39results about How to "Growing population" patented technology

Methods and systems for distributing a mobile device application for use in making and receiving payments utilizing a mobile device such as a mobile telephone (cellphone) or wireless connected personal digital assistant (PDA). A downloadable mobile device application, when installed on a compatible mobile device, is operative for communicating with a mobile financial transaction system (MFTS) that facilitates the making and receiving of payments via wireless mobile devices. The downloadable mobile device application is provided via a download system that downloads the application to mobile devices according to download procedures appropriate for a particular type of mobile device. When a payment is made to a payee having a mobile device, system communicates a message to the payee's mobile device that informs that a payment has been made and instructs the payee about the downloadable mobile device application. If the mobile device user/payee downloads and installs the mobile device application on his or her mobile device and provides enrollment information, interaction between the MFTS and the mobile device user/payee is permitted, and payment is provided to the mobile device user as user/payee.

Ex vivo and in vivo methods of expanding a population of stem and/or progenitor cells, while at the same time reversibly inhibiting differentiation of the stem and/or progenitor cells by providing the stem and/or progenitor cells with an effective amount of at least one copper chelate, so as to maintain a free copper concentration available to said cells substantially unchanged, to thereby expand the population of said stem and/or progenitor cells, while at the same time reversibly inhibit differentiation of said stem and/or progenitor cells.

Coatings for implantable medical devices and methods for fabricating the same are disclosed. The coating includes polycationic peptides, for example R7.

Provided herein is a method of controlling release rate of a bioactive agent from an implantable medical device comprising a coating, a coating on the implantable device and a method of making the coating.

Preparations of modified Fc fusion peptides that exhibit metabolically complete or near-complete oligosaccharide structures are provided. Also provided are methods for preparation of the modified Fc fusion peptides. These preparations exhibit enhanced serum half-life and are useful for treatment of a variety of diseases.

Methods, processes, uses, and pharmaceutical compositions are provided herein for mobilizing hematopoietic progenitor cells and/or cancer stem cells from bone marrow into peripheral blood, comprising the administration of an effective amount of an inhibitor of GTPases, such as a Cdc-42 specific inhibitor alone or in combination with one or more additional agents. Specifically, methods are disclosed for mobilizing hematopoietic stem cells into a subject's peripheral blood. In particular, embodiments of the method involve specific inhibition of the Cdc42 GTPase to increase the numbers of hematopoietic stem cells into a subject's peripheral blood of a subject.

Methods can be adapted for design of a sensitive monolayer for detection of hydrogen sulphide at room temperature with SAW/BAW devices. The sensitive monolayer can be synthesized based on chemical compounds, which belongs to a class of thiacalix[n]arenas, mercapto halides, mercapto alcohols and chloromethylated thiacalix[n]arenas. The sensitive monolayer can be directly immobilized or anchored at the surface of a piezoelectric quartz substrate in a covalently bonded manner by means of direct printing process. The piezoelectric quartz substrate can be activated in basic medium or in acid medium before the immobilization of the sensitive monolayer in order to increase the population of OH groups. Thus, the synthesized sensitive monolayer exhibits a high site density, fast response and long-term stability for H₂S sensing.

Methods for increasing blood flow and/or regenerating tissue using compounds which bind to the chemokine receptor CXCR4 are disclosed. Preferred embodiments of such compounds are of the formula Z-linker-Z′) wherein Z is a cyclic polyamine containing 9-32 ring members of which 2-8 are nitrogen atoms, said nitrogen atoms separated from each other by at least 2 carbon atoms, and wherein said heterocycle may optionally contain additional heteroatoms besides nitrogen and/or may be fused to an additional ring system; or Z is of the formula (I) wherein A comprises a monocyclic or bicyclic fused ring system containing at least one N and B is H or an organic moiety of 1-20 atoms; Z′ may be embodied in a form as defined by Z above, or alternatively may be of the formula —N(R)—(CR₂)n-X wherein each R is independently H or straight, branched or cyclic alkyl (1-6C), n is 1 or 2, and X is an aromatic ring, including heteroaromatic rings, or is a mercaptan; or Z is of the formula —Ar(Y)_j; wherein Ar is an aromatic or heteroaromatic moiety, and each Y is independently a non-interfering substituent and j is 0-3; “linker” represents a bond, alkylene (1-6C) or may comprise aryl, fused aryl, oxygen atoms contained in an alkylene chain, or may contain keto groups or nitrogen or sulfur atoms.

Disclosed are TGF-α polypeptides, related polypeptides, fragments and mimetics thereof useful in stimulating stem cell or precursor cell proliferation, migration and differentiation. The methods of the invention are useful to treat tissue injury as well as expand stem cell populations in, or obtained from, gastrointestinal, musculoskeletal, urogenital, neurological and cardiovascular tissues. The methods include ex vivo and in vivo applications.

Provided herein are computer-based methods for generating and using three-dimensional (3-D) structural models of target molecules and databases containing the models. The targets can be protein structural variants derived from genes containing polymorphisms. The models are generated using molecular modeling techniques and are used in structure-based drug design studies for identifying drugs that bind to particular structural variants in structure-based drug design studies, for designing allele-specific drugs and population-specific drugs and for predicting clinical responses in patients. Computer-based methods for predicting drug resistance or sensitivity via computational phenotyping are also provided. Databases containing protein structural variant models are also provided.

The expansion of a population of stem cells or progenitor cells, or precursors thereof, may be accomplished by disrupting or inhibiting p21^cip1/waf1 and/or p27, cyclin dependent kinase inhibitors. In the absence of p27 activity, progenitor cells move into the cell cycle and proliferate; whereas in the absence of p21 activity, stem cells move into the cell cycle and proliferate without losing their pluripotentiality (i.e., their ability to differentiate into the various cell lines found in the blood stream). Any type of stem cell or progenitor cell, or precursor thereof, including, but not limited to, hematopoietic, gastrointestinal, lung, neural, skin, muscle, cardiac muscle, renal, mesenchymal, embryonic, fetal, or liver cell may be used in accordance with the invention. The present invention provides a method of expanding a cell population, cells with decreased p27 and/or p21 activity, transgenic animals with a disrupted p27 and/or p21 gene, pharmaceutical compositions comprising the cells of the invention, and methods of using these cells in gene therapy (e.g., stem cell gene therapy) and bone marrow transplantation.

The present invention provides methods for treating a EGFR-mutant cancer in a patient by administering a selective CDK4/6 inhibitor described herein in combination or alternation with an EGFR-TKI to delay or reverse acquired resistance to previously administered EGFR-TKIs. In addition, methods for treating a EGFR-mutant cancer in a patient by administering a selective CDK4/6 inhibitor described herein in combination or alternation with an EGFR-TKI are provided wherein an intrinsically EGFR-TKI resistant EGFR-mutant cancer is sensitized to the effects of the EGFR-TKI.