Category: Publication Spotlight

The Eagle Bioscience’s Plasma Metanephrine ELISA Assay was utilized in a recent publication that focused on how social isolation exacerbates acute ozone inhalation induced pulmonary and systemic health outcomes . Check out the full text and abstract below.

Abstract

Psychosocially-stressed individuals might have exacerbated responses to air pollution exposure. Acute ozone exposure activates the neuroendocrine stress response leading to systemic metabolic and lung inflammatory changes. We hypothesized chronic mild stress (CS) and/or social isolation (SI) would cause neuroendocrine, inflammatory, and metabolic phenotypes that would be exacerbated by an acute ozone exposure. Male 5-week-old Wistar-Kyoto rats were randomly assigned into 3 groups: no stress (NS) (pair-housed, regular-handling); SI (single-housed, minimal-handling); CS (single-housed, subjected to mild unpredicted-randomized stressors [restraint-1 h, tilted cage-1 h, shaking-1 h, intermittent noise-6 h, and predator odor-1 h], 1-stressor/day*5-days/week*8-weeks. All animals then 13-week-old were subsequently exposed to filtered-air or ozone (0.8-ppm) for 4 h and immediately necropsied. CS, but not SI animals had increased adrenal weights. However, relative to NS, both CS and SI had lower circulating luteinizing hormone, prolactin, and follicle-stimulating hormone regardless of exposure (SI > CS), and only CS demonstrated lower thyroid-stimulating hormone levels. SI caused more severe systemic inflammation than CS, as evidenced by higher circulating cytokines and cholesterol. Ozone exposure increased urine corticosterone and catecholamine metabolites with no significant stressor effect. Ozone-induced lung injury, and increases in lavage-fluid neutrophils and IL-6, were exacerbated by SI. Ozone severely lowered circulating thyroid-stimulating hormone, prolactin, and luteinizing hormone in all groups and exacerbated systemic inflammation in SI. Ozone-induced increases in serum glucose, leptin, and triglycerides were consistent across stressors; however, increases in cholesterol were exacerbated by SI. Collectively, psychosocial stressors, especially SI, affected the neuroendocrine system and induced adverse metabolic and inflammatory effects that were exacerbated by ozone exposure.

Henriquez, Andres R., et al. “Social Isolation Exacerbates Acute Ozone Inhalation Induced Pulmonary and Systemic Health Outcomes.” Toxicology and Applied Pharmacology, vol. 457, 2022, p. 116295., https://doi.org/10.1016/j.taap.2022.116295.

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The Eagle Bioscience’s Biotinylated IGFBP-3 Recombinant Protein was highlighted in a recent publication that focused on how insulin like growth factor binding protein-3 induces senescence by inhibiting telomerase activity in MCF-7 breast cancer cells. Check out the full text and abstract below.

Abstract

Insulin-like growth factor binding protein-3 (IGFBP-3) has been known to inhibit the proliferation of various cell types in an insulin-like growth factor (IGF)-independent manner. In this study, we aimed to show that IGFBP-3 induces cellular senescence via suppression of telomerase activity, thereby inhibiting cancer cell proliferation. We found that the induction of IGFBP-3 in MCF-7 cells inhibited cell proliferation. Flow cytometry revealed that the percentage of non-cycling cells was higher in IGFBP-3-expressing cells than in controls. Induction of IGFBP-3 also resulted in morphological changes, such as a flattened cytoplasm and increased granularity, suggesting that IGFBP-3 induces senescence-like phenotype. The percentage of cells containing senescence-associated β-galactosidase activity was 3.3 times higher in IGFBP-3 expressing cells compared to control cells. Telomeric repeat amplification and real-time PCR showed that IGFBP-3 decreased telomerase activity by decreasing the expression of the RNA component (hTR) and catalytic protein component with reverse transcriptase activity (hTERT) of telomerase. These results suggest that IGFBP-3 functions as a negative regulator of breast cancer cell growth by inducing a senescence through the inhibition of telomerase activity.

Kwon, Ahreum, et al. “Insulin-like Growth Factor Binding Protein-3 Induces Senescence by Inhibiting Telomerase Activity in MCF-7 Breast Cancer Cells.” 2022, https://doi.org/10.21203/rs.3.rs-2081030/v1.

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The Eagle Bioscience’s Progesterone Saliva ELISA was utilized in a recent publication that explored the association between serum neurofilament light and glial fibrillary acidic protein levels. Check out the full text and abstract below.

Abstract

Recent investigations have identified water polo athletes as at risk for concussions and repetitive subconcussive head impacts. Head impact exposure in collegiate varsity women’s water polo, however, has not yet been longitudinally quantified. We aimed to determine the relationship between cumulative and acute head impact exposure across pre-season training and changes in serum biomarkers of brain injury. Twenty-two Division I collegiate women’s water polo players were included in this prospective observational study. They wore sensor-installed mouthguards during all practices and scrimmages during eight weeks of pre-season training. Serum samples were collected at six time points (at baseline, before and after scrimmages during weeks 4 and 7, and after the eight-week pre-season training period) and assayed for neurofilament light (NfL) and glial fibrillary acidic protein (GFAP) using Simoa^® Human Neurology 2-Plex B assay kits. Serum GFAP increased over time (e.g., an increase of 0.6559 pg/mL per week; p = 0.0087). Neither longitudinal nor acute pre-post scrimmage changes in GFAP, however, were associated with head impact exposure. Contrarily, an increase in serum NfL across the study period was associated with cumulative head impact magnitude (sum of peak linear acceleration: B = 0.015, SE = 0.006, p = 0.016; sum of peak rotational acceleration: B = 0.148, SE = 0.048, p = 0.006). Acute changes in serum NfL were not associated with head impacts recorded during the two selected scrimmages. Hormonal contraceptive use was associated with lower serum NfL and GFAP levels over time, and elevated salivary levels of progesterone were also associated with lower serum NfL levels. These results suggest that detecting increases in serum NfL may be a useful way to monitor cumulative head impact burden in women’s contact sports and that female-specific factors, such as hormonal contraceptive use and circulating progesterone levels, may be neuroprotective, warranting further investigations.

Huibregtse, Megan E., et al. “Association between Serum Neurofilament Light and Glial Fibrillary Acidic Protein Levels and Head Impact Burden in Women’s Collegiate Water Polo.” Journal of Neurotrauma, 2022, https://doi.org/10.1089/neu.2022.0300.

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The Eagle Bioscience’s High Sensitive CRP ELISA was highlighted in a recent publication that focused on firefighters with higher cardiorespiratory fitness demonstrate lower markers of cardiovascular disease risk. Check out the full text and abstract below.

Abstract

McAllister, Matthew J., et al. “Firefighters with Higher Cardiorespiratory Fitness Demonstrate Lower Markers of Cardiovascular Disease Risk.” Journal of Occupational & Environmental Medicine, vol. 64, no. 12, 2022, pp. 1036–1040., https://doi.org/10.1097/jom.0000000000002632.

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The Eagle Bioscience’s Human Prealbumin ELISA was utilized in a recent publication that focused on the growth biomarker for children with congenital heart disease. Check out the full text and abstract below.

Abstract

Background
Failure to thrive (FTT), defined as weight or height less than the lowest 2.5 percentile for age, is prevalent in up to 66% of children with congenital heart disease (CHD). Risk stratification methods to identify those who would benefit from early intervention are currently lacking. We aimed to identify a novel growth biomarker to aid clinical decision-making in children with CHD.

Methods
This is a cross-sectional study of patients 2 months to 10 years of age with any CHD undergoing cardiac surgery. Preoperative weight-for-age Z scores (WAZ) and height-for-age Z scores (HAZ) were calculated and assessed for association with preoperative plasma biomarkers: growth differentiation factor 15 (GDF-15), fibroblast growth factor 21, leptin, prealbumin, and C-reactive protein (CRP).

Results
Of the 238 patients included, approximately 70% of patients had WAZ/HAZ < 0 and 34% had FTT. There was a moderate correlation between GDF-15 and WAZ/HAZ. When stratified by age, the correlation of GDF-15 to WAZ and HAZ was strongest in children under 2 years of age and persisted in the setting of inflammation (CRP > 0.5 mg/dL). Diagnoses commonly associated with congestive heart failure had high proportions of FTT and median GDF-15 levels. Prealbumin was not correlated with WAZ or HAZ.

Conclusions
GDF-15 represents an important growth biomarker in children with CHD, especially those under 2 years of age who have diagnoses commonly associated with CHF. Our data do not support prealbumin as a long-term growth biomarker.

Paneitz, Dane C, et al. “Growth Differentiation Factor 15: A Novel Growth Biomarker for Children with Congenital Heart Disease.” World Journal for Pediatric and Congenital Heart Surgery, vol. 13, no. 6, 2022, pp. 745–751., https://doi.org/10.1177/21501351221118080.

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The Eagle Bioscience’s Creatine Microplate Assay was highlighted in a recent publication that explored the association of urinary biomarkers of smoking-related toxicants with lung cancer incidence in smokers. Check out the full text and abstract below.

Abstract

Cigan, Shannon S., et al. “Association of Urinary Biomarkers of Smoking-Related Toxicants with Lung Cancer Incidence in Smokers: The Multiethnic Cohort Study.” Cancer Epidemiology, Biomarkers & Prevention, 2023, https://doi.org/10.1158/1055-9965.epi-22-0569.

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The Eagle Bioscience’s Etanercept (Enbrel) ELISA was utilized in a recent publication that focused on the concentration of etanercept in human milk and infant outcomes. Check out the full text and abstract below.

Abstract

According to the National Institutes of Health, up to 23.5 million Americans (> 7% of the population) suffer from an autoimmune disease, and women are 2 times more likely to be diagnosed with an autoimmune disease than men.1,2 Medications such as etanercept (ETN) may be required for treatment of maternal disease during lactation. This can be problematic for lactating individuals due to the paucity of data on the safety of those medications for the nursing infant. Given that human milk is the recommended primary source of nutrition for infants until 6 months of age and a complementary source of nutrition until at least 12 months of age, it is critical to study medications that are used to treat autoimmune diseases during lactation

Bertrand, Kerri, et al. “The Concentration of Etanercept in Human Milk and Infant Outcomes.” The Journal of Rheumatology, 2022.

About Etanercept

Etanercept is a biopharmaceutical that treats autoimmune diseases by interfering with tumor necrosis factor (TNF, a soluble inflammatory cytokine) by acting as a TNF inhibitor. It has U.S. F.D.A. approval to treat rheumatoid arthritis, juvenile rheumatoid arthritis and psoriatic arthritis, plaque psoriasis and ankylosing spondylitis. TNF-alpha is the “master regulator” of the inflammatory (immune) response in many organ systems. Autoimmune diseases are caused by an overactive immune response. Etanercept has the potential to treat these diseases by inhibiting TNF-alpha.

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

Liver Transplant: antibody-mediated rejection monitored by C4d

Liver transplantation has become a routine treatment for children with end stage liver failure. Antibody-mediated rejection of the transplant can be monitored by C4d. This recent study utilized the Anti-Human C4d Antibody from Biomedica. Check out the abstract below.

Abstract

Liver transplantation has become a routine treatment for children with end stage liver failure. Recently, the long term survival of pediatric patients after liver transplantation has improved, with a life expectancy much longer than that of adult recipients, but also with longer exposition of the graft to various injuries, including immunological, inflammatory and others. Biochemical tests, although important, do not always reflect graft injury. The aim of our study was to analyze the histopathology of the graft in late protocol biopsies and correlate it with the clinical and biochemical status of these patients. We analyzed 61 protocol liver biopsies taken from 61 patients. Biopsies were taken 9.03-17.09 years (mean 12.68, median 11.74 years) after transplantation. Liver specimens were examined particularly for the presence and stage of liver fibrosis, inflammation, steatosis, and acute or chronic cellular and humoral rejection. We did not find any abnormalities in 26 (42.6%) liver specimens. None of the patients had signs of cellular or antibody mediated rejection or chronic rejection. In 23 liver biopsies (37.7%), we found non-specific lymphoid infiltrates. Another problem was fibrosis (equal to or more than three on the Ishak scale)-we found it in 17 patients, including seven liver specimens (11.5%) with severe fibrosis (Ishak 5-6). Conclusions: Various pathomorphological abnormalities were found in more than half of patients with a median 11.74 years post-transplant follow-up. Most of them presented normal laboratory liver tests at the same time, suggesting a slow subclinical process leading to pathomorphological abnormalities. No single factor for the development of these abnormalities was found, but our study supports the need for protocol liver biopsies even in patients with normal/almost normal biochemical liver tests.

Markiewicz-Kijewska M, Szymańska S, Pyzlak M, Kaliciński P, Teisseyre J, Kowalski A, Jankowska I, Czubkowski P, Ismail H. Liver Histopathology in Late Protocol Biopsies after Pediatric Liver Transplantation. Children (Basel). 2021 Aug 1;8(8):671. doi: 10.3390/children8080671. PMID: 34438562; PMCID: PMC8392008.

Anti-Human C4d Antibody Features

• Widely cited for ICH
• For kidney, heart, liver and other transplants

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The Eagle Bioscience’s Mouse Rat 25-OH Vitamin D ELISA was utilized in a recent publication that focused on how vitamin D and the ability to produce 1,25(OH)₂D is critical for protection from viral lung infection. Check out the full text and abstract below.

Abstract

Vitamin D supplementation is linked to improved outcomes from respiratory virus infection, and the COVID-19 pandemic renewed interest in understanding the potential role of vitamin D in protecting the lung from viral infections. Therefore, we evaluated the role of vitamin D using animal models of pandemic H1N1 influenza and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. In mice, dietary-induced vitamin D deficiency resulted in lung inflammation that was present prior to infection. Vitamin D sufficient (D+) and deficient (D−) wildtype (WT) and D+ and D− Cyp27B1 (Cyp) knockout (KO, cannot produce 1,25(OH)₂D) mice were infected with pandemic H1N1. D− WT, D+ Cyp KO, and D− Cyp KO mice all exhibited significantly reduced survival compared to D+ WT mice. Importantly, survival was not the result of reduced viral replication, as influenza M gene expression in the lungs was similar for all animals. Based on these findings, additional experiments were performed using the mouse and hamster models of SARS-CoV-2 infection. In these studies, high dose vitamin D supplementation reduced lung inflammation in mice but not hamsters. A trend to faster weight recovery was observed in 1,25(OH)₂D treated mice that survived SARS-CoV-2 infection. There was no effect of vitamin D on SARS-CoV-2 N gene expression in the lung of either mice or hamsters. Therefore, vitamin D deficiency enhanced disease severity, while vitamin D sufficiency/supplementation reduced inflammation following infections with H1N1 influenza and SARS-CoV-2.

Arora, Juhi, et al. “Vitamin D and the Ability to Produce 1,25(OH)2D Are Critical for Protection from Viral Infection of the Lungs.” Nutrients, vol. 14, no. 15, 2022, p. 3061., https://doi.org/10.3390/nu14153061.

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The Eagle Bioscience’s MedFrontier Intact FGF23 Assay highlighted in a recent publication that focused on the determination of FGF23 Levels for the diagnosis of FGF23-mediated hypophosphatemia. Check out the full text and abstract below.

Abstract

Fibroblast growth factor-23 (FGF23) measurement is a critical tool in the evaluation of patients with disordered phosphate homeostasis. Available laboratory reference ranges for blood FGF23 were developed using samples from normophosphatemic individuals. Reliance on such values can lead to misdiagnosis in patients with FGF23-mediated hypophosphatemia, such as X-linked hypophosphatemia (XLH) and tumor-induced osteomalacia (TIO), in whom pathology-driving FGF23 levels can be in the “normal range.” To determine FGF23 levels that are diagnostic for the identification of patients with FGF23-mediated hypophosphatemic disorders, we studied 149 patients with various disorders of FGF23-mediated and FGF23-independent hypophosphatemia and defined cut-off levels for both intact FGF23 (iFGF23) and C-terminal FGF23 (cFGF23) that can accurately distinguish between FGF23-mediated and FGF23-independent hypophosphatemia. In addition, to demonstrate the relationship between FGF23 and phosphate across the spectrum of human physiology, we assessed blood levels of FGF23 and phosphate in 434 patients with various forms of hypophosphatemia, hyperphosphatemia, and normophosphatemia. An intact FGF23 cut point of 27 pg/mL was 100% sensitive and specific in distinguishing FGF23-mediated from FGF23-independent hypophosphatemia, and a cFGF23 cut point of 90 RU/mL was 100% sensitive and specific in distinguishing specifically TIO from FGF23-independent hypophosphatemia. There was overlap in the cFGF23 range of 45–90 RU/mL between genetic forms of FGF23 excess and FGF23-independent hypophosphatemia, substantiating the superiority of iFGF23 over cFGF23 in making the diagnosis of FGF23-mediated hypophosphatemia. In this cohort, using the laboratory upper limit of normal for cFGF23 (180 RU/mL) would result in a misdiagnosis in more than half of patients with FGF23-mediated hypophosphatemia. In this, the largest study of FGF23 in chronic hypophosphatemia to date, we established iFGF23 and cFGF23 cut-off values to assist in the evaluation and diagnosis of hypophosphatemic conditions. © 2022 American Society for Bone and Mineral Research (ASBMR). This article has been contributed to by US Government employees and their work is in the public domain in the USA.

Hartley, Iris R., et al. “Determination of FGF23 Levels for the Diagnosis of FGF23‐Mediated Hypophosphatemia.” Journal of Bone and Mineral Research, vol. 37, no. 11, 2022, pp. 2174–2185., https://doi.org/10.1002/jbmr.4702.

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