The present invention relates to a normal-pressure hydrocephalus diagnosis composition and diagnosis marker detection method which use the level of expression of chitinase 3-like 1 (CHI3L1) in blood and, more specifically, to a normal-pressure hydrocephalus diagnosis composition and diagnosis kit which comprise a preparation for measuring the expression level of CHI3L1 protein or of mRNA encoding the protein, and to a normal-pressure hydrocephalus diagnosis method using same. According to the present invention, the expression level of CHI3L1 is significantly increased in patients with normal-pressure hydrocephalus. Thus, the present invention is excellent since it can rapidly and accurately diagnose normal-pressure hydrocephalus by analyzing the expression level of CHI3L1.

Various embodiments of the invention provide human kinases and phosphatases (KPP) polypeptides and polynucleotides which identify and encode KPP. Embodiments of the invention also provide expression vectors, host cells, antibodies, agonists, and antagonists. Other embodiments provide methods for diagnosing, treating, or preventing disorders associated with aberrant expression of KPP.

The present invention provides a method for screening for an autophagy activator or inhibitor comprising the steps of: (a) making a test material to be analyzed come into contact with cells containing Beclin 1 protein; and (b) analyzing the degree of phosphorylation at the 30.sup.th serine amino acid residue of the Beclin 1 protein. The test material is determined to be an autophagy activator when the phosphorylation of the Beclin 1 protein is up-regulated, and the test material is determined to be an autophagy inhibitor when the phosphorylation of the Beclin 1 protein is down-regulated. The present invention first establishes, by ULK1, the mechanism of phosphorylation at the 30.sup.th serine amino acid residue of Beclin 1.

This disclosure is directed to methods of methods of computing a composite measurement comprising employing two or more sub-instruments to measure one or more clinical symptoms of mitochondrial dysfunction or mitochondrial disease. This disclosure is also directed to methods of assessing and managing a subject with mitochondrial dysfunction or mitochondrial disease using a composite measurement.

Disclosed are biomarkers for Parkinson's disease (PD), including idiopathic PD (idPD). The present invention relates generally to assays, kits, compositions, solid supports and methods that measure a decrease in the expression or function of PLA2g6(L) variant of PLA2g6 (PARK 14) gene in a sample from the subject, including non-neuronal cells as a biomarker for preclinical (prodromal) or early stage Parkinson's disease (PD) and idiopathic PD (idPD), as well as assays, kits, compositions and methods that can detect the functional consequences of decreased expression of PLA2g6(L), including decreased store operated Ca2+ entry (SOCE), deficit of Ca2+ in endoplasmic reticulum stores, and autophagic dysfunction in the cells obtained from the subjects in preclinical (prodromal) and early stage PD diagnosis and for monitoring Parkinson's Disease progression.

The present disclosure provides methods of evaluating a subject, e.g., a subject at risk for or suffering from a pKal-mediated or bradykinin-mediated disorder, based on values (e.g., percentages) of intact and/or cleaved kininogen in a sample of the subject. Provided methods permit analysis of patients with plasma kallikrein-mediated angioedema (KMA), or other diseases mediated by pKal useful in the evaluation and treatment. Such methods can involve the use of a detection agent that preferentially binds cleaved kininogen or intact kininogen.

The present subject matter provides compositions, formulations and methods for preventing or reducing proliferation or migration of retinal cells or epithelial to mesenchymal transition in ocular cells or cells from other tissues.

The present disclosure provides methods of evaluating a subject, e.g., a subject at risk for or suffering from a pKal-mediated or bradykinin-mediated disorder, based on values (e.g., percentages) of intact and/or cleaved kininogen in a sample of the subject. Provided methods permit analysis of patients with plasma kallikrein-mediated angioedema (KMA), or other diseases mediated by pKal useful in the evaluation and treatment. Such methods can involve the use of a detection agent that preferentially binds cleaved kininogen or intact kininogen.

The present invention provides biomarkers, methods and kits for diagnosing latent tuberculosis (TB) in a subject exposed to TB, and methods and kits for monitoring the effectiveness of treatment for latent TB.

Disclosed are methods for diagnosing Lyme disease and distinguishing a new infection from a persistent infection of Borrelia burgdorferi in a subject.