Search PubMed⌕ Search

Biomedical subjects

M Osame

Publications and source records attributed to M Osame.

At least 181 records · Page 10Linked to original sources
PubMed1997

Human T-cell lymphotropic virus type 1 can infect primary rat retinal glial cells and induce gene expression of inflammatory cytokines.

PURPOSE: To examine whether or not retinal glial cells can be infected by human T-cell lymphotropic virus type 1 (HTLV-1) and test the possibility that HTLV-1-infected retinal glial cells are involved in the pathogenesis of HTLV-1 uveitis (HU). METHODS: We tested infection of HTLV-1 by a standard coculturing method using WKAH rat retinal glial cells and irradiated MT-2, a human T cell line that produces HTLV-1. Infection was confirmed by detecting the integrated HTLV-1 provirus, using polymerase chain reaction (PCR), viral gene expression, using reverse transcriptase-PCR (RT-PCR) and HTLV-1 p19 ELISA, and by identifying the HTLV-1-infected glial cells by immunofluorescence cytochemistry and in situ hybridization. Changes in cytokine gene expression were studied by RT-PCR. RESULTS: Using a semiquantitative PCR of HTLV-1 provirus sequence, we found that 2.6% of the retinal glial cells were infected at 3 days after infection, followed by a gradual decrease in the percentage with an extended period of culture up to 4 weeks. This time course of infection was also verified by RT-PCR and ELISA studies that detect viral mRNA expression and protein production, respectively. Expression of HTLV-1 gag protein and tax mRNA was detected in a part of glial cells by indirect immunofluorescence cytochemistry and in situ hybridization, respectively. RT-PCR analysis of cytokine gene expression revealed that gene expression of IL-6, CINC-1 (Gro, KC), and TNF-alpha were induced in these cells, with a peak at 3 weeks after infection. CONCLUSION: These results provided supportive evidence for the theory that the infection of retinal glial cells by HTLV-1 and subsequent production of inflammatory cytokines could be one contributing factor for the development of the unique clinical features of HU. A better understanding of the specific roles of the inflammatory cytokines in the pathogenesis of HU would be beneficial in the treatment and control of this disease.

Animals↗
PubMed1997

The effects of tobacco smoking on the short, middle, and long latency responses of the blink reflex in humans.

The three responses (R1, R2, and R3) of the electrically elicited blink reflex (BR) obtained in four normal human subjects were investigated before and after smoking both a filtered and an unfiltered cigarette. The changes observed in the BR were stronger and statistically more significant for the unfiltered than for the filtered cigarette, (p < 0.0001) and were more dramatic in R3 than R1 or R2. The action of nicotine on central pathways located at the interneuronal network of the brainstem, basal ganglia, and C fiber structures involved with this reflex seems to be the most likely mechanism for these findings.

Adult↗
PubMed1997

Depression of neuromuscular transmission in methylmercury-poisoned rats: a glass microelectrode and single fiber electromyography study.

Changes in neuromuscular transmission were examined in methylmercury (MeHg)-poisoned rats, given a total oral dose of 60 mg CH3HgCl at 5 mg/kg/day. A microelectrode study was done on the 21st day. The mean quantal content and mean values of the immediately available pool of ACh in the MeHg-poisoned rats were reduced as compared to those in the control rats, but the mean values for the release probability of ACh did not differ significantly. Stimulation single fiber electromyography (SFEMG) was done on the biceps femoris muscle at 1, 5, 10 and 20 Hz on the 28th day. Both a significant and consistent increase in jitter were found at increasing stimulation rates in the MeHg-poisoned rats. The SFEMG findings suggest presynaptic involvement due to accelerated depletion of ACh. We confirmed that neuromuscular transmission is depressed in MeHg-poisoned rats in vivo and in vitro.

Animals↗
PubMed1997

cis-Acting inhibitory elements within the pol-env region of human T-cell leukemia virus type 1 possibly involved in viral persistence.

Human T-cell leukemia virus type 1 (HTLV-1) remains latent throughout the life of the carrier, with cells containing the provirus and viral gene expression efficiently down-regulated. On a molecular level, exactly how viruses are down-regulated in vivo remains unresolved. We described here the possibility that down-regulation results from the presence of inhibitory elements within the gag-env region of the provirus in fresh peripheral blood mononuclear cells from carriers. In vitro experiments then revealed that potent cis-acting inhibitory elements (CIEs) are indeed contained in two discrete fragments from the pol region and weaker ones in the env region. The effect of CIEs is relieved by the HTLV-1 posttranscriptional regulator Rex through binding to the Rex-responsive element (RxRE), suggesting that Rex might interfere with pre-mRNA degradation and/or activate the export of mRNA molecules harboring both of the inhibitory elements and RxRE on the same RNA molecule. Thus, we propose the hypothesis that such functions of CIEs may be involved in HTLV-1 persistence.

Cell Line↗
PubMed1997

Abnormalities in the protein C anticoagulant pathway detected by a novel assay using human thrombomodulin.

We developed a novel assay using human thrombomodulin (TM), which detected overall abnormalities in the protein C anticoagulant pathway (PC pathway). This assay indicates the degree of inhibition of prothrombinase by TM, which is represented as the percentage of prothrombinase inhibition by 25 ng/ml of TM, termed PIP25 (Prothrombinase Inhibition Percentage). We examined PIP25 in plasma samples from patients with systemic lupus erythematosus (SLE) with or without lupus anticoagulant (LA), patients with Behcet's disease (BD), and patients with miscellaneous thrombotic vasculitis and compared these with the PIP25 of plasma samples from healthy volunteers in Japan. The PIP25S were significantly lower in SLE alone (35.5 +/- 12.8%, P = 0.036) and SLE with LA (33.0 +/- 13.3%, P = 0.030) and BD (33.3 +/- 13.4%, P = 0.010) than those in healthy volunteers (43.5 +/- 10.7%). There was no significance between healthy PIP25 and those with miscellaneous thrombotic vasculitis (44.2 +/- 8.4%, P = 0.823). These results suggest that the abnormalities of the protein C anticoagulant pathway were present in patients with SLE(LA) and BD.

Behcet Syndrome↗
PubMed1997

Idiopathic hypoparathyroidism with fungal seminal vesiculitis.

A 23-year-old man was suffering from high fever and general fatigue 6 months before admission. The levels of serum Ca and intact-parathyroid hormone (PTH) were low. His brain computed tomography (CT) revealed marked calcifications of the basal ganglia, and pelvis magnetic resonance imaging (MRI) showed inflammation of his seminal vesicle. His candida antigen titer was high and antibiotic therapy was unsuccessful. High fever persisted despite fluconazole treatment, however he recovered after treatment with fluconazole and vitamin D (alfacalcitol). Idiopathic hypoparathyroidism hinders the activation of vitamin D via insufficient PTH secretion, and vitamin D has some immunological effects. His decreased natural killer (NK) cell activity improved after alfacalcitol treatment. We suggest the possible immunological effects of vitamin D in this fungal infection.

Adult↗
PubMed1997

Nationwide survey of neurologic manifestations of acquired immunodeficiency syndrome in Japan.

To study the epidemiology of the neurologic manifestations of human immunodeficiency virus (HIV)-1 infection in Japan, we conducted two nationwide surveys. Of 1854 HIV-1 carriers, 578 had acquired immunodeficiency syndrome (AIDS) and 166 (28.7% of AIDS patients) had neurologic manifestations including HIV dementia (11.8%), myelopathy (3.6%) and peripheral neuropathy (2.6%). The incidence of neurologic manifestations in patients with HIV-1 infection through blood products was about 60% of that in patients with HIV-1 infection through sex or unknown routes. This nationwide survey showed that the incidence of neurologic manifestations in AIDS patients in Japan was consistent with that in other countries.

AIDS Dementia Complex↗
PubMed1997

Facioscapulohumeral muscular dystrophy: clinical diversity and genetic abnormalities in Japanese patients.

We studied 71 Japanese individuals, 42 patients (30 familial and 12 sporadic) suspected to have facioscapulohumeral muscular dystrophy (FSHD) and 29 family members, clinically and genetically using the chromosome 4qter DNA marker p13E-11. Early onset FSHD was detected in 7 patients, tortuosity of retinal arterioles and hearing impairment in 3 patients, progressive respiratory failure in 3 patients and limb-girdle type muscular weakness in 6 patients. Thirty-six (85.7%) FSHD patients, 3 asymptomatic family members and 1 of 35 healthy volunteers showed EcoRI digestion fragments shorter than 28kb. New mutations were detected in 25% of the patients with shorter EcoRI fragment. The age of disease onset appeared younger with successive generations in 6 parent-child pairs in FSHD families. We confirmed the existence of phenotypic and genetic diversities in Japanese patients with FSHD. It is still difficult to explain the phenotypic diversity merely by the size of the abnormal EcoRI fragment detected with the p13E-11 probe.

Arterioles↗
PubMed1997

[HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP)].

Human T lymphotropic virus type I(HTLV-I) is associated with the nonfatal neurologic disease, HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Many clinical signs of involvement outside the central nervous system (CNS) have been described in some patients with HAM/TSP and have triggered the discovery of some HTLV-I-associated concepts in the infected individuals without signs of CNS involvement. Most of these HTLV-I-associated diseases exhibit common possible viroimmunologic characteristics that include a distributional bias of HTLV-I activation between the blood flow and the affected lesions and accumulated cellular immune responses in the lesions. This review summarizes the recent perspectives of the molecular pathogenesis of HAM/TSP and other HTLV-I-associated diseases. Furthermore, the feasible pathogenic involvement of cellular interactions between infected cells and responding immunocompetent cells in the affected tissues is emphasized (bystander auto-aggressiveness).

Humans↗
PubMed1997

Neuropathology of HTLV-1-associated myelopathy (HAM/TSP).

In order to clarify pathogenesis of HAM/TSP, we performed a detailed neuropathologic analysis of seven autopsy patients with HAM/TSP. Inflammatory infiltrates of mononuclear cells and degeneration of myelin and axons were noted in the middle to lower thoracic spinal cords and were continuously extended to the entire spinal cord. Horizontal distribution of inflammatory lesions was symmetric at any spinal levels. Immunohistochemical analysis demonstrated T-cell dominance. The numbers of CD4+ T cells and CD8+ T cells were equally present in patients with shorter clinical course. Apoptosis of helper/inducer T cells were observed in the presence of TIA1+ cytotoxic T cells in these active inflammatory lesions. Inflammatory infiltrates were markedly decreased and CD8+/TIA1- T cells were predominated over CD4+ cells in patients with prolonged clinical course. HTLV-1 proviral DNA amounts in the freshly frozen spinal cord measured by quantitative PCR were well correlated with the numbers of infiltrated CD4+ cells. In situ PCR of HTLV-1 proviral DNA using multi-primary pairs demonstrated the presence of HTLV-1 infected cells exclusively in the mononuclear infiltrates of perivascular areas. From these findings, it is suggested that the target of the inflammatory process seen in HAM/TSP lesions may be HTLV-1 infected CD4+ T cells infiltrating the spinal cord.

Apoptosis↗