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S Kato

Publications and source records attributed to S Kato.

At least 793 records · Page 44Linked to original sources
PubMed1996

[Infantile onset chronic inflammatory demyelinating polyneuropathy with clinical course of 23 years; a case report].

We report a 23-year-old female with infantile onset chronic inflammatory demyelinating polyneuropathy. Muscle weakness was noticed when she was 1 year old, and, together with sensory disturbances, gradually progressed in an asymmetric manner. Nerve conduction studies disclosed slowing of conduction velocities, temporal dispersion, and decreased amplitude of compound muscle action potentials, the degrees of which were markedly different amongst different nerves even in the same limbs. The sural nerve biopsy showed various degrees of nerve fiber amongst different fascicles. Marked inter-nerve and intra-nerve differences of involvement and clinical improvement after steroid therapy supported the diagnosis of chronic inflammatory demyelinating polyneuropathy. It should be noted that even after a long clinical course of 23 years, her clinical symptoms remained asymmetrical and multi-focal lesions could be clearly demonstrated.

Adult↗
PubMed1996

[Recurrence of stones after extracorporeal shock wave lithotripsy].

During the 11-year period from September 1984 through August 1995, extracorporeal shock wave lithotripsy (ESWL) was performed on 5,558 patients using a Dornier HM3 apparatus. A recurrence questionnaire was sent out to 2,379 of those who had had complete elimination of the calculi and for whom at least 3 years had passed since the ESWL. The last day of follow-up was defined as follows: the day of completion of the questionnaire in the recurrence-free group (n = 787), the day when recurrence of calculi was diagnosed in the recurrence group (n = 415) and the day of the last visit to the outpatient clinic in the miscellaneous group (n = 1,133). The cumulative recurrence rates were calculated by the Kaplan-Meier equation. The resultant data were analyzed for statistically significant differences by the log rank test and the generalized Wilcoxon test. Ap value of < or = 0.05 was considered to indicate significance. The recurrence rate was examined for differences in relation to the following risk factors: the patients' age and sex, the stone location, size and number, the presence or absence of past history of lithiasis, the composition of the stone (s), and the presence or absence of urinary tract complications. The cumulative recurrence rates for the total cases were 2.0% at one year, 13.1% at 3 years, 23.9% at 5 years, 30.7% at 7 years and 40.7% at 10 years. Significantly higher recurrence rates were found for patients under 60 years of age, those with multiple stones and those with a past history of disease.

Female↗
PubMed1996

Ethanol-induced apoptosis and oxidative stress in hepatocytes.

This short review focuses on ethanol-induced oxidative stress and hepatocyte apoptosis. Apoptosis is increasingly recognized as a fundamental biological process that impacts on an early development, maturation, and acquisition of disease states of multicellular organisms. Although the occurrence of apoptosis has been identified for many decades, relatively recent acceptance of this principle is evidenced by remarkable increases in special conferences and presentations on this topic as well as its rapidly expanding volume of scientific literature. Oxidative stress is well recognized to be a key step in the pathogenesis of ethanol-associated liver injury. Ethanol administration induces an increase in lipid peroxidation either by enhancing the production of oxygen reactive species and/or by decreasing the level of endogenous antioxidants. Studies in our laboratory using a confocal laser scanning microscopic system strongly suggest that agents which inhibit ethanol-induced oxidative stress effectively attenuate hepatocyte death, i.e., apoptosis and necrosis. In addition, our investigations demonstrated that inhibitors of intracellular antioxidants exaggerate ethanol-associated hepatocyte apoptosis. Although the detailed mechanism still remains unknown, it is conceivable that an oxidant-dependent mechanism is largely involved in the process for ethanol-induced hepatocyte apoptosis.

Animals↗
PubMed1996

Ethanol-induced leukocyte adherence and albumin leakage in rat mesenteric venules: role of CD18/intercellular adhesion molecule-1.

The adherence and emigration of leukocytes have been implicated as a rate-limiting step in the microvascular disturbance in a variety of pathogenic events. The objective of the present study was to investigate leukocyte-endothelial cell adhesion and endothelial barrier function in rat mesenteric microvessels exposed to ethanol, which is known to cause inflammation and injury in various organs. Mesentery of male Wistar rats was used for intravital microscopic observations. Leukocyte adherence and albumin leakage were monitored in single postcapillary venules using the intravital fluorescence microscope. Superfusion of 50 mM ethanol elicited the leukocyte adherence and albumin leakage within 60 min. Pretreatment with a monoclonal antibody directed against either CD18 or intercellular adhesion molecule-1 (ICAM-1) significantly prevented the ethanol-induced increase in leukocyte adherence and decrease in barrier function of endothelium. These results suggest that ethanol-induced leukocyte adherence is mediated by CD18 on leukocytes and ICAM-1 on endothelial cells. The present study further supports that CD18/ ICAM-1-dependent leukocyte-endothelial adhesive interactions lead to macromolecular leakage in the postcapillary venules exposed to ethanol.

Animals↗
PubMed1996

Chronic ethanol consumption enhances endotoxin induced hepatic sinusoidal leukocyte adhesion.

In alcoholic liver disease, endotoxin has been postulated to play an important role in its pathogenesis. Endotoxin is known to lead to impediment of hepatic microcirculation, including the adhesion of leukocytes to sinusoidal endothelial cells. In this study, the effect of chronic ethanol consumption on the leukocyte adhesion elicited by endotoxin was examined. Male Wistar rats were pair-fed with a liquid diet containing ethanol or an isocaloric control diet for 6 weeks. The liver of anesthetized rats were placed on the nonfluorescent cover-glass for observation by an intravital inverted microscope equipped with a silicon intensified target camera. The red blood cell (RBC) velocity in hepatic sinusoids was measured by an off-line temporal correlation velocimeter (Capiflow, Sweden) after intravenous injection of fluorescein isothiocyanate-labeled rat RBC. RBC velocity in sinusoids was more severely disturbed in ethanol fed rats than in controls. Leukocytes were stained by the intravenous injection of carboxyfluorescein succinimidyl ester for a fluorographic observation of leukocyte adhesion. After lipopolysaccharide injection, the number of adherent leukocytes was significantly greater in ethanol-fed rats than in controls. Plasma tumor necrosis factor-alpha levels were also higher in ethanol-fed rats than in controls. These results suggest that chronic ethanol consumption aggravates endotoxin induced leukocytes adhesion that may result in hepatic microcirculatory disturbances. Leukocyte adhesion to the sinusoidal wall may be associated with increased in tumor necrosis factor-alpha levels.

Animals↗
PubMed1996

[Cord blood stem cell transplantation for a patient with acute myelogenous leukemia (M1)].

A five-year-old boy with acute myelogenous leukemia in relapse was treated by HLA-matched cord blood stem cell transplantation. The patient was preconditioned with 16 mg/kg of busulfan, 15 mg/kg of thiotepa and 90 mg/kg of cyclophosphamide and 2.45 x 10(7)/kg of cord blood mononuclear cells were infused to the patient on October 19th 1995 without the prophylaxis of graft-versus-host disease (GVHD). From the fifth day following the transplant, rG-CSF was administered at a dose of 300 micrograms/m2/day. Hematopoietic recovery was obtained as following; WBC over 1000/microliters was on +18 day, neutrophil over 500/microliters was on +20 day, reticulocyte over 20/1000 was on +28 day and platelet over 50 x 10(2) microliters was on +91 day. Engraftment was confirmed by DNA restriction fragment length polymorphism (VNTR) on +28 day. In spite of absence of prophylaxis of GVHD, the patient did not develop any signs of GVHD, and leukemia relapsed on +105 day. The patient died of leukemia relapse on +251 day. This is the first case of cord blood stem cell transplantation in Japan.

CD4-CD8 Ratio↗
PubMed1996

Platelet-activating factor receptor. Gene structure and tissue-specific regulation.

The human platelet-activating factor receptor gene exists as a single copy on chromosome 1. Two 5'-noncoding exons (Exon 1 and 2) has distinct transcription initiation sites and promoters. These exons are alternatively spliced to a common splice acceptor site on exon 3 that contains a total coding regions. The transcript 1 is expressed ubiquitously with an emphasis of differentiated eosinophilic cell line (Eol-1), and leukocytes. On the other hand, the transcript 2 is expressed tissue-specifically. The latter is not expressed in leukocytes or brain. The transcript 1 has three tandem repeats of NF-kappa B, and SP-1 site, and responded to various inflammatory reagents including PAF itself, lipopolysaccharide, or phorbol ester. By northern blotting of tissue or cells with various nutritional or hormonal treatments, the PAF receptor messages are up-regulated. Estrogen increased the expression of the PAF receptor in human endometrial glandular cells, and vitamin A (retinoic acid) or thyroid hormone treatment up-regulates the PAF receptor expression only tissues with transcript 2 By various in vivo and in vitro transcriptional assays (CAT reporter assay, gel mobility shift assay), we identified estrogen responsible element, and hormone responsive element. The PAF receptor hormone responsive element is composed of three direct repeated TGACCT-like hexamer motifs with 2 and 4 bp spaces, and the two upstream and two downstream motifs were identified as response elements for RA and T.

Animals↗
PubMed1995

Adenovirus-mediated gene transfer of dopamine D2 receptor cDNA into rat striatum.

A robust feature of mammalian aging associated with diminished motor control is the loss of dopamine D2 receptors from the neostriatum. Decline in this neurotransmitter receptor is also observed in neurodegenerative disorders, such as Huntington's disease and late-stage Parkinson's disease. We have constructed a replication-deficient adenoviral vector to transfer rat dopamine D2 receptor cDNA to brain as a possible therapeutic strategy. Using tissue culture cells infected with this vector, we detected dopamine D2 receptor mRNA by Northern analysis and functional receptor protein in membrane preparations as specific binding of the dopamine D2 receptor ligand, [3H]spiperone. In vivo demonstration involved autoradiographic analysis of [3H]spiperone binding in rat striatum following injection of the adenoviral vector. Dopamine D2 receptor expression was amplified markedly above normal concentrations in the injection site, whereas no increased expression was observed in sites receiving control treatments. These results demonstrate the potential of gene therapy using adenoviral vectors to transfer neurotransmitter receptor proteins to the brain to reverse deficiencies in specific neurodegenerative disorders.

Adenoviridae↗
PubMed1995

Activation of the estrogen receptor through phosphorylation by mitogen-activated protein kinase.

The phosphorylation of the human estrogen receptor (ER) serine residue at position 118 is required for full activity of the ER activation function 1 (AF-1). This Ser118 is phosphorylated by mitogen-activated protein kinase (MAPK) in vitro and in cells treated with epidermal growth factor (EGF) and insulin-like growth factor (IGF) in vivo. Overexpression of MAPK kinase (MAPKK) or of the guanine nucleotide binding protein Ras, both of which activate MAPK, enhanced estrogen-induced and antiestrogen (tamoxifen)-induced transcriptional activity of wild-type ER, but not that of a mutant ER with an alanine in place of Ser118. Thus, the activity of the amino-terminal AF-1 of the ER is modulated by the phosphorylation of Ser118 through the Ras-MAPK cascade of the growth factor signaling pathways.

Amino Acid Sequence↗
PubMed1995

Identification of the amino acid residues involved in selective agonist binding in the first extracellular loop of the delta- and mu-opioid receptors.

Effects of amino acid substitutions in the first extracellular loop region of the delta- and mu-opioid receptors were examined. Substitution of lysine-108 of the delta-receptor (delta K108) with asparagine improved affinity to [D-Ala2,MePhe4,Gly-ol5]enk ephalin (DAGO), a mu-selective peptide agonist, to be comparable with that of the mu-receptor. On the other hand, replacement of mN127 with lysine decreased the affinity to DAGO by approximately 15-fold. These results suggest that dK108 and mN127, which correspond to each other in the aligned amino acid sequences, mainly determine the difference in DAGO binding affinity between the delta- and mu-receptors.

Amino Acid Sequence↗
PubMed1995

A signal sequence detection system using secreted protease activity as an indicator.

We have developed a novel expression vector, pSSD1, to detect a cDNA fragment encoding a secretory signal sequence (Ss). This vector carries a cDNA fragment encoding the protease domain of human urokinase-type plasminogen activator (u-PA) as a reporter gene under the SV40 early promoter. We inserted cDNA fragments encoding various Ss between the promoter and the reporter gene of pSSD1. These plasmids were introduced into monkey COS7 cells to produce chimeric proteins. Only when the Ss was intact, was fibrinolytic activity detected in the culture medium of the transfected cells. Thus, this system may be useful for detecting the cDNAs encoding secreted proteins or type-I membrane proteins.

Amino Acid Sequence↗
PubMed1995

Inhibitory action of hypoxanthine on meiotic resumption of denuded pig follicular oocytes in vitro.

The present study was conducted to investigate the direct action of hypoxanthine, which has been reported to be present in pig follicular fluid, on spontaneous meiotic resumption of pig denuded oocytes in vitro. No oocytes, which were surrounded by a cumulus and some membrana granulosa cells directly adjacent to it from healthy antral follicles, underwent germinal vesicle breakdown (GVBD) when they were cultured in serum-supplemented 199 with or without 4 mM hypoxanthine. On the other hand, 81% of denuded oocytes prepared from such cumulus-oocyte-granulosa cell complexes showed GVBD after 24 h of culture. Hypoxanthine inhibited significantly this spontaneous resumption of meiosis in denuded oocytes. The inhibitory action of hypoxanthine was dose dependent at concentrations of 1-6 mM and was reversible following subsequent culture of the oocytes in hypoxanthine-free medium. However, premature chromosome condensation was observed in oocytes cultured in hypoxanthine-supplemented medium, and the oocytes released from the influence of hypoxanthine completed GVBD and reached the second metaphase slightly faster than those freshly isolated from the follicle. These results suggest that hypoxanthine inhibits spontaneous meiotic resumption of pig oocytes in vitro. However, the inhibitory action of hypoxanthine does not prevent all events involved in GVBD from occurring.

Animals↗
PubMed1995

Specific inhibitors of vacuolar type H(+)-ATPases induce apoptotic cell death.

Concanamycin A and bafilomycin A1 are known as strong inhibitors of the vacuolar type H(+)-ATPases in vitro. These inhibitors exhibited cytotoxic effects on twelve cell lines in cell viability assay. On the other hand, the F1F0-type H(+)-ATPase inhibitor oligomycin and the E1E2-type H(+)-ATPase inhibitor vanadate showed no cytotoxic effect. We show here that concanamycin A and bafilomycin A1 induce a significant increase in the proportion of fragmented DNA in agarose gel electrophoresis. Flow cytometric cell cycle analysis of WEHI 231 cells stimulated with concanamycin A revealed the increased percentage of apoptotic cells with hypodiploid DNA. These findings indicate that cell death induced by specific inhibitors of vacuolar type H(+)-ATPases occurs through apoptosis.

Animals↗
PubMed1995

Effects of benzoic acid and its analogues on insulin and glucagon secretion in sheep.

The effects of benzoic acid and its analogues on insulin and glucagon secretion were investigated in conscious sheep. Intravenous injections of benzoic acid increased plasma insulin and glucagon concentrations in a dose-dependent manner between 39-1250 mumol/kg, with ED50s for increasing both hormones of about 625 mumol/kg. Various derivatives of benzoic acid (625 mumol/kg) were administered and structure-activity relationships were examined. A single carboxylic group was essential for stimulating insulin and glucagon secretion, since both hormone responses were abolished with compounds in which the carboxylic group was replaced by sulfonic or phosphoric groups, or in which another carboxylic element was introduced (phthalic acids). Most of the compounds which introduced other elements (amino and hydroxy groups, and halogens) onto the benzene ring had an altered stimulating activity. Thus the pancreatic endocrine system can recognize the chemical structure of benzoic acid and its derivatives in detail and induce insulin and glucagon secretion in sheep.

Animals↗
PubMed1995

Human lung carcinogen-DNA adduct levels mediated by genetic polymorphisms in vivo.

BACKGROUND: Cancer risk from exposure to tobacco smoke varies widely from person to person, depending in part on the status of particular genes and acquired susceptibilities. Certain genes determine how cells activate and detoxify carcinogens. Activated carcinogen metabolites may bind to DNA and form DNA adducts (e.g., 7-methyl-2'-deoxyguanosine-3'-monophosphate [7-methyl-dGMP] and polycyclic aromatic hydrocarbons-dGMP [PAHs-dGMP]), many of which can induce genetic mutations. Thus, if individuals have an increased capacity to activate carcinogens, they might form more carcinogen-DNA adducts and subsequently have an increased risk of cancer. PURPOSE: Using DNA-adduct detection methods specific for 7-methyl-dGMP and PAH-dGMP, we sought to determine whether an inherited genetic susceptibility to cancer associated with certain carcinogen-metabolizing and detoxifying genes (e.g., cytochrome P450 and glutathione S-transferase) is related to DNA adduct formation in lung tissue. METHODS: Human lung tissues were collected randomly from 90 autopsy donors who were free of cancer. Levels of 7-methyl-dGMP, a metabolic product of N-nitrosamines, and PAH-dGMP adducts were determined in lung tissue specimens by use of micropreparative DNA purification steps combined with a 32P-postlabeling assay. Genetic polymorphisms (the presence of different genes and/or alleles) were determined for the cytochrome P450 genes, CYP2D6, CYP2E1, and CYP1A1, as well as for glutathione S-transferase M1 (GSTM1). Statistical differences among adduct levels for the study variables, including genotypes, were assessed by the two-sided Student's t test or the Mann-Whitney U test. RESULTS: Higher 7-methyl-dGMP adduct levels were associated with CYP2D6 genotypes (P = .01), consistent with the reports of the increased risk of lung cancer associated with this genotype. Higher adduct levels were also associated with CYP2E1 minor alleles (P = .05). In both cases, the association was attributed mostly to individuals with low serum cotinine levels (P = .004 and P = .05, respectively), suggesting that the effect of the genotypes is mostly in nonsmokers exposed to either passive tobacco smoke or to N-nitrosamine exposures other than tobacco smoke or to N-nitrosamine exposures other than tobacco smoke. Separately, the presence of PAH-dGMP adducts was associated with the GSTM1 null genotype (absence of the gene) (odds ratio = 8.6; 95% confidence interval = 1.03-100). CONCLUSIONS: This study finds that the levels of two different carcinogen-DNA adducts vary in lung tissue (an important target tissue) in association with three separate genetic polymorphisms (i.e., CYP2D6, CYP2E1, and GSTM1). CYP2D6 and CYP2E1 genotypes are associated with higher 7-methyl-dGMP levels, while the GSTM1 null genotype is associated with higher numbers of PAH-dGMP adducts. These findings suggest that genetic polymorphisms are predictive of carcinogen-DNA adduct levels and would thus be predictive of an individual's lifetime response to carcinogen exposure.

Adolescent↗
PubMed1995

Demonstration of human Borna disease virus RNA in human peripheral blood mononuclear cells.

BDV naturally infects horses and sheep, and causes sporadic neurological disease. Serological evidence suggests an association of BDV, or a related virus, with specific psychiatric diseases in humans. Here, by using a nested RT-PCR technique, we demonstrate that human BDV RNA is present in the PBMC of psychiatric patients. In an examination of a total of 60 patients from 5 wards of a hospital in Japan, the detection rate differed within each ward, ranging from 8% to > 50% (37% on the average). Of particular note was the finding that the human derived BDV sequences, which included deleted forms in about 23% of the positive samples, were slightly different from those derived from horse BDV. These results suggest urgent consideration of the measures to be taken to cope with the effects of blood transfusion. In addition, the detection of a high level of BDV in the PBMC of patients will help our understanding of the pathogenesis in the disease.

Antibodies, Viral↗
PubMed1995

Molecular cloning and expression of mouse mg(2+)-dependent protein phosphatase beta-4 (type 2C beta-4).

A full-length complementary DNA (cDNA) clone (pTK-3) encoding an isoform of Mg(2+)-dependent protein phosphatase beta (MPP beta-4) was isolated for the first time from a mouse melanocyte cDNA library. It was strongly suggested that the mRNA corresponding to the pTK-3 insert was a splicing variant of a single pre-mRNA that also encodes MPP beta-1 and -2 (T. Terasawa, T. Kobayashi, T. Murakami, M. Ohnishi, S. Kato, O. Tanaka, H. Kondo, H. Yamamoto, T. Takeuchi, and S. Tamura, 1993, Arch. Biochem. Biophys. 307, 342-349). The amino acid sequence of MPP beta-4 differed from those of MPP beta-1 and -2 only at the carboxyl terminal region. Analysis by reverse transcriptase polymerase chain reaction (RT-PCR) revealed that MPP beta-4 mRNA was expressed only in testis and intestine and not in other mouse tissues tested. Specific expression of the mRNA signals of two other isoforms of MPP beta, MPP beta-3 and -5 (a novel isoform), in testis and intestine was also demonstrated by the RT-PCR. The carboxyl terminal region of MPP beta-5 was found to have a chimera structure composed of part of MPP beta-1 and part of MPP beta-3. The recombinant MPP beta-3 and -4 and the putative MPP beta-5 expressed in Escherichia coli cells exhibited Mg(2+)-dependent and okadaic acid-insensitive protein phosphatase activities. It was demonstrated that the mRNA expression levels of MPP beta-3, -4, and -5 alter according to the maturation of mouse testis. These results suggest that the complex structure of MPP beta isoforms and their tissue- and developmental stage-specific expression reflect the variety of their physiological functions.

Alternative Splicing↗