Down-regulation of inducible nitric oxide synthase (iNOS) in rat with congenital hydronephrosis

BACKGROUND: Most of our knowledge concerning obstructive uropathy has been derived mainly from surgically manipulated animal models, and the pathogenesis of congenital obstructive hydronephrosis is not fully elucidated. Nitric oxide (NO) acts as an important biological modulator with diverse physiological functions, which can be either toxic or protective depending on the situation. NO is synthesized from l-arginine by nitric oxide synthase, and in the kidney iNOS is expressed spontaneously. The aim of our study is to investigate the expression of iNOS protein and its relationship with tubulointerstitial fibrosis and tubular cell apoptosis in congenital hydronephrosis. METHODS: We conducted histological studies on 18 kidneys of six-week-old-rats from an inbred colony of congenital hydronephrosis with reference to the histological grading of the affected kidney, tubulointerstitial fibrosis, renal tubular atrophy, and tubular cell apoptosis. Renal transforming growth factor-beta1 (TGF-beta1) level was determined by a sandwich ELISA assay and the expression of iNOS was analyzed by western blotting. RESULTS: Most of the hydronephrotic kidneys were markedly enlarged with dilatation of the collecting system, parenchymal thinning, tubular atrophy, interstitial infiltration and fibrosis. Renal TGF-beta1 level was higher in hydronephrotic kidneys than normal control kidneys (364.81 +/- 52.60 vs. 221.19 +/- 22.53 pg/mg protein, P < 0.05). Tubular apoptotic score in hydronephrotic kidneys was also significantly higher than in the normal control kidneys (1.97 +/- 0.42 vs. 0.14 +/- 0.02/HPF, P < 0.01). The expression of iNOS protein was lower in the affected kidneys compared with the normal control kidneys (8.79 +/- 0.78 vs. 14.00 +/- 0.83 arbitrary unit, P < 0.01). There was a negative correlation between iNOS expression and histological grading in congenital hydronephrosis. The iNOS expression also correlated negatively with renal interstitial fibrosis, TGF-beta1 level and tubular cell apoptosis. CONCLUSION: Our study confirmed the down-regulation of iNOS expression in affected kidneys from rats with congenital hydronephrosis, in which the cytoprotective effect of NO may be lost or weakened.     

钠摄入量对心力衰竭大鼠心脏肾素-血管紧张素系统与心钠素的影响

目的　观察钠摄入量对心力衰竭大鼠心脏局部肾素-血管紧张素系统与心钠素的影响 .方法　经动 -静脉分流术造成大鼠充血性心衰模型 ,分为心衰组、心衰限钠组、心衰补钠组 ,假手术大鼠为对照组 ,用放射免疫分析法和原位杂交技术分别测定各组血浆和心肌血管紧张素 、心钠素含量及心肌血管紧张素原 m RNA表达水平 (吸光度 A值 ) ,同时检测心功能 .结果　心衰限钠组心房和心室血管紧张素 含量(2 0 .1± 4 .5 )和 (2 7.3± 5 .9) ng· g- 1、血管紧张素原 m RNA表达 (6 .4± 1.2 )和 (12 .6± 2 .3)显著高于心衰组 (17.5± 3.6 )和 (2 0 .1± 3.7) ng· g- 1 ,(6 .2± 1.9)和 (8.6± 1.7) (P<0 .0 5 ,P<0 .0 1) ,心室心钠素 (42 3± 6 8) ng· g- 1 也显著高于心衰组 (337± 86 ) ng· g- 1 (P<0 .0 5 ) ,心房心钠素 (6 7± 19)μg· g- 1显著低于心衰组 (85± 15 ) μg· g- 1 (P<0 .0 5 ) ;心衰补钠组心房和心室血管紧张素原 m RNA表达水平、心室血管紧张素 和心钠素与心衰组无显著差别 ,心房血管紧张素 与对照组无显著差别 ,心房心钠素 (10 1± 17) μg· g- 1 显著高于心衰组 (P<0 .0 1) .结论　心衰时不同钠摄入量可通过改变心脏局部肾素 -血管紧张素系统与心钠素的平衡状态在心衰发展进程中发挥作用     

巨细胞病毒肝炎患儿血清细胞因子水平测定及其临床意义

目的　研究巨细胞病毒 (CMV)肝炎患儿血清干扰素 α(IFN α)、白细胞介素 8(IL 8)和肿瘤坏死因子 α(TNF α)水平的变化及其临床意义。方法　应用ELISA法检测 35例CMV肝炎患儿血清中上述三种细胞因子的含量 ,并对其两两之间进行了相关性分析。结果　CMV肝炎组患儿IFN α、IL 8、TNF α的含量分别为 (770 .3± 2 0 5 .4 )ng/L、(41.9± 2 2 .5 )ng/L和 (10 33.2± 388.5 )ng/L ,非常显著高于正常对照组 (P <0 .0 1)。相关性研究发现IFN α与TNF α呈显著正相关 (r =0 .35 6 ,P <0 .0 5 )。结论　血清细胞因子明显增高与CMV肝炎的病理变化和病损程度有着密切的联系     

Naturally occuring antibodies against nerve growth factor in human and rabbit sera: comparison between control and herpes simplex virus-infected patients

Antibodies against nerve growth factor (NGF) in sera were detected by enzyme-linked immunosorbent assays (ELISA), by their isolation after passage of sera through NGF immunoadsorbent columns and by their specificity to bind and immunoprecipitate mouse NGF as well as to stain by immunohistochemical methods cellular sites of NGF synthesis. Increased levels of anti-NGF antibodies were found in sera of herpes simplex virus (HSV)-infected patients but not in HSV-inoculated rabbits. As HSV latency is known to be promoted by NGF in vitro, these results may suggest that anti-NGF antibodies modulate the cytokine function of NGF and thus might play a role in HSV infection. The biological function of circulating antibodies against NGF, in general, is now open to future investigation.     

Cholesterol-based personal risk assessment in coronary heart disease

Using data from the National Health and Nutrition Examination Survey (NHANES II) 1976-1980, we demonstrate how cross-sectional total serum cholesterol surveillance data can be used by an individual to assess current and future personal cholesterol risk status. We propose statistical models, based on a person's current measured cholesterol level and the relationship between cross-sectional age and cholesterol percentile estimates, that will allow prediction of future cholesterol levels or the age at which specified cholesterol risk levels will be reached if no cholesterol-altering intervention is taken. These models incorporate the observed variation in the NHANES II data and expected intraperson biological variation and intralaboratory analytical variation. We illustrate the adequacy of the models using data from the longitudinal Framingham Study.     

基于虚拟仪器技术的高频电刀波峰因子检测与验证

提出了一种有效易行的高频电刀波峰因子检测系统的软、硬件设计方案。利用电磁感应原理接收电刀输出波形,由普通的数字示波器完成数据采集与数字化,基于虚拟仪器技术的PC端软件根据数据计算波峰因子。通过对高频电刀波峰因子的检测,最终验证波峰因子对电刀性能以及临床使用效果的重要性。     

牙根发育不良疾病的研究进展

牙根发育不良疾病是牙齿根部生理性发育出现障碍的疾病。其发病率为1%~10%,乳、恒牙列均可发生,其结果可导致牙根缺如或短根,严重者可造成牙齿过早脱落。国外学者将该疾病统称为短根异常疾病。其发病因素有遗传性疾病、全身性疾病、外源性因素和医源性因素等。     

环缩酚肽抑制视网膜表达VEGF及PECAM基因和血管增生

[目的]观察两种环缩酚肽衍生物(Hep-A和Hep-B)对氧诱导的小鼠视网膜表达血管内皮生长因子(VEGF)和细胞黏附分子(PECAM;ICAM-1;VCAM-1)基因的影响及血管增生的变化.[方法]建立氧诱导的血管增殖性视网膜病变模型,12 d开始给小鼠皮下注安慰剂(第1组,n=7)、Hep-A 10 mg/kg(第2组,n=6)或者Hep-B 10 mg/kg(第3组,n=6),每天两次.5 d后取出左侧眼,分离视网膜并抽提RNA,用荧光定量PCR测出上述基因含量,并分别求出每个靶基因与标准基因S16含量的比率;右眼经心脏荧光素灌注后取眼球做视网膜平铺片,用图像分析软件定量计算视网膜新生血管的面积.[结果]视网膜中VEGF/S16的mRNA比率为:第1组(0.554±0.050),第2组(0.355±0.037),第3组(0.287±0.051);PECAM/S16为:第1组(2.050±0.249),第2组(1.228±0.153),第3组(1.027±0.210).经ANOVA分析,第2组和第3组分别与第1组比较,视网膜中VEGF基因表达分别减少36%和48.2%(P=0.001);PECAM基因表达分别减少40.1%(P＜0.05)和49.9%(P＜0.01);而VCAM-1和ICAM-1表达无明显差异.视网膜平片检测视网膜新生血管面积:第1组为(1.06±0.03)mm2/眼,第2组为(0.17±0.01)mm2/眼,第3组为(0.11±0.01)mm2/眼;经ANOVA分析,第2组和第3组分别与第1组比较,视网膜新生血管的面积明显减少(P＜0.001).[结论]两种环缩酚肽衍生物均抑制氧诱导的小鼠视网膜表达VEGF和PECAM基因,并抑制其形成视网膜新生血管.     

胰岛素样生长因子1对新生大鼠缺氧缺血性脑损伤保护机制的研究

目的　建立单侧缺氧缺血性脑损伤 (HIBD)动物模型 ,研究胰岛素样生长因子 1(IGF 1)对HIBD的影响和可能机制。　方法　选择健康 7日龄Wistar大鼠 12 0只 ,建立HIBD模型 ,随机分成假手术组、HIBD组、HIBD后 0 .2mg/kg人基因重组IGF 1干预组 (RH IGF 1组 )、0 .0 6 6mg/kg人基因重组IGF 1干预组 (SRH IGF 1组 )及盐水对照组 (对照组 )。各组按观察时段进一步分为 2 4、4 8、72h组 ,每组 8只。各组于规定时刻观测脑形态学改变、谷氨酸 (Glu)含量、凋亡细胞计数、Bcl 2蛋白表达。　结果　 (1)HIBD 4 8h组Glu(116 2 .2± 10 8.1)mg/kg ,较假手术组(75 0 .9± 5 3.4 )mg/kg明显升高 (P <0 .0 5 ) ;HIBD组凋亡细胞计数 [2 4h :(7.6± 1.9) % ,4 8h(12 .6±1.2 ) % ,72h :(13.8± 0 .9) % ],较假手术组 [2 4h(2 .0± 0 .2 ) % ,4 8h(2 .0± 0 .3) % ,72h(2 .0±0 .2 ) % ]明显增加 (P均 <0 .0 5 )。 (2 )与对照组相比 ,RH IGF 1组脑组织病变减轻 ;干预 4 8h组Glu[SRH IGF 1组 (781.4± 5 4 .2 )mg/kg ,RH IGF 1组 (74 0 .5± 4 6 .6 )mg/kg],较对照组 (112 6 .6± 4 8.0 )mg/kg明显降低 (P均 <0 .0 5 ) ;RH IGF 1组凋亡细胞计数 [2 4h :(3.6± 0 .9) % ,4 8h(8.2± 2 .2 ) % ,72h(9.4± 1.4 ) % ],较对