Sample
Serum, cerebrospinal fluid, plasma
Intended Use
The Human GFAP ELISA is a sandwich enzyme immunoassay for the quantitative measurement of human Glial Fibrillary Acidic Protein (GFAP).
Features
− It is intended for research use only
− The total assay time is about 5 hours
− The kit measures GFAP in serum, cerebrospinal fluid (CSF) and plasma
− Assay format is 96 wells
− Quality Controls are human serum based
− Standard is purified native protein based
− Components of the kit are provided ready to use, concentrated or lyophilized
Contents of Kit
1.Antibody Coated Microtiter Strips, ready to use, 96 wells
2.Biotin Labelled Antibody, ready to use, 13 ml
3.Streptavidin-HRP Conjugate, ready to use, 13 ml
4.Master Standard, lyophilized, 1 vial
5.Quality Control HIGH, lyophilized, 1 vial
6.Quality Control LOW, lyophilized, 1 vial
7.Standard Diluent, ready to use, 9 ml
8.Dilution Buffer, ready to use, 13 ml
9.Wash Solution Conc. (10x), concentrated, 100 ml
10.Substrate Solution, ready to use, 13 ml
11.Stop Solution, ready to use, 13 ml
Storage
Store the complete kit at 2-8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).
Precision
Intra-assay (Within-Run) (n=8)
Inter-assay (Run-to-Run) (n=7)
Detection Limit
Limit of Detection (LOD) (defined as concentration of analyte giving absorbance higher than mean absorbance of blank* plus three standard deviations of the absorbance of blank: Ablank + 3x SDblank) is calculated from the real GFAP values in wells and is 0.045 ng/ml.
*Dilution Buffer is pipetted into blank wells.
General Description
Glial Fibrillary Acidic Protein (GFAP), as a member of the cytoskeletal protein family, is the principal 8-9 nm intermediate filament in mature astrocytes of the central nervous system (CNS). GFAP is a monomeric molecule with a molecular mass between 40 and 53 kDa and an isoelectric point between 5.7 and 5.8. GFAP is highly brain specific protein that is not found outside the CNS. Some studies showed that GFAP is released into the blood very soon after traumatic brain injury (TBI), that GFAP is related to brain injury severity and outcome after TBI and that GFAP is not released after multiple trauma without brain injury.
In the CNS following injury, either as a result of trauma, disease, genetic disorders, or chemical insult, astrocytes become reactive and respond in a typical manner, termed astrogliosis. Astrogliosis is characterized by rapid synthesis of GFAP. GFAP normally increases with age and there is a wide variation in collection and processing of human brain tissue. Thanks to the high brain specificity and early releasing from CNS after TBI, GFAP might be suitable marker for early diagnostics.
Citations
Publication ()
Have you cited DEIA7378 in a publication?
Let us know and earn a reward for your research.
Experimental autoimmune encephalomyelitis causes skeletal muscle dysfunction in mice
Boesch, J., Ramseier, P., Tisserand, S., Pierrel, E., Locatelli, G., & Summermatter, S.
Applications: ELISA
Reactive species: Mouse
"Abstract: Multiple sclerosis (MS) is a neuroinflammatory disease affecting the brain and spinal cord and characterized by demyelination, neurodegeneration and chronic inflammation. More than 90% of people with MS present with peripheral muscle dysfunction and a progressive decline in mobility. Current treatments attenuate the inflammatory processes but do not prevent disease progression. Therefore, there remains an unmet medical need for new and/or additional therapeutic approaches that specifically improve muscle function in this patient population. The development of novel treatments targeting skeletal muscle dysfunction in MS will depend on suitable preclinical models that can mimic the human musculoskeletal manifestations of MS. Using a non-invasive approach to assess muscle function, we demonstrate in vivo that Experimental Autoimmune Encephalomyelitis (EAE) impairs skeletal muscle strength. Our data reveal a 28.3% (p < 0.0001) lower muscle force in animals with EAE compared to healthy control mice during electrically evoked tetanic muscle contractions that occur at intervals of 0.25 s and thus mimic fatiguing tasks. As we conduct force measurements by direct transcutaneous muscle stimulation in anesthetized animals, our setup allows for the repeated evaluation of muscle function, and in the absence of primary fatigue or reduced nerve input which constitute important confounding factors in MS. Taken together, our data highlight important similarities between MS in humans and EAE in mice with regards to skeletal muscle contractile impairments, and provide first evidence for a non-invasive in-vivo setup that will enable the preclinical profiling of novel drug candidates directed at specifically improving muscle function in MS."
Article snippet: GFAP (Creative Diagnostics—Ref#DEIA7378), NF-L (*) and IGF-1 (*) ELISA were performed in cerebrospinal fluid (CSF) diluted 1/50 and 1/125, and in plasma diluted 1/5 in the sample diluent provided in each kit, respectively. 
Figure 1. Biomarkers of axonal damage, neuroinflammation, and muscle growth.
COA
Loading ......
