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101.
In the preceding paper, by means of selective agonists to gastrin (HG-17) and cholecystokinin (CCK-39), we evidenced the existence of "gastrin-type" receptors that could regulate histamine release and "CCK-type" receptors that could stimulate somatostatin release in isolated rabbit fundic non-parietal cells (F1 cells). Furthermore, these receptors could induce phosphoinositide breakdown. To confirm the involvement of these receptor types in these biological and biochemical processes, we used selective antagonists, L-364,718 (3-(benzoylamino)-benzodiazepine) specific to "CCK-A-type" receptor and L-365,260 (3-(acylamino)-benzodiazepine) specific to "gastrin/CCK-B-type" receptor. Neither L-364,718 nor L-365,260 alone caused any significant stimulation of [3H]inositol phosphate ([3H]InsP) production and release of histamine or somatostatin-like immunoreactivity (SLI). Each analogue inhibited in a dose-dependent manner [125I]HG-17 or [125I]CCK-39 binding to F1 cells, [3H]InsP accumulation and histamine and SLI release stimulated by HG-17 or CCK-39. L-365,260 appeared to be 30-70 times more potent than L-364,718 in inhibiting [125I]HG-17 binding to F1 cells, as well as HG-17-induced [3H]InsP accumulation and HG-17-or CCK-39-enhanced histamine release (IC50 values: approximately 5-20 nM for L-365,260 and approximately 200-1500 nM for L-364,718). In contrast, L-364,718 was 200 to 400 times more potent than L-365,260 in inhibiting [125I]CCK-39 binding to F1 cells, CCK-39-induced [3H]-InsP accumulation and SLI release stimulated by CCK-39 or HG-17 (IC50 values: approximately 0.3-1 nM for L-364,718 and 100-200 nM for L-365,260). These results led to conclude: (i) the existence of a "gastrin-type" receptor related to histamine release: (ii) the existence of a "CCK-A-type" receptor related to somatostatin release; (iii) the existence of "gastrin type" and "CCK-A-type" receptors linked to the phosphoinositide breakdown pathway. 相似文献
102.
103.
Jean E. de La Coussaye Bruno P. Bassoul Bernard Albat Pascale A. Peray Jean-Pierre Gagnol Jean-Jacques Eledjam Antoine Sassine 《Journal canadien d'anesthésie》1992,39(2):192-197
The intravascular injection of a large dose of bupivacaine induces electrophysiological cardiac impairment, mainly by slowing ventricular conduction velocity, and haemodynamic depression, by a decrease in myocardial contractility. When cardiotoxicity occurs, succinylcholine rapidly stops convulsions. However, the possible interactions between bupivacaine and succinylcholine on cardiac electrophysiology and haemodynamic status have never been investigated. Thus, we used an experimental electrophysiological model involving closed-chest dogs. Three groups (n = 6) of pentobarbital-anaesthetized dogs were given 0.2 mg.kg-1 atropine iv. Dogs in Group 1 were given saline. The others received 4 mg.kg-1 bupivacaine iv over ten seconds. Dogs in Group 2 were then given saline and those in Group 3 were then given 2 mg.kg-1 succinylcholine iv from one to two minutes after the administration of bupivacaine. The following electrophysiological variables were measured: heart rate represented by RR interval (RR), PR, atria-His (AH), and His-ventricle (HV) intervals, QRS duration, and QT interval corrected for heart rate (QTc). The following haemodynamic variables were measured: mean aortic pressure (MAoP), the peak of the first derivative of left ventricular pressure (LV dP/dt max), and LV end diastolic pressure (LVEDP). Comparison between Groups 1 and 2 showed that bupivacaine induced more than 100% HV interval lengthening and QRS widening (P less than 0.01), prolonged QTc interval by more than 25% (P less than 0.01), and decreased LV dP/dt max by more than 50% (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
104.
Perchellet Jean-Pierre; Kishore Gollamudi S.; Conrad Elizabeth A.; Boutwell R.K. 《Carcinogenesis》1982,3(10):1149-1158
Isolated epidermal cells were incubated with a variety of compoundsknown to interfere with or alter the ultrastructure of cellsurface receptors, and the ability of 12-O-tetradecanoyl-phorbol-13-acetate(TPA) to bind to these cells and induce epidermal ornithinedecarboxylase (ODC) activity was investigated. The - and ß-adrenergicantagonists, phentolamine and propranolol, and the cholinergicantagonist, atropine, which competed effectively for the bindingreceptors of [3H]dihydro--ergocryptine, [3H]dihydroalprenolol,and [14C]acetylcholine, did not inhibit the induction of ODCactivity by TPA or the specific binding of [3H]TPA to the cells.Neuraminidase treatments caused a time- and dose- related releaseof sialic acid from the cells and enhanced the stimulatory effectof cholera toxin on basal and TPA-induced ODC activities asmuch as the monosialoganglioside GM1. Neuraminidase and theother membrane-altering agents, fucosidase, galactosidase, galactoseoxidase, phospholipases A2 and C, and NaIO4, were used aloneand/or in various combinations in our studies. All treatmentstested inhibited the specific binding of several 125I-labeledhormones and epidermal growth factor to the cells. In contrast,none of these treatments was able, in the same cell system,to affect either the binding or the biological activity of TPA.Therefore, these results suggest that the primary interactionof TPA at the plasma membrane level as well as its biologicaleffect in the intact cell do not proceed through adrenergicor cholinergic receptors and do not require the integrity ofthe cell surface glycoconjugates and phospholipids. In addition,the inhibitory effect of retinoic acid on TPA-induced ODC activityremained unaffected by some of the above treatments, suggestingthat retinoic add is unlikely to interfere with TPA interactionsat the plasma membrane level. 相似文献
105.
Jean-Pierre Famaey Jeanine Fontaine Isabelle Seaman Jean Reuse 《Naunyn-Schmiedeberg's archives of pharmacology》1979,309(2):191-195
Summary High concentrations of antiinflammatory steroids (2.5–40 g/ml) reversibly inhibited the electrically induced contractions of the guinea-pig isolated ileum. At 40 g/ml they also reversibly inhibited contractions clicited by acetylcholine, histamine, nicotine and 5-hydroxytryptamine. PGE1 (2.5 ng/ml), PGE2 (2.5 ng/ml) and PGF2 (25 ng/ml) antagonized these effects.The inhibition of contractions elicited by direct agonists were less pronounced than those elicited by indirect or partly indirect agonists. The inhibitory effect of steroids may be related to non-specific actions on biological membranes. An overall sensitization of the smooth muscle by PG's may explain their antagonism to inhibition by steroids. 相似文献
106.
Karim Fizazi Stéphane Culine Andrew Kramar Robert J Amato Jeannine Bouzy Isan Chen Jean-Pierre Droz Christopher J Logothetis 《Journal of clinical oncology》2004,22(19):3868-3876
PURPOSE: The prognostic relevance of the rate of decline of serum alpha-fetoprotein (AFP) and human chorionic gonadotropin (HCG) during the first 3 weeks of chemotherapy for nonseminomatous germ cell tumors (NSGCT) was studied in the context of the International Germ Cell Cancer Collaborative Group (IGCCCG) classification. PATIENTS AND METHODS: Data from 653 patients prospectively recruited in clinical trials were studied. Tumor markers were obtained before chemotherapy and 3 weeks later. Decline rates were calculated using a logarithmic formula and expressed as a predicted time to normalization (TTN). A favorable TTN was defined when both AFP and HCG had a favorable decline rate, including cases with normal values. RESULTS: The median follow-up was 50 months (range, 2 to 151 months). Tumor decline rate expressed as a predicted TTN was associated with both progression-free survival (PFS; P <.0001) and overall survival (OS; P <.0001). The 4-year PFS rates were 64% and 38% in patients from the poor-prognosis group who had a favorable and an unfavorable TTN, respectively. The 4-year OS rates were 83% and 58%, respectively. This effect was independent from the initial tumor marker values, the primary tumor site, and the presence of nonpulmonary visceral metastases: tumor marker decline rate remained a strong predictor for both PFS (hazard ratio = 2.5; P =.01) and OS (hazard ratio = 4.6; P =.002) in patients from the IGCCCG poor-prognosis group in multivariate analysis. CONCLUSION: Early predicted time to tumor marker normalization is an independent prognostic factor in patients with poor-prognosis NSGCT and may be a useful tool in the therapeutic management of these patients. 相似文献
107.
Identification of HRK as a target of epigenetic inactivation in colorectal and gastric cancer. 总被引:3,自引:0,他引:3
108.
Jean-Pierre Valla Lise Bergeron Michelle Bidaut-Russell Marie St-Georges Nathalie Gaudet 《Journal of child psychology and psychiatry, and allied disciplines》1997,38(6):717-724
Reliability of the Dominic-R, a. questionnaire combining visual and auditory stimuli, was tested in 340 community children aged 6 to 11 years. Test-retest reliability of symptoms of, and of symptom scores of, DSM-III-R disorders including simple phobias, separation anxiety disorder, overanxious disorder, depression/dysthymia, attention deficit/ hyperactivity disorder, oppositional defiant disorder, and conduct disorder was assessed. Most symptoms yielded kappas greater than .40, and ICCs ranged from .74 to .81. In conclusion, reliability of the Dominic-R compares favourably with that of other child assessment questionnaires. 相似文献
109.
Carolyn R. Freeman B.S. M.B. FRCP Jean-Pierre Farmer M.D. FRCS José. Montes M.D. 《International journal of radiation oncology, biology, physics》1998,41(5):283-987
Developments in imaging and in neurosurgical techniques over the past decade have substantially altered the management of children with low-grade astrocytoma. Indications for surgery have become more clearly defined, and a larger proportion of children undergo complete or subtotal resection than in the past. Fewer receive adjuvant therapy, even though the options in this regard are more numerous now and theoretically likely to result in less morbidity than conventional external beam radiotherapy.
This review will address in particular the correlations between location, imaging appearance, and behavior that need to be more widely appreciated, and present recommendations regarding the management of these tumors. 相似文献
110.
Preclinical in vivo antitumor activity of vinflunine, a novel fluorinated Vinca alkaloid 总被引:1,自引:0,他引:1
Anna Kruczynski Francis Colpaert Jean-Pierre Tarayre Pierre Mouillard Jacques Fahy Bridget T. Hill 《Cancer chemotherapy and pharmacology》1998,41(6):437-447
Vinflunine, or 20′,20′-difluoro-3′,4′-dihydrovino‐relbine, is a novel Vinca alkaloid obtained by hemisynthesis using superacidic chemistry. The most impressive structural modification of this vinorelbine
derivative was the selective introduction of two fluorine atoms at the 20′ position, a part of the molecule previously inaccessible
by classic chemistry. The antitumor activity of vinflunine was evaluated against a range of transplantable murine and human
tumors. Vinflunine exhibited marked activity against murine P388 leukemia grafted i.v. when given i.p. in single or multiple
doses according to various schedules or in single i.v. or p.o. doses. Increases in life span achieved with vinflunine, as
assessed by T/C ratios, ranged from 200% to 457% and proved markedly superior to those of 129–186% obtained with the other
Vinca alkaloids tested. Against s.c.-implanted B16 melanoma, multiple i.p. administration of vinflunine proved active in terms
of both survival prolongation and tumor growth inhibition, with optimal T/C values and relative areas under the tumor growth
curves (rAUC) being 24% and 36%, respectively. The extent of this activity was superior to that noted for vinorelbine under
the same experimental conditions. Growth inhibition of human tumor xenografts LX-1 (lung) and MX-1 (breast) was also observed
following four weekly i.p. injections of vinflunine as reflected by optimal T/C values of 23% and 26%, respectively, and significant
differences in the rAUCs noted for treated versus control animals. It was also noticeable that vinflunine induced considerably
more prolonged inhibitory effects on tumor growth than did vinorelbine. These results demonstrate that vinflunine is well
tolerated and is definitively active against a range of experimental animal tumor models. Vinflunine activity has been documented
in terms of both survival prolongation and tumor growth inhibition, with definite superiority over vinorelbine being shown
in each tumor model evaluated.
Received: 13 July 1997 / Accepted: 21 October 1997 相似文献