Intrinsic Effects of Gold Nanoparticles on Oxygen–Glucose Deprivation/Reperfusion Injury in Rat Cortical Neurons

This study aimed to investigate the potential effects of gold nanoparticles (Au-NPs) on rat cortical neurons exposed to oxygen–glucose deprivation/reperfusion (OGD/R) and to elucidate the corresponding mechanisms. Primary rat cortical neurons were exposed to OGD/R, which is commonly used in vitro to mimic ischemic injury, and then treated with 5- or 20-nm Au-NPs. We then evaluated cell viability, apoptosis, oxidative stress, and mitochondrial respiration in these neurons. We found that 20-nm Au-NPs increased cell viability, alleviated neuronal apoptosis and oxidative stress, and improved mitochondrial respiration after OGD/R injury, while opposite effects were observed for 5-nm Au-NPs. In terms of the underlying mechanisms, we found that Au-NPs could regulate Akt signaling. Taken together, these results show that 20-nm Au-NPs can protect primary cortical neurons against OGD/R injury, possibly by decreasing apoptosis and oxidative stress, while activating Akt signaling and mitochondrial pathways. Our results suggest that Au-NPs may be potential therapeutic agents for ischemic stroke.

     

NaCl胁迫对藜麦幼苗生长及生理特性的影响

为探讨盐胁迫下两类不同地区藜麦品种幼苗的耐盐机制,该文利用不同浓度的NaCl溶液,对来自青海省海东市乐都区的'LD-13'(低盐地区)和来自青海省海西州乌兰县的'WL-192'(高盐地区)的2个藜麦品种的种子和幼苗进行盐胁迫处理,研究了种子萌发指标(发芽率、发芽势、发芽指数),生长指标(鲜重、根长、茎长)及生理指标(M...     

Probe droplet arrays generated in the capillary for microarray analysis

Microarray technology is a useful tool for nucleic acid detection and has been widely used in biology and related research fields. However, the procedure is labor intensive and time consuming. Microfluidic chip-based microarrays save time with better performance, but the low spot density and probe number limit its applications. To develop high performance microarrays with high spot density within a microchannel, a method is reported here for preparing microarrays in a capillary by generating probe droplet arrays. The probes in droplets are immobilized onto the inner wall of the capillary to form a one-dimensional probe array, and then a sample solution is introduced to hybridize with the probe array. The effect of the capillary's inner diameter was evaluated to realize a high-density probe array. The processes of array generation and probe immobilization were studied to avoid possible cross contamination. The background from probe immobilization during the array generation and incubation was quantified to assure sensitivity. Multiple sample detection was also demonstrated within one capillary. The capillary based microarray assay had high spot density, easy fabrication, fast detection, high sensitivity and multiple sample capacity.     

高浓度臭氧对蒙古栎叶片酚类物质含量和总抗氧化能力的影响

采用开顶箱(OTC)法,研究了高浓度臭氧(80±8 nmol·mol^-1)熏蒸处理对蒙古栎叶片 中总酚、类黄酮、单宁及丙二醛(MDA)含量的影响,使用1,1-二苯基苦基苯肼(DPPH) 法测定了蒙古栎叶片的总抗氧化能力.结果表明:蒙古栎叶片中总酚、类黄酮、缩合单宁和MDA的含量都有所增加,其中总酚和缩合单宁含量分别增加了48.17%和26.77%,差异显著（P<0.05）;类黄酮和MDA含量分别增加了24.66%和5.26%,差异不显著(P＞0.05);蒙古栎叶片总抗氧化能力显著增强(P<0.05),且与叶片中总酚和缩合单宁含量呈显著的正相关关系.     

断尾对胎生蜥蜴运动能力和选择体温的影响

尾自切是蜥蜴为了降低被捕食危险而采取的一种反捕食适应策略,但断尾可导致体重减轻、热量收支平衡改变,并影响蜥蜴的运动能力和体温调节.为检验断尾对蜥蜴运动能力和选择体温的影响,于2006年5月选取黑龙江省小兴安岭地区的一个胎生蜥蜴种群进行实验.结果表明:在30 ℃和24℃两个实验温度下,断尾后胎生蜥蜴的运动能力均明显下降,表现在停顿次数增多、最大可持续距离和最大疾跑速度减少等方面;断尾、温度和性别对胎生蜥蝎运动能力的影响在一定程度上是相互独立的,断尾是影响胎生蜥蜴运动能力的主要因素;断尾对胎生蜥蝎的选择体温没有显著影响.     

镶嵌式外固定架治疗长骨骨不连17例体会

目的：探讨长骨骨不连的一种治疗方法。方法：2007年1月至2009年8月,采用镶嵌式外固定架治疗17例长骨骨不连。本组17例,男11例,女6例,年龄16-64岁,平均31岁。2例为血源性骨髓炎病理性骨折后,股骨、胫骨各1例;6例为创伤性骨髓炎后骨折不愈,肱骨1例,股骨1例,胫骨4例;9例为手术后无感染性骨不连,肱骨2例,股骨2例,胫骨5例;7例有不同程度畸形,6例有1.5-8cm骨短缩,其中2例同时行骨痂延长术。结果：全部病人均获随访,随访时间9-20个月,以1975年天津全国骨科会议制定的骨折愈合标准为依据,本组17例病人均获得临床愈合,骨不连处平均愈合时间为4～9月（平均6.2月）,1例延长8cm,另1例延长6cm。结论：利用镶嵌式外固定架治疗长骨骨不连一种简单有效的方法。     

Facilitation versus depression in cultured hippocampal neurons determined by targeting of Ca2+ channel Cavbeta4 versus Cavbeta2 subunits to synaptic terminals

Ca(2+) channel beta subunits determine the transport and physiological properties of high voltage-activated Ca(2+) channel complexes. Our analysis of the distribution of the Ca(v)beta subunit family members in hippocampal neurons correlates their synaptic distribution with their involvement in transmitter release. We find that exogenously expressed Ca(v)beta(4b) and Ca(v)beta(2a) subunits distribute in clusters and localize to synapses, whereas Ca(v)beta(1b) and Ca(v)beta(3) are homogenously distributed. According to their localization, Ca(v)beta(2a) and Ca(v)beta(4b) subunits modulate the synaptic plasticity of autaptic hippocampal neurons (i.e., Ca(v)beta(2a) induces depression, whereas Ca(v)beta(4b) induces paired-pulse facilitation [PPF] followed by synaptic depression during longer stimuli trains). The induction of PPF by Ca(v)beta(4b) correlates with a reduction in the release probability and cooperativity of the transmitter release. These results suggest that Ca(v)beta subunits determine the gating properties of the presynaptic Ca(2+) channels within the presynaptic terminal in a subunit-specific manner and may be involved in organization of the Ca(2+) channel relative to the release machinery.     

Characterization of Ser338 phosphorylation for Raf-1 activation

Raf kinases are essential for regulating cell proliferation, survival, and tumorigenesis. However, the mechanisms by which Raf is activated are still incompletely understood. Phosphorylation plays a critical role in Raf activation in response to mitogens. The present study characterizes phosphorylation of Ser338, a crucial event for Raf-1 activation. Here we report that mutation of Lys375 to Met diminishes phosphorylation of Ser338 on both wild type Raf-1 in cells treated with epidermal growth factor (EGF) or 12-O-tetradecanoylphorbol-13-acetate (TPA) and a constitutively active mutant in which Tyr340/Tyr341 are replaced by 2 aspartic acids, a conserved substitution present in natural B-Raf. The loss of Ser338 phosphorylation in these Raf mutants is not engendered by a mutation-induced conformational change, inasmuch as mutation of another site (Ser471 to Ala) in the activation segment also abolishes Ser338 phosphorylation, whereas both the kinase-dead mutants of Raf-1 are phosphorylated well by active Pak1. Furthermore, our data demonstrate that EGF-stimulated phosphorylation of Ser338 is inhibited by Sorafenib, a Raf kinase inhibitor, but not by the MEK inhibitor U0126. Interestingly, a kinase-dead mutation and Sorafenib also markedly reduce phosphorylation of Ser445 on B-Raf, a site equivalent to Raf-1 Ser338. Finally, our data reveal that Ser338 is phosphorylated on inactive Raf-1 by an active mutant of Raf-1 when they are dimerized in cells and that artificial dimerization of Raf-1 causes Ser338 phosphorylation, accompanied by activation of ERK1/2. Altogether, our data suggest that Ser338 on Raf-1 is autophosphorylated in response to mitogens.