Category: Publication Spotlight

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).

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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.

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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.

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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).

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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.

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The Eagle Bioscience’s Serotonin ELISA Assay was utilized in a recent publication that explored how gut enterochromaffin cells drive visceral pain and anxiety. Check out the full text and abstract below.

Abstract

Gastrointestinal (GI) discomfort is a hallmark of most gut disorders and represents an important component of chronic visceral pain. For the growing population afflicted by irritable bowel syndrome, GI hypersensitivity and pain persist long after tissue injury has resolved². Irritable bowel syndrome also exhibits a strong sex bias, afflicting women three times more than men. Here, we focus on enterochromaffin (EC) cells, which are rare excitable, serotonergic neuroendocrine cells in the gut epithelium. EC cells detect and transduce noxious stimuli to nearby mucosal nerve endings but involvement of this signaling pathway in visceral pain and attendant sex differences has not been assessed. By enhancing or suppressing EC cell function in vivo, we show that these cells are sufficient to elicit hypersensitivity to gut distension and necessary for the sensitizing actions of isovalerate, a bacterial short-chain fatty acid associated with GI inflammation. Remarkably, prolonged EC cell activation produced persistent visceral hypersensitivity, even in the absence of an instigating inflammatory episode. Furthermore, perturbing EC cell activity promoted anxiety-like behaviors which normalized after blockade of serotonergic signaling. Sex differences were noted across a range of paradigms, indicating that the EC cell–mucosal afferent circuit is tonically engaged in females. Our findings validate a critical role for EC cell–mucosal afferent signaling in acute and persistent GI pain, in addition to highlighting genetic models for studying visceral hypersensitivity and the sex bias of gut pain.

Bayrer, James R., et al. “Gut Enterochromaffin Cells Drive Visceral Pain and Anxiety.” Nature, vol. 616, no. 7955, 2023, pp. 137–142., https://doi.org/10.1038/s41586-023-05829-8.

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The Eagle Bioscience’s Pepsinogen I ELISA Kit was highlighted in a recent publication that focused on the discrimination between precancerous gastric lesions and gastritis. Check out the full text and abstract below.

Abstract

Murphy, John, et al. “Discrimination between Precancerous Gastric Lesions and Gastritis Using a Gastric Cancer Risk Stratification Model.” Asian Pacific Journal of Cancer Prevention, vol. 24, no. 3, 2023, pp. 935–943., https://doi.org/10.31557/apjcp.2023.24.3.935.

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The Eagle Bioscience’s Calprotectin ELISA Assay was utilized in a recent publication that focused on the gut microbiota of people with asthma. Check out the full text and abstract below.

Abstract

Wilson, Naomi G., et al. “The Gut Microbiota of People with Asthma Influences Lung Inflammation in Gnotobiotic Mice.” IScience, vol. 26, no. 2, 2023, p. 105991.

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The Eagle Bioscience’s Rat IL-6 ELISA was highlighted in a recent publication that explored the protective effects of alfa lipoid acid on amiodarone induced hypothyroidism. Check out the full text and abstract below.

Abstract

Background: Amiodarone (AMD) is a highly effective antiarrhythmic agent. Its utilization is associated with toxic effects on thyroid gland. The aim of this research to evaluate the AMD chronic administration potential toxic impact on the thyroid gland and evaluate Alfa lipoic acid (α LA) possible protective impact.

Materials and methods: 40 adult male albino rats were equally separated into 4 groups, group I (control) given 1ml distilled water for 12 wks., group II (AMD tested group) received a single dose of 40 mg/kg /day AMD for 12 wks. Group III (AMD+ α-LA), where AMD was given as group II and a dose of 100 mg/kg of α-LA for 12 weeks, group IV received AMD in doses similar to group II, then the drug was withdrawn and the rats took no treatment for additional 4 weeks. All groups were sacrificed after 12 weeks except group IV after 16 weeks from the beginning of the experiment.

Results: In AMD treated group; the T3, T4 and catalase [CAT] serum levels were significantly reduced along with significant elevation in TSH, IL6 and malondialdehyde [MDA] level, light microscopic examination of AMD group showed cellular degeneration of follicles and colloid peripheral vacuolation along with strong positive immune reaction for Ki-67 declared in AMD group as compared to those of other groups. Additionally, electron microscopic studies supported these results. Conclusion: Chronic administration of AMD induced thyroid damage which could be improved by Co-supplementation of α-LA

Elshazly, Amal, et al. “Protective Effects of Alfa Lipoic Acid on Amiodarone Induced Hypothyroidism in Adult Male Albino Rats (a Biochemical, Histopathological and Immunohistochemical Study).” The Egyptian Journal of Hospital Medicine, vol. 90, no. 1, 2023, pp. 433–445.

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