Blog

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.

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

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.

If you have any questions about our Pepsinogen I ELISA Kit or our other offerings, please contact us here.

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.

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

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.

If you have any questions about our Rat IL-6 ELISA or our other offerings, please contact us here.

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.

If you have any questions about the Noradrenaline (Norepinephrine) Sensitive ELISA or our other offerings, please contact us here.

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.

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

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.

If you have any questions about the Proteinase 3 ELISA or our other offerings, please contact us here.