The Eagle Biosciences MedFrontier FGF23 (Human Intact FGF23) CLEIA ELISA Assay was used in a recently published study looking at the association between FGF23 levels and major adverse cardiovascular events (MACE) and mortality in patients with type 2 diabetes and normal or mildly impaired kidney function.

FGF23 is an endocrine hormone involved in vitamin D metabolism and phosphorous level regulation. Previous studies have shown a link between insulin resistance and an increase in FGF23, which researchers believe affects renal phosphorous handling and leads to a higher risk of MACE.

The study did find evidence of a connection with FGF23 levels and an increased risk of MACE or mortality in participating patients.

Read more about this study here.

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Study Citation:
Fibroblast Growth Factor 23 and Mortality in Patients With Type 2 Diabetes and Normal or Mildly Impaired Kidney Function
Stanley M.H. Yeung, S. Heleen Binnenmars, Christina M. Gant, Gerjan Navis, Ron T. Gansevoort, Stephan J.L. Bakker, Martin H. de Borst, Gozewijn D. Laverman
Diabetes Care Sep 2019, dc190528; DOI: 10.2337/dc19-0528

Eagle Biosciences partner Fianostics completed a study evaluating their Noggin and Asporin FluoBolt assays as biomarkers for non-alcoholic fatty liver disease (NAFLD). The study shows that NOGGIN and ASPORIN may be valuable biomarkers for the diagnosis of NAFLD patients and they may also mediate the favorable effect of vitamin E treatment, although mechanistic studies are needed. Further studies with higher patient numbers are also required to confirm these promising results. The study helps support that these highly sensitivity assays allow researchers to measure a decrease of both markers in samples from NAFLD patients. This measurement is not possible with less sensitive methods. This indicates that noggin and asporin may be valuable biomarkers for NAFLD diagnosis.

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FluoBolt Kits:
Noggin
Asporin

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The Eagle Biosciences NT-proCNP ELISA Assay Kit (manufactured by Biomedica) was used in a recent study published out of the University of Otago in Christchurch, New Zealand. This kit is used for the quantitative determination of NT-proCNP in human serum and plasma (EDTA, citrate, heparin). CNP, C-type natriuretic peptide, along with other natriuretic peptides, plays a role in regulatory mechanisms including blood pressure and body fluid homeostasis. It also serves as a biomarker.

Plasma C-Type Natriuretic Peptide: Emerging Applications in Disorders of Skeletal Growth

Abstract


Although studies in experimental animals show that blood levels of C-type natriuretic peptide (CNP) and its bioinactive aminoterminal propeptide (NTproCNP) are potential biomarkers of long bone growth, a lack of suitable assays and appropriate reference ranges has limited the application of CNP measurements in clinical practice. Plasma concentrations of the processed product of proCNP, NTproCNP – and to a lesser extent CNP itself – correlate with concurrent height velocity throughout all phases of normal skeletal growth, as well as during interventions known to affect skeletal growth in children. Since a change in levels precedes a measurable change in height velocity during interventions, measuring NTproCNP may have predictive value in clinical practice. Findings from a variety of genetic disorders affecting CNP signaling suggest that plasma concentrations of both peptides may be helpful in diagnosis, provided factors such as concurrent height velocity, feedback regulation of CNP, and differential changes in peptide clearance are considered when interpreting values. An improved understanding of factors affecting plasma levels, and the availability of commercial kits enabling accurate measurement using small volumes of plasma, can be expected to facilitate potential applications in growth disorders including genetic causes affecting the CNP signaling pathway.

Espiner, E.; Prickett, T.; Olney, Robert; (2019). Plasma C-Type Natriuretic Peptide: Emerging Applications in Disorders of Skeletal Growth. Horm. Res. Paediatr., 90:345–357. DOI: 10.1159/000496544

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The Eagle Biosciences Mouse / Rat Noradrenaline (Norepinephrine) ELISA was used in a recent study. This highly sensitive assay kit is part of our veterinary and neurobiology product lines. It is intended for the detection of noradrenaline (norepinephrine) in biological samples including serum, plasma, tissue, and cell culture samples of mice and rats.

Renal Denervation and CD161a Immune Ablation Prevent Cholinergic Hypertension and Renal Sodium Retention

Abstract


Cholinergic receptor activation leads to premature development of hypertension and infiltration of pro-inflammatory CD161a+/CD68+ M1 macrophages into the renal medulla. Renal inflammation is implicated in renal sodium retention and the development of hypertension. Renal denervation is known to decrease renal inflammation. To determine the role of CD161a+/CD68+ macrophages and renal sympathetic nerves in cholinergic-hypertension & renal sodium retention. Bilateral renal denervation (RND) and immune ablation of CD161a+ immune cells was performed in young prehypertensive SHR followed by infusion of either saline or nicotine (15mg/kg/day) for two weeks. Immune ablation was conducted by injection of unconjugated azide-free antibody targeting rat CD161a. Blood pressure was monitored by tail cuff plethysmography. Tissues were harvested at the end of infusion. Nicotine induced premature hypertension, renal expression of the sodium-potassium-chloride co-transporter (NKCC2), increases in renal sodium retention, and infiltration of CD161a+/CD68+ macrophages into the renal medulla of animals. All of these effects were abrogated or prevented by RND and ablation of CD161a+ immune cells. Cholinergic activation of CD161a+ positive immune cells leads to the premature development of hypertension in SHR, at least partly, through increased renal expression of NKCC2 and renal sodium retention. Effects on chemotaxis of CD161a+ macrophages to the renal medulla, decreased renal expression of NKCC2, and renal sodium retention appear to play a part in the prevention of cholinergic hypertension as a result of RND. The CD161a+ immune cells are necessary and essential for this pro-hypertensive nicotine-mediated inflammatory response. Cholinergic receptor activation leads to premature development of hypertension and infiltration of pro-inflammatory CD161a+/CD68+ M1 macrophages into the renal medulla. Renal inflammation is implicated in renal sodium retention and the development of hypertension. Renal denervation is known to decrease renal inflammation. To determine the role of CD161a+/CD68+ macrophages and renal sympathetic nerves in cholinergic-hypertension and renal sodium retention. Bilateral renal denervation (RND) and immune ablation of CD161a+ immune cells was performed in young prehypertensive SHR followed by infusion of either saline or nicotine (15mg/kg/day) for two weeks. Immune ablation was conducted by injection of unconjugated azide-free antibody targeting rat CD161a. Blood pressure was monitored by tail cuff plethysmography. Tissues were harvested at the end of infusion. Nicotine induced premature hypertension, renal expression of the sodium-potassium-chloride co-transporter (NKCC2), increases in renal sodium retention, and infiltration of CD161a+/CD68+ macrophages into the renal medulla of animals. All of these effects were abrogated or prevented by RND and ablation of CD161a+ immune cells. Cholinergic activation of CD161a+ positive immune cells leads to the premature development of hypertension in SHR, at least partly, through increased renal expression of NKCC2 and renal sodium retention. Effects on chemotaxis of CD161a+ macrophages to the renal medulla, decreased renal expression of NKCC2, and renal sodium retention appear to play a part in the prevention of cholinergic hypertension as a result of RND. The CD161a+ immune cells are necessary and essential for this pro-hypertensive nicotine-mediated inflammatory response.

Raikwar, NS;Braverman, C;Snyder, PM;Fenton, RA;Meyerholz, DK;Abboud, FM;Harwani, SC; (2019). Renal Denervation and CD161a Immune Ablation Prevent Cholinergic Hypertension and Renal Sodium Retention. Am. J. Physiol. Heart Circ. Physiol.. doi:10.1152/ajpheart.00234.2019.

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