The combination of clonidine (2 microg/kg) and ropivacaine 0.1% is associated with an improved quality of postoperative analgesia compared to plain 0.2% ropivacaine. The improved analgesic quality of the clonidine-ropivacaine mixture is achieved without causing any significant degree of postoperative sedation.

3.

No abstract

SummaryDown Syndrome (DS) is caused by the presence of three copies of the whole human chromosome 21 (HC21) or of a HC21 restricted region; the phenotype is likely to have originated from the altered expression of genes in the HC21. We apply the cDNA microarray method to the study of gene expression in human T lymphocytes with trisomy 21 in comparison to normal cells.Two patients with DS were investigated, along with two normal subjects as a control, all being tested in independent, duplicated cell culture experiments. The most consistent finding was the overexpression of the superoxide dismutase gene (SOD1), located on 21q, and of MHC DR beta 3 (HLA-DRB3), GABA receptor A gamma 2 (GABRG2), acetyltransferase Coenzyme, A 2 (ACAT2) and ras suppressor protein 1 (RSU1) genes. When the data were clustered according to chromosome localization, the HC21 gene set showed, on average, the highest expression in DS cells in all the experiments. Moreover, separate clustering of patients and controls was obtained when analysis was restricted to HC21 gene expression values.These findings reinforce the specific gene dosage theory for the pathogenesis of the DS phenotype, and show a consistent overexpression of the SOD1 gene on 21q.

Few cases of large-scale segmental paralogy have been reported in the human genome. We have identified a large (approximately 500 kb) segment on human chromosome (HC) 21 (21q22) that is triplicated on HC 1 (1p35) and HC 6 (6p12-21). We also identified a new member of CLIC (Chloride Intracellular Channel) family on 21q, namely CLIC6. All three segments appear to include three functional members of three different gene families: DSCR1-like (Down Syndrome Candidate Region 1-like), CLIC, and AML/Runt (Acute Myeloid Leukemia/Runt). Molecular evolution analysis shows a common evolutionary origin for the triplicated regions. This finding of a further large-scale genomic triplication that went undetected at previously systematic automated searches provides a new model for gene divergence study and underlines the need for new tools to effectively detect inter-chromosomal similarity. An algorithm to overcome current limitations is proposed.