EB病毒潜伏膜蛋白1在鼻咽癌细胞中通过ERK介导Ets-1表达

为了探讨EB病毒编码的潜伏膜蛋白1(LMP1)对核转录因子Ets-1表达和活化的影响,并证实细胞外信号调节激酶1/2（ERK1/2）参与了该过程,选用可调控表达LMP1的鼻咽癌细胞系L7,应用蛋白质印迹法检测Ets-1、p-ERK蛋白质表达,免疫共沉淀-蛋白质印迹法检测Ets-1磷酸化状态,使用ERK1/2特异性小分子阻断物PD98059作用后,蛋白质印迹法检测p-ERK、Ets-1表达及磷酸化变化.结果显示：在L7细胞中诱导性LMP1可促进p-ERK、Ets-1蛋白质表达及其苏氨酸残基磷酸化,在一定范围呈时间和剂量效应;通过PD98059对诱导性LMP1作用的干预发现,p-ERK大部分表达被阻断,而Ets-1表达及其苏氨酸磷酸化也被部分阻断,以上结果提示ERK部分介导了LMP1诱导Ets-1表达和活化.     

家蚕感染蛹虫草后的生理生化变化

蛹虫草分生孢子侵染5龄家蚕Bombyx mori后,家蚕血淋巴中总糖、海藻糖、蛋白质和甘油酯含量均有不同程度的下降,其中甘油酯含量下降最为明显。海藻糖酶活性在侵染初期也明显降低。接种后家蚕体内的保护酶超氧化物歧化酶、过氧化物酶和过氧化氢酶活性也有较大变化,其中超氧化物歧化酶活性上升最为明显,在4日内由441.841 U/mL升至601.255 U/mL。     

Effects of Dexmedetomidine and Oxycodone on Neurocognitive and Inflammatory Response After Tourniquet-Induced Ischemia–Reperfusion Injury

To evaluate the effects of dexmedetomidine (Dex) and oxycodone (Oxy) on neurocognitive and inflammatory response after tourniquet-induced ischemia–reperfusion (I/R) injury. C57/BL6 mice were used to construct the mouse model of tourniquet-induced I/R injury. Mice (n?=?48) were randomly divided into sham, I/R, Dex or Oxy group. Morris water maze test was performed to assess the spatial learning and memory function. The expression of NF-κB, TLR4, NR2B, M1 (CD68 and TNF-α) and M2 (CD206 and IL-10) polarization markers in mice hippocampus were detected by western blot or immunofluorescent staining. Spontaneous excitatory post-synaptic currents (sEPSCs) were recorded by electrophysiology. Dex treatment alleviated I/R-induced declines in learning and memory (p < 0.05), while Oxy had no significant effect on it. Compared with I/R group, Dex and Oxy treatment down-regulated the expression of NF-κB, TLR4, TNF-α and CD68 (all p < 0.05), while no significantly different was found in CD206 and IL-10. In addition, Dex treatment down-regulated the expression of NR2B and reduced the frequency and amplitude of sEPSCs in I/R model mice (all p < 0.05), while Oxy had no significant effect on them. Tourniquet-induced I/R could impair the neurocognitive function of mice. Dex treatment could alleviate I/R-induced neurocognitive disorder by inhibiting abnormal synaptic transmission in hippocampal neurons. Both Dex and Oxy could alleviate the inflammatory response likely by inhibiting the polarization of microglia toward M1 phenotype via TLR4/NF-κB pathway. Future studies are needed to further examine the effects of Dex on neurocognitive disorder after tourniquet-induced I/R injury and investigate the exact mechanism.

     

FERONIA is involved in phototropin 1-mediated blue light phototropic growth in Arabidopsis

Plant shoot phototropism is triggered by the formation of a light-driven auxin gradient leading to bending growth. The blue light receptor phototropin 1(phot1) senses light direction, but how this leads to auxin gradient formation and growth regulation remains poorly understood. Previous studies have suggested phot1’s role for regulated apoplastic acidification, but its relation to phototropin and hypocotyl phototropism is unclear. Herein, we show that blue light can cause phot1 to interact with...     

A Water‐Soluble Cu Complex as Molecular Catalyst for Electrocatalytic CO2 Reduction on Graphene‐Based Electrodes

A structurally simple molecular 1,10‐phenanthroline‐Cu complex on a mesostructured graphene matrix that can be active and selective toward CO₂ reduction over H₂ evolution in an aqueous solution is reported. The active sites consist of Cu(I) center in a distorted trigonal bipyramidal geometry, which enables the adsorption of CO₂ with η¹‐COO‐like configuration to commence the catalysis, with a turnover frequency of ≈45 s^?1 at ?1 V versus reversible hydrogen electrode. Using in situ infrared spectroelectrochemical investigation, it is demonstrated that the Cu complex can be reversibly heterogenized near the graphene surface via potential control. An increase of electron density in the complex is observed as a result of the interaction from the electric field, which further tunes the electron distribution in the neighboring CO₂. It is also found that the mesostructure of graphene matrix favored CO₂ reduction on the Cu center over hydrogen evolution by limiting mass transport from the bulk solution to the electrode surface.     

Two-component sensor RhpS promotes induction of Pseudomonas syringae type III secretion system by repressing negative regulator RhpR

The Pseudomonas syringae type III secretion system (T3SS) is induced during interaction with the plant or culture in minimal medium (MM). How the bacterium senses these environments to activate the T3SS is poorly understood. Here, we report the identification of a novel two-component system (TCS), RhpRS, that regulates the induction of P. syringae T3SS genes. The rhpR and rhpS genes are organized in an operon with rhpR encoding a putative TCS response regulator and rhpS encoding a putative biphasic sensor kinase. Transposon insertion in rhpS severely reduced the induction of P. syringae T3SS genes in the plant as well as in MM and significantly compromised the pathogenicity on host plants and hypersensitive response-inducing activity on nonhost plants. However, deletion of the rhpRS locus allowed the induction of T3SS genes to the same level as in the wild-type strain and the recovery of pathogenicity upon infiltration into plants. Overexpression of RhpR in the deltarhpRS deletion strain abolished the induction of T3SS genes. However, overexpression of RhpR in the wild-type strain or overexpression of RhpR(D70A), a mutant of the predicted phosphorylation site of RhpR, in the deltarhpRS deletion strain only slightly reduced the induction of T3SS genes. Based on these results, we propose that the phosphorylated RhpR represses the induction of T3SS genes and that RhpS reverses phosphorylation of RhpR under the T3SS-inducing conditions. Epistasis analysis indicated that rhpS and rhpR act upstream of hrpR to regulate T3SS genes.     

Targeted overexpression of inducible 6-phosphofructo-2-kinase in adipose tissue increases fat deposition but protects against diet-induced insulin resistance and inflammatory responses

Increasing evidence demonstrates the dissociation of fat deposition, the inflammatory response, and insulin resistance in the development of obesity-related metabolic diseases. As a regulatory enzyme of glycolysis, inducible 6-phosphofructo-2-kinase (iPFK2, encoded by PFKFB3) protects against diet-induced adipose tissue inflammatory response and systemic insulin resistance independently of adiposity. Using aP2-PFKFB3 transgenic (Tg) mice, we explored the ability of targeted adipocyte PFKFB3/iPFK2 overexpression to modulate diet-induced inflammatory responses and insulin resistance arising from fat deposition in both adipose and liver tissues. Compared with wild-type littermates (controls) on a high fat diet (HFD), Tg mice exhibited increased adiposity, decreased adipose inflammatory response, and improved insulin sensitivity. In a parallel pattern, HFD-fed Tg mice showed increased hepatic steatosis, decreased liver inflammatory response, and improved liver insulin sensitivity compared with controls. In both adipose and liver tissues, increased fat deposition was associated with lipid profile alterations characterized by an increase in palmitoleate. Additionally, plasma lipid profiles also displayed an increase in palmitoleate in HFD-Tg mice compared with controls. In cultured 3T3-L1 adipocytes, overexpression of PFKFB3/iPFK2 recapitulated metabolic and inflammatory changes observed in adipose tissue of Tg mice. Upon treatment with conditioned medium from iPFK2-overexpressing adipocytes, mouse primary hepatocytes displayed metabolic and inflammatory responses that were similar to those observed in livers of Tg mice. Together, these data demonstrate a unique role for PFKFB3/iPFK2 in adipocytes with regard to diet-induced inflammatory responses in both adipose and liver tissues.     

小鼠血管内膜增生模型的建立

该文主要介绍一种可以在小鼠中有效地诱导血管内膜增生的方法。该方法使用硅胶管嵌套小鼠股动脉,造成股动脉血管内膜增生。病理切片观察表明,实验组小鼠股动脉与假手术组相比出现了内膜层和中膜层不规则增厚,管腔狭窄,细胞排列紊乱,内膜炎症细胞浸润等。免疫组织化学染色显示内膜增生部分是由于血管平滑肌细胞（VsMCs）增生和基质积聚所致。该模型的建立对动脉粥样硬化病理机制研究和治疗药物的研发具有重要意义。