In this study, an analytical formulation of bone remodeling integrated with multiscale micromechanical models is proposed to investigate the effects of structural changes at the nanometer level (collagen scale) on those at higher levels (tissue scale).
The first stage of the analysis to show high level tissue contrast was performed between all malignant and normal sites from 101 margins (100 patients).
The most prominent charactistic of the human β-globin LCR is that it drives high level, tissue-specific, copy number-dependent and position-independent expression of linked transgenes in mice [1].
Nine clones showed high-level tissue plasminogen activator (tPA) production without amplification.
The libraries were grouped into 47 higher-level tissue categories (averaging across duplicates and triplicates).
Therefore, some TissueInfo categories were grouped together into higher-level tissue categories.
Six higher-level tissue categories were available for comparison between Gene Expression Atlas, SAGEmap, and TissueInfo (Table 1).
This procedure resulted in 48 higher-level tissue categories, 27 of which had EST counts in excess of 10,000 (the number of ESTs we accepted as the threshold for dataset size).
To compare different databases we grouped libraries into higher-level tissue categories, and calculated Pearson correlation coefficients for PEM scores for categories that were represented in all three databases.
After downloading, the libraries were grouped into 15 higher-level tissue categories (brain, prostate, kidney, colon, pancreas, ovary, breast, skin, peritoneum, stomach, blood, lung, liver, heart and vascular endothelium) and annotated according to their disease status (91 tumour tissues, 37 normal tissue libraries and four immortalised cell lines).
This would enable the use of complex regulatory regions, which, in contrast to the simple CMV enhancer-promoter system which was used, should confer high-level, tissue-specific and developmentally stable gene expression.
