European Journal of Pharmacology: Molecular Pharmacology最新文献

{"title":"Expression of endogenous muscarinic acetylcholine receptors in Chinese hamster ovary cells","authors":"Shou Zhen Wang,&nbsp;Sheng Zu Zhu,&nbsp;Esam E El-Fakahany","doi":"10.1016/0922-4106(95)90148-5","DOIUrl":"10.1016/0922-4106(95)90148-5","url":null,"abstract":"<div><p>Chinese hamster ovary (CHO) cells are commonly used for expression of the genes of cloned neurotransmitter receptors to study their pharmacology and coupling to signal transduction pathways. It is usually assumed that host cells do not endogenously express the specific receptor under consideration. We demonstrate in this report that CHO cells contain endogenous functional muscarinic acetylcholine receptors which, in some circumstances, might complicate interpretation of data related to the properties of exogenously expressed receptors.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"291 2","pages":"Pages R1-R2"},"PeriodicalIF":0.0,"publicationDate":"1995-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90148-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"53949184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Properties of TAN-67, a nonpeptide δ-opioid receptor agonist, at cloned human δ-and μ-opioid receptors","authors":"Richard J. Knapp ,&nbsp;Robert Landsman ,&nbsp;Sue Waite ,&nbsp;Ewa Malatynska ,&nbsp;Eva Varga ,&nbsp;Wajujahal Haq ,&nbsp;Victor J. Hruby ,&nbsp;William R. Roeske ,&nbsp;Hiroshi Nagase ,&nbsp;Henry I. Yamamura","doi":"10.1016/0922-4106(95)90134-5","DOIUrl":"https://doi.org/10.1016/0922-4106(95)90134-5","url":null,"abstract":"<div><p>2-methyl-4a α(3-hydroxyphenyl)-1,2,3,4,4a,5,12,12a α-octahydro-quinolino[2,3,3-<em>g</em>]isoquinoline (TAN-67) is a nonpeptidic δ-opioid receptor agonist. This report describes its receptor binding affinity and agonist potency at human and mouse δ and μ-opioid receptors. The binding affinities of TAN-67 and the cyclic enkephalin analog, [D-Pen², 4′-Cl-Phe⁴, <span>D</span>-Pen⁵]enkephalin (pCl-DPDPE) were measured by the radioligand binding inhibition studies at mouse and human variants of the δ and μ-opioid receptor using [³H]Naltrindole and [³H]<span>D</span>-Phe-<span><math><mtext>Cys  Tyr  D  Trp  Orn  Thr  Pen</mtext></math></span>-Thr-NH₂, respectively. TAN-67 showed high binding affinity (<em>K</em>_i = 0.647 nM) at the human δ-opioid receptor and high δ-opioid receptor binding selectivity (&gt; 1000-fold) relative to the human μ-opioid receptor. TAN-67 also showed high potency (EC₅₀ = 1.72 nM) for the inhibition of forskolin-stimulated cAMP accumulation at human δ-opioid receptors expressed by intact Chinese hamster ovary cells but low potency (EC₅₀ = 1520 nM) at human μ-opioid receptors expressed by intact B82 mouse fibroblast cells. The results show that TAN-67 has similar binding affinities, selectivity and potencies as pCl-DPDPE at human δ and μ-opioid receptors. These results combined with the nonpeptidic structure of TAN-67 suggest that this compound has therapeutic potential as a δ-opioid receptor agonist.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"291 2","pages":"Pages 129-134"},"PeriodicalIF":0.0,"publicationDate":"1995-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90134-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71780037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of hydrogen peroxide / L-histidine-induced DNA single- vs. double-strand breaks on poly(ADP-ribose)polymerase","authors":"Letizia Palomba,&nbsp;Andrea Guidarelli,&nbsp;Flaminio Cattabeni,&nbsp;Orazio Cantoni","doi":"10.1016/0922-4106(95)90139-6","DOIUrl":"10.1016/0922-4106(95)90139-6","url":null,"abstract":"<div><p><span>L</span>-Histidine markedly increases the ability of hydrogen peroxide to induce DNA cleavage and this effect is associated with a 3-aminobenzamide-inhibitable decline in NAD⁺ levels, an event which very likely reflects an enhanced stimulation of the enzyme poly(ADP-ribose)polymerase. 3-Aminobenzamide slowed down the removal of alkaline elution-detected strand breaks induced by either H₂O₂ alone (producing only DNA single-strand breaks) or associated with <span>L</span>-histidine (resulting in the formation of both single-strand breaks and DNA double-strand breaks), and the extent of inhibition was similar under the two experimental conditions. 3-Aminobenzamide did not affect the rate of rejoining of DNA double-strand breaks generated by the cocktail H₂O₂/<span>L</span>-histidine. The above results suggest that these double-strand breaks have hardly any effect on the induction of poly(ADP-ribose)polymerase activity, a conclusion that is consistent with the observation that the activity of this enzyme appears to be basically identical under conditions that abolish the formation of DNA double-strand breaks, in the absence of measurable variations in the level of induction of DNA single-strand breaks (e.g. in the presence of an excess of <span>L</span>-glutamine, a competitive inhibitor of <span>L</span>-histidine uptake). Finally, 3-aminobenzamide did not affect the toxicity of the oxidant, both in the absence and presence of <span>L</span>-histidine.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"291 2","pages":"Pages 167-173"},"PeriodicalIF":0.0,"publicationDate":"1995-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90139-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19545917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of a binding site for angiotensin IV on bovine aortic endothelial cells","authors":"Sylvie G. Bernier ,&nbsp;Guy Servant ,&nbsp;Manon Boudreau ,&nbsp;Alain Fournier ,&nbsp;Gaétan Guillemette","doi":"10.1016/0922-4106(95)90142-6","DOIUrl":"10.1016/0922-4106(95)90142-6","url":null,"abstract":"<div><p>We have characterized a specific binding site for angiotensin IV on bovine aortic endothelial cell membranes. Pseudo-equilibrium studies at 37°C for 2 h have shown that this binding site recognizes angiotensin IV with a high affinity (<em>K</em>_d=0.71; average of two experiments that yielded values of 0.71 and 0.72 nM). The binding site is saturable and relatively abundant with a maximal binding capacity of 0.59 pmol/mg protein (average of two experiments that yielded values of 0.39 and 0.78 pmol/mg of protein). Non-equilibrium kinetic analyses at 37°C revealed a calculated <em>K</em>_d of 59 pM (average of two experiments that yielded values of 67 and 50 pM). The binding site is pharmacologically distinct from the classic angiontensin receptors AT₁ or AT₂. An analysis of specificity showed that the binding site displays a high affinity for angiotensin IV, low affinities for angiotensin II, [Sar¹, Val⁵, Ala⁸]angiotensin II and does not recognize L-158,809 (5,7-dimethyl-2-ethyl-3-[(2′-(<em>H</em>-tetrazol-5-yl)[1,1′-biphenyl]-4-yl)methyl]-3<em>H</em>-imidazo [4,5-β]pyridine H₂O) and PD 123319 (1-[4-(dimethylamino)3-methylphenyl]methyl-5-(diphenylacety)4,5,6,7-tetrahydro-1<em>H</em>-imidazo[4,5-<em>c</em>]pyridine-6-carboxylic acid). A few unrelated hormones (bradykinin, [Arg⁸]vasopressin, endothelin-1, atrial natriuretic factor, isoproterenol and adrenocorticotropic hormone) were unable to inhibit any ¹²⁵I-angiotensin IV binding. The affinities of different structural analogues of angiotensin IV revealed that the N-terminal position is critical for receptor recognition and the C-terminal proline is also important. GTPγS and polyvinyl sulfate did not affect the binding, suggesting that the receptor is not coupled to a G-protein. The divalent cations Mg²⁺ and Ca²⁺ were shown to diminish the binding of ¹²⁵I-angiotensin IV. Cross-linking of ¹²⁵I-angiotensin IV to bovine aortic endothelial cell membranes in the presence of disuccinimidyl suberate, followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) revealed a major band of 186±12 kDa. The presence in high concentration of this angiotensin binding site an aortic endothelial cells suggests the existence of a novel mechanism involved in the control of vascular tone or vascular permeability.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"291 2","pages":"Pages 191-200"},"PeriodicalIF":0.0,"publicationDate":"1995-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90142-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19547033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional domains of the C-terminus of the rat angiotensin AT1A receptor","authors":"Anthony J. Balmforth,&nbsp;Alison J. Lee,&nbsp;Balwinder P.S. Bajaj,&nbsp;Catherine J. Dickinson,&nbsp;Philip Warburton,&nbsp;Stephen G. Ball","doi":"10.1016/0922-4106(95)90135-3","DOIUrl":"10.1016/0922-4106(95)90135-3","url":null,"abstract":"<div><p>Previous work has shown that truncating the carboxyl terminus (C-terminus) of the rat angiotensin AT_1A receptor to 309 amino acids abolishes G-protein coupling and receptor internalization. This suggests that domains responsible for these functions lie beyond amino acid 309 of the C-terminus. The objective of this study was to determine the effect on angiotensin AT_1A receptor function and regulation of deleting 41 amino acids from the C-terminus, which include the putative protein kinase C phosphorylation sites. Using site directed mutagenesis, the codon for Tyr³¹⁹ was converted to a stop codon and the resulting truncated receptor permanently expressed in cultured human kidney cells. The properties of the truncated receptor were compared to those of the full length receptor. Expression of the truncated receptor was confirmed by sodium dodecyl sulphate polyacrylamide gel electrophoresis analysis of photolabelled membrane preparations. Angiotensin II activation of both full length and truncated receptors resulted in mobilization of inositol phosphates. However, whereas this was associated with rapid internalization of the full length receptor, the truncated receptor failed to internalize. Furthermore, pretreatment of cells with phorbol 12-myristate 13-acetate, a direct activator of protein kinase C, markedly attenuated the full length, but not the truncated receptor's ability to mobilise inositol phosphates. Thus, we conclude that the domain between amino acids 309 &amp; 318 is important for G-protein coupling; that amino acids beyond 318 regulate internalization and one or more of the putative protein kinase C phosphorylation sites, present in the C-terminus of the angiotensin AT_1A receptor, actively regulate the receptor.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"291 2","pages":"Pages 135-141"},"PeriodicalIF":0.0,"publicationDate":"1995-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90135-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19545913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of AMPA receptor modulators on the production of arachidonic acid from striatal neurons","authors":"François Petitet,&nbsp;Jean-Charles Blanchard,&nbsp;Adam Doble","doi":"10.1016/0922-4106(95)90136-1","DOIUrl":"10.1016/0922-4106(95)90136-1","url":null,"abstract":"<div><p>The abilities of different compounds acting at α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors to modulate the overflow of [³H]arachidonic acid from rat striatal neurons were examined. The combination of AMPA (0.1 mM) and carbachol (1 mM) stimulated [³H]arachidonic acid production, this effect could be dose-dependently enhanced by the newly discovered allosteric modulator of AMPA receptors: cyclothiazide. Competitive (6-cyano-7-nitroquinoxaline-2,3-dione [CNQX] and 6-(1-imidazolyl)-7-nitroquinazoline-2,3-dione [YM 900]) and non-competitive antagonists, like 1-(amino-phenyl)-4-methyl-7,8-methylenedioxy-5<em>H</em>-2,3-benzodiazepine (GYKI 52466), antagonized the responses induced by either AMPA + carbachol or AMPA + carbachol + cyclothiazide. In order to appreciate the respective part of AMPA-versus kainate-preferring receptors experiments were performed with kainic acid (0.1 mM) and the more specific kainate agonist domoic acid (0.1 mM). Kainic acid behaves like AMPA, but the response induced by the combination domoic acid + carbachol could not be potentiated by cyclothiazide. On the contrary, concanavalin A potentiated the responses evoked by kainic acid or domoic acid (in combination with carbachol) but did not enhance the AMPA-evoked response. It could be concluded that both AMPA-and kainate-preferring receptors are present in cultured rat striatal neurons and that these two types of receptors were involved together with muscarinic receptors in the overflow of [³H]arachidonic acid.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"291 2","pages":"Pages 143-151"},"PeriodicalIF":0.0,"publicationDate":"1995-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90136-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19545914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Opiates inhibit ion conductances elicited by cell swelling and cAMP in cultured cells","authors":"Richard Callaghan,&nbsp;John R. Riordan","doi":"10.1016/0922-4106(95)90141-8","DOIUrl":"10.1016/0922-4106(95)90141-8","url":null,"abstract":"<div><p>The effect of several opiate compounds on I⁻ efflux was investigated in cultured cell lines. I⁻ efflux was evoked by two distinct stimuli, namely cell swelling and elevation of cellular cAMP levels by prostaglandin E₂. Cells expressing the multidrug resistance P-glycoprotein were found to have increased I⁻ efflux in response to hypo-osmotic challenge. This increased I⁻ efflux in P-glycoprotein containing cells was reduced to levels found in parental cells by the opiates morphine, pentazocine and naloxone. Addition of prostaglandin E₂ to T84 cells resulted in elevated cellular cAMP levels and a significant I⁻ efflux. This cAMP stimulated efflux was also inhibited by several opiates. None of the opiates was able to alter cAMP levels or protein kinase A mediated phosphorylation of immunoprecipitated cystic fibrosis transmembrane conductance regulator (CFTR) Cl⁻ channel in T84 cells. The ability of opiates to alter ion conductances is discussed in relation to the anti-diarrheal effects of these compounds.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"291 2","pages":"Pages 183-189"},"PeriodicalIF":0.0,"publicationDate":"1995-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90141-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19547032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thrombin triggers the de novo expression of an inducible NO synthase in porcine aortic valve endothelial cells","authors":"Erwin De Meyer ,&nbsp;Cor E. Van Hove ,&nbsp;Xiao Jie Feng ,&nbsp;Marc Rampart ,&nbsp;Arnold G. Herman","doi":"10.1016/0922-4106(95)90126-4","DOIUrl":"10.1016/0922-4106(95)90126-4","url":null,"abstract":"<div><p>The nitric oxide (NO) production by porcine aortic valve endothelial cells was estimated in cusps incubated at 37°C by measuring their cyclic GMP content and the nitrite levels of the incubation medium. After a stabilization period, incubations for 5 min with acetylcholine, bradykinin, ADP and bovine thrombin resulted in a receptor-mediated increase in cyclic GMP which could be blocked by EGTA, <span><math><mtext>N-ω-</mtext><mtext>nitro</mtext><mtext>-</mtext><mtext>L</mtext><mtext>-</mtext><mtext>arginine</mtext></math></span> methyl ester (L-NAME) and N^G-monomethyl-<span>L</span>-arginine (L-NMMA). Incubation with lipopolysaccharide (endotoxin) from <em>E. coli</em> O111:B4 or bovine thrombin for 5 h, dose-dependently increased nitrite production as well as cyclic GMP content. The elevated nitrite production was completely abolished in the presence of the protein synthesis inhibitor cycloheximide, was reduced by more than 50% by dexamethasone but was not affected by EGTA. L-NMMA dose-dependently reduced the increased nitrite production and cyclic GMP content. These results suggest that besides the presence of a constitutive NO synthase in porcine aortic valve endothelial cells thrombin, like lipopolysaccharide, triggers the de novo expression of an inducible Ca²⁺-independent NO synthase.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"291 2","pages":"Pages 67-72"},"PeriodicalIF":0.0,"publicationDate":"1995-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90126-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19546936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitogenic effect of serotonin in human small cell lung carcinoma cells via both 5-HT1A and 5-HT1D receptors","authors":"Maria G. Cattaneo ,&nbsp;Riccardo Fesce ,&nbsp;Lucia M. Vicentini","doi":"10.1016/0922-4106(95)90145-0","DOIUrl":"10.1016/0922-4106(95)90145-0","url":null,"abstract":"<div><p>We have recently shown that the mitogenic effect of serotonin (5-hydroxytryptamine, 5-HT) on human small cell lung carcinoma (SCLC) cells is at least partly due to stimulation of a 5-HT_1D receptor type. We now report that the 5-HT_1A receptor agonist R(+)-8-hydroxy-2-(di-<em>n</em>-propylamino)tetralin (8-OH-DPAT) is also capable of stimulating [³H]thymidine incorporation into SCLC GLC-8 cells, although with lower efficacy than 5-HT. The simultaneous administration of maximal doses of 8-OH-DPAT and the 5-HT_1D receptor agonist sumatriptan reproduced the maximal [³H]thymidine incorporation observed with 5-HT alone. The 5-HT_1A receptor antagonists spiperone and SDZ 216–525 completely abolished the effect of 8-OH-DPAT (IC₅₀ 30 nM for both drugs) behaving as pure antagonists. Accordingly, the two drugs partially inhibited the mitogenic effect of 5-HT. These data indicate that the mitogenic effect of 5-HT in SCLC cells involves both 5-HT_1A and 5-HT_1D receptor types.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"291 2","pages":"Pages 209-211"},"PeriodicalIF":0.0,"publicationDate":"1995-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90145-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19547036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Possible mechanism of oxygen radical production by human eosinophils mediated by K+ channel activation","authors":"Mitsuyo Saito ,&nbsp;Ichiro Hisatome ,&nbsp;Shigenori Nakajima ,&nbsp;Ryoichi Sato","doi":"10.1016/0922-4106(95)90147-7","DOIUrl":"10.1016/0922-4106(95)90147-7","url":null,"abstract":"<div><p>Quinidine hydrochloride, as potent K⁺ channel blocker, reduced luminol-dependent chemiluminescence products evoked by the addition of the calcium ionophore A23187 to eosinophils from patients with hypereosinophilic syndrome (<em>n</em> = 3) in a concentration-dependent manner (10⁻⁵ mM to 1.0 mM quinidine). A23187 is known to cause increasses in intracellular Ca²⁺ concentrations in eosinophils. Our results indicate that the production of reactive oxygen species by human eosinophils may be affected by Ca²⁺ -activated K⁺ channels.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"291 2","pages":"Pages 217-219"},"PeriodicalIF":0.0,"publicationDate":"1995-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90147-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19547038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}