A method of morphological reconstruction of biological activity in a tissue sample maps biological data resulting from analysis of tissue samples onto a 3-D morphological rendering of the biological sample. Each slice in a set of histological slices, indexed by a first index, is micro dissected into micro samples indexed by a pair of first and second indices. The indices are utilized to spatially map biological data to the 3-D rendering.

A method of morphological reconstruction of biological activity in a tissue sample maps biological data resulting from analysis of tissue samples onto a 3-D morphological rendering of the biological sample. Each slice in a set of histological slices, indexed by a first index, is micro dissected into micro samples indexed by a pair of first and second indices. The indices are utilized to spatially map biological data to the 3-D rendering.

A method of forming a metadatabase of minimal epitope profiles including: performing antibody activity profiling from an immunoglobulin fraction of a plurality of samples to form a data set of peptide profiles for each sample, comparing peptide profiles across different samples, assigning a diagnosis or disorder to differentially expressed meta-profiles, constructing a meta-database containing minimal epitope clusters, constructing a database of peptide frequencies, aligning peptides to define the sequence of minimal epitope, verifying the minimal epitope by harboring a connected identifier, providing an enriched affinity sample, and providing a source data for metadatabase a database underlying it.

A method of forming a metadatabase of minimal epitope profiles including: performing antibody activity profiling from an immunoglobulin fraction of a plurality of samples to form a data set of peptide profiles for each sample, comparing peptide profiles across different samples, assigning a diagnosis or disorder to differentially expressed meta-profiles, constructing a meta-database containing minimal epitope clusters, constructing a database of peptide frequencies, aligning peptides to define the sequence of minimal epitope, verifying the minimal epitope by harboring a connected identifier, providing an enriched affinity sample, and providing a source data for metadatabase a database underlying it.

Transcription in mammalian cells can be assessed at a genome-wide level, but it has been difficult to reliably determine whether individual transcripts are derived from the Plus- or Minus-strands of chromosomes. This distinction can be critical for understanding the relationship between known transcripts (sense) and the complementary antisense transcripts that may regulate them. Here we describe a technique that can be used to (i) identify the DNA strand of origin for any particular RNA transcript and (ii) quantify the number of sense and antisense transcripts from expressed genes at a global level. We examined five different human cell types and in each case found evidence for antisense transcripts in 2900 to 6400 human genes. The distribution of antisense transcripts was distinct from that of sense transcripts, was non-random across the genome, and differed among cell types. Antisense transcripts thus appear to be a pervasive feature of human cells, suggesting that they are a fundamental component of gene regulation.

Transcription in mammalian cells can be assessed at a genome-wide level, but it has been difficult to reliably determine whether individual transcripts are derived from the Plus- or Minus-strands of chromosomes. This distinction can be critical for understanding the relationship between known transcripts (sense) and the complementary antisense transcripts that may regulate them. Here we describe a technique that can be used to (i) identify the DNA strand of origin for any particular RNA transcript and (ii) quantify the number of sense and antisense transcripts from expressed genes at a global level. We examined five different human cell types and in each case found evidence for antisense transcripts in 2900 to 6400 human genes. The distribution of antisense transcripts was distinct from that of sense transcripts, was non-random across the genome, and differed among cell types. Antisense transcripts thus appear to be a pervasive feature of human cells, suggesting that they are a fundamental component of gene regulation.