HIV-1 glycoprotein 41 ectodomain induces activation of the CD74 protein-mediated extracellular signal-regulated kinase/mitogen-activated protein kinase pathway to enhance viral infection

Besides mediating the viral entry process, the human immunodeficiency virus (HIV-1) envelope protein gp41 can bind to many host cell components and regulate cell functions. Using a yeast two-hybrid system, we screened a human bone marrow cDNA library and identified a novel gp41-binding protein, CD74 (the MHC class II-associated invariant chain). Here, we report possible biological effects mediated by interaction between gp41 and CD74. We found that HIV-1 gp41 could bind directly to host CD74 in HIV-1-infected cells, and the peptide 6358 derived from gp41 loop region (aa 597-611) could effectively block the gp41-CD74 interaction. As a result of this binding, recombinant soluble gp41 and gp41 peptide 6358 activated the CD74-mediated ERK/MAPK pathway and significantly enhanced HIV-1 infection in vitro. Conversely, the enhancing effect could be suppressed by the recombinant CD74 extracellular domain. These results reveal a novel mechanism underlying gp41 mediation of HIV-1 infection and replication.     

Biodegradation of poly(ε-caprolactone) (PCL) by a new Penicillium oxalicum strain DSYD05-1

In this study, fungi isolated from soil were screened for their ability to form clear zones on agar plates with emulsified poly(ε-caprolactone) (PCL). The most active strain, designated as DSYD05, was identified as Penicillium oxalicum on the basis of morphological characteristics and phylogenetic analysis. Mutant DSYD05-1, obtained by ultraviolet-light mutagenesis from strain DSYD05, was more effective in PCL degradation. In liquid cultures of the mutant strain with PCL emulsion, DSYD05-1 showed the highest PCL-degrading activity after 4?days of cultivation. The products of PCL degradation were analysed by mass spectrometry; the results indicated that 6-hydroxyhexanoic acid was produced and assimilated during cultivation. The degradation of PCL film by DSYD05-1 was observed by scanning electron microscopy, and was indicative of a three-stage degradation process. The degradation of amorphous parts of the film preceded that of the crystalline center and then the peripheral crystalline regions. In addition, DSYD05-1 showed a wide range of substrate specificity, with capability to degrade PCL, poly(β-hydroxybutyrate), and poly(butylene succinate), but not poly(lactic acid), indicating that the strain could have potential for application in the treatment or recycling of bio-plastic wastes.     

电针诱导心肌缺血大鼠延髓头端腹外侧区nNOS和iNOS差异表达

许多研究表明,延髓头端腹外侧区(rostral ventrolateml medulla,RVLM)的NO/NOS系统参与心血管活动的中枢调节.本实验以结扎Wistar大鼠左冠状动脉前降支法建立急性心肌缺血(acute myocardial ischemia,AMI)动物模型,观察针刺"内关"穴改善AMI大鼠的心功能作用,同时检测大鼠RVLM区神经元型一氧化氮合酶(neuronal nitric oxide synthase,nNOS)和诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)表达的变化,进而探讨针刺治疗AMI的中枢机制.实验观察显示,AMI大鼠心功能各项指标减弱,伴随外周血去甲肾上腺素(norepinephrine,NE)和脑钠肽(brain natriuretic peptide,BNP)水平显著升高,同时RVLM区nNOS阳性神经元数和nNOS mRNA表达升高,而iNOS水平则降低.针刺"内关"穴(Pe 6)(每天30 min,连续5天)改善心功能,降低AMI大鼠血清中NE和BNP的水平,同时升高iNOS并降低nNOS在RVLM的表达.以上结果提示,针刺治疗心肌缺血的同时可以调节iNOS/NO和nNOS/NO在RVLM的变化,这可能与针刺通过调节RVLM区的NO含量进而降低交感传出,从而改善AMI大鼠的心功能有关.     

磷脂酶D和炎症的关系

磷脂酶Ｄ（ＰＬＤ）广泛存在于动物组织细胞中,并受各种胞外信号调节。其主要底物为磷脂酰胆碱（ＰＣ）。ＰＬＣ引起的ＰＣ水解是细胞内重要的信号转导途径。越来越多的证据表明ＰＬＤ和炎症有密切的关系。本文主要介绍ＰＬＤ在呼吸爆发、脱颗粒及花生四烯酸（ＡＡ）释放等方面的研究进展。     

Hypocrellin derivative with improvements of red absorption and active oxygen species generation

A novel diamino-substituted hypocrellin derived from hypocrellin B (HB) was synthesized by a mild method. The red absorption of the resulting product was significantly enhanced relative to the parent hypocrellins and any other hypocrellin derivatives, and the active oxygen species generating abilities were enhanced distinctly, which will remarkably improve its photodynamic therapy effectiveness.     

Improved ethanol yield and reduced Minimum Ethanol Selling Price (MESP) by modifying low severity dilute acid pretreatment with deacetylation and mechanical refining: 1) Experimental

ABSTRACT: BACKGROUND: Historically, acid pretreatment technology for the production of bio-ethanol from corn stover has required severe conditions to overcome biomass recalcitrance. However, the high usage of acid and steam at severe pretreatment conditions hinders the economic feasibility of the ethanol production from biomass. In addition, the amount of acetate and furfural produced during harsh pretreatment is in the range that strongly inhibits cell growth and impedes ethanol fermentation. The current work addresses these issues through pretreatment with lower acid concentrations and temperatures incorporated with deacetylation and mechanical refining. RESULTS: The results showed that deacetylation with 0.1 M NaOH before acid pretreatment improved the monomeric xylose yield in pretreatment by up to 20 % while keeping the furfural yield under 2 %. Deacetylation also improved the glucose yield by 10 % and the xylose yield by 20 % during low solids enzymatic hydrolysis. Mechanical refining using a PFI mill further improved sugar yields during both low- and high-solids enzymatic hydrolysis. Mechanical refining also allowed enzyme loadings to be reduced while maintaining high yields. Deacetylation and mechanical refining are shown to assist in achieving 90 % cellulose yield in high-solids (20 %) enzymatic hydrolysis. When fermentations were performed under pH control to evaluate the effect of deacetylation and mechanical refining on the ethanol yields, glucose and xylose utilizations over 90 % and ethanol yields over 90 % were achieved. Overall ethanol yields were calculated based on experimental results for the base case and modified cases. One modified case that integrated deacetylation, mechanical refining, and washing was estimated to produce 88 gallons of ethanol per ton of biomass. CONCLUSION: The current work developed a novel bio-ethanol process that features pretreatment with lower acid concentrations and temperatures incorporated with deacetylation and mechanical refining. The new process shows improved overall ethanol yields compared to traditional dilute acid pretreatment. The experimental results from this work support the techno-economic analysis and calculation of Minimum Ethanol Selling Price (MESP) detailed in our companion paper.     

Macrophage migration inhibitory factor (MIF) interacts with Bim and inhibits Bim-mediated apoptosis

The pro-apoptotic Bcl-2 family member Bim acts as a sensor for apoptotic stimuli and initiates apoptosis through the mitochondrial pathway. To identify novel regulators of Bim, we employed the yeast two-hybrid system and isolated the human gene encoding macrophage migration inhibitory factor (MIF), a ubiquitously expressed proinflammatory mediator that has also been implicated in cell proliferation, the cell cycle and carcinogenesis. The interaction between MIF and Bim was confirmed by both in vitro and in vivo protein interaction assays. Intriguingly, protein complexes between MIF and the three major Bim isoforms (BimEL/BimL/BimS) could be detected in HEK293 and K562 cells, especially in cells undergoing apoptosis. Moreover, exogenous expression of MIF partially inhibited Bim-induced apoptosis in HEK293 cells. SiRNA-mediated knockdown of MIF increased apoptosis in K562 cells exposed to the chemical oxidant diamide. Endogenous MIF may regulate the pro-apoptotic activity of Bim and inhibit the release of cytochrome c from mitochondria.     

PERMANENT GENETIC RESOURCES: A set of primer pairs for amplifying the complete mitochondrial DNA of endangered Chinese egret (Aves, Ardeidae, Egretta eulophotes)

The Chinese egret is a globally endangered species. Here we describe a set of primer pairs to amplify its entire mtDNA. The polymerase chain reaction products (1000–2000 bp) were successfully amplified by using this primer set and were then sequenced and aligned. The contiguous mtDNA sequences of the Chinese egret were assembled to be a circular molecule (17 579 bp). This primer set was also confirmed to be useful for six other species of ardeid birds. The versatility of this primer set will provide a groundwork for further studies on the genetic structure and molecular evolution of the ardeid species.     

The inhibitory effect of BSP-A1/-A2 on protein kinase C and tyrosine protein kinase

Bovine seminal plasma contains a group of similar proteins, namely BSP-A1, BSP-A2, BSP-A3, and BSP-30-kDa (collectively called BSP proteins), and they are secreted by the seminal vesicles. In our study, we purified the BSP-A1/-A2 through affinity chromatography and found for the first time that BSP-A1/-A2 can inhibit the activity of protein kinase C (PKC) and tyrosine protein kinase (TPK). The inhibition was dose dependent. When the PKC and TPK activities are expressed as the logarithm of percentage activity taking the activity in the absence of the BSP-A1/-A2 as 100%, there is a linear relationship between the their activities and the dose of BSP-A1/-A2.     

Evodiamine inhibits in vitro angiogenesis: Implication for antitumorgenicity

Evodiamine, the major bioactive compound isolated from Chinese herbal drug named Wu-Chu-Yu, has been reported to exhibit anti-tumor growth and metastasis. However, the effect of evodiamine on angiogenesis remains to be investigated. We used the fresh medium containing evodiamine or human lung adenocarcinoma cell (CL1 cells) derived conditioned media free of evodiamine to test their capability to induce in vitro angiogenesis, i.e., human umbilical vein endothelial cells (HUVECs) tube formation and invasion. We demonstrated that evodiamine could directly inhibit in vitro HUVECs tube formation and invasion. Locally administered evodiamine also inhibited the in vivo angiogenesis in the chick embryo chorioallantoic membrane (CAM) assay. The gene expression of vascular endothelial growth factor (VEGF) and the p44/p42 mitogen-activated protein kinase (MAPK, ERK) that correlated with endothelial cells angiogenesis were inhibited by evodiamine. We found that the evodiamine-treated CL1 cells derived conditioned medium showed decreased VEGF release and reduced ability of inducing in vitro tube formation. After the collection of conditioned media, the VEGF expression of remaining CL1 cells were determined by Western analyses and revealed that evodiamine decreased VEGF expression. Moreover, administration of recombinant human VEGF(165) (rhVEGF(165)) induced tube formation and ERK phosphorylation by HUVECs, and partially attenuated inhibitory effect of evodiamine. From these results, we suggested that evodiamine is a potent inhibitor of angiogenesis. The mechanism might involve at least the inhibition of VEGF expression, probably through repression of ERK phosphorylation.