Inhibition of tryptophan uptake in Aspergillus fumigatus by tryptamine

Summary The tryptophan uptake was inhibited considerably in tryptamine grown cells. This inhibition was due to feed-back inhibition and not to repression.The authors are greatful to Prof. V. V. Modi for his interest in this work. The award of research fellowship by M. S. University of Baroda to A. R. G. is greatfully acknowledged.     

丙烯睛—卤代羧酸共聚物热解过程的研究

采用付里叶变换红外光谱法在位连续测定了含羧酸及由代羧酸丙烯腈共聚物在低温热解时化学结构的变化，根据光谱特征峰随温度增加的变化规律。测定了裂解产物中残留的氰基量及环化度和环化序列长度。结果表明，溴代羧酸丙烯腈共聚物具有独特的性能。在可用于碳纤维原丝的共聚体中，是具有较大潜力的竞争者。     

12个草地早熟禾品种愈伤组织诱导体系的研究

 以生产中常见的12种草地早熟禾(Poa pratensis L.)成熟种子为外植体,对其愈伤组织诱导及愈伤组织增殖生长体系进行了优化试验.结果表明,在愈伤组织诱导试验中,单纯使用2,4-D时,不同品种愈伤组织诱导率在60%~93%之间,2,4-D质量浓度3 mg/L时12个早熟禾品种的愈伤组织诱导率均值最高,达到86%;在2,4-D基础上添加少量6-BA(0.1~0.2 mg/L)后,不同品种愈伤组织诱导率在30%~92%之间,12个品种的愈伤组织诱导率均值有所降低(3.1%~25.4%).在愈伤组织增殖试验中,单纯使用2,4-D时,不同品种愈伤组织增殖率在38%~164%之间,12个早熟禾品种的愈伤组织增殖率均值在3 mg/L 2,4-D时最高,达到81%;在3 mg/L 2,4-D基础上施加少量的6-BA(0.05~0.2 mg/L)后,愈伤组织增殖率均值有所降低,但存在品种的差异性.研究结果还显示,热激处理对部分草地早熟禾愈伤组织诱导及增殖有一定的促进作用.     

Smurf2单克隆抗体的制备与鉴定

Smad泛素调节因子家族的两个E3泛素连接酶成员Smurf1和Smurf2 (Smad ubiquitin regulatory factor 1 and 2)具有至少80％的同源性.为了更好地研究它们的功能,需要获得一个能区分Smurf1和Smurf2的单克隆抗体.选取Smurf2与Smurf1蛋白序列中仅有的非同源区域序列作为抗原免疫Bal b/C小鼠,成功制备若干株能稳定分泌抗Smurf2抗体的杂交瘤细胞株.对所获得的单克隆抗体的效价和特异性等进行一系列检测,结果表明该抗体能特异性地识别过表达及细胞内源Smurf2蛋白.此外该抗体能被应用于Western blot和免疫荧光实验,从而为深入研究Smurf2的细胞生物学功能提供了良好的实验基础.     

Synthesis, properties, and optical applications of noble metal nanoparticle-biomolecule conjugates

Noble metal nanoparticles, such as gold or silver nanoparticles and nanorods, exhibit unique photonic, electronic and catalytic properties. Functionalization of noble metal nanoparticles with biomolecules (e.g., protein and DNA) produces systems that possess numerous applications in catalysis, delivery, therapy, imaging, sensing, constructing nanostructures and controlling the structure of biomolecules. In this paper, the recent development of noble metal nanoparticle-biomolecule conjugates is reviewed from the following three aspects: (1) synthesis of noble metal nanoparticle-biomolecule systems by electrostatic adsorption, direct chemisorption of thiol derivatives, covalent binding through bifunctional linkers and specific affinity interactions; (2) the photonic properties and bioactivation of noble metal nanoparticle-biomolecule conjugates; and (3) the optical applications of such systems in biosensors, and medical imaging, diagnosis, and therapy. The conjugation of Au and Ag nanoparticles with biomolecules and the most recent optical applications of the resulting systems have been focused on.     

超强静磁场照射对小鼠抗氧化和免疫能力的影响

研究超强静磁场(USMF)连续照射对小鼠抗氧化和免疫能力的影响.采用12 T的超强静磁场每天照射小鼠2 h,连续7 d,测量小鼠肝脏和肾脏中丙二醛(MDA)的含量和过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、总抗氧化能力(T-AOC)和谷胱甘肽过氧化物酶(GSH-Px)的活力;测定胸腺、脾脏指数和脾脏中淋巴细胞转化率;检测外周血中白细胞数目.结果表明:超强静磁场可以显著增强肝脏中SOD和GSH-Px的活力以及肾脏中CAT,SOD,GSH-Px和总抗氧化能力;降低肝脏和肾脏中MDA含量;明显提高小鼠脾细胞淋巴转化率、胸腺指数和外周血中白细胞数目.超强静磁场对小鼠连续照射可以提高小鼠机体的抗氧化和免疫能力.     

Orai1 is an essential pore subunit of the CRAC channel

Stimulation of immune cells causes depletion of Ca2+ from endoplasmic reticulum (ER) stores, thereby triggering sustained Ca2+ entry through store-operated Ca2+ release-activated Ca2+ (CRAC) channels, an essential signal for lymphocyte activation and proliferation. Recent evidence indicates that activation of CRAC current is initiated by STIM proteins, which sense ER Ca2+ levels through an EF-hand located in the ER lumen and relocalize upon store depletion into puncta closely associated with the plasma membrane. We and others recently identified Drosophila Orai and human Orai1 (also called TMEM142A) as critical components of store-operated Ca2+ entry downstream of STIM. Combined overexpression of Orai and Stim in Drosophila cells, or Orai1 and STIM1 in mammalian cells, leads to a marked increase in CRAC current. However, these experiments did not establish whether Orai is an essential intracellular link between STIM and the CRAC channel, an accessory protein in the plasma membrane, or an actual pore subunit. Here we show that Orai1 is a plasma membrane protein, and that CRAC channel function is sensitive to mutation of two conserved acidic residues in the transmembrane segments. E106D and E190Q substitutions in transmembrane helices 1 and 3, respectively, diminish Ca2+ influx, increase current carried by monovalent cations, and render the channel permeable to Cs+. These changes in ion selectivity provide strong evidence that Orai1 is a pore subunit of the CRAC channel.     

Cell death in the nervous system

Neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease trigger neuronal cell death through endogenous suicide pathways. Surprisingly, although the cell death itself may occur relatively late in the course of the degenerative process, the mediators of the underlying cell-death pathways have shown promise as potential therapeutic targets.     

Interaction of Co, Mn, Mg and Al with d(GCCCATGGC) and d(CCGGGCCCGG): a spectroscopic study

Spectroscopic study of the interactions of metal ions, Co, Mn, Mg and Al with d(GCCCATGGGC) and d(CCGGGCCCGG) revealed the following. Metal ions Mn, Al and Mg at the lowest concentrations enhanced the t _m of oligomers, whereas Mn and Mg at higher concentrations decreased the t _m . Co enhanced the t _m of oligomers at higher concentrations. The studies have also indicated that Mn at lower concentrations displaced EtBr fluorescence, Mg and Co at moderate concentrations and Al only at higher concentrations. Addition of Co, Mn, Mg and Al altered the bands of the circulars dichroism (CD) spectra of the oligomers in a concentration-dependent manner. The CD spectra of d(GCCCATGGGC) and d(CCGGGCCCGG) indicated B and Z forms of DNA, respectively, in contrast to the A form observed in the crystal structures. Mg and Co at different ionic strength induced Z–B transition in d(CCGGGCCCGG), while Al at higher concentrations induced a Z–A transition. Mn did not induce any transition. This is the first report to show that Al causes structural transitions in sequence-specific oligomers and has strong binding ability with GC-rich euchromatin oligomers. Received 22 December 1997; received after revision 16 March 1998; accepted 16 March 1998