Category: Publication Spotlight

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 & 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).

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 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 Noradrenaline (Norepinephrine) Sensitive ELISA was utilized in a recent publication that focused on epinephrine versus vasopressin in an ovine model of perinatal cardiac arrest. Check out the full text and abstract below.

Abstract

Background: Current neonatal resuscitation guidelines recommend the use of epinephrine for bradycardia/arrest not responding to ventilation and chest compressions. Vasopressin is a systemic vasoconstrictor and is more effective than epinephrine in postnatal piglets with cardiac arrest. There are no studies comparing vasopressin with epinephrine in newly born animal models with cardiac arrest induced by umbilical cord occlusion.

Objective: To compare the effect of epinephrine and vasopressin on the incidence and time to return of spontaneous circulation (ROSC), hemodynamics, plasma drug levels, and vasoreactivity in perinatal cardiac arrest.

Design/Methods: Twenty-seven term fetal lambs in cardiac arrest induced by cord occlusion were instrumented and resuscitated following randomization to epinephrine or vasopressin through a low umbilical venous catheter.

Results: Eight lambs achieved ROSC prior to medication. Epinephrine achieved ROSC in 7/10 lambs by 8 ± 2 min. Vasopressin achieved ROSC in 3/9 lambs by 13 ± 6 min. Plasma vasopressin levels in nonresponders were much lower than responders after the first dose. Vasopressin caused in vivo increased pulmonary blood flow and in vitro coronary vasoconstriction.

Conclusions: Vasopressin resulted in lower incidence and longer time to ROSC compared to epinephrine in a perinatal model of cardiac arrest supporting the current recommendations for exclusive use of epinephrine in neonatal resuscitation.

Rawat, Munmun, et al. “Masked Randomized Trial of Epinephrine versus Vasopressin in an Ovine Model of Perinatal Cardiac Arrest.” Children, vol. 10, no. 2, 2023, p. 349.

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The Eagle Bioscience’s Dopamine ELISA Assay was utilized in a recent publication that focused on the diverging Parkinson’s Disease Pathology. Check out the full text and abstract below.

Abstract

Multiple neurodegenerative disorders, including Parkinson’s disease (PD) and Alzheimer’s disease-associated dementia (ADAD), are linked with dopaminergic (DA) neuron death and a resulting reduction in dopamine levels in the brain. DA neuron degeneration and the risk of developing PD is connected to genetic mutations affiliated with lysosomal function and protein degradation. Accessible human cellular models for PD-relevant genetic mutations are needed to investigate mechanisms of DA cell death and define points of therapeutic intervention. Human induced pluripotent stem cell (iPSC)-derived midbrain DA neurons offer a developmentally and physiologically relevant in vitro model for investigating PD pathogenic mechanisms across genetic backgrounds. In this study, we generated DA neurons using iPSCs from two clinically diagnosed PD patients, one harboring an inherited GBA^N370Smutation and the other a mutation in LRRK2^G2019S and compared pathophysiology against DA neurons from genetically engineered SNCA^A53T iPSCs and its isogenic apparently healthy normal (AHN) iPSCs. Our results present a novel phenotype for GBA^N370S and LRRK2^G2019Sderived DA neurons, showing that they produced and released significantly more dopamine compared to the AHN and SNCA^A53T mutant DA neurons. All mutant DA neurons developed deficient glucocerebrosidase (GCase) activity, increased mitochondrial stress, aberrant neuronal activity patterns, and increased α-synuclein accumulation. Together these data suggest potentially divergent origins of PD pathogenesis in GBA^N370S and LRRK2^G2019S DA neurons. In addition, compound screening confirmed that GCase modulators can rescue enzyme activity and impact neural activity across all DA mutant neurons, to varying degrees. These data demonstrate unique in vitro phenotypes associated with PD and suggest a diversity of underlying mechanisms across different genetic backgrounds. Together, the cell lines used in this study present a valuable tool for new therapeutic discovery.

Fathi, Ali, et al. Diverging Parkinson’s Disease Pathology between Patient-DerivedGBAn370s, LRRK2g2019sand EngineeredSNCAa53tIpsc-Derived Dopaminergic Neurons, 2023, https://doi.org/10.1101/2023.01.06.521264.

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The Eagle Bioscience’s Proteinase 3 ELISA was highlighted in a recent publication that explored how the PRTN3 variant correlates with increased autoantigen levels. Check out the full text and abstract below.

Abstract

A genome-wide association   study (GWAS) of patients with anti-neutrophil cytoplasmic antibodies (ANCAs) found an association between proteinase-3 ANCA (PR3-ANCA) and a single nucleotide polymorphism (rs62132293) upstream of PRTN3, encoding PR3. The variant (G allele) was shown to be an expression quantitative trait locus in healthy controls, but the clinical impact remains unknown. Longitudinally followed patients with ANCA and healthy controls were genotyped. Gene expression was quantified by real-time quantitative PCR from leukocyte RNA. Plasma PR3 was quantified by ELISA. Among patients, variant carriers had elevated leukocyte PRTN3 expression compared with noncarriers (C/G vs. C/C and G/G vs. C/C). Healthy controls had low PRTN3 regardless of genotype. Myeloperoxidase (MPO) expression did not differ by genotype. PRTN3 expression correlated with circulating PR3, and variant carriers had higher plasma PR3 compared with noncarriers. Among variant carriers, there was an increased risk of relapse in patients with PR3-ANCA versus MPO-ANCA. The risk allele marked by rs62132293 is clinically significant as it is associated with increased autoantigen and may, in part, explain increased relapse in PR3-ANCA. Our results underscore the role of autoantigen availability in ANCA vasculitis.

Chen, Dhruti P., et al. “PRTN3 Variant Correlates with Increased Autoantigen Levels and Relapse Risk in PR3-Anca versus MPO-Anca Disease.” JCI Insight, vol. 8, no. 4, 2023, https://doi.org/10.1172/jci.insight.166107.

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