No abstract available.
Diagnosis* ; Nervous System Diseases*

No abstract available.
Neurology*

The genome sequencing project has generated and will continue to generate enormous amounts of sequence data including 5 eukaryotic and about 60 prokaryotic genomes. Given this ever-increasing amounts of sequence information new strategies are necessary to efficiently pursue the next phase of the genome project-the elucidation of gene expression patterns and gene product function on a whole genome scale. In order to assign functional information to the genome sequence, DNA chip(or gene microarray) technology was developed to efficiently identify the differential expression pattern of independent biological samples. DNA chip provides a new tool for genome expression analysis that may revolutionize many aspects of biotechnology including new drug discovery and disease diagnostics.
Base Sequence ; Biotechnology ; Computational Biology ; Drug Discovery ; Gene Expression ; Genome ; Oligonucleotide Array Sequence Analysis

No abstract available.
Adrenocorticotropic Hormone* ; Infant ; Infant, Newborn ; Spasms, Infantile*

BACKGROUND: Although experimental and clinical evidences suggest that endothelin-1(ET-1) may play a pathophysiological role in ischemic heart disease, it is still controversial whether ET-1 produced during myocardial ischemia and reperfusion affects the extent of necrotic myocardium. This study was performed to investigate the role of ET-1 and the effect of ET antagonists in infarct size determination. METHODS: Male Wistar rats(260-400g) were anesthetized with pentobarbital(i.p. 50mg/kg) and ventilation was assisted via tracheostomy tube. The heart was exposed by midline incision and the left anterior descending coronary artery was ligated with 6-0 silk suture. The ligature was released after 1 hour and reperfusion was performed for 2 hours. In the first set of experiment, FRI139317(ET-A antagonist) was given as bolus i.v.(3mg/kg) 10 minutes before reperfusion, followed by continuous infusion(total 24mg/kg) throughout reperfusion. In the other protocol, bosentan(ET-A/ET-B antagonist ; 10mg/kg) was given 10 minutes before coronary occlusion as i.v. bolus. At the end of reperfusion, the heart was excised and stained with Evans blue dye(1% w/v) and triphenyltetrazolium chloride(TTC;1%) to distinguish infarct region(not stained by TTC and Evans blue), ischemic but viable myocardium(stained brick-red by TTC but not stained by Evans blue) and nonischemic myocardium(dyed by Evans blue). These three regions of myocardium were separated and weighed for analysis. Infarct size(in percent) was expressed as the ratio of infarct region to ischemic myocardium(i.e. infarct region plus ischemic but viable myocardium). RESULTS: In the first protocol, infarct region was 57.0 +/-3.8% of the ischemic myocardium in control(n=9) and 58.9+/-4.9% in FR139317 group(n=7) ; The difference was not significant statistically. Likewise, ET-A/ET-B antagonist bosentan given before coronary occlusion did not reduce infarct size significantly ; the ratio was 74.2+/-3.2% in control(n=7) and 69.5+/-2.0% in bosentan group(n=7). CONCLUSIONS: ET-A antagonist FR139317, given throughout reperfusion, did not reduce myocardial infarct size in rat. Bosentan(ET-A/ET-B antagonist) given just before coronary occlusion as i.v. bolus also did not reduce myocardial infarct size in rat.
Animals ; Coronary Occlusion ; Coronary Vessels* ; Endothelin-1 ; Endothelins* ; Evans Blue ; Heart ; Humans ; Ligation ; Male ; Myocardial Infarction* ; Myocardial Ischemia ; Myocardium ; Rats* ; Reperfusion* ; Silk ; Sutures ; Tracheostomy ; Ventilation

No abstract available.
Echocardiography ; Tuberous Sclerosis*

No abstract available.
Moyamoya Disease*

No abstract available.
Muscular Dystrophy, Duchenne*

No abstract available.
Muscular Atrophy*

No abstract available.
Brain* ; Child* ; Humans ; Magnetic Resonance Imaging* ; Seizures*