自由基相关细胞信号传导的研究进展

自由基是带有一个孤对电子的分子,具有很强的反应性。自由基可以直接与细胞组成成分发生反应,造成细胞损伤,如通过氧化线粒体DNA和线粒体心磷脂对线粒体造成氧化损伤,从而诱导细胞凋亡。此外,自由基还能影响包括Ca2+、蛋白质磷酸化、转录因子、Bcl-2基因等多种细胞信号传导。因此,自由基产生的生物学效应范围广泛,覆盖了从生理功能调节到影响诸多疾病的病程变化。该文从自由基的产生、清除及其对多种细胞信号传导的影响等方面对相关自由基的研究进展作简要的阐述,以期获得对自由基相关细胞信号传导研究进展较为全面的了解。     

p38MAPK在低氧高二氧化碳肺动脉平滑肌中的表达及三七皂苷单体Rb_1的干预

该实验旨在探讨三七皂苷单体Rb1对低氧高二氧化碳性肺动脉收缩的作用及其与p38MAPK信号通路的关系。原代培养雄性SD大鼠肺动脉平滑肌细胞(PASMCs),取第2~5代细胞,随机分为五组:常氧组(N组)、低氧高二氧化碳(1%O2,6%CO2)组(H组)、低氧高二氧化碳+8 mg/m LRb1组(RbL组)、低氧高二氧化碳+40 mg/m L Rb1组(RbM组)、低氧高二氧化碳+100 mg/m L Rb1组(RbH组)。孵育24 h后收集细胞,分别采用免疫印迹法测定p38MAPK磷酸化蛋白的表达水平,半定量逆转录–聚合酶链反应技术检测p38MAPK基因的表达水平。p-p38MAPK蛋白在N组表达弱阳性;较之H组,Rb1干预组(RbL、RbM、RbH组)表达均不同程度减弱,以RbM组最为显著,差异有统计学意义(P0.01);p38MAPK m RNA在N组表达较弱;与H组相比,RbL、RbM和RbH组中p38MAPK m RNA表达均不同程度下降,以RbM组最为显著(P0.01)。上述结果表明,p38MAPK信号通路可能介导大鼠低氧高二氧化碳性肺动脉收缩;三七皂苷单体Rb1可能通过抑制p38MAPK信号通路的表达而减轻低氧高二氧化碳性肺动脉收缩。     

基于ADS8332的生理信号采集系统电路设计

本文介绍了医学生理信号的的特点,根据其特点设计出了针对医学生理信号进行采集的电路。该电路设计实现了基于16位的高精度A/D 转换芯片ADS8332 的医学生理信号采集系统,以基于Cortex-M3 内核的32 位微控制器STM32F103RD作为采集控制芯片,该系统电路可以实现对最多16 个通道的模拟医学生理信号进行采集。此电路设计充分利用了ADS8332 的高精度、低功耗、高采样速率的特点以及片上集成功能,并配合了信号调理电路和相应的抗干扰措施,因此保证了医学生理信号的采集精度和系统的稳定性。     

TN-C在小细胞肺癌中的表达及STAT3对TN-C表达的影响

目的：探讨小细胞肺癌（SCLC）组织和小细胞肺癌细胞（H446）中肌糖蛋白-C（TN-C）的表达及STAT3对TN-C表达的影响。方法：应用免疫组化法检测58例小细胞肺癌和17例癌旁正常组织中TN-C的表达水平,应用RT-PCR和Western blotting法检测STAT-siRNA和STAT3过表达的H446细胞中TN-C的表达水平。结果：（1）小细胞肺癌组织中TN-C的表达水平显著高于癌旁正常组织（P〈0.05）;（2）在H446细胞中,TN-C和STAT3均呈现高表达;（3）STAT3-siRNA处理的H446细胞中STAT3和TN-C的表达均显著降低（P〈0.05）,而STAT3过表达的H446细胞中STAT3和TN-C的表达均显著上调（P〈0.05）。结论：TN-C在小细胞肺癌中的表达上调,可能受到STAT3的调控。     

D53： The Missing Link in Strigolactone Signaling

Strigolactones （SLs）, a group of small carotenoid-derived terpenoid lactones, have been recently identified as plant hormones controlling plant architecture through modulating shoot and root branching （Brewer et al., in the rhizosphere because of 2013）. SLs were first discovered their involvement in both symbiotic and parasitic interactions. Deficiencies in SL biosynthesis and perception lead to excessive growth of axillary bud, which is exemplified through various mutants such as max1, max2,     

FERONIA Receptor Kinase Controls Seed Size in Arabidopsis thaliana

Dear Editor,
Plants have evolved elaborate mechanisms by which cell elongation regulation is coupled to the environmental signals. The plasma membrane receptor kinase FERONIA （FER） has emerged as an important regulatory node in controlling cell elongation and hormone crosstalk （Guo et al., 2009; Deslauriers and Larsen, 2010; Duan et al., 2010; Yu et al.,     

Sucrose Induction of Anthocyanin Biosynthesis Mediated by DELLA

Dear Editor, While they affect all aspects of plant life, the exact molecu- lar mechanisms involved in sugar sensing and signaling are still mostly unknown. However, using the induction of antho- cyanin biosynthesis as a convenient readout and tool, the DELLA proteins can be identified as key positive regulators in sucrose-specific signaling and a point of integration of diverse metabolic and hormonal signals.     

Salicylic Acid Signaling Controls the Maturation and Localization of the Arabiclopsis Defense Protein ACCELERATED CELL DEATH6

ACCELERATED CELL DEATH6 （ACD6） is a multipass membrane protein with an ankyrin domain that acts in a positive feedback loop with the defense signal salicylic acid （SA）. This study implemented biochemical approaches to infer changes in ACD6 complexes and localization. In addition to forming endoplasmic reticulum （ER）- and plasma membrane （PM）-Iocalized complexes, ACD6 forms soluble complexes, where it is bound to cytosolic HSP70, ubiquitinated, and degraded via the proteasome. Thus, ACD6 constitutively undergoes ER-associated degradation. During SA signaling, the soluble ACD6 pool decreases, whereas the PM pool increases. Similarly, ACD6-1, an activated version of ACD6 that induces SA, is present at low levels in the soluble fraction and high levels in the PM. However, ACD6 variants with amino acid substitutions in the ankyrin domain form aberrant, inactive complexes, are induced by a SA agonist, but show no PM localization. SA signaling also increases the PM pools of FLAGELLIN SENSING2 （FLS2） and BRI1-ASSOClATED RECEPTOR KINASE 1 （BAK1）. FLS2 forms complexes ACD6; both FLS2 and BAK1 require ACD6 for maximal accumulation at the PM in response to SA signaling. A plausible scenario is that SA increases the efficiency of productive folding and/or complex formation in the ER, such that ACD6, together with FLS2 and BAK1, reaches the cell surface to more effectively promote immune responses.     

Negative Feedback Regulation of Auxin Signaling by ATHB8/ACL5-BUD2 Transcription Module

The role of auxin as main regulator of vascular differentiation is well established, and a direct correlation between the rate of xylem differentiation and the amount of auxin reaching the （pro）cambial cells has been proposed. It has been suggested that thermospermine produced by ACAULIS5 （ACL5） and BUSHY AND DWARF2 （BUD2） is one of the factors downstream to auxin contributing to the regulation of this process in Arabidopsis. Here, we provide an in-depth characterization of the mechanism through which ACL5 modulates xylem differentiation. We show that an increased level of ACL5 slows down xylem differentiation by negatively affecting the expression of homeodomain-leucine zipper （HD- ZIP） III and key auxin signaling genes. This mechanism involves the positive regulation of thermospermine biosynthesis by the HD-ZIP III protein ARABIDOPSIS THALIANA HOMEOBOX8 tightly controlling the expression of ACL5 and BUD2. In addition, we show that the HD-ZIP III protein REVOLUTA contributes to the increased leaf vascularization and long hypocotyl phenotype of acl5 likely by a direct regulation of auxin signaling genes such as LIKE AUXIN RESISTANT2 （LAX2） and LAX3. We propose that proper formation and differentiation of xylem depend on a balance between positive and negative feedback loops operating through HD-ZIP III genes.