No abstract available.
Precursor Cell Lymphoblastic Leukemia-Lymphoma*

No abstract available.
Leukemia* ; Molecular Biology*

No abstract available.
Growth Hormone*

No abstract available.
Humans* ; Pharmacokinetics*

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

The pathogenetic role of intrauterine infection to the neonatal pulmonary injury and bronchopulmonary dysplasia was assessed by studying the interleukin-6 (IL-6) level in the umbilical cord blood and the early morphologic changes of the neonatal lung. Patients were grouped into bronchopulmonary dysplasia (4 cases), chorioamnionitis without chronic lung injury (4 cases), and 6 cases without morphologic evidence of chronic lung injury or placental inflammation. IL-6 level of umbilical cord blood was higher in babies with bronchopulmonary dysplasia (17.7 pg/ml) compared to those with chorioamnionitis (4.7 pg/ml) or those with morphologically normal lung and placenta (6.2 pg/ml). Morphologic parameters of neonatal pulmonary injury were hyaline membrane, terminal bronchiole inflammation, terminal bronchiole regeneration, alveolar collapse and fibroblastic proliferation. Bronchiolar regeneration was the most peculiar feature seen in the lung with bronchopulmonary dysplasia. Alveolar collapse and interstitial fibroblastic reaction were commonly seen in bronchopulmonary dysplasia. The postnatal age at death was higher in those with bronchopulmonary dysplasia, although the occurrence of the morphologic changes was related with the chronicity of those lesions. These findings suggest that intrauterine infection is an aggravating factor for the neonatal pulmonary injury and bronchopulmonary dysplasia, although the early stage of the lung injury is not a definitive indicator for the progressive pulmonary damage leading to the bronchopulmonary dysplasia.
Bronchioles ; Bronchopulmonary Dysplasia* ; Chorioamnionitis ; Cytokines ; Female ; Fetal Blood ; Fibroblasts ; Humans ; Hyalin ; Hyaline Membrane Disease ; Infant, Newborn ; Inflammation ; Interleukin-6 ; Lung ; Lung Injury* ; Membranes ; Placenta ; Pregnancy ; Regeneration

No abstract available.
Chromosome Aberrations*

No abstract available.
Spermatozoa*

No abstract available.

On the contrary to congenital anomalies of intestinal rotation in pediatric patients, those in adults are generally nonsymptomatic and of little consequence. Occasionally, however, an adult may have midgut nonrotation and complain of chronic or recurrent abdominal pain. Intestinal nonrotation can be divided into complete or partial failure of rotation and into abnormalities affecting the proximal segment, the distal segment or both. We report herein a 43-year old female patient with symptomatic partial, cecocolic nonrotation.
Abdominal Pain ; Adult* ; Female ; Humans