An amino-acid taste receptor

The sense of taste provides animals with valuable information about the nature and quality of food. Mammals can recognize and respond to a diverse repertoire of chemical entities, including sugars, salts, acids and a wide range of toxic substances. Several amino acids taste sweet or delicious (umami) to humans, and are attractive to rodents and other animals. This is noteworthy because L-amino acids function as the building blocks of proteins, as biosynthetic precursors of many biologically relevant small molecules, and as metabolic fuel. Thus, having a taste pathway dedicated to their detection probably had significant evolutionary implications. Here we identify and characterize a mammalian amino-acid taste receptor. This receptor, T1R1+3, is a heteromer of the taste-specific T1R1 and T1R3 G-protein-coupled receptors. We demonstrate that T1R1 and T1R3 combine to function as a broadly tuned L-amino-acid sensor responding to most of the 20 standard amino acids, but not to their D-enantiomers or other compounds. We also show that sequence differences in T1R receptors within and between species (human and mouse) can significantly influence the selectivity and specificity of taste responses.     

一种烯丙位氧化方法的改进

以N-羟基-琥珀酰亚胺为促进剂,铬酐为氧化剂,在含水丙酮体系中对去氢表雄酮进行烯丙位氧化,合成了7-氧代-去氢表雄酮。降低了铬酐的用量,提高了反应得率。该方法也可以应用于其他△5-甾体化合物的烯丙位氧化中。     

An amino-acid substitution involved in phenylketonuria is in linkage disequilibrium with DNA haplotype 2

Phenylketonuria (PKU) is an autosomal recessive human genetic disorder caused by a deficiency of hepatic phenylalanine hydroxylase (PAH, phenylalanine 4-monooxygenase, EC 1.14.16.1). PKU is a common inborn error of amino-acid metabolism in caucasian populations and approximately 1 in 50 individuals are carriers of a PKU allele. To define the molecular basis of PKU, we characterized twelve restriction fragment-length polymorphism (RFLP) haplotypes of the PAH locus in the northern European population and observed that 90% of the PKU alleles in this population are confined to four common RFLP haplotypes. We have recently reported a splicing mutation in the PAH gene that is associated with RFLP haplotype 3 which is present at about 40% of mutant alleles. We now report the molecular lesion associated with the RFLP haplotype 2 mutant allele. This defect is caused by a C-to-T transition in exon 12 resulting in an amino-acid substitution (Arg to Trp) at residue 408 of PAH. Direct hybridization analysis of the point mutation using a specific oligonucleotide probe demonstrated that this mutation is also in linkage disequilibrium with RFLP haplotype 2 alleles that make up about 20% of mutant PAH genes.     

一种用于FMCW雷达系统的中频信号滤波器

调频连续波(FMCW)雷达是近年来在汽车主动防撞领域新兴的一种测距传感器,该雷达系统的中频信号处理中,滤波器是最关键的部分之一。基于对干扰杂波的分析,文章设计并实现了一种用于FMCW雷达系统的中频信号滤波器,该滤波器包含高通与低通模拟滤波单元及基于DSP的FIR数字滤波单元。仿真图形与实验结果表明,所设计的滤波器能有效完成对调制泄漏信号、高频杂波信号及离散杂波信号的滤除,有助于提高雷达系统测距及测速的准确性。     

Potassium conductances in hippocampal neurons blocked by excitatory amino-acid transmitters

Excitatory amino acids mediate fast synaptic transmission in the central nervous system through the activation of at least three distinct ionotropic receptors: N-methyl-D-aspartate (NMDA), the alpha-amino-3-hydroxy-5-methyl-isoxasole-4-propionate (AMPA)/quisqualate (QUIS) and the kainate subtypes (for reviews, see refs 1, 2). They also activate the additional QUIS 'metabotropic' receptor (sensitive to trans-1-amino-cyclopentyl-1,3-dicarboxylate, ACPD) linked to inositol phospholipid metabolism. We have used hippocampal slice cultures to study the electrophysiological consequences of the metabotropic response. We find that activation of an ACPD-sensitive QUIS receptor produces a 'slow' excitation of CA3 pyramidal cells, resulting from depression of a Ca2(+)-dependent K+ current and a voltage-gated K+ current. Combined voltage-clamp and microfluorometric recordings show that, although these receptors can trigger an increase in intracellular Ca2+ concentration, suppression of K+ currents is independent of changes in intracellular Ca2+. These effects closely resemble those induced by activating muscarinic acetylcholine receptors in the same neurons and suggest that excitatory amino acids not only act as fast ionotropic transmitters but also as slow neuromodulatory transmitters.     

Protein evolution: causes of trends in amino-acid gain and loss

Understanding how proteins evolve is important for determining the molecular basis of adaptation, for inferring phylogenies and for engineering novel proteins. It has been suggested that some amino acids were incorporated into the genetic code more recently than others and, after comparing pairs of closely related genomes, Jordan et al. report that 'recent' amino acids are becoming more common. They argue that this process has been going on since the genetic code first evolved to encompass all 20 amino acids. Here we provide evidence that the patterns observed conform with standard, nearly neutral theoretical expectations and require no new explanation. This reinforces the need for caution in the interpretation of results derived from closely related taxa.     

Single amino-acid changes in HIV envelope affect viral tropism and receptor binding

Infection by the human immunodeficiency virus (HIV) is initiated by the binding of its extracellular envelope glycoprotein, gp120, to the CD4 antigen on target cells. To map the residues of the HIV-1 glycoprotein that are critical for binding and to analyse the effects of binding on viral infectivity, we created 15 mutations in a region of gp120 that is important for binding to CD4 (refs 4,5). We find that substitution of a single amino acid (tryptophan at position 432) can abrogate CD4 binding and that virus carrying this mutation is non-infectious. By contrast, other amino-acid changes in the same region do not affect CD4 binding but restrict viral tropism: virions containing isoleucine substitutions at position 425 lose their ability to infect a monocyte cell line (U937 cells) but can still infect T-lymphocyte cell lines (CEM, SUP-T1) and activated human peripheral blood lymphocytes. These results indicate that cellular tropism of HIV can be influenced by a single amino-acid change in gp120.     

基于自由基链式反应改进干法烟气脱硫技术的方法

为了提高干法烟气脱硫反应的速率并改良脱硫产物,提出了一种基于自由基链式反应同步氧化烟气中NO和SO2的方法。对该方法的机理进行了分析,提出了利用添加剂引发烟气中链式反应的设想。分别选用双氧水、碳氢化合物、硝酸作为添加剂开展了实验研究。实验结果表明:利用链式反应同步氧化烟气中的NO和SO2是可行的。添加剂的选取很关键:双氧水和碳氢化合物由于自身消耗OH自由基,不能维持链式反应的进行;硝酸热解可有效地提供OH自由基,实现NO和SO2的同步氧化。优化反应条件有助于提高NO和SO2的氧化率。