[A report of three cases of epulis osteoplastica].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Y Takada.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
CDDP (100 mg bolus) was administered into the body cavity for cancerous pleural effusion and ascites, and its effectiveness and pharmacokinetics were studied. The cases treated consisted of 7 of gastric cancer, 1 of pancreas cancer, 2 of lung cancer and 2 of breast cancer. A decrease in body cavity fluid was observed in all cases. The cases in which treatment was effective were broken down into CR 2 cases, PR 8 cases and NC 2 cases, the efficacy rate being 83%. This procedure produced distinctly fewer side effects than intravenous administration. Disturbance of renal function and G.I. symptoms were negligible, but anemia was often found. The free-CDDP levels in the body cavity fluid remained of over 1.0 microgram/ml after 12 hours and those in plasma remained after 1 hour. Intracavitary administration thus seems an excellent method that enables a drug to act on cancer cells directly at high concentrations over many hours.
A case of pigmented, well differentiated, choroid plexus papilloma is reported. A 45-year-old man came to our hospital complaining of attacks of vertigo and nausea. Skull X-ray films and CT scan demonstrated a calcified tumor in the left middle fossa. Tumor removal was done, and it was found that the tumor occupied the inferior horn of the left lateral ventricle. Histological examination revealed well differentiated choroid plexus papilloma containing various shaped pigment granules in the cytoplasm. The pigment granules in the tumor cells were stained black by Fontana-Masson method for melanin. The stain was negative in a section subjected to oxidative bleach. Granules were PAS-positive and autofluorescence. Therefore, the pigment granules had properties of both melanin and lipofuscin. In the electron microscopic study the ultrastructural appearance of the pigment was similar to that of neuromelanin, but not to that of pre-melanosome of neural crest origin. The pigment in this case seemed to be formed by "melanization" of lipofuscin as Barden's theory of pseudo-peroxidation. There are several case reports of pigmented choroid plexus carcinoma. However, no case of pigmented, well differentiated choroid plexus papilloma has, so far, been reported.
A sensitive enzyme immunoassay was developed for the determination of urokinase in the plasma and urine. Normal human urine contained 2.68 +/- 0.36 u/ml of UK. Gel filtration of the mixture of normal urine resulted in 2 peaks in the profile, one with molecular weight of 32,000 and the other with molecular weight of 22,000. Patients with glomerulonephritis had higher UK levels. Kidneys with minimal changes and mild type or with the inactive phase of systemic lupus erythematosus (SLE) secreted relatively high levels of UK in the urine.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Ureidoglycollate lyase (UGL, EC 4.3.2.3), which catalyses the degradation of S(-)-ureidoglycollate to urea and glyoxylate, was found in the peroxisomes of marine fish (sardine and mackerel) liver. The enzyme highly purified from sardine liver had an Mr of about 121,000, with two identical subunits. When UGL was purified in the presence of 1 mM-EDTA, a much less active form was obtained. It was markedly activated by bivalent metal ions, particularly by Mn2+. The Mn2+-activated enzyme remained active when free Mn2+ was removed by gel filtration on Sephadex G-50, suggesting that UGL may be a metalloenzyme and the activation resulted from the binding of Mn2+ to the apoenzyme. UGL was found to be essential in peroxisomal urate degradation, since allantoate, the intermediate of urate catabolism, was found to be degraded to urea and glyoxylate in a two-step reaction catalysed by allantoicase (EC 3.5.1.5) and UGL via S(-)-ureidoglycollate as an intermediate in fish liver peroxisomes, but not in a one-step reaction as previously believed.
When Glu-plasminogen (plg) was activated by urokinase (UK) in the presence of fibrinogen or fibrin, B beta peptides (B beta 1-42) were released faster from fibrinogen than from fibrin (B beta 15-42). These results were contrary to faster release of B beta 15-42 from fibrin in the UK-activated clotted plasma in comparison to the release of B beta 1-42 from UK-activated plasma. The addition of plasma or lysine-Sepharose pass through fraction to the above system resulted in faster release of B beta peptides from fibrin than fibrinogen. The addition of alpha 2 antiplasmin (alpha 2AP) to the mixture of Glu-pig, UK and fibrinogen or fibrin resulted in faster release of B beta peptides from fibrin than from fibrinogen. These results indicate that fibrin protected plasmin from inactivation by alpha 2AP, leading to cleavage of Arg(42)-Ala(43) bond in beta-chain of fibrin which seems to be less susceptible to plasmin than the same bond in fibrinogen.
When Glu-plasminogen (Glu-plg) was activated by urokinase (UK) in the presence of fibrinogen or fibrinogen plus tranexamic acid (1 mM), or else tranexamic acid (1 mM), the activation as measured by the hydrolysis of S-2251 was enhanced by tranexamic acid or fibrinogen or both. When plasma or clotted plasma was activated by UK in the presence of 1 mM tranexamic acid, fibrinolysis was completely inhibited. When Lys-plg was activated by UK in the presence of tranexamic acid and fibrin or fibrinogen, fibrinolysis was completely inhibited by 1 mM tranexamic acid, but some inhibition of fibrinogenolysis was observed. The release of B beta 15-42 from fibrin in clotted plasma activated by UK was inhibited to some extent by 1 mM tranexamic acid. The release of B beta 15-42 from fibrin after UK-activation of Lys-plg was partly inhibited by tranexamic acid. In conclusion, tranexamic acid in the concentration of 1 mM enhanced amidolysis, but inhibted fibrinolysis measured by the generation of fibrin-degradation products. Fibrinogenolysis and the release of B beta 15-42 from fibrin were partly inhibited.
Polyclonal and three monoclonal anti-tissue plasminogen activator (a-t-PA) antibodies (1:3 C5, 1:3 G5 and 2:2 B10) were characterized by using enzyme immunoassay (EIA) in which beta-D-galactosidase was coupled to a-t-PA antibody. Monoclonal antibodies called 2:2 B10 and 1:3 G5, specific for both one-chain and two-chain t-PA, strongly bound to one-chain t-PA purified from cultured melanoma cell lines, but 1:3 C5 antibody bound weakly to such t-PA. When polyclonal t-PA antibody was used as the first reaction antibody immobilized on silicone pieces, few determinants were available for monoclonal antibody used in the second reaction due to previous interaction of these determinants in the first reaction. When t-PA levels in the plasma were determined, the presence of EDTA enhanced the sensitivity of t-PA determination by the present EIA technique. Plasma concentrations of t-PA were measured to be higher with 2:2 B10 monoclonal antibody than with polyclonal antibody as the first antibody. Tissue-PA was mainly detected in the endothelial cells, but not in the muscular layer of the inferior mesenteric artery when immunochemical technique was used with polyclonal t-PA antibody.
The rate of plasmin-catalyzed Glu-plasminogen to Lys-plasminogen conversion was faster in the presence of fibrin than in its absence when assayed by SDS-polyacrylamide gel electrophoresis followed by quantification of stained bands by densitometer. Experiments with the isozymes Glu-plasminogen I and Glu-plasminogen II showed that plasmin-catalyzed formation of Lys-plasminogen II was especially facilitated in the presence of fibrin.
When human plasma was activated by urokinase (UK) in the presence of thrombin, thrombin plus Ca++, Ca++ or in their absence and the plasmin activity was measured by the hydrolysis of S-2251, plasmin activity was higher in the presence of cross-linked or non cross-linked plasma clot. The results of similar experiments utilizing plasma after severe exercise indicated that the hydrolysis of S-2251 by plasma containing tissue plasminogen activator (t-PA) was also higher in cross-linked or non cross-linked plasma clot. Fibrinolysis was faster in thrombin-induced plasma clot, but was later shown significantly in plasma clot induced by thrombin and Ca++, whereas practically no fibrinogenolysis was shown in plasma. When Glu-plasminogen (Glu-plg) was activated by UK in the presence of cross-linked or non cross-linked fibrin and alpha 2 antiplasmin (alpha 2AP), fibrinolysis was faster in cross-linked fibrin than non cross-linked fibrin in the presence of alpha 2AP. No fibrinogenolysis was shown either. Plasmin activity measured by the hydrolysis of S-2251 was also higher in cross-linked or non cross-linked fibrin than in fibrinogen in the presence of alpha 2AP. These results indicate that enhanced activation of Glu-plg by UK or t-PA in the presence of fibrin was a more significant event than the inactivation of plasmin in the plasma clot or purified clot by alpha 2AP cross-linked to fibrin.
The specificities of extracellular and ribosomal serine proteinase from Bacillus natto, a food microorganism, were investigated. Both proteins have highly restricted and characteristic specificities. With the extracellular serine proteinase, initial cleavage site was observed at Leu15-Tyr16, secondary site at Ser9-His10 and additional cleavage sites at Gln4-His5 and His5-Leu6 in the oxidized insulin B-chain. Hydrolysis of proangiotensin with the extracellular serine proteinase was observed primarily at Phe8-His9 and secondary at Tyr4-Ile5. The extracellular serine proteinase has a Km of 0.08 mM and kcat of 3 S-1 for angiotensin hydrolysis. With the ribosomal proteinase, initial cleavage site of the oxidized insulin B-chain was observed at Leu15-Tyr16 and additional cleavage site at Phe24-Phe25. Hydrolysis of proangiotensin was observed at Tyr4-Ile5 bond with the ribosomal proteinase.
Chronological changes in diffuse brain swelling and brain oedema were studied in repeated CT studies following a closed head injury. These findings were compared with changes in intracranial pressure (ICP). The grades of diffuse brain swelling were classified into mild, moderate and marked according to the CT findings. Planimetry of low density areas of brain oedema was carried out on repeated CT images. Diffuse brain swelling was recognized in 71% of patients shortly after the head injury and subsided within days 3-5. Brain oedema first appeared 24 hours post injury and did not reach its maximum size and distribution before days 5-8. Thus, these two events can be clearly separated. The intracranial pressure reflected the course of the brain swelling and was not very high during the presence of maximum oedema.
Enhanced cisternal drainage was performed following early aneurysm surgery in patients with Hunt and Kosnik grades I-III, to effect continuous wash-out of subarachnoid blood clots and reduce symptomatic vasospasm. Following extensive evacuation of the cisternal blood clots, the Liliequist's membrane was opened extensively and a third ventriculostomy was effected by opening the lamina terminals. The drainage effect was considered as poor, moderate or fair, depending on the average amount of CSF drainage/day. SAH was graded into 0-III depending on the severity of cisternal haematoma in the pre-operative CT. No symptomatic vasospasm occurred in patients with SAH grade I. In SAH grade II + III patients symptomatic vasospasm occurred in 78, 60 and 42% of patients with a poor, moderate and fair drainage effect, respectively. Nine patients who developed symptomatic vasospasm were treated by hypertensive/hypervolemic therapy (HHT). The HHT was effective in 7 patients with fair and moderate CSF drainage and ineffective in 2 patients with poor a drainage effect. It seems, that enhanced post-operative cisternal drainage can reduce the incidence of symptomatic vasospasm and be of benefit to the outcome of early aneurysm surgery.
When human serum was incubated at 45 degrees C for 30 min, C3 and B were converted to C3b and Bb. Molecular weights of purified C3 and B were shown not to change after incubation at 50 degrees C. Spectropolarimetry indicated that the secondary structures of C3 and B changed after incubation at higher temperature. The titration of SH groups in the C3 molecule showed the liberation of an SH group. These results show that the alternative complement pathway is activated at raised temperatures without known activators such as zymosan or lipopolysaccharide (LPS). This may be due to the accelerated interaction of conformationally changed components of the alternative pathway such as C3 and B. Using this system, effects of various substances on the interaction of C3 and B in serum and the purified system were investigated. The addition of arginine and lysine resulted in the inhibition of the conversion of C3 and B in the serum at elevated temperature. Other amino acids such as anionic amino-acids and NaCl did not influence the conversion. In the purified system, only arginine and lysine prevented the conversion of C3 and B, when C3, B and D were incubated in the presence of Mg++ and amino-acids. Since lysine and arginine did not inhibit the enzymatic activity of D, these data suggest that arginine and lysine prevent the interaction of C3 and B in the serum at elevated temperatures.
Four cases of leptomeningeal dissemination of tumors were reported especially focused on their CT findings. These findings consisted of hydrocephalus and contrast enhancement of the quadrigeminal cistern, basal cisterns, Sylvian fissures, cerebro-cerebellar cortical sulci and ventricular wall. Although autopsy of 3 cases revealed diffuse subarachnoid tumor growth in the brain and spinal cord, not all lesions were demonstrated by CT. Therefore, CT findings varied greatly depending on case and course of the disease. Definite diagnosis of this disease could be done by CSF cytology.