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The Eagle Bioscience’s Anti-LKM1 ELISA Assay was utilized in a recent publication that focused on liver kidney microsome antibodies. Check out the full text and abstract below.

Abstract

Sanchez, Sandra, et al. “Liver Kidney Microsome Antibodies. Analysis of a Laboratory Series.” Practical Laboratory Medicine, vol. 33, 2023.

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The Eagle Bioscience’s Serotonin ELISA Assay was utilized in a recent publication that focused on patient-derived Enterococcus mundtii. Check out the full text and abstract below.

Abstract

The genus Enterococcus is commonly overpopulated in patients with depression compared to healthy control in the feces. Therefore, we isolated Enterococcus faecalis, Enterococcus durans, Enterococcus gallinarum, Enterococcus faecium, and Enterococcus mundtii from the feces of patients with comorbid inflammatory bowel disease with depression and examined their roles in depression in vivo and in vitro.

Of these Enterococci, E. mundtii NK1516 most potently induced NF-κB-activated TNF-α and IL-6 expression in BV2 microglia cells. NK1516 also caused the most potent depression-like behaviors in the absence of sickness behaviors, neuroinflammation, downregulated brain-derived neurotrophic factor (BDNF), and serotonin (5-HT) levels in the hippocampus of mice. Furthermore, E. mundtii NK1516 reduced the mRNA expression of Htr1a in the hippocampus. Its capsular polysaccharide (CP), but not cytoplasmic components, also caused depression-like behaviors and reduced BDNF and serotonin levels in the hippocampus. Conversely, this was not observed with Enterococcus mundtiiATCC882, a well-known probiotic, or its CP. Orally gavaged fluorescence isothiocyanate (FITC)-conjugated NK1516 CP was detected in the hippocampus of mice. The NK1516 genome exhibited unique CP biosynthesis-related genes (capD, wbjC, WecB, vioB), unlike that of ATCC882. These findings suggest that Enterococcus mundtii may be a risk factor for depression.

Joo, Min-Kyung, et al. “Patient-Derived Enterococcus Mundtii and Its Capsular Polysaccharides Cause Depression through the Downregulation of NF-ΚB-Involved Serotonin and BDNF Expression.” Microbes and Infection, 2023, p. 105116.

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The Eagle Bioscience’s Adrenaline ELISA Assay was utilized in a recent publication that explored the impact of epigallocatechin gallate (EGCG) ingestion on catecholamine metabolism during graded cycle exercise in humans. Check out the full text and abstract below!

Abstract

Purpose

Physical exercise is shown to mitigate catecholamine metabolites; however, it is unknown if exercise-induced increases in sympatho-adrenal activity or catecholamine metabolites are influenced by ingestion of specific catechins found within green tea. This study explored the impact of epigallocatechin gallate (EGCG) ingestion on catecholamine metabolism during graded cycle exercise in humans.

Methods

Eight males (22.4 ± 3.3 years, BMI:25.7 ± 2.4 kg.m²) performed a randomized, placebo-controlled, single-blind, cross-over trial after consumption (1450 mg) of either EGCG or placebo (PLAC) and performed graded cycling to volitional exhaustion. Venous bloods were taken at rest, 2 h post-ingestion and after every 3-min stage. Blood variables were analysed for catecholamines, catecholamine metanephrines and metabolic variables at rest, 2 h post-ingestion (POST-ING), peak rate of lipid oxidation (FATpeak), lactate threshold (LT) and peak rate of oxygen consumption (VO₂peak). Data were analyzed using SPSS (Version 26).

Results

Resting catecholamine and metanephrines were similar between trials. Plasma adrenaline (AD) was lower in ECGC treatment group between trials at FATpeak (P < 0.05), LT (P < 0.001) and VO₂peak (P < 0.01). Noradrenaline (NA) was lower under EGCG at POST (P < 0.05), FATpeak (P < 0.05), LT (P < 0.01) and VO₂peak (P < 0.05) compared to PLAC. Metanephrines, glucose and lactate increased similarly with exercise intensity in both trials. Lipid oxidation rate was 32% lower in EGCG at FATpeak (EGCG 0.33 ± 0.14 vs. PLAC 0.49 ± 0.11 g.min⁻¹, P < 0.05). Cycle time to exhaustion was similar (NS).

Conclusion

Acute EGCG supplementation reduced circulating catecholamines but not; metanephrine, glucose or lactates, response to graded exercise. Lower circulating catecholamines may explain a lower lipid oxidation rate.

Churm, R., Williams, L.M., Dunseath, G. et al. The polyphenol epigallocatechin gallate lowers circulating catecholamine concentrations and alters lipid metabolism during graded exercise in man: a randomized cross-over study. Eur J Nutr 62, 1517–1526 (2023).

If you have any questions about the Adrenaline ELISA Assay or our other offerings, please contact us here.

The Eagle Bioscience’s Glutathione Total Assay was utilized in a recent publication that explored how Diosmin mitigates dexamethasone-induced osteoporosis in vivo. Check out the full text and abstract below!

Abstract

Secondary osteoporosis is commonly caused by long-term intake of glucocorticoids(GCs), such as dexamethasone (DEX). Diosmin, a natural substance with potent antioxidant and anti-inflammatory properties, is clinically used for treating some vascular disorders. The current work targeted exploring the protective properties of diosmin to counteract DEX-induced osteoporosis in vivo. Rats were administered DEX (7 mg/kg) once weekly for 5 weeks, and in the second week, vehicle or diosmin (50 or 100 mg/kg/day) for the next four weeks. Femur bone tissues were collected and processed for histological and biochemical examinations. The study findings showed that diosmin alleviated the histological bone impairments caused by DEX. In addition, diosmin upregulated the expression of Runt-related transcription factor 2 (Runx2) and phosphorylated protein kinase B (p-AKT) and the mRNA transcripts of Wingless (Wnt) and osteocalcin. Furthermore, diosmin counteracted the rise in the mRNA levels of receptor activator of nuclear factor-kB ligand (RANKL) and the reduction in osteoprotegerin (OPG), both were induced by DEX. Diosmin restored the oxidant/antioxidant equilibrium and exerted significant antiapoptotic activity. The aforementioned effects were more pronounced at the dose level of 100 mg/kg. Collectively, diosmin has proven to protect rats against DEX-induced osteoporosis by augmenting osteoblast and bone development while hindering osteoclast and bone resorption. Our findings could be used as a stand for recommending supplementation of diosmin for patients chronically using GCs.

Arafa, El-Shaimaa A., et al. “Diosmin Mitigates Dexamethasone-Induced Osteoporosis in Vivo: Role of Runx2, Rankl/OPG, and Oxidative Stress.” Biomedicine &amp; Pharmacotherapy, vol. 161, 2023, p. 114461.

If you have any questions about the Glutathione Total Assay or our other offerings, please contact us here.

The Eagle Bioscience’s Lipid Peroxidase Assay was utilized in a recent publication that explored how hypercholesterolemia aggravates in-stent restenosis in rabbits. Check out the full text and abstract below!

Abstract

Competing Interest Statement

The authors have declared no competing interest.

Fishbein, Ilia, et al. Hypercholesterolemia Aggravates In-Stent Restenosis in Rabbits: A Mitigating Effect of Stent Surface Modification with CD47-Derived Peptide, 2023.

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The Eagle Bioscience’s Cortisol ELISA Assay was highlighted in a recent publication that focused on suppressive action of nesfatin-1 and nesfatin-1-like peptide on cortisol synthesis. Check out the full text and abstract below!

Abstract

Nasri, Atefeh, et al. Suppressive Action of Nesfatin-1 and Nesfatin-1-like Peptide on Cortisol Synthesis in Adrenal Cortex Cells, 2023, https://doi.org/10.21203/rs.3.rs-2595841/v1.

If you have any questions about the Cortisol ELISA Assay or our other offerings, please contact us here.

The Eagle Bioscience’s easYmer HLA-A*03:01 MHC Tetramers Kit was utilized in a recent publication that explored T cells specific for α-myosin drive immunotherapy-related myocarditis. Check out the full text and abstract below.

Abstract

Immune-related adverse events, particularly severe toxicities such as myocarditis, are major challenges to the utility of immune checkpoint inhibitors (ICIs) in anticancer therapy¹. The pathogenesis of ICI-associated myocarditis (ICI-MC) is poorly understood. Pdcd1^–/–Ctla4^+/– mice recapitulate clinicopathological features of ICI-MC, including myocardial T cell infiltration². Here, using single-cell RNA and T cell receptor (TCR) sequencing of cardiac immune infiltrates from Pdcd1^–/–Ctla4^+/– mice, we identify clonal effector CD8⁺ T cells as the dominant cell population. Treatment with anti-CD8-depleting, but not anti-CD4-depleting, antibodies improved the survival of Pdcd1^–/–Ctla4^+/– mice. Adoptive transfer of immune cells from mice with myocarditis induced fatal myocarditis in recipients, which required CD8⁺ T cells. The cardiac-specific protein α-myosin, which is absent from the thymus^3,4, was identified as the cognate antigen source for three major histocompatibility complex class I-restricted TCRs derived from mice with fulminant myocarditis. Peripheral blood T cells from three patients with ICI-MC were expanded by α-myosin peptides. Moreover, these α-myosin-expanded T cells shared TCR clonotypes with diseased heart and skeletal muscle, which indicates that α-myosin may be a clinically important autoantigen in ICI-MC. These studies underscore the crucial role for cytotoxic CD8⁺ T cells, identify a candidate autoantigen in ICI-MC and yield new insights into the pathogenesis of ICI toxicity.

Axelrod, M.L., Meijers, W.C., Screever, E.M. et al. T cells specific for α-myosin drive immunotherapy-related myocarditis. Nature 611, 818–826 (2022).

If you have any questions about the easYmer HLA-A*03:01 MHC Tetramers Kit or our other offerings, please contact us here.

The Eagle Bioscience’s Rituximab mAb-based ELISA was utilized in a recent publication that focused on how rituximab induced cytokine release with high concentrations of serum IP-10 concentrations is associated with infusion reactions. Check out the full text and abstract below.

Abstract

Monoclonal antibody induced infusion reactions (IRs) can be serious and even fatal. We used clinical data and blood samples from 37 treatment naïve patients with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL) initiating therapy for progressive disease with a single 50 mg dose of intravenous (IV) rituximab at 25 mg/h. Twenty-four (65 %) patients had IRs at a median of 78 min (range 35–128) and rituximab dose of 32 mg (range 15–50). IR risk did not correlate with patient or CLL characteristics, CLL counts or CD20 levels, or serum rituximab or complement concentrations. Thirty-five (95 %) patients had cytokine release response with a ≥ 4-fold increase in serum concentration of ≥ 1 inflammatory cytokine. IRs were associated with significantly higher post-infusion serum concentrations of gamma interferon induced cytokines IP-10, IL-6 and IL-8. IP-10 concentrations increased ≥ 4-fold in all patients with an IR and were above the upper limit of detection (40,000 pg/ml) in 17 (71 %). In contrast, to only three (23 %) patients without an IR had an ≥ 4-fold increase in serum concentrations of IP-10 (highest 22,013 pg/ml). Our data suggest that cytokine release could be initiated by activation of effector cells responsible for clearance of circulating CLL cells with IRs occurring in those with higher levels of gamma interferon induced cytokines. These novel insights could inform future research to better understand and manage IRs and understand the role of cytokines in the control of cytotoxic immune responses to mAb.

Moore, Jeremiah E., et al. “Rituximab Induced Cytokine Release with High Serum IP-10 (CXCL10) Concentrations Is Associated with Infusion Reactions.” Leukemia Research, vol. 129, 2023, p. 107072.

If you have any questions about our Rituximab mAb-based ELISA or our other offerings, please contact us here.