Abstract: Methods are disclosed for predicting the efficacy of a drug for treating an inflammatory disease in a human patient, including: obtaining a sample of cells from the patient; obtaining a gene expression profile of the sample in the absence and presence of in vitro modulation of the cells with specific cytokines and/or mediators; and comparing the gene expression profile of the sample with a reference gene expression profile, wherein similarities between the sample expression profile and the reference expression profile predicts the efficacy of the drug for treating the inflammatory disease in the patient.

Abstract: The invention relates to improved materials and methods for therapy to inhibit production of leukotrienes, and all therapeutic applications thereof.

Abstract: Linkage of myocardial infarction (MI) and a locus on chromosome 13q12 is disclosed. In particular, the FLAP gene within this locus is shown by genetic association analysis to be a susceptibility gene for MI and ACS, as well as stroke and PAOD. Pathway targeting for treatment and diagnostic applications in identifying those who are at risk of developing MI, ACS, stroke or PAOD, in particular are described. The invention also provides for compositions comprising a leukotriene synthesis inhibitor and a stating and methods of using these compositions to reduce C-reactive protein in a human subject at risk of MI, ACS, stroke and/or PAOD.

Abstract: Methods for diagnosis of asthma or a susceptibility to asthma based on detection of at-risk haplotypes associated with MAP3K9 are disclosed. Also methods for treatment of asthma or a susceptibility to asthma based on detection of at-risk haplotypes associated with MAP3K9 are disclosed. In particular, pathway targeting for treating individuals who are at-risk of developing asmtha are described. In certain aspects, MLK1 inhibitors are used in treatment methods.

Abstract: Linkage of myocardial infarction (MI) and a locus on chromosome 13q12 is disclosed. In particular, the FLAP gene within this locus is shown by genetic association analysis to be a susceptibility gene for MI and ACS, as well as stroke and PAOD. Pathway targeting for treatment and diagnostic applications in identifying those who are at risk of developing MI, ACS, stroke or PAOD, in particular are described.

Abstract: Linkage of myocardial infarction (MI) with a locus on chromosome 12q23 is disclosed. In particular, the LTA4H gene within this locus is shown by association analysis to be a susceptibility gene for MI. Methods for preventing and/or treating the recurrence of MI, in particular are described.

Abstract: The invention relates to methods for inducing a pro-asthma/pro-inflammatory like state in a resident tissue cell, comprising contacting the cell with one or more cytokines, e.g., IL-1?, TNF? or both. Methods are also disclosed for identifying genes that regulate responses to anti-inflammatory drugs, to methods for drug screening, and to methods for identifying genes that correlate with various pro-asthma/pro-inflammatory disease phenotypes.

Abstract: Linkage of myocardial infarction (MI) and a locus on chromosome 13q12 is disclosed. In particular, the FLAP gene within this locus is shown by genetic association analysis to be a susceptibility gene for MI and ACS, as well as stroke and PAOD. Pathway targeting for treatment and diagnostic applications in identifying those who are at risk of developing MI, ACS, stroke or PAOD, in particular are described.

Abstract: The present invention relates to methods for inducing a pro-asthma/pro-inflammatory like state in a resident tissue cell, comprising contacting the cell with IL-1?, TNF? or both. Methods are also disclosed for identifying genes that regulate responses to anti-inflammatory drugs, to methods for drug screening, and to methods for identifying genes that correlate with various pro-asthma/pro-inflammatory disease phenotypes.

Abstract: Methods of treating or preventing induction of asthma in a human patient are provided. The methods comprise administering to the human an anti-Fc?RII receptor protein ligand suspended in a pharmaceutically acceptable carrier in an amount sufficient to inhibit binding of IgE to an anti-Fc?RII receptor protein thereby treating or preventing induction of asthma in the human.

Abstract: Methods are disclosed for predicting the efficacy of a drug for treating hypertension in a patient, including: obtaining a sample of cells from the patient; obtaining a gene expression profile from the sample in the absence and presence of in vitro modulation of the cells with specific mediators; and comparing the gene expression profile of the sample with a reference gene expression profile, wherein similarity between the sample expression profile and the reference expression profile predicts the efficacy of the drug for treating hypertension in the patient.

Abstract: Methods of treating or preventing induction of asthma in a human patient are provided. The methods comprise administering to the human an anti-Fc&egr;RII receptor protein ligand suspended in a pharmaceutically acceptable carrier in an amount sufficient to inhibit binding of IgE to an anti-Fc&egr;RII receptor protein thereby treating or preventing induction of asthma in the human.

Abstract: Methods are disclosed for predicting the efficacy of a drug for treating an inflammatory disease in a human patient, including: obtaining a sample of cells from the patient; obtaining a gene expression profile of the sample in the absence and presence of in vitro modulation of the cells with specific cytokines and/or mediators; and comparing the gene expression profile of the sample with a reference gene expression profile, wherein similarities between the sample expression profile and the reference expression profile predicts the efficacy of the drug for treating the inflammatory disease in the patient.

Abstract: Methods are disclosed for predicting the efficacy of a drug for treating an inflammatory disease in a human patient, including: obtaining a sample of cells from the patient; obtaining a gene expression profile of the sample in the absence and presence of in vitro modulation of the cells with specific cytokines and/or mediators; and comparing the gene expression profile of the sample with a reference gene expression profile, wherein similarities between the sample expression profile and the reference expression profile predicts the efficacy of the drug for treating the inflammatory disease in the patient.

Abstract: The present invention relates to methods for inducing a pro-asthma/pro-inflammatory like state in a resident tissue cell, comprising contacting the cell with IL-1&bgr;, TNF&agr; or both. Methods are also disclosed for identifying genes that regulate responses to anti-inflammatory drugs, to methods for drug screening, and to methods for identifying genes that correlate with various pro-asthma/pro-inflammatory disease phenotypes.