The present invention relates to a method for predicting the prognosis of ischemic disease using an AGE-RAGE-based biomarker. The biomarker can be used as an indicator factor of the clinical severity of ischemic disease, can maximize the efficiency of stem-cell treatment by determination of the optimal timing of the stem-cell treatment on the basis of changes in the biomarker according to the severity of ischemic disease, and can also be used as a useful indicator factor for verifying efficacy after the stem-cell treatment.

Embodiments provide for devices and methods of use for detecting one or more biomarkers of rheumatic disease in a subject. In an example, a method includes detecting citrullinated human serum albumin (HSA) in a biological sample via obtaining the biological sample from a subject, applying the biological sample to a lateral flow device under conditions sufficient for formation of an immunocomplex comprising anti-HSA antibody coupled to citrullinated HSA that is in turn coupled to anti-citrullinated HSA autoantibody, determining a quantity of the immunocomplex, and managing rheumatic disease associated with the subject. In this way, rheumatic disease may be effectively managed based at least in part on amounts of citrullinated HSA detected via rapid point-of-care test methodology.

The present invention relates to a method for quantitative measurement of catechol estrogen bound protein in blood sample. By detecting adduction levels of binding sites of the catechol estrogen on the protein in blood sample, the catechol estrogen bound protein in the blood sample can be detected quantitatively and a limit of quantitation can be decreased.

A dry test piece for albumin measurement is based on the improved BCP method as a principle, and enables the measurement of albumin at a high sensitivity. The test piece includes a support; and a reagent holding layer provided on the support and on which a sample is spotted. The reagent holding layer contains a protein denaturation agent (component A), an SH reagent (component B), bromcresol purple (component C), and a nonionic surfactant (component D). In the reagent holding layer, a weight ratio (D/C) of the component D to the component C is 0.3 to 13, a content of the component C relative to an amount of the spotted sample is 0.4 μg/μL to 5.4 μg/μL, a content of the component D relative to the amount of the spotted sample is 25 μg/μL or less.

A method for determining an amount of functional albumin includes providing a test sample containing a defined amount of albumin of unknown binding capacity and a reference sample containing the same defined amount of albumin having a reference binding capacity, incubating the test and reference samples with a defined amount of at least one albumin-binding marker M under conditions that allow formation of complexes of the at least one albumin-binding marker M and albumin (M:A), removing the complexes, detecting a presence or an amount of unbound marker M in the samples after removal of the complex (M:A) through a first and a second test strips that allow for a determination of an amount of unbound marker M, and determining the amount of functional albumin based on the presence or the amount detected of marker M.

An assay method for detecting the presence or amount of human serum albumin vitamin D, C-reactive protein, or anti-transglutaminase autoantibody (ATA) immunoglobulin A (IgA) and/or ATA IgG in a sample using fluorescence resonance energy transfer (FRET).

A method for determining whether a subject has a disease or condition or is at risk of developing a disease or condition is disclosed. A method for determining whether a subject is at risk of developing an infectious disease or a complication thereof is also disclosed.

Method of determining therapeutic drug antibodies in a sample of bodily fluid of a subject receiving a medication containing a therapeutic drug antibodies against tumor necrosis factor alpha. The method is used in an lateral flow immunochromatographic test wherein the immunochromatographic bridging and binding in the test line comprises the use of an anti-idiotypic scFv fragment or Fab fragment fused to a carrier protein which is not involved in nor plays a role in the inherent or developed immune system. The fusion protein may contain human serum albumin, chicken ovalbumin, human haptoglobin or human alpha-1- antitrypsin. The immunological reaction is therefore not impaired, augmented or interfered by members of the complement system or by autoantibodies such as the rheumatoid factor. This is of particular importance and favorable when determining the concentration of tumor necrosis alpha blockers such as adalimumab or in-fliximab in serum or blood of patients.

Most chronic liver diseases are notoriously asymptomatic, until cirrhosis with clinical decompensation occurs. The use of early diagnosis strategies is vital to maintain patients in a symptom-free state and to delay decompensation, and thus improve the outcome. Albumin (HAS) undergoes several post-translational modifications in hepatocytes but clinical relevance of some of these modifications has been recently investigated in advanced liver diseases. Now, the inventors demonstrate that the binding capacities of some ligands, measured by inductively coupled plasma mass spectrometry (ICP-MS), are significantly different between cirrhotic patients and patients with no liver dysfunctions. The decreased binding capacities in cirrhotic patients were paralleled by the presence of significantly higher HSA isoforms Animal experimentations were also conducted to explore the precocity of HSA modifications in the course of chronic liver dysfunction. This allow the inventors to assume that the most important modifications of albumin structure due to liver dysfunction could be revealed by measuring the unbound fraction of specific ligands spiked in serum.

Embodiments of the instant disclosure relate to novel methods for treatment of a neurodegenerative disease or condition. In certain embodiments, methods of alleviating a neurodegenerative disease in a subject include administering an effective concentration of granulocyte macrophage colony stimulating factor (GM-CSF); monitoring an absolute number of at least one of leukocytes, concentration of at least one inflammatory cytokine, concentration of at least one neurodegenerative condition biomarker, or a combination thereof in the subject; and adjusting GM-CSF treatment regimens based the level of at least one of these parameters. In some embodiments, methods of alleviating a neurodegenerative condition in a subject can further include performing at least one cognition assessment test before and after GM-CSF treatment and adjusting the GM-CSF treatment regimen based on observations in the cognitive state of the subject before and after administration of GM-CSF.