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1.
J L Vatier Z Gao X M Fu-Cheng M T Vitre D A Levy G Cohen M Mignon 《The Journal of pharmacology and experimental therapeutics》1992,263(3):1206-1211
In light of evidence that certain aluminum-based antacids adhere to the gastric mucosa, we modified our previously described "artificial stomach" (AS) model by including a piece of hog stomach and compared the antacid activity of six aluminum-containing antacid products in the model with and without gastric mucosa. The activity of three of these, Maalox, Riopan and Supralox, was not significantly different in the two systems. In contrast, the activity of the other three, Aludrox, Phosphalugel and Simeco, was significantly greater with mucosa. Antacid activity of one product from each set (Supralox, Phosphalugel) was evaluated in two in vivo methods in human volunteers. For both antacids, results in vivo were similar to those obtained with the AS-containing mucosa. Without mucosa, in vivo and in vitro results were dissimilar for Phosphalugel, thus validating the modified AS. The difference between the two sets of antacids can be explained by 1) the fact that the Al:Mg ratio in the set affected by mucosa is greater than that of unaffected antacids, and 2) a weaker antacid load than in unaffected Supralox. We suggest that in an acid milieu, aluminum ions in antacids like Aludrox, Phosphalugel and Simeco are bound to sialic acid residues in mucus glycoproteins, thus retarding the transit of these antacids through both the AS and the real stomach and prolonging their activity in both situations. When the Al:Mg ratio is low or when the amount of antacid salts is large, aluminum ions tend to be buried in complexes, giving them less chance to interact with gastric mucus, so they transit the stomach more quickly. 相似文献
2.
Mechanisms of peptide YY release induced by an intraduodenal meal in rats: neural regulation by proximal gut 总被引:5,自引:0,他引:5
Fu-Cheng Xiaomei Anini Younes Chariot Jacques Castex Nathalie Galmiche Jean-Paul Rozé C. 《Pflügers Archiv : European journal of physiology》1997,433(5):571-579
Peptide YY (PYY) release in anaesthetized rats was studied during the 2 h following the intraduodenal administration of a
semi-liquid meal of 21 kJ. Surgical and pharmacological manipulations were performed in order to analyse the mechanisms of
PYY release. Postprandial PYY release was suppressed or strongly decreased by caecocolonectomy, truncal vagotomy, tetrodotoxin,
hexamethonium, sensory denervation by perivagal capsaicin, and by the NO-synthase inhibitor L-N-arginine methyl ester, while atropine, adrenergic blockers, antagonists of type-A or type-B cholecystokinin (CCK) receptors
or bombesin receptors had no effect. Comparing the digestive transit of the semi-liquid meal with the amount of PYY contained
in the small bowel wall showed that nutrients had not reached the area rich in cells containing PYY by 30 min, the time at
which there was a large PYY release in plasma. By 120 min, the meal front had travelled 72% of the small intestine length,
just beginning to reach the PYY-rich part of the ileum. We conclude that the main postprandial PYY release studied in this
model comes from ileal and colonic L-cells indirectly stimulated through a neural mechanism originating in the proximal gut
and involving sensory vagal fibres, nicotinic synapses and NO release, while CCK and bombesin do not seem to be physiologically
involved.
Received: 17 July 1996 / Received after revision: 11 October 1996 / Accepted: 18 October 1996 相似文献
3.
胃癌组织中p16,p53和P-糖蛋白的表达与预后 总被引:2,自引:0,他引:2
目的:探讨胃癌及癌前病变组织中p16,p53蛋白和P-糖蛋白(P-gP)的表达与预后的关系。方法应用免疫组化检测20例胃癌前病变、76例腺癌和10例正常组织中p16,p53和Pg-P的表达状况。结果p16,p53蛋白和P-gP在正常对照组、癌前病变组和腺癌组的阳性率分别为90%、705,50%;10%,20%,53%,0,5%,51%,p16,p53和P-gP在癌前病变与腺癌之间的阳性表达以及P16蛋白在临床分期Ⅰ和Ⅱb之间的表达均有显著差异(P<0.05),但与肿瘤与化无关,p53蛋白与P-gP阳性表达之间有显著相关(P<0.05)。结论p16,p53蛋白的异常表达与胃癌的发生有关,胃癌组织中p16蛋白的低表达和p53蛋白高表达均提示该患者预后较差,其中p53蛋白的高表达也提示该肿瘤细胞对某些化疗药物具有耐药性。 相似文献
4.
5.
Hui-Ping Zhang Ying Zhao Hui Li Guo-Dong Tang Hu Ai Nai-Xin Zheng Jing-Hua Liu Fu-Cheng Sun 《Medicine》2016,95(2)
In the setting of primary percutaneous coronary intervention (PCI), encountering with chronic total occlusion (CTO) in a noninfarct-related artery (IRA) is not a rare situation. Limited information on the impact of CTO on clinical outcomes in acute ST-elevation myocardial infarction (STEMI) patients undergoing primary PCI has raised more concerns. The aim of the present study was to evaluate the effect of concurrent CTO in a non-IRA on the clinical outcomes in patients with STEMI undergoing primary PCI.In the present prospective study, 555 consecutive patients with STEMI who underwent early primary PCI from January 2010 to December 2013 were included. The patients were divided into 2 groups: no CTO and CTO. Data on 12 months follow-up was obtained from 449 patients. The primary endpoint was the composite of hospitalization from angina, reinfarction, heart failure, or re-revascularization, and cardiac death at 12 months follow-up.Of the 555 patients, 75 (13.5%) had CTO in a non-IRA. Compared with patients in no CTO group, more patients in CTO group had hypertension (62.7% vs 46.5%, P = 0.009), diabetes (49.3% vs 35.0%, P = 0.024), and 3-vessel disease (52.0% vs 32.3%, P = 0.001). Patients with CTO had a lower left ventricular ejection fraction (LVEF) (40.1% ± 16.8% vs 54.3% ± 12.1%, P = 0.038), more presented with cardiogenic shock on admission (13.3% vs 4.8%, P = 0.008), compared with patients without CTO. Complete revascularization (CR) was less achieved in CTO group than in no CTO group (33.3% vs 49.1%, P = 0.013). The 12-month cardiac mortality rate was 14.5% versus 6.2% (P = 0.039), the incidence of 12-month primary endpoint was 38.7% versus 21.2% (P = 0.003) for CTO and no CTO group, respectively. Multivariate analysis revealed that after correction for baseline differences, CTO in a non-IRA (hazard ratio 4.183, 95% confidence interval 1.940–6.019, P = 0.001), cardiogenic shock on admission (hazard ratio 3.286, 95% confidence interval 1.097–9.845, P = 0.034), and 3-vessel disease (hazard ratio 2.678, 95% confidence interval 1.221–5.874, P = 0.014) remained an independent predictor of 1-year cardiac mortality in patients with STEMI undergoing primary PCI.CTO in a non-IRA in patients with STEMI undergoing primary PCI is associated with a poor prognosis. The presence of CTO in a non-IRA, cardiogenic shock on admission and 3-vessel disease might be an independent risk factor for greater 1-year cardiac mortality in patients with acute STEMI undergoing primary PCI. 相似文献
6.
Sun WP Li D Lun YZ Gong XJ Sun SX Guo M Jing LX Zhang LB Xiao FC Zhou SS 《Hypertension research》2012,35(2):180-185
Nicotinamide and catecholamines are both degraded by S-adenosylmethionine-dependent methylation. Whether excess nicotinamide affects the degradation of catecholamines is unknown. The aim of this study was to investigate the effect of nicotinamide on the methylation status of the body and methylation-mediated catecholamine degradation in both normotensives and hypertensives. The study was conducted in 19 normotensives and 27 hypertensives, using a nicotinamide-loading test (100?mg orally). Plasma nicotinamide, N(1)-methylnicotinamide, homocysteine (Hcy), betaine, norepinephrine, epinephrine, normetanephrine and metanephrine levels before and 5?h after nicotinamide loading were measured. Compared with normotensives, hypertensives had higher baseline (fasting) levels of plasma nicotinamide, Hcy and norepinephrine, but lower levels of plasma normetanephrine, a methylated norepinephrine derivative. Nicotinamide loading induced a significant increase in the levels of plasma N(1)-methylnicotinamide and norepinephrine, and a significant decrease in the levels of O-methylated epinephrine (metanephrine) and betaine, a major methyl donor, in both hypertensives and normotensives. Moreover, nicotinamide-loading significantly increased plasma Hcy levels, but decreased plasma normetanephrine levels in normotensives. The baseline levels of plasma epinephrine in hypertensives were similar to those of normotensives, but the post-nicotinamide-loading levels of plasma epinephrine in hypertensives were higher than those of normotensives. This study demonstrated that excess nicotinamide might deplete the labile methyl pool, increase Hcy generation and inhibit catecholamine degradation. It also revealed that hypertensives had an abnormal methylation pattern, characterized by elevated fasting plasma levels of unmethylated substrates, nicotinamide, Hcy and norepinephrine. Therefore, it seems likely that high nicotinamide intake may be involved in the pathogenesis of Hcy-related cardiovascular disease. 相似文献
7.
Hui-Ping Zhang Hu Ai Ying Zhao Hui Li Guo-Dong Tang Nai-Xin Zheng Fu-Cheng Sun Jing-Hua Liu 《The American journal of the medical sciences》2018,355(2):174-182
Background
There are little published data reporting the effect of coronary artery chronic total occlusion (CTO) percutaneous coronary intervention (PCI) on the prognosis of elderly patients with identified CTOs. We sought to evaluate the clinical effect of CTO PCI on the prognosis of elderly patients with CTOs.Methods
A total of 445 consecutive patients diagnosed with a CTO by angiography from January 2011 to December 2013 were enrolled. We compared long-term clinical outcomes between the elderly group (≥75 years; n = 120, 27.0%), and the nonelderly group (<75 years; n = 325, 73.0%) as well as between patients with unopened CTOs and patients with CTOs who were recanalized by PCI either during the index hospitalization or at a staged procedure within 30 days after discharge from the index hospitalization. The primary endpoint was defined as the composite of hospitalization from angina, reinfarction, heart failure or repeat revascularization and cardiac death at the 3-year follow-up.Results
More elderly CTO patients had left main (LM) disease (25.0 versus 15.1%, P = 0.015), 3-vessel disease (96.4% versus 73.8%, P < 0.001) and a Japan-CTO score ≥2 (36.7% versus 23.7%, P = 0.006) than nonelderly CTO patients. Furthermore, elderly patients had a higher syntax score than nonelderly patients (27.0 [25.0, 30.0] versus 26.0 [23.0, 30.0], P = 0.006). PCI was attempted for 33 out of 135 CTO lesions (24.4%) in the elderly group, and 127 out of 378 lesions (33.6%) in the nonelderly group (P = 0.049); however, there were no statistically significant differences in the CTO PCI success rates between the 2 groups (69.7% versus 82.7%, P = 0.097). The 3-year cardiac mortality rate was 15.0% and 4.6% (P < 0.011) for the elderly and nonelderly groups, respectively. Elderly patients with CTOs who were recanalized by PCI and those with unopened CTOs exhibited comparable 3-year cardiac mortality rates (15.0% versus 16.0%, P = 1.000). There was no significant difference in primary endpoint incidence (25.0% versus 33.0%, P = 0.486). Multivariate analysis revealed that after corrections for baseline and procedural differences, right coronary artery CTO (odds ratio = 4.600, 95% CI: 1.320-16.031; P = 0.017) and LM disease combined with 3-vessel disease (odds ratio = 4.296, 95% CI: 1.166-15.831; P = 0.028) were independent predictors of 3-year cardiac mortality among elderly patients with CTOs.Conclusions
Elderly patients with CTOs presented with seriously diseased coronary arteries and poor prognoses. CTO PCI did not seem to significantly improve long-term clinical outcomes among elderly patients with CTOs. Right coronary artery CTO and LM disease combined with 3-vessel disease might be independent predictors of 3-year cardiac mortality in elderly CTO patients. 相似文献8.
目的:观察丁酸钠对食管癌EC9706细胞增殖、细胞周期及NDRG1蛋白表达的影响.方法:采用0.5 mmol/L丁酸钠作用于食管癌EC9706细胞,用MTT法检测处理不同时间时细胞增殖的变化,采用流式细胞仪检测细胞周期的变化,采用免疫组化方法检测NDRG1蛋白表达的变化.结果:①MTT实验结果显示,丁酸钠作用1~5 d时各组吸光度均低于对照组,经统计学处理差异有显著性意义(P<0.05);丁酸钠不同作用时间的细胞增殖抑制率分别为:1 d组21.2%,3 d组23.5%,5 d组25.6%,且随作用时间延长抑制率升高.②细胞周期检测结果为(%):G1期细胞:对照组57.00±1.10,1 d组63.10±0.78,3 d组67.20±0.58,5 d组69.70±0.64;S期细胞:对照组25.30±0.27,1 d组20.20±0.66,3 d组20.40±0.82,5 d组20.90±0.50;M期细胞:对照组17.20±1.00,1 d组16.70±0.69,3 d组12.10±0.41,5 d组9.40±0.23.各组G1期结果分别与对照组结果比较,差异有显著性意义(P<0.01).③丁酸钠可上调NDRG1蛋白表达水平,随作用时间增长蛋白表达增强.结论:丁酸钠可抑制食管癌细胞增殖,这一作用可能与NDRG1蛋白表达增加有关. 相似文献
9.
骨髓间充质干细胞对肺损伤大鼠的治疗作用 总被引:5,自引:0,他引:5
目的:观察骨髓间充质干细胞(MSCs)对大鼠肺损伤的治疗作用.方法:将SD大鼠MSCs用DAPI标记后注入受体大鼠体内.将受体大鼠分为4组:肺损伤组、MSCs治疗组、MSCs对照组和正常对照组.2 wk后观察肺组织结构、植入细胞的变化,同时检测支气管肺泡灌洗液中层黏连蛋白、透明质酸以及肺组织羟脯氨酸含量的变化.结果:MSCs治疗组大鼠肺组织中可见少量DAPI标记的细胞,其中部分细胞表达广谱细胞角蛋白,肺间质增生减轻;支气管肺泡灌洗液中层黏连蛋白、透明质酸及肺组织羟脯氨酸的含量在肺损伤组均有明显升高(P<0.01),而在MSCs治疗组均有所下降(P<0.01).结论:MSCs可在损伤的大鼠肺组织中分化为肺泡上皮细胞,降低支气管肺泡灌洗液中层黏连蛋白、透明质酸及肺组织羟脯氨酸的含量,减轻大鼠肺损伤及纤维化的形成. 相似文献
10.
Comparison of the postprandial release of peptide YY and proglucagon-derived peptides in the rat 总被引:4,自引:0,他引:4
Younes Anini Xiaomei Fu-Cheng Jean Claude Cuber Alain Kervran Jacques Chariot C. Rozé 《Pflügers Archiv : European journal of physiology》1999,438(3):299-306
Endocrine L-cells of the distal intestine synthesize both peptide YY (PYY) and proglucagon-derived peptides (PGDPs), whose
release has been reported to be either parallel or selective. Here we compare the release mechanisms of PYY, glucagon-like
peptide-1 (GLP-1), and oxyntomodulin-like immunoreactivity (OLI) in vivo. Anaesthetized rats were intraduodenally (ID) given
either a mixed semi-liquid meal or oleic acid, or they received oleic acid or short chain fatty acids (SCFA) intracolonically
(IC). The ID meal released the three peptides with a similar time-course (peak at 30 min); ID oleic acid produced a progressive
release of PYY and OLI, while GLP-1 release was less. IC oleic acid or SCFA released smaller (but significant) amounts of
PYY but no OLI or GLP-1. Hexamethonium inhibited most of the response to the ID meal and ID oleic acid, but did not change
the PYY response to IC oleic acid. N
G
-nitro-l-arginine methyl ester (l-NAME, a nitric oxide synthase inhibitor) inhibited meal-induced PYY release and left OLI and GLP-1 unaffected. BW10 (a gastrin-releasing
peptide antagonist) had no effect on the meal-induced release of either peptide. These results suggest a parallel initial
release of PYY, OLI and GLP-1 after the ID meal, or oleic acid, by an indirect mechanism triggered in the proximal bowel,
using nicotinic synapses, and involving nitric oxide release for PYY and an unknown mediator for PGDPs. For PYY there is a
later phase of peptide release, probably induced by direct contact between nutrients and colonic L-cells.
Received: 8 January 1999 / Received after revision: 25 March 1999 / Accepted: 26 April 1999 相似文献