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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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We’re thrilled to announce that the MedFrontier Intact FGF23 Assay was featured in a recent publication! Details are available via the abstract and full-text access provided below.

Abstract

Multiple myeloma commonly manifests with symptoms arising from the involvement of various organs, particularly the bone and kidneys. In this report, we detail the case of a 44-year-old man who was diagnosed with multiple myeloma associated with reduced bone density. He exhibited clinical findings of osteomalacia due to Fanconi syndrome (characterized clinically by bone pain and proximal weakness and biochemically by elevated serum alkaline phosphatase, hypophosphatemia, hypouricemia, and glucosuria). With phosphate replacement, there was a notable improvement in bone pain, osteomalacia, and bone mineral density. Nevertheless, the patient continued to experience renal wasting of phosphate, uric acid, and glucose despite achieving remission from multiple myeloma for nearly 2 years. Our case highlights several important clinical features of myeloma-associated Fanconi syndrome, including the need to recognize this complication to appropriately treat the underlying bone disease while avoiding osteoclast inhibitors and the long-term persistence of the proximal renal tubulopathy despite achieving remission from myeloma and correction of osteomalacia.

Alireza Zomorodian, Naim M Maalouf, Long-term Evolution of Hypophosphatemia and Osteomalacia in a Patient With Multiple Myeloma, JCEM Case Reports, Volume 2, Issue 7, July 2024, luae137, https://doi.org/10.1210/jcemcr/luae137

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The Niacin Microtiter Plate Assay Kit was utilized in a recent study! Researchers developed a novel approach to study microglia, key immune cells in the CNS, under different conditions. Read on for a summary of this groundbreaking research!

Summary

Microglia are the resident macrophages of the central nervous system (CNS). Their phagocytic activity is central during brain development and homeostasis—and in a plethora of brain pathologies. However, little is known about the composition, dynamics, and function of human microglial phagosomes under homeostatic and pathological conditions. Here, we developed a method for rapid isolation of pure and intact phagosomes from human pluripotent stem cell-derived microglia under various in vitro conditions, and from human brain biopsies, for unbiased multiomic analysis. Phagosome profiling revealed that microglial phagosomes were equipped to sense minute changes in their environment and were highly dynamic. We detected proteins involved in synapse homeostasis, or implicated in brain pathologies, and identified the phagosome as the site where quinolinic acid was stored and metabolized for de novo nicotinamide adenine dinucleotide (NAD+) generation in the cytoplasm. Our findings highlight the central role of phagosomes in microglial functioning in the healthy and diseased brain.

Wogram, E et al. Rapid phagosome isolation enables unbiased multiomic analysis of human microglial phagosomes. Immunity. 57(9)p:2216-2231.e11 doi:10.1016/j.immuni.2024.07.019

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