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Biomedical subjects

S Matsuo

Publications and source records attributed to S Matsuo.

At least 181 records · Page 10Linked to original sources
PubMed1996

Effect of alcohol intake on the efficacy of interferon therapy in patients with chronic hepatitis C as evaluated by multivariate logistic regression analysis.

The effect of alcohol intake on the efficacy of interferon (IFN) therapy was evaluated retrospectively in patients with chronic hepatitis C diagnosed by liver histology and positive serum hepatitis C virus (HCV)-RNA. Patients included 119 given IFN therapy and 11 no IFN therapy. Serum HCV-RNA was measured 6 months after discontinuation of IFN therapy in 92 treated patients, 27.2% of whom showed disappearance of serum HCV-RNA. Multivariate logistic regression analysis revealed that this disappearance was affected by alcohol intake, the presence of its history (p < 0.05) or cumulative alcohol consumption (kg) (p < 0.01), and serum HCV-RNA levels (p < 0.001). The odds ratio associated with serum HCV-RNA still positive at 6 months was 7.018 (95% confidence interval: 1.444-34.062) and 1.004 (1.001-1.007) for the presence of alcohol intake history and the cumulative alcohol consumption, respectively. Other predictor variables-such as sex and age of patients, history of blood transfusion, HCV genotype, histological findings of the liver, and types of IFN-had no influence on the efficacy of the therapy. Cumulative alcohol consumption showed a negative correlation with serum HCV-RNA levels pretreatment, when the outcome variable was divided into two categories based on serum HCV-RNA levels: 10(6) copy/ml or less and 10(7) copy/ml or more. Alcohol intake was positively correlated with histological extent of alcoholic fibrosis, but affected neither grading nor staging of chronic viral hepatitis. We conclude that alcohol intake was a risk factor on the efficacy of IFN therapy in chronic hepatitis C patients. This effect was independent of serum HCV-RNA levels and histological findings specific for viral hepatitis in the liver.

Adult↗
PubMed1996

Contrast-enhanced radiographic computed tomographic findings in patients with straight back syndrome.

UNLABELLED: Straight back syndrome (SBS) is usually diagnosed by physical and chest radiographic findings. Radiographic computed tomographic (CT) findings are very useful for the diagnosis and the evaluation of its severity. The purpose is to evaluate the relationship between chest X-ray film and CT findings. SUBJECTS: We evaluated 26 patients (SBS group) and 11 normal subjects (control group). SBS group consisted of 15 patients without structural heart disease (group I) and 11 patients with other heart disease (group II). METHODS: (1) On the chest X-ray film, antero-posterior diameter (APD) of the thorax, transthoracic diameter (TTD), and APD/TTD ratio were measured. (2) On the CT image, three parameters were calculated; APD of the left atrium (LA diameter), APD/transverse diameter ratio of the heart (flattening ratio) and left side shift ratio of the heart (shifting ratio). (3) CT parameters were compared with APD/TTD ratio in patients and control group. RESULTS: (1) APD/TTD ratio was smaller in group I and II than control group (30.0 +/- 5.4, 30.5 +/- 4.0 v 44.6 +/- 2.7%, p < .001). (2) LA diameter was smaller in group I and II than control group (23.2 +/- 4.1, 26.0 +/- 8.6 v 30.0 +/- 6.5 mm, p < .01). Flattening ratio was also smaller in group I and II than control group (59.2 +/- 9.4, 61.8 +/- 8.6 v 75.4 +/- 13.2%, p < .01). Shifting ratio was greater in group I and II than control group (10.9 +/- 5.0, 11.9 +/- 4.5 v 8.4 +/- 4.0%, p < .01). (3) APD/TTD ratio correlated with LA diameter (r = .39, p < .05) and flattening ratio (r = .53, p < .001). APD/TTD ratio did not correlate with shifting ratio (r = -.27, NS). CONCLUSIONS: APD/TTD ratio correlated with LA diameter and flattening ratio rather than shifting ratio. LA diameter and flattening ratio on the CT image were more useful for evaluating the severity.

Adolescent↗
PubMed1995

N-ras mutation in 7,12-dimethylbenz[a]anthracene (DMBA)-induced erythroleukemia in Long-Evans rats.

Intravenous injections of 7,12-dimethylbenz[a]anthracene (DMBA) induce erythroblastic leukemia (erythroleukemia) with No.2 trisomy in Long-Evans rats. Activation of some oncogenes such as abl and Ha-ras has been reported to occur in relation to the secondary chromosomal translocations. In the present studies, a consistent type of mutation, A to T transversion in codon 61 of N-ras gene, was found in all of 6 cultured leukemia cell lines and 5 primary leukemias induced by DMBA. The N-ras mutation was also found in bone marrow cells of 2 out of 8 preleukemias. On the contrary, no mutation was observed in Ha- and Ki-ras genes in all leukemias and preleukemias. The consistent occurrence of above N-ras mutation in leukemias indicates that it plays an important role in DMBA-leukemogenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1995

Degradation of DNA in dried tissues by atmospheric oxygen.

Recently, DNA of extinct creatures have been brought into analyses. The difficulty in this field of research is DNA degradation. Oxidative damage is considered to be one of the causes of the DNA degradation. We studied how DNA in dried tissue was affected by atmospheric oxygen using freeze-dried rat liver as a model. In tissues exposed to oxygen, DNA degradation occurred within several months and the amount of 8-hydroxy-2'-deoxyguanosine in DNA rapidly increased. The DNA degradation was inhibited by lipid extraction prior to the exposure to atmospheric oxygen. Purified lambda phage DNA was not affected by oxygen. Cellular DNA and RNA were degraded slowly in nitrogen air. These results suggest that both atmospheric and endogenous oxygens play a role in DNA degradation in dried tissues.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1995

Posterior canal-activated vestibulocortical pathways in cats.

This study was undertaken to investigate vestibulothalamocortical pathways in anesthetized cats. Synaptic connections of posterior canal-activated excitatory vestibuloocular relay (PC) neurons to thalamic neurons were examined by a spike-triggered averaging technique. The averaged potentials evoked in the ventrobasal complex of the thalamus revealed a negative wave with latencies from 0.8 to 1.5 ms. Thirty-six thalamic neurons, which were activated by nose-up head rotation and by contralateral labyrinth stimulation, were mainly located in the ventrobasal complex. Thirteen of these neurons were antidromically activated from the anterior suprasylvian sulcus or postcruciate dimple of the cortex. These results suggest that the PC neurons participate, at least in part, in the vestibulocortical pathways contributing to spatial orientation.

Animals↗
PubMed1995

Relation between the trans-Golgi network and the Golgi stack on development of the Golgi apparatus of the ameloblast in developing rat molar tooth germs.

BACKGROUND: The problem of how the functional compartments of the Golgi apparatus organizes during cell differentiation to become a well-formed Golgi apparatus is as yet an unresolved issue. This study was designed to define the involvement of the trans-Golgi network (TGN) and the Golgi stack in organizing the Golgi apparatus. METHODS: The distribution of the TGN marker enzyme was examined in the ameloblast of developing rat molar tooth germs using cytochemistry with Co-enzyme A phosphatase (CoA Pase) and cytidine monophosphatase (CMPase). RESULTS: Typically formed Golgi apparatus was observed in the secretory ameloblast but not in the presecretory ameloblast. Organization of the Golgi apparatus through the presecretory ameloblast was noted. In the presecretory ameloblast, Golgi stacks of different sizes and clusters of small vesicles were located in the cytoplasm lateral to the nucleus. The saccules with enzymes marked for TGN were also observed in the cytoplasm lateral to the nucleus. These saccules were adjacent to the cluster of small vesicles and/or the Golgi stack. Upon cell differentiation, Golgi stacks were seen in line along the long axis of the cell, and the file of the stacks in the cytoplasm lateral to the nucleus was formed. The positive saccule was seen in a parallel line equal to the length of the Golgi stacks. CONCLUSIONS: In organizing the Golgi apparatus, the development process of the TGN and the Golgi stack appear to be different, and new Golgi stacks seem to be formed through the accumulation of small vesicles near the pre-existing TGN.

Ameloblasts↗
PubMed1995

Repression of involucrin gene expression by transcriptional enhancer factor 1 (TEF-1).

Involucrin is one of the precursor proteins of keratinocyte cornified envelope that is formed beneath the inner surface of the cell membrane during terminal differentiation. Although involucrin is specifically expressed in the upper squamous cells of the epidermis, the precise regulatory mechanism of involucrin gene expression remains unknown. Transcriptional enhancer factor 1 (TEF-1), which binds to SV40 enhancer, is a nuclear protein expressed in various types of cells including keratinocytes. Immunohistochemical study has revealed that TEF-1 protein is highly expressed on the basal cell layer of the epidermis. To examine the possible regulatory mechanism of involucrin gene expression by TEF-1 protein, we analysed involucrin promoter activity of the INV-CAT vector, which was constructed by connecting the 5' upstream region of the involucrin gene (-801 bp upstream from the transcription start site and downstream including the untranslated first exon) to the chloramphenicol acetyltransferase (CAT) reporter gene. The INV-CAT vector was transfected to SV40-transformed human keratinocytes (SVHK). Cotransfection of the TEF-1 expression vector significantly repressed INV-CAT promoter activity in a dose-dependent manner. The repression was also observed by transfection of the GAL4-TEF-1 vector, which was constructed by replacement of the TEF-1 DNA binding domain by the GAL4 activator domain. This suggests that TEF-1-induced repression is due to interference/squelching of a limiting transcriptional intermediary factor that is essential for involucrin expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗
PubMed1995

Transforming growth factor beta 1 inhibits IL-3- and IL-4-dependent mouse connective tissue-type mast cell proliferation.

Transforming growth factor beta 1 (TGF beta 1) is a regulator of cell proliferation and differentiation. Using a mouse peritoneal cell-derived mast cell culture system, we investigated the effects of TGF beta 1 on mast cell proliferation. TGF beta 1 inhibited IL-3- and IL-4-dependent connective tissue-type mast cell proliferation. The effect was concentration dependent: 50% inhibition was observed with 1.0 ng/ml TGF beta 1 and the maximal inhibitory effect (no proliferation), was observed with 10 ng/ml. Flow cytometric analysis suggested that the inhibitory effect of TGF beta 1 was due to blocking of both G1 and G2 phases. Both control and TGF beta 1-treated mast cells showed similar histamine release induced by the calcium ionophore, A23187. TGF beta 1 seems to be an important negative regulator of connective tissue-type mast cell proliferation with apparently no appreciable effect on mast cell function.

Animals↗
PubMed1995

Liver injuries induced by herbal medicine, syo-saiko-to (xiao-chai-hu-tang).

Four patients treated with the herbal medicine syo-saiko-to (xiao-chai-hu-tang) exhibited acute drug-induced liver injury. The latent period was one and a half to three months. All of the patients showed a rise in aminotransferases after readministration or challenge test. The liver histology revealed centrilobular confluent necrosis or spotty necrosis, microvesicular fatty change, acidophilic degeneration, and a granuloma. Cholestasis was seen in two patients. The results of the [13C]aminopyrine breath test, performed in one patient, were low before the challenge test and even lower after the challenge. These findings suggest that the herbal medicine syo-saiko-to may induce acute injury or the hepatocellular pattern with variable cholestasis.

Chemical and Drug Induced Liver Injury↗
PubMed1995

Enhancement of FK-506 activities by ganglioside (GM3) in vivo.

Influence of FK-506 and ganglioside (GM3) on acquired immunity to Hymenolepis nana reinfection was examined in BALB/c mice. Treatment of mice with FK-506 abolished the acquired immunity to challenge infection with eggs of H. nana when the agent was injected inraperitoneally at daily doses of 9.0 to 11.0 mg/kg (but not 8.5 mg/kg) on days -1, 0, 1, 2, and 3 relative to the challenge. Intravenous injection of GM3 at a daily dose of 10.0 mg/kg could not produce an immunosuppressive effect on the acquired immunity. Combination treatment with 8.5 mg/kg/day FK-506 and 10.0 mg/kg/day of GM3 inhibited the acquired immunity. These results suggest that GM3 will be a good candidate for a clinical supplementary immunosuppressive agent.

Animals↗
PubMed1995

Generation of effector T cells in Hymenolepis nana-infected, FK-506-treated BALB/c mice.

FK-506 administered into mice daily at a dose of 10.0 mg/kg (but not 1.0 and 5.0 mg/kg) caused suppression of protective immunity to Hymenolepis nana, when the agent was injected intraperitoneally during the induction phase of protective immunity. Daily administration of 10.0 mg/kg FK-506, during the course of larval development from challenge, also suppressed protective immunity. Inhibition of protective immunity was only observed in mice that received FK-506 for 6 days at a daily dose of 10.0 mg/kg and were challenged 24 h after the final FK-506 injection. FK-506 did not inhibit formation of effector cells that mediate delayed-type hypersensitivity (DTH) to H. nana egg antigen when the agent was administered intraperitoneally at a dose of 10.0 mg/kg/day for 6 days before cell preparation. However, FK-506 did inhibit DTH effector cell activation when cells prepared from infected, saline-injected mice were transferred into 10.0 mg/kg FK-506-treated recipient mice. These results strongly indicate that FK-506 cannot inhibit the generation of effector cells but will suppress their function in vivo.

Animals↗
PubMed1995

Finer mapping of neutralizing epitope(s) on the C-terminal of Japanese encephalitis virus E-protein expressed in recombinant Escherichia coli system.

In order to localize denaturation-resistant neutralizing epitope(s) in the C-terminal 180 amino acids of Japanese encephalitis (JE) virus E-protein, four recombinant clones encoding different or overlapping nucleotide sequences were constructed by PCR from a recombinant plasmid pS22. The amplified fragments were cloned into PCR 1000 vector, and then transferred into Escherichia coli expression vector pRIT2T. The inserted genes were expressed as fusion proteins with protein-A and examined for their antigenicity and immunogenicity by Western blotting and mouse immunization, respectively. Among the four recombinant fusion proteins, the highest neutralizing antibody titre was obtained by the one expressed by the recombinant clone pRIT2T-B3, which carried the coding sequence of amino acid number 373-399 of JE virus E protein. The results indicated that this short region of 27 amino acids sequence near the C-terminal of JE virus E protein possesses neutralizing epitope(s). These data should assist in the design of an efficient subunit vaccine against JE virus infection in future.

Animals↗
PubMed1995

Pathogenic significance of interleukin-6 in a patient with antiglomerular basement membrane antibody-induced glomerulonephritis with multinucleated giant cells.

We report a patient with anti-glomerular basement membrane disease who developed renal failure associated with systemic manifestations, including acute-phase inflammatory reactions and plasmacytosis. Renal tissue obtained by an open surgical biopsy showed circumferential cellular crescents, multinucleated giant cells, and exudation of fibrin in all glomeruli. Immunofluorescence microscopy demonstrated deposition of immunoglobulin G, C3, and membrane attack complex along glomerular capillary walls. Multinucleated giant cells were suggested to be macrophage-monocyte lineage because they were CD68 positive. Bone marrow aspiration showed an increase of plasma cells. Immunostaining showed intensive expression of interleukin-6 (IL-6) in practically every part of the renal sites involving multinucleated cells, crescents, tubules, and infiltrating cells, suggesting that one of the sources of systemically elevated IL-6 was the kidney. Serum IL-6, anti-glomerular basement membrane antibody, and acute-phase proteins were markedly elevated, and returned dramatically to the normal level after corticosteroid therapy and plasmapheresis. We believe that IL-6 played an important role in the development of many symptoms in the present case.

Aged↗
PubMed1995

Thyrotropin-releasing hormone in treatment of intractable epilepsy: neurochemical analysis of CSF monoamine metabolites.

The efficacy of thyrotropin-releasing hormone in children with intractable epilepsy was investigated and changes in cerebrospinal fluid monoamine metabolites were analyzed. The 18 patients had either West syndrome (12 patients) or Lennox-Gastaut syndrome (6 patients), which was intractable to antiepileptic drug therapy and to adrenocorticotrophic hormone. Thyrotropin-releasing hormone-tartrate was administered for 4 weeks. Before and after the thyrotropin-releasing hormone administration, cerebrospinal fluid was collected and analyzed for 5-hydroxyindoleacetic acid, kynurenine, homovanillic acid, and 3-methoxy-4-hydroxyphenyl glycol. The patients were classified into 3 groups, based on seizure frequency and electroencephalographic effects: cessation of seizures and seizure discharges (very effective; group A), reduction of seizures and/or seizure discharges (effective; group B), and no changes in frequency of seizures or discharges (not effective; group C). There were 6 patients in group A, 3 in group B, and 9 in group C. There were no significant differences in monoamine metabolites before and after the thyrotropin-releasing hormone therapy. A trial of thyrotropin-releasing hormone for the treatment of intractable epilepsy is warranted and further study is required on the mechanism of the antiepileptic action of thyrotropin-releasing hormone.

Child↗