梗阻性黄疸肝肾细胞内胆汁酸活度的变化

本实验运用离子选择性微电极技术直接测定了鼠胆道梗阻前后肝、肾细胞内的胆汁酸活度。结果表明，胆道梗阻２周，肝、肾细胞内胆汁酸活度明显升高，其中肝细胞内达５．４６ｍｍｏｌ／Ｌ，肾细胞内达０．３７ｍｍｏｌ／Ｌ，已达到或接近体外膜损害浓度，提示胆汁酸可能是梗阻性黄疸引起肝、肾细胞超微结构损害的因素之一。     

应用生物技术选育黑优粘系列新品种的研究

本文报道了糯稻黑糯14号(♀)和粘稻特优粘9号(♂)的杂交,并应用生物技术和通过多种现代测试仪器对后代植株的检测,已成功地选育出“黑优粘”系列新品种。这些新品种具有营养价值高和产量也较高的优点。     

生物芯片的应用

生物芯片的应用是将探针固定于芯片上 ,利用核酸链间的分子杂交 ,鉴定DNA和蛋白质的一种新技术。尽管生物芯片仅仅出现几年 ,但它带来的信息却蕴藏着生物学中结构与功能的内在联系 ,其应用具有十分巨大的潜力 ,它已在功能基因组研究、新药研究、物种改良和医学诊断、军事科学等方面提供或正在提供极有价值的信息 ,已成为科学家们手中的有力武器     

Study on the distribution of active centers in novel low Ti-loading MgCl2-supported Ziegler-Natta catalyst

Novel MgCl2-supported Ziegler-Natta (Z-N) catalysts prepared using a new one-pot ball milling method caneffectively control the amounts of Ti-loading in the catalysts. Complex GPC data on polypropylene synthesized by thesenovel catalysts were analyzed using the method of fitting the molecular weight distribution (MWD) curves with a multipleFlory-Schulz function. It was found that multiple active centers exist in these novel catalysts. Detailed study of the effects ofthe Ti-loadings in the catalysts on the distribution of the active centers showed that the Ti-loadings in the novelMgCl2-supported Z-N catalysts might affect the proportion of each type of active centers; and might be the main factorresponsible for the effect of the Ti-loadings on the microstructure, the molecular weight and molecular weight distributionwidth of the resultant polymer, the catalytic activity and polymerization kinetics.     

Post-exercise ingestion of different amounts of protein affects plasma insulin concentration in humans

Abstract

The synergistic stimulating effect of combined intake of carbohydrate and protein on plasma insulin concentration has been reported previously. However, it remains unclear whether the amount of protein ingested after exercise affects the concentrations of plasma insulin and amino acids. This study of trained men compared the effects of post-exercise co-ingestion of carbohydrate plus different amounts of whey protein hydrolysates (WPHs) with carbohydrate alone on (1) blood biochemical parameters of carbohydrate metabolism during the post-exercise phase, and (2) endurance performance. Eight trained men exercised continuously for 70 min. Immediately after exercise and 30, 60, 90, and 120 min later, the participants received supplements containing: (1) 17.5 g carbohydrate, (2) 3.0 g WPHs and 17.5 g carbohydrate (L-WPH), or (3) 8.0 g WPHs and 17.5 g carbohydrate (H-WPH). After a 2-h recovery period, the participants performed an endurance performance test. The concentrations of blood glucose were lower and plasma insulin significantly higher in the H-WPH trial compared with the carbohydrate trial. The concentrations of plasma amino acids were increased in a dose-dependent manner following ingestion of different amounts of WPHs with carbohydrate. Endurance performance was not significantly different between the three trials. Co-ingestion of carbohydrate and H-WPH was more effective than ingestion of carbohydrate alone for stimulating insulin secretion and increasing the availability of plasma amino acids. These results suggest that plasma concentrations of amino acids during the recovery period are determined by the amount of dietary protein ingested, and that it is necessary to increase the concentration of plasma amino acids above a certain level to stimulate insulin secretion.     

Acute taurine supplementation enhances thermoregulation and endurance cycling performance in the heat

Abstract

This study investigated the effects of oral taurine supplementation on cycling time to exhaustion at a fixed-intensity and thermoregulation in the heat. In a double-blind, randomised crossover design, 11 healthy males participated in a time to exhaustion test in the heat (35°C, 40% RH), cycling at the power output associated with ventilatory threshold, 2?h after ingesting: Taurine (50?mg?kg^?1) or placebo (3?mg?kg^?1?maltodextrin). Core and mean skin temperature, mean sweat rate, heart rate, rating of perceived exertion (RPE), thermal comfort and thermal sensation were measured during exercise and blood lactate concentration (B[La]) was measured after exercise. Taurine supplementation increased time to exhaustion by 10% (25.16 min vs. 22.43 min, p?=?0.040), end sweat rate by 12.7% (687?nL?min^?1 vs. 600?nL?min^?1, p?=?0.034) and decreased B[La] by 16.5% (5.75?mmol?L^?1 vs. 6.85?mmol?L^?1, p?=?0.033). Core temperature was lower in the final 10% of the time to exhaustion (38.5°C vs. 38.1°C, p?=?0.049). Taurine supplementation increased time to exhaustion and local sweating, while decreasing RPE and core temperature in the later stages of exercise, as well as reducing post-exercise B[La]. This study provides the evidence of taurine's role in thermoregulatory processes. These findings have implications for the short-term preparation strategies of individuals exercising in the heat. Based on these findings, a single dose of taurine 2?h prior to training or competition would provide an ergogenic and thermoregulatory effect.     

Urea production during prolonged swimming

Male interscholastic swimmers (n = 8) completed a 4572 m training swim in 62 ±1.1 min (x ± s.e.) with terminal heart rate and blood lactate of 152 ± 6 beats min^‐1 and 6.9±0.89 mM, respectively. Sweat rate (0.48±0.0951. h^‐1) was lower than similar intensity cycling (1.5±0.13 1. h^‐1) or running (1.1 ± 0.14 l.h^‐1). Post‐swim serum urea N (11.6±0.71 mM) was elevated (P<0.05) vs pre‐swim (4.6±0.39 mM). Post‐swim urine volume (860±75 ml 24 h^‐1) was reduced (P<0.07) and resulted in an elevated (P<0.05), but delayed (24–84 h), post‐exercise urea N excretion. Although the reduced urine and sweat production during the swim undoubtedly contributed to the elevated serum urea, there must be another explanation because together they could only account for 38% of the observed increase. On the basis of the magnitude of serum urea increase, it appears that the swim caused an increase in urea production (amino acid oxidation). The failure to observe larger increases in urinary urea during recovery indicates that either urea excretion following exercise continues for prolonged periods of time (>48 h) or another significant mode of nitrogen excretion exists.     

Optimization of insulin-mediated creatine retention during creatine feeding in humans

Abstract

The aim of this study was to determine whether creatine ingested in combination with relatively small quantities of essential amino acids, simple sugars, and protein would stimulate insulin release and augment whole-body creatine retention to the same extent as a large bolus of simple sugars. Seven young, healthy males underwent three randomized, 3-day experimental trials. Each day, 24-h urine collections were made, and on the second day participants received 5 g creatine + water (creatine trial), 5 g creatine + ～95 g dextrose (creatine + carbohydrate) or 5 g creatine + 14 g protein hydrolysate, 7 g leucine, 7 g phenylalanine, and 57 g dextrose (creatine + protein, amino acids, and carbohydrate) via naso-gastric tube at three equally spaced intervals. Blood samples were collected at predetermined intervals after the first and third naso-gastric bolus. After administration of the first and third bolus, serum insulin concentration was increased by 15 min (P < 0.05) in the creatine + carbohydrate and creatine + protein, amino acids, and carbohydrate trials compared with creatine alone, and plasma creatine increased more following creatine alone (15 min, P < 0.05) than in the creatine + carbohydrate and creatine + protein, amino acids, and carbohydrate trials. Urinary creatine excretion was greater with creatine alone (P < 0.05) than with creatine + carbohydrate and creatine + protein, amino acids, and carbohydrate. Administration of creatine + protein, amino acids, and carbohydrate can stimulate insulin release and augment whole-body creatine retention to the same extent as when larger quantities of simple sugars are ingested.     

补充不同剂量支链氨基酸对运动大鼠下丘脑5-羟色胺及其前体的影响

观察补充支链氨基酸(BCAA)后大鼠力竭游泳运动恢复期下丘脑细胞外液BCAA、游离色氨酸(f-Trp)和5-羟色胺(5-HT)的变化,分析补充BCAA是否能够提高大鼠的运动能力,比较补充BCAA的效果,探索补充BCAA的最佳剂量。方法:将32只大鼠随机分为对照组、小剂量补充组[1.25g/(kg·BW-1)]、中剂量补充组[2.5g/kg·BW-1)]和大剂量补充组[5g/(kg·BW-1)],每组8只。BCAA补充方案为:每天上午补充一次,每周6次(周日暂停),持续6周。6周后,在大鼠进行力竭游泳运动前一天下午取大鼠尾血测试血氨。采用毛细管电泳-激光诱导荧光法检测大鼠下丘脑细胞外液BCAA、f-Trp和5-HT的浓度。结论:血氨随着BCAA补充剂量的增加而升高,小剂量补充BCAA对机体血氨的生成无影响;补充BCAA能提高大鼠力竭游泳运动能力,但并不随BCAA补充剂量的增加而提高;补充BCAA可能提高了血浆BCAA与f-Trp竞争通过血脑屏障的能力且具有推迟和减少脑5-HT生成的作用;小剂量[1.25g/(kg·BW-1)]补充BCAA对提高大鼠运动能力效果最佳。     

Long-term high fructose and saturated fat diet affects plasma fatty acid profile in rats

As the consumption of fructose and saturated fatty acids (FAs) has greatly increased in western diets and is linked with an increased risk of metabolic syndrome, the aim of this study was to investigate the effects of a moderate (10 weeks) and a prolonged (30 weeks) high fructose and saturated fatty acid (HFS) diet on plasma FA composition in rats. The effects of a few weeks of HFS diet had already been described, but in this paper we tried to establish whether these effects persist or if they are modified after 10 or 30 weeks. We hypothesized that the plasma FA profile would be altered between 10 and 30 weeks of the HFS diet. Rats fed with either the HFS or a standard diet were tested after 10 weeks and again after 30 weeks. After 10 weeks of feeding, HFS-fed rats developed the metabolic syndrome, as manifested by an increase in fasting insulinemia, total cholesterol and triglyceride levels, as well as by impaired glucose tolerance. Furthermore, the plasma FA profile of the HFS group showed higher proportions of monounsaturated FAs like palmitoleic acid [16:1(n-7)] and oleic acid [18:1(n-9)], whereas the proportions of some polyunsaturated n-6 FAs, such as linoleic acid [18:2(n-6)] and arachidonic acid [20:4(n-6)], were lower than those in the control group. After 30 weeks of the HFS diet, we observed changes mainly in the levels of 16:1(n-7) (decreased) and 20:4(n-6) (increased). Together, our results suggest that an HFS diet could lead to an adaptive response of the plasma FA profile over time, in association with the development of the metabolic syndrome.