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Biomedical subjects

T Horie

Publications and source records attributed to T Horie.

At least 145 records · Page 8Linked to original sources
PubMed1999

Therapy-related megakaryoblastic leukemia with pituitary involvement following treatment for non-Hodgkin's lymphoma.

A case of a 66-year-old Japanese man developed therapy-related megakaryoblastic leukemia with pituitary involvement after chemotherapy for non-Hodgkin's lymphoma. Alkylating agents had been administered for the treatment of non-Hodgkin's lymphoma and 6 years later, megakaryoblastic leukemia with myelofibrosis and myelodysplasia developed. The blast cells expressed CD41, and immature antigens also. These findings were compatible with therapy-related megakaryoblastic leukemia. An autopsy revealed blast-cell infiltration into multiple organs including the posterior pituitary lobe. Therapy-related megakaryoblastic leukemia is very rare, and pituitary involvement may be associated with immaturity of blast cells.

Antigens, CD↗
PubMed1999

[Crohn's disease with the onset resembling systemic lupus erythematosus].

We described a 37-year-old man with Crohn's disease (CD) resembling systemic lupus erythematosus (SLE) at his disease onset. He was admitted to the municiple Akiru Hospital in October 1986 by fever, aphtous oral ulcerations, sore throat and polyarthralgia. Hematologic examination showed leukocytopenia, lymphocytopenia, positive tests for antinuclear antibody, anti-DNA antibody and LE cell phenomenon. He has had episodes of convulsion and conciousness loss of unknown etiology when he was 17 years old. The diagnosis of SLE was made, and oral medication of prednisolone was started. Several weeks later, most of symptoms and autoantibodies disappeared, although the oral aphtous ulcerations and leukocytopenia remained. In May 1987, he admitted to the other hospital because of bloody vomiting. Endoscopic examination showed the esophagial ulceration, and histology of biopsied-specimen was nonspecific esophagitis. The combination of prednisolone and oral cyclophosphamide or methotrexate was employed thereafter. However, the leukocytopenia, oral aphtous ulceration and esophagial ulceration continued in spite of these treatments. All the immunosuppressive treatment was stopped at March 1992. In October 1995, he admitted to our hospital because of body weight loss and continuous diarrhea with occasional bloody stool. Barium enema and endoscopic examination of the colon revealed the findings compatible with CD. The patient responded favorably to methylprednisolone pulse therapy followed by oral sulphasalazine. This case indicated that cases with inflammatory bowel diseases like CD could show similar clinical signs and symptoms to SLE, and in some cases of CD might satisfied the classification of criteria for SLE.

Administration, Oral↗
PubMed1999

Effect of beta-agonists on production of cytokines by activated T cells obtained from asthmatic patients and normal subjects.

Intracellular levels of cAMP were found to regulate T cell activity. We examined whether beta2-agonists altered cytokine production and cyclic adenosine monophosphate (cAMP) accumulation in concanavalin A (ConA)-activated peripheral T cells from asthmatic patients. Procaterol and isoproterenol weakly decreased the ConA-elicited interleukin (IL)-4 and IL-5 secretion; however, the inhibitory effect of procaterol on the ConA-induced IL-2 secretion was inferior to that of isoproterenol in normal controls and was little in asthmatics. The intracellular accumulation of cAMP by procaterol was not altered compared with that by isoproterenol. Results suggest that there is a qualitative difference between procaterol- and isoproterenol-induced cAMP accumulation in T cells.

Adrenergic beta-Agonists↗
PubMed1999

Evaluation of expression of CD15 and sCD15 in non-small cell lung cancer.

Changes in cell membrane carbohydrate antigens play an important role in metastatic potential associated with carcinogenesis and in prognostic factors. We investigated immunohistochemically the expression of CD15 and sialyl CD15 (sCD15) in lung cancer tissue by using Leu-M1 antibody and MXKM-93 antibody, respectively, and then assessed the relationship between their expression and the patient outcome. Lung cancer tissue expression of CD15 was significantly higher in adenocarcinoma (55.9%) and squamous cell carcinoma (44.7%) than in small cell carcinoma (10%) (p=0.01, p=0.006). Expression of sCD15 was significantly higher in adenocarcinoma (52.9%) than in squamous cell carcinoma (10.5%) or small cell carcinoma (10%) (p<0. 0001, p=0.016). No association was found between CD15 expression and clinical stage, but sCD15 expression increased with clinical stage (stage I+II vs. III+IV: 16.7% vs. 39.6%; p=0.049). Expression of CD15 (1.5%) was significantly lower than expression of sCD15 (12.3%) in normal surrounding tissue. Examination of associations with outcome in NSCLC revealed that expression of sCD15 in resected cases, and expression of CD15 in non-resected cases were significantly correlated with shortening of median survival time (p<0.05). When associations with prognostic factors were assessed by univariate analysis, expression of sCD15 was found to be correlated with distant metastasis, and expression of CD15 with decrease in performance status (PS). In the multivariate analysis by the Cox proportional hazard model, sCD15 and CD15 negativity contributed to longer survival time after PS and clinical stage. The results of a combination assay of CD15 and sCD15 showed that expression of both carbohydrate antigens significantly shortened survival time in both the resected and non-resected group (log-rank test, p<0.05). This combination assay also appeared to be extremely useful in predicting the outcome in all clinical stages of NSCLC.

Adenocarcinoma↗
PubMed1999

[Clinical outcomes in low grade follicular lymphoma].

Twenty-six patients with follicular small-cleaved lymphoma (FSCL) and 16 patients with follicular mixed lymphoma (FML) were treated at the Nichidai Itabashi Hospital between 1981 and 1995. The 5-year overall survival rate was 74.3% and 70.0% for the FSCL and FML patients, respectively. Of the patients with stage III-IV FSCL, 9 were assigned to a "watchful waiting" follow-up course and 13 were treated with a single alkylating agent or CHOP therapy. The 5-year failure-free survival rate was 66.7% and 33.0%, respectively. Of the patients with stage II-IV FML, 6 were treated with CHOP or MACOP-B protocol. The complete response rate for this group was only 33.3%, and none of the patients were in remission for more than 2 years. Histological transformation into diffuse aggressive lymphoma was observed in 7 patients, with the median time from diagnosis to transformation at 50 months. Three of those patients were successfully treated with intensive chemotherapy after transformation.

Adult↗
PubMed1999

[A case of chronic myelogenous leukemia presenting multiple extramedullary tumors localized in cranial dura].

A 64-year-old woman had been given a diagnosis of Ph-positive chronic myelogenous leukemia (Ph+ CML) in October 1992 and accordingly treated with interferon-alpha busulfan, and hydroxyurea. She was admitted to our hospital with a one-day history of consciousness disturbance on May 30, 1993. Two weeks before admission, she had received chemotherapy consisting of vincristine and predonisolone because of progressive thrombocytopenia, basophilia, and leukocytosis accompanied by a heightened degree of cell immaturity in peripheral blood and bone marrow. Cranial computerized tomography on admission disclosed tumoral masses in the left frontal lobe and the right temporal lobe. Moreover, lumbar puncture ezinkns disclosed blastoid cells in cerebrospinal fluid. Based on these laboratory findings, the diagnosis was blastic crisis CML, 46XX t(9; 22; 17) (q34; q11; q23), cytogenetic aberration and extramedulary brain disease Although the patient underwent the same combined chemotherapy again, her unconsciousness did not resolve. She died of cerebellar herniation on the 7th hospital day. Post mortem examination revealed three extramedullary tumors localized in cranial dura. This was a rare case of CML presenting multiple extramedullary tumors localized in cranial dura.

Blast Crisis↗
PubMed1999

[Histopathological findings of coronary arteries in cases with acute coronary syndromes].

A histopathological study of coronary arteries in patients with acute coronary syndromes was carried out. The results of this study are as follows: 1. A high incidence of thrombus formation, corresponding to the site of the infarction, was observed in cases with acute myocardial infarction. 2. Coronary thrombi containing plaque components such as foam cells, cholesterol clefts, and fractured intimal collagen fibers were detected. 3. Patients who succumbed suddenly after coronary attack had ruptured atheromatous plaque only, but not a thrombus. As these patients showed severe stenosis with recanalization in 2 of the 3 main coronary arteries, the rupture of the plaque caused significant occlusion of the remaining coronary artery. 4. Increase of intra-plaque pressure resulting from a honeycomb-like accumulation of foam cells, cholesterin clefts, and blood infiltration from lumen to plaque through the injured endothelial cells is the cause of rupture of the atheromatous plaque. This rupture into the lumen might precede, and be responsible for formation of the thrombus and onset of acute coronary syndromes.

Angina Pectoris↗
PubMed1999

p38 Mitogen-activated protein kinase regulates IL-8 expression in human pulmonary vascular endothelial cells.

The aim of this study was to examine the role of p38 mitogen-activated protein (MAP) kinase in interleukin (IL)-8 expression in tumour necrosis factor (TNF)-alpha- and IL-1alpha-stimulated human pulmonary vascular endothelial cells. To this end, the phosphorylation and activation of p38 MAP kinase and the effect of SB 203580, a specific inhibitor of p38 MAP kinase activity, on p38 MAP kinase activity and IL-8 expression in TNF-alpha- and IL-1alpha-stimulated human pulmonary vascular endothelial cells were examined. TNF-alpha- and IL-1alpha- induced phosphorylation and activation of p38 MAP kinase and IL-8 expression in human pulmonary endothelial cells. Inhibition of TNF-alpha- and IL-1alpha-induced p38 MAP kinase activity by SB 203580 inhibited TNF-alpha- and IL-1alpha-induced IL-8 protein production as well as IL-8 messenger ribonucleic acid (mRNA) expression, indicating that SB 203580 was effective at the transcriptional level. These results indicate that p38 mitogen-activated protein kinase plays an important role in the tumour necrosis factor-alpha- and interleukin-1alpha-activated signalling pathway which regulates interleukin-8 expression in human pulmonary vascular endothelial cells.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed1999

[Merocyanine 540-mediated photodynamic therapy inhibits P-glycoprotein (P-gp) activity in adriamycin-resistant K562 cells].

The photosensitizing dye merocyanine 540 (MC540) has been used in preclinical models and in a phase I clinical trial in the U.S.A. for the extracorporeal purging of autologous bone marrow grafts contaminated with leukemia or lymphoma. In this communication, we report MC540-mediated photodynamic therapy (PDT) was effective in purging leukemic cells expressing P-gp. When K562 and K562/ADM were exposed to MC540 (15 micrograms/ml) and white light (145.8 kJ/m2), the concentration of K562 and K 562/ADR was reduced by 1.8 and 3.0 log, respectively. Using flow cytometry and confocal laser scan microscopy, MC540 and calcein-AM were bound intracellularly and effluxed by P-gp in K562/ADM. In K562/ADM, calcein-AM efflux was inhibited by P-gp modulator, cyclosporin A (5 microM) and verapamil (15 micrograms/ml). In contrast, MC540 efflux was inhibited by cyclosporin A but not verapamil. Furthermore, MC540-mediated PDT inhibited efflux of calcein-AM and MC540, and induced the accumulation of dyes in K562/ADM. We conclude that MC540 is a substrate of P-gp and that MC540-mediated PDT is useful for purging MDR cells through inhibition of P-gp activity.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

[Medical treatment for bronchial stenosis due to endobronchial tuberculosis].

It is needless to say that early diagnosis and appropriate treatment for endobronchial tuberculosis are most important, and bronchoscopic examination is necessary for early diagnosis. Although endobronchial tuberculosis frequently causes bronchial stenosis, there are no specific therapies to prevent the complication. To determine the effectiveness of corticosteroids in the prevention of complication of endobronchial tuberculosis, this study was undertaken. 18 patients with endobronchial tuberculosis whose bronchoscopic findings showing ulcer formation or endobronchial polyp, out of 35 patients with endobronchial tuberculosis who were treated in Nihon University hospital from 1996 to 1998, were evaluated to determine the effectiveness of corticosteroids in the prevention of bronchial stenosis. We divided the patients into 2 groups: 11 who received systemic chemotherapy for tuberculosis only, and 7 who received systemic chemotherapy combined with oral corticosteroid. No significant differences distinguished the groups with respect to duration of positive sputum culture or reduction of respiratory symptoms. However, a significant alleviation of bronchial stenosis was observed in the patients who received systemic chemotherapy combined with oral corticosteroid. This study suggested that corticosteroid therapy in addition to standard chemotherapy for tuberculosis was effective for prevention of complication of endobronchial tuberculosis, such as bronchostenosis.

Administration, Oral↗
PubMed1999

A prostaglandin E1 analog, OP-1206, alleviates 5-fluorouracil-induced injury of rat small intestine.

5-Fluorouracil (5-FU) often causes the gastrointestinal toxicity, including enterocolitis. We investigated effects of OP-1206 (17S, 20-dimethyl-trans-delta2-prostaglandin E1) on 5-FU-induced leukocyte infiltration and epithelial barrier dysfunction of rat small intestine. Myeloperoxidase (MPO) activity of the small intestine was assayed as an index of leukocyte infiltration. Intestinal epithelial permeability was determined by the small intestinal absorption of a paracellular permeation marker, fluorescein isothiocyanate-labeled dextran (molecular weight; 4,400) (FD-4) using the in situ closed intestinal loop technique. The MPO activity and FD-4 permeation were significantly increased by the administration of 5-FU to rats for 4 days, while on the coadministration of 5-FU and OP-1206, they were similar to those of control rats treated with saline solution alone, respectively. These observations indicate that OP-1206 reduced the leukocyte infiltration and the change in epithelial permeability of rat small intestine induced by 5-FU.

Alprostadil↗
PubMed1998

InsP3, but not novel Ca2+ releasers, contributes to agonist-initiated contraction in rabbit airway smooth muscle.

1. To examine the contributions of the putative Ca2+ releasers, inositol 1,4,5-trisphosphate (InsP3), cyclic ADP ribose (cADPR), and nicotinate adenine dinucleotide phosphate (NAADP), to carbachol (CCh)-induced contraction in airway smooth muscle, we measured force development of permeabilized rabbit tracheal smooth muscle, human bronchial smooth muscle and guinea-pig ileum longitudinal smooth muscle. 2. In the presence of 50 microM GTP, CCh and InsP3 contracted alpha-toxin-permeabilized tracheal smooth muscle dose dependently; the EC50 values for CCh and InsP3 were 1.84 microM and 363 microM, and the maximum responses (normalized to the 30 mM caffeine response) to 100 microM CCh and to 800 microM InsP3 were 206 +/- 13.4 % (mean +/- S.E.M.) and 84.4 +/- 5.3 %, respectively. 3. However, cADPR (10-300 microM), beta-NAD+ (2.5 mM), FK506 (30 microM) and NAADP (100 microM) neither contracted the strip by themselves nor affected the subsequent CCh (1 microM) response. alpha-Toxin-permeabilized bronchial smooth muscle and ileum smooth muscle also responded to caffeine, InsP3 and CCh but not to cADPR. 4. Both 100 microM 8-amino-cADPR, a selective cADPR antagonist, and 100 microM thionicotinamide-NADP, a selective NAADP antagonist, failed to inhibit the CCh response, although procaine abolished the caffeine, InsP3 and CCh responses in the permeabilized tracheal smooth muscle. 5. Although inhibition of the caffeine response by 30 microM ryanodine was nearly complete, approximately 30 % of the InsP3 (300 microM) plus GTP (50 microM) response was retained, and the resultant response disappeared after the caffeine response was evoked in the presence of ryanodine. 6. Heparin (300 microg ml-1) blocked InsP3 (300 microM) and CCh (3 microM) responses in beta-escin-permeabilized tracheal smooth muscle, while Ruthenium Red (100 microM) partially inhibited the CCh response. 7. Collectively, InsP3 but not cADPR or NAADP plays a key role in CCh-initiated contraction, and InsP3 utilizes a single compartment of the caffeine/ryanodine-sensitive stored Ca2+ in airway smooth muscle.

Adenosine Diphosphate Ribose↗
PubMed1998

Cooling and rewarming-induced IL-8 expression in human bronchial epithelial cells through p38 MAP kinase-dependent pathway.

p38 mitogen-activated protein kinase (MAP) kinase is activated by various stresses; however, little is known about cold stress which has been shown to cause various inflammatory diseases. In the present study, we examined the effect of cold stimulation on interleukin-8 (IL-8) expression and a role of p38 MAP kinase in IL-8 expression in human bronchial epithelial cells (BEC) in order to clarify the mechanism in hypothermic temperature-induced inflammation. The results showed that cold stimulation induced tyrosine phosphorylation of p38 MAP kinase but not IL-8 expression. IL-8 expression in BEC was induce when the temperature of incubation changed from 1 degree C to 37 degrees C (cooling and rewarming). The specific p38 MAP kinase inhibitor SB 203580 inhibited cooling and rewarming-induced IL-8 expression, indicating that cooling and rewarming-induced IL-8 expression in BEC was mediated through p38 MAP kinase-dependent pathway.

Bronchi↗
PubMed1998

Analysis of exploratory eye movement in a patient with lupus psychosis.

The psychiatric and cognitive condition of a patient with lupus psychosis was evaluated. Using a device that detects the corneal reflection of infrared light, the patterns of eye tracking movements were recorded before the onset of lupus psychosis, after remission, and again 1 year later. Electroencephalographic findings and cerebrospinal fluid levels of both interferon alpha and interleukin-6 were also obtained longitudinally. Electroencephalographic findings and clinical signs were correlated to the levels of interferon alpha in cerebrospinal fluid. Analysis of exploratory eye movements revealed marked decreases in the number of eye fixation, mean eye-scanning length and total eye-scanning length. Even though the lupus psychosis resolved and the electroencephalographic findings became normal, the eye movement patterns showed remaining deterioration. It was concluded that analysis of exploratory eye movements in patients with systemic lupus erythematosus may be useful in diagnosing lupus psychosis, and may also present a diagnostic clue to subclinical lupus psychosis.

Adult↗
PubMed1998

Successful methotrexate therapy for adult Still's disease with marked thrombocytopenia.

A 34-year-old Japanese woman developed spiking fever, splenomegaly, arthritis, neutrophilia, hyperferritinaemia (22517 ng/ml), elevated C-reactive protein (9.1 mg/ml) and severe thrombocytopenia (1.7 x 10(4)/microl). The patient had depressed antithrombin III activity and abnormally high concentrations of both fibrin degradation products and thrombin-antithrombin complexes. This condition was resistant to high-dose prednisolone therapy (120 mg/day) and non-steroidal anti-inflammatory drugs. We initiated oral methotrexate therapy (7.5 mg/week, orally) with a favourable outcome. The patient's spiking fever subsided on the first day of methotrexate administration. Elevated levels of ferritin and C-reactive protein in the sera rapidly normalised. Methotrexate rapidly improved the disease state which suggested that methotrexate act via modulation of cytokine production or secretion.

Administration, Oral↗