Author: Eagle Biosciences

Osteoprotegerin (OPG) is a glycoprotein that plays a crucial role in regulating bone metabolism. It is a decoy receptor for the receptor activator of nuclear factor-kappa B ligand (RANKL), which is involved in the process of bone resorption. OPG is primarily produced by osteoblasts (bone-forming cells) but can also be found in other tissues like endothelial cells, smooth muscle cells, and certain immune cells.

OPG is an important regulator not just for bone metabolism but also in inflammation. It modulates immune cell activity, cytokine production, and tissue remodeling in response to inflammation. Elevated OPG levels can be a sign of ongoing inflammatory processes in diseases such as rheumatoid arthritis, atherosclerosis, and other autoimmune disorders.

Biomedica’s Osteoprotegerin ELISA Assay Kit (BI-20403) was highlighted in a recent study! The study assessed serum OPG levels during acute inflammatory states induced by a bacterial or viral infection in children. The researchers investigated whether OPG increases during acute inflammatory states and if its levels correlate with other biomarkers. Click below for the full publication, where you can find the abstract and key findings!

Giannakopoulos, Aristeidis, et al. “Osteoprotegerin in infection-induced acute inflammatory states in children.” Heliyon, vol. 10, no. 6, Mar. 2024, https://doi.org/10.1016/j.heliyon.2024.e27565.

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The Testosterone ELISA Assay Kit was employed in a recent study that explored the effects of cluster vs. traditional sets complex training on physical performance adaptations of trained male volleyball players. Check out the details and access the full findings below.

Abstract

This study aimed to examine the impact of different set configurations during combination of resistance and plyometric training (complex [COX]) on jumping ability, power output, strength, and hormonal adaptations in young male volleyball players after a 6-week training period. A randomized controlled trial was conducted with twenty-four trained male volleyball players under the age of 19, who were assigned to one of two groups for lower-body COX training: cluster sets (CS-COX: n = 8) or traditional sets (TS-COX: n = 8), with an additional active control group (CON: n = 8). The players underwent evaluations for countermovement vertical jump (CMVJ), spike jump (SPJ), T-test change of direction speed (T-test CODS), one repetition maximum (1RM) in the back squat and leg press, and the Wingate Anaerobic Test before and after the 6-week training intervention (12 sessions in total). Blood samples were also collected before and after training to assess resting testosterone and cortisol responses. Following the training, both the CS-COX and TS-COX groups exhibited significantly greater (p = 0.001) changes than the CON group in the variables, while similar improvements in maximal strength, mean power output, and testosterone adaptations were observed following the training (p < 0.05). Moreover, the CS-COX group demonstrated greater improvements in CMVJ (effect size [ES] = 0.36), SPJ (ES = 0.06), T-test CODS (ES = -0.60), and peak power output (ES = 0.72), along with greater reductions in resting cortisol (ES = -0.30) levels compared to the TS-COX group after the 6-week intervention (p < 0.05). In conclusion, the results indicate that incorporating cluster sets during COX training sessions led to more favorable changes in bio-motor ability, peak power output, and cortisol adaptations, with greater consistency and uniformity in adaptations among the players compared to traditional set configurations.

Rong, Bo, and Chen Xiu. “Effects of cluster vs. traditional sets complex training on physical performance adaptations of trained male volleyball players.” Journal of Sports Science and Medicine, 1 Dec. 2024, pp. 822–833, https://doi.org/10.52082/jssm.2024.822.

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Frailty is a syndrome characterized by the gradual decline in physical function, strength, and endurance, typically associated with aging. Frailty increases the risk of falls, fractures, disability, and death, making early detection and intervention critical. The onset of frailty is often subtle and difficult to identify in its early stages, which is why there is increasing interest in finding reliable biomarkers for its detection.

Sclerostin has emerged as a potential biomarker for the early detection of frailty due to its involvement in both bone metabolism and muscle function. Studies suggest that changes in sclerostin levels are associated with age-related declines in skeletal muscle mass, strength, and function — all of which are central components of frailty.

Biomedica’s Sclerostin ELISA Kit was used in a first time study that explored the association between circulating sclerostin levels and frailty. Click below for the full publication, where you can find the abstract and key findings!

Baek, Ji Yeon, et al. “Elevated circulating Sclerostin levels in frail older adults: Implications beyond bone health.” Endocrinology and Metabolism, vol. 40, no. 1, 28 Feb. 2025, pp. 73–81, https://doi.org/10.3803/enm.2024.2100.

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The BI-CAT Adrenaline & Noradrenaline ELISA Assay Kit was utilized in a recent study that focused on if low-dose glucagon is needed and effective in preventing fasted exercise-induced hypoglycaemia in type 1 diabetes. Check out the abstract and full text details below!

Abstract

Aim: The aim of this study is to evaluate and compare the plasma glucose (PG) response during spontaneous fasted morning moderate-intensity exercise with and without injection of subcutaneous glucagon in adults with type 1 diabetes (T1D) treated with an automated insulin delivery (AID) system.

Methods:
Ten adults (four female) with T1D (age 50 [42–67] years, diabetes duration: 22 [14–44] years, HbA1c: 55 [47–69] mmol/mol) treated with the MiniMed™ 780G AID system participated in a proof-of-concept two-period, crossover trial. Fasting participants undertook a 45 min bout of continuous moderate-intensity (~60% V̇O_2peak) exercise on a cycle ergometer followed by 1 h of rest. Before exercise, 150-μg glucagon was administered subcutaneously on visit 1 (GLUC) but not on visit 2 (NO-GLUC). Temporary target on the AID was activated 15 min before until 15 min after exercise cessation. Blood samples were taken at 5- and 15-min intervals for measuring PG and biomarkers. Data were analysed using paired t tests or repeated measures ANOVA.

Results
Time in range (3.9–10.0 mmol/L) was 100% on both study visits. No hypoglycaemia (<3.9 mmol/L) occurred in either arm. The GLUC arm had significantly higher mean PG (p = 0.01), area under the PG curve (p = 0.01), coefficient of variation (p < 0.01), peak PG (p = 0.01) and PG at the end of exercise (p < 0.01). No differences in endogenous gluco-regulatory hormones were observed between visits.

Conclusion
Adults with T1D treated with the MiniMed™ 780G can perform spontaneous fasted moderate-intensity exercise without hypoglycaemia. Therefore, glucagon was not needed for prevention of hypoglycaemia in such situations.

Lundemose, Sissel Banner, et al. “Is low‐dose glucagon needed and effective in preventing fasted exercise‐induced hypoglycaemia in type 1 diabetes treated with the minimed 780g, an automated insulin delivery system?” Diabetes, Obesity and Metabolism, 27 Nov. 2024, https://doi.org/10.1111/dom.16103.

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The Mouse Albumin ELISA Assay Kit was utilized in a recent study! The study demonstrates the beneficial role of early immune activation during stress, revealing that the immune system could protect against psychological insults. Access the abstract and full text below.

Abstract

Psychological stress and its sequelae pose a major challenge to public health. Immune activation is conventionally thought to aggravate stress-related mental diseases such as anxiety disorders and depression. Here, we sought to identify potentially beneficial consequences of immune activation in response to stress. We showed that stress led to increased interleukin (IL)-22 production in the intestine as a result of stress-induced gut leakage. IL-22 was both necessary and sufficient to attenuate stress-induced anxiety behaviors in mice. More specifically, IL-22 gained access to the septal area of the brain and directly suppressed neuron activation. Furthermore, human patients with clinical depression displayed reduced IL-22 levels, and exogenous IL-22 treatment ameliorated depressive-like behavior elicited by chronic stress in mice. Our study thus identifies a gut-brain axis in response to stress, whereby IL-22 reduces neuronal activation and concomitant anxiety behavior, suggesting that early immune activation can provide protection against psychological stress.

Xia, Mengyu, et al. “Elevated IL-22 as a result of stress-induced gut leakage suppresses septal neuron activation to ameliorate anxiety-like behavior.” Immunity, vol. 58, no. 1, Jan. 2025, https://doi.org/10.1016/j.immuni.2024.11.008.

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The L-Ornithine ELISA Assay Kit was utilized in a recent study! The study shows the benefits of combined liver and retinal OAT supplementation for the treatment of GACR. For more details, reference the abstract and access to the full text below.

Abstract

Gyrate atrophy of the choroid and retina (GACR) is due to ornithine aminotransferase (OAT) deficiency, which causes hyperornithinemia, leading to retinal pigment epithelium, followed by choroidal and retinal degeneration. Adeno-associated virus serotype 8 (AAV8) vector-mediated OAT (AAV8-OAT) liver gene transfer reduces ornithinemia in the Oat^−/− mouse model of GACR and improves retinal function and structure. Since OAT is expressed in various tissues including the retina, we investigated the efficacy of restoration of OAT expression in either retina or liver or both tissues on the retinal phenotype of Oat^−/− mice. Intravenous and subretinal administration of AAV8-OAT resulted in intraocular and liver OAT expression with reduced ornithinemia after intravenous AAV8-OAT administration, while intraocular ornithine levels were significantly reduced only following combined gene delivery. Accordingly, only Oat^−/− animals treated with combined intravenous and subretinal AAV8-OAT administrations showed significant improvements in both retinal morphology and function. This work shows the benefits of combined liver and retinal OAT supplementation for the treatment of GACR.

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We’re excited to announce that the Noradrenaline (Norepinephrine) Sensitive ELISA was featured in a recent publication! Check out access the abstract and full text below.

Abstract

Spinal cord injury triggers leukocyte mobilization from the peripheral circulation to the injury site, exacerbating spinal cord damage. Simultaneously, bone marrow hematopoietic stem cells (HSCs) and splenic leukocytes rapidly mobilize to replenish the depleted peripheral blood leukocyte pool. However, current treatments for spinal cord injuries overlook interventions targeting peripheral immune organs and tissues, highlighting the need to develop novel drugs capable of effectively regulating peripheral immunity and treating spinal cord injuries. In this study, we designed, synthesized, and characterized novel Ejiao carbon dots (EJCDs) that inhibit myeloid cell proliferation and peripheral migration by promoting HSC self-renewal, and distinct differentiation into erythroid progenitors in vitro and in vivo. Additionally, EJCDs attenuate the immune response in the spleen, leukocytes’ reservoir, following spinal cord injury by diminishing the local infiltration of monocytes and macrophages while promoting motor function recovery. These effects are mediated through the downregulation of CCAAT enhancer binding protein-β expression in the spleen and the upregulation of FZD4 protein expression in Lin⁻ Sca-1⁺ c-kit⁺ cells (LSKs) within the bone marrow. Our findings demonstrate that EJCDs effectively reduce myeloid cell infiltration post-spinal cord injury and promote neurological recovery, making them promising therapeutic candidates for treating spinal cord injuries.

Li, Junjin, et al. “Novel carbon dots with dual modulatory effects on the bone marrow and spleen as a potential therapeutic candidate for treating spinal cord injury.” Bioactive Materials, vol. 45, Mar. 2025, pp. 534–550, https://doi.org/10.1016/j.bioactmat.2024.11.032.

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The Eagle Bioscience’s Noradrenaline ( Norepinephrine) High Sensitive ELISA was utilized in a recent publication that focused on how β₁-adrenergic receptor links sympathetic nerves to T cell exhaustion. Check out the full text and abstract below!

Abstract

CD8⁺ T cells are essential components of the immune response against viral infections and tumors, and are capable of eliminating infected and cancerous cells. However, when the antigen cannot be cleared, T cells enter a state known as exhaustion¹. Although it is clear that chronic antigen contributes to CD8⁺ T cell exhaustion, less is known about how stress responses in tissues regulate T cell function. Here we show a new link between the stress-associated catecholamines and the progression of T cell exhaustion through the β₁-adrenergic receptor ADRB1. We identify that exhausted CD8⁺ T cells increase ADRB1 expression and that exposure of ADRB1⁺ T cells to catecholamines suppresses their cytokine production and proliferation. Exhausted CD8⁺ T cells cluster around sympathetic nerves in an ADRB1-dependent manner. Ablation of β₁-adrenergic signaling limits the progression of T cells towards the exhausted state in chronic infection and improves effector functions when combined with immune checkpoint blockade (ICB) in melanoma. In a pancreatic cancer model resistant to ICB, β-blockers and ICB synergize to boost CD8⁺ T cell responses and induce the development of tissue-resident memory-like T cells. Malignant disease is associated with increased catecholamine levels in patients^2,3, and our results establish a connection between the sympathetic stress response, tissue innervation and T cell exhaustion. Here, we uncover a new mechanism by which blocking β-adrenergic signaling in CD8⁺ T cells rejuvenates anti-tumor functions.

Globig, AM., Zhao, S., Roginsky, J. et al. The β₁-adrenergic receptor links sympathetic nerves to T cell exhaustion. Nature 622, 383-392 (2023).

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The Eagle Bioscience’s easYmer H2-Db MHC Tetramer was highlighted in a recent publication that focused on killing tumor-associated bacteria with a liposomal antibiotic and how it generates neoantigens that induce anti-tumor immune responses. Check out the full text and abstract below!

Abstract

Increasing evidence implicates the tumor microbiota as a factor that can influence cancer progression. In patients with colorectal cancer (CRC), we found that pre-resection antibiotics targeting anaerobic bacteria substantially improved disease-free survival by 25.5%. For mouse studies, we designed an antibiotic silver-tinidazole complex encapsulated in liposomes (LipoAgTNZ) to eliminate tumor-associated bacteria in the primary tumor and liver metastases without causing gut microbiome dysbiosis. Mouse CRC models colonized by tumor-promoting bacteria (Fusobacterium nucleatum spp.) or probiotics (Escherichia coliNissle spp.) responded to LipoAgTNZ therapy, which enabled more than 70% long-term survival in two F. nucleatum-infected CRC models. The antibiotic treatment generated microbial neoantigens that elicited anti-tumor CD8⁺ T cells. Heterologous and homologous bacterial epitopes contributed to the immunogenicity, priming T cells to recognize both infected and uninfected tumors. Our strategy targets tumor-associated bacteria to elicit anti-tumoral immunity, paving the way for microbiome–immunotherapy interventions.

Wang, M., Rousseau, B., Qiu, K. et al. Killing tumor-associated bacteria with a liposomal antibiotic generates neoantigens that induce anti-tumor immune responses. Nat Biotechnol (2023).

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