Provided herein are methods and devices related to inducing a population of self-renewing or senescent stem cells, to produce one or more beneficial factors for the treatment of a disease or disorder in an individual. Also provided are compositions and methods for inducing senescence, useful for inducing senescence in a population of stem cells, in order to produce one or more beneficial factors for the treatment of a disease or disorder in an individual. Methods and devices to control and customize the production of the beneficial factors for the requirements of a disease or disorder being treated are described. Also provided are factor production units for the production of the beneficial factors, and devices for the delivery of the beneficial factors to an individual in need.

Methods and compositions are provided for assessing (e.g., diagnosing), treating, and preventing diseases, especially cancer, and particular lung cancer, using lung cancer markers (LCM). Individual LCM and panels comprising multiple LCM are provided for these and other uses. Methods and compositions are also provided for determining or predicting the effectiveness of a treatment or for selecting a treatment using LCM. Methods and compositions are further provided for modulating cell function using LCM. Also provided are compositions that modulate LCM (e.g., antagonists or agonists), such as antibodies, proteins, small molecule compounds, and nucleic acid agents (e.g., RNAi and antisense agents), as well as pharmaceutical compositions thereof. Further provided are methods of screening for agents that modulate LCM, and agents identified by these screening methods.

The present invention provides an aptamer containing a sequence shown by the following formula (1) or formula (2):

TABLE-US-00001 (1) GGGGCCUCC-N.sub.1-GGACYAAACC (2) GGGGCCUCC-N.sub.1-GGACWYAAACC
wherein N.sub.1 shows 3 to 24 bases in length, Y is C or U, and W is A or U (uracil is optionally thymine), wherein the aptamer binds to a disintegrin and metalloproteinase with thrombospondin motifs-5 (ADAMTS5).

A method of determining the pre-eclampsia status of a pregnant subject, comprising providing a biological sample obtained from the subject; and determining the presence or absence, and/or level, of one or more of Type XVII collagen alpha 1, leptin, neprilysin, Filamin B and Scavenger receptor class B member 1 in the biological sample, and preferably comparing the level determined with a control.

An ADAMTS13 mutant protein having an improved escaping rate against an autoantibody and a composition that is suitable for preventing or treating thrombotic diseases are disclosed. By efficiently avoiding autoantibodies known to have high binding affinity to the main domain of ADAMTS13, the ADAMTS13 variant protein of the present invention can be used as an effective therapeutic composition for various thrombotic diseases, such as TTP (thrombotic thrombocytopenic purpura), in which the presence of such autoantibodies is the main etiology, and can stably maintain the biological activity thereof when administered into a body. In addition, a newly identified site within ADAMTS13, which is recognized by an autoantibody can be used in screening novel ADAMTS13 variants having an improved autoantibody escaping rate by applying a combination of various mutations within the corresponding site.

The present invention relates to the field of fibrosis and inflammation and more particularly to the use of ADAM12 (A Disintegrin and Metalloproteinase 12) inhibitors to prevent or treat inflammation-induced fibrosis. The present invention also relates to the use of ADAM12 as a marker for inflammation-induced fibrosis and to the ablation of ADAM12 expressing cells as therapeutic approach to interfere with the development of pro-fibrotic cells.

Disclosed are methods and systems for the analysis activity of enzyme disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) in a sample. The methods and systems disclosed herein can be useful for diagnosis of thrombotic thrombocytopenic purpura in a patient.

The invention generally relates to methods of testing the effectiveness of a von Willebrand factor (VWF) in treating von Willebrand disease (VWD) in a subject comprising measuring VWF cleavage fragments in a blood sample from the subject before and after treatment. In particular, the invention relates to methods of measuring VWF cleavage fragments, wherein an increase in VWF cleavage fragments after the treatment indicates that endogenous a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) in the subject is cleaving the VWF and wherein a decrease or absence of VWF cleavage fragments after the treatment indicates that endogenous ADAMTS13 in the subject is not cleaving the VWF.

The present invention relates to detecting cleavage activity of an enzyme. The various aspects of the invention include an enzyme detection device, kit, method and use for detecting or measuring the presence in a test sample of the activity of an enzyme capable of cleaving a substrate. The invention also relates to indicator and binding molecules useful for carrying out the invention. The enzyme substrate contains a hidden binding site which is only revealed upon cleavage by the enzyme.

Methods for quantifying the amount of drug present in a prodrug composition are provided.