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Biomedical subjects

M Osame

Publications and source records attributed to M Osame.

At least 235 records · Page 13Linked to original sources
PubMed1996

[Medullary infarction due to vertebral dissecting aneurysm in a patient with Behçet's disease].

A 65-year-old man with Behçet's disease was admitted to our hospital because of an acute left occipital headache and truncal ataxia. He had been treated with prednisolone since the age of 40. MRI showed a hyperintense lesion on T2-weighted images on the left of the medulla oblongata. Left vertebral angiogram showed findings consistent with a dissection at the V4 segment of the artery. After admission, the patient showed marked improvement and was discharged 1 month later without neurological deficits. This is a very rare case of medullary infarction due to vertebral dissecting aneurysm in a patient with Behçet's disease.

Aged↗
PubMed1996

[Dural arteriovenous fistulas of the posterior fossa associated with lateral sinus thrombosis presenting as progressive visual impairment].

A 62-year-old man was admitted because of progressive visual impairment since 2 months ago. Ophthalmological examination revealed impaired visual acuity with papillary edema in both eyes. Right carotid angiograms showed dural arteriovenous fistulas of the lateral sinus mainly fed by the right occipital artery. On the angiograms, the right transverse sinus was completely occluded. Endovascular embolization via jugular vein and via occipital artery was performed. Dural AVF disappeared and visual acuity was improved with normalized intracranial tension.

Arteriovenous Fistula↗
PubMed1996

[Clinical features of allergic granulomatosis and angiitis (Churg-Strauss syndrome). Association with asthma symptoms].

We reported clinical and laboratory findings of 5 patients with Churg-Strauss syndrome (CSS), especially association with asthma symptoms. Subjects included 3 males and 2 females with a mean age of 53.8 year-old. In all 5 patients symptoms of neuropathy; mononeuritis multiplex and in some patients, other vasculitic symptoms; fever, diarrhea, abdominal pain and skin eruptions, were noted. These clinical features and laboratory findings; marked peripheral eosinophilia and elevation of serum ECP were normalized after steroid therapy. We investigated the relation between the occurrence of CSS and the symptoms of asthma. The mean duration of asthma in this series was 17.2 years, and 4 cases were atopic and one was non-atopic asthma. In previous publications, asthmatic symptoms were severe at the onset of the disease and progressed thereafter. In our 5 cases, however, the severities of bronchial asthma were mild of two cases, moderate of two and severe of only one, moreover severe asthmatic attacks were shown in only 2 cases when the manifestation of systemic vasculitis occurred. In conclusion, although CSS has been thought that one of complications of bronchial asthma, the occurrence of CSS are not necessarily correlated with symptoms of bronchial asthma.

Adult↗
PubMed1996

[A case of paranasal sinusitis-cavernous sinusitis with ophthalmoplegia externa].

A 15-year-old man was admitted because of diplopia and bilateral ptosis which occurred a few days after initial clinical signs, such as fever up, nausea, vomiting and headache. His pupils were anisocoric (Rt. phi 3.5 mm < Lt. phi 6.0 mm). In his left eye, light reflex was absent and its movements were limited in all directions. Brain MRI revealed the findings of paranasal sinusitis in bilateral ethmoidal and sphenoidal sinuses and swelling of bilateral cavernous sinus. Combination of intravenous antibiotic therapy and drainage improved his clinical symptoms and MRI findings. It was diagnosed as the inflammation originated in the sphenoid and ethmoid sinuses, which extended to the cavernous sinus and then involved III, IV, and VI cranial nerves. In conclusion, MRI was very useful to detect the cavernous sinusitis secondary to sphenoidal sinusitis.

Adolescent↗
PubMed1995

Human T-cell leukemia virus type-1 (HTLV-1) Tax is expressed at the same level in infected cells of HTLV-1-associated myelopathy or tropical spastic paraparesis patients as in asymptomatic carriers but at a lower level in adult T-cell leukemia cells.

Patients with human T-cell leukemia virus type-1 (HTLV-1)-associated myelopathy (HAM/TSP) generally harbor a much greater population of HTLV-1-infected T cells in peripheral blood mononuclear cells (PBMCs) than asymptomatic carriers. These cells are not malignant but frequently proliferate clonally. To investigate the possibility that higher expression of the viral activator Tax induces preferential proliferation of infected nonmalignant T cells in HAM/TSP patients, the expression of Tax mRNA in fresh PBMCs was analyzed by reverse transcriptase-mediated polymerase chain reaction. Total amount of Tax mRNA was higher in HAM/TSP patients than in carriers, but the expression level was almost the same as that in asymptomatic carriers when compared per infected cell. The expression levels in adult T-cell leukemia patients were significantly lower than those in HAM/TSP patients and asymptomatic carriers. These results indicate that tax gene is not expressed at a continuously high level in HAM/TSP patients who carry a high population of infected T cells, even in those with clonally proliferated infected T cells.

Base Sequence↗
PubMed1995

Midkine is present in the early stage of cerebral infarct.

Expression of midkine (MK), a growth factor with neurotrophic activities, was examined immunohistochemically in experimental cerebral infarct of rats. From postoperative day 1 to day 7 after the onset of infarct, anti-MK immunoreactivity was observed in the surrounding ischemic zone of the infarct but not in the necrotic lesion. The immunoreactive material was identified to be MK by Western blotting. On day 14, anti-MK immunoreactivity became negative. Absence of MK in the normal brain was verified both by immunohistochemical staining and Western blotting. The induced expression of MK is an early event: increased expression of glial fibrillary acidic protein (GFAP), a marker of astrocytes, started on day 4 and continued to day 14. These findings suggest that MK is produced around the site of nerve damage and plays a role as a reparative neurotrophic factor during the early phase of cerebral infarct.

Animals↗
PubMed1995

Cardiac involvement in mitochondrial diseases. A study on 17 patients with documented mitochondrial DNA defects.

BACKGROUND: Mutations of mitochondrial DNA have been demonstrated as causes of human mitochondrial diseases. While these disorders typically involve multiple organs, the effect of mitochondrial mutations on the heart has not been systematically studied. METHODS AND RESULTS: We studied mitochondrial mutations and cardiac changes in 17 patients with Kearns-Sayre syndrome; ocular myopathy; myoclonus epilepsy with ragged red fibers (MERRF); and mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS). Cardiac involvement was evaluated by chest radiograph, ECG, His-bundle electrogram, and echocardiogram. All 3 patients with Kearns-Sayre syndrome had large deletions of mitochondrial DNA and disturbances in cardiac conduction. ECG abnormalities were found in 2 of 6 patients with ocular myopathy who showed large deletions of mitochondrial DNA. All 3 patients with MERRF had an A-to-G mutation at nucleotide position 8344; 2 had cardiomegaly, asymmetrical septal hypertrophy, and diffuse hypokinesis of the left ventricle. One patient with asymmetrical septal hypertrophy developed dilated cardiomyopathy 2 years later. All 5 patients with MELAS had an A-to-G mutation at nucleotide position 3243, and 2 had symmetrical left ventricular hypertrophy with or without abnormal wall motion. CONCLUSIONS: The clinical features of cardiac involvement in mitochondrial diseases vary in the different subgroups of these disorders. Particular mitochondrial mutations can cause characteristic cardiac abnormalities.

Adult↗
PubMed1995

Detection of human T-lymphotropic virus type I (HTLV-I) tax RNA in the central nervous system of HTLV-I-associated myelopathy/tropical spastic paraparesis patients by in situ hybridization.

Autopsy specimens from 3 patients with human T-lymphotropic virus (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) were examined for the presence of HTLV-I in the central nervous system (CNS). In situ hybridization using an HTLV-I tax RNA probe detected cells containing HTLV-I RNA in spinal cord and cerebellar sections. HTLV-I infected cells were located within the white matter and, in particular, within the anterior and lateral funiculi of the spinal cord. Consistent with previously described HAM/TSP pathology, there were perivascular infiltrates in these CNS specimens. Significantly, HTLV-I RNA was not localized to these infiltrates but was detected deeper within the neural tissue. Furthermore, phenotypic analysis demonstrated that at least some of the infected cells were astrocytes. While previous polymerase chain reaction studies have demonstrated the presence of proviral HTLV-I in CNS specimens, here we provide evidence for the in situ expression of HTLV-I RNA in the CNS of HAM/TSP patients.

Aged↗
PubMed1995

Detection of HTLV-I provirus by in situ polymerase chain reaction in mononuclear inflammatory cells in skeletal muscle of viral carriers with polymyositis.

We tested for HTLV-I proviral DNA in skeletal muscle from patients with polymyositis infected with HTLV-I using the in situ polymerase chain reaction. We found the HTLV-I provirus in some of the CD4-positive cells in HTLV-I-positive polymyositis cases but not in HTLV-I-negative polymyositis ones. We could not detect HTLV-I within the muscle fibers. We suggest that HTLV-I-associated polymyositis is not due to direct, persistent infection of the muscle fiber by the virus, but to a T-cell-mediated immunological process triggered by the HTLV-I-infected cells.

Adult↗
PubMed1995

Differential effect of TGF-beta 1 on the in vitro activation of HTLV-I and the proliferative response of CD8+ T lymphocytes in patients with HTLV-I-associated myelopathy (HAM/TSP).

While considerable information is available on the pathogenesis of human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP), fundamental questions remain unanswered. In particular the clinicopathological uniformity of the disorder among patients remains poorly understood. The potential role of TGF-beta as a preferential immune regulator in the CNS and the functional heterogeneity of TGF-beta has led us to assess the possible involvement of this cytokine in the pathogenic process. To investigate this, the modulatory effects of TGF-beta 1 on HTLV-I-induced in vitro phenomena were evaluated using fractionated lymphocytes from patients with HAM/TSP. It could be shown that the proliferative response of CD8+ cells against cultured and irradiated autologous CD4+ cells possessing HTLV-I antigens was significantly inhibited by TGF-beta 1. However, the in vitro activation of HTLV-I, which was evaluated by spontaneous proliferation of CD4+ cells, was unaffected by TGF-beta 1. The induction of intracytoplasmic HTLV-I antigens in cultured CD4+ cells was facilitated by TGF-beta 1 in a dose-dependent manner. These findings suggest that TGF-beta may have a critical role in localized viral activation within the CNS in patients with HAM/TSP.

Adult↗
PubMed1995

In situ polymerase chain reaction detection of HTLV-I provirus and expression of the p53 tumor suppressor gene in infiltrating cells in skeletal muscle from a patient with adult T cell leukemia.

We report the pathological changes in skeletal muscle from a patient with acute adult T cell leukemia (ATL). HTLV-I provirus was detected in infiltrating cells using in situ polymerase chain reaction in frozen sections. Furthermore, aberrant expression of the p53 protein was observed in the infiltrating cells. As p53 protein was not observed in mononuclear inflammatory cells in patients with polymyositis, expression of the p53 protein was considered to be one of the characteristic findings in ATL cells. This is the first direct detection of ATL cells in skeletal muscle.

Gene Expression↗
PubMed1995

Magnetic resonance tomographic angiography: diagnostic value in trigeminal neuralgia.

A combination of MRI, MR angiography and MR tomographic angiography (MRTA) was used to study the relationship of the root exit zone of the trigeminal nerve to surrounding vascular structures in seven patients with trigeminal neuralgia (TN) and ten patients with no evidence at a lesion in this region. MRTA is the technique for showing the relationship between vessels, cranial nerves and brain stem. MRTA clearly demonstrated the presence of a vessel at the root exit zone of the trigeminal nerve in all patients with TN. In the ten other patients, examination of 20 trigeminal nerves revealed that only one nerve (5%) was in contact with a vessel at the root exit zone. This study supports vascular compression of trigeminal nerves as a cause of TN, and demonstrates the value of MRTA as noninvasive technique for demonstrating compression.

Arteries↗
PubMed1995

HTLV-I from Iranian Mashhadi Jews in Israel is phylogenetically related to that of Japan, India, and South America rather than to that of Africa and Melanesia.

A new endemic focus of human T-lymphotropic virus type I (HTLV-I) was recently reported among Mashhadi Jews, a group of immigrants from northeastern Iran to Israel. We extracted DNAs from fresh peripheral blood mononuclear cells (PBMCs) and/or gargle mouthwash from 10 HTLV-I carriers, who consisted of members of one family, and HTLV-I-associated myelopathy (HAM) and adult T-cell leukemia (ATL) patients. Long terminal repeat (LTR) regions of proviral DNAs were sequenced and analyzed phylogenetically. In a phylogenetic tree, all the Mashhadi HTLV-I isolates belonged to subtype A, one of the three subtypes of the cosmopolitan type of HTLV-I, and made a tight cluster distinct from the other isolates of subtype A from Japan, India, the Caribbean Basin, and South America. Although a few nucleotide substitutions were observed among the clones sequenced, no characteristic sequence variation was found in different disease manifestations, even in one family or different sources of DNA preparation.

Adult↗
PubMed1995

Cardiac dystrophin abnormalities in Becker muscular dystrophy assessed by endomyocardial biopsy.

Duchenne and Becker muscular dystrophy (DMD/BMD) are allelic variants caused by mutations in gene-encoding dystrophin. Abnormal expression of dystrophin in skeletal muscle has been shown to correlate with severity of disease. However, in BMD the severity of skeletal and cardiac involvement are not well correlated. We studied the immunostaining pattern of cardiac dystrophin in endomyocardial biopsy specimens from 83 patients with heart disease. Immunohistochemical assessment of dystrophin in four patients with BMD and cardiomyopathy showed a variable distributions of myocytes with continuous, discontinuous, or absent membrane immunostaining patterns. These patterns were obviously different from patterns of other heart diseases. We conclude that the discontinuous immunostaining pattern of cardiac dystrophin is characteristic of BMD and that an absent pattern may be associated with more severe cardiac dysfunction. Because genetic analysis cannot determine the correct diagnosis in 35% of DMD/BMD cases, we recommend routine examination of immunostaining patterns of dystrophin in endomyocardial biopsy specimens in patients with cardiomyopathy suspected to be the result of BMD.

Adult↗
PubMed1995

Contralateral early blink reflex in patients with HTLV-I associated myelopathy/tropical spastic paraparesis.

Thirty-two Japanese patients with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) were studied by means of the electrically elicited blink reflex and three responses (R1, R2, R3) were registered. 69% of the patients displayed a uni- or bilateral crossed R1 response (R1k) as compared to 11% in the control group. A positive correlation between R1k and an exaggerated jaw jerk reflex was found in the patients. Central abnormalities of the nervous system with diminished presynaptic inhibition acting in the interneuronal input of the brainstem of HAM/TSP patients was the most likely cause. It could lead to the unmasking of crossed trigemino-facial pathway reflex which is present in the normal population from birth. These results strongly support the supraspinal involvement of the central nervous system (CNS) in HAM/TSP more than usually thought.

Action Potentials↗
PubMed1995

Familial spastic paraplegia with mental impairment and thin corpus callosum.

We described four patients in two families of unique familial spastic paraplegia (FSP) which was thought to be possibly autosomal recessive inheritance. All four patients had quite similar manifestations. Gait disturbance started at their second decade, then spastic paraparesis and mental deterioration progressed slowly. Cerebellar ataxia and sensory loss in the distal parts of four extremities were also slightly presented. In all patients, cranial MRI revealed marked thin corpus callosum with mild changes in the region of periventricular white matter and in the gray matter. Biopsied sural nerves of all patients showed chronic axonal degeneration with mild decrease of both large and small myelinated fibers. Electron microscopic study demonstrated crystalline-like inclusion bodies in the cytoplasm of Schwann cells in all patients. Despite extensive investigation for metabolic disorder, we could not find any abnormality. However an etiology have not established at the time presented, the combination of these clinical features suggested that the disorder could represent a specific clinical entity.

Adult↗