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Biomedical subjects

Y Niho

Publications and source records attributed to Y Niho.

At least 127 records · Page 7Linked to original sources
PubMed1998

Large granular lymphocytic leukaemia with a mixed T-cell/B-cell phenotype.

We report a case of large granular lymphocytic leukaemia (LGLL) with mixed T-cell/B-cell phenotypes. The LGLL cells expressed T-cell markers such as CD1, CD2, CD3, CD5, CD7, CD8 and CD57. The CD8+ LGLL cells coexpressed B-cell markers including CD20 and PCA-1, and a fraction of purified CD8+ LGLL cells secreted double isotypes of immunoglobulins (IgG-kappa and IgA-kappa). Both TCRB and IGH genes were clonally rearranged. The LGLL cells could be divided into at least three subpopulations that were cytogenetically distinct, and all subpopulations involved the 11q23. The expression of both T- and B-cell markers on the LGLL cells suggests the involvement of a putative common lymphoid progenitor in leukaemic transformation.

Aged↗
PubMed1998

Early viral complications following CD34-selected autologous peripheral blood stem cell transplantation for non-Hodgkin's lymphoma.

A patient with non-Hodgkin's lymphoma who received a CD34-selected autologous peripheral blood stem cell transplant (PBSCT) developed cytomegalovirus retinitis, adenovirus-associated haemorrhagic cystitis (HC) and fatal herpes simplex virus pneumonia. Depletion of mature T cells from the graft and a persistent decrease in CD4+ lymphocytes following PBSCT may have predisposed this patient to such viral infections. Infusion of cryopreserved autologous PBSC (containing mature T cells) was effective for adenovirus-associated HC. Immunosuppression and resultant viral infections may affect patients receiving CD34-selected autologous transplantation.

Adenoviridae Infections↗
PubMed1998

Effect of thrombopoietin on proliferation of blasts from CD7-positive acute myelogenous leukaemia.

We investigated the effect of thrombopoietin (TPO) on the growth of leukaemic blasts from 30 acute myelogenous leukaemia (AML) patients according to the surface expression of CD7 and CD34: 10 patients were CD7 positive (CD7+), nine were CD7 negative/CD34+ (CD7-/CD34+) and the remaining 11 were CD7-/CD34-. Significant growth response of leukaemic blasts to TPO was observed in 10/10 CD7+, 5/9 CD7-/CD34+ and 2/11 CD7-/CD34- AML cases using 3H-thymidine incorporation. Synergistic stimulatory effects of TPO with stem cell factor (SCF), interleukin-3 (IL-3), granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor were observed in both TPO-responding cases (9/17) and TPO-non-responding cases (8/13). In a leukaemic blast colony assay. significant growth response to TPO was observed in 5/6 CD7+ and 4/17 CD7-AML cases examined. However, the effect of TPO on the growth of CD7+ leukaemic blasts was not so potent as that of IL-3 and SCF, both of which support the proliferation of primitive haemopoietic progenitors. Expression of c-mpl (TPO receptor) was significantly higher in CD7+ AML cases than in CD7- cases, suggesting a relationship between expression of c-mpl and proliferative response to TPO. These data indicate that CD7+ leukaemic blasts express functional TPO receptors and proliferate in response to TPO. These observations also imply that CD7 expression on AML blasts may indicate involvement of leukaemic progenitors at an early stage of multipotent haemopoietic stem cells.

Adolescent↗
PubMed1998

Beta2-glycoprotein I-dependent and -independent anticardiolipin antibody in non-obese diabetic (NOD) mice.

In the present study we investigate whether or not anticardiolipin antibody (aCL) is produced in NOD mice, which is a representative animal model of insulin-dependent diabetes mellitus (IDDM). We found that IgG class aCL appeared in 6.9% of non-diabetic NOD mice at weeks 5-15. The rates increased with age to 31.6% at weeks 16-25 and 71.9% at weeks 26-35. In addition, the titre and incidence of aCL were higher in diabetic mice than in non-diabetic mice. It was also found that aCL in NOD mice involved beta2-glycoprotein I (beta2-GPI)-dependent and -independent aCL, when beta2-GPI was added to the aCL assay system. The IgG subclass of both beta2-GPI-dependent and -independent aCL belonged exclusively to IgG2a. In addition, immunohistochemical studies revealed the predominant accumulation of IgG2a- or IgG3-positive B lymphocytes within insulitis. These results suggest that the autoimmunity in NOD mice may thus be associated with Th1 predominant immunological response. In conclusion, aCL with multiple antigenic specificity were produced in NOD mice along with the development of insulitis and diabetes. NOD mice should thus be added to the list of animal models possessing antiphospholipid antibody.

Animals↗
PubMed1998

Action of interleukin-3 on the proliferation of leukaemic progenitor cells from patients with acute myeloblastic leukaemia.

In the present study, we examined the effects of interleukin-3 (IL-3) on the proliferation of leukaemic progenitor cells from 11 Japanese patients with acute myeloblastic leukaemia (AML), including the effect of its combination with granulocyte/macrophage colony-stimulating factor (GM-CSF) or granulocyte colony-stimulating factor (G-CSF). The results showed that IL-3 sufficiently stimulated the proliferation of AML progenitor cells in almost all the cases examined, and that the stimulation pattern of IL-3 was similar to that of GM-CSF, although different from that of G-CSF. Furthermore, IL-3 worked synergistically with G-CSF, whereas IL-3 and GM-CSF together were less actively synergistic (P < 0.05). These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.

Adolescent↗
PubMed1998

Proliferation of CD3+ B220- single-positive normal T cells was suppressed in B-cell-deficient lpr mice.

It is known that lpr mice develop systemic lymphadenopathy and lupus erythematosus-like autoimmune disease that are associated with the accumulation of CD4- CD8- (double-negative; DN) CD3+ B220+ abnormal T cells as well as normal mature CD4+ or CD8+ single-positive (SP) CD3+ T cells. In order to clarify the role of B cells in the lymphoproliferation and autoimmunity of lpr mice, we created B-cell-deficient C57BL/6 (B6) lpr mice (B6lpr/lpr microMT/microMT) by crossing B6lpr/lpr mice with B6 microMT/microMT mice in which the B-cell development was arrested at pre-B stage owing to a targeted disruption of the immunoglobulin mu heavy-chain gene locus. In the B-cell-deficient B6-lpr mice, both lymphadenopathy and splenomegaly were markedly suppressed. Although the accumulation of both CD3+ B220- SP normal T cells and CD3+ B220+ DN abnormal T cells was inhibited in the B-cell-deficient lpr mice, the decrease in numbers of CD3+ B220- SP normal T cells occurred more strikingly than that of the CD3+ B220+ DN abnormal T cells. Glomerulonephritis did not develop in the B-cell-deficient lpr mice over 40 weeks. The present results indicate that the B cells thus play a crucial role in the extensive proliferation of normal CD3+ B220- mature SP T cells rather than the accumulation of abnormal DN T cells.

Animals↗
PubMed1998

Analysis of CD40 ligand gene mutations in patients with primary biliary cirrhosis.

An elevated immunoglobulin (Ig)M concentration in serum is a common and distinctive feature of primary biliary cirrhosis (PBC). Little is known, however, about the mechanism of hyper-IgM in PBC. CD40 ligand (CD40L) has a crucial role in immunoglobulin class switching in B cells. Mutations in the gene encoding CD40L are known to induce X-linked hyper-IgM syndrome. To identify mutations in the gene for CD40L in PBC patients, we analyzed CD40L gene mutations, using reverse transcription (RT)-PCR single-strand conformation polymorphism (SSCP) analysis. No mutations were detected in cDNA from any of 24 PBC patients by the RT-PCR-SSCP technique. These data suggest that other, unidentified mechanisms are involved in hyper-IgM in PBC patients.

Aged↗
PubMed1998

Fas/Fas ligand and hematopoietic progenitor cells.

Fas antigen is a receptor that crosslinks with a ligand or antibody initiating a signal transduction cascade that leads to apoptosis. During normal hematopoiesis, Fas antigen is not expressed on CD34+ cells, including premature hematopoietic progenitor cells. Functioning Fas antigen expression is induced by several hematopoietic regulators. These changes may appear not only in the process of differentiation of hematopoietic progenitor cells, but also as a negative feedback mechanism that controls chaotic proliferation of these cells. These findings suggest that the Fas/Fas ligand system is closely related to the maintenance of homeostasis during the process of normal hematopoiesis. Furthermore, increased Fas antigen expression is observed on CD34+ cells from patients with aplastic anemia, suggesting that it might cause bone marrow suppression. The use of Fas-mediated apoptosis of malignant cells as a tool for eliminating hematologic malignancies is promising. Increased Fas ligand expression is observed on natural killer lymphoma cells and may be associated with the pathogenesis of failure of several organs. The Fas/Fas ligand system plays an important role in the physiologic and pathologic processes of hematopoiesis. The development of treatments using this system are forthcoming.

Antigen-Antibody Reactions↗
PubMed1998

Radiofrequency catheter ablation of left ventricular outflow tract tachycardia: report of two cases.

Idiopathic ventricular tachycardia (VT) originating from the left ventricular outflow tract (LVOT) is rare. We report two patients whose QRS configuration during VT commonly showed an inferior axis and monophasic R waves in all the precordial leads. The mechanism of these VTs appeared to be triggered activity. From mapping and ablation, the origin of these VTs was determined to be in the most posterior LVOT, corresponding to the aortomitral continuity (left fibrous trigone).

Catheter Ablation↗
PubMed1998

Hemophagocytic syndrome associated with fulminant ulcerative colitis and presumed acute pancreatitis.

We herein report a case of hemophagocytic syndrome that developed in a 25-yr-old man with fulminant ulcerative colitis and presumed acute pancreatitis. Physical examination on admission showed a chronically ill, delirious patient with an upper abdominal mass. Peripheral blood showed progressive pancytopenia and bone marrow aspirate smears revealed hypocellular bone marrow with an increase of histiocytes showing prominent hemophagocytosis. Plain abdominal radiography revealed toxic megacolon. Both ultrasound and computed tomography showed the enlargement of the pancreas, thus indicating presumed acute pancreatitis. No apparent neoplasms or viral or bacterial infections, which are normally reported to be the cause of hemophagocytic syndrome, were detected. The patient was successfully treated with high doses of prednisolone and gamma-globulin.

Acute Disease↗
PubMed1998

Analysis of the granulocyte colony-stimulating factor receptor gene structure using PCR-SSCP in myeloid leukemia and myelodysplastic syndrome.

The membrane-proximal cytoplasmic region of the granulocyte colony-stimulating factor receptor (G-CSFR) is known to be essential for the proliferation signal, with a more distal region being required for the differentiation signal. Such a separation of functional domains raises the possibility that mutations occurring at these regions may contribute to cell proliferation in the absence of differentiation, this being the most important characteristic in acute leukemia cells. Therefore, we analysed the structural abnormalities at the transmembrane and cytoplasmic region of G-CSFR in a significant number of patients with various myeloid malignancies. When we examined the genomic DNA of G-CSFR obtained from 41 patients with acute myelogenous leukemia (AML), 18 with chronic myelogenous leukemia (CML), 7 with myelodysplastic syndrome (MDS), 2 with chronic myelomonocytic leukemia and 1 with chronic neutrophilic leukemia, we found a polymorphism in 3 patients, but no significant pathogenic mutations in any patients. The screening for this polymorphism in 100 hematologically normal controls revealed that it may be useful as a linkage marker for population and family studies, because the heterozygosity index is at a high level (0.055). While there have been several reports discussing the leukemogenic potential of mutations in the cytokine/hematopoietin receptor superfamily, genetic alterations in the transmembrane and cytoplasmic region of G-CSFR do not seem to play a pathogenic role in leukemia.

Humans↗
PubMed1998

[Clinical study of itraconazole for systemic fungal infections complicated with hematological malignancies--multicenter cooperative study. West-Japan Systemic Fungal Infection Study Group].

Itraconazole, an oral antifungal agent, was evaluated for the clinical efficacy and safety in patients documented or suspected of systemic fungal infection (SFI) complicated with hematological malignancies. The data was also evaluated according to serological tests and fungal culture. Out of a total of 79 patients, the clinical efficacy of itraconazole was evaluated in 52 patients, comprising 4 patients with proven SFI, 33 with clinical SFI, and 15 with suspected SFI. The overall efficacy was 67.3% (35/52), in which 25.0% in the established SFI group (1/4), 78.8% in the clinical SFI group (26.33), and 53.3% in the suspected SFI (8/15). When assessed according to the severity of SFI, the effectiveness rates were 75.0% in the mild group (15/20), 76.2% in the moderate group (16/21), and 36.4% in the severe group (4/11), resulting in significantly higher rates in the mild and the moderate groups than in the severe group (p = 0.0479). Out of the 10 patients who were switched from the previous antifungals, 7 patients were judged as showing marked or good responses. All of these patients were switched from intravenous fluconazole therapy. With respect to the safety of itraconazole, among 79 patients eligible for safety evaluation, adverse events such as hepatic dysfunction, increase in GOT and/or GPT, nausea and vomiting, and chest pain were observed in 6 patients (7.6%), and itraconazole may have been associated with them. As a conclusion, itraconazole proved to be effective and safe on SFI developed in patients with various hematological malignancies.

Administration, Oral↗
PubMed1998

Role of IL-10 in the crossregulation of prostaglandins and cytokines in monocytes.

In the present study we have focused mainly on the role of IL (interleukin)-10 in the crossregulation of prostaglandins and cytokines in human monocytes. We first determined the effects of tumor necrosis factor-alpha (TNF-alpha) and IL-10 on monocyte prostaglandin E2 (PGE2) production. Unstimulated monocytes constitutively produced a small but significant amount of PGE2 in the culture supernatants. Both TNF-alpha and lipopolysaccharide (LPS) caused a remarkable increase in monocyte PGE2 production. On the other hand, IL-10 alone was without effect on constitutive PGE2 production but drastically inhibited LPS-induced PGE2 production in monocytes. Moreover, this inhibitory effect of IL-10 was not simply attributable to its inhibition of TNF-alpha production in LPS-stimulated monocytes. Next, we determined the effect of PGE2 on TNF-alpha mRNA expression in monocytes. Treatment of monocytes with or without PGE2 showed no detectable TNF-alpha mRNA. Activation of monocytes by LPS resulted in a remarkable accumulation of TNF-alpha mRNA and PGE2 efficiently inhibited this expression. Finally, we determined the effect of PGE2 on IL-10 mRNA expression in monocytes. Similar to TNF-alpha mRNA, unstimulated monocytes showed no detectable IL-10 mRNA. Interestingly, PGE2 alone drastically induced IL-10 mRNA. Besides, activation of monocytes by LPS resulted in a remarkable accumulation of IL-10 mRNA, and PGE2 further enhanced this expression. These results indicate that TNF-alpha and PGE2 are key molecules for the induction of IL-10 in monocytes, and that IL-10, in turn, plays a crucial role in terminating the inflammatory cascade via downregulation of production of proinflammatory molecules including TNF-alpha and PGE2.

Cells, Cultured↗
PubMed1998

Interaction of mRNAs for angiotensin II type 1 and type 2 receptors to vascular remodeling in spontaneously hypertensive rats.

We administered angiotensin II (Ang II) receptor type 1 (AT1) blockade (losartan, 40 mg x kg-1 x d-1), type II receptor (AT2) blockade (PD123319, 100 mg x kg-1 x d-1), or angiotensin-converting enzyme (ACE) inhibitor (enalapril, 30 mg x kg-1 x d-1) to spontaneously hypertensive rats (SHR) from 10 to 20 weeks of age. Control SHR and Wister-Kyoto rats (WKY) received a placebo for the same period. At the end of treatment, losartan and enalapril were both found to have significantly reduced the arterial systolic blood pressure and the collagen concentration to the level of WKY, whereas PD123319 had no effect. Enalapril and PD123319 significantly reduced the media cross-sectional area of the aorta in comparison to that of untreated SHR, which was still larger than that of the WKY; however, losartan did not change it. Using reverse transcription-polymerase chain reaction, we next examined the mRNA expressions for ACE, AT1 receptor, and AT2 receptor in experimental animals. We observed significantly enhanced mRNA expression for AT1 and AT2 receptors and ACE in untreated SHR compared with WKY. The AT1 mRNA level was also significantly decreased in the SHR treated with either losartan or enalapril, whereas the AT2 mRNA level was significantly decreased in the SHR treated with either PD123319 or enalapril in comparison to untreated SHR. The level of ACE mRNA was significantly decreased only in the SHR treated with enalapril. These results indicate that AT1 receptor, but not AT2 receptor, plays a crucial role in the remodeling of matrix tissue, while AT2 receptor may play a role in the development of hypertrophy of smooth muscle in aorta in SHR, and that the reduction of hypertrophy of smooth muscle does not fully account for the suppression of hypertension.

Angiotensin Receptor Antagonists↗
PubMed1998

Isoproterenol-induced creatine kinase leakage in Langendorff-perfused rat heart associated with significant myocardial edema.

Since the mechanism of creatine kinase (CK) leakage induced by beta-adrenoceptor activation remains unclear, we studied the effects of incremental application (10(-9) to 10(-4) M) of isoproterenol (ISP) on the CK efflux from Langendorff-perfused isolated rat hearts under aerobic conditions. Tissue water content was estimated after the perfusion experiment. ISP-induced dose-dependent CK leakage was noted in a sigmoidal fashion, which showed low temperature-dependency (Q10 of 2.41), sensitivity to cepharantine (10(-6) M) and propranolol (10(-7) to 10(-6) M) without any signs of demand ischemia or oxidant stress. CK liberation was not replicated at all by maneuvers activating cAMP-dependent protein kinase (A-kinase). Myocardial edema noted in the control ISP application was ameliorated by exposure to 10(-6) M propranolol or cepharantine (i.e., significant fall in tissue water content; p < 0.05). Histological study revealed nonspecific myocardial fiber swelling and separation without any myocyte necrosis for all the perfusion groups. These results suggest that ISP-induced CK leakage in this model is not mediated by beta-adrenoceptor stimulation, subsequent A-kinase activation or related demand ischemia, but is attributed most to the direct effects of ISP augmenting sarcolemmal CK and water permeability.

Adrenergic beta-Agonists↗
PubMed1998

[Interstitial cystitis in case of primary Sjögren's syndrome].

A 53-year-old woman who had xerostomia for ten years was admitted to our hospital because of refractory lower abdominal pain and pollakisuria of five years duration. Although she had undergone surgical treatments including cholecystectomy, ovarian cystectomy and groin hemiorrhaphy, she still suffered from abdominal symptoms. A diagnosis of interstitial cystitis was confirmed by hydraulic distention during a cystoscopic examination and by histopathological examination of the bladder. Her symptoms disappeared soon after the cystoscopic procedure, which also had a therapeutic effect of interstitial cystitis. Laboratory findings revealed hypergammaglobulinemia, a high titer of rheumatoid factor, positive anti-nuclear antibody, and positive anti-SS-A/Ro antibody. She was diagnosed as having primary Sjögren's syndrome based on the results of a gum test (8.5 ml/ 10 min), sialography (Stage II), and a positive minor salivary gland biopsy. Starting one month after the hydraulic distention, her abdominal symptoms gradually reappeared along with elevation of her serum IgG level. These features were markedly improved with 30 mg/day of oral prednisolone, which was then successfully tapered. These results suggested that interstitial cystitis in this case was caused by immunological abnormalities associated with Sjögren's syndrome.

Cystitis, Interstitial↗
PubMed1998

[Fanconi anemia].

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Apoptosis↗