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游离空肠段肠腺分泌规律及病理学变化 被引量:2
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作者 何发尧 王跃建 +4 位作者 马玲国 张剑利 唐隽 陈伟雄 曾勇 《中国耳鼻咽喉头颈外科》 北大核心 2005年第5期323-326,共4页
目的探讨游离空肠段肠腺分泌规律及其相应的病理学变化,为临床应用于气管重建提供依据。方法通过建立腹壁下去神经游离空肠的肠分泌动物实验模型,包括A组(无支架组)、B组(游离空肠联合镍钛合金内、外支架组)及C组(游离空肠联合镍钛合金... 目的探讨游离空肠段肠腺分泌规律及其相应的病理学变化,为临床应用于气管重建提供依据。方法通过建立腹壁下去神经游离空肠的肠分泌动物实验模型,包括A组(无支架组)、B组(游离空肠联合镍钛合金内、外支架组)及C组(游离空肠联合镍钛合金外支架组),对比其术后肠分泌量的变化以及相应的病理学变化。结果①A、B、C三组术后早期肠分泌量增高,1月后肠分泌量显著减少并趋于稳定;B组和C组均比A组的分泌量大(P<0.05),1月后逐渐接近A组;B、C两组对比肠分泌量无显著差异(P>0.05);②移植空肠上皮腺体萎缩,肠黏膜上皮层变薄,微绒毛大部分脱落,部分吸收细胞空泡变性和坏死,杯状细胞减少;其中以B组改变最明显。结论去外源神经犬空肠段随着肠腺萎缩,肠腺分泌逐渐减少,术后60天左右趋于低水平;推断游离空肠重建气管是可行的。 展开更多
关键词 游离空 分泌 病理学 外源神经 肠腺萎缩
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卞嵩京辨治慢性萎缩性胃炎肠上皮化生经验 被引量:11
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作者 杨强 祝其荣 卞嵩京 《上海中医药杂志》 2015年第10期20-21,共2页
总结整理卞嵩京治疗慢性萎缩性胃炎肠上皮化生的临床经验。认为其病因为中阳不足、痰凝血瘀,辨证分为中阳虚寒、中虚气滞、寒凝瘀阻及气阴两虚,治以温养中阳、活血止痛。并举验案1则。
关键词 慢性萎缩性胃炎化生 胃癌 胃脘痛 临证经验 卞嵩京
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Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer 被引量:40
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作者 ChuanZhang NobutakaYamada +3 位作者 Yun-LinWu Minwen TakeshiMatsuhisa NorioMatsukura 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第6期791-796,共6页
AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gast... AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and Hpylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pyloripositivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylorinegativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylon positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer. 展开更多
关键词 Helicobacter pylori Glandular atrophy Intestinal metaplasia Early gastric cancer
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