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M Yoshida

Publications and source records attributed to M Yoshida.

At least 955 records · Page 53Linked to original sources
PubMed1997

Experimental diabetes upregulates the expression of uretereral endothelin receptors.

We investigated the binding characteristics of endothelin (ET) receptors in the ureters of rats with experimentally induced diabetes and diuresis. Receptor binding experiments demonstrated an upregulation in the expression of [125I]ET-1 binding sites in the diabetic rat ureter but not in the diuretic rat ureter. ET-1, ET-3, IRL 1620, and BQ 610 inhibited [125I]ET-binding to the rat ureter consistent with the predominance of ETA receptors in these tissues. The subtype specificity of ET receptors in ureteral tissues was confirmed with inhibition data obtained from cloned human ETA and ETB receptors.

Animals↗
PubMed1997

Systemic immediate-type reactions to gelatin included in Japanese encephalitis vaccines.

Three children had systemic immediate-type reactions to Japanese encephalitis (JE) vaccine which contains gelatin as a stabilizer. We found that all the children had anti-gelatin IgE in their sera. Further, two of the three also had experienced systemic allergic reactions to gelatin-containing foods before the vaccination. We assume that the systemic allergic reactions to JE vaccines might be caused by gelatin in the JE vaccine.

Anaphylaxis↗
PubMed1997

X-ray characteristics of wrists in calcium pyrophosphate crystal deposition disease. Is pseudogout a major cause of scapholunate advanced collapse?

Deposition of calcium pyrophosphate dihydrate (CPPD) crystals has been considered to be a cause of scapholunate advanced collapse (SLAC) wrist. The aim of this study was to look at X-ray changes in wrist joints affected by CPPD crystal deposition disease and to determine whether crystal deposition is a cause of SLAC wrist. A total of 150 wrists of 78 patients with CPPD crystal deposition disease were examined. In our population of Japanese patients with CPPD crystal deposition disease, the incidence of SLAC wrist was very low, and no case of Stage III SLAC wrist was found. We therefore conclude that SLAC wrist is not a radiographic characteristic of CPPD crystal deposition disease and that pyrophosphate crystal deposition cannot be a major cause of SLAC wrist.

Aged↗
PubMed1997

Subcutaneous extensor tendon rupture associated with calcium pyrophosphate dihydrate crystal deposition disease of the wrist.

We report a patient with rupture of the ring extensor tendon associated with calcium pyrophosphate dihydrate crystal deposition disease of the wrist. Crystal deposits were noted in synovium and the triangular fibrocartilage complex. Histological examination revealed chronic synovitis with foreign body giant cell reaction to crystals. The cause of the tendon rupture was synovitis due to crystal deposition.

Aged↗
PubMed1997

Angioimmunoblastic lymphadenopathy-like T-cell lymphoma. A case report and immunologic study.

BACKGROUND: Angioimmunoblastic lymphadenopathy (AILD) is rare in the head and neck and its definition remains controversial. METHOD: A case of AILD with an ulcer of the lateral pharyngeal wall was studied for viral infection, immunohistologic findings and T-cell receptor (TCR) V beta rearrangement. RESULTS: We observed elevation of antibodies against herpes simplex virus and herpes zoster virus as well as Epstein-Barr virus considered closely associated with AILD. The affected neck lymph node showed a preponderance of T-cells, predominantly CD4+ over CD8+ T-cells and all V beta gene families were expressed in the T-cells without enhancement of any particular TCR gene usage. CONCLUSION: Viral infection may occur easily in patients with AILD, possibly owing to immunodeficiency. Assessment of TCR V beta gene usage indicated T-cells to non-specifically become lymphomatous in AILD-like T-cell lymphoma.

Aged↗
PubMed1997

Preferential infiltration by activated eosinophils in allergic sinusitis.

Although Type I allergy is a trigger for provoking chronic inflammation, whether allergic sinusitis (AS) can be distinguished from sinusitis due to chronic infection is still debated. This study was performed to characterize inflammatory cells in AS and to determine whether patients with AS differ from patients with chronic suppurative sinusitis (CSS). 5 patients with AS and 10 patients with CSS were investigated. Cellular infiltration was studied using immunohistochemistry with monoclonal antibodies using CD3, CD4, CD8, CD25, major basic protein (BMK13), eosinophil cationic protein (EG2), neutrophil elastase, and tryptase. There were no differences in CD3+, CD4+, CD25+, and tryptase+ cells between the groups. Whereas the total number of eosinophils (BMK13+) also did not significantly differ, the number of activated eosinophils (EG2+) was significantly higher (P < 0.05) in patients with AS. Furthermore, a statistically significant increase in the percentage of activated eosinophils to total eosinophils (P < 0.05) was observed in patients with AS. In contrast, the number of neutrophil elastase+ cells was significantly higher (P < 0.05) in patients with CSS. These results suggest that patients with AS can be distinguished immunohistochemically from patients with CSS, with AS being distinguished by activated eosinophil infiltration.

Adolescent↗
PubMed1997

Effects of acute treatment and long-term treatment with MK-801 against amygdaloid kindled seizures in rats.

Effects of both acute and long-term treatments with a non-competitive NMDA-antagonist, MK-801, were studied in rats in order to investigate whether NMDA receptors would be involved in the maintenance of kindling. Intraperitoneally administered MK-801 at doses of 0.5, 1.0 and 2.0 mg/kg inhibited fully amygdaloid kindled seizures (stage 5) behaviorally and significantly reduced the duration of after discharge and postictal spikes in a dose-dependent manner. Long-term (28 days) administration of MK-801 at three dosages neither abolished behavioral kindled seizures nor significantly altered generalized seizure thresholds. However the after discharge duration and postictal spikes were significantly reduced in rats treated with MK-801 at doses of 0.5 and 1.0 mg/kg, while no significant alterations were observed in rats treated with saline or MK-801 at a dose of 2.0 mg/kg. Acute effects of MK-801 suggested that NMDA receptors were involved in the maintenance of kindling. On the other hand, long-term treatments with MK-801 remained to show such an unequivocal effect.

Amygdala↗
PubMed1997

Rare but important adverse effects of all-trans retinoic acid in acute promyelocytic leukemia and their management.

Several adverse effects have been reported to occur after clinical application of all-trans retinoic acid (RA) in acute promyelocytic leukemia (APL). Except for severe side effects including retinoic acid syndrome, the mechanism of action of RA on adverse effects remains unclear. Here we describe some rare adverse effects and their management. We reviewed the English literature, and we added our cases of endocrine and metabolic adverse effects, such as hypercalcemia, male infertility, bone marrow necrosis, fibrosis and acute pancreatitis. We also described our cases of thromboembolic events, RA-dependent growth of pathologic cells including Sweet's syndrome, erythema nodosum, hyperhistaminemia, granulomatous proliferation, and mild cases of pulmonary complications. In addition, we reviewed the efficacy of RA administration for other types of leukemia or myelodysplastic syndrome. RA and chemotherapeutic agents might induce complete remission, but we obtained a response in only one case of M2 in the third relapse. During RA administration the patient should be monitored for these adverse effects, and early diagnosis and appropriate treatment are important.

Antineoplastic Agents↗
PubMed1997

Hyperdiploid myeloma cell as an indicator of poor prognosis and drug refractoriness.

Although almost 40% of patients with multiple myeloma respond to initial chemotherapy, myeloma with no response to initial chemotherapy remains a serious problem. To understand the characteristics of drug-refractoriness of myeloma, fresh tumor cells from 13 untreated myeloma patients were fixed and stained with anti-human immunoglobulins and propidium iodide for subsequent flow cytometric analysis of DNA content. More than 10% of myeloma cells were hyperdiploid in eight cases (hyperdiploid + cases) while less than 10% of myeloma cells were hyperdiploid in five cases (hyperdiploid - cases). The proportion of hyperdiploid cells among all myeloma cells was highly correlated with incidence of myeloma cells with morphologically abnormal nuclei such as those with multiple-nuclei or convoluted nuclei (P = 0.001). Among the eight hyperdiploid + cases, two (2/8) showed good response to subsequent chemotherapy while four of five hyperdiploid - cases (4/5) responded well. Cases with poor response had more hyperdiploid myeloma cells (average 25.7% of all myeloma cells) than sensitive cases (average 6.8%), suggesting a contribution of hyperdiploid myeloma cells to primary drug resistance (P = 0.065). The 3 year survival rate of hyperdiploid+cases was 0% while that of the control group was 41.9%. These results suggest that myeloma cells with abnormal nuclear morphology may show hyperdiploidy and poor response to chemotherapy.

Adult↗
PubMed1997

Infections in patients with hematological diseases: recent advances in serological diagnosis and empiric therapy.

Recent advances in the diagnosis and therapy of infections in patients with hematological diseases are reviewed. In general, 40-60% of febrile episodes lack clinical or microbiological evidence of infection and are thus treated empirically. Among the cases of microbiologically documented bacteremia treated in our department, the incidence of Gram-negative bacteria was high (47.1%) and the incidence of Gram-positive bacteremia is increasing. To improve the diagnostic rate of Gram-negative sepsis, the measurement of plasma endotoxin was performed. Of 147 febrile neutropenic episodes, endotoxemia was observed in 58 (39.5%) and the causative microorganisms of these infections were deemed Gram-negative bacteria. The measurement of plasma (1-->3)-beta-D-glucan, a ubiquitous component of fungi, was also performed for making early diagnosis of deep mycosis; the sensitivity of this assay was 90% and the specificity was 100%. The detection of (1-->3)-beta-D-glucan appears to be useful as a screening test of deep mycosis. The effects of the concomitant use of granulocyte-colony stimulating factor (G-CSF) and empiric antibiotic therapy for febrile neutropenia were studied in a randomized fashion. G-CSF did not affect the rate of the response to the empiric antibiotic therapy, although a significant effect of G-CSF on neutrophil recovery was observed. Guidelines for empiric antibiotic and antifungal therapy combined with serological diagnosis are proposed.

Bacterial Infections↗
PubMed1997

Influence of combined use of selenious acid and SH compounds in parenteral preparations.

The influence of the combined use of selenious acid and SH compounds (glutathione (GSH) and cysteine (Cys), or ascorbic acid (Asc)) on cultured venous vascular cells was investigated experimentally. When cultured human umbilical venous vascular endothelial cells were exposed to 10 microM of selenious acid combined with 0.5 mM-GSH or 0.5 mM-Cys, the release rates of [3H]-adenine and lactate dehydrogenase (LDH) from cells into the medium increased significantly as compared with after exposure to selenious acid alone, and damage to the vascular endothelial cells was found to be intensified. Addition of 1 microM of selenious acid simultaneously with 0.5 mM-GSH or 0.5 mM-Cys showed no differences in toxicity for the vascular endothelial cells as compared with the addition of selenious acid alone. On the other hand, simultaneous exposure to 10 microM of selenious acid and 1 mM-Asc induced no significant differences in the release rates of [3H]-adenine and LDH, and no damage was observed to the vascular endothelial cells. These results suggest that simultaneous addition of selenious acid together with GSH or Cys, which have the SH-group, may cause damage to the vascular endothelial cells. Therefore careful attention is warranted in total parenteral nutrition (TPN).

Ascorbic Acid↗
PubMed1997

Cytokines and lipopolysaccharide enhance basal and thrombin-stimulated production of PGI2 by cultured human pulmonary artery smooth muscle cells.

We evaluated the thrombin-stimulated production of prostacyclin (PGI2) by cultured human pulmonary artery smooth muscle cells (HPASMC) that were pretreated with cytokines (IL-1 beta, TNF alpha) and lipopolysaccharide (LPS). Cultured HPASMC, obtained from autopsied cases, were identified as smooth muscle cells by immune staining with mouse anti-human alpha-smooth muscle actin monoclonal IgG. A 3 hour incubation of HPASMC with LPS, IL-1 beta, or TNF alpha followed by a 10 min exposure to 2 U/ml thrombin was sufficient to generate a greater amount of PGI2 than observed in control cells. The increase in PGI2 production peaked after 8 h in the IL-1 beta- and TNF alpha-treated HPASMC, and continued to increase for 24 h in the LPS-treated HPASMC. We then investigated the effect of incubation time of thrombin on PGI2 production in HPASMC pretreated with cytokines or LPS for 24 h. PGI2 production by LPS- and cytokine-treated HPASMC peaked after a 15 min exposure to thrombin. In contrast, the exposure of LPS- or IL-1 beta-treated HPASMC to buffer seemed to increase the release of PGI2 for up to 30 min of incubation. However, the PGI2 released was less than that in the thrombin-stimulated HPASMC. After incubation with various concentrations of LPS or cytokines, the production of PGI2 by thrombin-stimulated HPASMC showed significant, dose-dependent increases beginning at 0.1 microgram/ml of LPS, 20 U/ml of IL-1 beta, and 50 U/ml of TNF alpha. We conclude that LPS, IL-1 beta, and TNF alpha enhanced both the basal and thrombin-stimulated production of PGI2 by HPASMC. This enhanced production of PGI2 might help in lowering the pulmonary vascular tone and modifying pulmonary hemodynamics in cytokine- or endotoxin-mediated inflammation and acute injury of the lung.

Actins↗
PubMed1997

Azelastine suppresses the release of arachidonic acid metabolites from cultured human umbilical vein endothelial cells.

We investigated the effects of azelastine, an anti-allergic agent, on the release of arachidonic acid metabolites from cultured human umbilical vein endothelial cells (HUVEC). High performance liquid chromatography (HPLC) revealed that HUVEC treated with 10(-5) M azelastine released smaller amounts of arachidonic acid metabolites into the medium than control HUVEC. Azelastine significantly reduced the release of prostaglandin F2 alpha (PGF2 alpha), leukotriene B4 (LTB4) and 5-hydroxy-eicosatetraenoic acid (5-HETE) by HUVEC. These results suggest that azelastine may inhibit contraction of bronchial smooth muscle cells and reduce bronchial inflammation by suppressing the release of arachidonic acid metabolites from vascular endothelial cells.

Anti-Allergic Agents↗
PubMed1997

Thickness of the basement membrane of bronchial epithelial cells in lung diseases as determined by transbronchial biopsy.

The thickness of the basement membranes of bronchial epithelial cells varies under various pathological conditions. It has been reported that this membrane is thickened in patients with bronchial asthma. By light microscopy, this parameter was measured in biopsy specimens of bronchial mucosa obtained by fibre-optic bronchoscopy. These specimens were obtained from 171 patients who had undergone bronchial biopsy between 1984 and 1994. It was demonstrated that the thickness of the basement membrane of bronchial epithelial cells was weakly correlated with the patient's age, when thickness was examined in patients with lung cancer (r = 0.242, P = 0.0268). The basement membranes in patients with bronchial asthma (8.193 +/- 1.362 mu, mean +/- SEM) were significantly thicker than those without bronchial asthma (5.145 +/- 0.233 mu) (P = 0.0180, Mann-Whitney's U-test). In addition, it is noteworthy that the basement membranes in patients with diabetes mellitus (7.217 +/- 0.753 mu) were also significantly thicker than those without diabetes mellitus (4.968 +/- 0.235 mu) (P = 0.0038, Mann-Whitney's U-test). The background or underlying pathophysiology in such patients should be studied further, with attention directed towards the thickness of the bronchial basement membrane in bronchial biopsy specimens.

Aged↗
PubMed1997

Thrombopoietin alone stimulates the early proliferation and survival of human erythroid, myeloid and multipotential progenitors in serum-free culture.

We examined the effects of recombinant human thrombopoietin (TPO, c-Mpl ligand) on the proliferation and differentiation of human haemopoietic progenitors other than megakaryocytic progenitors using serum-free cultures. TPO alone supported the generation of not only megakaryocytic (MK) but also blast cell (blast) colonies from cord blood CD34+ cells. Delayed addition of a cytokine cocktail (cytokines; interleukin (IL)-3, IL-6, stem cell factor, erythropoietin, granulocyte-macrophage colony-stimulating factor, and TPO) to cultures with TPO alone on day 7 induced various colonies including granulocyte-macrophage (GM) colonies, erythroid bursts (E), granulocyte-erythrocyte-macrophage-megakaryocyte (GEMM) colonies. Replating experiments of blast colonies supported by TPO alone for culture with cytokines revealed that approximately 60% of the blast colonies contained various haemopoietic progenitors. Single cell cultures of clone-sorted CD34+ cells indicated that TPO supported the early proliferation and/or survival of both primitive and committed haemopoietic progenitors. In serum-free suspension cultures, TPO alone significantly stimulated the production of progenitors for MK, GM, E and GEMM colonies as well as long-term culture-initiating cells. These effects were completely abrogated by anti-TPO antibody. These results suggest that TPO is an important cytokine in the early proliferation of human primitive as well as committed haemopoietic progenitors, and in the ex vivo manipulation of human haemopoietic progenitors.

Antigens, CD34↗