过氧化氢脱毒前后小桐子油饼营养成分分析

小桐子(Jatropha curcas Linn.)又名麻疯树,属于大戟科(Euphorbiaceae)麻疯树属(Jatropha Linn.)植物,在中国西南各省均有大规模种植基地。小桐子树皮和叶片具有多种生物活性[1-2];种子含丰富油脂,可作为生物柴油的原料[3]。小桐子油饼是一种在小桐子生物柴油生产过程中大量产生的副产品,其中的蛋白质含量较高、氨基酸组成合理,是优     

The involvement of hydrogen peroxide in abscisic acid-induced activities of ascorbate peroxidase and glutathione reductase in rice roots

We have monitored the changes in antioxidant enzyme activities and H₂O₂ concentrations in roots of rice (Oryza sativa L., cv. Taichung Native 1) seedlings treated with exogenous abscisic acid(ABA). Decrease in superoxide dismutase (SOD) and catalase (CAT) activities was observed in rice roots in the presence of ABA. However, ascorbate peroxide (APX) and glutathione reductase (GR) activities were increased after the ABA treatment. ABA treatment resulted in an increase in H₂O₂ concentrations in rice roots. Pre-treatment with dimethylthiourea, a chemical trap for H₂O₂, and diphenyleneiodonium chloride (DPI), a well known inhibitor of NADPH oxidase, inhibited ABA-induced accumulation of H₂O₂ and ABA-induced activities of APX and GR. ABA-induced accumulation of H₂O₂ was found to be prior to ABA-induced activities of APX and GR. Our results suggest that H₂O₂ is involved in ABA-induced APX and GR activities in rice roots.     

MicroRNAs are dynamically regulated and play an important role in LPS-induced lung injury

Acute lung injury is characterized by an increase of inflammatory reaction and severe lung edema. Even if there have been great advances in the identification of genes and signaling pathways involved in acute lung injury, the fundamental mechanisms of initiation and propagation of acute lung injury have not been understood completely. A growing amount of evidence indicates that microRNAs (miRNAs) are involved in various human diseases. However, the expression profile and function of miRNAs in acute lung injury have not been investigated. Here, using real-time polymerase chain reaction analysis, we show that a collection of miRNAs is dynamically regulated in lipopolysaccharide (LPS)-induced mouse acute lung injury. Among them, miR-199a and miR-16 are the most significantly down-regulated miRNAs. To study the role of miR-199a and miR-16 in acute lung injury, an over-expression of miR-199a or miR-16 assay was performed in LPS-treated A549 cells, and then the expression of inflammatory factors was analyzed. Over-expression of miR-199a could not alter the expression level of interleukin (IL)-6 and tumor necrosis factor-alpha (TNFα), while up-regulation of miR-16 could significantly down-regulate IL-6 and TNFα expression level. Using bioinformatic analysis, we show that a 3' untranslational region (UTR) of IL-6 and TNFα contains the binding sites of miR-16. Accordingly, over-expression of miR-16 could significantly suppress the luciferase activity of reporter fusion with the binding sites of TNFα in its 3'UTR region, suggesting that miR-16 played its role in LPS-induced lung inflammation by a direct manner. In this study, we show for the first time that miRNAs are dynamically regulated and play an important function in LPS-induced lung injury.     

Involvement of hydrogen peroxide in heat shock- and cadmium-induced expression of ascorbate peroxidase and glutathione reductase in leaves of rice seedlings

Hydrogen peroxide (H2O2) is considered a signal molecule inducing cellular stress. Both heat shock (HS) and Cd can increase H2O2 content. We investigated the involvement of H2O2 in HS- and Cd-mediated changes in the expression of ascorbate peroxidase (APX) and glutathione reductase (GR) in leaves of rice seedlings. HS treatment increased the content of H2O2 before it increased activities of APX and GR in rice leaves. Moreover, HS-induced H2O2 production and APX and GR activities could be counteracted by the NADPH oxidase inhibitors dipehenylene iodonium (DPI) and imidazole (IMD). HS-induced OsAPX2 gene expression was associated with HS-induced APX activity but was not regulated by H2O2. Cd-increased H2O2 content and APX and GR activities were lower with than without HS. Cd did not increase the expression of OsAPX and OsGR without HS treatment. Cd increased H2O2 content by Cd before it increased APX and GR activities without HS. Treatment with DPI and IMD effectively inhibited Cd-induced H2O2 production and APX and GR activities. Moreover, the effects of DPI and IMD could be rescued with H2O2 treatment. H2O2 may be involved in the regulation of HS- and Cd-increased APX and GR activities in leaves of rice seedlings.     

免疫复合物参与冻伤大鼠冻结-融化损伤的研究

目的：了解体液免疫在冻结性冻伤损伤病理生理过程中的作用,为冻结性冻伤的预防和治疗提供依据。方法：实验采用Wistar大鼠冻结性冻伤模型,在冻伤前及冻伤后4h、1d、3d和5d测量三种免疫球蛋白（IgG、IgA和IgM）、两种补体（C3和C4）和血清循环免疫复合物的含量;用免疫荧光标记技术检测骨骼肌中的组织免疫复合物含量;用免疫粘附法观察红细胞表面免疫复合物含量变化。结果：大鼠冻伤后血清IgG急剧下降,冻后4h下降至最低值。IgA在冻伤后1d达到最低。血清IgM浓度在冻伤后逐渐增高,冻后5d继续上升。血清循环免疫复合物浓度在冻后逐渐增高,冻后1d达峰值,为冻前的28、8倍（P〈0.01）。冻伤后1d大鼠骨骼肌开始出现免疫复合物沉积。红细胞表面免疫复合物含量明显高于冻前,冻后3d达到高峰（P〈0．01）。结论：研究结果表明,冻结性冻伤是一种免疫复合物相关性疾病,对此国内、外尚未见报道。     

Gangliosides play an important role in the organization of CD82-enriched microdomains

Four-transmembrane-domain proteins of the tetraspanin superfamily are the organizers of specific microdomains at the membrane [TERMs (tetraspanin-enriched microdomains)] that incorporate various transmembrane receptors and modulate their activities. The structural aspects of the organization of TERM are poorly understood. In the present study, we investigated the role of gangliosides in the assembly and stability of TERM. We demonstrated that inhibition of the glycosphingolipid biosynthetic pathway with specific inhibitors of glucosylceramide synthase [NB-DGJ (N-butyldeoxygalactonojirimycin) and PPMP (D-threo-1-phenyl-2-hexadecanoylamino-3-morpholino-1-propanol.HCl)] resulted in specific weakening of the interactions involving tetraspanin CD82. Furthermore, ectopic expression of the plasma-membrane-bound sialidase Neu3 in mammary epithelial cells also affected stability of the complexes containing CD82: its association with tetraspanin CD151 was decreased, but the association with EGFR [EGF (epidermal growth factor) receptor] was enhanced. The destabilization of the CD82-containing complexes upon ganglioside depletion correlated with the re-distribution of the proteins within plasma membrane. Importantly, depletion of gangliosides affected EGF-induced signalling only in the presence of CD82. Taken together, our results provide strong evidence that gangliosides play an important role in supporting the integrity of CD82-enriched microdomains. Furthermore, these results demonstrate that the association between different tetraspanins in TERM is controlled by distinct mechanisms and identify Neu3 as a first physiological regulator of the integrity of these microdomains.     

麻疯树中ADP核糖基化因子基因的克隆和表达

从麻疯树cDNA文库中筛选到包含完整编码序列的ADP核糖基化因子的cDNA序列,命名为Jc-arf．其长度为887bp,开放阅读框546bp,推测的编码蛋白含181个氨基酸残基,具有典型的GTP结合蛋白家族的特点：P框（GLDAAGKT）、G’框（DVGGQ）和G框（NKQDL）。序列分析显示,Jc-arf矿接近于人类ClassI型arf基因,其蛋白序列与多种植物ARF有很高的同源性。半定量RT-PCR结果显示,Jc-arf的表达具有一定的组织特异性,在花中最丰富。PEG、低温、NaCl胁迫下,Jc-arf的表达受PEG和低温的诱导,而对NaCl胁迫不敏感。     

Polycystin-1 may play an important role in mechanical modulation of bone growth and healing

Mechanical stress is known to modulate bone growth and healing. However, the mechanisms underlying the mechanotransduction are not fully understood. Previous studies show that PC1 is a promising candidate among proteins that may play a role in the mechanotransduction process as it has been shown to function as a flow sensor in renal epithelium and it is known to be important for the growth of for skeletal development. We hypothesized that PC1 plays an important role in bone responses to mechanical stress. PC1 is required for the proliferation, differentiation and survival of periosteal osteochondroprogenitor cells upon mechanical stimulation of bone. Using both genetically manipulated animal models and animals undergoing are necessary to test this hypothesis.     

Neurotrophins play an important role in the perineural invasion and distant metastasis of malignant tumor

Neurotrophins (NTs) family was first discovered in nervous system and it regulates the proliferation and differentiation of many neural cell types in the peripheral and central nervous system.Due to their perineural invasive characters, certain part of malignant tumor cases was first diagnosed because of nerve paralysis or idiopathic neuralgia caused by perineural invasion. For this reason, the study on the association between NTs and perineural invasion of malignant tumor aroused the attention of many researchers. Increasing evidence indicates that NTs and their receptors, Trks, play important roles in malignant cells, especially the exhibiting perineural invasive phenotype. It was suggested that NTs produced by neural tissue can act as a chemotactic factor, and tumor cells in which the overexpression of Trks' exists seem to be selected to invade the perineural space. Except for contributing to perineural invasion of malignant tumor, accumulated evidence proved NTs now also significantly associated with the metastasis of malignant tumor. Overexpression of NTs or Trks often correlated with the tumorigenesis, angiogenesis and anoikis resistance in these malignancies, contributing significantly to the metastasis and poor prognosis.In summary, besides its role in development and function of nervous system, NTs also play an important role in the perineural invasion and metastasis of malignant tumor. Considering the role that NTs played in malignant tumor, we believe that further studies between NTs and malignant tumor are necessary. Research on the role of NTs pathway might allow advancements in this field.     

Glycosylphosphatidylinositol-anchored proteins play an important role in the biogenesis of the Alzheimer's amyloid beta-protein.

The Alzheimer's amyloid protein (Abeta) is released from the larger amyloid beta-protein precursor (APP) by unidentified enzymes referred to as beta- and gamma-secretase. beta-Secretase cleaves APP on the amino side of Abeta producing a large secreted derivative (sAPPbeta) and an Abeta-bearing C-terminal derivative that is subsequently cleaved by gamma-secretase to release Abeta. Alternative cleavage of the APP by alpha-secretase at Abeta16/17 releases the secreted derivative sAPPalpha. In yeast, alpha-secretase activity has been attributed to glycosylphosphatidylinositol (GPI)-anchored aspartyl proteases. To examine the role of GPI-anchored proteins, we specifically removed these proteins from the surface of mammalian cells using phosphatidylinositol-specific phospholipase C (PI-PLC). PI-PLC treatment of fetal guinea pig brain cultures substantially reduced the amount of Abeta40 and Abeta42 in the medium but had no effect on sAPPalpha. A mutant CHO cell line (gpi85), which lacks GPI-anchored proteins, secreted lower levels of Abeta40, Abeta42, and sAPPbeta than its parental line (GPI+). When this parental line was treated with PI-PLC, Abeta40, Abeta42, and sAPPbeta decreased to levels similar to those observed in the mutant line, and the mutant line was resistant to these effects of PI-PLC. These findings provide strong evidence that one or more GPI-anchored proteins play an important role in beta-secretase activity and Abeta secretion in mammalian cells. The cell-surface GPI-anchored protein(s) involved in Abeta biogenesis may be excellent therapeutic target(s) in Alzheimer's disease.     

Cell-wall polysaccharides play an important role in decay resistance of Sphagnum and actively depressed decomposition in vitro

Sphagnum-dominated peatlands head the list of ecosystems with the largest known reservoirs of organic carbon (C). The bulk of this C is stored in decomposition-resistant litter of one bryophyte genus: Sphagnum. Understanding how Sphagnum litter chemistry controls C mineralization is essential for understanding potential interactions between environmental changes and C mineralization in peatlands. We aimed to separate the effects of phenolics from structural polysaccharides on decay of Sphagnum. We measured aerobic microbial respiration of different moss litter types in a lab. We used chemical treatments to step-wise remove the chemical compounds thought to be important in decay-resistance in three taxonomically distant moss genera. We also focused on the effect of Sphagnum-specific cell-wall pectin-like polysaccharides (sphagnan) on C and N mineralization. Removing polymeric lignin-like phenolics had only negligible effects on C mineralization of Sphagnum litter, but increased mineralization of two other bryophyte genera, suggesting a minor role of these phenolics in decay resistance of Sphagnum but a major role of cell-wall polysaccharides. Carboxyl groups of pectin-like polysaccharides represented a C-source in non-Sphagnum litters but resisted decay in Sphagnum. Finally, isolated sphagnan did not serve as C-source but inhibited C and N mineralization instead, reminiscent of the effects reported for phenolics in other ecosystems. Our results emphasize the role of polysaccharides in resistance to, and active inhibition of, microbial mineralization in Sphagnum-dominated litter. As the polysaccharides displayed decay-inhibiting properties hitherto associated with phenolics (lignin, polyphenols), it raises the question if polysaccharide-dominated litter also shares similar environmental controls on decomposition, such as temperature or nutrient and water availability.     

Complement and the alternative pathway play an important role in LPS/D-GalN-induced fulminant hepatic failure

Fulminant hepatic failure (FHF) is a clinically severe type of liver injury with an extremely high mortality rate. Although the pathological mechanisms of FHF are not well understood, evidence suggests that the complement system is involved in the pathogenesis of a variety of liver disorders. In the present study, to investigate the role of complement in FHF, we examined groups of mice following intraperitoneal injection of LPS/D-GalN: wild-type C57BL/6 mice, wild-type mice treated with a C3aR antagonist, C5aR monoclonal antibody (C5aRmAb) or CR2-Factor H (CR2-fH, an inhibitor of the alternative pathway), and C3 deficient mice (C3^−/− mice). The animals were euthanized and samples analyzed at specific times after LPS/D-GalN injection. The results show that intraperitoneal administration of LPS/D-GalN activated the complement pathway, as evidenced by the hepatic deposition of C3 and C5b-9 and elevated serum levels of the complement activation product C3a, the level of which was associated with the severity of the liver damage. C3a receptor (C3aR) and C5a receptor (C5aR) expression was also upregulated. Compared with wild-type mice, C3^−/− mice survived significantly longer and displayed reduced liver inflammation and attenuated pathological damage following LPS/D-GalN injection. Similar levels of protection were seen in mice treated with C3aR antagonist,C5aRmAb or CR2-fH. These data indicate an important role for the C3a and C5a generated by the alternative pathway in LPS/D-GalN-induced FHF. The data further suggest that complement inhibition may be an effective strategy for the adjunctive treatment of fulminant hepatic failure.     

Early production and scavenging of hydrogen peroxide in the apoplast of sunflower plants exposed to ozone

The present work set out to define the processes involved in the early O3-induced H2O2 accumulation in sunflower plants exposed to a single pulse of 150 ppb of O3 for 4 h. Hydrogen peroxide accumulation only occurred in the apoplast and this temporally coincided with the fumigation period. The inhibitor experiments suggested that both the plasma membrane-bound NAD(P)H oxidase complex and cell-wall NAD(P)H PODs contributed to H2O2 generation. To investigate the mechanisms responsible for O3-induced H2O2 accumulation further, both production and scavenging of H2O2 were investigated in the extracellular matrix after subcellular fractionation. The results indicated that H2O2 accumulation is a complex and highly regulated event requiring the time-dependent stimulation and down-regulation of differently located enzymes, some of which are involved in H2O2 generation and degradation, not only during the fumigation period but also in the subsequent recovery period in non-polluted air. Owing to the possible interplay between H2O2 and ethylene, the time-course of ethylene emission was analysed too. Ethylene was rapidly emitted following O3 exposure, but it declined to control values as early as after 4 h of exposure. The early contemporaneous detection of increased ethylene and H2O2 levels after 30 min of exposure does not allow a clear temporal relationship between these two signalling molecules to be established.     

Vibrio fischeri lux genes play an important role in colonization and development of the host light organ

The bioluminescent bacterium Vibrio fischeri and juveniles of the squid Euprymna scolopes specifically recognize and respond to one another during the formation of a persistent colonization within the host's nascent light-emitting organ. The resulting fully developed light organ contains brightly luminescing bacteria and has undergone a bacterium-induced program of tissue differentiation, one component of which is a swelling of the epithelial cells that line the symbiont-containing crypts. While the luminescence (lux) genes of symbiotic V. fischeri have been shown to be highly induced within the crypts, the role of these genes in the initiation and persistence of the symbiosis has not been rigorously examined. We have constructed and examined three mutants (luxA, luxI, and luxR), defective in either luciferase enzymatic or regulatory proteins. All three are unable to induce normal luminescence levels in the host and, 2 days after initiating the association, had a three- to fourfold defect in the extent of colonization. Surprisingly, these lux mutants also were unable to induce swelling in the crypt epithelial cells. Complementing, in trans, the defect in light emission restored both normal colonization capability and induction of swelling. We hypothesize that a diminished level of oxygen consumption by a luciferase-deficient symbiotic population is responsible for the reduced fitness of lux mutants in the light organ crypts. This study is the first to show that the capacity for bioluminescence is critical for normal cell-cell interactions between a bacterium and its animal host and presents the first examples of V. fischeri genes that affect normal host tissue development.