Abstract: Systems and methods for inhibiting atherosclerosis using FoxP3+ CD8 T-cells (TcREG). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (TcREG) through introduction of a low-dose of a RANK agonist such as RANKL. The RANKL was found to best work when provided in accordance with a schedule resulting in a pulsed administration.

Abstract: Systems and methods for inhibiting atherosclerosis using FoxP3+ CD8 T-cells (TcREG). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (TcREG) through introduction of a low-dose of a RANK agonist suck as RANKL. The RANKL was found to best work when provided in accordance with a schedule resulting in a pulsed administration.

Abstract: Systems and methods for inhibiting atherosclerosis using FoxP3+ CD8 T-cells (TcREG). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (TcREG) through introduction of a low-dose of a RANK agonist such as RANKL. The RANKL was found to best work when provided in accordance with a schedule resulting in a pulsed administration.

Abstract: Systems and methods for treating osteogenesis imperfecta using FoxP3+ CD8 T-cells (TcREG). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (TcREG) through introduction of a low-dose of a RANK agonist such as RANKL. The RANKL was found to best work when provided in accordance with a schedule resulting in a pulsed administration.

Abstract: Systems and methods for inhibiting atherosclerosis using FoxP3+ CD8 T-cells (TcREG). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (TcREG) through introduction of a low-dose of a RANK agonist suck as RANKL. The RANKL was found to best work when provided in accordance with a schedule resulting in a pulsed administration.

Abstract: Systems and methods for inhibiting bone loss using FoxP3+ CD8 T-cells (TcREG). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (TcREG) through introduction of a low-dose of a RANK agonist such as RANKL. The RANKL was found to best work when provided in accordance with a schedule resulting in a pulsed administration.

Abstract: Systems and methods for inhibiting bone loss using FoxP3+ CD8 T-cells (TcREG). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (TcREG) either in vivo or ex vivo. The FoxP3+ CD8 T-cells (TcREG) are provided to the patient to subsequently regulate osteoclast function, thereby establishing a bi-directional regulatory loop between osteoclasts and FoxP3+ CD8 T-cells (TcREG).

Abstract: Methods of identifying targets for designing a therapeutic agent are disclosed. These methods comprise: determining an amino acid sequence of one or more polypeptides of each isolate of a plurality of isolates of a biological system; identifying covariance pairs of amino acid residues; establishing a network comprising the covariance pairs; and identifying one or more hub residue positions, wherein a hub residue position comprises a target for designing a therapeutic agent if the hub residue position has a rank order in the 40th percentile or greater. In other aspects, methods are disclosed for selecting a therapy for an infectious disorder.

Abstract: Systems and methods for inhibiting bone loss using FoxP3+ CD8 T-cells (TcREG). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (TcREG) either in vivo or ex vivo. The FoxP3+ CD8 T-cells (TcREG) are provided to the patient to subsequently regulate osteoclast function, thereby establishing a bi-directional regulatory loop between osteoclasts and FoxP3+ CD8 T-cells(TcREG).

Abstract: Disclosed are methods for detecting cellulose in cellulosic materials and producing alcohol using cellulosic materials. More particularly, disclosed are methods for producing alcohol in a cell-free system by contacting pyruvate with enzymes from a minimal enzymatic pathway. Also disclosed are methods of producing pyruvate by culturing a microorganism under hypoxic conditions. Disclosed are methods for detecting cellulose in a sample using Congo red dye.

Abstract: Methods for predicting a response of a virus to an antiviral therapy are provided.

Abstract: The present invention generally relates to a computer-implemented method for predicting a response of a virus to antiviral therapy, and finds particular use in predicting a response of a Hepatitis C or Hepatitis B virus isolated from a patient.

Abstract: Methods of identifying targets for designing a therapeutic agent are disclosed. These methods comprise: determining an amino acid sequence of one or more polypeptides of each isolate of a plurality of isolates of a biological system; identifying covariance pairs of amino acid residues; establishing a network comprising the covariance pairs; and identifying one or more hub residue positions, wherein a hub residue position comprises a target for designing a therapeutic agent if the hub residue position has a rank order in the 40th percentile or greater. In other aspects, methods are disclosed for selecting a therapy for an infectious disorder.

Abstract: Methionine aminopeptidases catalyse the co-translational removal of amino terminal methionine residues from nascent polypeptide chains. A newly-discovered enzyme, designated methionine aminopeptidase type-3 (MetAP-3), has a substrate specificity which is similar to MetAP-1 and MetAP-2, although it is not inhibited by fumagillin, an irreversible inhibitor of MetAP-2. MetAP-3 also preferentially localizes to mitochondria, unlike MetAP-1 and MetAP-2, which accumulate in the cytoplasm. One embodiment of the present invention relates to human cDNAs encoding polypeptides comprising MetAP-3. Other embodiments of the invention relate to nucleic acid molecules derived from these cDNAs, including complements, homologues, and fragments thereof, and methods of using these nucleic acid molecules, to generate polypeptides and fragments thereof.

Abstract: Methionine aminopeptidases catalyse the co-translational removal of amino terminal methionine residues from nascent polypeptide chains. A newly-discovered enzyme, designated methionine aminopeptidase type-3 (MetAP-3), has a substrate specificity which is similar to MetAP-1 and MetAP-2, although it is not inhibited by fumagillin, an irreversible inhibitor of MetAP-2. MetAP-3 also preferentially localizes to mitochondria, unlike MetAP-1 and MetAP-2, which accumulate in the cytoplasm. One embodiment of the present invention relates to human cDNAs encoding polypeptides comprising MetAP-3. Other embodiments of the invention relate to nucleic acid molecules derived from these cDNAs, including complements, homologues, and fragments thereof, and methods of using these nucleic acid molecules, to generate polypeptides and fragments thereof.

Abstract: The present invention relates to a human cDNA encoding a methionine aminopeptidase type-3 (MetAP-3) protein. The invention also relates to nucleic acid molecules associated with or derived from this cDNA including complements, homologues and fragments thereof, and methods of using these nucleic acid molecules, to generate, for example, polypeptides and fragments thereof. The invention also provides methods of using the nucleic acids, for example, to produce a protein and fragments thereof and to screen for compounds or compositions that preferentially or specifically effect the activity of a MetAP-3 protein.

Abstract: 2-19 polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing 2-19 polypeptides and polynucleotides in therapy, and diagnostic assays for such.

Abstract: EF-7 polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing EF-7 polypeptides and polynucleotides in therapy, and diagnostic assays for such.