Author: Eagle Biosciences

We’re excited to share that the Noradrenaline (Norepinephrine) Sensitive ELISA Assay Kit was featured in a recent publication! The study explored the link between Alzheimer’s Disease and osteoporosis using mouse models. Discover the abstract and access the full text below.

Abstract

Alzheimer’s disease (AD) and osteoporosis often coexist in the elderly. Although observational studies suggest an association between these two diseases, the pathophysiologic link between AD and skeletal health has been poorly defined. We examined the skeletal phenotype of 5xFAD mice, an AD model with accelerated neuron-specific amyloid-β accumulation causing full-blown AD phenotype by the age of 8 months. Micro-computed tomography indicated significantly lower trabecular and cortical bone parameters in 8-month-old male, but not female, 5xFAD mice than sex-matched wild-type littermates. Dynamic histomorphometry revealed reduced bone formation and increased bone resorption, and quantitative RT-PCR showed elevated skeletal RANKL gene expression in 5xFAD males. These mice also had diminished body fat percentage with unaltered lean mass, as determined by dual-energy X-ray absorptiometry (DXA), and elevated Ucp1 mRNA levels in brown adipose tissue, consistent with increased sympathetic tone, which may contribute to the osteopenia observed in 5xFAD males. Nevertheless, no significant changes could be detected between male 5xFAD and wild-type littermates regarding the serum and skeletal concentrations of norepinephrine. Thus, brain-specific amyloid-β pathology is associated with osteopenia and appears to affect both bone formation and bone resorption. Our findings shed new light on the pathophysiologic link between Alzheimer’s disease and osteoporosis.

Jung, Ay, Cyr et al. Amyloid-β neuropathology induces bone loss in male mice by suppressing bone formation and enhancing bone resoptioin. Bone Rep. 2024. 21:101771 DOI: 10.1016/j.bonr.2024.101771

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An innovative study leveraged multiple ELISA kits from our portfolio to investigate the impact of head-out cold water immersion on thyroid hormone concentrations. The researchers used a range of kits, such as the Free Triiodothyronine (fT3) ELISA, Triiodothyronine T3 ELISA Assay Kit, Free Thyroxine (fT4) ELISA Assay Kit, Thyroxine (T4) ELISA Assay Kit, and Thyroid Stimulating Hormone ELISA Assay Kit. Find the abstract and access to the full text below.

Abstract

This study tested the hypothesis that acute moderate normobaric hypoxia augments circulating thyroid hormone concentrations during and following 1 h of cold head-out water immersion (HOWI), compared with when cold HOWI is completed during normobaric normoxia. In a randomized crossover single-blind design, 12 healthy adults (27 ± 2 yr, 2 women) completed 1 h of cold (22.0 ± 0.1°C) HOWI breathing either normobaric normoxia (F⁢IO2 = 0.21) or normobaric hypoxia (F⁢IO2 = 0.14). Free and total thyroxine (T3) and triiodothyronine (T4), and thyroid-stimulating hormone (TSH) concentrations were measured in venous blood samples obtained before (baseline), during (15-, 30-, and 60 min), and 15 min following HOWI (post-), and were corrected for changes in plasma volume. Arterial oxyhemoglobin saturation and core (rectal) temperature were measured continuously. Arterial oxyhemoglobin saturation was lower during hypoxia (90 ± 3%) compared with normoxia (98 ± 1%, P < 0.001). Core temperature fell from baseline (normoxia: 37.2 ± 0.4°C, hypoxia: 37.2 ± 0.4°C) to post-cold HOWI (normoxia: 36.4 ± 0.5°C, hypoxia: 36.3 ± 0.5°C, P < 0.001) in both conditions but did not change differently between conditions (condition × time: P = 0.552). Circulating TSH, total T3, free T4, total T3, and free T4 concentrations demonstrated significant main effects of time (all P ≤ 0.024), but these changes did not differ between normoxic and hypoxic conditions (condition × time: all P ≥ 0.163). These data indicate that acute moderate normobaric hypoxia does not modify the circulating thyroid hormone response during 1 h of cold HOWI.

Keeler JM, et al. Acute moderate normobaric hypoxia does not modify circulating thyroid hormone concentrations induced by 1 h of head-out cold-water immersion. Journal of Applied Physiology. 2024 136(6):1400-1409. https://doi.org/10.1152/japplphysiol.00061.2024

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In their latest research, scientists utilized the Creatinine Microplate Assay Kit to shed light on why lung cancer is more prevalent among African Americans compared to Whites, even when both groups have similar smoking habits. See the abstract and full text below.

Abstract

Background: After accounting for smoking history, lung cancer incidence is greater in African Americans than Whites. In the multiethnic cohort, total nicotine equivalents (TNE) are higher in African Americans than Whites at similar reported cigarettes per day. Greater toxicant uptake per cigarette may contribute to the greater lung cancer risk of African Americans.

Methods: In a nested case–control lung cancer study within the Southern Community Cohort, smoking-related biomarkers were measured in 259 cases and 503 controls (40% White; 56% African American). TNE, the trans-3-hydroxycotinine/cotinine ratio, 4-(methylnitrosamino)-1–3-(pyridyl)-1-butanol (NNAL), mercapturic acid metabolites of volatile organic compounds, phenanthrene metabolites, cadmium (Cd), and (Z)-7-(1R,2R,3R,5S)-3,5-dihydroxy-2-[(E,3S)-3-hydroxyoct-1-enyl]cyclopenyl]hept-5-enoic acid were quantified in urine. Unconditional logistic regression was used to estimate the ORs and 95% confidence intervals (CI) for each biomarker and lung cancer risk.

Results: TNE, NNAL, and Cd were higher in cases than controls (adjusted for age, race, sex, body mass index, and cigarettes per day). Among cases, these levels were higher in African Americans compared with Whites. After accounting for age, sex, body mass index, and pack-years, a one-SD increase in log-TNE (OR = 1.30; 95% CI, 1.10–1.54) and log-NNAL (OR = 1.27; 95% CI, 1.03–1.58 with TNE adjustment) was associated with lung cancer risk. In this study, in which NNAL concentration is relatively high, the association for log-TNE was attenuated after adjustment for log-NNAL.

Conclusions: Smoking-related biomarkers provide additional information for lung cancer risk in smokers beyond smoking pack-years.

Murphy, Guillermo, Thomson et al. Association of urinary biomarkers of tobacco exposure with lung cancer risk in African American and White cigarette smokers in the Southern Community Cohort Study. Cancer Epidemiol Biomarkers Prev. (2024) https://doi.org/10.1158/1055-9965.EPI-23-1362

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In a recent study on fibrous dysplasia (FD), researchers employed the Free Soluble RANKL ELISA from Biomedica! Researchers developed a comprehensive genetic profile of FD bone marrow stromal cells and examined various cytokines connected to disease severity. Check out the abstract and full text below to learn more.

Abstract

Fibrous dysplasia (FD) is a mosaic skeletal disorder caused by somatic activating variants of GNAS encoding for Gαs and leading to excessive cyclic adenosine monophosphate signaling in bone-marrow stromal cells (BMSCs). The effect of Gαs activation in the BMSC transcriptome and how it influences FD lesion microenvironment are unclear. We analyzed changes induced by Gαs activation in the BMSC transcriptome and secretome. RNAseq analysis of differential gene expression of cultured BMSCs from patients with FD and healthy volunteers, and from an inducible mouse model of FD, was performed, and the transcriptomic profiles of both models were combined to build a robust FD BMSC genetic signature. Pathways related to Gαs activation, cytokine signaling, and extracellular matrix deposition were identified. To assess the modulation of several key secreted factors in FD pathogenesis, cytokines and other factors were measured in culture media. Cytokines were also screened in a collection of plasma samples from patients with FD, and positive correlations of several cytokines to their disease burden score, as well as to one another and bone turnover markers, were found. These data support the pro-inflammatory, pro-osteoclastic behavior of FD BMSCs and point to several cytokines and other secreted factors as possible therapeutic targets and/or circulating biomarkers for FD.

Michel, Z et al. Transcriptomic Signature and Pro-Osteoclastic Secreted Factors of Abnormal Bone-Marrow Stromal Cells in Fibrous Dysplasia. Cells 2024, 13, 774. https://doi.org/10.3390/cells13090774

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Take a look at this new study that employed our Noradrenaline (Norepinephrine) Sensitive ELISA! The research focused on exploring the impact of sympathetic regulation on aging-related osteoarthritis. Check out the abstract and full text below.

Abstract

Introduction: Osteoarthritis (OA) is a progressive disease that poses a significant threat to human health, particularly in aging individuals: Although sympathetic activation has been implicated in bone metabolism, its role in the development of OA related to aging remains poorly understood. Therefore, this study aimed to investigate how sympathetic regulation impacts aging-related OA through experiments conducted both in vivo and in vitro.

Methods: To analyze the effect of sympathetic regulation on aging-related OA, we conducted experiments using various mouse models. These models included a natural aging model, a medial meniscus instability model, and a load-induced model, which were used to examine the involvement of sympathetic nerves. In order to evaluate the expression levels of β1-adrenergic receptor (Adrβ1) and sirtuin-6 (Sirt6) in chondrocytes of naturally aging OA mouse models, we performed assessments. Additionally, we investigated the influence of β1-adrenergic receptor knockout or treatment with a β1-adrenergic receptor blocker on the progression of OA in aging mice and detected exosome release and detected downstream signaling expression by inhibiting exosome release. Furthermore, we explored the impact of sympathetic depletion through tyrosine hydroxylase (TH) on OA progression in aging mice. Moreover, we studied the effects of norepinephrine(NE)-induced activation of the β1-adrenergic receptor signaling pathway on the release of exosomes and miR-125 from chondrocytes, subsequently affecting osteoblast differentiation in subchondral bone.

Results: Our findings demonstrated a significant increase in sympathetic activity, such as NE levels, in various mouse models of OA including natural aging, medial meniscus instability, and load-induced models. Notably, we observed alterations in the expression levels of β1-adrenergic receptor and Sirt6 in chondrocytes in OA mouse models associated with natural aging, leading to an improvement in the progression of OA. Critically, we found that the knockout of β1-adrenergic receptor or treatment with a β1-adrenergic receptor blocker attenuated OA progression in aging mice and the degraded cartilage explants produced more exosome than the nondegraded ones, Moreover, sympathetic depletion through TH was shown to ameliorate OA progression in aging mice. Additionally, we discovered that NE-induced activation of the β1-adrenergic receptor signaling pathway facilitated the release of exosomes and miR-125 from chondrocytes, promoting osteoblast differentiation in subchondral bone.

Conclusion: In conclusion, our study highlights the role of sympathetic innervation in facilitating the transfer of exosomal miR-125 from osteoarthritic chondrocytes, ultimately disrupting subchondral bone homeostasis and exacerbating cartilage damage in aging mice. These findings provide valuable insights into the potential contribution of sympathetic regulation to the pathogenesis of aging-related OA.

Zhiyuan Guan, et al. Sympathetic innervation induces exosomal miR-125 transfer from osteoarthritic chondrocytes, disrupting subchondral bone homeostasis and aggravating cartilage damage in aging mice. Journal of Advanced Research. 2024. https://doi.org/10.1016/j.jare.2024.03.022.

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Two Creatinine Detection Kits, the Urine Creatinine Detection Kit and Creatinine Serum Detection Kit, were utilized in a recent study! This study explored whether adherence to the National Institute for Occupational Safety and Health (NIOSH) heat stress guidelines could prevent reductions in glomerular filtration rate (GFR) under varying heat conditions. Check out the abstract and full text below.

Abstract

We tested the hypothesis that compliance with the National Institute for Occupational Safety and Health (NIOSH) heat stress recommendations will prevent reductions in glomerular filtration rate (GFR) across a range of wet-bulb globe temperatures (WBGTs) and work-rest ratios at a fixed work intensity. We also tested the hypothesis that noncompliance would result in a reduction in GFR compared with a work-rest matched compliant trial. Twelve healthy adults completed five trials (four NIOSH compliant and one noncompliant) that consisted of 4 h of exposure to a range of WBGTs. Subjects walked on a treadmill (heat production: approximately 430 W) and work-rest ratios (work/h: 60, 45, 30, and 15 min) were prescribed as a function of WBGT (24°C, 26.5°C, 28.5°C, 30°C, and 36°C), and subjects drank a sport drink ad libitum. Peak core temperature (TC) and percentage change in body weight (%ΔBW) were measured. Creatinine clearance measured pre- and postexposure provided a primary marker of GFR. Peak TC did not differ among NIOSH-compliant trials (P = 0.065) but differed between compliant versus noncompliant trials (P < 0.001). %ΔBW did not differ among NIOSH-compliant trials (P = 0.131) or between compliant versus noncompliant trials (P = 0.185). Creatinine clearance did not change or differ among compliant trials (P ≥ 0.079). Creatinine clearance did not change or differ between compliant versus noncompliant trials (P ≥ 0.661). Compliance with the NIOSH recommendations maintained GFR. Surprisingly, despite a greater heat strain in a noncompliant trial, GFR was maintained highlighting the potential relative importance of hydration.

Hess, Baker, Tarr et al. Creatinine clearance is maintained in a range of wet-bulb globe temperatures an work-rest ratios during simulated occupational heat stress. Am J Physiol Renal Physiol. 2024. https://doi.org/10.1152/ajprenal.00089.2024

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The Human Recombinant Superoxide dismutase PPFs from StressMarq Biosciences Inc. were used in a recent study! Scientists demonstrated that nanoassemblies may potentially modulate the activity and structure of SOD1. Check out the abstract and full text below.

Abstract

The misfolding and aggregation of superoxide dismutase 1 (SOD1) and its mutants has been implicated in amyotrophic lateral sclerosis (ALS). In this study, we have created three peptide conjugates with the antioxidant pentacyclic terpene celastrol and examined their interactions with SOD1 and its mutants A4V and G93A. The peptides YYIVS, MPDAHL, and GSGGL are derived from natural sources and are known for their inherent antioxidant properties. Docking studies revealed that most conjugates showed strong binding with the metal binding and electrostatic loops as well as the β1, β5, and β6 hydrophobic core of SOD1. The conjugates were synthesized and self-assembled into nanoassemblies. Surface plasmon resonance studies further confirmed the binding interactions of the nanoassemblies with the SOD1 proteins. The nanoassemblies were found to internalize into HEK293T cells. The HEK 293T cells were then transfected with GFP fused WT (Wild Type), A4V and G93A SOD1 mutants. Flow cytometry revealed that treatment with celastrol-peptide nanoassemblies, affected the fluorescence of the SOD1 protein, implying their role in modulating SOD1, particularly for the mutants. N–Acetyl–Leu–Leu–Norleucinal (ALLN) induced SOD1 aggregation was also affected upon treatment with the nanoassemblies. These results suggest that the nanoassemblies may potentially modulate the activity and structure of SOD1.

Goncalves BG, et al. Design and investigation of celastrol-peptide nanoassemblies and their binding interactions with superoxide dismutase 1 and its mutants. Nano Select. 2024. https://doi.org/10.1002/nano.202400042

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Check out this recent study that utilized our Dopamine Sensitive ELISA! This study aimed to evaluate whether Cyperus esculentus extract (CEE) could mitigate the adverse effects of sertraline (SRT) on neuronal health and cognitive function in adult male albino rats. Check out the abstract and full text below.

Abstract

Chronic use of sertraline (SRT) for depression treatment can elevate oxidative stress, potentially leading to neuropathy. Cyperus esculentus extract (CEE) has demonstrated neuroprotective properties against oxidative imbalance, memory impairment, and neural degeneration. Adult male albino rats (40 rats) were placed into four groups: control (GI), CEE (200 mg/kg/day, orally) (GII), SRT (20 mg/kg/day, intraperitoneal) (GIII), and SRT+CEE (GIV). The rats’ spatial learning was assessed using a multiple T-maze after four weeks. Subsequently, rats were euthanized, and brain tissue samples were collected to assess oxidative stress indicators, monoamine oxidase, and dopamine. Brain tissue samples were also examined histologically and immunohistochemically for synaptophysin. SRT significantly increased monoamine oxidase activity, leading to oxidative stress, reduced dopamine levels, and neuronal degeneration in the brain. Treatment with SRT resulted in a decrease in the expression of synaptophysin in the cerebral cortex, dentate gyrus of the hippocampus, and cornu ammonis. These changes, in turn, led to impaired spatial learning. Co-treatment with CEE ameliorated changes in the levels of monoamine oxidase, dopamine, and synaptophysin, restored the redox balance, and improved spatial learning. CEE demonstrated a protective effect against sertraline-induced oxidative damage, preserving neurons, synaptogenesis, and spatial learning. These findings suggest CEE’s potential positive impact on sertraline-related neurodegeneration.

Badr, N. S., Samak, N. M., & Barakat, A. I. (2024). Cyperus esculentus extract mitigates sertraline-induced behavioral and histopathological changes in the brain of rats. Egyptian Journal of Basic and Applied Sciences, 11(1), 162–182. https://doi.org/10.1080/2314808X.2024.2327816

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