General Pharmacology-the Vascular System最新文献

{"title":"Buspirone, a 5-HT1A receptor agonist, dilates the perfused rat uterine vascular bed through α1-adrenoceptor blockade","authors":"Ayotunde S.O Adeagbo ,&nbsp;Elizabeth A Kadavil ,&nbsp;Mariam Yousif ,&nbsp;Mabayoje A Oriowo","doi":"10.1016/S0306-3623(01)00073-8","DOIUrl":"10.1016/S0306-3623(01)00073-8","url":null,"abstract":"<div><p>In the perfused rat uterine vascular bed, 5-hydroxytryptamine (5-HT) produced dose-dependent vasoconstrictor responses. Buspirone, a selective 5-HT_1A receptor agonist, was not effective at low doses but produced a response at high doses. When perfusion pressure was raised with phenylephrine, responses to 5-HT were enhanced while buspirone produced dose-dependent vasodilator responses. Buspirone did not produce vasodilation when perfusion pressure was raised with vasopressin or U46619. Buspirone-induced vasodilator responses were not affected by selective 5-HT_1A receptor antagonists, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4,5]-decane-7,9-dione (BMY 7378) and <em>N</em>-<em>tert</em>-butyl-3-(4-[2-methoxyphenyl]piperazin-1-yl)-2-phenylpropanamide (WAY 100478), indicating that specific 5-HT_1A receptors might not be involved in buspirone-induced vasodilation. Buspirone (3×10⁻⁵ M) and prazosin (3×10⁻⁹ M) antagonized noradrenaline-induced constriction with dose ratios of 19.1±2.9 and 11.7±2.1, respectively. The dose ratio of these antagonists in combination was 46.6±8.1. Since the combination ratio is closer to the sum of their individual dose ratios less 2 (i.e. DR_p+DR_b−2) than it is to the product of their individual dose ratios, our data suggest an interaction of buspirone with α₁-adrenoceptors. Buspirone also protected adrenoceptors against inactivation by phenoxybenzamine confirming that buspirone interacted with α₁-adrenoceptors. We concluded that buspirone-induced vasodilation of the perfused rat uterine vascular bed is mediated through blockade of α₁-adrenoceptors rather than through 5-HT_1A receptors.</p></div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 5","pages":"Pages 357-362"},"PeriodicalIF":0.0,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(01)00073-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73633181","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":"Novel therapeutic approach by culture filtrate of Cryptococcus neoformans var. gattii (CneF) in experimental immune complex glomerulonephritis","authors":"Abbas Mirshafiey,&nbsp;Farhad Mehrabian,&nbsp;Alireza Razavi,&nbsp;Mohammad R Shidfar,&nbsp;Saeed Namaki","doi":"10.1016/S0306-3623(00)00075-6","DOIUrl":"10.1016/S0306-3623(00)00075-6","url":null,"abstract":"<div><p>The present study was undertaken to determine the therapeutic effect of the culture filtrate of <em>Cryptococcus neoformans</em> var. <em>gattii</em> (CneF) in experimental immune complex glomerulonephritis. Bovine serum albumin (BSA) nephritis was induced in rats by a subcutaneous immunization and daily intravenous administration of BSA. CneF solution at three different doses (36, 54, and 90 mg/kg based on carbohydrate concentration) was administered intraperitoneally at regular 72-h intervals for 4 weeks. Onset of treatment was day 65, and urinary protein was measured at different intervals. Animals were euthanized on day 107. Serum and urine determinants were measured at the time of sacrifice and kidney specimens were examined. Results of this experiment showed that CneF therapy could significantly reduce the urinary protein excretion, blood urea nitrogen (BUN), plasma concentration of triglyceride, and increase the serum HDL cholesterol in treated rats vs. nontreated controls. Moreover, there was significant difference in glomerular changes between treated and nontreated groups. These observations show that the beneficial effect of CneF may be related to decreased number of glomerular leukocytes. Our findings suggest that treatment with CneF as a new antiinflammatory compound can reduce proteinuria, suppress the development of glomerular lesions, and exert lipid-lowering property in a rat model of immune complex glomerulonephritis.</p></div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 5","pages":"Pages 311-319"},"PeriodicalIF":0.0,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(00)00075-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79303945","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":"Activation of caspase cascades in Korean mistletoe (Viscum album var. coloratum) lectin-II-induced apoptosis of human myeloleukemic U937 cells","authors":"Myung-Sunny Kim ,&nbsp;Hong-Seob So ,&nbsp;Kang-Min Lee ,&nbsp;Ji-Sun Park ,&nbsp;Jae-Hoon Lee ,&nbsp;Seong-Keun Moon ,&nbsp;Do-Gon Ryu ,&nbsp;Sang-Young Chung ,&nbsp;Byung-Hak Jung ,&nbsp;Yong-Kyu Kim ,&nbsp;Goo Moon ,&nbsp;Raekil Park","doi":"10.1016/S0306-3623(01)00072-6","DOIUrl":"10.1016/S0306-3623(01)00072-6","url":null,"abstract":"<div><p>Mistletoe lectins are of high biological activity and exert cytotoxic effects. We have previously shown that Korean mistletoe, <em>Viscum album</em> var. <em>coloratum</em>, lectin-II specifically induces apoptotic cell death in cancer cells, not normal lymphocytes. The destructive mechanism by mistletoe lectins on tumor cells was mediated by activation of c-JUN N-terminal kinase (JNK)/stress-activated protein kinase. Herein, we investigated the involvement of caspase cascade and its proteolytic cleavage effects on biosubstrates of human myeloleukemic U937 cells by <span>d</span>-galactoside and <em>N</em>-acetyl-galactosamine-specific Korean mistletoe lectin-II. Mistletoe lectin-II induced ladder pattern DNA fragmentation and activation of caspase-3, -8, and -9 of U937 cells, but not caspase-1 protease, in a time- and dose-dependent manner. Consistent with catalytic activation of protease, both poly(ADP-ribose) polymerase (PARP) and protein kinase C-δ (PKC-δ) are also cleaved in mistletoe lectin-II-treated U937 cells. An inhibitor of caspase-3-like protease, DEVD-CHO peptide, significantly inhibited mistletoe lectin-II-induced apoptosis, PARP cleavage, and fragmentation of DNA. These results provide the evidence that Korean mistletoe lectin-II induces apoptotic death of U937 cells via activation of caspase cascades.</p></div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 5","pages":"Pages 349-355"},"PeriodicalIF":0.0,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(01)00072-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83291533","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":"Mechanisms of endothelin-1-induced contraction in isolated placental veins from normal full-term and preterm pregnancies","authors":"Victoria Gallardo ,&nbsp;M.Antonieta Cruz ,&nbsp;Patricia Miguel ,&nbsp;Gonzalo Carrasco ,&nbsp;Clemente González","doi":"10.1016/S0306-3623(00)00070-7","DOIUrl":"10.1016/S0306-3623(00)00070-7","url":null,"abstract":"<div><p>This study characterizes the reactivity of human chorionic plate vein in full-term (39.4±0.3 weeks of gestation) and preterm (34.4±0.6 weeks of gestation) pregnancy to endothelin-1 (ET-1) and attempts to characterize ET-1 receptor subtype, and the contribution of nitric oxide and cyclooxygenase products in these responses. In placental veins from full-term and preterm pregnant women, cumulative addition of ET-1 (10⁻¹⁰–10⁻⁶ M) caused marked and long-lasting concentration-dependent contractile responses. The mean EC₅₀ and <em>E</em>_max values for ET-1-induced venoconstriction did not differ between the full-term and preterm pregnancy groups. In the veins from preterm placental preparations, the ET_A receptor-selective antagonist cyclo(<span>d</span>-α-aspartyl-<span>l</span>-propyl-<span>d</span>-valyl-<span>l</span>-leucyl-<span>d</span>-tryptophyl (BQ123) reduced the ET-1-induced contraction by 28.6±2.4%, compared to a decline in tension of 51.2±4.2% in the full-term placental vessels. The ET_B receptor-selective antagonist, <em>N</em>-[<em>N</em>-[<em>N</em>-[2,6-dimethyl-1piperidinyl)carbonyl]-4-methyl-<span>l</span>-leucyl]-1-(methoxycarbonyl)-<span>d</span>-tryptophyl]-<span>d</span>-norleucinemonosodium (BQ788), did not influence ET-1-induced contraction in placental vein from both pregnancy groups in terms of maximal contraction and sensitivity. Pretreatment with the cyclooxygenase inhibitor, indomethacin (1 μM) and the nitric oxide synthase inhibitor <em>N</em>^w-nitro-<span>l</span>-arginine (NOLA, 100 μM) did not significantly affect either the EC₅₀ or the maximum contraction to ET-1 in veins from normal full-term and preterm preparations. The results of this study suggest that there is no correlation between ET-1-induced vasoconstriction and gestational age and that this vasoconstriction is mediated predominantly via ET_A receptor subtype in both groups of pregnant women, independent of NO and eicosanoids.</p></div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 5","pages":"Pages 295-301"},"PeriodicalIF":0.0,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(00)00070-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81283865","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 role of cyclic nucleotides and calcium in the relaxation produced by amrinone in rat aorta","authors":"Andrea van der Zypp ,&nbsp;Mary Rechtman ,&nbsp;Henryk Majewski","doi":"10.1016/S0306-3623(00)00071-9","DOIUrl":"10.1016/S0306-3623(00)00071-9","url":null,"abstract":"<div><p>(1) The vasorelaxation produced by the phosphodiesterase 3 (PDE3) inhibitor, amrinone was investigated in isolated rat aorta denuded of endothelium. In the presence of extracellular Ca²⁺, amrinone, milrinone and 3-isobutyl-1-methylxanthine (IBMX), relaxed endothelium-denuded rat aortic rings constricted with phenylephrine. While the actions of milrinone and IBMX were inhibited by the protein kinase G (PKG) inhibitor, Rp-8-Bromo guanosine-3′,5′ monophosphothioate (Rp-8-Br-cGMPS; 0.5 mM), that of amrinone was only slightly affected; whereas the protein kinase A (PKA) inhibitor, Rp-adenosine-3′,5′ cyclic monophosphothioate (Rp-cAMPS; 0.5 mM) had no effect on any agent. (2) Amrinone (100 μM) inhibited ⁴⁵Ca²⁺ influx through receptor- or store-operated Ca²⁺ channels following stimulation with phenylephrine (1 μM) or thapsigargin (1 μM). In contrast, amrinone had no effect on KCl (120 mM)-stimulated Ca²⁺ influx. (3) In the absence of extracellular Ca²⁺, amrinone (30 μM) inhibited the constriction produced by phenylephrine, 5-hydroxytryptamine (5HT) and U46619, and this effect was not affected by Rp-cAMPS or Rp-8-Br-cGMPS. (4) The intracellular mechanism of action of amrinone may involve the phospholipase C (PLC)-inositol 1,4,5 trisphosphate (IP₃)-intracellular Ca²⁺ signal transduction pathway. However, amrinone (100 μM) had no effect on either basal- or noradrenaline (100 μM)-stimulated PLC activity. Similarly, IP₃ stimulated a concentration-dependent release of Ca²⁺ from rat brain microsomes that was not affected by amrinone (30 and 100 μM). (5) In conclusion, the vasorelaxant action of amrinone does not involve adenosine 3′,5′ cyclic monophosphate (cAMP) or involve guanosine 3′,5′ cyclic monophosphate (cGMP) but may include an inhibition of Ca²⁺ influx through receptor- or store-operated Ca²⁺ channels, although it does not directly affect intracellular Ca²⁺ release.</p></div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 4","pages":"Pages 245-253"},"PeriodicalIF":0.0,"publicationDate":"2000-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(00)00071-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79496718","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":"Abstracts from 7th Biannual Conference on Vascular Endothelium: source and target of inflammatory mediators; June 24–July 3, 2000, Knossos Royal Village, Crete, Greece","authors":"","doi":"10.1016/S0306-3623(00)00069-0","DOIUrl":"https://doi.org/10.1016/S0306-3623(00)00069-0","url":null,"abstract":"","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 4","pages":"Pages 273-294"},"PeriodicalIF":0.0,"publicationDate":"2000-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(00)00069-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91609004","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":"Insulin effects on the sympathetic contraction of rabbit ear arteries","authors":"Angel Luis Garcı́a-Villalón,&nbsp;Nuria Fernández,&nbsp;Luis Monge,&nbsp;Marı́a Angeles Martı́nez,&nbsp;Bernardino Gómez,&nbsp;Godofredo Diéguez","doi":"10.1016/S0306-3623(00)00063-X","DOIUrl":"https://doi.org/10.1016/S0306-3623(00)00063-X","url":null,"abstract":"<div><p>Electrical field stimulation (4 Hz, 0.2 ms, 70 V supramaximal voltage, 10 s duration) produced contraction of perfused rabbit central ear arteries, and this contraction was reduced by incubation with insulin (0.6–200 mU/ml). This inhibitory effect of insulin was not significantly modified by removing the endothelium, or by treatment with <em>N</em>^W-nitro-<span>l</span>-arginine (<span>l</span>-NA, 10⁻⁴ M), meclofenamate (10⁻⁵ M), ouabain (10⁻⁶ M), or cocaine (10⁻⁵ M). Insulin (200 mU/ml) did not modify the vascular contraction due to exogenous norepinephrine (10⁻⁸–10⁻⁴ M) nor the relaxation due to acetylcholine (10⁻⁸–10⁻⁴ M). This suggests that insulin may reduce vascular contraction by sympathetic stimulation, and this effect is not dependent on endothelial nitric oxide, prostanoids, or Na⁺–K⁺ pump activation.</p></div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 4","pages":"Pages 221-226"},"PeriodicalIF":0.0,"publicationDate":"2000-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(00)00063-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91641234","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":"Interactions between agmatine and polyamine uptake pathways in rat pulmonary artery endothelial cells","authors":"Pavel Babál ,&nbsp;Mykhaylo Ruchko,&nbsp;Jack W. Olson,&nbsp;Mark N. Gillespie","doi":"10.1016/S0306-3623(00)00072-0","DOIUrl":"https://doi.org/10.1016/S0306-3623(00)00072-0","url":null,"abstract":"<div><p>Agmatine, a product of arginine metabolism in vascular endothelial cells, is structurally similar to the natural polyamines, putrescine, spermidine and spermine. To test the hypothesis that agmatine and polyamines interacted at the level of the polyamine transporter, we determined if polyamines competed with agmatine for import and whether interventions modulating polyamine import exerted coordinate effects on agmatine uptake. Multiple lines of evidence were obtained to suggest that agmatine enters pulmonary artery endothelial cells (PAECs) via the polyamine transporter, though its intracellular disposition after uptake appears different from the natural polyamines.</p></div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 4","pages":"Pages 255-261"},"PeriodicalIF":0.0,"publicationDate":"2000-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(00)00072-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91641236","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":"Pharmacokinetics of verapamil in lactating rabbits","authors":"Carlos Solans ,&nbsp;José Javier Aramayona ,&nbsp;Miguel Angel Bregante ,&nbsp;Lorenzo José Fraile ,&nbsp;Silvia Rueda ,&nbsp;Marı́a Angeles Garcia","doi":"10.1016/S0306-3623(00)00066-5","DOIUrl":"https://doi.org/10.1016/S0306-3623(00)00066-5","url":null,"abstract":"<div><p>In this work, we have studied the pharmacokinetics and milk penetration of verapamil following intravenous administration in lactating rabbits. Milk-to-serum drug concentration ratios (M/B_obs) have been determined using area under the milk and serum concentration–time profiles, and the resulting values have then been compared with those obtained by theoretical classical diffusion milk transfer models that were described by Fleishaker et al. [J. Pharm. Sci. 76 (1987) 189.], Atkinson and Begg [Br. J. Clin. Pharmacol. 25 (1990) 495.], and Stebler and Guentert [Pharm. Res. 9 (1992) 1299.]. The pharmacokinetic profile of verapamil in lactating rabbits following endovenous administration is described in the form of a two-compartment model. Moreover, we detected an important milk transfer after endovenous administration of verapamil in lactating rabbits. M/B_obs was near 15. The classical diffusional models mentioned were not able to predict this extensive transfer of verapamil into rabbit milk. However, when the classical Fleishaker equation was modified and a stepwise regression was carried out, we found that the M/B_obs value could be predicted using the plasma and milk protein binding.</p></div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 4","pages":"Pages 237-243"},"PeriodicalIF":0.0,"publicationDate":"2000-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(00)00066-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91641237","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":"Hwansodan protects PC12 cells against serum-deprivation-induced apoptosis via a mechanism involving Ras and mitogen-activated protein (MAP) kinase pathway","authors":"Myung-Sunny Kim ,&nbsp;Hong-Seob So ,&nbsp;Ji-Sun Park ,&nbsp;Kang-Min Lee ,&nbsp;Byung-Soon Moon ,&nbsp;Ho-Sub Lee ,&nbsp;Tae-Young Kim ,&nbsp;Seong-Keun Moon ,&nbsp;Raekil Park","doi":"10.1016/S0306-3623(00)00065-3","DOIUrl":"https://doi.org/10.1016/S0306-3623(00)00065-3","url":null,"abstract":"<div><p>Hwansodan has been used as a prescription for senile and vascular dementia in Oriental medicine. We investigated the neuroprotective effects of Hwansodan water extract on the apoptotic death of PC12 cells by serum deprivation. Hwansodan significantly rescued PC12 cells from apoptotic death by serum deprivation in a dose-dependent manner. The nuclear staining of PC12 cells clearly showed that Hwansodan attenuated nuclear condensation and fragmentation, which represents typical neuronal apoptotic characteristics. Hwansodan also prevents DNA fragmentation and caspase-3-like protease activation in serum-deprived PC12 cells and induces the tyrosine phosphorylation of proteins around 44 kDa, which was identified as ERK1 with electrophoretic gel mobility shift by Western blot. In addition, MEK inhibitor PD98059 and Ras inactivator, α-hydroxyfarnesylphosphonic acid and mevastatin, attenuated the neuroprotective effects of Hwansodan in serum-deprived PC12 cells. These results indicate that Ras/MEK/ERK signaling pathway plays a role in neuroprotective effects of Hwansodan in serum-deprived PC12 cells.</p></div>","PeriodicalId":12607,"journal":{"name":"General Pharmacology-the Vascular System","volume":"34 4","pages":"Pages 227-235"},"PeriodicalIF":0.0,"publicationDate":"2000-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0306-3623(00)00065-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91609369","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}