Eagle Biosciences Histamine ELISA Assay Kit used in a recent study. This kit is part of our Immunology Assay Kit line which is a line of highly sensitive and specific kits used for the detection of a variety of samples in serum, plasma, tissue, urine, and saliva.

Histamine deficiency aggravates cardiac injury through miR-206/216b-Atg13 axis-mediated autophagic-dependant apoptosis


Histamine is a widely distributed biogenic amine involved in the regulation of an array of biological processes. Serum histamine level is markedly elevated in the early stages of acute myocardial infarction, whereas the role it plays remains unclear. Histidine decarboxylase (HDC) is the unique enzyme responsible for histamine production, and cardiac injury is significantly aggravated in HDC knockout mice (HDC−/−), in which histamine is deficient. We also observed that autophagy was highly activated in cardiomyocytes of HDC−/− mice post acute myocardial infarction (AMI), which was abolished by compensation of exogenous histamine. The in vivo and in vitro results showed that acting through histamine 1 receptor, histamine increased miR-206 and miR-216b, which worked in concert to target to Atg13, resulting in the reduction of autophagy activation under hypoxia and AMI condition. Further study revealed that Atg13 interacted with FADD to promote the activation of caspase-8 and cell apoptosis. Taken together, these data unveil a novel intracellular signaling pathway involved in histamine regulating myocardial autophagy and apoptosis under hypoxia and AMI condition, which might help to more comprehensively evaluate the usage of histamine receptor antagonists and to develop new therapeutic targets for myocardial infarction.

Ding, Suling, et al. “Histamine Deficiency Aggravates Cardiac Injury through MiR-206/216b-Atg13 Axis-Mediated Autophagic-Dependant Apoptosis.” Cell Death & Disease, vol. 9, no. 6, 7 June 2018, p. 694., doi:10.1038/s41419-018-0723-6.

Eagle Biosciences announces the expansion of our line of Gastrointestinal Assays to include a Lactoferrin ELISA Assay Kit as well as a TNF-Alpha Stool ELISA Assay Kit. These kits add to our world class line of stool assays that include Zonulin, Pancreatic Elatase, Blastocystis, and NGAL

Lactoferrin ELISA Assay TNF-Alpha ELISA Assay
Size: 1×96 wells Size: 1×96 wells
Sensitivity: 0.369 ng/mL Sensitivity: 10 pg/mL
Incubation: 1.5 hours Dynamic Range: 10-500 pg/mL
Sample: Stool Incubation: 4.5 hours
Size: 15 mg Sample: Plasma, Serum, Stool

What is Lactoferrin and TNF-Alpha?

Lactoferrin is a protein found in a monomer or tetramer, that is involved in iron homeostasis, innate defense against microbial infections, anti-inflammatory activity, regulation of cellular growth and differentiation and protection against cancer. Elevated levels of lactoferrin are associated with Inflammatory Bowel Disease (IBD) such as Ulcerative Colitis (UC) or Crohn’s Disease (CD).

TNF-Alpha’s primary role is the regulation of immune cels. It stimulates apoptotic cell death, cell proliferation, and differentiation, inhibits tumor genesis and viral replication. Elevated levels of TNF-Alpha are found in patients suffering from Crohn’s Disease (CD), Ulcerating Colitis (UC), or Rheumatoid Arthritis (RA).

Eagle Bioscience’s Total Testosterone ELISA Assay Kit was used in a recent study. This kit is part of our line of Steroid Assay Kits which is a line of highly sensitive and specific assays used to detect a variety of samples in serum, plasma, tissue, urine, and saliva.

Impact of resistance training on body composition and metabolic syndrome variables during androgen deprivation therapy for prostate cancer: a pilot randomized controlled trial


Prostate cancer patients on androgen deprivation therapy (ADT) experience adverse effects such as lean mass loss, known as sarcopenia, fat gain, and changes in cardiometabolic factors that increase risk of metabolic syndrome (MetS). Resistance training can increase lean mass, reduce body fat, and improve physical function and quality of life, but no exercise interventions in prostate cancer patients on ADT have concomitantly improved body composition and MetS. This pilot trial investigated 12 weeks of resistance training on body composition and MetS changes in prostate cancer patients on ADT. An exploratory aim examined if a combined approach of training and protein supplementation would elicit greater changes in body composition.


A 12-week resistance training intervention effectively improved sarcopenia, body fat %, strength and quality of life in hypogonadal prostate cancer patients, but did not change MetS or physical function. PRO did not offer additional benefit in improving body composition.

Dawson, Jacqueline K., et al. “Impact of Resistance Training on Body Composition and Metabolic Syndrome Variables during Androgen Deprivation Therapy for Prostate Cancer: a Pilot Randomized Controlled Trial.” BMC Cancer, vol. 18, no. 1, 3 Apr. 2018, p. 368., doi:10.1186/s12885-018-4306-9.

Yale Researchers Identify Target for Novel Malaria Vaccine

Yale University

A team of researchers has developed a vaccine against malaria infection targeting a unique protein produced by malaria parasites. Plasmodium macrophage migration inhibitory factor (PMIF) suppresses the infection fighting cells that respond to threats and protect the body against reinfection. PMIF is critical for the completion of the parasite life cycle, specifically the transmission to new hosts. An RNA based vaccine developed by the researchers protects against reinfection in mice. The next step is to develop a vaccine that could be used for individuals who have never been infected with malaria. Researchers also have noted that the PMIF protein has been conserved over various strains of malaria, and therefore it should be nearly impossible for the virus to develop a resistance to the vaccine. 

Read More.

Why measure zonulin?

The zonulin biomarker is a pre-haptoglobin (pre-HP2) protein found in the gut. It is responsible for the permeability of the mucosal barrier of the intestines. When zonulin binds to the epithelial cells of the intestines a signal cascade is induced. This cascade disassembles the paracellular tight junctions of the intestinal wall. The tight junctions of the intestinal walls are one of two ways that allow molecules to transfer from the gut lumen to the bloodstream and vice versa. When zonulin levels in the gut increase and go out of balance, these junctions open wider and stay open longer. These widened entry points allow larger macromolecules into the bloodstream or into the gut lumen. The molecules that pass through these breaches can increase the body’s natural immune reaction, causing inflammation and a number of autoimmune diseases.

Diseases Associated with increased Zonulin levels:

  • Type-1 Diabetes
  • Rheumatoid Arthritis
  • Celiac Disease
  • Liver Disease 

The Eagle Biosciences 8-Isoprostane ELISA Assay Kit was utilized in a recent research project. This kit is part of our Oxidative Stress Assay Kit line which is a line of highly sensitive and specific assays used to detect a variety of samples in serum, plasma, tissue, urine, and saliva.

Effect of flavoring chemicals on free radical formation in electronic cigarette aerosols


Flavoring chemicals, or flavorants, have been used in electronic cigarettes (e-cigarettes) since their inception; however, little is known about their toxicological effects. Free radicals present in e-cigarette aerosols have been shown to induce oxidative stress resulting in damage to proliferation, survival, and inflammation pathways in the cell. Aerosols generated from e-liquid solvents alone contain high levels of free radicals but few studies have looked at how these toxins are modulated by flavorants.


Our results suggest that flavoring agents play an important role in either enhancing or inhibiting the production of free radicals in flavored e-cigarette aerosols. This information is important for developing regulatory strategies aimed at reducing potential harm from e-cigarettes.

Bitzer, Zachary T, et al. “Effect of Flavoring Chemicals on Free Radical Formation in Electronic Cigarette Aerosols.” Free Radical Biology and Medicine, vol. 112, 20 May 2017, p. 200., doi:10.1016/j.freeradbiomed.2017.10.315.

A next generation cancer therapy helps immune cells detect, and destroy cancer cells. This therapy works by evading two mechanisms that cancer cells use to evade macrophages, cells whose job it is to eat and destroy cancerous cells.

“The researchers [at Brigham and Women’s Hospital] tested the supramolecular therapeutic in animal models of aggressive forms of breast cancer and skin cancer, comparing their drug directly with a drug currently available in the clinic. Mice that were untreated formed large tumors by Day 10. Mice treated with currently available therapies showed decreased tumor growth. But mice treated with the new supramolecular therapy had complete inhibition of tumor growth. The team also reported an increase in survival and a significant reduction in metastatic nodes.”

This treatment is skill in the testing phases but it hold potential for future applications.

Read More.

The Eagle Biosciences Humanized Anti HER-2 ELISA Assay Kit detect levels of Trastuzumab (Herceptin) in human serum and plasma.

What is HER-2?

The Human Epidermal Growth Factor Receptor 2 gene (HER-2) can play a role in the development of breast cancer. This gene codes for a protein that are receptors on breast cells and helps the cell grow and divide normally. When regulation of the HER-2 gene gets disrupted or too many copies of the HER-2 gene are present in the cell, this can lead to an increased amount of the HER-2 protein on the cell surface. This causes the cell to start growing out of control and can develop into a tumor. Trastuzumab (Herceptin) is a drug that blocks the ability of the HER-2 protein on the surface of cells to receive chemical signals telling the cell to grow. This can slow or stop the growth of these breast cells and can also signal the immune system that these cells need to be destroyed. Measuring the levels of this drug in serum or plasma are important for evaluating the effectiveness of drug therapy.

Key Advantages of EagleBio’s Anti HER-2 ELISA

  • Excellent Specificity
  • High Sensitivity
  • Precise results under 2 hours

Eagle Bioscience’s Calprotectin ELISA Assay Kit was recently used in a study dealing with bone loss in relation to arthritis and other inflammatory diseases. The Calprotectin ELISA Assay is part of our line of Gastrointestinal Assays which is a line of highly sensitive and specific kits used to detect the concentration of a variety of samples in serum, plasma, tissue, urine, and saliva.

Blood-induced bone loss in murine hemophilic arthropathy is prevented by blocking the iRhom2/ADAM17/TNFα pathway


Hemophilic arthropathy (HA) is a debilitating degenerative joint disease that is a major manifestation of the bleeding disorder Hemophilia A. HA typically begins with hemophilic synovitis (HS) that resembles inflammatory arthritides such as rheumatoid arthritis (RA) and frequently results in bone loss in patients. A major cause of RA is inappropriate release of the pro-inflammatory cytokine tumor necrosis factor α (TNFα) by the TNFα convertase (TACE, also referred to as ADAM17) and its regulator, iRhom2. Therefore, we hypothesized that iRhom2/ADAM17-dependent shedding of TNFα also has a pivotal role in mediating HA. Here, we show that addition of blood or its components to macrophages activates iRhom2/ADAM17-dependent TNFα shedding, providing the premise to study the activation of this pathway by blood in the joint in vivo. For this, we turned to hemophilic FVIII-deficient mice (F8-/- mice), which develop a hemarthrosis following needle puncture injury with synovial inflammation and significant osteopenia adjacent to the affected joint. We found that needle puncture-induced bleeding leads to increased TNFα levels in the affected joint of F8-/- mice. Moreover, inactivation of TNFα or iRhom2 in F8-/- mice reduced the osteopenia and synovial inflammation that develops in this mouse model for HA. Taken together, our results suggest that blood entering the joint activates the iRhom2/ADAM17/TNFα pathway, thereby contributing to osteopenia and synovitis in mice. Therefore, this pro-inflammatory signaling pathway could emerge as an attractive new target to prevent osteoporosis and joint damage in HA patients.

Haxaire, Coline, et al. “Blood-Induced Bone Loss in Murine Hemophilic Arthropathy Is Prevented by Blocking the iRhom2/ADAM17/TNFα Pathway.” Blood, 18 May 2018, 

Multiple genes have been found to be linked to the cause Alzheimer’s disease and result in the disease in different ways. This connection can help better identify targets for prevention therapy by recognizing the different ways the genes lead to neuronal death.

Neurons, astrocytes, oligodendrocytes, and microglial cells are all different cell types found in the brain, specific gene variants had different proportions of these cells in the brain. Scientists at the Washington School of Medicine in St. Louis are working on figuring out how each gene is different and what it does in the brain can help the understanding of how it leads to disease and the best ways to treat it.


Dryden J. Genes linked to Alzheimer’s contribute to damage in different ways. The Source. June 8, 2018.