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Biomedical subjects

M Osame

Publications and source records attributed to M Osame.

At least 433 records · Page 24Linked to original sources
PubMed1989

Electroencephalographic abnormalities in human T-cell lymphotropic virus type I-associated myelopathy.

Thirty-six patients with human T-cell lymphotropic virus type I (HTLV-I)-associated myelopathy were studied by electroencephalogram. Twenty-two of 36 patients showed mild to moderate electroencephalographic abnormalities, ranging from poor organization or slowing of the background activity to theta bursts and/or spikes. None of these abnormalities were considered specific for HTLV-I-associated myelopathy. These electroencephalographic abnormalities had no apparent relationship to duration or severity of illness, nor to HTLV-I antibody titers in the cerebrospinal fluid. We document electroencephalographic changes in HTLV-I-associated myelopathy. Our data are consistent with previous reports describing the fact that involvement of regions above the spinal cord may exist in HTLV-I-associated myelopathy.

Adult↗
PubMed1989

Increased replication of HTLV-I in HTLV-I-associated myelopathy.

To estimate the replication of the human T-cell leukemia virus type I (HTLV-I) in patients with HTLV-I-associated myelopathy (HAM), or tropical spastic paraparesis (TSP), HTLV-I DNA integrated into lymphocyte genomes was analyzed by Southern blot hybridization. HTLV-I DNA was detected in 125 (82%) of 153 patients and most showed random integration. This incidence was much higher than the 29% found in asymptomatic carriers. Therefore, HAM/TSP development is associated with a high level of HTLV-I replication. In addition, lymphocytes from 3 patients with HAM/TSP showed monoclonal integration of HTLV-I DNA, indicating adult T-cell leukemia.

Adult↗
PubMed1989

Annulate lamellae-soleplate nuclei associations in skeletal muscle fibers of rats during chronic high-dose exposure to neostigmine.

To investigate annulate lamellae (AL) with nuclear changes, ultrastructural time course studies were done of the reversible end-plate myopathy in the soleus muscles of rats exposed chronically to a high dose of the anticholinesterase drug neostigmine. At the earliest stage (2 hours) in which severe subjunctional damage involving a nuclear lesion (nuclear pyknosis) was prominent, AL profiles were undetectable. At the intermediate stage (7, 21 days), in which the subjunctional organelles tended to cluster and nuclear pyknosis often accompanied degenerative features, most AL laid near the surface of the abnormal nuclei, where there were signs of elimination or formation of pores, as well as a progression of changes leading to the loss of pores. At the late stage (56 days), in which muscle repair was nearly completed and euchromatic nuclei usually were found, there was a concomitant enhanced formation of false nuclear inclusions and of the AL profiles in these sites. Pores are packed on nuclear envelopes, which detach themselves from the nucleus and take the same profile as AL. This phenomenon can be envisioned not only in the euchromatic but also in the abnormal (pyknotic or degenerated) nuclei. Following nuclear reconstitution, the nuclear envelope folding is accelerated to induce the usual pattern of AL organization, i.e., budding from the invaginated nuclear envelope.

Animals↗
PubMed1989

Morphogenesis of nuclear inclusions in the soleplate region of rat skeletal muscle fibers following chronic daily administration of neostigmine.

In the course of ultrastructural investigations of motor endplate pathology mediated by calcium ions, intranuclear sarcoplasmic inclusions, either membrane-free (true type) or membrane-delimited (false type), were observed during chronic daily high-dose exposure to the anticholinesterase neostigmine. At the stage in which subjunctional components, including soleplate nuclei, were severely damaged (day 7), the true nuclear inclusions were frequently associated with the disrupted nuclear envelope (fragmentation, vesiculation etc.) and nuclear pores. At a subsequent stage, in which muscle repair was accelerated and most soleplate nuclei were less severely affected (day 21), formation of the false inclusions in these nuclei was enhanced. Analysis of serial sections of the less severely affected nuclei, where only a true inclusion type was present, revealed no sign of invaginated nuclear envelopes or other membranes enclosing the inclusions. Our findings indicate that morphogenesis of true inclusions depends upon the severity of nuclear degeneration, i.e., in severely affected nuclei there is disruption in the nuclear envelope and/or nuclear pores, while in less severely affected nuclei, either a pinched-off invagination or diffusion of excessive sarcoplasmic proteins into the nucleus via nuclear pores occurs.

Animals↗
PubMed1989

Germanium myopathy: clinical and experimental pathological studies.

Pathological examinations were carried out on the skeletal muscle of a patient with germanium intoxication. The prominent histochemical finding was vacuolar myopathy with lipid excess, increased acid phosphatase activity and decreased cytochrome c oxidase activity. Ultrastructural lesions revealed a mitochondrial abnormality, autophagic vacuoles and accumulation of high electron-dense materials in deformed mitochondria and at the periphery of lipid droplets. Furthermore, the toxic effect of germanium on skeletal muscle was confirmed by the experimentally induced germanium myopathy, which showed autophagic degeneration, decreased cytochrome c oxidase activity and a mitochondrial abnormality with high electron-dense materials.

Child, Preschool↗
PubMed1989

Preclinical detection in Japanese families with myotonic dystrophy using polymorphic DNA markers.

Myotonic dystrophy (DM) is a genetic disease inherited by an autosomal dominant trait and characterized by multi-organ disorders. Although its biochemical basis has been unknown, the DM locus is closely linked to D19S19 and APOC2 on the long arm of chromosome 19 both in Japanese and Caucasian populations. Linkage studies of Japanese DM families using these polymorphic DNA markers detected two asymptomatic gene carriers in two unrelated families.

Adult↗
PubMed1989

Hyperestrogenemia in neuromuscular diseases.

In order to elucidate the relationship between certain neuromuscular diseases and gonadal hormones, we measured the levels of serum estrogens and other sex-related hormones. The values were compared with those for age-matched controls. The cases, comprising bulbospinal muscular disease of the Kennedy-Alter-Sung type, Kugelberg-Welander disease, amyotrophic lateral sclerosis, and Duchenne muscular dystrophy, were all euthyroid males. The baseline levels of serum estrone were significantly higher in all of the patients than in age-matched normal subjects. Serum baseline testosterone, LH and FSH levels were all essentially normal, except low FSH levels in Duchenne muscular dystrophy. Since our patients had no overweight, liver or glandular abnormalities, we presume that the elevated serum estrone levels have resulted from increased peripheral androgen-to-estrogen conversion.

Adolescent↗
PubMed1989

Nasu-Hakola disease (membranous lipodystrophy). Clinical, histopathological and biochemical studies of three cases.

We report 3 cases of Nasu-Hakola disease found in 2 families. These cases had identical clinical features with progressive spastic paraplegia and severe dementia after adolescence. They had no history of any skeletal symptoms, but roentgenographs of their bones presented characteristic evidence of polycystic osteodysplasia. All cases revealed not only manifestations of this condition in the central nervous system, but also peripheral neuropathy with axonal degeneration. The membranous structures in the adipose tissues appeared histochemically to be composed of a kind of compound glycolipid or glycoprotein. Histopathologically, the biopsied rectum showed the infiltration of many histiocytes in the mucosa and ultrastructurally, the granules in these histiocytes showed many membrane-bound vacuoles of different sizes. Interestingly, the histochemical reactivity of the material in the granules was very similar to that of membranous structures in adipose tissues. In the biochemical analysis of lipids in affected adipose tissues, no marked abnormalities were found in the patients. Nasu-Hakola disease is not a typical form of lysosomal storage disease, because lysosomal enzyme activities remain normal and there is no accumulation of urinary oligosaccharides and lipids, no vacuolation of lymphocytes, and no hepatosplenomegaly. However, histochemical findings suggest that the lysosomes may be secondarily involved in this disease, and that the formation of membranous structures might be related to the disturbance of glycolipid or glycoprotein metabolisms.

Adipose Tissue↗
PubMed1989

Type IIa hyperlipoproteinemia masquerading as cerebrotendinous xanthomatosis.

We describe an adult patient with type IIa hyperlipoproteinemia, presenting with Achilles tendon xanthomas, cataracts, dementia, ataxia, pyramidal tract signs, and peripheral neuropathy, which are commonly seen in cerebrotendinous xanthomatosis (CTX). However, the diagnosis of CTX was excluded on the basis of the cholestanol level and the normal cholestanol/cholesterol ratio in his serum and tendon. The pathomechanism for some of the clinical manifestations in type IIa hyperlipoproteinemia and CTX might be caused by a common biochemical disturbance.

Aged↗
PubMed1989

Immune dysfunction in hypophosphatemic vitamin D-resistant rickets: immunoregulatory reaction of 1 alpha(OH) vitamin D3.

We investigated immunologic function in six cases with hypophosphatemic vitamin D-resistant rickets (VDRR) before and after treatment with 1 alpha-hydroxycholecalciferol (1 alpha(OH) vitamin D3). All cases suffered frequent episodes of infection, which tended to be more severe in the older patients. OKT9-, OKT10-, and OKM1-positive cells and adenosine deaminase (ADA) were significantly increased, whereas numbers and activity of natural killer (NK) cells were lower than normal before treatment. After administration of 1 alpha(OH) vitamin D3, however, the susceptibility to infection apparently decreased, and NK cell number and activity increased in all patients. ADA was also significantly decreased and remained in the normal range after treatment. These results suggest that vitamin D plays a role in the impaired immunoregulatory functions of NK cells in VDRR. Furthermore, ADA may be one parameter reflecting this immunologic impairment.

Adenosine Deaminase↗
PubMed1989

In vitro modulation of lymphocyte proliferation by prednisolone and interferon-alpha in patients with HTLV-I-associated myelopathy (HAM).

One of the hallmarks of human T-lymphotropic virus type I (HTLV-I) infection is the proliferation in vitro of peripheral blood lymphocytes (PBLs) in the absence of growth factors. This phenomenon, the autologous proliferative response (APR), involves spontaneous growth of HTLV-I-infected T-cells and proliferation of T-cells in response to the infected cells. We studied the modulating effect of prednisolone (PSL) and interferon-alpha (IFN) on APR of PBLs obtained from five patients with HTLV-I-associated myelopathy (HAM). APR was significantly inhibited by PSL and IFN suggesting that APR is important in the pathogenesis of HAM.

Adult↗
PubMed1989

Activated T lymphocytes in cerebrospinal fluid of patients with HTLV-I-associated myelopathy (HAM/TSP).

In order to detect activated T lymphocytes in the cerebrospinal fluid (CSF) of patients with human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP), we studied CSF lymphocytes in untreated patients with HAM/TSP and other neurological diseases (OND). Dual-immunofluorescence staining technique was performed using fluorescence microscopy. No significant difference in the CD4+/CD8+ ratio of CSF lymphocytes was observed between HAM/TSP patients and patients with OND. However, both CD4+ and CD8+ CSF lymphocytes of HAM/TSP patients contained higher percentages of HLA-DR-positive cells than those of patients with OND (P less than 0.05), suggesting that the activated CSF T lymphocytes were composed of both CD4+ and CD8+ subsets in patients with HAM/TSP.

Antibodies, Monoclonal↗
PubMed1989

Determination of urine thiocyanate in patients with amyotrophic lateral sclerosis.

It has been reported that amyotrophic lateral sclerosis-Parkinsonism-dementia in Guam might be related to the eating of Cycas seeds, which contain cyanide. Based on this assumption, we determined the urinary thiocyanate excretion level in patients with ALS and compared this with that of other neurological diseases. The assay method was designed to use column chromatography with Amberlite IRA 402. The thiocyanate level was determined using pyridine-barbiturate method. The 24-h thiocyanate level was higher in the ALS patients of the middle stages than in the normal control group (Wilcoxon's test, P less than 0.02). There were no significant differences between the ALS patient groups of the early and terminal stages, Kugelberg-Welander disease group, Duchenne type muscular dystrophy group and control group. From these results, we concluded that ALS patients were contaminated with cyanide or thiocyanate and that, along with rapid muscular atrophy, the thiocyanate excretion levels were high.

Adult↗
PubMed1989

Retinal vasculitis in human T-lymphotropic virus type I associated myelopathy.

Human T-lymphotropic virus type I (HTLV-I) has been recently found to be associated with slowly progressive myelopathy. We have seen 12 patients with HTLV-I associated myelopathy (HAM), three of whom showed retinal vasculitis. In addition two patients had ocular symptoms of vitreous opacity. Retinal vasculitis in these patients appears to be phlebitis and sheathing of retinal veins in the periphery of the fundus.

Female↗
PubMed1989

HTLV-I-associated myelopathy and adult T-cell leukemia cases in a family.

Familial cases of HTLV-I-associated myelopathy (HAM) and adult T-cell leukemia (ATL), developing in a daughter and father, respectively, are reported. The coexistence of both diseases in a family has not been reported before. This supports the recent findings that ATL and HAM may be brought about by an identical virus on an apparently different immunogenetic background.

Adult↗