共查询到20条相似文献,搜索用时 62 毫秒
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《中国药房》2017,(36):5136-5139
目的:研究草木犀药材的生药学。方法:从原植物形态、性状特征、显微特征和药材浸提物的紫外光谱、药材粉末的红外光谱方面对草木犀进行定性鉴别。结果:草木犀药材根横切面可见辐射型维管束中有19束射线;茎横切面髓部占整个横切面的4/5;小叶片横切面主脉维管束正上方有栅栏组织通过;叶柄横切面呈心形,内有3个大小不等的维管束成三角形排列;叶表皮分布有细胞组成的腺毛和单细胞非腺毛;组织解离中叶可见草酸钙方晶的晶纤维,不定式气孔,叶柄有腺毛和非腺毛表面可见疣状突起,螺纹导管;提取物紫外光谱图、药材粉末二阶导数红外光谱图特征明显。结论:该研究所建标准可用于草木犀药材的生药学鉴别。 相似文献
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《沈阳药科大学学报》2015,(7):548-555
目的对东北银莲花属6种药材多被银莲花、黑水银莲花、反萼银莲花、阴地银莲花、毛果银莲花、细茎银莲花进行系统的生药学鉴定。方法采用性状、显微的方法对银莲花属6种植物进行了较全面的研究。结果通过性状、显微鉴别,最终得到结论,a.性状的主要区别为:根茎形状、颜色、断面质地、断面颜色及气味有明显不同;b.显微横切片的主要区别为:维管束个数及导管个数明显不同;c.显微粉末主要区别为:粉末颜色、表皮细胞颜色、导管种类及大小有明显区别。结论银莲花属6种植物的药材性状、显微特征有明显区别,为鉴别银莲花属植物,开发药源提供了参考。 相似文献
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Buruli Ulcer (BU) is a neglected, necrotizing skin disease, caused by M. ulcerans, that can leave patients with prominent scars and lifelong disability. M. ulcerans produces a diffusible lipid toxin, mycolactone, essential for bacterial virulence. Prevention is difficult as little is known about disease transmission and there is no vaccine. There have been several recent advances in the field. These include sequencing of the bacterial genome and of the giant plasmid responsible for mycolactone synthesis, better understanding of the bacterial lifecycle and of the mechanism of action of the toxin. This work has revealed a number of possible vaccine candidates, some of which are shared with other mycobacteria, e.g. M. tuberculosis, while other targets are unique to M. ulcerans. In this review, we discuss several M. ulcerans vaccine targets and vaccination methods, and outline some of the gaps in our understanding of the bacterium and the immune response against it. 相似文献
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胃溃疡与十二指肠溃疡是消化系统最常见的疾病.结合患者的病史和临床表现,正确选择药物是治疗的关键.临床药师在药物疗效、药物相互作用以及药物不良反应的认识方面具有自身的优势.本文通过报道临床药师参与1例胃十二指肠溃疡患者的诊疗过程,反映临床药师在合理用药及为患者提供药学服务方面发挥了重要作用. 相似文献
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Baron JH 《The Mount Sinai journal of medicine, New York》2000,67(1):58-62
Indigestion and heartburn have been described for thousands of years, but it was only in the 16th century that the disease peptic ulcer was established by autopsy. At first, only gastric ulcers were identified. In the 18th century, duodenal ulcers, most of which were fatal cases after perforation or hemorrhage, were seen. In the 19th century, when autopsy became a common, even routine, hospital procedure, uncomplicated acute and chronic ulcers were found and then correlated with symptoms. Thus, our current clinical understanding dates from the 1820s, by which time peptic ulcers were being reported in the U.S. It is unclear why gastric ulcers were not diagnosed at The Mount Sinai Hospital until 1873 and duodenal ulcers until 1885. However, after that time both conditions were diagnosed frequently, and they rapidly became common and were treated medically and surgically. 相似文献
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Baron JH 《The Mount Sinai journal of medicine, New York》2000,67(1):63-67
From the late 19th century, Mount Sinai gastroenterologists declared their scepticism of the efficacy of all recommended treatments of peptic ulcer, and looked forward to trials which could distinguish between sequence and consequence, between association and causation. The rationale of all the early studies was to reduce gastric acidity, but it soon became clear that any neutralization by single doses of antacids was brief and ineffective. Winkelstein s demonstration that patients with duodenal ulcer had higher acidities not only before and after meals but also through the night hours led him to introduce a new treatment, the alkalinized intragastric milk drip together with atropine. One of the earliest controlled clinical trials at Mount Sinai compared different antacid regimes and showed that pH values above 3.5 were achieved in only about half of the patients on the various drips. When the new anticholinergic drugs were developed in the 1950s, they were found to produce sustained hypoacidity and were tried as maintenance treatment, as an alternative to acid-lowering operations. The third Mount Sinai approach was to attack the machinery of the acid-producing cell itself by an inhibitor of the enzyme producing hydrogen ions. In 1939, this enzyme had been thought to be carbonic anhydrase, but when Janowitz and Hollander tested its inhibitor, acetazolamide, and showed marked but very brief acid inhibition, they concluded that its action was too brief to be therapeutically useful. The problem was to be solved decades later by H2 receptor blockers from Britain and H+K+ATPase inhibitors from Sweden. 相似文献
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