Provided is a method for evaluating the progression of glioma in an individual comprising monitoring the levels of circulating exosomes that are positive for survivin and a glial marker (such as glial fibrillary acidic protein). An increase in the level of such exosomes is indicative of poor prognosis. Levels of circulating exosomes that are positive for survivin and glial marker can also be used for evaluating the efficacy of a therapy for glioma in an individual, and modifying the therapy or introducing additional therapy if levels of such exosomes are found to be increasing.

Disclosed are a means which enables simple and rapid detection of the presence or absence, and of the degree, of homologous recombination activity in an individual, and a means which is useful for detection and treatment of homologous recombination-restored cancer for which no treatment means is available at present. The nucleic acid construct of the present invention comprises: (1) a promoter region; (2) a mutant gene sequence containing a cleavage site in a gene sequence encoding a protein; and (3) a base sequence composed of a first homologous region and a second homologous region, the base sequence being capable of replacing, by homologous recombination, a partial region in the mutant gene sequence of (2), the partial region containing the cleavage site. The nucleic acid construct of the present invention can be used as a measurement reagent or kit for homologous recombination activity, a diagnostic agent for homologous recombination-deficient cancer, a therapeutic agent for homologous recombination-restored cancer, or the like.

Disclosed is a method for determination of the metastatic and/or invasive potential of a malignant neoplasm The method comprises measuring the electric activity of cells from the neoplasm and ranking the measured activity relative to measurement values of electric activity in cancer cells from cancers with known metastatic activity and/or invasiveness. Thereby the electric activity functions as a surrogate measure for metastatic activity and/or invasiveness.

The present disclosure is directed to disclosed compounds that increase cystic fibrosis transmembrane conductance regulator (CFTR) activity as measured in human bronchial epithelial (hBE) cells.

The present disclosure is based, in part, on the discovery that disclosed compounds such as those having Formula (IIIa), (III), or (IV) can increase cystic fibrosis transmembrane conductance regulator (CFTR) activity as measured in human bronchial epithelial (hBE) cells.

Provided herein is a dual cell aggregate culture of retinal epithelial cells and photoreceptors for use as a research tool, such as the screening of compounds or model for study of retinal diseases, as well as a therapeutic for treating ocular diseases.

A β.sub.1-ADR agonist prodrug compound, which is hydrolysable in vivo to release a β1-ADR agonist compound, and which prodrug compound contains a group which imparts greater lipophilicity and CNS bioavailability to the prodrug compound relative to the β1-ADR agonist compound.

Provided are age-modified cells and method for making age modified cells by reducing or increasing the level of genomic nucleic acid methylation in the cells. The aging and/or maturation process can be accelerated or reduced and controlled for young, aged, mature and/or immature cells, such as a somatic cell, a stem cell, a stem cell-derived somatic cell, including an induced pluripotent stem cell-derived cell, by reducing or increasing the level of genomic nucleic acid methylation in the cells. Methods described by the present disclosure can produce age-appropriate cells from a somatic cell or a stem cell, such as an old cell, young cell, immature cell, and/or a mature cell. Such age-modified cells constitute model systems for the study of late-onset diseases and/or disorders.

The methods and kits described herein are based, in part, to the discovery of a phenotype representing a fully-reprogrammed iPS cell and several reprogramming intermediates. The methods and kits described herein permit identification of fully-reprogrammed iPS cells and further permits one of skill in the art to monitor the emergence of iPS cells during the reprogramming process. The methods/kits can also be performed using real time using live cell imaging. Also described herein are methods for screening candidate reprogramming agents by monitoring the emergence of fully-reprogrammed iPS cells in the presence and absence of such an agent.

Methods for assaying antigen-specific T-cell activation in vitro, comprising the steps of (a) providing a phagocytable particle, having a candidate antigen polypeptide tightly associated thereto, wherein the particle with the associated polypeptide has been subjected to a denaturing wash resulting in an endotoxin level low enough to not interfere with the subsequent steps; (b) providing a viable antigen-presenting cell; (c) contacting the washed particle with the antigen-presenting cell under conditions allowing phagocytosis of the particle by the antigen-presenting cell; (d) providing a T-cell sample to be assayed comprising viable T-cells; (e) contacting the T-cell sample with the antigen-presenting cell contacted with the particle under conditions allowing specific activation of T-cells in response to an antigen presented by an antigen-presenting cell; and (f) determining the degree of T-cell activation in the T-cell sample.