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Biomedical subjects

M Yagisawa

Publications and source records attributed to M Yagisawa.

At least 19 recordsLinked to original sources

[A case of sleep apnea syndrome due to a nasopharyngeal tumor].

Obstructive Sleep Apnea Syndrome (OSAS) is children is commonly caused by upper airway obstruction, such as that caused by adeno-tonsillar hypertrophy. We report a rare case of SAS due to a nasopharyngeal tumor. The patient was a 10-year-old boy who complained of snoring and sleep apnea. The tumor was found in the nasopharynx and mesopharyngeal space. We diagnosed this case as OSAS by overnight sleep study (Apnea Hypopnea Index: AHI = 19.67). The tumor was removed under general anesthesia. Histopathology revealed features of nasopharyngeal angiofibroma. After removal of the tumor, his symptoms resolved completely. A follow-up overnight sleep study confirmed resolution of OSAS. At the last follow up, conducted 17 months after the operation there were no signs of tumor recurrence.

Angiofibroma

Activation of human monocyte functions by tumor necrosis factor: rapid priming for enhanced release of superoxide and erythrophagocytosis, but no direct triggering of superoxide release.

Tumor necrosis factor (TNF), like granulocyte-macrophage colony-stimul ating factor (GM-CSF), rapidly primed human monocytes for enhanced release of superoxide (O-2) stimulated by receptor-mediated agonists, N-formyl-methionyl-leucyl-phenylalanine (FMLP) and concanavalin A (Con A), but not by phorbol myristate acetate (PMA), which bypasses the receptors to stimulate the cells. The optimal priming was obtained by pretreatment of suspended monocytes with 10 U/mL TNF for 10 minutes at 37 degrees C. The potency of the maximal priming effect was TNF> GM-CSF, and the combined effect of TNF and GM-CSF was greater than that of each cytokine alone. GM-CSF induced an increase in cytoplasmic pH but TNF did not. These findings suggest that TNF and GM-CSF activate monocytes through different mechanisms. TNF and GM-CSF by themselves never triggered O-2 release in suspended monocytes or monocytes adherent to endothelial cells, although both cytokines triggered massive release of O-2 in human neutrophils. In additions, TNF and GM-CSF induced tyrosine phosphorylation of a 42-kD protein in neutrophils but not in monocytes. These findings suggest that the TNF-receptor- or GM-CSF-receptor-mediated signaling pathways for triggering O-(2) release is active in neutrophils but inactive or defective in monocytes. TNF also enhanced phagocytosis of sialidase-treated autologous erythrocytes by monocytes, and this effect was further potentiated in the presence of autologous fresh serum. The significant enhancement of erythrophagocytosis was obtained at 1 U/mL TNF. At this concentration of TNF, the expression of C3bi-receptor (CD11b/CD18) was upregulated. These findings show that TNF rapidly primes human monocytes for enhanced release of O-(2) and erythrophagocytosis and suggest that TNF activates monocytes through autocrine or paracrine mechanisms at the inflammatory sites inasmuch as TNF is primarily produced by activated monocytes/macrophages.

Adult

[Pharmacokinetic, bacteriological and clinical studies on cefozopran in neonates and premature infants. A study of cefozopran in the perinatal co-research group].

The following results were obtained in pharmacokinetic, bacteriological and clinical investigations of a cephem antibiotic for injection, cefozopran (SCE-2787, CZOP), administered to neonates and premature infants. 1. Pharmacokinetics (1) Half-lives (T 1/2's) of CZOP in 0-day-old (less than 24 hours after birth) neonates and premature infants were longer than those in 1-day-old or older infants. When half-lives were compared between 0-day-old neonates and 0-day-old premature infants, longer half-lives were observed in premature infants. (2) When CZOP was intravenously administered to 1-day-old or older neonates and premature infants at a dose of 20 mg/kg, no differences were noted in blood concentrations between neonates and premature infants from 30 minutes to 6 hours after administration as well as T 1/2's. (3) Blood concentration of CZOP administered at doses of 10, 20 and 40 mg/kg were dose-dependent. (4) Urine excretion rates of CZOP administered to 1-day-old or older neonates and premature infants were approximately 30 to 60% in the first 6 hours after administration. Urine excretion rates in 0-day-old neonates and premature infants were low. 2. Clinical results (1) Of a total of 136 cases to which CZOP was administered, clinical efficacy evaluation was possible in 96 cases, and safety evaluation in 132 cases. (2) The clinical efficacy rates were 78.6% (22/28) in 28 cases in which causative organisms were detected (Group A), and 97.1% (66/68) in 68 cases in which no such organisms were detected (Group B), with the total efficacy rate (Groups A and B) of as high as 91.7% (88/96). (3) Bacteriological evaluations were made with 33 strains isolated from the 28 cases of Group A. Elimination rates for Gram-positive and Gram-negative bacteria were 88.2% (15/17) and 92.3% (12/13), respectively, with the total elimination rate of 90.0% (27/30). No microbial substitution was noted. (4) As an adverse reaction, diarrhea was noted in one case (0.8%). Abnormal laboratory test values were noted in 15 cases (12.3%) including eosinophilia, elevated GPT, and elevated gamma-GTP. All of these abnormalities were transitory, and none of them critical. As a result of above pharmacokinetic and clinical investigations, CZOP is considered to be highly useful in the treatment of indicated infections in neonates and premature infants. It appears that 20 mg/kg of CZOP can be administered by intravenous injection or intravenous drip infusion to neonates and premature infants aged 0-day (less than 24 hours after birth) once or twice daily, to those aged 1 (24 or more hours after birth) to 7 days twice or three times daily, and to those aged 8 or more days three to four times daily, and that the dose can be increased up to 40 mg/kg in cases of critical or intractable infections.

Bacterial Infections

Tyrosine phosphorylation of vav protooncogene product in primary human myelogenous leukemic cells stimulated by granulocyte colony-stimulating factor.

Granulocyte colony-stimulating factor(G-CSF), but not granulocyte-macrophage CSF(GM-CSF), induced tyrosine phosphorylation of 95-kDa protein in 13 cases of primary human acute myelogenous leukemic cells. Electrophoretic mobility of 95-kDa phosphoprotein and the protooncogene product p95vav was identical. In addition, p95vav was tyrosine-phosphorylated only in G-CSF-stimulated cells. In contrast to primary leukemic cells, amount of p95vav was under detectable level and G-CSF did not induce tyrosine phosphorylation of 90-100-kDa proteins in human neutrophils. These results indicate specific involvement of vav product in signaling pathway of G-CSF in primary human leukemic cells.

Amino Acid Sequence

Biological characteristics of chronic eosinophilic leukemia cells with a t(2;5)(p23;q35) translocation.

We studied the biological features of eosinophils in a patient with chronic eosinophilic leukemia and a unique t(2:5)(p23;q35) translocation. Microscopic and cytochemical studies revealed no particular abnormalities, although more than 90% of the peripheral eosinophils had a density lighter than 1.080 g/ml. Clonogenic assay disclosed that myeloid progenitor cells possessed the translocation, although in vitro eosinophilopoiesis seemed normal, and there were also hematopoietic cells with a normal karyotype. In a surface marker study, EG1 was positive on 34.0% of the eosinophils, while EG2 positivity was only 0.5%. Eosinophilopoietic growth factors and adhesion molecules were virtually absent with the exception of GM-CSF and CD11b. Functional studies showed that chemotaxis for C5a was normal, although that for IL-2 or FMLP was attenuated. In addition, leukotriene C4 production was decreased while O2- production was intact. These findings indicated that our patient's eosinophils were not in an activated state despite their extreme hypodensity, and suggested that the leukemic eosinophils had slight defects of cellular function. These characteristics may have saved the patient from the multiple organ damage which occurs in typical hypereosinophilic syndrome.

Adult

Stimulation and priming of human neutrophils by IL-1 alpha and IL-1 beta: complete inhibition by IL-1 receptor antagonist and no interaction with other cytokines.

Together, interleukin-1 alpha (IL-1 alpha) and IL-1 beta primed human neutrophils for enhanced release of superoxide (O2-) stimulated by chemotactic peptide, chemokine, and plant lectin, and alone, each triggered O2- release in a dose-dependent manner. The maximal priming and triggering effect was obtained by high concentrations (50 to 500 ng/mL) of IL-1 alpha or IL-1 beta, though IL-1 beta was more effective than IL-1 alpha at suboptimal concentrations. Priming effect of IL-1 was very rapid and maximal within 10 minutes, whereas O2- release triggered by IL-1 was gradual and continued for 90 to 120 minutes. Combined stimulation of human neutrophils with IL-1 plus granulocyte colony-stimulating factor (G-CSF) or granulocyte-macrophage CSF (GM-CSF) resulted in additive priming effect, and combined stimulation of neutrophils with IL-1 plus G-CSF, GM-CSF, or tumor necrosis factor (TNF) resulted in additive triggering effect, even when the maximal concentration of each cytokine was used. These priming and triggering effects of IL-1 alpha and IL-1 beta on the respiratory burst in human neutrophils were completely inhibited by IL-1 receptor antagonist (IL-1ra). Furthermore, only the net effect of IL-1 was inhibited by IL-1ra, even when human neutrophil was stimulated with IL-1 plus other cytokines to release O2-. Present results indicate that IL-1 does stimulate the respiratory burst activity in human neutrophils via receptor-mediated mechanism and suggest that the post-IL-1-receptor signaling pathways linked to the activation system of the respiratory burst are independent from those utilized by other cytokines in human neutrophils.

Adult

Current status of type 2 (non-insulin-dependent) diabetic subjects on dialysis therapy in Japan.

According to a national survey of dialysis patients in Japan conducted by the Japanese Society for Dialysis Therapy, there were 1,033 patients on dialysis in the Shiga area which has a population of about 1.2 million. Of these 1,033 dialysis patients 140 were the result of diabetic nephropathy. From four hospitals affiliated to Shiga University of Medical Science the medical records of 90 diabetic subjects on dialysis therapy were reviewed and various clinical parameters were analysed and compared with those of patients with chronic glomerulonephritis. Since only one patient had Type 1 (insulin-dependent) diabetes, the remaining 89 with Type 2 (non-insulin-dependent) diabetes were used for this study. The significantly different variables between patients with Type 2 diabetes and chronic glomerulonephritis were age (60.4 vs 54.6 years, p < 0.05), BMI (22.4 vs 20.6 kg/m2, p < 0.001), cardiothoracic ratio (56.4 vs 53.3%, p < 0.001), mean blood pressure (110 vs 117 mmHg, p < 0.05), serum creatinine (9.0 vs 11.5 mg/dl, p < 0.001), serum urea-N (98.2 vs 115.5 mg/dl, p < 0.001), serum total protein (6.0 vs 6.5 g/dl, p < 0.001) and serum albumin (3.5 vs. 3.9 g/dl, p < 0.001). Serum levels of cholesterol and triglyceride were not significantly different between two groups, though the prevalence of electrocardiogram abnormalities, oedema, neuropathy, myocardial infarction and cerebrovascular diseases was significantly higher in the Type 2 diabetic group. These results suggested that Type 2 diabetic patients with end-stage renal disease were older, more malnourished, fluid overloaded and multi-morbid as a result of vasculopathy and neuropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure

Serum erythropoietin titers in hematological malignancies and related diseases.

Serum erythropoietin (Epo) titers in patients with various hematological malignancies and related diseases were determined by radioimmunoassay. Serum Epo titer was inversely correlated with hemoglobin concentration in iron deficiency anemia, aplastic anemia, myelodysplastic syndromes (MDS), acute leukemia, malignant lymphoma, multiple myeloma and myelofibrosis, but there was no correlation between serum Epo titer and hemoglobin concentration in chronic myelogenous leukemia or polycythemias. Serum Epo titers in aplastic anemia were much higher than those in iron deficiency anemia. Serum Epo titers in MDS, malignant lymphoma and multiple myeloma differed considerably among patients. Serum Epo titers in untreated polycythemia vera were significantly lower than in treated polycythemia vera or secondary polycythemia.

Anemia

[Changes in bone marrow MRI patterns in aplastic anemia before and after successful treatment with ATG].

In order to evaluate the usefulness of MRI in estimating bone marrow cellularity, we performed MRI of the lumbar spine in two patients with severe aplastic anemia, before and after successful treatment with antithymocyte globulin (ATG). Case 1, a 25-year-old man with idiopathic aplastic anemia, was treated with ATG 6 months after the onset. One month after treatment, his peripheral blood count and bone marrow cellularity recovered, and the MRI bone marrow pattern became normal. Case 2, a 78-year-old woman with drug-induced aplastic anemia, was treated with ATG 4 months after the onset. Three months after treatment, her peripheral blood count improved. Five months after treatment, her bone marrow cellularity recovered and the MRI bone marrow pattern was normal for her age. Seven months after treatment, when her peripheral blood count was almost normal, we observed hypercellular bone marrow restoration at the periphery of the vertebrae. MRI seems to be an effective method of evaluating bone marrow recovery in aplastic anemia.

Adult

[Immunoblastic lymphadenopathy-like T cell lymphoma accompanied by autoimmune hemolytic anemia].

A 62-year-old man was admitted to our hospital because of generalized lymphadenopathy, fever and skin eruptions. The histology of the right cervical lymph nodes showed immunoblastic lymphadenopathy (IBL)-like T cell lymphoma. His laboratory data were as follows: hemoglobin concentration 7.1 g/dl, red blood cells 1,850,000/microliters, reticulocytes 4.2%, total bilirubin 2.6mg/dl, direct bilirubin 0.5mg/dl, haptoglobin less than 10mg/dl, positive Coombs test. He was diagnosed as having IBL-like T cell lymphoma accompanied by autoimmune hemolytic anemia. He was successfully treated with combination chemotherapy (Pro-MACE), and lymph node swelling and hemolytic anemia disappeared. He has been in complete remission for more than 1 year.

Anemia, Hemolytic, Autoimmune

[alpha-Interferon in the treatment of essential thrombocythemia].

Two patients with essential thrombocythemia were successfully treated by administering native alpha-interferon (alpha-IFN). One patient was a 38-year-old man in whom thrombocytosis was found accidentally. His platelet count on admission was 880,000/microliters and megakaryocytes increased. Three million units of alpha-IFN was administered subcutaneously everyday, and the platelet count decreased gradually to about 500,000/microliters within 2 weeks. The other patient was a 66-year-old woman who visited our hospital complaining of tenderness and swelling of the fingertips. Her platelet count was 1,610,000/microliters, and megakaryocytes increased and showed abnormal morphology. Six million units of alpha-IFN was administered subcutaneously every other day. The tenderness and swelling of the fingertips disappeared soon after the beginning of alpha-IFN administration. The platelet count decreased to about 500,000/microliters within 10 days, but she developed itching of the skin over the entire body. Therefore, alpha-IFN treatment was discontinued. It was suggested that alpha-IFN suppresses not only the maturation and proliferation of the progenitors of megakaryocytes but also the production of platelets from megakaryocytes. Administration of alpha-IFN should be considered in treating patients with essential thrombocythemia, because effects appear soon and alpha-IFN does not induce a second malignancy.

Adult

The role of natural killer cells in human tonsillar tissue focussing on the change of tonsillar tissue with aging.

The natural killer (NK) activity of tonsillar lymphocytes is low and NK-cells are small in number. In tonsillar tissue, NK-cells were present in the germinal center, which is where B-cells are located. This suggests that B-cells are related to NK-cells. Judging from the rates of augmentation of NK-activity of INF-alpha, INF-beta, and from the fact that there is no difference in the rate of NK-activity augmentation between tonsillar and peripheral blood lymphocytes with IFN added, it is highly unlikely that there is much difference between the ratios of pre-NK cells and NK-cells. The fact that the NK-activity augmentation in the tonsil rose to approximately double that of peripheral blood on the addition of IL-2 suggests that the percentage of immature NK-cells is high in the tonsil. This supposition is in agreement with the morphological findings. In the infected and child tonsil, it is probable that NK-cells are at an immature stage, that NK-activity is low, that B-cells are active, and that immunoglobulin production is in progress.

Adult

Laryngeal lymphangioma--case report.

Laryngeal lymphangioma is extremely rare. We have been able to find only seventeen cases reported in world literature. We recently, treated a patient suffering from laryngeal lymphangioma in our department. The female patient, aged 36, complained of hoarseness for several months. Indirect laryngoscopy revealed a growth on her right false vocal cord. Under general anesthesia, tracheostomy and laryngofissure were performed for removal of this neoplasm. The tumor was microscopically diagnosed as lymphangioma. The symptoms disappeared after surgery and there has been no recurrence. The pertinent literature on this rare disease is reviewed.

Adult