Biomedical subjects

M Satoh

Publications and source records attributed to M Satoh.

At least 469 records · Page 26Linked to original sources

PubMed1996

[Pediatric fiberoptic bronchoscopy via the laryngeal mask airway].

Fiberoptic bronchoscopy was performed on 11 children aged from 6 months to 3 years and weighing between 2.1 and 12.5 kg using the laryngeal mask airway (LMA). The LMA allows observation of subglottic stenosis which can not be seen under tracheal intubation. The smaller prototype of the fiberoptic bronchoscope whose diameter is 1.8mm has no provision for angulation at the tip. However, using the LMA as a guide it was easy to reach the subglottic stenosis even using this smaller bronchoscope.

Anesthesia, General↗

PubMed1995

Control of gallbladder contractions by cholecystokinin through cholecystokinin-A receptors in the vagal pathway and gallbladder in the dog.

The mechanism of CCK action on gallbladder contractions in the physiological condition is unclear. Gallbladder contractions were monitored by means of chronically implanted force transducers in conscious dogs. Postprandial gallbladder contractions were partially inhibited by atropine and hexamethonium, and completely inhibited by devazepide. In vitro contractile response of canine gallbladder muscle strips to CCK-8 was also studied. CCK-8-induced muscle strip contraction was atropine and tetrodotoxin resistant, but was completely eliminated by devazepide. The existence of CCK receptors in the vagal nerve and gallbladder was examined by means of autoradiography. Forty-eight hours after ligation of the abdominal vagus, CCK-8 binding sites were found to accumulate in the subdiaphragmatic vagal nerve immediately proximal to the ligature, and similar binding sites were also found in the gallbladder smooth muscle layer. These binding sites were displaced by the addition of 10(-7) mol/1 unlabeled CCK-8 and devazepide, but L-365,260 had no effect. In conclusion, it is considerable that postprandial CCK-induced gallbladder contractions are controlled through CCK-A receptors both on the vagal nerve in stimulating endogenous release of acetylcholine and on the gallbladder directly to stimulate muscle contraction in the dog.

Animals↗

PubMed1995

Pharmacological study of dihydroetorphine in cloned mu-, delta- and kappa-opioid receptors.

We investigated the binding characteristics of dihydroetorphine, 7,8-dihydro-7 alpha-[1-(R)-hydroxy-1-methylbutyl]-6, 14-endoethanotetrahydro-oripavine, and its effect on the inhibitory system of cyclic AMP production using cloned mu-, delta- and kappa-opioid receptors expressed on Chinese hamster ovary cells. The Ki values of dihydroetorphine for the mu-, delta- and kappa-opioid receptors were 4.5 x 10(-10). 1.8 x 10(-9) and 5.7 x 10(-10) M, respectively. On the other hand, those of morphine were 1.9 x 10(-9), 1.4 x 10(-6) and 1.3 x 10(-7) M, respectively. Through all of these three types of opioid receptors, dihydroetorphine inhibited forskolin (10 microM)-stimulated cyclic AMP production via pertussis toxin-sensitive G protein(s), and the inhibitory effects were antagonized by co-application with opioid receptor antagonists. The IC50 values of dihydroetorphine for the inhibition of cyclic AMP production through the mu-, delta- and kappa-opioid receptors were 4.2 x 10(-11), 8.6 x 10(-10) and 4.3 x 10(-9) M. respectively. On the other hand, those of morphine were 2.6 x 10(-8), 2.6 x 10(-6) and 1.9 x 10(-6) M, respectively. These results indicate that dihydroetorphine, unlike morphine which preferentially binds the mu-opioid receptor, binds not only mu- but also delta- and kappa-opioid receptors with high affinity and acts as a more potent agonist than morphine for all of the three types of receptors.

Animals↗

PubMed1995

Quantitative contribution of the acid production to the intracellular acidification in human neutrophils stimulated by N-formyl-methionyl-leucyl-phenylalanine.

A chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (fMLP), induced an acidification of cytosol by about 0.05 pH units in 30 sec followed by an alkalinization in human neutrophils. The quantitative contribution of acid production to the acidification was studied. The superoxide (O2-) production stimulated by fMLP was not involved in the acidification because the production of acids in neutrophils from patients with chronic granulomatous disease who do not produce O2-, was the same as that in normal neutrophils. The intracellular acidification was completely inhibited by deoxyglucose, suggesting that energy metabolism enhanced upon stimulation by fMLP might be the main source of the acidification. Although enhancement of the lactate formation by fMLP was 0.8 nmol/10(6) cells, which could lower intracellular pH by 0.08 pH units, the lactate production could not explain the initial acidification because the production of lactate started at 1 min after the stimulation while the intracellular acidification began immediately after the stimulation. Mitochondrial respiratory inhibitors such as KCN and rotenone had no effects on the fMLP-induced intracellular acidification. The fMLP-induced production of CO2 in 30 sec through the hexose monophosphate shunt was only 2.6 pmol/10(6) cells, which was calculated to decrease intracellular pH by only 0.0014. Thus, changes of energy metabolism induced by fMLP does not explain the acidification.

Acids↗

PubMed1995

Anti-nuclear antibody production and immune-complex glomerulonephritis in BALB/c mice treated with pristane.

The pathogenesis of systemic lupus erythematosus is thought to be primarily under genetic control, with environmental factors playing a secondary role. However, it has been shown recently that intraperitoneal injection of pristane (2,6,10,14-tetramethylpentadecane) induces autoantibodies typical of lupus in BALB/c mice, a strain not usually considered to be genetically susceptible to the disease. In this study, the induction of autoimmune disease by pristane was investigated. BALB/c mice receiving pristane were tested for autoantibody production and histopathological evidence of glomerulonephritis. Six of 11 mice developed IgM anti-single-stranded DNA antibodies shortly after receiving pristane and 4 developed IgM anti-histone antibodies, but anti-double-stranded DNA antibodies were absent. IgG anti-DNA and anti-histone antibodies were absent. In contrast, the lupus-associated anti-nuclear ribonucleoprotein/Sm and anti-Su autoantibodies produced by these mice were predominantly IgG. In addition to autoantibodies, most of the mice developed significant proteinuria. Light microscopy of the kidney showed segmental or diffuse proliferative glomerulonephritis. Electron microscopy showed subepithelial and mesangial immune-complex deposits and epithelial foot process effacement. Immunofluorescence revealed striking glomerular deposition of IgM, IgG, and C3 with a mesangial or mesangiocapillary distribution. Thus, pristane induces immune-complex glomerulonephritis in association with autoantibodies typical of lupus in BALB/c mice. These data support the idea that lupus is produced by an interplay of genetic and environmental factors and that unlike the MRL or (NZB x W)F1 mouse models, in which genetic susceptibility factors are of primary importance, environmental factors are of considerable importance in the autoimmune disease of pristane-treated BALB/c mice.

Animals↗

PubMed1995

Galactosylgloboside expression in seminoma. Inverse correlation with metastatic potential.

BACKGROUND: Altered glycosylation is a common phenotype expressed in essentially all types of human cancer and has been found to be correlated closely with the invasive and metastatic properties of a given tumor. Because there was no prognostic information concerning aberrant glycosylation of seminoma, the authors studied this topic. METHODS: Glycosphingolipid (GSL) composition of orchiectomy samples of seminoma were analyzed systematically. GSL patterns from seminoma samples of the following three groups were compared after a 44-month postoperative period: Stage I disease with no evidence of metastasis during the 44-month postoperative period, Stage I with metastatic relapse during this period, and Stage II with retroperitoneal lymph node metastasis. Unknown GSLs detected were analyzed chemically by 1H-nuclear magnetic resonance spectroscopy and mass spectrometry. RESULTS: All nonmetastatic seminomas (n = 12) contained a GSL band that was identified as galactosylgloboside (Gb5; Gal beta 1-->3GalNAc beta 1-->3Gal alpha 1-->4 Gal beta 1-->4Glc beta 1-->1Cer). All metastatic seminomas (n = 5) lacked this GSL, although the sample sizes were admittedly small. CONCLUSION: Only the presence or absence of galactosylgloboside (Gb5), but of no other GSL or gangliosides, clearly correlated with metastatic potential in patients with seminoma. This observation is useful in the estimation of prognosis of patients with seminoma, especially those with Stage I disease.

Adult↗

PubMed1995

Expression of type I interleukin-1 receptor mRNA and its regulation in cultured astrocytes.

The expression of type I interleukin-1 receptor (IL-1RI) mRNA enriched astrocytes and microglia was investigated by Northern blot analysis. IL-1RI mRNA was expressed in untreated astrocytes, but not in microglia. This expression was markedly suppressed by a treatment with isoproterenol, a beta-adrenoceptor agonist (1 x 10(-8) to 1 x 10(-6) M). This suppression was clearly reversed by propranolol, a beta-adrenoceptor antagonist. Dibutyryl cAMP (dbcAMP) also suppressed the expression of IL-1RI mRNA. The suppression by isoproterenol or dbcAMP was blocked by H8 or H89, inhibitors of cAMP-dependent protein kinase. The present results suggest that IL-1RI mRNA expression in cultured astrocytes may be regulated by intracellular cAMP, elevated upon the activation of beta-adrenoceptors as an example, and cAMP-dependent protein kinase.

Adrenergic beta-Agonists↗

PubMed1995

Cloning of boar SPMI gene which is expressed specifically in seminal vesicle and codes for a sperm motility inhibitor protein.

Boar semen contains a seminal plasma motility inhibitor (SPMI) that blocks the motility of demembranated-reactivated spermatozoa as well as of intact spermatozoa. In this paper, we describe the primary structure of SPMI, the coding of boar SPMI cDNA gene and its expression in various porcine tissues. Nucleotide sequence analysis of the 645-bp SPMI cDNA predicts a coded polypeptide of 137 amino acid residues which includes a 21-residue signal peptide and a 116-residue secreted protein. The amino acid sequence of SPMI was found to be highly homologous to AQN-3, a member of spermadhesin family proteins of boar that bind to spermatozoa. Expression of the boar SPMI gene detected by Northern blot analysis revealed that its expression is very abundant in seminal vesicles and specific to this tissue.

Amino Acid Sequence↗

PubMed1995

Inhibition of TNF-triggering activity of lipopolysaccharide by a proteinaceous factor from normal mouse liver extract.

Recent studies have revealed that animals have evolved a wide range of protective systems against the deleterious effects of LPS, but the molecular mechanisms in the barrier functions of liver against enterobacterial LPS, particularly in mammals, are poorly understood. In this study, we extracted a soluble fraction from the liver of normal mice (normal liver extract, NLE) and examined its effect on biologic activities of LPS. Preincubation of NLE and LPS suppressed serum-dependent TNF induction (TNF-triggering activity) of LPS; the effect was dose-dependent and overcome by increasing LPS concentration, but treatment of macrophages with NLE showed no effect. Separation by ultrafiltration and protease sensitivity demonstrated that the factor(s) in NLE was a protein(s). We tentatively called this liver LPS-inactivating factor (LLIF). LPS inactivation by LLIF was temperature-dependent and required the coexistence of divalent cations. LLIF also suppressed a synthetic lipid A analogue, ONO-4007. Pretreatment of LPS with serum rendered LPS refractory to the action of LLIF. However, LLIF was unable to inhibit limulus amebocyte lysate activation by LPS. Direct interaction of LLIF and lipid A was evident by the method of [1-14C]ONO-4007 binding to solid-phase LLIF, but treatment of [1-14C]ONO-4007 with LLIF generated no degradative products. These results suggest that LLIF probably interacts with the lipid A portion of LPS and interferes with the association of LPS and LBP (LPS-binding protein) in serum, and that LLIF may be one of the protective molecules in liver against the gastrointestine-derived LPS.

Acute-Phase Proteins↗

PubMed1995

Induction of NCAM expression in mouse olfactory keratin-positive basal cells in vitro.

The expression of neural cell adhesion molecule (NCAM) by olfactory keratin+ basal cells was investigated in vitro. In primary cultures from embryonic day 14.5 or newborn mouse olfactory epithelium (OE), flat keratin+ basal cells were negative for NCAM-immunostaining. Transforming-growth factor-beta 1, beta 2 (TGF-beta 1, beta 2) or a high concentration of Ca2+ induced these cells to express NCAM. We obtained a cell line, designated DBC1.2, from embryonic day 14.5 mouse OE. All DBC1.2 cells were positive for keratin-immunostaining, whereas nearly all cells were negative for NCAM-immunostaining. Therefore, DBC1.2 cells seemed to derive from dark basal cells. DBC1.2 cells were also induced to express NCAM by the treatment with TGF-beta s or a high Ca2+ concentration. Western blotting revealed that the components of the NCAM expressed by DBC1.2 were 120 and 140 kDa, but not 180 kDa, isoforms. Since NCAM is the cell adhesion molecule mainly expressed in nervous tissues, these results suggest a cell lineage relationship or interactions between olfactory keratin+ basal cells and olfactory sensory neurons.

Aging↗

PubMed1995

Effects of leukemia inhibitory factor on the differentiation of astrocyte progenitor cells from embryonic mouse cerebral hemispheres.

The effects of leukemia inhibitory factor (LIF) on the differentiation and proliferation of astrocyte progenitor cells in an enriched culture were studied. The astrocyte progenitor cells obtained from embryonic mouse cerebral hemispheres were enriched by subculturing twice in serum-free medium containing epidermal growth factor (EGF). They exhibited a flat, non-process-bearing morphology and were negative for glial fibrillary acidic protein (GFAP), a specific marker for astrocytes. Culture of the cells with LIF resulted in the expression of GFAP and in the inhibition of growth. These results suggest that LIF promotes the differentiation of astrocyte progenitor cells.

Animals↗

PubMed1995

Involvement of botulinum C3-sensitive GTP-binding proteins in alpha 1-adrenoceptor subtypes mediating Ca(2+)-sensitization.

The mechanisms of alpha 1-adrenoceptor agonist-mediated sensitization of the contractile apparatus of smooth muscle to Ca2+ were studied in beta-escin-permeabilized thoracic arterial smooth muscle of rabbit. Addition of norepinephrine (10 microM) plus guanosine 5'-triphosphate (GTP, 50 microM) significantly enhanced Ca2+ sensitivity as compared with the addition of 0.3 microM Ca2+ alone (pCa6.5). In beta-escin-skinned smooth muscle of chloroethylclonidine-treated tissues, the enhancement of Ca(2+)-contraction produced by norepinephrine or clonidine was completely inhibited by guanosine 5'-O-(beta-thiodiphosphate) (GDP beta-S, 1 mM). In addition, Clostridium botulinum C3, which inactivates low molecular weight GTP-binding protein families, abolished norepinephrine- or clonidine-induced Ca(2+)-sensitization, but did not affect clonidine-induced translocation of protein kinase C to the membrane. The norepinephrine-enhanced Ca2+ sensitivity was partially reversed by a pretreatment with a selective myosin light chain kinase inhibitor (8R*, 9S*, 11S*)-(-)-9-hydroxy-9-methoxycarbonyl-8-methyl-14-n- propoxy-2,3,9,10-tetrahydro-8,11-epoxy,1H,8H,11H-2,7b,11a- triazadibenzo[a,g]cycloocta[cde]trinden-1-one (KT5926, 500 nM), but those of clonidine and in the chloroethylclonidine-treated tissues norepinephrine were not. These results suggest that Ca(2+)-sensitization produced by the activation of the alpha 1-adrenoceptor subtypes is linked via a low molecular weight GTP-binding protein (Rho), and the regulations of phosphorylation in contractile elements.

ADP Ribose Transferases↗

PubMed1995

Absence of autoantigen Ku in mature human neutrophils and human promyelocytic leukemia line (HL-60) cells and lymphocytes undergoing apoptosis.

The Ku autoantigen is a heterodimer of 70- and 80-kD proteins recognized by autoantibodies from patients with systemic lupus erythematosus and related diseases that is the DNA-binding component of a DNA-dependent protein kinase. The catalytic activity of DNA-dependent protein kinase is carried by a 350-kD subunit (p350). In light of the recently described role of Ku in repairing double-strand DNA breaks, we investigated the regulation of Ku and p350 levels in neutrophils, a terminally differentiated cell type destined to undergo apoptosis. Since the appearance of double-strand DNA breaks is characteristic of apoptosis, we were interested in the possibility that Ku might oppose programmed cell death. Analysis of peripheral blood cells by flow cytometry using anti-Ku and anti-p350 monoclonal antibodies revealed that neutrophils were unstained, whereas resting (G0) lymphocytes were positive. The absence of Ku in mature neutrophils was confirmed by Western blotting and enzyme-linked immunosorbent assay for Ku antigen. In contrast, the human promyelocytic leukemia line, HL-60, which undergoes differentiation toward neutrophils after dimethylsulfoxide treatment, was positive for Ku and p350. In view of the short lifespan of neutrophils and the prolonged half-life of Ku and p350 (> 5 d), these data suggested that Ku was actively degraded during myeloid differentiation. Analysis of HL-60 cells by flow cytometry revealed that Ku staining was bimodal. Cells in G1/G0, S, or G2/M were all stained positively, whereas cells with a subdiploid DNA content characteristic of apoptosis were Ku negative. Similar results were obtained with phytohemagglutin-stimulated human lymphocytes. These data suggest that the Ku antigen is actively degraded in both myeloid cells destined to undergo apoptosis and apoptotic lymphocytes, raising the possibility that degradation of Ku may help to prevent the inappropriate repair of fragmented nuclear DNA during apoptosis.

Antibodies, Monoclonal↗

PubMed1995

Intracisternal administration of interleukin-1 beta attenuates naloxone-precipitated withdrawal in morphine-dependent mice.

The effect of central administration of interleukin-1 beta on naloxone-precipitated withdrawal in morphine-dependent mice was studied. The degree of physical dependence on morphine was estimated by counting the number of jumps precipitated by naloxone, one of the typical withdrawal signs. Intracisternal (i.c.) administration of interleukin-1 beta (0.01-1 ng/5 microliters per mouse) to morphine-dependent mice 30 min prior to the injection of naloxone (10 mg/kg i.p.) decreased the number of jumps in a dose-dependent manner. The effect of interleukin-1 beta (1 ng) was significantly antagonized when it was co-administered with interleukin-1 receptor antagonist (1 microgram/mouse). These results suggest that centrally administered interleukin-1 beta could attenuate naloxone-precipitated withdrawal in morphine-dependent mice via interleukin-1 receptors in the brain. Co-administration of alpha-melanocyte-stimulating hormone (300 ng/mouse) or alpha-helical corticotropin-releasing factor (CRF)-(9-41), a CRF receptor antagonist (300 ng/mouse), with interleukin-1 beta also antagonized the inhibitory effect of interleukin-1 beta (1 ng). Moreover, i.c. administration of CRF (200 ng/mouse) significantly decreased the number of jumps.

Animals↗

PubMed1995

Pristane induces high titers of anti-Su and anti-nRNP/Sm autoantibodies in BALB/c mice. Quantitation by antigen capture ELISAs based on monospecific human autoimmune sera.

Autoantibodies to Su and anti-nRNP/Sm are common in human and murine systemic lupus erythematosus (SLE), and are also produced by BALB/c mice with SLE-like autoimmunity induced by pristane. Antigen capture ELISAs employing monospecific human autoimmune IgG were developed to quantitate the production of anti-Su and anti-nRNP/Sm autoantibodies in 77 sera from BALB/c mice with pristane-induced autoimmunity. The sensitivity and specificity of the anti-Su antigen capture ELISA were 100% compared with immunoprecipitation of 35S-labeled cellular proteins. All 16 immunoprecipitation positive sera were positive in the anti-nRNP/Sm antigen capture ELISA (100% sensitivity), whereas 55/61 immunoprecipitation negative sera were negative by ELISA (90% specificity). The 6/61 immunoprecipitation negative sera that were ELISA positive were probably true positives because subsequent sera obtained from the same mice were positive by both techniques. Thus, the antigen capture ELISA may be somewhat more sensitive than immunoprecipitation. The titers of anti-Su and anti-nRNP/Sm positive antibodies in the sera were as high as 1:25,000-1:250,000 by ELISA, suggesting that autoantibodies may be produced in pristane-primed BALB/c mice at levels comparable to those seen in spontaneous autoimmune disease. We conclude that antigen capture ELISAs based on human autoimmune sera were highly sensitive and specific for detecting murine anti-Su and anti-nRNP/Sm antibodies. This technique will be useful for quantitating antibodies in murine autoimmune disease models, since antigen capture ELISA avoids the use of denatured or recombinant antigens, permitting antibodies recognizing tertiary and quaternary structures to be detected.

Animals↗

PubMed1995

DAMGO, a mu-opioid receptor selective ligand, distinguishes between mu-and kappa-opioid receptors at a different region from that for the distinction between mu- and delta-opioid receptors.

The structural basis of opioid receptors (OPRs) for the subtype-selective binding of DAMGO, a mu-opioid receptor selective ligand, was investigated using chimeric mu/kappa-OPRs. Replacement of the region from the middle of the fifth transmembrane domain to the C-terminal of mu-OPR with the corresponding region of mu-OPR remarkably decreased the binding affinity to DAMGO, while the reciprocal chimera revealed the high affinity to DAMGO. These results indicate that DAMGO distinguishes between mu- and mu-OPRs at the region around the third extracellular loop, different from the case of the distinction between mu-and delta-OPRs in which the region around the first extracellular loop is important. Furthermore, displacement studies revealed that the region around the third extracellular loop is involved in the discrimination between mu- and kappa-OPRs not only by peptidic mu- selective ligands but also by non-peptidic ligands, such as morphine and naloxone.

Amino Acid Sequence↗

PubMed1995

Alpha 2-adrenoceptor-mediated inhibition of capsaicin-evoked release of glutamate from rat spinal dorsal horn slices.

It is known that the descending noradrenergic system suppresses nociceptive transmission in the spinal dorsal horn. To determine whether noradrenaline-alpha-adrenoceptor systems exert inhibitory influence on the release of glutamate from the nociceptive primary afferents, the effects of alpha-adrenoceptor agonists on the capsaicin (3 microM)-evoked release of glutamate from rat spinal dorsal horn slices were examined using an on-line continuous monitoring system for glutamate. The application of alpha 2-agonists clonidine (0.1-10 microM) and ST-91 (1 and 10 microM), respectively, decreased the capsaicin-evoked release of glutamate in a concentration-dependent manner. The partial alpha 2-agonist oxymetazoline (1 and 10 microM) produced a slight inhibition in the evoked release of glutamate. In contrast, the alpha 1-agonist phenylephrine (1 and 10 microM) did not show any significant effects on the evoked release of glutamate. The inhibitory action of 10 microM clonidine on the evoked glutamate release was antagonized by the alpha 2-antagonist yohimbine (1 microM) but not by the opioid antagonist naloxone (10 microM). These findings suggest that noradrenaline, probably released from the descending inhibitory system, reduces the release of glutamate from the capsaicin-sensitive primary afferent terminals through alpha 2-adrenoceptors.

Adrenergic alpha-Agonists↗

PubMed1995

Expression of insulin receptor-related receptor mRNA in the rat brain is highly restricted to forebrain cholinergic neurons.

Insulin receptor-related receptor (IRR) is a member of the insulin receptor family. However, its endogenous ligand and the physiological roles of IRR are unknown. To elucidate the physiological roles of IRR in the brain, we examined the expression of its mRNA in the rat brain by in situ hybridization. In contrast to the widespread expression of insulin receptor and insulin-like growth factor-1 receptor mRNAs in the brain, the expression of IRR mRNA was highly restricted to the forebrain cholinergic neurons. All the forebrain cholinergic neurons expressed IRR mRNA. The present findings indicate that IRR has a selective role in the brain for forebrain cholinergic function.

Animals↗