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  • 1
    Electronic Resource
    Electronic Resource
    Corticosteroid effect on early beta-adrenergic down-regulation durign circulatory shock: Hemodynamic study and beta-adrenergic receptor assay (1995)
    Springer
    Intensive care medicine 21 (1995), S. 204-210 
    Details
    ISSN: 1432-1238
    Keywords: Steroids ; Methylprednisolone ; Down-regulation ; Up-regulation ; Catecholamines ; Hemodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objectives The steroid effect on critically ill patients remains controversial. The aim of this study is to characterize the effect of methylprednisolone on the heart in a beta-adrenergically downregulated condition. Design A prospective hemodynamic study and retrospective receptor assay. Setting Multidisciplinary ICU in a university hospital. Subjects 42 patients who required pulmonary arterial catheters and an additional 4 corpses who were available for study within 3 h of their deaths. Intervention Intravenous methylprednisolone (10 mg/kg). Measurements and results We pursued a hemodynamic study following a glucocorticoid administration. In patients who had undergone a long term (〉72 h) catecholamine treatment, the cardiac index increased. In patients who had undergone a short term (1–72 h) catecholamine treatment and in patients with no record of catecholamine administration, the cardiac index showed no remarkable change. Among the corpuses, who died soon after their arrival, and the patients, who later died in the ward and were available for further study, we measured beta-adrenergic receptor density in the left ventricular myocardium. It was found that receptor density was decreased after long term catecholamine treatment. Methylprednisolone, on the other hand increased the receptor density. Conclusion Methylprednisolone improved the cardiac index, intriguingly, in patients with long term catecholamine treatment in circulatory shock. Myocardial beta-adrenergic receptor also increased in number after the administration of methylprednisolone. However, the hemodynamic improvement caused by methylprednisolone was not observed in patients without beta-adrenergic down-regulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01701473
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  • 2
    Electronic Resource
    Electronic Resource
    Modification of glycophorin A during oxidation of erythrocyte membrane
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 1023 (1990), S. 413-420 
    Details
    ISSN: 0005-2736
    Keywords: (Human erythrocyte membrane) ; Glycophorin A ; Lipid oxidation ; Oxidative damage ; Proteolysis ; Tritium labeling
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0005-2736(90)90134-A
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  • 3
    Electronic Resource
    Electronic Resource
    New benzofurans related to egonol from immature seeds of Styrax obassia
    Amsterdam : Elsevier
    Phytochemistry 27 (1988), S. 1224-1226 
    Details
    ISSN: 0031-9422
    Keywords: 2-methylbutanoate. ; Styrax obassia ; egonol: benzofuran ; glucoside ; styrocaceae
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0031-9422(88)80314-5
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  • 4
    Electronic Resource
    Electronic Resource
    Down-regulation of membrane immunoglobulin-associated proteins, MB-1, B29 and Lyn, in AIDS-lymphomas and related conditions (1994)
    Springer
    Virchows Archiv 424 (1994), S. 553-561 
    Details
    ISSN: 1432-2307
    Keywords: AIDS ; Lymphoma ; Epstein-Barr virus Tyrosine kinase ; Immunoglobulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract B-lymphocytes infected with Epstein-Barr virus (EBV) can proliferate in immunocompromized hosts to form lymphomas (MLs). Similar MLs are produced in mice with severe combined immune deficiency (SCID) by transfusion of human lymphocytes infected with EBV (SCID-EBV-positive BML). Mb-1 and B29 are recently found transmembrane proteins associated with membrane immunoglobulins (mIg) on the surface of B cells. Lyn is a src family gene product expressed in B cells submembranously, in association with mIg, possibly through Mb-1/B29 heterodimer. These mIg-associated proteins (Mb-1, B29 and Lyn) are known to mediate antigenic stimulation through mIgs. We noted recently that Lyn is decreased selectively in around a half of SCID-EBV-positive BMLs. We extended this line of investigation to other mIg-associated proteins. Five acquired immunodeficiency syndrome (AIDS)-MLs and ten SCID-EBV-positive BMLs were first analysed by immunohistochemistry for the expression of Mb-1, B29 and Lyn. It was found that in AIDS-MLs, all the mIg-associated proteins were heavily down-regulated. In SCID-EBV-positive BMLs, Mb-1 was down regulated in six of ten, B29 in nine of ten and Lyn in six of ten, whereas no down-regulation was noted in eight EBV-free B MLs that were also maintained in SCID mice. An additional flow-cytometric study of two SCID-EBV-positive and two EBV-negative BMLs showed similar down-regulation in the former cases exclusively. Whereas mIg was also decreased in three of five SCID-EBV positive BMLs, it did not necessarily match the decrease of mIg-associated proteins, which contrasts with the recent finding that mIgs coexist with Mb-1 or B29. Some EBV-encoded proteins may activate host molecules located downwardly; this, in turn, may lead to the suppression of these upwardly-located mIg-associated proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00191443
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  • 5
    Electronic Resource
    Electronic Resource
    Role of alpha1A adrenoceptor subtype in production of the positive inotropic effect mediated via myocardial alpha, adrenoceptors in the rabbit papillary muscle: influence of selective alpha1A subtype antagonists WB 4101 and 5-methylurapidil (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 345 (1992), S. 578-585 
    Details
    ISSN: 1432-1912
    Keywords: WB 4101 ; 5-Methylurapidil ; Alpha1 adrenoceptors ; Positive inotropic effect ; [3H]CGP-12177 ; Rabbit papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to elucidate the contribution of alpha1A subtype to the positive inotropic effect mediated by myocardial alpha, adrenoceptors, the influence of the alpha1A selective antagonists WB 4101 and 5-methylurapidil on the alpha,-mediated positive inotropic effect (induced by phenylephrine in the presence of a beta adrenoceptor blocking agent bupranolol) was assessed in the isolated rabbit papillary muscle. WB 4101 (10−9-10−7mol/l) shifted the concentration-response curve of the alpha,-mediated positive inotropic effect to the right in parallel, but the slope of Schild plot did not meet the competitive antagonism: WB 4101 shifted the curve by log one unit at 10−9 mol/1, whereas it did not cause further shift at higher concentrations of 10−8 and 10−7 mol/l. WB 4101 did not affect the beta adrenoceptor-mediated positive inotropic effect. 5-Methylurapidil (10−9 to 10−7 mol/l) shifted the curve of alpha1-mediated positive inotropic effect to the right and downwards in a concentration-dependent manner; the slope of Schild plot calculated at the level of 20% of the maximum response to phenylephrine was close to unity. 5-Methylurapidil at 3 × 10−7 mol/1 abolished the alpha1-mediated positive inotropic effect. In addition, 5-methylurapidil inhibited the beta adrenoceptor-mediated positive inotropic effect in the same concentration range as it antagonized the alpha1-mediated positive inotropic effect, indicating that 5-methylurapidil is not selective for myocardial alpha, adrenoceptors. In the membrane fraction derived from the rabbit ventricular muscle, 5-methylurapidil displaced the specific binding of [3H]CGP-12177 with high affinity, whereas WB 4101 did not affect the [3H]CGP-12177 binding in the concentration range that it antagonized the alpha,-mediated positive inotropic effect. The present results indicate that alpha1A adrenoceptor subtype plays a role in production of the positive inotropic effect mediated by myocardial alpha, adrenoceptors, but the extent is less than that mediated by alpha1B subtype in the rabbit ventricular myocardium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168952
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  • 6
    Electronic Resource
    Electronic Resource
    Pronounced direct inhibitory action mediated by adenosine A1 receptor and pertussis toxin-sensitive G protein on the ferret ventricular contraction (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 282-289 
    Details
    ISSN: 1432-1912
    Keywords: Adenosine ; Phenylisopropyladenosine ; Adenosine receptors ; Negative inotropic effect ; G proteins ; Ferret ventricular myocardium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An adenosine A1 receptor agonist R-N6-phenylisopropyladenosine (R-PIA) elicited a pronounced negative inotropic effect with the EC50 value of 0.69 μmol/1 in the presence of a β-adrenoceptor blocking agent bupranolol (0.3 μmol/1) in the isolated ferret papillary muscle. The negative inotropic effect of R-PIA was not associated with changes in cyclic AMP level. Adenosine and other A1 receptor agonists also elicited a negative inotropic effect. DPCPX (1,3-dipropyl-8-cyclopentyl xanthine) antagonized the negative inotropic effect of R-PIA in a competitive manner (pA2 value = 8.4). The inhibitory action of R-PIA was markedly attenuated in the ventricular muscle preparation isolated from ferrets pretreated with pertussis toxin that caused ADP-ribosylation of 39 kDa proteins in the membrane fraction. In the membrane fraction derived from the ferret ventricle, [3H]-DPCPX bound to a single binding site in a saturable and reversible manner with high affinity (Kd value = 1.21±0.41 nmol/l; B max = 12.8±3.02 fmol/mg protein; n = 7). The binding characteristics of [3H]-DPCPX in the rat ventricle (Kd value = 1.51 ±0.09 nmol/l; B max = 12.7±1.47 fmol/mg protein; n = 5) were similar to those in the ferret. On the other hand, the content of Go, a major pertussis toxin-sensitive G protein in the ferret heart, was much higher in the ferret than in the rat ventricle. The present results indicate that adenosine receptors may play an important role in the inhibitory regulation of ventricular contractility in the ferret in contrast to other mammalian species. The signal transduction process subsequent to agonist binding to A1 receptors including the pertussis toxin-sensitive G protein and ion channels may be responsible for the unique inhibitory action of adenosine in this species.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169157
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  • 7
    Electronic Resource
    Electronic Resource
    Potent inhibitory action of chlorethylclonidine on the positive inotropic effect and phosphoinositide hydrolysis mediated via myocardial alpha1-adrenoceptors in the rabbit ventricular myocardium (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 343 (1991), S. 669-673 
    Details
    ISSN: 1432-1912
    Keywords: Chlorethylclonidine ; Alpha1-adrenoceptors ; Positive inotropic effect ; [3H]prazosin binding ; Phosphoinositide hydrolysis ; Rabbit papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of the alphalb-adrenoceptor-selective antagonist chlorethylclonidine on the alpha1-adrenergic positive inotropic effect and the phosphoinositide hydrolysis induced by phenylephrine was investigated in the rabbit ventricular myocardium. Pretreatment of membrane fractions derived from the rabbit ventricular muscle with 10−5 mol/l chlorethylclonidine decreased the specific binding of [3H]prazosin (at a saturating concentration of 10−9 mol/l) from the control value of 11.27±0.48 to 4.18±1.87 fmol/mg protein. The inhibition by adrenaline of the binding of [3H]prazosin (slope factor and affinity) was not affected by chlorethylclonidine. The positive inotropic effect of phenylephrine (in the presence of 3 × 10−7 mol/l bupranolol) was inhibited by chlorethylclonidine in a concentration-dependent manner (10−7−10−5 mol/l) and abolished by 10−5 mol/l chlorethylclonidine. The concentration of chlorethylclonidine to inhibit the phenylephrine-induced maximum response to 50% was 2.4 × 10−6 mol/l. The accumulation of [3H]inositol monophosphate and [3H]inositol trisphosphate induced by 10−5 mol/l phenylephrine was inhibited by chlorethylclonidine in the same concentration range. These findings indicate that the myocardial alpha1-adrenoceptors mediating a positive inotropic effect in the rabbit ventricular myocardium may belong to the chlorethylclonidine-sensitive alpha1b-subtype, and that the subcellular mechanism of action involve phosphoinositide hydrolysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00184301
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  • 8
    Electronic Resource
    Electronic Resource
    Pharmacological characteristics of adenosine-induced inhibition of dog ventricular contractility: dependence on the pre-existing level of β-adrenoceptor activation (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 344 (1991), S. 70-78 
    Details
    ISSN: 1432-1912
    Keywords: Adenosine ; Phenylisopropyladenosine ; Negative inotropic effect ; Cyclic AMP ; Ventricular myocardium of the dog
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experiments were carried out to characterize the adenosine-induced negative inotropic effect in relation to the extent of β-adrenoceptor activation in the isolated dog left ventricular myocardium. Adenosine and R-N6-phenylisopropyladenosine inhibited the positive inotropic effect of isoprenaline (10−7 mol/1 and lower) about 20% of its maximal response, which was antagonized by an A1 adenosine receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine in a concentration-dependent manner. The negative inotropic effect of adenosine disappeared and that of R-N6-phenylisopro-pyl-adenosine decreased when the isoprenaline concentration was elevated to the level higher than 10−7 mol/1. Adenosine deaminase (1.5 U/ml) that abolished the negative inotropic effect of adenosine enhanced the effect of R-N6-phenylisopropyladenosine, indicating that endogenous adenosine released by high isoprenaline concentration (10−6 mol/1) modulates the interaction. The maximal response to adenosine and R-N6-phenylisopro-pyladenosine determined in the presence of 10−7 mol/1 isoprenaline was 50% of that of carbachol which elicited the maximal inhibition even in the presence of 10−6 mol/1 isoprenaline. The negative inotropic effects of R-N6-phenylisopropyladenosine and carbachol were additive to the maximal response equivalent to that of carbachol. The difference in the efficiency between the adenosine and muscarinic receptor agonists may be partly ascribed to the difference in densities of the respective receptors in the dog ventricular myocardium. The negative inotropic effect of R-N6-phenylisopropyladenosine in the presence of isoprenaline was associated with decrease in cyclic AMP levels elevated previously by isoprenaline. The elevation of cyclic AMP levels caused by isoprenaline (3 × 10−7 mol/1) was abolished by R-N6-phenylisopro-pyladenosine (10−4 mol/1), while the contractile response was reduced only by 30% with R-N6-phenylisopro-pyladenosine. In the absence of β-adrenoceptor stimulation R-N6-phenylisopropyladenosine elicited a negative inotropic effect without changes in cyclic AMP levels, but this effect was less than 10% of the basal force of contraction. It is concluded that in the dog ventricular myocardium adenosine receptors play a role for the inhibitory regulation of contractility, which is influenced markedly by the pre-existing level of β-adrenoceptor activation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00167384
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  • 9
    Electronic Resource
    Electronic Resource
    Age-related changes in alpha1-adrenoceptors in rat prostate (1995)
    Springer
    Urological research 22 (1995), S. 389-392 
    Details
    ISSN: 1434-0879
    Keywords: Alpha1-adrenoceptor ; Age-related change ; Rat prostate ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The age-related changes in the density of alpha1-adrenoceptors in the dorsolateral lobe of the rat prostate were evaluated in Wistar rats at 8, 52, and 104 weeks of age. [3H]YM617, a newly senthesized alpha1-adrenergic blocker, was used as the ligand. The mean maximum number of binding sites, or alpha1-adrenoceptor density (Bmax)±SE of 104-week-old rats (11.0±1.2 fmol/mg protein) was significantly lower than that in the 8-week-old rats (37.0±4.3 fmol/mg protein) and 52-week-old rats (37.2±3.4 fmol/mg protein) respectively, P〈0.01. In contrast, mean affinity (Kd) values±SE of these groups showed no significant differences (8-week-old rats, 115.8±9.1; 52-week-old rats, 100.5±5.8; and 104-week-old rats, 116.4±9.8 pM). Mean volumes±SE of muscle cells of the prostate were 3.7±1.1x103 μm3 at 8 weeks, 30.0±6.2x103 μm3 at 52 weeks, and 18.6±8.2x103 μm3 at 104 weeks. Volumes for 8-week-old rats were significantly smaller than those for 52-week-old (P〈0.01) and 104-week-old rats (P〈0.05). However, the mean area density of the muscle cells showed no difference among the three groups: 20.1±2.2% at 8 weeks, 27.3±2.9% at 52 weeks and 20.3±3.4% at 104 weeks. In conclusion, the density of YM617-binding sites (alpha1-adrenoceptors) in 104-week-old rats was lower than in 8- and 52-week-old rats. Muscle volume in the rat prostate was larger in rats aged 52 and 104 weeks than in 8-week-old rats, but no correlation was found between alpha1-adrenoceptor density and the muscle volume or muscle density in aging.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296882
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  • 10
    Electronic Resource
    Electronic Resource
    Tumorigenicity of mouse BALB/c 3T3 fibroblast cells which express Epstein-Barr virus-encoded LMP1 and show normal growth phenotypes in vitro is correlated with loss of transforming growth factor-β1-mediated growth inhibition (1999)
    Springer
    Archives of virology 144 (1999), S. 241-257 
    Details
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary.  Latent membrane protein 1 (LMP1) encoded by the Epstein-Barr virus (EBV) genome is known to induce loss of contact inhibition and the anchorage-independent growth in rodent fibroblasts and increased expression of cell-surface activation markers and cell adhesion molecules in human B lymphocytes. To analyze the role of LMP1 in tumorigenicity, we prepared BALB/c 3T3 clones (B3LP) expressing LMP1. These B3LP cells showed non-transformed phenotypes in vitro which were characterized by normal cell morphology, contact inhibition in growth and anchorage-dependent growth. The activity of NF-κB induced generally in several cell lines after transfer of the LMP1 gene was not detected in B3LP cells. However, B3LP expressing LMP1 at moderate levels lost sensitivity to growth arrest by transforming growth factor-β1(TGF-β1) and formed tumors in severe combined immune deficiency mice. Cells expressing the truncated form of LMP1 and expressing LMP1 at low level were sensitive to TGF-β1-mediated growth arrest and did not form tumors in mice. Therefore, cells expressing LMP1 at moderate but not at low levels formed tumors in mice and lost sensitivity to TGF-β1. Our results suggest that loss of TGF-β1-mediated growth inhibition is an important event for the tumorigenicity of LMP1-expressing cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007050050501
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