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The ICAD partners (i.e. contributors of the data) have sole access to the pooled database for 12 months (March 2011-Feb 2012), after which time the database is open to any approved user (see http://www.mrc-epid.cam.ac.uk/Research/Studies/ for more information on the procedures for using ICAD).
We have previously demonstrated that the hepatitis C virus core protein, which not only encodes the viral nucleocapsid but has a number of properties enabling persistent viral infection, induces gene expression of ICAD, thereby increasing steady-state levels of the ICAD protein [ 15].
To examine potential regulatory sequences involved in ICAD gene expression, a 1 kb 5′-upstream region of the ICAD gene was sequenced and analyzed.
In this study, we identified a functional promoter of the human ICAD gene and investigated the role of c-Myc and N-Myc in regulation of the ICAD promoter.
Absence of a TATA-like sequence upstream of the transcription start site has also been reported for the mouse ICAD gene, suggesting that TATA-less promoters might be a common feature in transcriptional regulation of the ICAD gene.
A 5′-upstream region of the ICAD gene was amplified by PCR using primers based on the genomic DNA sequence of the human ICAD gene (GenBank accession No. NM_004401).
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In the ICaD-ARQ scheme, the SUs retransmit erroneous packets in busy timeslots only.
In this case, the ICaD-ARQ-PS scheme performs exactly as in the perfect CSI case.
We first describe the basic idea of the ICaD-ARQ scheme.
To practise the ICaD-ARQ scheme, we should estimate the optimal beamforming weight vector g b ∗ for accessing busy timeslots.
When the ICaD-ARQ-QS scheme is applied, the average delay decreases with the increase of the threshold Q.
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