[Blood grouping and crossmatching].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Tamura.
Explore the source record for details and available documents.
In May, 1946, one hundred two children were detected to have inoculated tuberculosis on their arms among the primary school children in Hyogo prefecture who had received anti-typhoid vaccine on the same spot. Of the 102 patients in the past 25 years, 26 (25%) developed secondary tuberculosis. One of these inoculated tuberculosis patients, 53-years-old woman, was admitted for pleuritis tuberculosa in September, 1989. She had not been included in secondary tuberculosis group. The relationship between her past inoculated tuberculosis and the pleurisy has not been proved. However, this pleurisy would have been developed in case it was caused by the past tuberculosis after 43 years.
A 23-year-old man was admitted with progressively disturbed vision and easy fatigability. CT scans demonstrated an enhanced mass in the sellar region. Physical and endocrinological examinations revealed atrophy of both optic nerves, temporal field cuts in both eyes, and panhypopituitarism. Concentrations of human chorionic gonadotropin (HCG) in the serum and cerebrospinal fluid were 12 and 33IU/L, respectively. On November 11, 1987, the tumor was partially removed using the transsphenoidal approach. The histological diagnosis was germinoma with syncytiotrophoblastic giant cells. Following postoperative craniospinal irradiation (whole brain, 30Gy; local, 18Gy; spinal canal 28Gy), CT scans showed no residual tumor and the HCG levels decreased until they were undetectable. Eighteen months later, the patient complained of abdominal pain. His serum HCG level had increased to 2,554 IU/L. CT scans of the abdomen revealed multiple low density areas in the liver. Chest X-ray was negative. A Ga scintigram disclosed only liver metastasis. Administration of a chemotherapy was started on June 26, 1989. Cisplatin and etoposide in doses of 20mg and 40mg respectively were given for 5 consecutive days in one course. Following four courses of the combined chemotherapy, the tumor entirely disappeared on CT scans and the HCG level returned to normal. The patient is now able to work well without evidence of recurrence. Multiple liver metastases of an intracranial germ cell tumor had been fatal in previous reports. This may be the first case with liver metastases in which the victim is still alive. The present case indicates that combined chemotherapy with cisplatin and etoposide is effective for extraneural metastases of an intracranial germ cell tumor.
N-isopropyl-I-123-p-iodoamphetamine (123I-IMP) is taken up by the capillary endothelial cells during the first pulmonary pass and is released from the lung. To evaluate the effect of the 123I-IMP retention on diffuse lung disease, we studied prolonged 123I-IMP clearance from lung in 5 non-smoking control volunteers and 15 patients with various diffuse lung diseases. The time-activity curve for 60 min after the injection of 111 MBq of 123I-IMP was described as follows: C(t) = A1e-k1t + A2e-k1t (A1, A2: intercepts; K1, K2: slopes of the exponential components). 123I-IMP clearance was delayed in the patient group and K2 was significantly lower. There was a significant correlation between K2 and Ga-computer activity index on the 67Ga scintigraphy in the patient group. K2 was also correlated with %Dlco on the pulmonary function test. Our study suggests that the delayed clearance and retention of 123I-IMP in the diseased lung are influenced by the pathological activity in the lung lesion.
An endogenous inhibitor of monoamine oxidase (MAO) was separated by gel-filtration from 105,000 g supernate of T4-treated rat liver cytosol. The inhibition by this inhibitor was concentration-dependent and more potent for A-form MAO than for B-form MAO. The mode of inhibition was competitive either with 5-hydroxytryptamine or beta-phenylethylamine. The molecular weight of this inhibitor was estimated to be 600-700 by gel filtration. The pI value was determined to be 3.0 by isoelectric focusing. This inhibitor was proved to be heat-stable and resistant to protease treatment. MAO inhibition activity was much lower in the cytosol of thyroidectomized, non-T4-treated rats than T4-treated rats, suggesting that this inhibitor is induced by thyroid hormone T4. MAO activity in rat liver might be regulated by the level of this inhibitor.
The effect of Ca2+ or Mg2+ on cytochrome b5 reduction by porcine liver microsomes was examined using trypsin-solubilized cytochrome b5 as a substrate. The reduction of exogenous cytochrome b5 by microsomes was low at 1.2 microM cytochrome b5 (3.9 or 2.7 nmol/min/mg protein, respectively, with NADH or NADPH). The addition of CaCl2 greatly enhanced either NADH-dependent or NADPH-dependent cytochrome b5 reduction. At 2 mM CaCl2, the reduction rate was increased to 23- or 18-fold of control, respectively with NADH or NADPH. The concentration for half-maximal effect (EC50) was 0.5 or 0.6 mM in the NADH or NADPH systems, respectively. MgCl2 also stimulated cytochrome b5 reduction with a EC50 value of 1.0 mM in the NADH system or 0.6 mM in the NADPH system. The comparison with the result with KCl indicated that the activation by CaCl2 or MgCl2 is caused mainly by their divalent cation moiety. The Km value for cytochrome b5 was decreased and the Vmax was increased by calcium with either the NADH- or the NADPH-dependent system. NADH-ferricyanide reductase activity was not affected by calcium, but NADPH-ferricyanide reductase activity was stimulated as well as NADPH-cytochrome c reductase activity. In the presence of Triton X-100, divalent cations were inhibitory in NADH-dependent cytochrome b5 reduction, and in contrast, stimulative in NADPH-dependent reaction. These findings suggest that the activation of cytochrome b5 reduction by divalent cations in the NADH system is mainly due to an increasing accessibility of the substrate, and in the NADPH system, in addition to this, a direct effect of divalent cations on NADPH-cytochrome P450 reductase is also involved.
Administration of human granulocyte colony-stimulating factor (hG-CSF) to mice with cyclophosphamide (CPA)-induced neutropenia for 4 consecutive days from the day after the CPA dosing (100 mg/kg) resulted in a dose-dependent increase in the peripheral blood neutrophil count 6 hours after the final hG-CSF injection. Within the hG-CSF dose range of 0.1 to 10 micrograms per mouse per day, there was a strong linear relationship (r greater than .9) between the logarithm of the dose and the peripheral blood neutrophil count in the treated mice. Using the same hG-CSF preparation, 38 experiments indicated that the regression lines are highly reproducible. Such an association never occurred with intact mice, and 100 mg/kg of CPA induced the highest response to hG-CSF. This linear relationship between the two variables allows us to determine the biologic potency of a test hG-CSF preparation relative to a reference standard using a parallel line assay, with a coefficient of precision of around .2. When assayed by this bioassay procedure, which we have termed CPA-mouse assay, natural hG-CSF and recombinant hG-CSF (produced by Chinese hamster ovary cells) were nearly equipotent in specific biologic activity. These results confirm the CPA-mouse assay as an especially useful assay method for quantifying the in vivo activity of hG-CSF.
A mixed glioma and sarcoma in a 3-month-old infant is presented as a rare case of gliosarcoma with a good response to treatment. This congenital case is quite different from those in adults: the tumor cells were mainly composed of sarcomatous elements; glial components were not anaplastic without obvious endothelial hyperplasia, but presented as reticulin-free islands, mimicking a reactive glioma in a sarcoma. It may be termed "sarcoglioma" to distinguish from a classic gliosarcoma. The origin of the rare mixed tumor may be related to a dysgenesis of both mesenchymal and glial elements.
An immunohistochemical study was performed to observe cellular proliferation on the surface of implanted intraocular lenses (IOLs) in rabbit eyes. Rabbits were killed at intervals of 3 days and 1, 2, and 4 weeks after the operation. The IOLs were removed and examined by an immunoperoxidase staining method using antifibronectin (anti-FN) antibodies. The FN immunoreactivity was detected in macrophages and giant cells attached to the IOL surface. Prominent staining was observed in these cells 1 week after the operation, and staining for FN was less intense in the specimens obtained 2 and 4 weeks after implantation. These findings suggest that FN is produced by macrophages and giant cells on the IOL surface and may play an important role in cellular adhesion and motility. FN immunoreactivity decreased with time, which might be related to cellular activity.
The prognosis of recurrent IV-ventricle ependymoma in children is poor. Three cases of recurrent ependymoma were treated with combination chemotherapy using cis-diamine dichloro platinum (II) (CDDP) and methyl-6-(3-(2-chloroethyl)-3-nitrosoureido)-6-deoxy-alpha-D-glucopyrano side (MCNU). The patients were 2-, 3-, and 6-year-old boys. The interval between the first operation with irradiation and recurrence was 1 year and 5 months to 2 years. Two cases showed a recurrence at the original site; in the other case, a right sylvian tumor deposit was found via computed tomography. The therapeutic regiment for recurrent ependymomas was as follows: (1) the tumor was debulked if possible; (2) additional local irradiation of 30 Gy was administered; (3) combined treatment of 100 mg/m2 CDDP and 80 mg/m2 MCNU over 24 h was given 5 times with an interval of 6 weeks between treatments. The patients tolerated the therapy well with only mild side effects. Remission lasted 1 year in two patients and has lasted for 8 months in one.
Seventy-five formalin-fixed and 18 alcohol-fixed pituitary adenomas were studied immunohistochemically using antibodies to keratin, vimentin, neurofilaments (NFs), glial fibrillary acidic protein, desmin, actin, S-100 protein and a variety of pituitary hormones. The pituitary adenoma cells were positive for keratin, vimentin and NFs (68 kDa and 160 kDa) and in a few instances there was co-expression of these three types of intermediate filaments (IMFs). The pattern of keratin-specific staining showed diffuse cytoplasmic or patchy paranuclear reactivity and of NF- or vimentin-specific staining showed fibrillar or patchy paranuclear reactivity. The patchy staining seemed to decorate the fibrous body. There was no correlation between the distribution of IMFs and pituitary hormones in pituitary adenomas except that melanocyte-stimulating-hormone-positive reactivity was limited to the NF-positive adenomas. The pattern of IMF staining did not depend on hormone production in adenomas.
An influenza A subtype cross-reactive CTL clone (A-11) was established following stimulation of A/PR/8 virus-immune spleen cells of Balb/C (H-2d) mice. This T cell clone lysed target cells infected with influenza viruses of the H1, H2, or H3 subtypes, and recognizes a conserved epitope on the NS1 protein. The clone is restricted by the H-2Ld allele. Adoptive transfer of A-11 significantly reduced virus titers in the lungs of mice infected with influenza A viruses of the H1, H2, or H3 subtypes. These results suggest that the conserved epitope on NS1 which is recognized by A-11 may be a useful component to consider for inclusion in experimental cross-reactive influenza vaccines.
Explore the source record for details and available documents.
The major cellular components on intraocular lenses experimentally implanted in the rabbit eye and in the mouse peritoneal space were examined. They consisted of macrophages and their metamorphosed epithelioid cells with occasional formations of foreign-body giant cells from the fusion of the macrophage-related cells. Lymphocytes, individually and in clusters, were also seen on the lenses implanted in the mouse peritoneal space but rarely on those implanted in the rabbit eye. Macrophages, epithelioid cells, and giant cells exhibited active phagocytosis on the implanted intraocular lenses. These cells phagocytized not only minor foreign particles such as artificially fed latex or carbon colloids but also living cells including erythrocytes, leukocytes, and lymphocytes. The nuclear pattern of the giant cell formation process initially assumed a centrally located nuclear distribution of a foreign-body giant cell type, and then a peripherally located Langhans type distribution when the number of nuclei reached about five in both the mouse peritoneal space and the rabbit eye chamber. Ultra-large giant cells containing a number of nuclei, however, were only observed on lenses implanted in the rabbit eye, demonstrating a difference between the two environments.
Three-piece poly(methyl methacrylate) intraocular lenses (IOLs) were implanted in rabbit eyes with and without lens extraction to examine the cellular response on the IOL surface without the effects of the residual lens cortex. Each rabbit had extracapsular lens extraction (ECCE) with IOL implantation in the posterior chamber of one eye. In the second eye, the IOL was implanted in the anterior chamber without lens extraction. The lenses were removed and studied with light microscopy and scanning electron microscopy one week after surgery. Light microscopic findings revealed a similar cellular response on the surface of the IOLs in both groups. Scanning electron microscopy suggested that the cellular adhesiveness on the IOL surface in the eyes without lens extraction was weaker than in the eyes that had ECCE. Cells on the IOLs in the eyes without lens extraction were flatter and had membranous pseudopodia. It appears that the cells on the IOL surface were caused by a foreign body reaction and that their adhesiveness to the IOL was affected by residual lens cortex.
A method of separating neutrophils from the peripheral blood of rats with 95% purity is described. To determine the role of antigenic stimulation in neutrophil function, neutrophils from germ-free (GF) rats were compared with those of conventional (CV) rats. Neutrophil counts were lower in GF rats but the total number of monocytic cells was the same. To measure phagocytic killing, superoxide anion production was determined and found to be lower in GF neutrophils (2.1 +/- 0.5 nmol/min/10(6) cells) than in CV neutrophils (9.5 +/- 2.9 nmol/min/10(6) cells). Myeloperoxidase activity was found to be twofold higher in GF neutrophils. When a recombinant human granulocyte colony-stimulating factor (rhG-CSF) was intravenously injected, superoxide production did not change in either GF or CV neutrophils, but the myeloperoxidase activity of neutrophils in both types of rats decreased. rhG-CSF increased the number of neutrophils in both GF (10-fold) and CV rats (three- to fourfold).
(1) Continuous intravenous infusion (2-10 micrograms/kg/min) of nitroglycerin (TNG) was administered to 20 neonates consisting of 17 with refractory congestive heart failure and 3 with PFC (Persistent Fetal Circulation). (2) At doses of 2-4 micrograms/kg/min, there were no significant changes in heart rate or systemic blood pressure. (3) At doses of 2-4 micrograms/kg/min, the CVP was significantly reduced and urinary output increased. (4) Echocardiograms revealed a significant decrease in LVS at 4-5 micrograms/kg/min. In addition, the EF and cardiac output were significantly increased at 2-5 micrograms/kg/min. (5) The right ventricle systolic time interval (STI) was reduced significantly at 2 micrograms/kg/min. The left ventricle STI was not reduced below doses of 4 micrograms/kg/min. (6) In the dose range 2-5 micrograms/kg/min, TNG is an effective and safe vasodilator in the treatment of refractory congestive heart failure or PFC in neonates.
We used CT to make a quantitative evaluation of the pontine volumes of 55 patients with adult-onset cerebellar degeneration and compared the results with their clinical records. Patients with pontine atrophy showed significantly more autonomic dysfunction and extrapyramidal signs; their other clinical features did not differ from patients without pontine atrophy. After dividing the patients into 2 groups, those with and without autonomic dysfunction or extrapyramidal signs, we found that those with these manifestations also had pontine atrophy, a later onset and shorter duration of the disease, and impairment of higher brain functions. The group without these manifestations had relatively normal pontine volume, a greater familial tendency for cerebellar degeneration, and longer duration of the disease. Our results suggest that quantitative volume evaluation of the pons by CT is important for the clinical categorization of cerebellar degeneration.