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Biomedical subjects

M Osame

Publications and source records attributed to M Osame.

At least 361 records · Page 20Linked to original sources

Neuropathology of HTLV-I-associated myelopathy--a report of two autopsy cases.

A neuropathological analysis was performed in two autopsy cases of HTLV-I-associated myelopathy. The thoracic spinal cords were most severely affected and the histopathological findings consisted of mononuclear cell infiltration, marked destruction of myelin and axons and astrocytic gliosis. More than half the infiltrated cells were positive for pan-T cell marker; B cells were sparse in the parenchyma and subarachnoid spaces. CD4 and CD8 positive cells were found in the early stages of the lesions. CD8, however, predominated over CD4 in the other stages. It appeared that a chronic inflammatory process had started at the middle to lower thoracic cord and had extended gradually in both directions. The middle thoracic spinal cord is known to have the poorest blood supply, and the horizontal distribution of inflammatory cells at this region correlated with the most distal supply of the anterior spinal artery.

Aged↗

[Markedly elevated serum neopterin levels in patients with hemophagocytic histiocytosis].

The authors measured serum neopterin by HPLC in 3 patients with hemophagocytic histiocytosis (HH) with DIC which occurred during the clinical course of T cell malignant lymphoma (T-ML). Extremely high levels of serum neopterin (754.3 +/- SD 467.3 pmol/ml) were found in the patients, about 200, 13 and 10 times higher than that of normal subjects, non-HH DIC patients and non-HH/DIC T-ML patients. Moreover their serum soluble interleukin-2 receptor levels were markedly elevated. These results indicate that markedly raised serum neopterin would be a sensitive parameter for activation of the mononuclear phagocyte system closely associated with T-cell activation and may serve as a useful diagnostic marker for HH.

Adult↗

[The significance and limit of thermography at present].

Thermography has been reported to be usefull in the detection and characterization of nervous diseases. Recently, however, some papers report that it is not useful. In this paper, problems including its history, and measures to solve them are discussed. It is proposed that methods to distinguish patients from normal subjects and information that cannot be obtained by other tests, are needed.

Arterial Occlusive Diseases↗

[Bronchopneumonopathy in HTLV-1 associated myelopathy (HAM) and non-HAM HTLV-1 carriers].

Human T-cell leukemia virus type 1 (HTLV-1) causes not only adult T-cell leukemia (ATL), but also HTLV-1 associated myelopathy, a recently described slowly progressive spastic paraparesis, in its carrier state. Pulmonary involvement has been reported in HAM patients. Based on bronchoalveolar lavage or histological examination, the pulmonary involvement has been characterized by accumulation of T-cells, especially activated T-cells, in the lung. We reviewed our data on pulmonary involvement in HAM, which suggested that the characteristic pulmonary involvement observed in HAM was not restricted to HAM patients, but was also observed in non-HAM HTLV-1 carriers. Based on the data, we report that HAM is a systemic disease and that HTLV-1 causes characteristic pulmonary involvement, which we termed HTLV-1 associated bronchopneumonopathy (HAB).

Bronchoalveolar Lavage Fluid↗

[A case of motor neuron disease with IgM gammopathy which showed anti-cerebrum antibody].

A patient, 50-year-old female, developed progressive weakness of lower extremities, and gait disturbance for 2 years. Neurological examination revealed hyperreflexia with pathological reflex, fasciculation in the limbs and tongue, muscle weakness and atrophy in distal limbs, but no sensory disturbance. Needle EMG showed neurogenic findings compatible with motor neuron disease (MND). Laboratory data showed polyclonal IgM hyperimmunoglobulinemia, positive several autoimmune antibodies including antisingle strand DNA antibody (Ab), ENAab, SS-A ab and RA. There were no antibodies for gangliosides and Myelin-associated glycoprotein (MAG), but positive antibody for 54KD protein of cerebral gray and white matter. The clinical manifestations including gait disturbance and muscle weakness, and serum IgM level were moderately improved by plasmapheresis which is considered important for consideration of causes of MND.

Autoantibodies↗

Inhibitory effect of maternal antibody on mother-to-child transmission of human T-lymphotropic virus type I. The Mother-to-Child Transmission Study Group.

In order to evaluate the protective role of the maternal antibody against mother-to-child transmission of HTLV-I, we followed a total of 780 children born to HTLV-I carrier mothers by investigating the level of anti-HTLV-I antibody transferred in utero, decline of the maternal antibody and seroconversion in post-natal life. The anti-HTLV-I antibody was positively detected within the first 3-6 months of life and declined at 6-12 months after birth in all children. After the maternal antibody declined, seroconversion occurred in some of the children following either breast feeding or bottle feeding. The seroconversion rates of short-term (less than or equal to 6 months) and long-term (greater than or equal to 7 months) breast feeders were 4.4% (4/90 cases) and 14.4% (20/139 cases), and the rate of bottle feeders was 5.7% (9/158 cases). Long-term breast feeding yielded more seroconverters than short-term breast feeding; 14.4% (20/139 cases) vs. 4.4% (4/90 cases), RR = 3.68, p = 0.018. The seroconversion rate of short-term breast feeders was nearly equal to that of bottle feeders; 4.4% (4/90 cases) vs. 5.7% (9/158 cases), RR = 0.770, p = 0.471. When neonatal lymphocytes were cultured with breast milk cells of HTLV-I carrier mothers, the in vitro infection of HTLV-I was inhibited by the addition of HTLV-I-seropositive cord-blood plasma. Our results suggest that the maternal antibody may inhibit HTLV-I infection by short-term breast feeding but not by long-term breast feeding after decline of the maternal antibody.

Adolescent↗

Atherogenic risk factors in cerebrotendinous xanthomatosis.

In a study of coronary artery disease in patients with cerebrotendinous xanthomatosis (CTX), we documented the presence or absence of atherogenic risk factors and performed detailed analyses of serum lipid and lipoprotein profiles. Four of the seven patients examined had coronary arterial narrowing and/or obstruction, but multiple atherogenic risk factors were not found in any of these patients. Total cholesterol (T.ch) levels and low density lipoprotein-cholesterol (LDL-ch) levels were lower, and high density lipoprotein2-cholesterol (HDL2-ch) levels were higher in CTX patients than in controls. Triglyceride and very low density lipoprotein (VLDL) levels were significantly lower in the former. Indices correlating with the risk of atherosclerosis, such as the atherogenic index, and the ratios of apolipoprotein B/apolipoprotein AI, HDL2-ch/LDL-ch, HDL2-ch/HDL3-ch, indicated that CTX serum was, in fact, 'anti-atherogenic'. However, coronary artery disease is frequently seen in patients with CTX. This discrepancy suggests the existence of a unique mechanism by which atherosclerosis is induced in patients with CTX. We discuss a mechanism of disturbed lipoprotein metabolism which might be responsible for the deposition of sterols in the tissues of patients with CTX.

Adult↗

Relative prevalence and risk factors of HTLV-I and HTLV-II infection in US blood donors.

The clinical significance of human T-cell lymphotropic virus type II (HTLV-II) infection, unlike that of HTLV-I, is unknown, and the major known association of HTLV-II seropositivity is with intravenous drug abuse. Screening of blood donors for HTLV-I, now routine in North America, does not distinguish this retrovirus from HTLV-II. To find out more about the seroepidemiology of and risk factors for HTLV I and II, blood from 480,000 volunteer donors in five geographically separate US urban centres was tested for antibodies to HTLV-I/II and HIV-1. Confirmed HTLV-I/II seropositive donors were then followed up by DNA amplification to distinguish type I from type II and by interviews focusing on possible risk factors. HTLV seroprevalence was 3.3 times greater than that for HIV-1 (0.043% vs 0.013%). DNA amplification on 65 of the 207 HTLV-I/II seropositive donors revealed that 34 (52%) had HTLV-II infection and 28 (43% had HTLV-I; 3 samples were uninformative. Interviews of 49 donors showed that whereas HTLV-I was principally associated with donor origin from endemic regions, the major risk factor for HTLV-II infection was intravenous drug use. The surprisingly high rate of HTLV-II infection in US blood donors raises important public health and donor counselling issues since HTLV-I infection is associated with adult T-cell leukaemia and a neurological disorder while the pathogenicity of HTLV-II is as yet unclear.

Adult↗

Immunocytochemical study on endothelial markers with the cerebral vessel from a patient with familial moyamoya disease.

The immunocytochemical study of thrombomodulin (TM), a newly recognized anticoagulant endothelial surface protein, was performed with a surgical specimen of a superficial temporal artery (STA) obtained from a 29-year-old woman with familial moyamoya disease. The staining of TM showed positive immunoreactivity in smaller vessels in the surrounding connective tissue of the specimen, whereas negative in STA. Immunoelectronmicroscopically the luminal plasma membrane of endothelial cells was positive for TM. These staining pattern was the same as that in controls. She concurrently suffered from von Willebrand disease type I, and she had two cerebral hemorrhagic attacks. A quantitative defect of the von Willebrand factor in the endothelium was demonstrated immunocytochemically.

Adult↗

Increased expression of thrombomodulin on the cultured human umbilical vein endothelial cells and mouse hemangioma cells by cyclic AMP.

We previously reported that the expression of thrombomodulin on the MEG-01, a cell line from human megakaryoblastic leukemia, was increased by agents that increase intracellular cAMP. In this paper we examine the effect of these agents on cultured human umbilical vein endothelial cells (HUVEC) and mouse hemangioma cells. Incubation of the cells with 3 mM dibutyryl cAMP (dbcAMP) increased functionally active thrombomodulin by about 2-fold on HUVEC and 4-fold on hemangioma cells. This effect was observed from 1 hour after the incubation and continued up to 24 hours. Dot hybridization of mRNA demonstrated a dose dependent increase in thrombomodulin mRNA in response to dbcAMP. Treatment of HUVEC with 20 microM forskolin or 100 microM isobutylmethylxanthine (IBMX) also increased cell-surface thrombomodulin on HUVEC. These agents prevented the interleukin I (IL-I) or tumor necrosis factor (TNF)-induced decrease in thrombomodulin on HUVEC. These data suggest that the expression of thrombomodulin on HUVEC and mouse hemangioma cells may be regulated by intracellular cAMP level.

1-Methyl-3-isobutylxanthine↗

Arthritis in patients infected with human T lymphotropic virus type I. Clinical and immunopathologic features.

Ten patients with chronic inflammatory arthropathy and the human T lymphotropic virus type I (HTLV-I) are described. These patients showed chronic persistent oligoarthritis, associated with proliferative synovitis, in large joints. The place of birth or residence of these patients was within the area endemic for adult T cell leukemia (ATL) and HTLV-I. The age at onset of articular symptoms tended to be higher in these patients than in typical rheumatoid arthritis patients. Anti-HTLV-I antibodies were detected in both sera and synovial fluids from all patients. Western blot analysis revealed antibodies to viral gag proteins (p19, p24, and p28). Atypical lymphocytes with nuclear indentations, consistent with ATL-like cells, were observed in both synovial fluid and synovial tissue. Furthermore, HTLV-I proviral DNA was integrated into the DNA of synovial fluid cells and synovial tissue cells. These findings suggest that HTLV-I might be involved in the pathogenesis of this unique arthropathy.

Aged↗

Concentration of activated T lymphocytes in extracorporeal blood circulation for plasma separation.

To investigate whether the proportion of activated T lymphocytes changes in an extracorporeal blood flow, we compared paired samples collected at the inlet and outlet lines of an artificial circuit for plasma separation, using a dual-immunofluorescence flow cytometric technique. In our series of materials from patients with rheumatoid arthritis or systemic lupus erythematosus, the percentages of HLA-DR-positive cells in both CD4+ (P less than 0.01, n = 6) and CD8+ (P less than 0.05, n = 10) subsets were significantly increased in the outlet lines compared with the inlet lines, suggesting that activated T lymphocytes pass through an extracorporeal blood circuit more easily than resting T lymphocytes.

Adult↗

Human acid maltase-deficient myogenic cell transformation with origin-defective SV40: characterization of a cloned line.

A clonal human skeletal muscle cell line showing acid maltase deficiency (AMD) was established through the transfection of origin-defective SV40 DNA. The low acid alpha-glucosidase activity and glycogenosomes in this clone corresponded to AMD. This clone, in spite of loading glycogenososmes, was competent not only as to proliferation without contact inhibition but also as to myogenic differentiation to some extent. Dexamethasone promoted the formation by the transformant of multinucleated myotubes, which expressed acetylcholine receptors. The existence of glycogenosomes did not seem to affect the proliferation or differentiation of myoblasts. The aberrant acid alpha-glucosidase expressed in the transformed myogenic clone was shown to be biochemically identical to that in AMD fibroblasts. This transformant should be of great value for investigating the pathogenesis of AMD because of the possibility of supplying semi-permanently a uniform myogenic cell line expressing AMD.

Adolescent↗

Experimental germanium myopathy.

The long-term administration of germanium dioxide (GeO2) to rats produced Ge myopathy characterized by the formation of ragged-red fibers. The earliest pathological changes in experimental Ge myopathy were a decrease in cytochrome c oxidase activity and accumulation of high electron-dense materials in mitochondria. These findings suggest that a mitochondrial dysfunction may be most important in the genesis of experimental Ge myopathy, which could be a useful animal model for the investigation of and therapeutic trials for human mitochondrial myopathies.

Animals↗

Polyneuropathy induced by m-tolyl methyl carbamate intoxication.

A 55-year-old woman who attempted suicide by ingesting 200 ml of m-tolyl methyl carbamate (MTMC) is reported. She was comatose for 3 days and, upon recovery, had notable paraesthesia in her lower limbs and difficulty in walking. Neurological examination revealed sensorimotor polyneuropathy. Sural nerve biopsy revealed marked axonal degeneration with a moderate decrease of myelinated fibres.

Carbamates↗

Cardiomyopathy, mental retardation, and autophagic vacuolar myopathy. Abnormal MRI findings in the head.

A 21-year-old man with childhood-onset mental retardation, non-obstructive hypertrophic cardiomyopathy, and vacuolar myopathy is presented. A histopathological study of biopsied skeletal muscle showed lysosomal glycogen storage mimicking acid maltase deficiency, but biochemical analysis showed normal acid alpha-glucosidase activity. Glycogenosomes were also recognized in endothelial cells on electronmicroscopic examination of biopsied skeletal muscle. Magnetic resonance imaging (MRI) findings in the head revealed the involvement of the central nervous system. This is a new type of lysosomal glycogen storage disease with multisystemic involvement. The specific biochemical defect in this disorder remains to be elucidated.

Adult↗