[A case report of ischemic colitis, gangrene type].
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Biomedical subjects
Publications and source records attributed to S Handa.
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Griseolic acid inhibited cAMP phosphodiesterase (PDE) at low concentrations, the I50 being of the order of 0.01-0.1 microM. Administration of griseolic acid to rats increased the cAMP level in liver and plasma several-fold. It increased glycogen degradation in mouse liver and stimulated lipolysis in isolated rat fat cells. Griseolic acid did not block the adenosine-elicited accumulation of cAMP in guinea pig brain slices. It had no effect on cAMP-dependent protein kinase from rat liver nor on the adenyl cyclase from rat brain.
To investigate the value of the 12-lead ECG and two-dimensional echocardiography (2DE) in the distinction of left circumflex (LCX) from right coronary artery (RCA) disease, we analyzed the location of Q waves, infarct lesions, and coronary artery narrowings in 26 patients with angiographically documented single-vessel disease. Q waves in leads II, III, and aVF were associated with the posterior wall (PW) lesions at the papillary muscle level. Extensive lesions from the PW to the posterior septum (PS) identified RCA disease, while extension to the lateral wall (LW) identified LCX disease. Eleven of 12 patients with high posterior infarction (tall R wave in V1) were found to have extensive LW lesions and 10 of these had coronary narrowings in or proximal to the obtuse marginal branch of LCX. All 6 patients with high posterior infarction and high lateral infarction (Q in I or aVL) had infarct lesions extending from the LW to the anterior wall (AW) and were associated with LCX disease with a large obtuse marginal branch. Of 10 patients with Q waves in V6, the apical LW and PW were involved in 7 and either segment in 3. Nine of these 10 patients had LCX disease. It is concluded that the location of Q waves in inferior infarction could aid in recognizing infarct extension and underlying coronary artery disease.
Hepatic aryl hydrocarbon hydroxylase (AHH)-inducing potency of toxic polychlorinated aromatic hydrocarbons such as polychlorinated dibenzofurans (PCDFs), 3,4,5,3',4',5'-hexachlorobiphenyl (HCB) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was studied in four inbred strains of mice with different phenotypes of Ah locus, i.e., AHH-responsive strains: C57BL/6N and AKR/Ms Qdj, and AHH-nonresponsive strains: DBA/2Cr Slc and Qdj; DDD. Eight individual PCDF isomers or TCDD were administered IP in doses of 30 micrograms/kg; HCB was given in a dose of 120 micrograms/kg. In AHH-nonresponsive strains of mice, only TCDD significantly induced hepatic AHH activity, while in AHH-responsive strains, 2,3,7,8-tetrachlorodibenzofuran(2,3,7,8-TCDF), 1,2,3,7,8-pentachlorodibenzofuran(1,2,3,7,8-PCDF), 2,3,4,7,8-pentachlorodibenzofuran(2,3,4,7,8-PCDF), and TCDD significantly enhanced the enzyme activity, and the induced AHH activities with the three PCDF isomers were about 30-65% of those of TCDD. These results indicate that AHH responsiveness in mice segregates with the induction of AHH activity by PCDF isomers and may also segregate with the toxic potency of the isomers; i.e., toxic potencies of 2,3,7,8-TCDF, 1,2,3,7,8-PCDF, and 2,3,4,7,8-PCDF in AHH-responsive strains of mice may be much greater than those in AHH-nonresponsive strains of mice. Taking into account both the potent AHH inducibility and the high bioaccumulation of 2,3,7,8-TCDF, 1,2,3,7,8-PCDF, and 2,3,4,7,8-PCDF, these three PCDF isomers should be given greater attention with regard to environmental contamination.
Changes in left ventricular (LV) diastolic indices after left ventriculography (LVG) with iopamidol or urografin were studied in 42 subjects. Increase in heart rate and decrease in LV systolic pressure were more significant with urografin than with iopamidol (p less than 0.05 to 0.001). LV end-diastolic pressure was elevated more with urografin than with iopamidol (p less than 0.005 to 0.05) 1 to 3 minutes after LVG. LV peak negative dP/dt decreased significantly with urografin immediately (10 to 15 seconds, -511 and 30 seconds, -376 mm Hg/sec; p less than 0.0005 to 0.02), but with iopamidol it did not decrease significantly after LVG. Time constant, T, was elongated with iopamidol (10 to 15 seconds, +13 and 30 seconds, +6 msec; p less than 0.0005), but this elongation was significantly less than urografin (10 to 15 seconds, +34; 30 seconds, +25; 1 minute, +15; and 2 minutes, +10 msec; p less than 0.05 to 0.0005). We conclude that iopamidol disturbed LV diastolic function to a lesser degree than did urografin.
A patient with malignant lymphoma who developed congestive heart failure, conduction disturbances and myocardial infarction is presented. Two-dimensional echocardiography revealed marked thickening of the left ventricular wall, where the gallium scan correspondingly showed an abnormal accumulation. Irradiation to the mediastinum resulted in a dramatic decrease in ventricular wall thickness and disappearance of the gallium accumulation. Postmortem examination confirmed previous lymphomatous involvement of the myocardium. Combined techniques, including echocardiography and gallium scan, can be valuable for noninvasive detection and follow-up of myocardial involvement in patients with malignant lymphoma.
A series of underivatized sulfoglycolipids (SM4g, lyso-SM4g, SM4s, SM3, SM2, SB2, and SB1a) from various tissues were analyzed by both positive (POS-SI-MS) and negative (NEG-SI-MS) secondary ion mass spectrometry. By POS-SI-MS were detected the molecular ions of sulfoglycolipids in the form with sodium or potassium together with some fragment ions useful for the carbohydrate sequence determination. The analysis of monosulfogangliotriaosyl- or monosulfogangliotetraosylceramide and bis-sulfoglycolipid was difficult due to noise in the high mass region. On the other hand, NEG-SI-MS of sulfoglycolipids gave more intense signals from molecular ion of (M-H)- for monosulfoglycolipids and [M-H+Na)-H)- for bis-sulfoglycolipid. Many fragment ions useful for the elucidation of the carbohydrate sequences were also obtained with significant intensities. The fragmentation was assessed to occur at the glycosidic linkages to form ions of the oligosaccharides with or without ceramide. These ions were useful for sugar sequencing and also for distinguishing the differences in the position of the sulfate group. The intensities of saccharide ions without sulfate were lower than those with sulfates. In the case of SB2 and SB1a, containing 2 mol of sulfate ester groups, the molecular ion was detected as [M-H+Na)-H)-. Also, fragment ions with 2 mol of sulfate were detected as the sodium-additive form. It was concluded that NEG-SI-MS is a very useful technique for the structural elucidation of higher sulfoglycolipids.
A simple and rapid method for the analysis of lipids on a thin layer chromatography (TLC) plate by matrix-assisted secondary ion mass spectrometry (SI-MS) is reported. Analysis was performed without elution of the sample from the TLC plate. Mass spectra obtained by this method are free from interference due to the TLC plate absorbent and reagents used for the detection of the spots. About 1 micrograms of lipids applied on a TLC plate can be analyzed by this method. On scanning the plate, mass chromatograms of each lipid were obtained based on its migration distance along the plate.
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This is a report of abnormal endocardial structures on the left ventricular wall as visualized by two-dimensional echocardiography (2-D echo) in patients with systemic lupus erythematosus. Abnormal endocardial structures, arising from the left ventricular endocardium and appearing to proliferate into the cavity, were found in 11 (20%) of 54 patients. The most frequently involved site was posterobasal left ventricular wall in the parasternal long-axis view, and the posterolateral segment of the left ventricle including the anterior and posterior papillary muscles in the parasternal short-axis view. M-mode echocardiograms, simultaneously recorded with 2-D echo, revealed abnormal structures of increased intensity adjacent to the endocardium with thicknesses of 4 approximately 7 mm. Most of the abnormal endocardial structures were observed in patients in the active phase by 2-D echo, and they appeared to regress with steroid therapy. In one autopsy case, fibrous endocardial thickening suggesting healed endocarditis was present in the anterior papillary muscle as observed by 2-D echo. Their location and response to steroid therapy suggests that these abnormal echoes could represent Libman-Sacks endocarditis.
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