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.

This invention provides methods for diagnosing Alzheimer's disease in a symptomatic human subject, and for determining whether a human subject is predisposed to becoming afflicted with Alzheimer's disease. These methods employ the steps of (a) culturing a subject's lymphocytes with a suitable basement membrane matrix to permit the lymphocytes to aggregate; (b) measuring the resulting lymphocyte aggregation; and (c) based on such measurement, either diagnosing Alzheimer's disease or determining a predisposition to it, as appropriate.

A method of making triterpenoids from petri dish cultured Antrodia cinnamomea includes: A. providing petri dish cultured Antrodia cinnamomea in an extracting container; B. providing a supercritical solvent to the extracting container to obtain an Antrodia cinnamomea extract; sending the Antrodia cinnamomea extract to a chromatographic column to separate impurities and triterpenoids from the Antrodia cinnamomea extract, and removing the impurities, and collecting the triterpenoids containing fraction; and C. testing the bioactivity of the triterpenoids containing fraction by cytotoxicity test, cell morphology analysis, cell cycle and apoptosis test, and cell motility test to find an anti-cancer effect of the triterpenoids.

The present invention relates to a method for determining the relief of the skin surface of a subject, and hence the degree of maturation of the said skin surface. Methods for identifying active agents, raw materials and formulation are also provided.

The present disclosure relates to methods for screening test samples or substances that are capable of inducing or reducing nucleolar hypertrophy in cancer cells. The present disclosure further provides methods of contacting isolated cancer cells with a test sample or a substance that can induce nucleolar hypertrophy in a cancer cell. The present disclosure further provides methods for contacting an isolated cancer cell characterized by nucleolar hypertrophy with a test sample or substance that can reduce the nucleolar hypertrophy. One benefit to the method of screening disclosed herein can be the identification of test samples or substances capable of reducing nucleolar hypertrophy. Another benefit to the method of screening disclosed herein can be the identification of those combinations of test samples, substances, or combinations or series thereof, which are suitable or optimal for treating specific cancers in patients.

Provided are assay systems for determining the therapeutic or toxic effect of a putative drug based on assaying its activity in cells which have been differentiated in vitro from stem cells, and induced to display a phenotype that resembles a disease to be treated.

The present invention provides methods of treating Alport syndrome in a subject by the administration of an agent that can block the activation of RAC1/CDC42 members of the rho family of small GTPases. Such agents include, but are not limited to, the endothelin receptor antagonists such as bosentan and letairis and neutralizing antibodies to endothelin-1. Such administration prevents invasion of the glomerular capillary tufts by mesangial lamellipodial/filopodial processes, blocks mesangial process invasion abrogates the deposition of laminin 211 in the GBM, and prevents the activation of maladaptive expression of proteins known to contribute to glomerular disease progression.

In vitro methods and kits for modulating and studying mechanical movement of hepatic bile canaliculi lumen through activation or inhibition of the Rho-kinase molecular regulation pathway. In vitro methods and kits for modulating lumen opening and clearing using matrix metalloproteinases, as well as diagnostic methods based upon the same.

Methods of treating kidney disease and protecting podocytes from injury are provided. Methods of screening agents for the treatment of kidney disease are also provided. In addition, methods of identifying structural or functional defects in a patient's podocytes and methods of identifying kidney disease causing agents in a patient's biological sample are also provided.

Embodiments may provide capability to predict the 10-year risk of local recurrence of ductal carcinoma in situ (DCIS) conditions or other non-invasive carcinomas in situ. Embodiments may evaluate the severity and frequency of numerical and structural CA present within DCIS, and may assign a quantitative centrosomal amplification score (CAS) to each sample. For example, a method of determining the risk profile of a carcinoma in situ in a patient may comprise determining severity and frequency of numerical and structural centrosome amplification present within a sample of a carcinoma in situ from the patient and determining at least one centrosome amplification score (CAS) value for the sample based on the determined severity and frequency of numerical and structural centrosome amplification in the sample, wherein the determined at least one CAS value provides a measure of a level of a 10-year risk of local recurrence associated with the carcinoma in situ.