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Biomedical subjects

Y Niho

Publications and source records attributed to Y Niho.

At least 145 records · Page 8Linked to original sources
PubMed1998

[Utilization of a direct sandwich ELISA kit for rapid diagnosis of adenovirus hemorrhagic cystitis in a patient with adult T-cell leukemia].

We report on a case of adenovirus hemorrhagi cystitis that developed in a 49-year-old woman during intensive chemotherapy for adult T-cell leukemia. Although rapid etiologic diagnosis is essential for the effective management of viral hemorrhagic cystitis, the isolation of adenovirus from urine is often too time-cousuming. We detected the adenovirus antigen in the patient's urine using an Adenoclone direct sandwich ELISA kit (Cambridge Bio Science), which is commonly employed for the diagnosis of adenovirus conjunctivitis. Treatment consisted of intravenous vidarabine and bladder irrigation, which resulted in prompt clinical improvement. The Adenoclone kit was useful for the rapid etiologic diagnosis of adenovirus hemmorrhagic cystitis.

Adenoviridae Infections↗
PubMed1998

Attachment of hepatitis C virus to cultured cells: a novel predictive factor for successful interferon therapy.

In order to identify reliable predictive factors for the response to interferon (IFN) therapy, we examined 52 patients with chronic hepatitis C virus (HCV) infection who underwent IFN therapy. Titers of free virions that were not complexed with antibodies were determined by immunoprecipitation of the pretreatment sera with antihuman immunoglobulin. Cell attachment titers were determined by inoculating HPB-Ma cells, a human T-cell line, with the patients' pretreatment sera. A sustained remission was achieved in 9 out of 28 patients with genotype 1b infection and in 18 out of 24 patients with genotype 2 infection. The free virion titers and the cell attachment titers correlated well with the serum HCV RNA levels in patients with genotype 1b infection (r = 0.817, P < 0.001; r = 0.802, P < 0.001, respectively), but not in those with genotype 2 infection. They exhibited a high correlation with the responsiveness to IFN in all patients combined (P < 0.001). A multiple logistic regression analysis was performed to identify the factor most significantly associated with the response to IFN among all confounding factors. The analysis indicated that the cell attachment is the most reliable predictive factor regarding a favorable response to IFN therapy in patients with chronic HCV infection.

Adult↗
PubMed1998

Increased plasma epinephrine but not reduced heart rate variability leads to ventricular arrhythmias in patients with acute myocardial infarction.

Ventricular arrhythmia observed in the acute stage of myocardial infarction is profoundly related to the autonomic balance. To investigate prediction of ventricular arrhythmia, heart rate variability and plasma catecholamine concentration were simultaneously measured for a week in 17 consecutive patients with first anterior or anteroseptal Q wave infarction treated without specific coronary intervention. The cross-sectional plot of coefficient of variance (= standard deviation of N-N interval/mean N-N interval x 100; %) as a function of plasma epinephrine on the day of admission remained lower than the standard average. Ventricular premature contractions increased in proportion to the plasma epinephrine concentration. In the first week of hospitalization, plasma epinephrine concentration and frequency of premature contraction decreased exponentially, whereas the coefficient of variance showed a modest decline. Ventricular tachycardia refractory to xylocaine with rate accelerating with persistence was observed only in patients with the peak epinephrine concentration > 375 pg/ml. Plasma epinephrine concentration rather than coefficient of variance during sleep after the first acute episode is more closely related to the following triggered ventricular arrhythmia.

Aged↗
PubMed1998

[Pneumatosis cystoides intestinalis associated with intravenous pulse cyclophosphamide treatment for systemic lupus erythematosus].

Pneumatosis cystoides intestinalis (PCI) is an uncommon disease manifestation characterized by the presence of air in the bowel wall. PCI is sometimes observed in patients with progressive systemic sclerosis or mixed connective tissue disease but extremely rare in patients with systemic lupus erythematosus (SLE). We here report a patient with SLE who developed PCI after the treatment with intravenous cyclophosphamide (IVCY). This is the first case that association between IVCY and PCI was suggested. A 51-year-old woman with a 24-year history of SLE was admitted to our hospital because of skin ulcers in the lower legs. She had been receiving prednisolone orally. Laboratory findings on the present admission showed a elevated titer of anti-double stranded DNA antibody and positive LE test. She was successfully treated with three pulses of methylprednisolone followed by two IVCY together with vasodilators for her disease activity of SLE including skin manifestation. Just after the second IVCY, abdominal distention was gradually developed without any other abdominal symptoms, including abdominal pain. Abdominal radiography and computed tomography revealed pneumoperitoneum and multiple intramural air collections which involved the ascending colon primarily. Gastrointestinal series, however, showed no evidence of intestinal perforation. The diagnosis of PCI was made radiologically. After she was treated with a combined therapy with intravenous hyperalimentation and breathing with high concentration of oxygen for three weeks, PCI and pneumoperitoneum disappeared. It would be necessary that IVCY is carefully administrated, especially for the patients under the risk of PCI, such as collagen diseases.

Cyclophosphamide↗
PubMed1998

Improvement of systemic lupus erythematosus activity by the association of delayed onset Cushing's syndrome.

We describe a 43-year-old woman with systemic lupus erythematosus (SLE) who had complete resolution of all SLE symptoms as a result of hypercortisolemia induced by a glucocorticoid-producing adenoma of the left adrenal gland. After an adrenalectomy, she developed an SLE exacerbation, characterized by photosensitivity, polyarthralgia, and hemolytic anemia, which required intensive steroid therapy. This is the first report of a patient with SLE entering apparent remission due to excessive adrenal secretion of glucocorticoids.

Adult↗
PubMed1997

Effect of the chimeric soluble granulocyte colony-stimulating factor receptor on the proliferation of leukemic blast cells from patients with acute myeloblastic leukemia.

The biological roles of the soluble granulocyte colony-stimulating factor (G-CSF) receptor, which arises as a result of alternative RNA splicing, are as yet unknown. In this study, we examined the in vitro effect of a chimeric protein composed of the extracellular region of a murine G-CSF receptor and the human IgG1 Fc region because a human natural soluble G-CSF receptor was not available. First, we found that this chimeric soluble G-CSF receptor could inhibit the biological activity of G-CSF on normal bone marrow colony formation. Because G-CSF also plays an important role in the proliferation of leukemic blast cells, we next examined the effect of the soluble G-CSF receptor on leukemic blast colony formation in 10 acute myeloblastic leukemia cases. Although G-CSF stimulated the proliferation of leukemic progenitor cells to form leukemic blast colonies, the chimeric soluble G-CSF receptor completely inhibited this stimulatory effect. Furthermore, the chimeric soluble G-CSF receptor also inhibited spontaneous leukemic blast colony formation in two cases. Because a high concentration of G-CSF was observed in the supernatants of leukemic blast cells from these two cases, it seems likely that the soluble G-CSF receptor cut off the autocrine growth mechanism of leukemic blast cells mediated by G-CSF. These findings suggest the possibility that the soluble G-CSF receptor could be used in a clinical application for acute myeloblastic leukemia patients in the future.

Animals↗
PubMed1997

Role of the vav proto-oncogene product (Vav) in erythropoietin-mediated cell proliferation and phosphatidylinositol 3-kinase activity.

The vav proto-oncogene product (Vav), which is specifically expressed in hematopoietic cells, contains multiple structural motifs commonly used by intracellular signaling molecules. Although a variety of stimuli including erythropoietin (Epo) have been shown to tyrosine phosphorylate Vav, little is known about the Vav signal transduction pathway. Here, we have investigated the role of Vav in the Epo signaling pathway by characterizing its interaction with other proteins, using the human Epo-responsive cell line, F-36P. Immunoprecipitation and immunoblot analyses have demonstrated that Vav was associated with the Epo receptor (EpoR) in an Epo-independent manner and was tyrosine-phosphorylated after Epo stimulation. Furthermore, two phosphotyrosine proteins (pp70 and pp100) co-immunoprecipitated with the regulatory subunit of phosphatidylinositol 3-kinase (PI3-kinase) (p85) were identified as EpoR and Vav, respectively. The interaction between Vav and p85 was shown to be mediated through the SH2 domains of p85 by an in vitro binding assay and confirmed by the presence of in vitro PI3-kinase activity associated with Vav. Treatment of the cells with antisense-vav and -p85 abrogated Epo-induced cell proliferation and PI3-kinase activity. Finally, we found that JAK2 was associated with Vav in vivo and that Vav could be tyrosine-phosphorylated by activated JAK2 in vitro. These results suggest the possible role of JAK2 for tyrosine phosphorylation of Vav and involvement of Vav and PI3-kinase in Epo-induced proliferative signals.

Cell Cycle Proteins↗
PubMed1997

Regulation by interleukin-10 and interleukin-4 of cyclooxygenase-2 expression in human neutrophils.

Neutrophils are important effector cells of acute inflammation because of their potential capacity to synthesize various proinflammatory mediators, and inhibition of their production is expected to result in anti-inflammatory effects. In this study, we investigate the effects of the anti-inflammatory cytokines, interleukin-10 (IL-10) and IL-4, on prostanoid synthesis in human neutrophils. Neutrophils isolated from healthy donors constitutively produced a small amount of prostaglandin E2 (PGE2) without any stimulations, whereas they produced a large amount of PGE2 after lipopolysaccharide (LPS) stimulation. IL-10 and IL-4 selectively inhibited their LPS-induced PGE2 production. Inhibition by both cytokines occurred at an early stage of LPS stimulation. Anti-IL-10 treatment of LPS-stimulated neutrophils resulted in enhanced PGE2 production. LPS-induced PGE2 and thromboxane B2 (TXB2) production in aspirin-treated neutrophils was significantly inhibited by IL-10, IL-4, and NS-398. Moreover, IL-10 and IL-4 inhibited LPS-induced cyclooxygenase (COX) activity in neutrophils. Western blot and immunocytochemical analysis showed that COX-2 protein was clearly induced in LPS-stimulated neutrophils and that its induction was inhibited by both IL-10 and IL-4. Moreover, both of these cytokines inhibited COX-2 mRNA expression in LPS-stimulated neutrophils. These results raise the possibility that these two cytokines may both offer potent clinical utility as anti-inflammatory agents in the future.

Cells, Cultured↗
PubMed1997

Membrane tumor necrosis factor-alpha (TNF-alpha) expressed on HTLV-I-infected T cells mediates a costimulatory signal for B cell activation--characterization of membrane TNF-alpha.

The 26-kDa membrane tumor necrosis factor-alpha (TNF-alpha) expressed on activated CD4(+) T cells is a novel candidate for the functional membrane molecule in T-B cell interactions. We found that normal human T cells, when infected with human T cell lymphotropic virus type I (HTLV-I) in vitro, were induced to express the 26-kDa membrane TNF-alpha. The infected T cells, through this molecule, activated autologous B cells to produce immunoglobulin (Ig)M in a contact-dependent manner, which was partially inhibited by anti-TNF-alpha antibody (Ab). IgG synthesis was not stimulated, however, probably because of lack of CD40 ligand expression on the infected T cells. Anti-TNF-alpha Ab treatment stimulated the secretion of interleukin (IL)-2 and interferon gamma (IFN-gamma) in the infected T cells. These effects were not induced by anti-TNF receptor Ab treatment. Anti-TNF-alpha Ab also induced the elevation of intracellular calcium concentration in the infected T cells. These results suggest that T cells expressing membrane TNF-alpha can be directly stimulated through this molecule. Thus, it is suggested that the 26-kDa membrane TNF-alpha on HTLV-I-infected T cells plays a role in polyclonal B cell activation and may be involved in the pathogenesis of some HTLV-I-associated diseases. Additionally, our results suggest a novel mechanism by which cytokine production can be modulated in these T cells through membrane TNF-alpha on their surface.

Antigen Presentation↗
PubMed1997

Effect of (-)-epigallocatechin gallate on leukemic blast cells from patients with acute myeloblastic leukemia.

Information on the anti-carcinogenic effect of EGCG, the main constituent of the polyphenols present in Japanese green tea leaves, has recently been accumulating. In this report, we evaluate the effect of EGCG on leukemic blast cells from AML patients. The results showed that EGCG inhibited the proliferation of AML cells in all cases examined. Since AML cells might proliferate by autocrine or paracrine growth mechanisms, we also examined the effect of EGCG on the production of GM-CSF from AML cells. Although EGCG did not directly inhibit the production of GM-CSF, it did inhibit the effect of TNF-alpha or TPA, both of which stimulated AML cells to produce GM-CSF. On the other hand, the modulation of receptors for growth factors might play a role in the proliferation or carcinogenesis of AML cells. We also found that EGCG inhibited the modulation of c-kit, a receptor for stem cell factor, on leukemic cells. These findings suggested that EGCG might be available as a new therapeutic tool for AML patients.

Blast Crisis↗