Methods and materials are described for human genome prophylaxis and therapy of diseases using myoblast transfer. These methods result in gene transcript changes in multiple pathways. Linking the myoblast transfer technology development from DMD, cardiomyopathy, and Type-II diabetes, the myoblast transfer demonstrably mediates its effect through transfer of the normal myoblast nuclei that supply the complete human genome, in addition to just replenishing the missing gene(s) or the aberrant gene(s). The replacement genes then transcribe to produce the necessary proteins or factors for genetic repair. A variety of uses of this technology are described, including that for disease treatment, disease prevention, drug discovery, and selection of superior cells and clones for therapy

The present invention is based on the discovery of genetic polymorphisms that are associated with cardiovascular disorders, particularly acute coronary events such as myocardial infarction and stroke, and genetic polymorphisms that are associated with responsiveness of an individual to treatment of cardiovascular disorders with statin. In particular, the present invention relates to nucleic acid molecules containing the polymorphisms, variant proteins encoded by such nucleic acid molecules, reagents for detecting the polymorphic nucleic acid molecules and proteins, and methods of using the nucleic acid and proteins as well as methods of using reagents for their detection.

Disclosed are compositions and methods for determining aberrant cardiac function or a predisposition to aberrant cardiac function, said method comprising detecting a fragment of βII spectrin associated with aberrant cardiac function or a predisposition to aberrant cardiac function in a sample derived from a subject, wherein the detection is indicative of aberrant cardiac function in the subject.

Biomarkers and/or risk assessments identify patients having an increased risk of certain clinical disease states including, for example, CHD, type 2 diabetes, dementia, or all-cause death (ACD) using NMR signal to measure a level of “GlycA” in arbitrary units or in defined units (e.g., μmol/L) that can be determined using a defined single peak region of proton NMR spectra. The GlycA measurement can be used as an inflammation biomarker for clinical disease states. The NMR signal for GlycA can include a fitting region of signal between about 2.080 ppm and 1.845 ppm of the proton NMR spectra.

In various embodiments methods are provided for identifying a mammal having an elevated risk for an adverse cardiac event (e.g. an MI) and/or determining the prognosis for the mammal. In certain embodiments the methods comprise determining, or causing to be determined, the presence and/or level of antibodies that bind a malondialdehyde acetaldehyde adduct (MAA adduct) in a biological sample from the mammal, where an elevated level of anti-MAA adduct antibodies, as compared to the level found in a normal healthy mammal is an indicator that that said mammal has one or more atherosclerotic lesions and/or is at elevated risk for a myocardial infarction.

A method of inhibiting hypercoagulation and/or thrombosis in a subject having or at risk of hypercoagulation or thrombosis includes administering to the subject an amount of a composition effective to inhibit MRP-8/14 and/or MRP-14 binding to platelet CD36 and inhibit hypercoagulation and/or thrombosis in the subject.

The present invention relates to methods of diagnosing an inflammatory disorder in a patient, as well as methods of monitoring the progression of an inflammatory disorder and/or methods of monitoring a treatment protocol of a therapeutic agent or regimen. The invention also relates to assay methods used in connection with the diagnostic methods described herein.

This invention provides mass spectrometry (MS) compatible nanomaterials for the selective capture and enrichment of low abundance proteins as well as MS analysis of different proteoforms of proteins, particularly cardiac proteins and different proteoforms of cardiac troponin I (cTnI) arising from post-translational modifications and sequence variations. The surface of superparamagnetic nanoparticles is functionalized with probe molecules that specifically bind to the desired protein. In an embodiment, the nanoparticles are functionalized with probe molecules having high affinity and selectivity for cTnI within the human cardiac troponin complex. This allows for MS-analysis and characterization of cTnI proteoforms from human heart tissue lysates and human blood or serum samples, and provides an accurate assay for detection of cTnI with molecular details. Such assays are useful for accurate diagnosis of acute coronary syndrome and chronic diseases, including acute myocardial infarction and other cardiac injuries, as well as risk stratification and outcome assessment for patients.

The invention relates to methods for the diagnosis of ischemia or ischemic tissue damage, methods for predicting the progression of ischemia in a patient having suffered an ischemic event, for determining the prognosis of a patient having suffered an ischemic event and for determining the risk that a patient suffering from stable coronary disease suffers a recurrent ischemic event based on the detection of the levels of glycosylated Apo J. The invention relates as well to a method for the determination of glycosylated Apo J in a sample.

Biomarkers, methods, devices, reagents, systems, and kits used to assess an individual for the prediction of risk of developing a primary or secondary Cardiovascular (CV) event over a 4 year period are provided.