The influence of alcohol-containing and alcohol-free beverages on lipid levels and lipid peroxides in serum of rats

It is an established fact that moderate consumption of alcoholic beverages leads to some positive biochemical changes in blood that are widely regarded as indicators of improved prevention of atherosclerosis. However, at present, there are different opinions regarding the biologically active compounds of alcoholic beverages that bring about these changes. This experiment was conducted on 60 male Wistar rats, which were divided into five groups, each of which contained 12 rats: four experimental groups (EG1, EG2, EG3, EG4) and one control group (CG). During 4 weeks, all groups of rats were fed basal diet (BD) supplemented with dry red wine (EG1), beer (EG2), lyophilized dry red wine (EG3), or lyophilized beer (EG4). The rats of the CG were fed BD only. The rats of EG1 and EG2 were fed BD supplemented daily with 2.0 mL of wine and 6.0 mL of beer, respectively. The rats of EG3 and EG4 were fed BD supplemented daily with lyophilized wine and lyophilized beer at a concentration corresponding to an intake of 2.0 mL of original wine and 6.0 mL of original beer, respectively. Before and after completion of the trial, a wide range of laboratory tests including lipids and lipid peroxides were performed. The results of this investigation reveal that both original and lyophilized wine and beer exercise statistically significant beneficial lipidemic and antioxidant effects by reducing total cholesterol (TC), low density lipoprotein cholesterol, triglycerides, and lipid peroxides (P < 0.05 for all) and by elevating the high density lipoprotein cholesterol:TC ratio. There were no statistically significant differences in the results between groups fed BD supplemented with original wine and beer versus groups fed BD supplemented with lyophilized wine and beer. Therefore, it can be concluded that the biologically active compound of these beverages is their dry matter containing inter alia polyphenols in relatively high concentrations.     

大鼠脑血管颈内动脉系肾上腺素能神经起源的观察

应用免疫组织化学技术,观察了30只Wistar大鼠脑血管颈内动脉系肾上腺素能神经的起始核团。正常组脑血管颈内动脉系均可见棕褐色的免疫反应阳性纤维。手术1组作一侧颈上神经节切除术,同侧大脑前动脉、大脑中动脉和大脑后动脉的阳性纤维较正常组减少约2／3,对侧同部位动脉的阳性纤维约减少1／3;手术Ⅱ组作双侧颈上神经节切除术,双侧大脑前动脉、大脑中动脉和大脑后动脉的阳性纤维基本消失。结果提示：脑血管一侧颈内动脉系的肾上腺素能神经纤维起源于双侧颈上神经节。讨论了交感神经对脑血管可能的作用。     

A Marked Increase in Free Copper Levels in the Plasma and Liver of LEC Rats: An Animal Model for Wilson Disease and Liver Cancer

Most of copper present in rat plasma and liver binds to caeruloplasmin and metallothionein, respectively, and is not redox active. However, free forms of copper including loosely bound forms to other molecules are redox active. We assessed the free copper in Long-Evans rats with a cinnamon-like coat color (LEC rats), an animal model of Wilson disease and liver cancer. Compared to those of control rats, the liver and plasma of LEC rats showed a marked elevation of free copper, especially at the stage of acute hepatitis, in parallel with an increase of total copper levels in the livers and a decrease of plasma caeruloplasmin (ferroxidase I) activity. At the onset of jaundice, the total copper levels, however, decreased in liver, but increased in plasma, while free copper levels in both liver and plasma remained higher. Free iron levels in both liver and plasma were also determined and did not change significantly, except for the case of plasma in jaundiced rats. The data are consistent with a proposal in which increased levels of redox active free copper in the liver of LEC rats catalyze Fenton-type reactions, producing a large flux of hydroxyl radicals that would play an important role in the observed liver dysfunction, leading to acute hepatitis, and, finally, hepatocarcinoma. This is the first demonstration that the free copper may participate in the pathophysiology of the LEC rats and Wilson disease.     

Nicotine Is More Efficient than Cotinine at Passing the Blood–Brain Barrier in Rats

1. Nicotine and its main metabolite, cotinine, were reported to have distinct behavioral activities in mammals.2. In this study, cotinine was synthesized without detectable nicotine contamination to compare the ability of nicotine and cotinine to pass the blood–brain barrier (BBB)in rats.3. The alkaloids were extracted from plasma and brain tissues by methanol, identified by thin-layer chromatography, and quantified by high-pressure liquid chromatography and radioimmunoassays.4. Consistently, the three methods showed that the passage of cotinine was time, route of administration, and dose dependent and that nicotine was more efficient than cotinine to pass the BBB.5. The results suggest that these alkaloids may have central activities that probably result from their actions at distinct molecular levels.     

磁共振波谱成像结合扩散加权成像在脑胶质瘤及脑转移瘤鉴别诊断中的意义

目的:评估磁共振波谱成像(Proton Magnetic Resonance Spectroscopy,1H-MRS)联合磁共振扩散加权成像(Diffusion Weighted Imaging,DWI)在鉴别脑胶质瘤及孤立的脑转移瘤中的作用。方法:应用3.0T磁共振扫描仪,对临床手术确诊及组织病理学诊断证实的49例脑肿瘤患者(35例多形性胶质母细胞瘤,14例脑转移瘤)进行常规磁共振成像、磁共振波谱成像及磁共振扩散加权成像,并并对获得的数据进一步测量瘤内及瘤周区的代谢比、N-乙酰天门冬氨酸(NAA)、胆碱(Cho)、肌酸(Cr)值以及表观弥散系数(ADC值),分析两肿瘤组之间不同参数的统计学差异。此外,我们研究了感兴趣区域(ROI)的大小对肿瘤区域的病变扩散性能潜在影响。结果:胶质母细胞瘤瘤周N-乙酰天门冬氨酸(NAA)、肌酸(Cr),胆碱(Cho)/Cr,Cho/NAA和r CBV显著高于颅内转移瘤(P0.05);ADC值在两肿瘤组之间无显著差异(P0.05)。结论:在瘤周区1H-MRS有助于鉴别胶质母细胞瘤与单发的脑转移瘤。在瘤内扩散性的定量特性依赖ROI大小的设置。     

精神疲劳状态下脑组织血氧饱和度的近红外光谱分析

目的:研究精神疲劳状态下脑组织血氧饱和度的变化规律。方法:从某军校随机抽取25名被试,采用模拟飞行任务负荷构建精神疲劳模型,采用NASA-TLX量表评价模型。实验全程使用近红外光谱技术对被试脑组织血氧饱和度进行实时监测;实验前后分别对被试的作业绩效水平进行评估。结果:任务后NASA-TLX量表评分明显高于任务前(P0.01);任务前后作业绩效发生变化,反应能力测试的正确率下降(P0.01),错误率上升(P0.01);任务负荷后脑组织血氧饱和度相对于静息状态升高(P0.05)。结论:精神疲劳状态会影响被试的作业绩效。疲劳后脑组织血氧饱和度水平受被试动机以及代偿机制的影响高于静息水平。     

早期介入微弹簧圈栓塞治疗脑动脉瘤破裂的疗效及预后分析

目的:研究分析早期介入微弹簧圈栓塞治疗脑动脉瘤破裂的疗效及预后。方法:选取我院2011年至2014年期间收治的脑动脉瘤破裂患者96例作为研究对象。根据数字法随机分成观察组及对照组各48例,观察组患者在入院3d之内实施微弹簧圈栓塞形式介入治疗,对照组治疗时间为入院3 d后。对比两组患者临床治疗疗效、并发症发生情况、以及术后6个月的改良Rankin量表(m RS)、改良型日常生活能力(MBI)评分。结果:观察组的栓塞效果显著好于对照组,差异有统计学意义(P0.05)。观察组术后6个月的m RS评分显著低于对照组,且MBI评分显著高于对照组,差异均有统计学意义(均P0.05)。观察组的并发症发生率均显著低于对照组,差异均有统计学意义(均P0.05)。结论:入院3d之内利用微弹簧圈栓塞对脑动脉瘤破裂实施早期介入治疗,具有较好的疗效及预后,值得临床重视。     

邻苯二甲酸二(2-乙基己基)酯对大鼠胎盘组织的影响

目的:探讨孕期不同剂量邻苯二甲酸二(2-乙基己基)酯(DEHP)暴露对大鼠胎盘组织形态学和超微结构的影响,以推断DEHP对胎盘结构和功能的损害。方法:健康雌性Wistar大鼠40只,随机分为4组,妊娠第11日起每日给予DEHP灌胃,剂量分别为:对照组(玉米油)、低剂量组(100 mg/kg)、中剂量组(500 mg/kg)和高剂量组(1000 mg/kg),妊娠第19日处死孕鼠,取胎盘组织分别做HE染色和电镜制片,观察各剂量组胎盘形态学及超微结构的变化。结果:各剂量组胎盘形态学和超微结构的变化与DEHP摄入量呈负相关,低剂量组胎盘无明显改变;中剂量组胎盘缩小,空泡化细胞增多,微观结构显示胞质内线粒体水肿;高剂量组胎盘迷路带血窦扩张淤血严重,滋养细胞变性、坏死。结论:DEHP可导致大鼠胎盘形态结构发生改变,这种病理改变是胎盘功能减退的形态学基础,可直接影响胚胎发育和妊娠结局。     

Estrogen and n-3 polyunsaturated fatty acid supplementation have a synergistic hypotriglyceridemic effect in ovariectomized rats

The n-3 polyunsaturated fatty acids (PUFAs), EPA and DHA, as well as estrogen have been shown to decrease circulating levels of triglyceride (TG), but their underlying mode of action is unclear. The purpose of this study was to determine the effects of n-3 PUFA consumption and estrogen injection on TG metabolism. Rats (n = 48) were fed a modified AIN-93G diet with 0, 1, or 2 % EPA + DHA relative to the total energy intake during 12 weeks. At 8 weeks, rats were ovariectomized (OVX), and after a 1-week recovery, rats were injected with either 17β-estradiol-3-benzoate (E₂) or corn oil for the last 3 weeks. The n-3 PUFA consumption and E₂ injection independently decreased the hepatic expressions of sterol regulatory element-binding protein 1, acetyl-CoA carboxylase 1, fatty acid synthase (FAS), and diacylglycerol acyltransferase 2 (DGAT2) (P < 0.05). There were interactions between n-3 PUFA consumption and E₂ injection on hepatic expression of FAS and DGAT2. In addition, n-3 PUFA consumption and E₂ injection up-regulated the expression of AMP-activated protein kinase (AMPK), phosphorylated AMPK, peroxisomal proliferator-activated receptor α, and carnitine palmitoyltransferase 1 in liver and skeletal muscle. E₂ injection increased the expression of estrogen receptor α and β in skeletal muscle and liver, but n-3 PUFA consumption increased the expression of both receptors only in skeletal muscle. The present study suggests that the hypotriglyceridemic effects of n-3 PUFA consumption and E₂ injection could be due to the down-regulation of hepatic TG synthesis and up-regulation of TG oxidation in liver and skeletal muscle in OVX rats.