[A case of lymphoblastic crisis in chronic myelogenous leukemia showing pre-T cell phenotype].
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Biomedical subjects
Publications and source records attributed to T Goto.
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A case of chondromyxoid fibroma of the skull is reported. A 20-year-old boy visited our clinic on December, 1982 because of a recurrent forehead tumor. He had a 4 X 4 X 1.5 cm tumor on the right side of forehead and a 3 X 3 X 0.5 cm tumor on the left. Neurological examination showed no abnormalities. Skull X-ray film showed a large round radiolucent area with clear sclerotic margin in the frontal bone and right orbit. Right carotid angiogram showed marked posterior displacement of the anterior cerebral artery, but no tumor stain. Plain CT scan showed a mass with iso to low density area in the frontal region. It was markedly and irregularly enhanced with contrast media. Surgery was performed entirely in the epidural space, and the tumor was completely removed. The post-operative clinical course was uneventful. Histologically, the three components of chondroid, myxomatous and fibrous tissues in this tumor led to the diagnosis of "chondromyxoid fibroma."
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The transfer of cefoperazone into exudates from excoriated skin wounds was studied in 13 adolescent and adult patients. Subjects were given an intravenous bolus injection of 50 mg/kg of body weight. Concentrations of cefoperazone in serum and in exudate fluids were determined by bioassay using Escherichia coli as the test organism. Mean (+/- SD) cefoperazone concentration in serum reached 333.3 +/- 103.3 micrograms/ml 30 minutes after the injection and decreased to 16.4 +/- 5.7 micrograms/ml eight hours after the injection. In exudate fluids, the peak value was 52.7 +/- 22.1 micrograms/ml at one hour. Eight hours after the injection, the mean concentration in the exudate was 10.7 +/- 7.2 micrograms/ml, which was considerably above the minimum inhibitory concentrations for important pathogens.
Clinical study on cefpiramide (CPM, SM-1652), a new cephalosporin antibiotic, was carried out and the following results were obtained. CPM was intravenously administrated at a daily dose of 2 g to 8 cases including 2 cases with intrauterine infection, 3 cases with adnexitis, 2 cases with intrapelvic infection and 1 case with external genital infection. All cases responded to the drug, and marked response was seen in 2 cases, moderate response in 6 cases. Neither side effects nor abnormal values in clinical laboratory findings attributable to the drug were seen.
Production of bityrosine (2,2'-dihydroxy-5,5'-bis (beta-carboxy-beta-aminoetyl)-diphenyl) was established in horseradish peroxidase-H2O2-tyrosine system at pH 9.2 by mass and NMR spectrometries.
The ATP-independent type I and the ATP-dependent type II DNA topoisomerase of the yeast Saccharomyces cerevisiae have been purified to near homogeneity, and the purification procedures are reported. Both purified topoisomerases are single subunit enzymes with monomer weights of Mr = 90,000 and 150,000 for the type I and type II enzyme, respectively. Sedimentation and gel filtration data suggest that the type I enzyme is monomeric and the type II enzyme is dimeric. Similar to other purified eukaryotic topoisomerases, the yeast type I enzyme does not require a divalent cation for activity, but is stimulated 10-20-fold in the presence of 7-10 mM Mg(II) or Ca(II). Mn(II) is about 25% as efficient as Mg(II) in this stimulation but Co(II) is inhibitory. The yeast type II topoisomerase has an absolute requirement for a divalent cation: Mg(II) is the most effective, whereas Mn(II), Ca(II), or Co(II) supports the reaction to a lesser extent. The type II enzyme also requires ATP or dATP; the nonhydrolyzable ATP analogues adenylyl imidodiphosphate and adenylyl (beta,gamma-methylene)diphosphonate are potent inhibitors. Both yeast topoisomerases are completely inhibited by N-ethylmaleimide at 0.5 mM. In addition, the type II enzyme, but not the type I enzyme, is inhibited to various extents by coumermycin, ethidium, and berenil. Both topoisomerases are nuclear enzymes; no topoisomerase specific to mitochondria has been detected.
A method for measurement of renin concentration (PRC) in human plasma has been developed and validated experimentally and theoretically. Like most of the previous methods, the present method is based on a radioimmunoassay of angiotensin I generated during incubation of plasma with an excess of renin substrate. In the present study we used, as the substrate, sheep angiotensinogen partially purified from anephric sheep plasma by ammonium sulfate fractionation and pepstatin-aminohexyl-agarose chromatography. The advantage of using sheep substrate is that it has an exceptionally high affinity for human renin. The partially purified substrate, which contained no detectable renin activity, improved the sensitivity, allowing quantification of renin in low-renin plasma. Possible interfering influences of plasma proteins on the radioimmunoassay were eliminated by the introduction of a simple deproteinization step. For determination of total renin concentration (TRC), inactive renin was activated by exposing plasma to low pH or trypsin. Normal values of PRC and TRC after careful selection of assay conditions were 2.9 +/- 0.4 and 33.9 +/- 6.1 ng angiotensin I X ml-1 X h-1, respectively. As an illustrative example of usefulness of the assay, PRC determination of a patient with a ectopic renin-secreting tumor is presented.
The ultrastructure of photoreceptors in two species of chaetognaths, Sagitta crassa and Spadella schizoptera, was studied by electron microscopy using a goniometer specimen stage as well as by freeze-fracture techniques. In contrast to earlier descriptions, the photoreceptor is made up of a stack of lamellae with pores. The lamellae, each 30-45 nm in thickness, are piled one on top one another at intervals of 10-20 nm. The lamellar surface is often perpendicular to the incident light. The pores are 35-55 nm in diameter and arranged in an orderly square lattice with a center-to-center distance of 80-95 nm. These perforated lamellar structures, resembling annulate lamellae, are entirely new as photoreceptive structures.
The gene TOP2 encoding yeast topoisomerase II has been cloned by immunological screening of a yeast genomic library constructed in the phage lambda expression vector, lambda gt11. The ends of the message encoded by the cloned DNA fragment were delimited by the Berk and Sharp procedure (S1 nuclease mapping) for the 5' end and mapping of the polyA tail portion of a cDNA fragment for the 3' end. The predicted size of the message agrees with the length of the message as determined by Northern blot hybridization analysis. The identity of the gene was confirmed by expressing the gene in E. coli from the E. coli promoter lac UV5 to give catalytically active yeast DNA topoisomerase II. Disruption of one copy of the gene in a diploid yeast creates a recessive lethal mutation, indicating that the single DNA topoisomerase II gene of yeast has an essential function.
This is a report concerning 13 autistic children who have been followed up from their early infancy to adulthood. Some intake variables, such as speech development at the age of 5, were correlated with the outcome status. As a result, we showed that a higher level of speech development at age 5 did not necessarily lead to a better outcome in social adaptability. We showed also that any of the variables we examined, such as the presence of brain organic abnormality, the duration of schooling and the duration of medical treatment, were not factors in determining a good or poor prognosis. We concluded that a rather poor outcome seen in our subjects might be due to the particular situation in Japan throughout this study period, and not a reflection of the real natural history of early infantile autism.
The distribution, density, and histochemical subtype of mast cells were studied in the respiratory tract of rats with bleomycin-induced pulmonary fibrosis. In normal rats, mast cell densities were highest in the trachea and lowest in the bronchus and parenchyma. Two histochemically distinct mast cell populations were identified in the mucosa adjacent to the tracheal cartilage, but elsewhere only a single population of typical connective tissuelike mast cells was found. After intratracheally administered bleomycin, lung histamine levels (micrograms/g wet weight) increased as much as 14-fold by Day 50. Pulmonary mast cell changes were present early in the fibrotic process, and by Day 14 the mast cell density in the parenchyma was 10 times normal. These parenchymal mast cells were histochemically of the connective tissue type. Thus, pronounced mast cell hyperplasia occurs during the evolution of experimental pulmonary fibrosis. This model provides a powerful tool to study pulmonary mast cells and to identify their role in fibrotic disease.
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The present study was designed to investigate the effects of the Ca-antagonist, nifedipine, on receptor-mediated renal vascular responses to vasoconstrictors (angiotensin II, norepinephrine and vasopressin) and vasodilators (bradykinin and prostaglandin E2). Renal blood flow was estimated by noncannulating electromagnetic flowmetry in anesthetized rabbits. Vasoactive substances were infused directly into the renal artery. After the intravenous administration of nifedipine (50 micrograms/kg), decreases in renal blood flow in response to angiotensin II infused at rates of 2.5, 5 and 10 ng/kg/min were attenuated by 64% (p less than 0.01), 45% (p less than 0.05) and 42% (p less than 0.05), respectively. Decreases in renal blood flow in response to vasopressin infused at rates of 10, 20 and 50 mU/kg/min were also attenuated by nifedipine, 50% (p less than 0.05), 57% (p less than 0.05) and 38% (p less than 0.05), respectively. However, renal vasoconstrictor responses to norepinephrine (25, 50 and 100 ng/kg/min) did not change significantly after the administration of nifedipine. Increases in renal blood flow induced by the intrarenal infusion of bradykinin (2.5, 5 and 10 ng/kg/min) and prostaglandin E2 (20, 50 and 100 ng/kg/min) were not affected by nifedipine. These results suggest that receptor-mediated vasoconstrictor responses of the renal vascular bed to angiotensin II and vasopressin are produced mainly by Ca++ influx but that of norepinephrine is not. Furthermore, it is confirmed that the renal vasodilator effect of bradykinin and prostaglandin E2 is not altered by nifedipine in anesthetized rabbits.
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Responses in urinary kallikrein and kinin excretion and systolic blood pressure to MK 421, SA 446 or captopril were studied in normotensive rats fed on a regular or a low sodium diet to assess the role of renal kallikrein-kinin system in their hypotensive effect. MK 421, SA 446 or captopril were infused at a rate of 6 mg/kg/day by osmotic minipump implanted intraperitoneally for up to 6 days. The magnitude of fall in systolic blood pressure was greater on a low sodium diet when compared to on a regular diet, whereas the pattern of the fall was similar on both diets. The magnitude of falls in plasma angiotensin II and aldosterone concentration induced by MK 421, SA 446 and captopril was not significantly different between both regular and low sodium diets. Urinary kallikrein and kinin excretion and sodium excretion were increased during infusion of MK 421, SA 446 or captopril on a low sodium diet, however any significant changes were not found in each of them on a regular diet. The present results suggest that on a low sodium diet the augmented hypotensive response to angiotensin converting enzyme inhibitors in the rats might be due to the enhanced renal kallikrein-kinin system in addition to suppressed renin-angiotensin system.