肾上腺皮质激素对心房钠尿肽基因表达的促进作用

给完整的及切除肾上腺的雌性 Wistar 大鼠分別注射地塞米松、去氧皮质酮或地塞米松加去氧皮质酮;冷酚法提取心房总 RNA,用α-~(32P)标记的大鼠心房肽 cDNA 探针与之杂交。完整大鼠接受地塞米松和切除肾上腺后接受地塞米松加去氧皮质酮的大鼠,心房肽基因转录产物增加2倍,其余组无显著变化。结果提示糖皮质激素可促进心房肽基因表达,但此作用依赖于盐皮质激素的同时存在,单纯盐皮质激素不能增强该基因的表达。     

兔边缘系统隔区呼吸相关神经元

本实验在42只家兔给与 Urethane 半量麻醉,在边缘系统隔区用玻璃微电极方法记录了60个自发的呼吸相关神经元单位放电:吸气型30个单位;呼气型16个单位;跨时相型14个单位。断双侧迷走神经,静脉注入尼克刹米后,呼吸相关神经元单位放电与呼吸节律变化具有伴随性,呈正相关。窒息可以诱发隔区神经元呼吸节律放电。延髓第四脑室局部注入2%Sod。pentothal 后,随呼吸节律抑制、隔区呼吸相关神经元单位放电立即消失。上述结果提示:到达边缘系统隔区的呼吸信息在自主功能及情绪活动的协调方面,可能被认为是有意义的。     

兔核移植胚胎起始发育的超微结构研究

对兔核移植胚胎起始发育的超微结构变化进行电镜观察,并与供体桑椹胚细胞,受体卵母细胞及同期正常受精胚胎的超微结构进行比较,“原核”期兔核移植胚胎的超微结构明显不同于供体桑椹胚细胞及受体卵母细胞的超微结构,而与同期正常受精胚胎相似,但有些核移植胚胎中皮质反应,及核仁和线粒体中出电子致密的网眼结构,与正常受精卵存在差别,分裂至２－细胞期时,与正常２－细胞胚超微结构更相似,结果提示,兔胚胎细胞核移植后,供     

低氧低二氧化碳对大鼠脑血流的调节作用

低氧下脑血流与急性高原病有关,许多研究已证明,低氧不适应者的ＣＢＦ明显高于低氧适应者,而高原世居者则低于海平正常值。低氧下低动脉血二氧化碳分压有对抗低氧扩血管及降低ＣＢＦ的作用。因此研究低氧下低ＰａＣＯ２对ＣＢＦ的调节作用对于研究急性高原病的防治及其机理分析具有重要意义。本项研究目的：（１）揭示低氧下低ＰａＣＯ２与ＣＢＦ之间的关系;（２）通过增加通气量使ＰａＣＯ２下降至合适水平,以保护脑血流维持在     

低浓度氢清除法测定大鼠局部脑血流量

利用氢清除法测量动物局部脑血流量已被广泛应用于研究中。本文采用低于爆炸范围下限的３％Ｈ２浓度,它可以与任何比例的氮氧气体安全混合,且可避免吸纯氢期间的短暂缺氧,更为严格地控制了实验条件,增加了安全和准确性。本工作对吸１００％Ｈ２和吸３％Ｈ２以及吸３％Ｈ２１－１．５ｍｉｎ和吸３％Ｈ２５ｍｉｎ测得脑血流量分析作了比较,结果表明短期低浓度氢清除法能较好地反映动物的局部脑血流量。     

辽宁蛙科一新种：无尾目

１９８６－１９８７年４月在辽宁省桓仁县采到２５只成蛙。其鉴别特征为,头宽大于头长;鼓膜约为眼径的１／２;背侧褶细而折曲;胫长于足;趾间全蹼,缺刻浅;雄性无声囊,无雄性线。此蛙与林蛙其它种均有明显区别,故定为新种,桓仁林蛙Ｒａｎａ ｈｕａｎｒｅｎｅｎｓｉｓ ｓｐ．ｎｏｖ．     

电刺激兔肾脏传入神经对血压,心率及加压素释放的影响

本工作以兔为实验对象,观察电刺激肾脏传入神经（ＡＲＮ）对血压、心率、颈交感神经放电、以及加压素（ＡＶＰ）合成和释放的影响,并对ＡＲＮ进入中枢的通路作了观察。结果显示,电刺激ＡＲＮ可以引起血压下降、心率减慢、颈交感神经放电抑制等反应,ＡＲＮ的兴奋还可使下丘脑的视上核、室旁核中的ＡＶＰ含量增加,垂体中ＡＶＰ含量下降,血浆ＡＶＰ水平升高。硝普钠的降压实验和静脉注射ＡＶＰ受体阻断剂ＡＶＰａ的实验均证实了Ａ     

Sequence,structure and function-based classification of the broadly conserved FAH superfamily reveals two distinct fumarylpyruvate hydrolase subfamilies

Fumarylacetoacetate hydrolase (FAH) superfamily proteins are found ubiquitously in microbial pathways involved in the catabolism of aromatic substances. Although extensive bioinformatic data on these proteins have been acquired, confusion caused by problems with the annotation of these proteins hinders research into determining their physiological functions. Here we classify 606 FAH superfamily proteins using a maximum likelihood (ML) phylogenetic tree, comparative gene-neighbourhood patterns and in vitro enzyme assays. The FAH superfamily proteins used for the analyses are divided into five distinct subfamilies, and two of them, FPH-A and FPH-B, contain the majority of the proteins of undefined function. These subfamilies include clusters designated FPH-I and FPH-II, respectively, which include two distinct types of fumarylpyruvate hydrolase (FPH), an enzyme involved in the final step of the gentisate pathway. We determined the crystal structures of these FPH enzymes at 2.0 Å resolutions and investigate the substrate binding mode by which these types of enzymes can accommodate fumarylpyruvate as a substrate. Consequentially, we identify the molecular signatures of the two types of FPH enzymes among the broadly conserved FAH superfamily proteins. Our studies allowed us to predict the relationship of unknown FAH superfamily proteins using their sequence information.     

土地流转背景下不同经营规模青田稻鱼共生系统的环境影响差异——基于碳足迹的实证研究

在快速工业化和城镇化的影响下,农业文化遗产的保护与管理正面临着适龄劳动力大量外流、土地抛荒、传统知识体系难以维持等诸多威胁与挑战。推动土地流转、进行适度规模经营,可在农业文化遗产的保护中产生积极作用。土地流转在给遗产地带来经济效益的同时,对当地生态环境产生的影响变化同样值得关注,但现有研究却少有涉及。本研究以全球重要农业文化遗产——浙江青田稻鱼共生系统为例,将不同经营规模的稻鱼共生系统分为小农户经营模式和规模化经营模式,运用生命周期法对两种模式的碳足迹进行核算。结果表明: 小农户经营模式和规模化经营模式的碳足迹分别为6510.80和5917.00 kg CO₂-eq·hm^-2,单位产值碳足迹分别为0.13和0.10 kg CO₂-eq·yuan^-1。与小农户经营模式相比,规模化经营模式温室气体排放更少,单位产值的环境影响更小。农户扩大经营规模后,当地温室气体排放减少了4097.20 kg CO₂-eq。农业生产过程中积累的CH₄在碳足迹中占比最大,农业生产资料中复合肥是仅次于CH₄的第二大温室气体排放来源。对于小农户经营模式,饲料中使用的玉米和小麦也对温室气体排放有重要的影响。因此,推动土地适度规模经营,有利于传统农业系统实现经济效益和环境效益的双赢,对于农业文化遗产保护具有重要作用。     

Enhanced Phase II Detoxification Contributes to Beneficial Effects of Dietary Restriction as Revealed by Multi-platform Metabolomics Studies

Dietary restriction (DR) has many beneficial effects, but the detailed metabolic mechanism remains largely unresolved. As diet is essentially related to metabolism, we investigated the metabolite profiles of urines from control and DR animals using NMR and LC/MS metabolomic approaches. Multivariate analysis presented distinctive metabolic profiles and marker signals from glucuronide and glycine conjugation pathways in the DR group. Broad profiling of the urine phase II metabolites with neutral loss scanning showed that levels of glucuronide and glycine conjugation metabolites were generally higher in the DR group. The up-regulation of phase II detoxification in the DR group was confirmed by mRNA and protein expression levels of uridinediphospho-glucuronosyltransferase and glycine-N-acyltransferase in actual liver tissues. Histopathology and serum biochemistry showed that DR was correlated with the beneficial effects of low levels of serum alanine transaminase and glycogen granules in liver. In addition, the Nuclear factor (erythroid-derived 2)-like 2 signaling pathway was shown to be up-regulated, providing a mechanistic clue regarding the enhanced phase II detoxification in liver tissue. Taken together, our metabolomic and biochemical studies provide a possible metabolic perspective for understanding the complex mechanism underlying the beneficial effects of DR.It has been known for more than 70 years that dietary restriction (DR)¹ can extend the life span and delay the onset of age-related diseases, based on an early rodent study showing such effects (1). However, not until the 1980s was DR recognized as a good model for studying the mechanism of or inhibitory measures for aging (2). So far, extensive studies employing model organisms such as yeasts, nematodes, fruit flies, and rodents have shown that DR has beneficial effects in most of the species studied (for a review, see Ref. 3). Most notably, a recent 20-year-long study showed that monkeys, the species closest to humans, also benefit from DR similarly (4). Although there has not been (or could not have been) a systematic study on the effects of DR on the human life span, several longitudinal studies strongly suggest that changes in dietary intake can affect the life span and/or disease-associated marker values greatly (5–7).This inverse correlation between dietary intake and long-term health strongly indicates that DR''s effects should involve metabolism, and that DR elicits the reorganization of metabolic pathways. It also seems quite natural that something we eat should affect the body''s metabolism. Despite this seemingly straightforward relationship between diet and metabolism, the mechanisms underlying the beneficial effects of DR are anything but simple. Intensive efforts, spanning decades, to understand the mechanisms of DR have identified several genes that might mediate the effects of DR, such as mTOR, IGF-1, AMPK, and SIRT1 (for a review, see Ref. 8). Still, most of them are involved in early nutrient-sensing steps, and specific metabolic pathways, especially those at the final steps actually responsible for the effects of DR, are largely unknown.This might be at least partially due to the fact that previous studies have focused mostly on genomic or proteomic changes induced by DR, instead of looking at changes in metabolism or metabolites directly. Metabolomics, which has gained much interest in recent years (9–11), might be a good alternative for addressing the mechanistic uncertainty of DR''s effects, with the direct profiling of metabolic changes elicited by environmental factors. In contrast to genomics or proteomics, which often employ DNA or proteins extracted from particular tissues, metabolomics studies mostly employ body fluids (i.e. urine or blood), which can reflect the metabolic status of multiple organs, enabling investigations at a more systemic level. In particular, urine has been used extensively to study the mechanism of external stimuli (i.e. drugs or toxic insults) at most major target organs, such as the lung, kidney, liver, or heart (12–18). Still, metabolomics studies of DR effects have been very limited. A few previous ones reported the changes in phenomenological urine metabolic markers with DR, without identification and/or validation of specific metabolic pathways reflected at the actual tissue or enzyme level (19, 20). Therefore, those studies fell short of providing a mechanistic perspective on DR''s effects. In addition, they employed either NMR or LC/MS approaches without validation across the two analytical platforms.Among the metabolic pathways that can directly affect the integrity of multiple organs, and hence long-term health, are phase II detoxification pathways (21). Typically, lipophilic endo/xenobiotics are metabolized first by a phase I system, such as cytochrome P450, which modifies the compounds so that they have hydrophilic functional groups for increased solubility. In many cases, though, these modifications might increase the reactivity of the compounds, leading to cellular damage. The phase II detoxification systems involve conjugation reactions that attach charged hydrophilic molecular moieties to reactive metabolites, thus facilitating the elimination of the harmful metabolites from body, ultimately reducing their toxicity (22). These systems are thus especially important in protecting cellular macromolecules, such as DNA and proteins, from reactive electrophilic or nucleophilic metabolites. The enzymes involved in these processes include glutathione-S-transferase (GST), sulfotransferase, glycine-N-acyltransferase (GLYAT), and uridinediphospho-glucuronosyltransferase (UGT), with the last enzyme being the most prevalent (23). The beneficial effects of phase II reactions have been particularly studied in relation to the mechanism of healthy dietary ingredients. It is well believed that many such foods can prevent cancers (hence the term “chemoprevention”) by inducing phase II detoxification systems (24–26). Although DR also substantially reduces the incidence of cancers, the exact mechanism remains elusive.Here, we employed multi-platform metabolomics to obtain metabolic perspectives on the beneficial effects of DR on rats. Our results about urine metabolomics markers suggest that DR enhances the phase II detoxification pathway, which was confirmed by means of conjugation metabolite profiling and changes in mRNA/protein expression levels of phase II enzymes in actual liver tissues. A possible molecular mechanism was also addressed through the exploration of Nuclear factor (erythroid-derived 2)-like 2 (Nrf-2) pathway activation upon DR. We believe the current study provides new metabolic insights into DR''s beneficial effects, as well as a workflow for studying DR''s effects from a metabolic perspective.