Granulocytic sarcoma of the jaw.
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Biomedical subjects
Publications and source records attributed to M Takagi.
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The authors have carried out the laboratory and clinical studies of cefotetan (CTT), and obtained the following results. The antibacterial activities of CTT were measured by the plate dilution method against the clinical isolates of S. aureus, E. coli, K. pneumoniae, S. marcescens and Salmonella sp. The susceptibility distribution of S. aureus to CTT was at concentration of 6.25-12.5 micrograms/ml and the peak of that was obtained at 6.25 micrograms/ml with an inoculum size of 10(6) cells/ml. And the peaks of susceptibility distribution of E. coli and K. pneumoniae to CTT were obtained at less than 0.1 microgram/ml respectively, and that of S. marcescens was obtained at 6.25-12.5 micrograms/ml with an inoculum size of 10(6) cells/ml. The growth of all strains of Salmonella sp. was inhibited at concentration of less than 0.1 microgram/ml. As for pharmacokinetic study, CTT was given by intravenous bolus injection and drip infusion for 30 minutes at a single dose of 20 mg/kg. After intravenous bolus injection of 20 mg/kg of CTT, the mean peak serum level was 175.0 +/- 7.0 micrograms/ml at 15 minutes after injection, and half-life time was 3.53 hours. After 30 minutes drip infusion of 20 mg/kg of CTT, the mean serum concentration was 106.0 +/- 6.0 micrograms/ml at end of infusion, half-life time was 2.41 hours. The mean urinary excretion rates were 49.4% and 64.2% up to 8 hours after drip and bolus injection of 20 mg/kg of CTT, respectively. CTT was given 15 cases with bacterial infection. Daily doses of CTT were from 15.0 to 107.0 mg/kg. Clinical results obtained were excellent and good responses in 12 of 15 cases (80.0%). No side effects were obtained except for 2 cases with elevation of GOT and GPT, and 1 case with eosinophilia.
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The authors have carried out the laboratory and clinical studies of cefpiramide (CPM). The results were as follows; The sensitivity was estimated by plate dilution method on 27 strains of S. aureus and P. aeruginosa, 26 strains of E. coli, 25 strains of K. pneumoniae and 13 strains of Proteus sp. isolated from patients. The distribution of S. aureus was 0.78 approximately 6.25 micrograms/ml and the peak of distribution was 1.56 micrograms/ml. The distribution of E. coli was 0.78 approximately 50 micrograms/ml and the peak of distribution was 0.78 and 25 micrograms/ml. The growth of 24% of K. pneumoniae was not inhibited at concentration of more than 50 micrograms/ml. The distribution of Proteus sp. was 6.25 approximately 100 micrograms/ml. The growth of 77.8% of P. aeruginosa was inhibited at concentration of less than 3.13 micrograms/ml. CPM was given by intravenous administration for 5 minutes and drip infusion for 30 minutes at a single dose of 20 mg/kg of CPM to each 2 children respectively. After intravenous administration of CPM, the mean peak serum level was 200.5 +/- 37.5 micrograms/ml at 15 minutes, 44.3 +/- 0.9 micrograms/ml at 6 hours, 19.9 +/- 0.3 micrograms/ml at 12 hours respectively. Half-life time was 4.2 hours. After drip infusion of CPM, the mean peak serum level was 150.5 +/- 14.5 micrograms/ml at end of infusion, 23.6 +/- 3.3 micrograms/ml at 6 hours and 8.2 +/- 2.0 micrograms/ml at 12 hours respectively. Half-life time was 3.8 hours. The mean urinary excretion rate was 23.15%, 28.2% up to 12 hours after intravenous administration and drip infusion respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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The introduction of trimodal combination therapy (surgery + radiation + intraarterial infusion) for maxillary carcinoma resulted in a change in the sites of recurrence and no satisfactory improvement in the local control rate. To examine the cause of these phenomena, external carotid angiography was performed on 51 patients prior to the start of the therapy and the results of the treatment were studied. Angiographic findings indicated that maxillary carcinoma is fed not only by the maxillary artery, but also by the internal carotid, facial, transverse facial and other arteries from the external carotid artery. The multiplicity of feeders causes irregular distribution of the intraarterially infused antimetabolites. Irregular and local low distribution of antimetabolites may well bring about the high rate of recurrence. The results of intraarterial transcatheter TC-99m-MAA injection were also in accord with the angiographic findings.
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Complex carbohydrates in eosinophils from human, rabbit, and rat marrow were identified and localized by cytochemical and radioautographic methods. The high iron diamine-thiocarbohydrazide-silver proteinate (HID-TCH-SP), low iron diamine (LID)-TCH-SP, and periodate (PA)-TCH-SP methods were used for the localization of sulfate, sulfate and carboxyl, and vicinal glycol- containing complex carbohydrates, respectively. Golgi vesicles and small precursor granules (0.2-0.4 micrometer in diameter) demonstrated strong HID-TCH-SP staining and labeled intensely after a 10-minute pulse with 35SO4(2). Crystalloid-free or immature specific granules (0.5-0.9 micrometers in diameter) labeled heavily after a 60-minute incubation and 60-minute chase with 35SO4(2). Immature granules were graded according to their HID-TCH-SP staining. Type I granules demonstrated strong rim staining and similar or somewhat less central staining, whereas type 2 granules only demonstrated rim staining, and type 3 granules lacked staining. Fully mature crystalloid-containing granules lacked staining. LID-TCH-SP similarly stained the HID-positive sulfated material in cytoplasmic granules. PA-TCH-SP stained some Golgi vesicles and diffusely stained all precursor granules and type 1 granules. Weaker staining was observed in type 2 granules and staining was very weak or absent in type 3 and crystalloid-containing granules. In early eosinophils, tubulovesicular structures (TVS) were observed rosetting and contacting precursor and type 1 granules. These TVS contained material with strong PA-TCH-SP staining but lacked HID-TCH-SP or LID-TCH-SP-reactive acidic glycoconjugates. Flattened Golgi saccules or early eosinophils stained weakly or not at all with the PA-TCH-SP method. Small granules and TVS in late (bilobed) eosinophils displayed PA-TCH-SP reactivity and lacked HID-TCH-SP staining but differed from TVS in early eosinophils in that they were not associated as rosettes with specific granules. These results indicate that sulfated and vicinal glycol-containing complex carbohydrates are differently disturbed in immature specific granules of eosinophils and presumably become masked to staining as the granule matures.
In the rat kidney the presence of the kallikrein-like pro-phe-argnaphthylester esterase activity was demonstrated by a simultaneous coupling azo dye method. The enzyme was identified as a serine-protease because it was inhibited by preincubation with diisopropyl-fluorophosphate and unaffected by sodium iodoacetate. Since kallikrein is a serine-protease and prophe-arg-naphthylester is a synthetic and sensitive substrate for kallikrein, the enzyme activity revealed by this method was considered to represent kallikrein, although non-kallikrein esterase activity is not totally excluded. The enzyme activity was localized mainly in the outer stripe of the outer medulla, with focal extensions primarily only in the lower half of the cortex corresponding to the medullary rays.
Pyridoxal(5')diphospho(1)-alpha-D-glucose was used to reconstitute glycogen phosphorylase beta (1,4-alpha-D-glucan:orthophosphate alpha-D-glucosyltransferase, EC 2.4.1.1) from rabbit muscle, replacing the natural pyridoxal 5'-phosphate coenzyme. Incubation of the reconstituted enzyme alone resulted in the gradual cleavage of the synthetic cofactor to pyridoxal 5'-phosphate, which caused slow reactivation of the enzyme. The addition of maltopentaose or glycogen altered the mode of cleavage; the cofactor was rapidly decomposed to pyridoxal 5'-diphosphate. The radioactive glucose moiety released from pyridoxal(5')diphospho(1)-alpha-D-[14C]glucose was incorporated into the outer chain of glycogen, forming an alpha-1,4-glucosidic linkage. These results show that the glucosyl transfer reaction discovered mimics the normal catalysis of this enzyme, and they strongly support the catalytic mechanism in which the coenzyme phosphate acts as a catalyst by direct interaction with the phosphate of the substrate, forming the pyrophosphate-like transition intermediate.
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The present study has applied the low iron diamine (LID) method at the ultrastructural level to demonstrate acid glycoconjugates. We have examined rat epiphyseal cartilage, human bone marrow, rat tracheal glands, and mouse sublingual glands stained with LID prior to embedment. The LID staining appeared to require postosmication for adequate visualization at the electron microscope level. Thiocarbohydrazide-silver proteinate (TCH-SP) staining of thin sections variably enhanced LID reactive sites. LID-TCH-SP stained carboxyl and sulfate groups of glycosaminoglycans in the extracellular cartilage matrix, secretory granules, and expanded Golgi saccules of chondrocytes. In human bone marrow, LID-TCH-SP variably stained the cytoplasmic granules, known to contain sulfated glycosaminoglycans, and the external surface of the plasma membrane of leukocytes. Moderately strong LID staining was observed in secretory granules in mucous tubules of rat tracheal glands, known to contain sulfated glycoproteins, and in acinar cells of mouse sublingual glands, known to contain a sialoglycoprotein. The lack of sulfated glycoconjugates in acinar cells of the mouse sublingual gland was confirmed by their failure to stain with the high iron diamine method. Thus these studies indicate that the LID and LID-TCH-SP methods are useful for the ultrastructural localization of carboxylated and sulfated glycoconjugates in extracellular and intracellular sites.
In order to clarify the risk factors for stroke from an epidemiological viewpoint, 314 men (aged 50-79) in the fishing village of Ushibuka were evaluated over an 8-year period (1970-1978) by means of multivariate analysis. At the systematic re-examination in 1970, the following 11 variables were determined: age, systolic blood pressure, electrocardiographic (ECG) abnormalities, serum cholesterol, serum triglyceride, serum alpha-lipoprotein fraction, serum albumin, serum uric acid, drinking habits, smoking habits and body mass index. Thirty men experienced stroke during the 8-year period. The mean value of age, systolic blood pressure and serum uric acid were significantly higher in men who experienced stroke, while serum cholesterol, triglyceride, alpha-lipoprotein fraction and albumin were not seen as statistically significant. The high level of serum uric acid correlated with the high incidence of stroke. According to stepwise discriminant analysis of the 11 variables. ECG abnormalities, systolic blood pressure and serum uric acid discriminated 73.9% of the men who experienced stroke. In conclusion, a high serum uric acid concentration is noted to be an important risk factor for stroke in the fishing village of Ushibuka where high intake of fish protein is common.
Twenty-eight patients with esophageal carcinoma and one or more separate primary carcinomas in other organs were treated from 1960 to 1980, representing 8.3 per cent of the 339 cases of esophageal carcinoma observed during this period. The most frequent sites of the additional tumors were the oral cavity and pharynx (11 patients) and the stomach (12 patients). Awareness of the frequent combination of esophageal carcinoma with other primary neoplasms in the sites mentioned may lead to the detection of small curable malignant tumors.