神经节苷脂GM1 对缺血缺氧后谷氨酸及其转运体神经元的作用

目的: 探讨神经节苷脂GM1 对新生大鼠缺氧缺血性脑病保护作用及其可能的机理。方法: 通过建立新生鼠缺氧缺血性脑病动物模型, 应用免疫组化方法, 观察缺血缺氧后不同时期脑组织中谷氨酸及其转运体阳性神经元的动态变化, 以及GM1 对其的影响。结果: 缺血缺氧后6 h 、1 、3 d 大脑皮层和纹状体中谷氨酸阳性神经元明显减少, 而谷氨酸转运体阳性神经元有所增加,GM1 组脑组织损伤明显减轻, 谷氨酸神经元及谷氨酸转运体神经元较单纯缺氧缺血组明显增多。结论: 神经节苷脂GM1 对谷氨酸神经元具有保护作用, 可能是通过部分提高谷氨酸转运体的表达而发挥作用。     

Early Postnatal Exposure to a Low Dose of Nanoparticulate Silver Induces Alterations in Glutamate Transporters in Brain of Immature Rats

Due to strong antimicrobial properties, silver nanoparticles (AgNPs) are used in a wide range of medical and consumer products, including those dedicated for infants and children. While AgNPs are known to exert neurotoxic effects, current knowledge concerning their impact on the developing brain is scarce. During investigations of mechanisms of neurotoxicity in immature rats, we studied the influence of AgNPs on glutamate transporter systems which are involved in regulation of extracellular concentration of glutamate, an excitotoxic amino acid, and compared it with positive control—Ag citrate. We identified significant deposition of AgNPs in brain tissue of exposed rats over the post-exposure time. Ultrastructural alterations in endoplasmic reticulum (ER) and Golgi complexes were observed in neurons of AgNP-exposed rats, which are characteristics of ER stress. These changes presumably underlie substantial long-lasting downregulation of neuronal glutamate transporter EAAC1, which was noted in AgNP-exposed rats. Conversely, the expression of astroglial glutamate transporters GLT-1 and GLAST was not affected by exposure to AgNPs, but the activity of the transporters was diminished. These results indicate that even low doses of AgNPs administered during an early stage of life create a substantial risk for health of immature organisms. Hence, the safety of AgNP-containing products for infants and children should be carefully considered.     

Spinal Glutamate Transporters Are Involved in the Development of Electroacupuncture Tolerance

Background: Electroacupuncture (EA) tolerance is a gradual decline in EA antinociception because of its repeated or prolonged use. This study aims to explore the role of spinal glutamate transporters (GTs) in EA tolerance (EAT). Methods: Rats were treated with EA once per day for eight consecutive days, and their L4-5 spinal cords were collected at days 0, 2, 4, 6 and 8. The levels of three spinal GTs and their mRNAs were detected with Western blot and pPCR, respectively. Then, riluzole, a positive GT regulator, was administered intrathecally in order to observe its effect on EA analgesia after repeated EA. Results: The expression levels of the spinal GTs increased at days 2 and 4, and gradually decreased as the times of EA increased. At day 8, no difference was observed in the spinal GTs between the sham treatment and the EA treatment. Intrathecal administration of riluzole dose-dependently attenuated the decreased EA analgesia. Conclusion: These results indicated the participation of the spinal GTs in EAT.     

EAAC1 Gene Deletion Increases Neuronal Death and Blood Brain Barrier Disruption after Transient Cerebral Ischemia in Female Mice

EAAC1 is important in modulating brain ischemic tolerance. Mice lacking EAAC1 exhibit increased susceptibility to neuronal oxidative stress in mice after transient cerebral ischemia. EAAC1 was first described as a glutamate transporter but later recognized to also function as a cysteine transporter in neurons. EAAC1-mediated transport of cysteine into neurons contributes to neuronal antioxidant function by providing cysteine substrates for glutathione synthesis. Here we evaluated the effects of EAAC1 gene deletion on hippocampal blood vessel disorganization after transient cerebral ischemia. EAAC1^−/− female mice subjected to transient cerebral ischemia by common carotid artery occlusion for 30 min exhibited twice as much hippocampal neuronal death compared to wild-type female mice as well as increased reduction of neuronal glutathione, blood–brain barrier (BBB) disruption and vessel disorganization. Pre-treatment of N-acetyl cysteine, a membrane-permeant cysteine prodrug, increased basal glutathione levels in the EAAC1^−/− female mice and reduced ischemic neuronal death, BBB disruption and vessel disorganization. These findings suggest that cysteine uptake by EAAC1 is important for neuronal antioxidant function under ischemic conditions.     

Inhibition of GTRAP3-18 May Increase Neuroprotective Glutathione (GSH) Synthesis

Glutathione (GSH) is a tripeptide consisting of glutamate, cysteine, and glycine; it has a variety of functions in the central nervous system. Brain GSH depletion is considered a preclinical sign in age-related neurodegenerative diseases, and it promotes the subsequent processes toward neurotoxicity. A neuroprotective mechanism accomplished by increasing GSH synthesis could be a promising approach in the treatment of neurodegenerative diseases. In neurons, cysteine is the rate-limiting substrate for GSH synthesis. Excitatory amino acid carrier 1 (EAAC1) is a neuronal cysteine/glutamate transporter in the brain. EAAC1 translocation to the plasma membrane promotes cysteine uptake, leading to GSH synthesis, while being negatively regulated by glutamate transport associated protein 3-18 (GTRAP3-18). Our recent studies have suggested GTRAP3-18 as an inhibitory factor for neuronal GSH synthesis. Inhibiting GTRAP3-18 function is an endogenous mechanism to increase neuron-specific GSH synthesis in the brain. This review gives an overview of EAAC1-mediated GSH synthesis, and its regulatory mechanisms by GTRAP3-18 in the brain, and a potential approach against neurodegeneration.     

音频编解码技术及应用

首先分析了在各个不同的历史阶段为满足不同的需求而提出的各种音频编解码器,讨论了最常见编解码器的特征和性能。然后考虑了它们对当前和未来移动通信需求的适应性,比较了各种音频编解码器的性能。最后给出了一些音频编解码器在移动通信系统中的应用。     

紫茎泽兰同时制备活性炭及高热值燃气实验研究

以紫茎泽兰为原料,通过物理活化同时制得活性炭和高热值燃气。考察了活化温度、时间、CO2流量对多孔碳产品吸附性能和得率的影响。通过响应曲面法得到实验优化工艺条件:活化温度980℃,活化时间130min,CO2流量400mL/min,所制得活性炭碘吸附值和得率分别为1002mg/g,15.79%。制得的多孔碳BET比表面积、孔容和平均孔径分别为1076m2/g、0.63mL/g、2.36nm。在此优化条件下得到高热值燃气,燃气热值达11542.32kJ/m3。     

Impaired Glutathione Synthesis in Neurodegeneration

Glutathione (GSH) was discovered in yeast cells in 1888. Studies of GSH in mammalian cells before the 1980s focused exclusively on its function for the detoxication of xenobiotics or for drug metabolism in the liver, in which GSH is present at its highest concentration in the body. Increasing evidence has demonstrated other important roles of GSH in the brain, not only for the detoxication of xenobiotics but also for antioxidant defense and the regulation of intracellular redox homeostasis. GSH also regulates cell signaling, protein function, gene expression, and cell differentiation/proliferation in the brain. Clinically, inborn errors in GSH-related enzymes are very rare, but disorders of GSH metabolism are common in major neurodegenerative diseases showing GSH depletion and increased levels of oxidative stress in the brain. GSH depletion would precipitate oxidative damage in the brain, leading to neurodegenerative diseases. This review focuses on the significance of GSH function, the synthesis of GSH and its metabolism, and clinical disorders of GSH metabolism. A potential approach to increase brain GSH levels against neurodegeneration is also discussed.     

低码率音频编码技术综述

介绍了当今主流低码率音频编码标准及其关键技术,包括EAAC 及其SBR技术,PS技术,AMR-WB 及TCX技术,G.729.1及嵌入式分层编码技术.