[Digital subtraction angiography in neonates and children].
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Biomedical subjects
Publications and source records attributed to M Sudo.
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This study was performed to measure regional myocardial blood flow (MBF) quantitatively using dynamic positron emission tomography (PET) and O-15 water. The subjects consisted of two normal volunteers, four patients with normal coronary angiograms (CAG), two patients with angina pectoris (3-vessel disease) and three patients with myocardial infarction. O-15 water (15-20 mCi) was injected via the cubital vein in a bolus, and dynamic PET was performed. MBF was calculated according to the method of Iida. The region of interest (ROI) was selected on the left ventricular wall (septum, anterior and lateral walls) and MBF was calculated in each ROI. In normal volunteers, MBF was 1.07 to 1.17 ml/g/min. It was 0.96 to 1.02 ml/g/min in patients with normal CAG, and 0.53 to 0.64 ml/g/min in patients with angina pectoris in the ischemic area. In patients with myocardial infarction, MBF was so diminished in the infarcted area as detected by 2-DE or ECG that the absolute value was almost 0 ml/g/min. In patients with angina pectoris, there was no definite defect on the MBF image, but we could estimate the severity of coronary stenosis by quantifying the MBF. The clinical advantages of this method include estimation of the severity of coronary arterial stenosis in the resting state.
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Inflammatory peritoneal exudates from 11 patients with purulent peritonitis or non-perforative appendicitis were analyzed by gas chromatography mass spectrometry (GC-MS) for their content of 5S, 12R-dihydroxy-6,14-cis-8,10-trans-eicosatetraenoic acid (LTB4) and its omega-oxidized catabolite, 5S,12R,20-trihydroxy-6,8,10,14-eicosatetraenoic acid (20-OH-LTB4). Eleven samples of peritoneal exudates were examined. LTB4 and 20-OH-LTB4 were demonstrated only in the samples from patients with purulent peritonitis. LTB4 was detected in 4 samples, and 20-OH-LTB4 was detected in 6 samples by GC-MS with selected ion monitoring. In addition, a nearly full spectrum corresponding to that of synthetic 20-OH-LTB4 was obtained with 3 samples. Neither LTB4 nor 20-OH-LTB4 were detected in samples from patients with non-perforative appendicitis. LTB4 or 20-OH-LTB4 may be related to the pathophysiological mechanism of purulent inflammations.
The biosynthesis of 5(S), 12(R)-dihydroxy-6,14-cis-8,10-trans-eicosatetraenoic acid, leukotriene B4, by human polymorphonuclear leukocytes was examined in relation to age. The leukotriene B4 production by polymorphonuclear leukocytes from umbilical cords, infants, and adults was assayed using high pressure liquid chromatography. The specificity of the leukotriene B4 assay was examined by gas chromatography mass spectrometry. Polymorphonuclear leukocytes from 10 umbilical cords, 24 infants and children, and 10 adults were examined for their ability to synthesize leukotriene B4, in vitro after stimulation by the ionophore A23187 or platelet-activating factor. Among the infants and children, there was a slight age-dependent increase of leukotriene B4 production by polymorphonuclear leukocytes in response to ionophore A23187, but it was not statistically significant. Leukotriene B4 production by polymorphonuclear leukocytes in the umbilical cords and infants was not significantly lower than that of polymorphonuclear leukocytes in adults in response to both ionophore A23187 and platelet-activating factor under our experimental conditions.
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We determined the myocardial metabolic rate for glucose (MMRGlc) in the ischemic or infarcted myocardium using 18-F-fluorodeoxyglucose (18-FDG) with positron emission tomography (PET), and studied energy metabolism in the ischemic myocardium. In some cases, we compared glucose metabolism images by 18-FDG with myocardial blood flow images using 15-oxygen water. Two normal subjects, seven patients with myocardial infarction and four patients with angina pectoris were studied. Coronary angiography was performed within two weeks before or after the PET study to detect ischemic areas. PET studies were performed for patients who did not eat for 5 to 6 hours after breakfast. Cannulation was performed in the pedal artery to measure free fatty acid, blood sugar, and insulin. After recording the transmission scan for subsequent correction of photon attenuation, blood pool images were recorded for two min. after the inhalation of carbon monoxide (oxygen-15) which labeled the red blood cells in vivo. After 20 min., oxygen-15 water (15 to 20 mCi) was injected for dynamic scans, and flow images were obtained. Thirty min. after this procedure, 18-FDG (5 to 6 mCi) was injected, and 60 min later, a static scan was performed and glucose metabolism images were obtained. Arterial blood sampling for the time activity curve of the tracer was performed at the same time. According to the method of Phelps et al, MMRGlc was calculated in each of the region of interest (ROI) which was located in the left ventricular wall. MMRGlc obtained from each ROI was 0 to 17 mg/100 ml/min. In normal subjects MMRGlc was 0.4 to 7.3 mg/100 ml/min.(ABSTRACT TRUNCATED AT 250 WORDS)
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Delipidation of carp liver mitochondria by treatment with methyl ethyl ketone (MEK) or Triton X-100 and then perchlorate greatly reduced MAO activities. Treatment with only Triton X-100 resulted in less reduction in activity. The Km values of the remaining activities were similar regardless of these treatments. The sensitivities towards clorgyline and l-deprenyl of the remaining activity in the Triton X-100-treated residue and the phospholipase C-treated carp brain mitochondria were found to be unchanged, but those of the activity remaining in the MEK-treated residue were similarly decreased. No evidence was obtained suggesting conversion of carp MAO to either MAO-A or MAO-B by the modification of the mitochondrial lipid environment by the treatments employed.
The DNA region having homology between Marek's disease virus and herpesvirus of turkey was assigned to the restriction map of Marek's disease virus by Southern blot hybridization. Under moderate conditions at the level of 15% mismatching, homology was found to be distributed throughout the Marek's disease virus genome. The long inverted-repeat regions (TRL and IRL), which are considered to play a significant role in tumorigenicity, did not show any homology to herpesvirus of turkey DNA.
Basophil histamine release induced by allergens (house dust and Candida albicans) and anti-IgE was examined in 31 patients with bronchial asthma in relation to patient age, age at onset of the disease and serum IgE levels. Basophils from patients under 40 years of age generally released a significantly large amount of histamine by stimulation with house dust and anti-IgE. On the other hand, histamine release from patients over 41 years of age was generally not marked when the cells were incubated with house dust and anti-IgE, although, in some cases, the release induced by C. albicans was fairly marked. Basophils from patients under 30 years of age at onset were reactive to house dust and anti-IgE, while the cells from patients over 41 years of age at onset tended to be reactive only to C. albicans. Basophils from patients with low serum IgE levels were less reactive than the cells from patients with high levels of IgE to house dust and anti-IgE. C. albicans-induced release of histamine did not correlate with serum IgE levels.
Candida albicans-induced histamine release from basophils was studied in 54 patients with bronchial asthma in comparison with the release caused by house dust and anti-IgE. The release of histamine induced by C. albicans and that induced by house dust were closely related to the serum levels of specific IgE antibodies as expressed by RAST scores. A correlation of C. albicans-induced histamine release with the release caused by anti-IgE was not generally observed. On the other hand, a close correlation was found between house dust- and anti-IgE-induced histamine release. It was suggested from these results that the differences between C. albicans- and house dust-induced histamine release might be due to the different antigenicity of the two allergens.
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