Renal growth after neonatal urinary tract infection

This study presents the result of 12–21 years' follow-up in a group of children with neonatal urinary tract infection (onset within 1 month after birth) in whom early renal growth retardation was noted without concomitant classical renal scarring. In all cases the neonatal infection was diagnosed and treated within a few days of onset and the patients were closely supervised thereafter. Renal length, parenchymal thickness and area were measured at urography. At first follow-up (22 children, mean age 4.1 years) a significant reduction of renal parenchymal thickness was noted. Long-term follow-up (18 patients, mean age 17 years) demonstrated a normalization of renal size in the entire group, although less complete in the subgroup with reflux. There were two major findings in the present study. Firstly, renal growth retardation was seen after neonatal infection, both with and without reflux. Secondly, normalization of renal size in previously small kidneys was demonstrated, suggesting that growth retardation can be a reversible phenomenon. The tendency for such normalization was slightly more marked in children without reflux. Reduction of parenchymal thickness without calyceal deformity, therefore, does not necessarily mean irreversible damage, and differentiation between permanent scarring and temporary growth retardation can thus only be made at later follow-up, possibly not until after puberty. The demonstration of renal growth retardation in spite of early diagnosis and treatment emphasizes the great vulnerability of the kidney in the newborn.     

Hypoxia effects on vascular endothelial growth factor derived epithelial cells of nasal polyps]

OBJECTIVE: To understand the role of nasal mucous epithelial cells to hypoxia in early stage of nasal polyps(NP) formation. METHODS: Epithelial cells of NP and inferior turbinate (IT) were cultured without serum under normal oxygen and hypoxia, and stimulus of inflammatory cytokines. Erythropoietin (EPO) was regarded as hypoxia mark, and expression of vascular endothelial growth factor(VEGF) mRNA and protein derived from epithelial cells were detected respectively by in situ hybridization and ELISA. RESULTS: 1. Under hypoxia, EPO mRNA was expressed intensely in epithelial cells from NP and IT, and there was no significant difference between both of them. This result suggested that EPO might be regarded as a hypoxic mark. 2. The ability of producing VEGF mRNA increased with cytokines stimulation, especially under hypoxia. Protein level of VEGF from epithelial cells of NP and IT increased with cytokines stimulation, especially in hypoxia and was time-dependent. CONCLUSION: Epithelial cells actively produce vast VEGF under hypoxia. The VEGF induced by hypoxia of the mucosa in middle meatus is of importance in the formation of nasal polyps(NP) in early stage, which may be the major cause of NP formation in middle meatus.     

Effects of galanin on insulin and glucagon secretion in the rat

Galanin-like immunoreactivity has been visualized in nerve fibers in the islets of Langerhans, suggesting an involvement of galanin in the neural regulation of islet function. In this study, we investigated the effects of galanin on basal and stimulated insulin and glucagon secretion by infusing the peptide at three different dose rates in rats. We also studied the direct effect of galanin on insulin secretion from freshly isolated rat islets. At 320 pmol/kg/min, but not at 20 or 80 pmol/kg/min, galanin lowered basal plasma insulin levels. In contrast, basal plasma glucagon levels were lowered by galanin already at 20 and 80 pmol/kg/min. Furthermore, galanin inhibited both glucose- and arginine-induced insulin release at all three dose levels, whereas arginine-induced glucagon release was not affected by galanin. Glucose-stimulated insulin secretion from isolated rat islets was dose-dependently suppressed by galanin (10^-6-10^-8M). Therefore, it is concluded that galanin in rats inhibits insulin secretion, both in vivo and in vitro, and that at lower dose levels, the peptide also inhibits basal glucagon release.     

仙草消毒液杀灭微生物效果与毒性的试验观察

仙草消毒液为含 3 0 %乙醇的植物消毒剂 ,其中包括五味子、细辛、丁香等成分 ,p H6.0 1。为了解其杀灭微生物效果及其毒性 ,进行了载体定量杀菌试验及毒性试验。结果 ,1∶ 1的水稀释液对金黄色葡萄球菌作用2分钟 ,1∶ 2的稀释液对金黄色葡萄球菌作用 8分钟 ,以其原液对白色念珠菌作用 2 min,平均杀灭率均大于99.90 %。小牛血清对其杀灭效果有影响 ,原液经 5 4℃存放 14天 ,杀菌效果无明显变化。以其原液对雌、雄小鼠经口 LD50 >5 0 0 0 mg/Kg,对大耳白兔一次眼、皮肤刺激试验平均积分指数为 0 ,微核试验阴性 ,蓄积毒性试验为弱蓄积毒性     

肾上腺素能β1受体亚型特异性抗体的制备及鉴定

【目的】制备和鉴定 β1受体亚型特异性抗体。【方法】人工合成 β1受体细胞膜外第二环 197 2 2 2位氨基酸序列作为抗原。连接钥孔冒贝血蓝蛋白 (KLH)增加抗原性后免疫兔获得抗血清。通过凝胶双扩散实验和ELISA法鉴定其效价 ;通过免疫荧光法及ELISA法鉴定其特异性 ;通过离体蛙心灌流实验鉴定其药理活性。【结果】该抗血清效价高 (分别为 1∶6 4和 1∶10 6)、特异性强 ,能和心肌 β1受体发生特异性结合 (1∶10 4 ～ 1∶10 5) ,为异丙肾上腺素的非竞争性拮抗剂。 (pD2 ′ =1 6 2 )。【结论】成功制备的 β1受体亚型特异性抗体可能成为进一步研究 β1受体分布、功能和定量的有力工具。     

微卫星改变与肺癌发生发展的关系

目的 :研究肺癌组织中第 3号染色体短臂 (3P)和第 9号染色体短臂 (9P)上微卫星标志物的改变与肺癌发生发展的关系。方法 :应用聚合酶链反应 (PCR)结合微卫星银染法检测 5 6例肺癌和 2 3例良性肺部病变 3P和 9P上的微卫星标志物的改变。结果 :5 6例肺癌组织标本中 3P上有微卫星改变 2 6例 ,检出率 46% ,9P上有微卫星改变的 2 3例 ,检出率为 41% ,5 6例肺癌组织中 ,3P和 9P上有微卫星改变的 3 9例 ,检出率 69 6% ,2 3例肺部良性疾病组织中均未出现微卫星标志物改变。肺癌组织标本中 3P上的微卫星改变与肺癌的分化程度有关 ,低分化肺癌的微卫星改变较高、中分化肺癌的微卫星改变明显增多 (P <0 .0 1)。而 9P上的微卫星改变与淋巴结转移有关 ,有淋巴结转移的肺癌组织标本上微卫星改变较不伴淋巴结转移的微卫星改变检出率明显增多 ,(P <0 .0 5 )。结论 :3P和 9P上的微卫星改变与肺癌发生、发展和转移密切相关 ,检测肺癌组织 3P和 9P上的微卫星改变对肺癌的早期诊断和判断有无淋巴结转移有一定的价值     

大鼠MMP-13重组腺病毒载体的构建

目的　构建大鼠MMP1 3重组腺病毒载体。方法　将MMP1 3cDNA目的片段插入腺病毒柯氏质粒中 ,再将此质粒与腺病毒DNA末端蛋白复合物共转染 2 93细胞 ,通过同源重组构建MMP1 3 重组腺病毒载体。结果　MMP1 3 重组腺病毒载体经PCR鉴定正确 ,包装纯化后 ,检测病毒滴度为 4× 1 0 9PFU/ml。结论　成功地构建了RatMMP1 3 重组腺病毒载体 ,为下一步行MMP 1 3转基因治疗低顺应性膀胱的研究提供了条件     

7例睾丸静脉和2例卵巢静脉变异的解剖学研究

目的：了解睾丸静脉和卵巢静脉的变异。方法：观测了73具（146侧）成人尸体（男58，女15）两种静脉的形态结构。结果：发现两种静脉有变异者7例，其中睾丸静脉5例，卵巢静脉2例，另外，作者还对变异与国内文献作了比较。结论：本研究为探讨睾丸静脉和卵巢静脉曲张发生原因及治疗等提供解剖学资料。     

放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.     

双侧自发性气胸伴左膈疝1例

患者,女,52岁,因突发呼吸困难5h入院,既往有肺结核病史20a,慢性支气管炎病史10a。X线表现:右肺外带异常透亮,并见压缩肺组织边缘,肺压缩约50%,压缩之肺组织上部见致密斑点影(见图1)。气管纵隔明显左移,左膈明显升高达左胸中部,经透视证实为左膈疝,疝入胸腔组织为胃(见胃泡)。左肺野上部透亮度明显增加,并见清晰光滑边缘,结合透视证实为左肺自发性气胸。双侧胸廓较对称,未见明显塌陷改变。X线诊断:右肺陈旧TB;双侧自发性气胸伴左膈疝形成。讨论:自发性气胸是指在无外伤和人为因素的情况下,肺组织及脏层胸膜突然破裂而引起的胸腔积气。自发…