A strategy for finding regions of similarity in complete genome sequences

MOTIVATION: Complete genomic sequences will become available in the future. New methods to deal with very large sequences (sizes beyond 100 kb) efficiently are required. One of the main aims of such work is to increase our understanding of genome organization and evolution. This requires studies of the locations of regions of similarity. RESULTS: We present here a new tool, ASSIRC ('Accelerated Search for SImilarity Regions in Chromosomes'), for finding regions of similarity in genomic sequences. The method involves three steps: (i) identification of short exact chains of fixed size, called 'seeds', common to both sequences, using hashing functions; (ii) extension of these seeds into putative regions of similarity by a 'random walk' procedure; (iii) final selection of regions of similarity by assessing alignments of the putative sequences. We used simulations to estimate the proportion of regions of similarity not detected for particular region sizes, base identity proportions and seed sizes. This approach can be tailored to the user's specifications. We looked for regions of similarity between two yeast chromosomes (V and IX). The efficiency of the approach was compared to those of conventional programs BLAST and FASTA, by assessing CPU time required and the regions of similarity found for the same data set. AVAILABILITY: Source programs are freely available at the following address: ftp://ftp.biologie.ens. fr/pub/molbio/assirc.tar.gz CONTACT: vincens@biologie.ens.fr, hazout@urbb.jussieu.fr      

A comparison of the illness beliefs of people with angina and their peers: a questionnaire study

Background

Systolic compression of a coronary artery by overlying myocardial tissue is termed myocardial bridging. Myocardial bridging usually has a benign prognosis, but some cases resulting in myocardial ischemia, infarction and sudden cardiac death have been reported. We are reporting a case of myocardial bridging which was complicated with acute myocardial infarction associated with inappropriate blood donation.

Case presentation

A 33 year-old-man was admitted to our emergency with acute anteroseptal myocardial infarction after a blood donation. The electrocardiography showed sinus rhythm and was consistent with an acute anteroseptal myocardial infarction. We decided to perform primary percutanous intervention (PCI). Myocardial bridging was observed in the mid segment of the left anterior descending coronary artery on coronary angiogram. PCI was canceled and medical follow up was decided. Blood transfusion was made because he had a deep anemia. A normal hemaglobin level and clinical reperfusion was achieved after ten hours by blood transfusion. At the one year follow up visit, our patient was healthy and had no cardiac complaints.

Conclusions

Myocardial bridging may cause acute myocardial infarction in various clinical conditions. Although the condition in this case caused profound anemia related acute myocardial infarction, its treatment and management was unusual.     

Enhancement of HERG K(+) currents by Cd(2+) destabilization of the inactivated state

We have studied the functional effects of extracellular Cd(2+) on human ether-a-go-go-related gene (HERG) encoded K(+) channels. Low concentrations (10-200 &mgr;M) of extracellular Cd(2+) increased outward currents through HERG channels; 200 &mgr;M Cd(2+) more than doubled HERG currents and altered current kinetics. Cd(2+) concentrations up to 200 &mgr;M did not change the voltage dependence of channel activation, but shifted the voltage dependence of inactivation to more depolarized membrane potentials. Cd(2+) concentrations >/=500 &mgr;M shifted the voltage dependence of channel activation to more positive potentials. These results are consistent with a somewhat specific ability of Cd(2+) to destabilize the inactivated state. We tested the hypothesis that channel inactivation is essential for Cd(2+)-induced increases in HERG K(+) currents, using a double point mutation (G628C/S631C) that diminishes HERG inactivation (Smith, P. L., T. Baukrowitz, and G. Yellen. 1996. Nature (Lond.). 379:833-836). This inactivation-removed mutant is insensitive to low concentrations of Cd(2+). Thus, Cd(2+) had two distinct effects on HERG K(+) channels. Low concentrations of Cd(2+) caused relatively selective effects on inactivation, resulting in a reduction of the apparent rectification of the channel and thereby increasing HERG K(+) currents. Higher Cd(2+) concentrations affected activation gating as well, possibly by a surface charge screening mechanism or by association with a lower affinity site.