Search PubMed⌕ Search

Biomedical subjects

J Satoh

Publications and source records attributed to J Satoh.

At least 127 records · Page 7Linked to original sources
PubMed1992

[Detection of anti-HCV antibody, anti-GOR antibody and autoantibodies in sera of patients with non-A, non-B liver diseases].

Anti-HCV antibody, anti-GOR antibody and autoantibodies were measured in sera of 41 patients with non-A, non-B liver diseases. Anti-HCV antibody (C100-3) was positive in 73.1% of the patients. On the other hand, anti-GOR antibody, rheumatoid factor, anti-ssDNA antibody and anti-dsDNA antibody was positive in 56%, 26.8%, 12.1% and 2.4% of the patients, respectively. In 70.7% of the patients, at least one of these four antibodies was positive. No relationship was observed in both positive rate and antibody titers among these different antibodies. On the other hand, positive rates of anti-HCV and anti-GOR antibody were higher in patients with persistently elevated serum ALT. Anti-GOR antibody appears to be a kind of autoantibody since it recognizes liver cell protein which has amino acid sequence partly similar to an epitope of HCV protein. Therefore, it could be speculated that the frequent appearance of antibodies against self constituents may be related to the chronic inflammation of the liver induced by HCV infection.

Autoantibodies↗
PubMed1992

[A case of advanced gastric cancer with liver metastasis completely responding to a combined immunochemotherapy with UFT, mitomycin C and lentinan].

A 74-year-old man with advanced gastric cancer of Borrmann type III and liver metastasis was treated by combined administration of UFT (400 mg/day, p. o.), Mitomycin C (14 mg/body/4w., i.v.) and Lentinan (2 mg/w., i.v.). Five and half months after the therapy, endoscopic examination and ultrasonography showed the primary and liver-metastatic lesions had completely disappeared. Ten months after the therapy, total gastrectomy and intraoperative liver wedge biopsy were performed and complete disappearance of cancer cells was histologically confirmed. The total dose of UFT, MMC and LNT administered until the operation was 76.4 g, 42 mg and 74 mg, respectively. However, the patient eventually died of the recurrence of liver metastases three years after the initial immunochemotherapy.

Adenocarcinoma↗
PubMed1991

Expression and induction of intercellular adhesion molecules (ICAMs) and major histocompatibility complex (MHC) antigens on cultured murine oligodendrocytes and astrocytes.

Expression of intercellular adhesion molecule-1 (ICAM-1), ICAM-2-like molecule (Lgp55), and class I/II major histocompatibility complex (MHC) antigens (H-2 and Ia) was investigated in cultures of murine oligodendrocytes and astrocytes. Under unstimulated conditions, low levels of ICAM-1 expression were observed on astrocytes (less than 20%), but not on oligodendrocytes. Lgp55 was expressed intensely on oligodendrocytes (greater than 90%) and to a lesser degree on astrocytes (greater than 70%). A weak class I MHC (H-2) immunoreactivity was identified on both oligodendrocytes and astrocytes (50-70%). Class II MHC (Ia) antigen was undetectable on both cell types. After 48-hr exposure to immune mediators that include interferon-gamma (IFN-gamma), 500 U/ml, and supernatant from concanavalin A (Con A)-activated spleen cells, ICAM-1 expression was markedly increased on astrocytes (greater than 80%), but not on oligodendrocytes. Lgp55 expression on both cell types was not altered. Induction of H-2 antigen expression by immune mediators was quite high on both cell types (greater than 95%), while Ia antigen induction was low on astrocytes (less than 50%) and did not occur on oligodendrocytes. Cell type-specific expression and induction of ICAMs and MHC antigens by immune mediators may play roles in lymphocyte-glial cell interactions at the sites of inflammation in the central nervous system (CNS).

Animals↗
PubMed1991

Parvalbumin-immunoreactive neurons in the human central nervous system are decreased in Alzheimer's disease.

Immunohistochemical localization of the Ca(2+)-binding protein parvalbumin (PV) was investigated in the adult human central nervous system (CNS). The antiserum against purified rat skeletal muscle PV specifically recognized certain neuronal populations and their processes. Strongly positive were Purkinje, basket and stellate cells of the cerebellum, cerebral cortical nonpyramidal cells, and neurons in the thalamic reticular and ventrolateral nuclei, subthalamic nucleus, lateral and medial geniculate bodies, vestibular and cochlear nuclei, spinal trigeminal nucleus, cuneate and gracile nuclei, and dorsal nucleus of Clarke. Negative were cortical pyramidal neurons, neurons of the autonomic nerves, and neurons in the caudate nucleus, putamen, dentate nucleus, inferior olive, and substantia gelatinosa. The number and size of PV-immunoreactive neurons were significantly decreased in Alzheimer's disease. However, the decrease was not disease specific.

Adult↗
PubMed1991

Lymphokine-activated killer (LAK) and adherent LAK (A-LAK) activity in multiple sclerosis.

The cytotoxic activity of lymphokine-activated killer (LAK) cells against enriched cultures of oligodendrocytes (OL) was investigated in multiple sclerosis (MS) and controls. Human LAK cells, derived from macrophage-depleted peripheral blood mononuclear cells (PBMC) and incubated with recombinant human interleukin-2 (IL-2) (20-80 U/ml), mediated high levels of cytotoxicity against Raji cells but low levels of cytotoxicity against primary cultures of bovine OL. Cytotoxicity was not enhanced by incubation with a high level of IL-2 (500 U/ml). No statistically significant differences in LAK cell activity against bovine OL were observed among the study groups. Enriched adherent LAK (A-LAK) cells mediated greater levels of cytotoxicity against both bovine OL and tumor cell lines than unfractionated LAK cells. Flow cytometric analysis indicated that A-LAK effector cells were CD4-, CD8+, and CD16+. Furthermore, A-LAK cells mediated lysis of OL derived from several different animal species. Our results suggest that LAK and A-LAK cells can mediate cytolysis of OL in culture similar to that observed with a number of different tumor cell lines. However, no significant difference in cytolysis was identified between MS and control groups in this study.

Adult↗
PubMed1991

Cytolysis of oligodendrocytes is mediated by killer (K) cells but not by natural killer (NK) cells.

The cytotoxic activity of killer (K) cells against enriched cultures of bovine oligodendrocytes (BOL) was investigated in multiple sclerosis (MS) and controls. Human K cells mediated cytotoxicity to primary cultures of BOL in the presence of anti-BOL antiserum in all study groups, while BOL were resistant to human natural killer (NK) cells. Cytotoxic activity was significantly reduced in MS when compared to age-matched normal controls but not when compared to other neurologic disease (OND) patients. K cell-mediated lysis of BOL could also be induced with anti-galactocerebroside antibody but not with other antibodies including those specific for OL antigens (myelin basic protein, proteolipid apoprotein, and 2',3'-cyclic nucleotide 3'-phosphodiesterase). Enrichment of the effector population indicated that antibody-dependent cell-mediated cytotoxicity (ADCC) to BOL was mediated by large granular lymphocytes, and the effector population was further characterized by flow cytometry. The effector cells mediating ADCC could be inhibited by protein A of Staphylococcus aureus, and by K562 cells in cold competition assay. These observations indicate that oligodendrocytes are resistant to NK cells but are susceptible to cytolysis mediated by K cells. This may represent a potentially important immune mechanism in the pathogenesis of MS.

Adult↗
PubMed1991

Clinical and neuropathological findings in severe athetoid cerebral palsy: a comparative study of globo-Luysian and thalamo-putaminal groups.

We divided cases of severe athetoid cerebral palsy originating perinatally into two groups neuropathologically, the "globo-Luysian group" (GL) and the "thalamo-putaminal group" (TP). The major abnormal sites in GL were the pallidum and subthalamic nucleus, and in TP the thalamus and putamen. The lesions in TP were more widespread and frequently accompanied by fibrillary gliosis in the central gray matter of the midbrain, and subthalamic nuclei were dominantly devastated. Concerning the etiology, GL and TP were related to perinatal severe jaundice and neonatal asphyxia, respectively. The patients in TP showed lower mental ability and suffered from more intractable convulsions than those in GL. In GL, rigidospasticity was frequently demonstrated with fluctuation of athetoid movements, while in TP various abnormalities of muscle tone were observed, with rather restricted athetosis.

Adolescent↗
PubMed1991

Cytokine-induced expression of intercellular adhesion molecule-1 (ICAM-1) in cultured human oligodendrocytes and astrocytes.

We investigated the expression of intercellular adhesion molecule-1 (ICAM-1) on primary cultures of human adult oligodendrocytes and astrocytes. Under unstimulated conditions, low levels of ICAM-1 immunoreactivity were identified on both oligodendrocytes (less than 50%) and astrocytes (less than 30%). After 48 hours' exposure to immune mediators, such as culture supernatant of phytohemagglutinin (PHA)-stimulated lymphocytes, interferon gamma (IFN-gamma; 1,000 U/ml), tumor necrosis factor alpha (TNF-alpha; 2,000 U/ml), interleukin-1 alpha (IL-1 alpha; 1,000 U/ml) and lipopolysaccharide (LPS; 50 micrograms/ml), ICAM-1 expression on both cell types was markedly increased in terms of intensity and cell numbers. IFN-gamma and culture supernatant of PHA-stimulated lymphocytes were the most potent inducers of ICAM-1 among the mediators tested, while TNF-alpha, IL-alpha and LPS were less effective, although variations were observed among cultures derived from different donors. Cytokine-induced expression of ICAM-1 on glial cells may play a role in mediating lymphocyte-glial cell interactions at sites of inflammation in the central nervous system.

Adult↗
PubMed1991

Neurochemical and immunocytochemical studies of catecholamine system in the brindled mouse.

The distribution of immunoreactive catecholamine neurons and fibers was investigated in brindled mottled mouse, a murine model of Kinky hair syndrome (KHS), using antisera against tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase (DBH). In all mice, including normal littermate controls, a transient increase of TH-immunoreactive neurons (TH-IN) was observed in the cerebral cortex during the second postnatal week. The numbers of TH-IN were more pronounced in hemizygous brindled males (MObr/y). In addition, TH-IN appeared and rapidly increased in number in the striatum of MObr/y after postnatal day 11 (P11). Striatal TH-IN were rarely detected in controls. After cupric chloride (CuCl2) treatment, TH-IN in the striatum of some of the MObr/y mice became less conspicuous. In the substantia nigra and ventral tegmental area where TH-IN are normally present, no differences either in the immunostaining of TH-IN or the pattern of TH immunoreactive fibers were detected between MObr/y and controls. In MObr/y, a superficial plexus of DBH immunoreactive fibers was more pronounced than in controls but there were no DBH immunoreactive neurons in the cerebral cortex or striatum in any of the mice examined. Neurochemical analysis revealed a marked decrease in norepinephrine levels and increase of serotonin and its metabolites in the brain in MObr/y. Together, these data suggest that the unusual expression of TH-IN in MObr/y represents perturbations of normal development of catecholamine neurons in this copper deficient mutant mouse.

Animals↗
PubMed1991

Inhibition of autoimmune diabetes in NOD mice with serum from streptococcal preparation (OK-432)-injected mice.

We have recently reported that systemic and chronic administration of recombinant tumour necrosis factor alpha (TNF-alpha), as well as streptococcal preparation (OK-432), inhibits development of insulin-dependent diabetes mellitus (IDDM) in NOD mice and BB rats, models of IDDM. In this study we examined whether serum containing endogenous TNF induced by OK-432 injection could inhibit IDDM in NOD mice. Treatment twice a week from 4 weeks of age with OK-432-injected mouse serum, which contained endogenous TNF (75U), but not IL-1, IL-2 and interferon-gamma (IFN-gamma) activity, reduced the intensity of insulitis and significantly inhibited the cumulative incidence of diabetes by 28 weeks of age in NOD mice, as compared with the incidence in non-treated mice (P less than 0.01) and in mice treated with control serum (P less than 0.02). This inhibitory effect of the serum was diminished, although not significantly, by neutralization of serum TNF activity with anti-mouse TNF antibody. In the mice treated with the serum from OK-432-injected mice, Thy-1.2+ or CD8+ spleen cells decreased (P less than 0.01) and surface-Ig+ (S-Ig+) cells increased (P less than 0.05), whereas the proliferative response of spleen cells to concanavalin A (P less than 0.01) and lipopolysaccharide (P less than 0.05) increased. The results indicate that the inhibition by OK-432 treatment of IDDM in NOD mice was partially mediated by serum factors including endogenous TNF.

Animals↗
PubMed1990

Inhibition of type 1 diabetes in BB rats with recombinant human tumor necrosis factor-alpha.

We previously reported that streptococcal preparation (OK-432), which is a TNF inducer, inhibits insulitis and development of autoimmune diabetes in nonobese diabetic (NOD) mice and Bio-Breeding (BB) rats, as animal models of insulin-dependent diabetes mellitus. We have recently shown that recombinant human (h)TNF-alpha also suppresses development of diabetes in NOD mice. In this study we have extended our observation on TNF to BB rats in order to see whether TNF generally inhibits autoimmune diabetes. A total of 5 x 10(4) U of rhTNF-alpha was administered i.p., twice a week to male and female BB rats from 4 to 27 wk of age. The cumulative incidence of diabetes by 27 wk of age in nontreated rats was 36.4% (8/22), whereas that in hTNF-alpha-treated rats was 0% (0/21) (p less than 0.001). The hTNF-alpha-treated rats did not lose body weight and maintained normal blood glucose concentrations. Immunologic and histologic examinations were performed at the end of the experiment. Spleen cell cytotoxicities for NK-sensitive YAC-1 and rat insulinoma (RINm5F) cells in hTNF-alpha-treated rats significantly decreased in comparison with nontreated and nondiabetic BB rats. Intensity of insulitis was also inhibited in hTNF-alpha-treated rats. Interestingly, a huge hepatomegaly and splenomegaly was found in two of the 21 hTNF-alpha-treated rats. The latter consisted of W3/13dull+ and W3/25dull+ cells, which did not exhibit cytotoxicity for either YAC-1 or RINm5F cells. These results indicate that the chronic and systemic administration of TNF has a regulatory role in autoimmune diabetes in BB rats as well as in NOD mice, and that these animals may have a defect in TNF-mediated immunoregulation.

Animals↗
PubMed1990

Tyrosine hydroxylase-immunoreactive neurons in the mouse cerebral cortex during the postnatal period.

Using specific antiserum against tyrosine hydroxylase, the key enzyme in catecholamine synthesis, we found tyrosine hydroxylase immunoreactive neurons (TH-IN) in the cerebral cortex of Swiss Webster mice. They were found in the deeper layers of the cerebral isocortex in all the mice examined up to 60 days postnatal (P60). However, they appeared to be more numerous in early postnatal days. On P3 and P5, a few neurons with faintly stained perikarya were detected in the layer V and VI. The number and intensity of TH-IN increased gradually after P7, reaching to the maximum between P10 and P14 and then gradually decreased. Many of these neurons were multipolar but some were bipolar. Significance of TH-IN in the cortex and their apparent increase in immunoreactivity during the second postnatal week is not certain. Such an increase may be a transient increase in activity or phenotypic expression of tyrosine hydroxylase (TH) by young neurons in response to as yet unknown intrinsic environmental changes during this particular period of the brain development.

Aging↗
PubMed1990

Mechanism of action of a streptococcal preparation (OK-432) in prevention of autoimmune diabetes in NOD mice. Suppression of generation of effector cells for pancreatic B cell destruction.

We have previously reported that treatment with a streptococcal preparation (OK-432), one of the biologic response modifiers, inhibits insulitis and development of autoimmune diabetes in nonobese diabetic (NOD) mice and Bio-Breeding rats used as animal models of insulin-dependent diabetes mellitus (IDDM). We studied the mechanism by which OK-432 inhibited development of IDDM in NOD mice. In female NOD mice diabetes spontaneously developed from 10 to 15 wk of age and the cumulative incidence of diabetes amounted to 74.7% at 30 wk of age. NOD mice, however, never developed diabetes over the observation period of up to 45 wk of age when they were i.p. injected with 0.1 mg of OK-432 weekly from 4 to 15 wk of age. OK-432 treatment in younger age had a stronger inhibitory effect on the development of diabetes. Diabetes was transferred to young, irradiated mice by spleen cells of nontreated, adult mice, but barely transferred by those of OK-432-treated mice. Furthermore, these spleen cells of OK-432-treated mice did not suppress transfer of diabetes by diabetic mice spleen cells. Treatment with cyclophosphamide promoted development of diabetes in nontreated NOD mice due to removal of suppressor cells. However, cyclophosphamide did not show the promotive effect in OK-432-treated mice. Taken together, these results indicate that OK-432 treatment prevented development of diabetes mainly by suppression in generation of the effector cells for pancreatic B cell destruction. The same OK-432 treatment did not suppress the immune response to exogenous AG such as xenogeneic SRBC and allogeneic tumor cells. The study suggests that BRM in the natural environment such as streptococci may suppress induction and progression of autoimmunity and be useful for the immunotherapy of human IDDM.

Animals↗
PubMed1990

Absence of natural killer (NK) cell activity against oligodendrocytes in multiple sclerosis.

The cytotoxicity of natural killer (NK) cells directed to enriched cultures of bovine oligodendrocytes was investigated in multiple sclerosis (MS) patients and controls. Macrophage-depleted peripheral blood lymphocytes were used as effector cells in a 4-h 51Cr release assay. No significant cytotoxic activity to oligodendrocytes was identified in either MS or control groups. In contrast, a definite cytotoxic activity directed toward K562 cells was observed in the study populations. No statistically significant difference was observed between chronic progressive or stable MS, other neurological diseases (OND), and normal controls. These results indicate that NK cell activity directed toward intact bovine oligodendrocytes is not significantly different between MS and control groups and question the significance of studies employing K562 cells as the target in NK assays in MS. Furthermore, these observations suggest that NK-mediated cytotoxicity against oligodendrocytes is unlikely to be a specific mechanism mediating demyelination in MS.

Analysis of Variance↗
PubMed1990

[Alzheimer's neurofibrillary tangles in a 52-year-old patient with severe brain damage].

A woman, who had been developmentally delayed since her birth, further deteriorated after she got an episode of high fever of unknown origin at 2 years of age. At the age of 52 years, she died of liver cancer after a long-standing HB virus carrier state. Neuropathological examination revealed brain atrophy, narrowed white matter, myelin pallor, fibrillary gliosis and status marmoratus of the thalamus. These findings suggested the primary cause of the brain pathology in this case to be a developmental destructive process which should have taken place in the early stage of brain development. In addition, neurofibrillary tangles (NFT) were noticed in the hippocampus, locus ceruleus and nucleus basalis of Meynert, but no senile plaques were found anywhere. These NFT changes seemed to be closely resembling to those of the Fukuyama type congenital muscular dystrophy. But the reason why NFT occur in this case is still obscure and probably different from that in the Down syndrome or in physiological senility.

Brain↗
PubMed1989

An autopsy case of atypical infantile motor neuron disease with hyaline intraneuronal inclusions.

We describe a 5-year-old boy who had had a progressive motor weakness with bulbar palsy and spasticity of the lower extremities since age 3 years and who died of bronchopneumonia after about two and a half years of the illness. Neuropathologic examination revealed combined degenerative processes in the upper and lower motor neurons, the spinocerebellar and olivocerebellar systems, and the ventral thalamic nuclei. Lewy body-like intraneuronal hyaline inclusions, which ultrastructurally showed irregular accumulations of trilaminar membranous profiles, were detected in the spinal anterior horn, Clarke's dorsal nucleus, facial nerve nucleus, inferior olivary nucleus, and substantia nigra. This case could be considered as a unique form in the group of the infantile motor neuron diseases associated with multi-systemic degenerations in the central nervous system.

Brain↗
PubMed1989

Recombinant human tumor necrosis factor alpha suppresses autoimmune diabetes in nonobese diabetic mice.

We previously reported that administration of a streptococcal preparation (OK-432) inhibited insulitis and development of autoimmune diabetes in nonobese diabetic (NOD) mice and BB rats as animals models of insulin-dependent diabetes mellitus. In this study, we screened various cytokines that could be induced by OK-432 in vivo, for their preventive effect against diabetes in NOD mice. Among recombinant mouse IFN gamma, human IL1 alpha, human IL2, mouse granulocyte-macrophage colony-stimulating factor and human TNF alpha, only human TNF alpha suppressed insulitis and significantly (P less than 0.001) inhibited development of diabetes. NOD mice were the lowest producers of the mRNA of TNF and serum TNF on stimulation with OK-432 or with IFN gamma plus LPS, compared with C57BL/6, C3H/He, and Balb/c mice. The results imply a role for low productivity of TNF in the pathogenesis of autoimmune diabetes in NOD mice.

Animals↗