomic approaches for the investigation of mechanisms underlying the beneficial effects of magnesium supplementation. Clinical Trials Registration: ClinicalTrials.gov NCT02837328.

Hypomagnesemia due to two novel TRPM6 mutations

2015 ◽  
Vol 28 (11-12) ◽  
Author(s):  
Michelle Coulter ◽  
Caroline Colvin ◽  
Bruce Korf ◽  
Ludwine Messiaen ◽  
Benjamin Tuanama ◽  
...  
Keyword(s):  
Clinical Presentation ◽  
Seizure Activity ◽  
Neonatal Period ◽  
Serum Magnesium ◽  
Magnesium Concentration ◽  
Magnesium Supplementation ◽  
Generalized Seizures ◽  
Neonatal Hypoparathyroidism ◽  
Hispanic Male ◽  
Oral Magnesium

AbstractAlthough most hypocalcemia with hypomagenesemia in the neonatal period is due to transient neonatal hypoparathyroidism, magnesium channel defects should also be considered.We report a case of persistent hypomagnesemia in an 8-day-old Hispanic male who presented with generalized seizures. He was initially found to have hypomagnesemia, hypocalcemia, hyperphosphatemia and normal parathyroid hormone. Serum calcium normalized with administration of calcitriol and calcium carbonate. Serum magnesium improved with oral magnesium sulfate. However, 1 week after magnesium was discontinued, serum magnesium declined to 0.5 mg/dL. Magnesium supplementation was immediately restarted, and periodic seizure activity resolved after serum magnesium concentration was maintained above 0.9 mg/dL. The child was eventually weaned off oral calcium and calcitriol with persistent normocalemia. However, supraphysiologic oral magnesium doses were necessary to prevent seizures and maintain serum magnesium at the low limit of normal.As his clinical presentation suggested primary renal magnesium wastage,Two novel

scholarly journals Abnormal upregulation of cardiovascular disease biomarker PLA2G7 induced by proinflammatory macrophages in COVID-19 patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yang Li ◽  
Yongzhong Jiang ◽  
Yi Zhang ◽  
Naizhe Li ◽  
Qiangling Yin ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Normal Limit ◽  
Genomic Analysis ◽  
High Rate ◽  
Hub Gene ◽  
Viral Loads ◽  
Protein Levels ◽  
Nasal Swabs ◽  
Positive Rate ◽  
Validation Stage

AbstractHigh rate of cardiovascular disease (CVD) has been reported among patients with coronavirus disease 2019 (COVID-19). Importantly, CVD, as one of the comorbidities, could also increase the risks of the severity of COVID-19. Here we identified phospholipase A2 group VII (PLA2G7), a well-studied CVD biomarker, as a hub gene in COVID-19 though an integrated hypothesis-free genomic analysis on nasal swabs (n = 486) from patients with COVID-19. PLA2G7 was further found to be predominantly expressed by proinflammatory macrophages in lungs emerging with progression of COVID-19. In the validation stage, RNA level of PLA2G7 was identified in nasal swabs from both COVID-19 and pneumonia patients, other than health individuals. The positive rate of PLA2G7 were correlated with not only viral loads but also severity of pneumonia in non-COVID-19 patients. Serum protein levels of PLA2G7 were found to be elevated and beyond the normal limit in COVID-19 patients, especially among those re-positive patients. We identified and validated PLA2G7, a biomarker for CVD, was abnormally enhanced in COVID-19 at both nucleotide and protein aspects. These findings provided indications into the prevalence of cardiovascular involvements seen in patients with COVID-19. PLA2G7 could be a potential prognostic and therapeutic target in COVID-19.

Contribution of Growth Arrest-Specific 5/miR-674 to the Hypothalamus Pituitary Adrenal Axis Regulation Effect by Electroacupuncture following Trauma

2021 ◽  
pp. 1-13
Author(s):  
Jing Zhu ◽  
Chunxia Guo ◽  
Pingping Lu ◽  
Shuijin Shao ◽  
Bing Tu
Keyword(s):  
Hpa Axis ◽  
Interleukin 1 ◽  
Growth Arrest ◽  
Luciferase Assay ◽  
Function Evaluation ◽  
Protein Levels ◽  
Adrenal Axis ◽  
Post Surgery ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

<b><i>Background:</i></b> Electroacupuncture (EA) can improve trauma-induced hypothalamus pituitary adrenal axis (HPA) hyperactivity. However, the mechanism underlying the EA effect has not been fully understood. <b><i>Methods and Study Design:</i></b> This study was undertaken to explore the role of hypothalamic growth arrest-specific 5 (Gas5) in the regulation of EA on HPA axis function post-surgery. Paraventricular nuclear Gas5 levels were upregulated in rats using an intracerebroventricular injection of pAAV-Gas5. Primary hypothalamic neurons and 293T cells were cultured for miRNA and siRNAs detection. Radioimmunoassay, PCR, Western blot, and immunohistochemistry were used for HPA axis function evaluation. <b><i>Results:</i></b> The overexpression of Gas5 abolished the effect of EA on the regulation of trauma-induced HPA axis hyperactivity. Using a bioinformatics analysis and dual luciferase assay, we determined that miRNA-674 was a target of Gas5. Additionally, miRNA-674 levels were found to have decreased in trauma rats, and this effect was reversed after EA intervention. TargetScan analysis showed that serum and glucocorticoid inducible kinase 1 (SGK1) were targets of miR-674. Moreover, we found that SGK1 protein levels increased in trauma rats and SGK1 expression inhibition alleviated HPA axis abnormality post-surgery. EA could improve the number of hypothalamus iba-1 positive cells and hypothalamic interleukin 1 beta protein expression. <b><i>Conclusions:</i></b> Our study demonstrated the involvement of the hypothalamic Gas5/miRNA-674/SGK1 signaling pathway in EA regulation of HPA axis function after trauma.

scholarly journals Effects of spinal manipulative therapy on inflammatory mediators in patients with non-specific low back pain: a non-randomized controlled clinical trial

2021 ◽  
Vol 29 (1) ◽  
Author(s):  
Julita A. Teodorczyk-Injeyan ◽  
John J. Triano ◽  
Robert Gringmuth ◽  
Christopher DeGraauw ◽  
Adrian Chow ◽  
...  
Keyword(s):  
Low Back Pain ◽  
Back Pain ◽  
Inflammatory Mediators ◽  
Interleukin 1 ◽  
Spinal Manipulative Therapy ◽  
Controlled Clinical Trial ◽  
Low Back ◽  
Manipulative Therapy ◽  
Randomized Controlled ◽  
Link Type

Abstract Background The inflammatory profiles of patients with acute and chronic nonspecific low back pain (LBP) patients are distinct. Spinal manipulative therapy (SMT) has been shown to modulate the production of nociceptive chemokines differently in these patient cohorts. The present study further investigates the effect(s) of SMT on other inflammatory mediators in the same LBP patient cohorts. Methods Acute (n = 22) and chronic (n = 25) LBP patients with minimum pain scores of 3 on a 10-point numeric scale, and asymptomatic controls (n = 24) were recruited according to stringent exclusion criteria. Blood samples were obtained at baseline and after 2 weeks during which patients received 6 SMTs in the lumbar or lumbosacral region. The in vitro production of tumor necrosis factor (TNFα), interleukin-1 β (IL-1β), IL-6, IL-2, interferon ɣ (IFNɣ), IL-1 receptor antagonist (IL-1RA), TNF soluble receptor type 2 (sTNFR2) and IL-10 was determined by specific immunoassays. Parametric as well as non-parametric statistics (PAST 3.18 beta software) was used to determine significance of differences between and within study groups prior and post-SMT. Effect size (ES) estimates were obtained using Cohen’s d. Results Compared with asymptomatic controls, SMT-related change scores were significant (P = 0.03–0.01) in reducing the production levels of TNFα in both patient cohorts and those of IL-6, IFNɣ and sTNFR2 (P = 0.001–0.02) in patients with chronic LBP. Above-moderate to large ES (d > 0.6–1.4) was observed for these mediators. Compared with respective baselines, a significant post-SMT reduction (P = 0.01) of IL-6 production was detected only in patients with chronic LBP while a significant increase of IL-2 production (P = 0.001 vs. control, and P = 0.004 vs. chronic LBP group) and a large ES (d = 0.87) were observed in patients with acute LBP. Pain and disability scores declined significantly (P < 0.001) in all LBP patients, and were positively correlated (P = 0.03) with IFNɣ and IL-2 levels in the acute LBP cohort. Conclusion The short course of SMT treatments of non-specific LBP patients resulted in significant albeit limited and diverse alterations in the production of several of the mediators investigated in this study. This exploratory study highlights the potential of SMT to modulate the production of inflammatory components in acute and chronic non-specific LBP patients and suggests a need for further, randomized controlled clinical trials in this area. Trial registration This study was prospectively registered April 2012 with Clinical Trials.gov (#NCT01766141). https://register.clinicaltrials.gov/prs/app/action/SelectProtocol?sid=S0003ZIL&selectaction=Edit&uid=U0001V74&ts=2&cx=-axvqtg

scholarly journals Role of Cathepsin S in Periodontal Inflammation and Infection

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
S. Memmert ◽  
A. Damanaki ◽  
A. V. B. Nogueira ◽  
S. Eick ◽  
M. Nokhbehsaim ◽  
...  
Keyword(s):  
Periodontal Diseases ◽  
Interleukin 1 ◽  
Critical Role ◽  
Gingival Tissue ◽  
Cathepsin S ◽  
Protein Levels ◽  
Periodontal Inflammation

Cathepsin S is a cysteine protease and regulator of autophagy with possible involvement in periodontitis. The objective of this study was to investigate whether cathepsin S is involved in the pathogenesis of periodontal diseases. Human periodontal fibroblasts were cultured under inflammatory and infectious conditions elicited by interleukin-1β and Fusobacterium nucleatum, respectively. An array-based approach was used to analyze differential expression of autophagy-associated genes. Cathepsin S was upregulated most strongly and thus further studied in vitro at gene and protein levels. In vivo, gingival tissue biopsies from rats with ligature-induced periodontitis and from periodontitis patients were also analyzed at transcriptional and protein levels. Multiple gene expression changes due to interleukin-1β and F. nucleatum were observed in vitro. Both stimulants caused a significant cathepsin S upregulation. A significantly elevated cathepsin S expression in gingival biopsies from rats with experimental periodontitis was found in vivo, as compared to that from control. Gingival biopsies from periodontitis patients showed a significantly higher cathepsin S expression than those from healthy gingiva. Our findings provide original evidence that cathepsin S is increased in periodontal cells and tissues under inflammatory and infectious conditions, suggesting a critical role of this autophagy-associated molecule in the pathogenesis of periodontitis.

Serum Magnesium, Blood Pressure, and Risk of Hypertension and Chronic Kidney Disease Progression in the CRIC Study

Hypertension ◽  
2021 ◽  
Author(s):  
Simon Correa ◽  
Xavier E. Guerra-Torres ◽  
Sushrut S. Waikar ◽  
Finnian R. Mc Causland
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Disease Progression ◽  
Lower Risk ◽  
Serum Magnesium ◽  
Hazard Ratio ◽  
Adjusted Hazard Ratio ◽  
Ckd Progression ◽  
Baseline Serum

Magnesium is involved in the regulation of blood pressure (BP). Abnormalities in serum magnesium are common in chronic kidney disease (CKD), yet its association with the development of hypertension and CKD progression in patients with CKD is unclear. We analyzed data from 3866 participants from the CRIC Study (Chronic Renal Insufficiency Cohort). Linear regression assessed the association of serum magnesium with baseline systolic BP (SBP) and diastolic BP (DBP). Logistic regression explored the association of serum magnesium with various definitions of hypertension. Cox proportional hazards models explored assessed the risk of incident hypertension and CKD progression. Mean serum magnesium was 2.0 mEq/L (±0.3 mEq/L). Higher magnesium was associated with lower SBP (−3.4 mm Hg [95% CI, −5.8 to −1.0 per 1 mEq/L]) and lower DBP (−2.9 mm Hg [95% CI, −4.3 to −1.5 per 1 mEq/L]). Higher magnesium was associated with a lower risk of American Heart Association–defined hypertension (SBP≥130 mm Hg or DBP≥80 mm Hg) at baseline (adjusted hazard ratio, 0.65 [95% CI, 0.49–0.86 per 1 mEq/L]), a lower risk of suboptimally controlled BP (SBP≥120 mm Hg or DBP≥80 mm Hg; adjusted odds ratio, 0.58 [95% CI, 0.43–0.78 per 1 mEq/L]). In time-to-event analyses, higher baseline serum magnesium was associated with a nominally lower risk of incident CRIC-defined hypertension (adjusted hazard ratio, 0.77 [95% CI, 0.46–1.31 per 1 mEq/L]). Higher magnesium was associated with a significantly lower risk of CKD progression (adjusted hazard ratio, 0.68 [95% CI, 0.54–0.86 per 1 mEq/L]). In patients with CKD, higher serum magnesium is associated with lower SBP and DBP, and with a lower risk of hypertension and CKD progression. In patients with CKD, whether magnesium supplementation could optimize BP control and prevent disease progression deserves further investigation.

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