Category: Publication Spotlight

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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Take a look at this recent study that utilized our Mouse/Rat 25-OH Vitamin D ELISA Assay Kit! Researchers set out to examine the effects of the loss of Galnt11 on vitamin D homeostasis and bone composition in mice. Check out the abstract and the full text below.

Abstract

O-glycosylation is a conserved posttranslational modification that impacts many aspects of organismal viability and function. Recent studies examining the glycosyltransferase Galnt11 demonstrated that it glycosylates the endocytic receptor megalin in the kidneys, enabling proper binding and reabsorption of ligands, including vitamin D–binding protein (DBP). Galnt11-deficient mice were unable to properly reabsorb DBP from the urine. Vitamin D plays an essential role in mineral homeostasis and its deficiency is associated with bone diseases such as rickets, osteomalacia, and osteoporosis. We therefore set out to examine the effects of the loss of Galnt11 on vitamin D homeostasis and bone composition. We found significantly decreased levels of serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, consistent with decreased reabsorption of DBP. This was accompanied by a significant reduction in blood calcium levels and a physiologic increase in parathyroid hormone (PTH) in Galnt11-deficient mice. Bones in Galnt11-deficient mice were smaller and displayed a decrease in cortical bone accompanied by an increase in trabecular bone and an increase in a marker of bone formation, consistent with PTH-mediated effects on bone. These results support a unified model for the role of Galnt11 in bone and mineral homeostasis, wherein loss of Galnt11 leads to decreased reabsorption of DBP by megalin, resulting in a cascade of disrupted mineral and bone homeostasis including decreased circulating vitamin D and calcium levels, a physiological increase in PTH, an overall loss of cortical bone, and an increase in trabecular bone. Our study elucidates how defects in O-glycosylation can influence vitamin D and mineral homeostasis and the integrity of the skeletal system.

E. Tian et al. Loss of the glycosyltransferase Galnt11 affects vitamin D homeostasis and bone composition. Journal of Biological Chemistry. Volume 300. Issue 4. 2024. https://doi.org/10.1016/j.jbc.2024.107164

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A recent study utilized two ELISAs from Eagle Biosciences, our Estradiol ELISA and Progesterone ELISA! The research aimed to find out if low oxygen levels during sleep affect blood fat levels differently in men and women. Check out the abstract and full text below.

Abstract

Obstructive sleep apnoea is characterized by chronic intermittent hypoxaemia and is independently associated with an increased risk of metabolic comorbidities (e.g. type II diabetes and ischaemic heart disease). These comorbidities could be attributable to hypoxaemia-induced alterations in blood lipid profiles. However, it remains unclear whether intermittent hypoxaemia alters triglyceridaemia differently between biological sexes. Therefore, we used a randomized crossover design to examine whether 6 h of moderate intermittent hypoxaemia (15 hypoxaemic cycles/h, 85% oxyhaemoglobin saturation) alters plasma triglyceride levels differently between men and women after a high-fat meal. Relative to men, women displayed lower levels of total triglycerides, in addition to denser triglyceride-rich lipoprotein triglycerides (TRL-TG; mainly very low-density lipoprotein triglycerides and chylomicron remnant triglycerides) and buoyant TRL-TG (mainly chylomicron triglycerides) during normoxia (ambient air) and intermittent hypoxaemia (sex × time: all P ≤ 0.008). Intermittent hypoxaemia led to higher triglyceride levels (condition: all P ≤ 0.016); however, this effect was observed only in men (sex × condition: all P ≤ 0.002). Compared with normoxia, glucose levels were higher in men and lower in women during intermittent hypoxaemia (sex × condition: P < 0.001). The different postprandial responses between biological sexes occurred despite similar reductions in mean oxyhaemoglobin saturation and similar elevations in insulin levels, non-esterified fatty acid levels and mean heart rate (sex × condition: all P ≥ 0.185). These results support growing evidence showing that intermittent hypoxaemia impacts men and women differently, and they might help to explain biological sex-related discrepancies in the rate of certain comorbidities associated with intermittent hypoxaemia

Goulet N. et al. Biological sex-related differences in the postprandial triglyceride response to intermittent hypoxaemia in young adults: a randomized crossover trial. Journal of Physiology. Jan 2024. doi:10.1113/JP285430

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Eagle Bioscience’s is excited to report that our Human Albumin ELISA Assay Kit utilized in a recent study. In this study, researchers identify a beneficial role for the heme-binding protein hemophilin (Hpl) produced by the non-pathogenic bacterium Haemophilus haemolyticus against its close relative, the opportunistic respiratory tract pathogen non-typeable Haemophilus influenzae (NTHi). Check out the abstract and full text below.

Abstract

Iron acquisition is a key feature dictating the success of pathogen colonization and infection. Pathogens scavenging iron from the host must contend with other members of the microbiome similarly competing for the limited pool of bioavailable iron, often in the form of heme. In this study, we identify a beneficial role for the heme-binding protein hemophilin (Hpl) produced by the non-pathogenic bacterium Haemophilus haemolyticus against its close relative, the opportunistic respiratory tract pathogen non-typeable Haemophilus influenzae (NTHi). Using a mouse model, we found that pre-exposure to H. haemolyticus significantly reduced NTHi colonization of the upper airway and impaired NTHi infection of the lungs in an Hpl-dependent manner. Further, treatment with recombinant Hpl was sufficient to decrease airway burdens of NTHi without exacerbating lung immunopathology or systemic inflammation. Instead, mucosal production of the neutrophil chemokine CXCL2, lung myeloperoxidase, and serum pro-inflammatory cytokines IL-6 and TNFα were lower in Hpl-treated mice. Mechanistically, H. haemolyticus suppressed NTHi growth and adherence to human respiratory tract epithelial cells through the expression of Hpl, and recombinant Hpl could recapitulate these effects. Together, these findings indicate that heme sequestration by non-pathogenic, Hpl-producing H. haemolyticus is protective against NTHi colonization and infection.

Fulte S, Atto B, McCarty A, Horn KJ, Redzic JS, Eisenmesser E, Yang M, Marsh RL, Tristram S, Clark SE. 2024. Heme sequestration by hemophilin from Haemophilus haemolyticus reduces respiratory tract colonization and infection with non-typeable Haemophilus influenzae. mSphere 9:e00006-24. https://doi.org/10.1128/msphere.00006-24

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Clostridium Difficile Toxin AB Qualitative ELISA Assay Kit was utilized in a recent study! Researchers demonstrated that treatment with the microbial metabolite urolithin A (UroA) attenuates Clostridioides difficile infection (CDI) induced adverse effects on the colon epithelium in a preclinical model of CDI-induced colitis. Check out the abstract and full text below.

Abstract

Clostridioides difficile is a Gram-positive, anaerobic, spore-forming bacterium responsible for antibiotic-associated pseudomembranous colitis. Clostridioides difficile infection (CDI) symptoms can range from diarrhea to life-threatening colon damage. Toxins produced by C. difficile (TcdA and TcdB) cause intestinal epithelial injury and lead to severe gut barrier dysfunction, stem cell damage, and impaired regeneration of the gut epithelium. Current treatment options for intestinal repair are limited. In this study, we demonstrate that treatment with the microbial metabolite urolithin A (UroA) attenuates CDI-induced adverse effects on the colon epithelium in a preclinical model of CDI-induced colitis. Moreover, our analysis suggests that UroA treatment protects against C. difficile-induced inflammation, disruption of gut barrier integrity, and intestinal tight junction proteins in the colon of CDI mice. Importantly, UroA treatment significantly reduced the expression and release of toxins from C. difficile without inducing bacterial cell death. These results indicate the direct regulatory effects of UroA on bacterial gene regulation. Overall, our findings reveal a novel aspect of UroA activity, as it appears to act at both the bacterial and host levels to protect against CDI-induced colitis pathogenesis. This research sheds light on a promising avenue for the development of novel treatments for C. difficile infection.

Ghosh S, Erickson D, Chua MJ, Collins J, Jala VR. 2024. The microbial metabolite urolithin A reduces Clostridioides difficile toxin expression and toxin-induced epithelial damage. mSystems 9:e01255-23. https://doi.org/10.1128/msystems.01255-23

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Check out this recent publication that utilized our Calprotectin ELISA Assay Kit! This study examined whether patient-derived materials could predict individual clinical responsiveness to the Janus kinase (JAK) inhibitory, tofacitinib, prior to treatment initiation. Find the abstract and full text below.

Abstract

Background & Aims: Despite increasing therapeutic options in the treatment of ulcerative colitis (UC), achieving disease remission remains a major clinical challenge. Nonresponse to therapy is common and clinicians have little guidance in selecting the optimal therapy for an individual patient. This study examined whether patient-derived materials could predict individual clinical responsiveness to the Janus kinase (JAK) inhibitor, tofacitinib, prior to treatment initiation.

Method: In 48 patients with UC initiating tofacitinib, we longitudinally collected clinical covariates, stool, and colonic biopsies to analyze the microbiota, transcriptome, and exome variations associated with clinical responsiveness at week 24. We established patient-derived organoids (n = 23) to determine how their viability upon stimulation with proinflammatory cytokines in the presence of tofacitinib related to drug responsiveness in patients. We performed additional biochemical analyses of organoids and primary tissues to identify the mechanism underlying differential tofacitinib sensitivity.

Results: The composition of the gut microbiota, rectal transcriptome, inflammatory biomarkers, and exome variations were indistinguishable among UC patients prior to tofacitinib treatment. However, a subset of patient-derived organoids displayed reduced sensitivity to tofacitinib as determined by the ability of the drug to inhibit STAT1 phosphorylation and loss of viability upon cytokine stimulation. Remarkably, sensitivity of organoids to tofacitinib predicted individual clinical patient responsiveness. Reduced responsiveness to tofacitinib was associated with decreased levels of the cationic transporter MATE1, which mediates tofacitinib uptake.

Conclusions: Patient-derived intestinal organoids predict and identify mechanisms of individual tofacitinib responsiveness in UC. Specifically, MATE1 expression predicted clinical response to tofacitinib.

Jang KK, Ercelen D, Cen Feng JYC, et al. Tofacitinib uptake by patient-derived intestinal organoids predicts individual clinical responsiveness. bioRxiv [Preprint]. 2024 Mar 6:2024. doi: 10.1101/2024.03.02.583137

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Check out this recent article that utilized our H. pylori Qualitative ELISA! This study aimed to determine the association of H. Pylori infection among acne vulgaris (AV) patients and correlate it with disease activity. Find the abstract and full text below.

Abstract

Background: Helicobacter pylori (H. pylori) is a gastric Gram-negative, spiral-shaped microaerophilic pathogen. H. pylori may play a potential pathogenic role in extra-intestinal diseases such as hepatobiliary, respiratory, and dermatological disorders. The latter included chronic urticaria, psoriasis and rosacea. The first report in literature on the relationship between H. pylori and acne vulgaris (AV), found association between severe AV and H. pylori infection. There are very limited data in AV patients addressing the impact of H. pylori infection on various severities. In this context, the aim of the present work was to determine the association of H. Pylori infection among AV patients and correlate it with the disease severity.

Methods: This case-control study included 45 Patients with AV and 45 age and sex matched healthy volunteers as a control group. H. pylori antigen in stool and serum H. pylori antibody IgG using commercially available ELISA kits was tested in all included subjects.

Results: The percentage of participants with a positive H. pylori antigen in stool and positive H. pylori antibody in serum in the whole study population was 35/90 (38. 9%) and 41/90 (45. 6%). On comparing between the percentagesof positive H. pylori antigen in stool and positive H. pylori antibody in serum between the patients with AV and healthy controls, a highly statistically significant difference was found between the two groups (P<0.001, P=0.006). On comparing between the percentages of positive H. pylori antigen in stool and positive H. pylori antibody in serum in the patients with different grades of acne severity and healthy controls, the rate of positive H. pylori antigen in stool and positive H. pylori Ab in serum was significantly associated with severity of acne comparing with healthy controls (p<0. 001).

Conclusion: The rate of H. pylori infection in patients with AV is high so it may influence the pathogenesis of this skin disease. Patients with severe AV had higher rates of H. pylori antigen in stool and H. pylori antibody in serum as compared to the patients with mild AV and healthy controls.

ahmed afify, Hanan Mohamed Ahmed Saleh, Abeer Farrag et al. Helicobacter pylori and acne vulgaris: is there a relationship?, 08 January 2024, PREPRINT (Version 1) available at Research Square https://doi.org/10.21203/rs.3.rs-3835029/v1

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Check out this recent study that utilized our Noradrenaline (Norepinephrine) Sensitive ELISA! The researchers aimed to develop a method to innervate human pluripotent stem cell (hPSC)-based 3D organoids, particularly focusing on the autonomic sympathetic nervous system’s regulation of the heart. Check out the abstract and full text below.

Abstract

The technology of human pluripotent stem cell (hPSC)-based 3D organoid/assembloid cultures has become a powerful tool for the study of human embryonic development, disease modeling and drug discovery in recent years. The autonomic sympathetic nervous system innervates and regulates almost all organs in the body, including the heart. Yet, most reported organoids to date are not innervated, thus lacking proper neural regulation, and hindering reciprocal tissue maturation. Here, we developed a simple and versatile sympathetic neuron (symN)-innervated cardiac assembloid without the need for bioengineering. Our human sympathetic cardiac assembloids (hSCAs) showed mature muscle structures, atrial to ventricular patterning, and spontaneous beating. hSCA-innervating symNs displayed neurotransmitter synthesis and functional regulation of the cardiac beating rate, which could be manipulated pharmacologically or optogenetically. We modeled symN-mediated cardiac development and myocardial infarction. This hSCAs provides a tool for future neurocardiotoxicity screening approaches and is highly versatile and modular, where the types of neuron (symN or parasympathetic or sensory neuron) and organoid (heart, lung, kidney) to be innervated may be interchanged.

Nadja Zeltner, Hsueh-Fu Wu, Kenyi Saito-Diaz et al. A modular platform to generate functional sympathetic neuron-innervated heart assembloids, 21 March 2024, PREPRINT (Version 1) available at Research Square https://doi.org/10.21203/rs.3.rs-3894397/v1

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The StressMarq Biosciences, Inc. Alpha B Crystallin ELISA was utilized in a recent publication! The study aimed to investigate the potential peripheral myelin protein 2 (P2) and Alpha B-crystallin (aBC) as predictive biomarkers in Guillain-Barré syndrome (GBS). Check out the abstract and full text below!

Abstract

Objectives: The study aimed to investigate the potential of peripheral myelin protein 2 (P2) and Alpha B-crystallin (αBC) as predictive biomarkers in Guillain-Barré syndrome (GBS). Given the unpredictability of GBS prognosis, the need for specific and reliable biomarkers for disease development and intensity assessment is crucial.

Material and Methods: A prospective observational study was conducted on a cohort of 220 individuals diagnosed with GBS at a tertiary general hospital in South India. P2 and αBC levels in cerebrospinal fluid (CSF) were quantified using ELISA assay kits. The study spanned from March 2021 to April 2023, with participants aged 18–60 years. The study protocol adhered to ethical standards, and the Brighton criteria were employed for GBS diagnosis. CSF samples were collected at admission and two weeks post-onset. Data analysis utilised SPSS, and statistical significance was set at p < 0.05.

Results: Upon admission, mean P2 levels were 2.2 ± 0.5 ng/mL, and αBC levels were 9.8 ± 2.3 ng/mL. After two weeks, P2 increased to 4.8 ± 0.8 ng/mL, and αBC increased to 15.1 ± 2.3 ng/mL. A positive correlation was observed between the rise in P2 and αBC levels and enhanced muscle strength at 4 weeks and 6 months.

Conclusion: The study suggests a significant increase in P2 and αBC levels in GBS patients, correlating with improved muscle strength. P2 and αBC ratios in CSF between the second and first weeks may serve as prognostic markers for GBS. Limitations include a small sample size and the absence of a control group, necessitating caution in generalizability.

Amalakanti S, Arepalli KVR, Jillella JP. Utility of cerebrospinal fluid protein biomarkers in predicting the outcome of Guillain-Barre syndrome. South Asian J Health Sci. 2024;1:27–30. doi: 10.25259/SAJHS_18_2023

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The Biomedica Sclerostin ELISA Assay Kit was utilized in a recent publication! This study assessed the associations between serum and bone sclerostin levels and biomarkers of bone turnover and bone histomorphometry. Check out the abstract and full text below.

Abstract

The pathophysiology of chronic kidney disease-mineral and bone disorder (CKD-MBD) is not well understood. Specific factors secreted by osteocytes are elevated in the serum of adults and pediatric patients with CKD-MBD, including FGF-23 and sclerostin, a known inhibitor of the Wnt signaling pathway. The molecular mechanisms that promote bone disease during the progression of CKD are incompletely understood. In this study, we performed a cross-sectional analysis of 87 pediatric patients with pre-dialysis CKD and post-dialysis (CKD 5D). We assessed the associations between serum and bone sclerostin levels and biomarkers of bone turnover and bone histomorphometry. We report that serum sclerostin levels were elevated in both early and late CKD. Higher circulating and bone sclerostin levels were associated with histomorphometric parameters of bone turnover and mineralization. Immunofluorescence analyses of bone biopsies evaluated osteocyte staining of antibodies towards the canonical Wnt target, β-catenin, in the phosphorylated (inhibited) or unphosphorylated (active) forms. Bone sclerostin was found to be colocalized with phosphorylated β-catenin, which suggests that Wnt signaling was inhibited. In patients with low serum sclerostin levels, increased unphosphorylated “active” β-catenin staining was observed in osteocytes. These data provide new mechanistic insight into the pathogenesis of CKD-MBD and suggest that sclerostin may offer a potential biomarker or therapeutic target in pediatric renal osteodystrophy.

Laster M. et al. Sclerostin, Osteocytes, and Wnt Signaling in Pediatric Renal Osteodystrophy. Nutrients. 2023 Sep 25;15(19):4127. doi: 10.3390/nu15194127

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