Differentiation-associated ganglioside changes in chronic myelogenous leukemia cells.
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Biomedical subjects
Publications and source records attributed to S Sakamoto.
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A new antibiotic cefminox (CMNX, MT-141) was administered to 54 patients with severe infections accompanying various hematological diseases. The rate of effectiveness was 55.3% on the whole. Mild liver dysfunction was observed in 3 cases, which recovered quickly following the stop of the administration.
There have been very few reports of studies on histological abnormalities of the umbilical cord. In the present study, we have investigated various abnormalities of the cord with special emphasis on the cord vasculature and the vestigial remnants based on developmental abberations. The incidence of single umbilical artery was 1/509 (0.2%), by which no special relation was signified between the single artery and the occurrence of congenital malformations of the neonate. Supernumerary umbilical vessels were found in 5/509 (1.0%) of the cases examined. Three out of five revealed the umbilical cord with two arteries and two veins, while two of them showed the umbilical cord with the normal 3 vessels associated with an accessory fourth vessel. It is of a great interest to note that fetal distress with or without fetal acidosis was demonstrated in all cases with the accessory fourth vessel, whereas the presence of supernumrary umbilical vessels was least related to the occurrence of congenital malformations of the neonates. The incidence of vestigial remnants was 30/509 (5.9%). The vestigial remnants were classified into two groups according to their epithelial pattern, i.e. flat epithelium and cuboidal or columnar epithelium. The vestigial remnants with flat epithelium type, considered to originate in the allantoic duct, were found in 2/3 (66.7%) of all cases with vestigial remnants. The vestigial remnants with cuboidal or columnar epithelium, considered to originate in the omphalomesenteric duct, were found in 1/3 (33.3%) of all cases with vestigial remnants, one of which case was associated with congenital malformation of omphalocele of the neonate.
The effects of nifedipine were examined in dogs with flow-limiting dynamic and fixed coronary stenoses. During dynamic coronary stenosis, produced by an intraluminal microballoon occluder which preserved active vasomotion in a stenosed segment of a proximal left circumflex coronary artery, intracoronary infusion of nifedipine (0.01 and 0.1 microgram/kg/min) increased coronary blood flow (CBF) by 15 +/- 5.0% (P less than .05) and 50 +/- 11.6% (P less than .01), respectively (mean +/- S.E.) and reduced stenosis resistance (SR) resulting in the alleviation of myocardial ischemia due to preferential vasodilation of large coronary arteries. In contrast, nifedipine (1.0 microgram/kg/min) did not increase CBF and reduced distal coronary pressure associated with intensified SR mainly due to arteriolar vasodilation. During fixed coronary stenosis created by external application of an occluder device, all doses of nifedipine failed to affect CBF and SR. Intravenous nifedipine (3 micrograms/kg) caused a biphasic response during dynamic coronary stenosis; an initial transient decrease and a late sustained increase in CBF concomitant with a transient augmentation and a subsequent prominent reduction of SR. These results suggest that nifedipine is capable of preferentially dilating large epicardial coronary arteries and reducing stenosis severity resulting in the relief of myocardial ischemia during pliable coronary stenosis, and this mechanism may contribute to the beneficial effects of nifedipine in clinical ischemic syndrome.
Five patients with right ventricular dysplasia (RVD) and 28 patients with predominantly left sided dilated cardiomyopathy (DCM) were studied. RVD was characterised by syncope, recurrent sustained ventricular tachycardia, which typically had a left bundle branch block pattern on the surface electrocardiogram, right heart failure, and faint or absence of the right ventricular free wall on the myocardial scintigraphy. Two-dimensional echocardiographic, radionuclide angiographic, and contrast ventriculographic studies were typical of the right ventricular abnormalities in both Uhl's anomaly and arrhythmogenic right ventricular dysplasia. Two of them were died suddenly. Pathologic examinations showed "parchment-like" thinning of portions of the right ventricular free wall and its replacement by adipose tissue, although such degenerations were not found in the septum and the left ventricle. By contrast, DCM was characterised by exertional dyspnea and short run ventricular tachycardia, most of which had a right bundle branch block pattern. Ten of them had left ventricular myocardial defects on the scintigraphy, of whom five died suddenly. Hemodynamic data showed that left ventricular dysfunction was predominant more than right ventricle. Thus we postulate that these two syndromes are manifestations of a congenital, pathophysiologic process - the "involved right or left ventricle" syndrome.
An autopsy case of hypertrophic obstructive cardiomyopathy with extensive myocardial fibrosis is reported in a 43-year-old male. His mother died suddenly at 55. At the age of 39 the patient felt fatigue and feverish sensation followed by dyspnea and palpitation on exertion. He responded to beta-blocker and was discharged on the 51st hospital day. He died suddenly during his work three years and one month after discharge. The heart weighs 700 g. The thickness of the ventricular septum measures up to 3.2 cm, and that of the left ventricular posterior wall 2.2 cm. Subaortic endocardium is moderately thickened. Many patchy fibroses of various sizes and broad linear fibroses are mainly observed in the ventricular septum and in the left ventricular free wall. Microscopic examination shows severe fascicular disarray of hypertrophied myocardial fibers in the ventricular septum and in a part of the left ventricular anterior wall. Pericardial fibrosis, granulation tissue with many capillaries, and slight lymphocytic infiltrate are also noted. These findings suggest that the patient have both congenital hypertrophic cardiomyopathy and myocarditis. There are following possibilities as regards the relation between the two: first, haphazard association of cardiomyopathy with myocarditis; secondly, myocarditis triggered the onset or progression, or both, of cardiomyopathy. He also had liver cirrhosis, probably alcoholic, which appears to accelerate the progression of myocardial disarray and fibrosis.
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A 46-year-old woman was admitted to our hospital for evaluation of oppressive chest pain and ECG abnormalities. Her ECG on admission showed old inferior myocardial infarction. Chest radiography on admission indicated cardiomegaly (cardiothoracic ratio was 60%). The echocardiogram showed compression of the right atrium, right ventricle, and tricuspid annulus by a tumor which was located between the liver and the heart. The tumor's echo density was heterogenous. Cardiac computed tomography showed compression of the tricuspid annulus by the tumor which was located anterior to the right atrium and the right ventricle. The tumor registered 65.1 HU and was not enhanced by contrast medium. These findings strongly suggested a giant right coronary aneurysm filled with thrombus, and this diagnosis was confirmed at surgery and pathologically. Coronary aneurysms are rarely diagnosed during life, and usually are incidental findings during coronary arteriography performed to evaluate myocardial infarction or angina pectoris. The coronary aneurysm of the present case was clearly and easily recognized using computed tomography and appeared as a pericardial tumor. Computed tomography may be helpful for observing the growth of tumor and thrombus formation within it.
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In order to evaluate the effects of aging on platelet alpha-adrenergic receptor function, we have examined the binding of [3H]dihydroergocryptine ( [3H]DHE), a nonselective alpha-adrenergic antagonist, to crude platelet membrane at 25 degrees C in 28 subjects of various ages (mean 48, range 21-77 years) and platelet aggregatory response to epinephrine in other 32 subjects of various ages (mean 51, range 27-82 years). The average values of the binding capacity and affinity for [3H]DHE showed 218 +/- 56 fmol/mg protein (mean +/- SD) and 1.80 +/- 0.20 nM, respectively. There was a significant correlation between the binding capacity for [3H]DHE and age (r = 0.654, p less than 0.001). On the contrary, no significant correlation was found between the binding affinity for [3H]DHE and age (r = 0.273, p greater than 0.1). Exaggerated aggregatory response to epinephrine with advancing age was also demonstrated in this study (r = 0.716, p less than 0.001). Thus, the demonstration of increased alpha-adrenergic receptor capacity in aging man offers a possible explanation for the observed age-associated hyperactivity of the platelets to epinephrine.
The organ culture of neonatal mouse calvaria produced both collagenase and collagenase inhibitor. The inhibitor was purified by a series of column chromatographies: DEAE-cellulose and CM-cellulose ion-exchange chromatography, concanavalin A-Sepharose and heparin-Sepharose affinity chromatography, and finally by Sephacryl S-200 gel filtration. The purified inhibitor migrated as a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis and had a molecular mass of 28,000. The inhibitor was purified 140-fold to a specific activity of 163 units/mg with a yield of 18% over the first step of the purification by DEAE-cellulose chromatography. The inhibitor stained positively for carbohydrate with periodic acid-Schiff's reagent indicating, in conjunction with its affinity to concanavalin A, that the inhibitor is a glycoprotein. In addition to mouse bone collagenase, this inhibitor also inhibited chick bone, rat bone, rabbit corneal, and human gingival collagenase, but did not inhibit bacterial collagenase.
Mechanisms for the development of functional tricuspid regurgitation (TR) were studied in 41 patients by ultrasound. The severity of TR was classified into 4 grades according to the extent of the regurgitant signal by pulsed Doppler echocardiography (echo). No TR signal was detected in 11 patients; the grade of TR was 1+ in 9 patients, 2+ in 10, 3+ in 8 and 4+ in 9. Using 2-dimensional echo, the tricuspid anular area was estimated from a horizontal and a sagittal diameter of the anulus, and systolic configurations of the tricuspid valve was observed. The tricuspid anular area corrected for body surface area increased with the grade of TR. Anterior displacement of the tips of the tricuspid leaflets was seen in 10 patients with TR of 2+ or greater severity, and its frequency also increased with the grade of TR. Loss of coaptation was seen in 3 patients with 4+ TR and malaligned coaptation was seen in 4 patients with TR of variable degrees. Tricuspid anular dilatation and anterior displacement of the tricuspid leaflet tips causes a separation between the leaflet tips and appears to be the main mechanisms for the development of functional TR. Malaligned coaptation also plays a role in the development of functional TR.
A 32-year-old woman with asymptomatic primary biliary cirrhosis had autoimmune hemolytic anemia associated with reticulocytopenia and thrombocytopenia despite an intensely erythroid bone marrow. Her anemia was successfully treated with oral prednisolone and intravenous pulse methylprednisolone, with a rapid response of reticulocytosis and sustained erythrocytosis. Tiopronin therapy was later initiated and resulted in fever, rash, exacerbation of the liver disease, and positive direct and indirect antiglobulin tests.