Current cases in which epitope mimicry is considered a component cause of autoimmune disease: Guillain-Barré syndrome

Some patients develop Guillain-Barré syndrome (GBS) after the administration of bovine gangliosides. Patients with GBS subsequent to Campylobacter jejuni enteritis frequently have IgG antibody to GM1 ganglioside. Miller Fisher syndrome (MFS), a variant of GBS, is associated with IgG antibody to GQ1b ganglioside. Molecular mimicry between GM1 and lipopolysaccharide of C. jejuni isolated from patients with GBS, and between GQ1b and C. jejuni lipopolysaccharides from patients with MFS have been demonstrated. The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies. This sugar mimicry is one possible cause of the Guillain-Barré and Miller Fisher syndromes; however, unidentified host factors may contribute to the development of these syndromes.     

HAR1 mediates systemic regulation of symbiotic organ development

Symbiotic root nodules are beneficial to leguminous host plants; however, excessive nodulation damages the host because it interferes with the distribution of nutrients in the plant. To keep a steady balance, the nodulation programme is regulated systemically in leguminous hosts. Leguminous mutants that have lost this ability display a hypernodulating phenotype. Through the use of reciprocal and self-grafting studies using Lotus japonicus hypernodulating mutants, har1 (also known as sym78), we show that the shoot genotype is responsible for the negative regulation of nodule development. A map-based cloning strategy revealed that HAR1 encodes a protein with a relative molecular mass of 108,000, which contains 21 leucine-rich repeats, a single transmembrane domain and serine/threonine kinase domains. The har1 mutant phenotype was rescued by transfection of the HAR1 gene. In a comparison of Arabidopsis receptor-like kinases, HAR1 showed the highest level of similarity with CLAVATA1 (CLV1). CLV1 negatively regulates formation of the shoot and floral meristems through cell-cell communication involving the CLV3 peptide. Identification of hypernodulation genes thus indicates that genes in leguminous plants bearing a close resemblance to CLV1 regulate nodule development systemically, by means of organ-organ communication.     

Essential role for TIRAP in activation of the signalling cascade shared by TLR2 and TLR4

Signal transduction through Toll-like receptors (TLRs) originates from their intracellular Toll/interleukin-1 receptor (TIR) domain, which binds to MyD88, a common adaptor protein containing a TIR domain. Although cytokine production is completely abolished in MyD88-deficient mice, some responses to lipopolysaccharide (LPS), including the induction of interferon-inducible genes and the maturation of dendritic cells, are still observed. Another adaptor, TIRAP (also known as Mal), has been cloned as a molecule that specifically associates with TLR4 and thus may be responsible for the MyD88-independent response. Here we report that LPS-induced splenocyte proliferation and cytokine production are abolished in mice lacking TIRAP. As in MyD88-deficient mice, LPS activation of the nuclear factor NF-kappaB and mitogen-activated protein kinases is induced with delayed kinetics in TIRAP-deficient mice. Expression of interferon-inducible genes and the maturation of dendritic cells is observed in these mice; they also show defective response to TLR2 ligands, but not to stimuli that activate TLR3, TLR7 or TLR9. In contrast to previous suggestions, our results show that TIRAP is not specific to TLR4 signalling and does not participate in the MyD88-independent pathway. Instead, TIRAP has a crucial role in the MyD88-dependent signalling pathway shared by TLR2 and TLR4.     

薄层分离-分光光度法测定夹竹桃枝中三萜类化合物的质量分数

为测定夹竹桃中总三萜的质量分数,以齐墩果酸为对照品,5％的香草醛-冰醋酸溶液和高氯酸为显色剂,采用薄层色谱分离-分光光度法在550 nm波长处测定样品吸光度.用正交试验法优化了显色反应条件,适宜的展开剂组成为氯仿∶丙酮=10∶3,对照品在10～200μL/mL范围呈良好线性关系,其回归方程为Y=0.007 0C+0.0...     

Recent Advances in Protein Extraction and Chiral Separation of Biomolecules

Introduction Surfactant self-assemblies, such as reverse micelles ormicroemulsions, create unique environments in or-ganic solvents. These aggregates display a range of in-teresting physico-chemical properties that havebrought about great potential in mod…     

塔克拉玛干沙漠周边地区暖季气温、降水的变化特征及其响应分析

气温和降水是最重要的气候要素,与人们的生产、生活联系也最为紧密.通过对塔克拉玛干沙漠周边地区9个气象站34年逐月气温、降水资料分析研究,发现该地区暖季气温和降水有明显的上升趋势.暖季气温增加了约0.30℃,暖季对年气温变化的影响不如冷季大.暖季降水量约增加了7.30mm,暖季降水暖季降水量占全年降水量的82.96%,决定了年降水变化趋势.暖季气温对降水存在明显的逆动响应关系.     

An efflux transporter of silicon in rice

Silicon is an important nutrient for the optimal growth and sustainable production of rice. Rice accumulates up to 10% silicon in the shoot, and this high accumulation is required to protect the plant from multiple abiotic and biotic stresses. A gene, Lsi1, that encodes a silicon influx transporter has been identified in rice. Here we describe a previously uncharacterized gene, low silicon rice 2 (Lsi2), which has no similarity to Lsi1. This gene is constitutively expressed in the roots. The protein encoded by this gene is localized, like Lsi1, on the plasma membrane of cells in both the exodermis and the endodermis, but in contrast to Lsi1, which is localized on the distal side, Lsi2 is localized on the proximal side of the same cells. Expression of Lsi2 in Xenopus oocytes did not result in influx transport activity for silicon, but preloading of the oocytes with silicon resulted in a release of silicon, indicating that Lsi2 is a silicon efflux transporter. The identification of this silicon transporter revealed a unique mechanism of nutrient transport in plants: having an influx transporter on one side and an efflux transporter on the other side of the cell to permit the effective transcellular transport of the nutrients.     

国产夹竹桃枝中化学成分的研究

采用硅胶柱色谱、Sephadex LH-20柱色谱等方法分离纯化国产夹竹桃(Nerium indicum Mill)枝,根据理化性质和波谱数据对其化学成分进行结构鉴定.结果表明,从夹竹桃枝中分离并鉴定了4个化合物,分别为16β,17β-环氧-12β-羟基-孕甾-4,6-二烯-3,20-二酮;12β-羟基-孕甾-4,6,16-三烯-3,20-二酮;20(s)21-二羟基-孕甾-3,12-二酮;3β,14β-二羟基-5β-强心甾-20(22)-烯.化合物1～4均为首次从国产夹竹桃中分离得到.