Biomedical subjects

T Murayama

Publications and source records attributed to T Murayama.

At least 127 records · Page 7Linked to original sources

PubMed1998

Effects of alkaline protease or restrictocin deficient mutants of Aspergillus fumigatus on human polymorphonuclear leukocytes.

Several substances including proteases and restrictocin have been suggested as candidates for virulence determinants in invasive pulmonary aspergillosis. However, the roles of such substances are not well understood. This study compared the in vitro suppressive effects of Aspergillus fumigatus culture filtrates (ACFs), on the functions of human polymorphonuclear leukocytes (PMNLs), the principal cells in the host defence against aspergillus hyphae, from a clinically isolated wild-type and isogenic mutant strains which lack production of elastolytic alkaline protease (Alp) and/or restrictocin. ACFs were obtained by culturing conidia of each strain in Medium- 199 at 37 degrees C for 5 days. ACFs of the wild-type significantly (p<0.01) suppressed chemotaxis, superoxide anion (O2-) release and PMNL-mediated hyphal damage, compared with the control (Medium-199). ACFs of the mutant strains that lack Alp or restrictocin significantly (p<0.01) suppressed chemotaxis and O2(-)-release, but did not suppress hyphal damage, compared with the control. The wild-type significantly (p<0.01) suppressed chemotaxis of PMNLs compared with the mutant strains lacking Alp or restrictocin, whereas there were no significant differences in suppression of O2(-)-release and hyphal damage by PMNLs. ACF of a mutant strain that lacks both Alp and restrictocin had much less activity, but significantly (p<0.01) suppressed chemotaxis of PMNLs compared with the control. In conclusion, alkaline protease and restrictocin may play roles in the suppressive effect of Aspergillus fumigatus culture filtrates on the functions of human polymorphonuclear leukocytes. Other antiphagocytic substances produced by Aspergillus fumigatus remain to be identified.

Allergens↗

PubMed1998

Polypoid bronchial lesions due to Scedosporium apiospermum in a patient with Mycobacterium avium complex pulmonary disease.

A 69 yr old female was hospitalized for further examination of abnormal shadows on chest radiographs. She had a history of tuberculous pleurisy, rheumatoid arthritis and gold-induced interstitial pneumonia. On admission she still suffered from rheumatoid arthritis. A chest computed tomography scan on admission showed clusters of small nodules in subpleural regions of both lungs combined with bronchiectasis. Mycobacterium avium complex was cultured repeatedly from the sputum. Bronchoscopic examination disclosed white-yellow polypoid lesions in the orifice of the left B4 bronchus. Cultures of the brushing specimen of the polypoid lesions and bronchial aspirates from the B4 bronchus yielded smoky-grey mycelial colonies that were later identified as Scedosporium apiospermum. It was concluded that the polypoid bronchial lesions due to Scedosporium apiospermum were formed in the preexisting dilated bronchus caused by Mycobacterium avium complex pulmonary disease.

Aged↗

PubMed1998

The actions of NO in the central nervous system and in thymocytes.

Nitrogen monoxide (NO) has been suggested to be involved in many physiological and pathological functions. In rat hippocampus, chemical NO donors stimulated noradrenaline release in the presence of thiols such as dithiothreitol and L-cysteine. S-Nitrosocysteine, which is proposed to be a stable and endogenous S-nitrosothiol molecule, stimulated noradrenaline release by itself. The effect of S-nitrosothiol on noradrenaline release was calmodulin-dependent and cyclic GMP-independent. S-Nitrosocysteine was incorporated into the slice via the L-type-like amino acid transporter. These findings suggest the physiological significance of S-nitrosocysteine on neurotransmitter release and propose the existence of a specific uptake system of S-nitrosothiols in neuronal tissues. In rat thymocytes, chemical NO donors inhibited DNA synthesis. Hydrocortisone treatment in vivo inhibited DNA synthesis via the expression of the inducible NO synthase protein, and the accumulation of NO and cyclic GMP. Although it is known that glucocorticoids regulate inducible NO synthase expression negatively in several types of cells in vitro, glucocorticoid treatment in vivo regulates the expression positively. In primary cultured rat glial cells, a combination of cytokines stimulated production of nitrite via expression of inducible NO synthase. In these cells, simultaneous addition of endothelin decreased inducible NO synthase expression induced by cytokines. On the other hand, pretreatment with endothelin for 24 hr enhanced the inducible NO synthase expression. Endothelin has two effects on inducible NO synthase expression, positive and negative, depending on treatment time. The actions of NO on the hippocampus and thymocytes and the regulation of inducible NO synthase expression in glial cells are discussed.

Adjuvants, Immunologic↗

PubMed1998

The effects of T-588, a novel cognitive enhancer, on noradrenaline uptake and release in rat cerebral cortical slices.

Previously, we reported that (R)-(-)-1-(benzo[b]thiophen-5-yl)-2-[2-(N,N-diethylamino)-ethoxy]e thanol hydrochloride (T-588), a novel cognitive enhancer, stimulated noradrenaline (NA) release from rat cerebral cortical slices. In this study, we investigated the effects of T-588 on NA uptake and release, compared to the effects of desipramine, a blocker of the NA carrier on the plasma membrane. Both T-588 and desipramine caused dose-dependent inhibition of [3H]NA uptake into the slices. Addition of 3 mM T-588 stimulated [3H]NA release from the prelabeled slices even in the presence of 10 microM desipramine, which inhibited NA uptake completely. Tyramine, which accelerates NA carrier-mediated release, also stimulated [3H]NA release, and tyramine-stimulated release was inhibited by desipramine. These findings indicated that T-588-stimulated NA release was not mediated by 1) inhibition of reuptake or 2) reverse transport mediated by NA carriers. Reserpine, which interacts with the intracellular vesicular transport system, increased [3H]NA efflux from slices. High K+-, not T-588-, stimulated [3H]NA release was shifted upward by reserpine. These findings suggest that T-588 evokes NA release by a mechanism similar to that induced by reserpine. T-588 might act as a cognitive enhancer via neurotransmitter release in the brain.

Adrenergic Uptake Inhibitors↗

PubMed1998

[Interrelationship between human cytomegalovirus infection and chemokine].

Human cytomegalovirus (HCMV) infection is frequently associated with AIDS patients and immunocompromised recipients of organ transplants. The progression of HCMV infection is related to a complex interrelation of virus replication with the host immune system, including soluble and cellular factors. A chemokine, interleukin-8 (IL-8), is essentially involved in neutrophil-mediated tissue injury. Moreover, several chemokine receptors are co-receptor for HIV entry. Hence, we investigated the effects of IL-8 on HCMV replication in human embryonic fibroblasts, MRC-5 cells. IL-8 augmented both infectious virus production and replication of HCMV, with concomitant increases in the levels of both the HCMV pp71 genome and the synthesis of the HCMV late antigen. The enhancing effect of IL-8 was observed at concentration from 0.1 ng to 10 ng of IL-8/ml, showing a dose-response relationship similar to that observed in the neutrophil chemotactic activity of IL-8. IL-8 did not enhance the growth of MRC-5 cells, indicating that IL-8 enhanced HCMV replication and virus production without affecting the proliferation of host cells. We also found that HCMV selectively induced transcripts of CXCR-1 in fibroblasts by RT-PCR, but significant numbers of binding sites could not be detected on HCMV infected cells by using 125I-labeled IL-8. Thus, IL-8 may enhance HCMV replication in fibroblasts through interaction with small number of CXCR-1. Furthermore, HCMV infection induced IL-8 gene transcription in a human monocytic cell line, THP-1, leading to IL-8 secretion. It is unlikely that HCMV infection enhanced IL-8 production indirectly by inducing the production of some soluble factors, because virus-free filtrated HCMV or UV-irradiated HCMV infected supernatants failed to induce IL-8 production. The functional analysis of the IL-8 gene revealed that both AP-1 and NF-kB factor-binding element were involved in conferring the responsiveness to HCMV. Moreover, electrophoretic mobility shift assay demonstrated that the formation of AP-1 and NF-kB complex was observed upon HCMV infection. These results suggest that IL-8 produced upon HCMV infection, may aggravate HCMV infection by enhancing its replication. Thus, IL-8 and CXCR-1 might be a novel target for intervention therapy for opportunistic HCMV infection.

Antigens, CD↗

PubMed1998

[Eosinophilic cystitis induced by tranilast: a case report].

We report a patient with tranilast-induced eosinophilic cystitis who had no allergies, but had been administered tranilast to reduce prednisolone. A 62-year-old man presented with macroscopic hematuria and bladder irritative symptoms. The patient had a past medical history of idiopathic thrombocytopenic purpula and had been treated with 15 mg of prednisolone since 1980. He had been receiving 300 mg of tranilast for the past 18 months. Urinalysis revealed a marked increase in eosinophils (4 x 10(4)/ml). A cystoscopic examination revealed reddish mucosa throughout the bladder. A retrograde cystogram showed incomplete bilateral vesicoureteral reflux. Histological examinations of biopsied bladder specimens revealed a marked increase in the number of eosinophils (1,126/mm2), but not of mast cells (12/mm2). The symptoms resolved within one week after cessation of tranilast.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1998

Leiomyoma of the spermatic cord extending along the vas deferens.

We report an unusual case of a leiomyoma of the spermatic cord. The tumor did not present as a mass but presented as a hard structure along the spermatic cord. To our knowledge, this is the first case report of a leiomyoma of the spermatic cord with such an unusual appearance.

Aged↗

PubMed1998

[Retroperitoneal Castleman's disease: a case report].

We report a case of retroperitoneal Castleman's disease. A 57-year-old woman was referred for evaluation of microscopic hematuria. Computed tomography demonstrated a small solid retroperitoneal mass. The mass was surgically resected and the histopathological diagnosis of the resected tissue was hyalin vascular type of Castleman's disease. Although retroperitoneal Castleman's disease is an uncommon disease. We should always consider this tumor in the differential diagnosis of retroperitoneal tumors.

Castleman Disease↗

PubMed1998

[Rapid tapering of cyclosporine for cytogenetic relapse shortly after bone marrow transplantation in a patient with chronic myeloid leukemia].

A 53-year-old female case of cytogenetically relapsed chronic myeloid leukemia after allogeneic bone marrow transplantation (BMT) who achieved remission by withdrawal of immunosuppressant is reported. On day 690 of this presentation she is well and alive with performance status of 100%. She had episodes of cyclic oscillation of her neutrophil count during hydroxyurea therapy lasting 1 year before transplantation. Increase of the neutrophils at the time of BMT might have contributed to her early relapse on day 207. Withdrawal of immunosuppressant was successful at least in this case.

Bone Marrow Transplantation↗

PubMed1998

[Molecular mechanism of interleukin-8 gene expression].

Evidence is accumulating that interleukin-8 (IL-8), discovered as a potent neutrophil chemotactic factor, plays a crucial role in establishing acute neutrophil-mediated inflammation by exerting various activities against non-leukocytic as well as leukocytic cells. Various types of cells can rapidly produce a large amount of IL-8 upon stimulation with inflammatory stimuli, such as lipopolysaccharide, IL-1, and tumor necrosis factor (TNF). However, IL-8 production is tightly regulated at several levels, particularly at the transcriptional levels to prevent aberrant production. Our previous experiments demonstrated that IL-8 gene transcription requires the cooperative activation of a transcription factor, NF-kappa B, with an additional transcription factor, AP-1 or NF-IL6, depending on types of cells and stimuli. In addition, we recently observed that infection with Helicobacter pylori or cytomegalovirus activated NF-kappa B, therapy inducing IL-8 protein secretion as well as IL-8 gene transcription. Moreover, IL-8, in turn, enhanced cytomegalovirus replication and infectious virion production. Collectively, these results suggest the potential involvement of IL-8 in the pathology of bacterial or viral infection.

Cytomegalovirus↗

PubMed1998

[Multicentric Castleman's disease with lymphoid interstitial pneumonia and polyneuropathy].

A 51-year-old woman was admitted to a local hospital because of pneumonia, and received a diagnosis of cervical lymphadenopathy, anemia, and hyperimmunoglobulinemia with suspected multicentric Castleman's disease (MCD). At the age of 53 she was transferred to our hospital because of numbness and muscle weakness. Polyclonal hyperimmunoglobulinemia was observed, and biopsy specimens of lymph node tissue revealed infiltration of plasma cells in the interfollicular areas, thus leading to a diagnosis of MCD. A chest computed tomography scan revealed diffuse nodular shadows in all lung fields, and a transbronchial lung biopsy disclosed infiltration of plasma cells in the alveolar septa. Together, these findings indicated lymphoid interstitial pneumonia (LIP). Polyneuropathy was diagnosed by neurological examination and nerve conduction studies. Treatment with prednisolone and cyclophosphamide was ineffective against LIP probably because the patient had coexising pulmonary fibrosis. Since pulmonary complications of MCD determine its prognosis, their early detection and treatment are essential.

Castleman Disease↗

PubMed1998

[Anesthesia for abdominal surgery after percutaneous transluminal coronary angioplasty (PTCA)].

From December 1989 to October 1996, 1,318 PTCAs (percutaneous transluminal coronaly angioplasty) were performed for AMI (acute myocardial infarction) or postinfarction angina in our institute. Within 7 days to 71 days after successful PTCA, five patients who had been diagnosed as cholelithiasis or gastric cancer were operated under general anesthesia. Performed operations were cholecystectomy in the first patient, subtotal gastrectomy in the second, third and fourth patients, and total gastrectomy and cholecystectomy in the fifth patient. There was no serious cardiac complication during the operations and perioperative period. PTCA is considered to have decreased cardiac complications in patients with ischemic heart disease having undergone abdominal surgery.

Abdomen↗

PubMed1997

Endothelin enhances lipopolysaccharide-induced expression of inducible nitric oxide synthase in rat glial cells.

Lipopolysaccharide is known to stimulate production of nitrite via expression of inducible nitric oxide (NO) synthase in not only macrophages but also glial cells. We found that in glial cell cultures lipopolysaccharide-stimulated inducible NO synthase expression and nitrite accumulation were synergistically enhanced by pretreatment with endothelin, whereas endothelin itself did not induce these responses. Pretreatment with endothelin-1, endothelin-3, and the selective endothelin type B (ETB) receptor agonist IRL 1620 caused the same effect with similar potencies, suggesting that the synergism was mediated via the endothelin ETB receptor. A protein kinase C inhibitor, calphostin C, suppressed endothelin-3-enhanced inducible NO synthase expression. Pretreatment with either endothelin-3 or phorbol ester enhanced lipopolysaccharide-induced production of tumor necrosis factor-alpha (TNF-alpha). Simultaneous addition of TNF-alpha increased lipopolysaccharide-stimulated inducible NO synthase expression. These results suggest that the increase in inducible NO synthase expression by endothelin was due to the elevated TNF-alpha production via protein kinase C. Our findings present the possibility that endothelin is implicated in neurotoxicity via enhancement of inducible NO synthase expression.

Animals↗

PubMed1997

The alpha chemokine, interleukin 8, inhibits the antiviral action of interferon alpha.

Interferon (IFN) exhibits a potent antiviral activity in vitro and plays a major role in the early defense against viruses. Like IFN, the proinflammatory chemokine, interleukin (IL)-8, is induced by viruses and appears in circulation during viral infections. In an in vitro cytopathic effect assay for IFN, we found that IL-8 can inhibit IFN-alpha activity in a dose-dependent manner. This action was reversed by specific monoclonal antibodies to IL-8. The chemokine was able to attenuate the IFN-mediated inhibition of viral replication as determined by measuring infectious virus yield. IL-8 also diminished the ability of IFN to inhibit an early stage of viral replication since IL-8 attenuated the inhibition of the formation of viral proteins. It appeared that IL-8 interfered with a late rather than an early step of IFN-mediated pathway such as early gene expression. The IL-8 inhibitory action on IFN-alpha antiviral activity was associated with reduced 2',5'-A oligoadenylate synthetase activity, a pathway well correlative with the anti- encephalomyocarditis virus action of IFN-alpha. Understanding pathways that antagonize IFN action may lead to novel approaches to potentiate endogenous and therapeutic IFN.

2',5'-Oligoadenylate Synthetase↗

PubMed1997

Characterization of type 3 ryanodine receptor (RyR3) of sarcoplasmic reticulum from rabbit skeletal muscles.

We investigated type 3 isoform (RyR3) of ryanodine receptor in rabbit skeletal muscles using an antibody specific for RyR3. By Western blot analysis and by immunoprecipitation, a single polypeptide for RyR3 was detected in sarcoplasmic reticulum vesicles from rabbit diaphragm but not in those from back muscle. The molecular mass was slightly smaller than that of RyR1, the major isoform in skeletal muscles. Each of RyR1 and RyR3 formed a homotetramer in rabbit diaphragm. RyR3 had a single class of [3H]ryanodine binding sites of high affinity (KD = 1.6 nM). From the Bmax of the binding, the content of RyR3 was estimated to be only 0.6% of RyR1 in rabbit diaphragm. -3H-Ryanodine binding to RyR3 was biphasically dependent on Ca2+, as is true of RyR1, and was stimulated further by adenine nucleotide, caffeine, or high salt concentration. Procaine and ruthenium red inhibited the binding. RyR3 was more resistant to Mg2+ inhibition than RyR1. Interestingly, RyR3 showed about a 7-fold lower Ca2+ sensitivity for activation than RyR1. Comparison with the counterparts in bullfrog skeletal muscles indicates that the Ca2+ sensitivities of RyR3 homologs are similar to each other, whereas those of RyR1 homologs are species-specific.

Animals↗

PubMed1997

Interleukin-8 selectively enhances cytopathic effect (CPE) induced by positive-strand RNA viruses in the human WISH cell line.

Interleukin-8 (IL-8), a proinflammatory chemokine, is induced by viruses and appears in circulation during viral infections. We found that IL-8 enhanced cytopathic effect induced by the positive strand RNA virus, encephalomyocarditis virus (EMCV), in the human WISH cell line. The enhancement was dependent on IL-8 dose and virus dose and was reversible by specific monoclonal antibodies to IL-8. The chemokine was also able to increase EMC viral RNA synthesis and infectious virus yield. This IL-8 enhancing action was not observed in the case of the negative strand RNA virus, vesicular stomatitis virus (VSV), in WISH cells. We examined the activity of constitutive 2',5'-oligoadenylate synthetase (OAS), a pathway that was implicated in protection from EMCV but not VSV. The IL-8 action in EMCV-infected cells, unlike VSV-infected cells, was associated with decreased OAS activity in a manner that was independent of OAS gene expression. Understanding mechanisms of cytokine enhancement of viral activity may lead to novel ways to control viral infections.

2',5'-Oligoadenylate Synthetase↗

PubMed1997

Nuclear factor Y controls the basal transcription activity of the mouse platelet-derived-growth-factor beta-receptor gene.

To determine the regulatory mechanism of the expression of the mouse platelet-derived growth factor (PDGF) beta-receptor gene, a 1.9-kb 5' flanking genomic fragment was cloned and analyzed. Site-directed mutagenesis of a CCAAT motif, located 60 bp upstream of the transcriptional-start site, completely abolished the promoter activity [Ballagi, A. E., Ishisaki, A., Nelin, J.-O. & Funa, K. (1995) Biochem. Biophys. Res. Commun. 210, 165-1751. The sequence around the intact CCAAT motif was protected by in vitro DNase-I-footprinting analysis. Electrophoresis-mobility-shift assays with anti-[nuclear factor Y(NF-Y)]Ig revealed binding of the NF-Y complex to the CCAAT box. Furthermore, the double-stranded oligonucleotides corresponding to the sequence around the CCAAT motif were conjugated with DNA-affinity magnetic beads. The binding proteins were affinity purified and identified as the NF-Y transcription factor by western blotting. Our results indicate that NF-Y controls the basal transcription activity of the mouse PDGF beta-receptor gene.

3T3 Cells↗

PubMed1997

Effects of R(-)-1-(benzo[b]thiophen-5-yl)-2-[2-N,N-diethylamino)ethoxy]ethan ol hydrochloride (T-588), a novel cognitive enhancer, on noradrenaline release in rat cerebral cortical slices.

We investigated the effects of R(-)-1-(benzo[b]thiophen-5-yl)-2-[2-(N,N-diethylamino)ethoxy]ethan ol hydrochloride (T-588), a novel cognitive enhancer, on noradrenaline (NA) release from rat cerebral cortical slices in vitro. Addition of T-588 in an assay mixture stimulated [3H]NA release from prelabeled slices in the presence or absence of extracellular CaCl2, and in the presence of the Ca2+/calmodulin antagonists N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide and trifluoperazine. T-588 stimulated NA release with a time lag of about 1 min, and the high level of release was maintained for at least 10 min, whereas maximal KCl-evoked NA release was observed within 1 min after the addition of KCl, and the effect declined subsequently. The effect of T-588 was reversible (pretreatment with T-588 showed no effect on NA release after two washes by centrifugation). We also compared the effects of T-588 and N-ethylmaleimide (NEM), a sulfhydryl alkylating agent known to stimulate neurotransmitter release in several types of cells. The addition of NEM stimulated NA release irreversibly from the slices in a Ca2+-independent manner, and the effect of NEM, but not that of T-588, was inhibited by the simultaneous addition of dithiothreitol, a sulfhydryl group reducing agent. The addition of T-588, which stimulated NA release by itself, inhibited the NA release by 0.6 mM NEM, although the effect of T-588 was additive in the presence of 0.2 mM NEM. These findings suggest that T-588 stimulates NA release from rat cerebral cortical slices in a Ca2+- and calmodulin-independent manner, possibly via an NEM-sensitive factor(s), although the mechanism of the effects of T-588 seems to be different from that of NEM.

Animals↗