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Growth Inhibitors (growth + inhibitor)
Selected AbstractsResponse of the freshwater alga Chlorella vulgaris to trichloroisocyanuric acid and ciprofloxacin,ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 1 2008Xiangping Nie Abstract The effects of trichloroisocyanuric acid (TCCA) and ciprofloxacin (CPFX) on the freshwater alga Chlorella vulgaris were assessed by toxicity bioassays and by the values of biomarkers in phase I and phase II. The biomarkers included growth rate, concentration of chlorophyll a, activities of 7-ethoxyresorufin- O -dealkylases (EROD), glutathione S -transferase (GST), catalase (CAT), and total glutathione (GSH). Ciprofloxacin was a weaker growth inhibitor than TCCA but, at a concentration of greater than 12.5 mg/L, decreased the growth of C. vulgaris. Concentration of chlorophyll a showed a similar trend. The 96-h median effective concentration (EC50; i.e., 50% reduction in growth relative to the control) of CPFX was 20.6 mg/L. Trichloroisocyanuric acid was a strong growth inhibitor and, at concentrations of greater than 0.80 mg/L, caused 100% inhibition on 24-h exposure. The 96-h EC50 of TCCA was 0.313 mg/L. Ciprofloxacin and TCCA affected the phase I and phase II enzyme activities differently. On exposure to CPFX, both EROD and GSH decreased at low CPFX concentrations (<5.0 mg/L) and increased at high CPFX concentrations (>12.5 mg/L), and CAT and GST exhibited induction at low concentrations and inhibition at high concentrations. In TCCA exposure, GST activity was significantly stimulated, and GSH concentration was increased. Catalase activity increased only at TCCA concentrations of greater than 0.12 mg/L, and no change in EROD activity was observed. [source] Transforming growth factor-,1 expression is up-regulated in maturation-stage enamel organ and may induce ameloblast apoptosisEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 2 2009Masahiro Tsuchiya Transforming growth factor-,1 (TGF-,1) regulates a variety of cellular responses that are dependent on the developmental stage and on the origins of the cell or the tissue. In mature tissues, and especially in tissues of epithelial origin, TGF-,1 is generally considered to be a growth inhibitor that may also promote apoptosis. The ameloblast cells of the enamel organ epithelium are adjacent to and responsible for the developing enamel layer on unerupted teeth. Once the enamel layer reaches its full thickness, the tall columnar secretory-stage ameloblasts shorten, and a portion of these maturation-stage ameloblasts become apoptotic. Here we investigate whether TGF-,1 plays a role in apoptosis of the maturation-stage ameloblasts. We demonstrate in vitro that ameloblast lineage cells are highly susceptible to TGF-,1-mediated growth arrest and are prone to TGF-,1-mediated cell death/apoptosis. We also demonstrate in vivo that TGF-,1 is expressed in the maturation-stage enamel organ at significantly higher levels than in the earlier secretory-stage enamel organ. This increased expression of TGF-,1 correlates with an increase in expression of the enamel organ immediate-early stress-response gene and with a decrease in the anti-apoptotic Bcl2 : Bax expression ratio. We conclude that TGF-,1 may play an important role in ameloblast apoptosis during the maturation stage of enamel development. [source] Natural killer cell-mediated ablation of metastatic liver tumors by hydrodynamic injection of IFN, gene to miceINTERNATIONAL JOURNAL OF CANCER, Issue 6 2007Tetsuo Takehara Abstract Interferon (IFN) , is a pleiotropic cytokine acting as an antiviral substance, cell growth inhibitor and immunomodulator. To evaluate the therapeutic efficacy and mechanisms of IFN, on hepatic metastasis of tumor cells, we hydrodynamically injected naked plasmid DNA encoding IFN,1 (pCMV-IFNa1) into Balb/cA mice having 2 days hepatic metastasis of CT-26 cells. Single injection of pCMV-IFNa1 efficiently enhanced the natural killer (NK) activity of hepatic mononuclear cells, induced production of IFN, in serum and led to complete rejection of tumors in the liver. Mice protected from hepatic metastasis by IFN, therapy displayed a tumor-specific cytotoxic T cell response and were resistant to subcutaneous challenge of CT-26 cells. NK cells were critically required for IFN,-mediated rejection of hepatic metastasis, because their depletion by injecting anti-asialo GM1 antibody completely abolished the antimetastatic effect. To find whether NK cells are directly activated by IFN, and are sufficient for the antimetastatic effect, the responses to IFN, were examined in SCID mice lacking T cells, B cells and NKT cells. IFN, completely rejected hepatic metastasis in SCID mice and efficiently activated SCID mononuclear cells, as evidenced by activation of STAT1 and a variety of genes, such as MHC class I, granzyme B, tumor necrosis factor-related apoptosis-inducing ligand and IFN,, and also enhanced Yac1 lytic ability. Study of IFN, knockout mice revealed that IFN, was not necessary for IFN,-mediated NK cell activation and metastasis protection. In conclusion, IFN, efficiently activates both innate and adaptive immune responses, but NK cells are critically required and sufficient for IFN,-mediated initial rejection of hepatic metastasis of microdisseminated tumors. © 2006 Wiley-Liss, Inc. [source] The role of vascular endothelial growth inhibitor in wound healingINTERNATIONAL WOUND JOURNAL, Issue 1 2007Article first published online: 5 APR 200 No abstract is available for this article. [source] TGF-, control of cell proliferationJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2005Shuan S. Huang Abstract This article focuses on recent findings that the type V TGF-, receptor (T,R-V), which co-expresses with other TGF-, receptors (T,R-I, T,R-II, and T,R-III) in all normal cell types studied, is involved in growth inhibition by IGFBP-3 and TGF-, and that TGF-, activity is regulated by two distinct endocytic pathways (clathrin- and caveolar/lipid-raft-mediated). TGF-, is a potent growth inhibitor for most cell types, including epithelial and endothelial cells. The signaling by which TGF-, controls cell proliferation is not well understood. Many lines of evidence indicate that other signaling pathways, in addition to the prominent T,R-I/T,R-II/Smad2/3/4 signaling cascade, are required for mediating TGF-,-induced growth inhibition. Recent studies revealed that T,R-V, which is identical to LRP-1, mediates IGF-independent growth inhibition by IGFBP-3 and mediates TGF-,-induced growth inhibition in concert with T,R-I and T,R-II. In addition, IRS proteins and a Ser/Thr-specific protein phosphatase(s) are involved in the T,R-V-mediated growth inhibitory signaling cascade. The T,R-V signaling cascade appears to cross-talk with the T,R-I/T,R-II, insulin receptor (IR), IGF-I receptor (IGF-IR), integrin and c-Met signaling cascades. Attenuation or loss of the T,R-V signaling cascade may enable carcinoma cells to escape from TGF-, growth control and may contribute to the aggressiveness and invasiveness of these cells via promoting epithelial-to-mesenchymal transdifferentiation (EMT). Finally, the ratio of TGF-, binding to T,R-II and T,R-I is a signal controlling TGF-, partitioning between two distinct endocytosis pathways and resultant TGF-, responsiveness. These recent studies have provided new insights into the molecular mechanisms underlying TGF-,-induced cellular growth inhibition, cross-talk between the T,R-V and other signaling cascades, the signal that controls TGF-, responsiveness and the role of T,R-V in tumorigenesis. © 2005 Wiley-Liss, Inc. [source] K vitamins, PTP antagonism, and cell growth arrestJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2002Brian I. Carr The main function of K vitamins is to act as co-factors for ,-glutamyl carboxylase. However, they have also recently been shown to inhibit cell growth. We have chemically synthesized a series of K vitamin analogs with various side chains at the 2 or 3 position of the core naphthoquinone structure. The analogs with short thio-ethanol side chains are found to be more potent growth inhibitors in vitro of various tumor cell lines. Cpd 5 or [2-(2-mercaptoethanol)-3-methyl-1,4-naphthoquinone] is one of the most potent. The anti-proliferation activity of these compounds is antagonized by exogenous thiols but not by non-thiol antioxidants. This suggests that the growth inhibition is mediated by sulfhydryl arylation of cellular glutathione and cysteine-containing proteins and not by oxidative stress. The protein tyrosine phosphatases (PTP) are an important group of proteins that contain cysteine at their catalytic site. PTPs regulate mitogenic signal transduction and cell cycle progression. PTP inhibition by Cpd 5 results in prolonged tyrosine phosphorylation and activation of several kinases and transcription factors including EGFR, ERK1/2, and Elk1. Cpd 5 could activate ERK1/2 either by signaling from an activated EGFR, which is upstream in the signaling cascade, or by direct inhibition of ERK1/2 phosphatase(s). Prolonged ERK1/2 phosphorylation strongly correlates with Cpd 5-mediated growth inhibition. Cpd 5 can also bind to and inhibit the Cdc25 family of dual specific phosphatases. As a result, several Cdc25 substrates (Cdk1, Cdk2, Cdk4) involved in cell cycle progression are tyrosine phosphorylated and thereby inhibited by its action. Cpd 5 could also inhibit both normal liver regeneration and hepatoma growth in vivo. DNA synthesis during rat liver regeneration following partial hepatectomy, transplantable rat hepatoma cell growth, and glutathione-S-transferase-pi expressing hepatocytes after administration of the chemical carcinogen diethylnitrosamine, are all inhibited by Cpd 5 administration. The growth inhibitory effect during liver regeneration and transplantable tumor growth is also correlated with ERK1/2 phosphorylation induced by Cpd 5. Thus, Cpd 5-mediated inhibition of PTPs, such as Cdc25 leads to cell growth arrest due to altered activity of key cellular kinases involved in signal transduction and cell cycle progression. This prototype K vitamin analog represents a novel class of growth inhibitor based upon its action as a selective PTP antagonist. It is clearly associated with prolonged ERK1/2 phosphorylation, which is in contrast with the transient ERK1/2 phosphorylation induced by growth stimulatory mitogens. © 2002 Wiley-Liss, Inc. [source] 1,1-bis(3,-indolyl)-1-(p -methoxyphenyl)methane activates Nur77-independent proapoptotic responses in colon cancer cellsMOLECULAR CARCINOGENESIS, Issue 4 2008Sung Dae Cho Abstract 1,1-Bis(3,-indolyl)-1-(p -methoxyphenyl)methane (DIM-C-pPhOCH3) is a methylene-substituted diindolylmethane (C-DIM) analog that activates the orphan receptor nerve growth factor-induced-B, (NGFI-B,, Nur77). RNA interference studies with small inhibitory RNA for Nur77 demonstrate that DIM-C-pPhOCH3 induces Nur77-dependent and -independent apoptosis, and this study has focused on delineating the Nur77-independent proapoptotic pathways induced by the C-DIM analog. DIM-C-pPhOCH3 induced caspase-dependent apoptosis in RKO colon cancer cells through decreased mitochondrial membrane potential which is accompanied by increased mitochondrial bax/bcl-2 ratios and release of cytochrome c into the cytosol. DIM-C-pPhOCH3 also induced phosphatidylinositol-3-kinase-dependent activation of early growth response gene-1 which, in turn, induced expression of the proapoptotic nonsteroidal anti-inflammatory drug-activated gene-1 (NAG1) in RKO and SW480 colon cancer cells. Moreover, DIM-C-pPhOCH3 also induced NAG-1 expression in colon tumors in athymic nude mice bearing RKO cells as xenografts. DIM-C-pPhOCH3 also activated the extrinsic apoptosis pathway through increased phosphorylation of c- jun N-terminal kinase which, in turn, activated C/EBP homologous transcription factor (CHOP) and death receptor 5 (DR5). Thus, the effectiveness of DIM-C-pPhOCH3 as a tumor growth inhibitor is through activation of Nur77-dependent and -independent pathways. © 2007 Wiley-Liss, Inc. [source] Characterization of three members of the Arabidopsis carotenoid cleavage dioxygenase family demonstrates the divergent roles of this multifunctional enzyme familyTHE PLANT JOURNAL, Issue 6 2006Michele E. Auldridge Summary Arabidopsis thaliana has nine genes that constitute a family of putative carotenoid cleavage dioxygenases (CCDs). While five members of the family are believed to be involved in synthesis of the phytohormone abscisic acid, the functions of the other four enzymes are less clear. Recently two of the enzymes, CCD7/MAX3 and CCD8/MAX4, have been implicated in synthesis of a novel apocarotenoid hormone that controls lateral shoot growth. Here, we report on the molecular and genetic interactions between CCD1, CCD7/MAX3 and CCD8/MAX4. CCD1 distinguishes itself from other reported CCDs as being the only member not targeted to the plastid. Unlike ccd7/max3 and ccd8/max4, both characterized as having highly branched phenotypes, ccd1 loss-of-function mutants are indistinguishable from wild-type plants. Thus, even though CCD1 has similar enzymatic activity to CCD7/MAX3, it does not have a role in synthesis of the lateral shoot growth inhibitor. Rather, it may have a role in synthesis of apocarotenoid flavor and aroma volatiles, especially in maturing seeds where loss of function leads to significantly higher carotenoid levels. [source] Regulation of TGF-, signaling and its roles in progression of tumorsCANCER SCIENCE, Issue 3 2003Kohei Miyazono Transforming growth factor-, (TGF-,) is a potent growth inhibitor of most types of cells; therefore, perturbations of TGF-, signaling are believed to result in progression of various tumors. On the other hand, TGF-, has been shown to act as an oncogenic cyto-kine through induction of extracellular matrices, angiogenesis, and immune suppression. A wide variety of effects of TGF-p are mediated by physical interaction of signal transducer Smad proteins with various transcription factors. Among these, Runx3 plays a pivotal role in prevention of gastric cancer. TGF-, signaling is regulated by various mechanisms in the cytoplasm and nucleus. Inhibitory Smads (l-Smads) repress TGF-, signaling mainly by interacting with activated TGF-, receptors. Smad ubiquitin regulatory factors (Smurfs) play important roles in facilitating the inhibitory signals induced by l-Smads. In addition, the transcrip-tional co-repressors c-Ski and SnoN interact with Smads, and repress transcription induced by TGF-,. Abnormalities of these regulators of TGF-, signaling may thus participate in the progression of various tumors. (Cancer Sci 2003; 94: 230,234) [source] Tenascin-R and axon growth-promoting molecules are up-regulated in the regenerating visual pathway of the lizard (Gallotia galloti)DEVELOPMENTAL NEUROBIOLOGY, Issue 7 2008Dirk M. Lang Abstract It is currently unclear whether retinal ganglion cell (RGC) axon regeneration depends on down-regulation of axon growth-inhibitory proteins, and to what extent outgrowth-promoting substrates contribute to RGC axon regeneration in reptiles. We performed an immunohistochemical study of the regulation of the axon growth-inhibiting extracellular matrix molecules tenascin-R and chondroitin sulphate proteoglycan (CSPG), the axon outgrowth-promoting extracellular matrix proteins fibronectin and laminin, and the axonal tenascin-R receptor protein F3/contactin during RGC axon regeneration in the lizard, Gallotia galloti. Tenascin-R and CSPG were expressed in an extracellular matrix-, oligodendrocyte/myelin- and neuron-associated pattern and up-regulated in the regenerating optic pathway. The expression pattern of tenascin-R was not indicative of a role in channeling or restriction of re-growing RGC axons. Up-regulation of fibronectin, laminin, and F3/contactin occurred in spatiotemporal patterns corresponding to tenascin-R expression. Moreover, we analyzed the influence of substrates containing tenascin-R, fibronectin, and laminin on outgrowth of regenerating lizard RGC axons. In vitro regeneration of RGC axons was not inhibited by tenascin-R, and further improved on mixed substrates containing tenascin-R together with fibronectin or laminin. These results indicate that RGC axon regeneration in Gallotia galloti does not require down-regulation of tenascin-R or CSPG. Presence of tenascin-R is insufficient to prevent RGC axon growth, and concomitant up-regulation of axon growth-promoting molecules like fibronectin and laminin may override the effects of neurite growth inhibitors on RGC axon regeneration. Up-regulation of contactin in RGCs suggests that tenascin-R may have an instructive function during axon regeneration in the lizard optic pathway. © 2008 Wiley Periodicals, Inc. Develop Neurobiol, 2008 [source] Biological warfare in the garden pond: tadpoles suppress the growth of mosquito larvaeECOLOGICAL ENTOMOLOGY, Issue 1 2003Allie Mokany Abstract. 1. Although tadpoles and mosquito larvae may compete for scarce resources in natural freshwater systems, the mechanisms involved in such competition remain largely unstudied. 2. Replicated artificial ponds were set up to examine the role of pathogenic interference (water-borne growth inhibitors) in two tadpole,mosquito systems from south-eastern Australia. One system comprised taxa that are commonly sympatric in freshwater ponds (tadpoles of Limnodynastes peronii and larvae of Culex quinquefasciatus) while the other comprised species that co-occur in brackish water ponds (tadpoles of Crinia signifera and larvae of Ochlerotatus australis). 3. Water that had previously contained tadpoles suppressed the rates of survival and pupation of mosquito larvae in both systems. Fungicide reduced or eliminated this effect, suggesting that the growth inhibitors may be fungal organisms (possibly the yeast Rhodotorula glutinis) from tadpole faeces. Fungicide also enhanced growth rates of tadpoles. 4. These results suggest that interference competition between tadpoles and mosquito larvae is mediated by other organisms in some ecological systems. [source] Liver cell proliferation requires methionine adenosyltransferase 2A mRNA up-regulationHEPATOLOGY, Issue 6 2002Covadonga Pañeda Regulation of liver cell proliferation is a key event to control organ size during development and liver regeneration. Methionine adenosyltransferase (MAT) 2A is expressed in proliferating liver, whereas MAT1A is the form expressed in adult quiescent hepatocytes. Here we show that, in H35 hepatoma cells, growth factors such as hepatocyte growth factor (HGF) and insulin up-regulated MAT2A expression. HGF actions were time- and dose-response dependent and required transcriptional activity. Mitogen-activated protein (MAP) kinase and phosphatidylinositol 3-phosphate kinase (PI 3-K) pathways were required for both HGF-induced cell proliferation and MAT2A up-regulation. Furthermore, in H35 cells treated with HGF, the inhibition of these pathways was associated with the switch from the expression of fetal liver MAT2A to the adult liver MAT1A isoform. Fetal liver hepatocytes exhibited an identical response pattern. Treatment of H35 hepatoma cells with MAT2A antisense oligonucleotides decreased cell proliferation induced by HGF; this decrease correlated with the decay in MAT2A messenger RNA (mRNA) levels. Finally, growth inhibitors such as transforming growth factor (TGF) , blocked HGF-induced MAT2A up-regulation while increasing MAT1A mRNA levels in H35 cells. In conclusion, our results show that MAT2A expression not only correlates with liver cell proliferation but is required for this process. [source] Decomposition of Allelopathic Plants in SoilJOURNAL OF AGRONOMY AND CROP SCIENCE, Issue 3 2005T. D. Xuan Abstract Higher plants with strong allelopathic properties are commonly incorporated into soil for weed-control purposes. To understand the phytotoxic variation in the soil, which can be utilized for weed control through the use of allelopathic plants, the decomposition of alfalfa (Medicago sativa L. cv. Rasen) and kava (Piper methysticum L.) after soil amendment were evaluated. Both alfalfa and kava strongly inhibited barnyardgrass and monochoria growth for up to 10 days (80,100 % weed control). After 20,25 days, the magnitude of inhibition was drastically reduced, but was still effective (50 % weed control). A number of phenolic acids were detected in the soil even 50 days after incorporation in low concentration, but their concentrations reached a maximum after 10,15 days and were efficacious until 20,25 days. Phenolic acids varied between alfalfa and kava. The variations in electrical conductivity (EC) and osmotic pressure (OP) were strongly related to chemicals and toxic compounds exuded into the soil during decomposition and were proportional to the magnitude of inhibition observed, whereas pH did not appear to be correlated with inhibition. The decomposition of several unknown inhibitors present in kava was also analysed and assessed. Our findings indicate that these growth inhibitors were almost disintegrated in soil after 10 days, but strong inhibition was detected until 25 days after amendment. Results from this study demonstrate that chemicals released from allelopathic plants incorporated into soil are toxic and cause inhibition of certain species and could be exploited as a biological tool for weed management. [source] K vitamins, PTP antagonism, and cell growth arrestJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2002Brian I. Carr The main function of K vitamins is to act as co-factors for ,-glutamyl carboxylase. However, they have also recently been shown to inhibit cell growth. We have chemically synthesized a series of K vitamin analogs with various side chains at the 2 or 3 position of the core naphthoquinone structure. The analogs with short thio-ethanol side chains are found to be more potent growth inhibitors in vitro of various tumor cell lines. Cpd 5 or [2-(2-mercaptoethanol)-3-methyl-1,4-naphthoquinone] is one of the most potent. The anti-proliferation activity of these compounds is antagonized by exogenous thiols but not by non-thiol antioxidants. This suggests that the growth inhibition is mediated by sulfhydryl arylation of cellular glutathione and cysteine-containing proteins and not by oxidative stress. The protein tyrosine phosphatases (PTP) are an important group of proteins that contain cysteine at their catalytic site. PTPs regulate mitogenic signal transduction and cell cycle progression. PTP inhibition by Cpd 5 results in prolonged tyrosine phosphorylation and activation of several kinases and transcription factors including EGFR, ERK1/2, and Elk1. Cpd 5 could activate ERK1/2 either by signaling from an activated EGFR, which is upstream in the signaling cascade, or by direct inhibition of ERK1/2 phosphatase(s). Prolonged ERK1/2 phosphorylation strongly correlates with Cpd 5-mediated growth inhibition. Cpd 5 can also bind to and inhibit the Cdc25 family of dual specific phosphatases. As a result, several Cdc25 substrates (Cdk1, Cdk2, Cdk4) involved in cell cycle progression are tyrosine phosphorylated and thereby inhibited by its action. Cpd 5 could also inhibit both normal liver regeneration and hepatoma growth in vivo. DNA synthesis during rat liver regeneration following partial hepatectomy, transplantable rat hepatoma cell growth, and glutathione-S-transferase-pi expressing hepatocytes after administration of the chemical carcinogen diethylnitrosamine, are all inhibited by Cpd 5 administration. The growth inhibitory effect during liver regeneration and transplantable tumor growth is also correlated with ERK1/2 phosphorylation induced by Cpd 5. Thus, Cpd 5-mediated inhibition of PTPs, such as Cdc25 leads to cell growth arrest due to altered activity of key cellular kinases involved in signal transduction and cell cycle progression. This prototype K vitamin analog represents a novel class of growth inhibitor based upon its action as a selective PTP antagonist. It is clearly associated with prolonged ERK1/2 phosphorylation, which is in contrast with the transient ERK1/2 phosphorylation induced by growth stimulatory mitogens. © 2002 Wiley-Liss, Inc. [source] A structure/function study of polyaminoamide dendrimers as silica scale growth inhibitorsJOURNAL OF CHEMICAL TECHNOLOGY & BIOTECHNOLOGY, Issue 6 2005Konstantinos D Demadis Abstract Dendrimers have attracted immense attention during the last decade due to their interesting properties both from a basic and an applied research viewpoint. Encapsulation of metal nanoparticles for catalysis, drug delivery and light harvesting are only some applications of dendrimers that are breaking new ground. A novel application of dendrimer technology is described in the present paper that relates to industrial water treatment. Industrial water systems often suffer from undesirable inorganic deposits. These can form either in the bulk or on metallic surfaces, such as heat exchangers or pipelines. Silica (SiO2) scale formation and deposition is a major problem in high-silica-containing cooling waters. Scale prevention rather than removal is highly desired. In this paper, benchtop screening tests on various silica inhibition chemistries are reported, with emphasis on materials with a dendrimeric structure. Specifically, the inhibition properties of commercially available STARBURST® polyaminoamide (PAMAM) dendrimers generations 0.5, 1, 1.5, 2, and 2.5 are investigated in detail together with other commonly-used scale inhibitors. Experimental results show that inhibition efficiency largely depends on structural features of PAMAM dendrimers such as generation number and nature of the end groups. PAMAM dendrimers are effective inhibitors of silica scale growth at 40 ppm dosage levels. PAMAM dendrimers also act as silica nucleators, forming SiO2,PAMAM composites. This occurs because the SiO2 formed by incomplete inhibition interacts with cationic PAMAM-1 and -2. The general scope of silica formation and inhibition in industrial waters is also discussed. Copyright © 2005 Society of Chemical Industry [source] INHIBITION OF FOODBORNE PATHOGENS AND SPOILING BACTERIA BY ESSENTIAL OIL AND EXTRACTS OF ERIGERON RAMOSUS (WALT.) B.S.P.JOURNAL OF FOOD SAFETY, Issue 2 2009ATIQUR RAHMAN ABSTRACT The antibacterial potential of essential oil and methanolic extracts of Erigeron ramosus (Walt.) B.S.P. was evaluated. Thirty-one components representing 95.3% of the total oil were identified, of which ,-caryophyllene (24.0%), ,-humulene (14.5%), 1,8-cineole (9.0%), eugenol (7.2%), globulol (7.1%), caryophyllene oxide (5.2%), ,-cadinene (5.0%), ,-copaene (4.9%) and widdrol (2.0%) were the major components. The antibacterial activity of essential oil and methanolic extracts of E. ramosus was determined in vitro using the agar diffusion method and minimum inhibitory concentration determination test against 14 (seven gram-positive and seven gram-negative) foodborne bacteria. The essential oil (5 µL/mL, corresponding to 1,000 ppm/disc), methanol extract and its different organic subfractions (7.5 µL/mL, corresponding to 1500 ppm/disc) of E. ramosus displayed a great potential of antibacterial activity against all gram-positive bacteria: Staphylococcus aureus (ATCC 6538 and KCTC 1916), Listeria monocytogenes (ATCC 19116, ATCC 19118, ATCC 19166 and ATCC 15313) and Bacillus subtilis ATCC 6633 and four gram-negative bacteria: Pseudomonas aeruginosa KCTC 2004, Enterobacter aerogenes KCTC 2190 and Escherichia coli (0157:H7 ATCC 43888 and ATCC 8739). The zones of inhibition of different concentrations of essential oil and methanolic extracts against the tested bacteria were found in the range of 10.1,22.3 mm, and MIC values were recorded between 62.5 and 500 µg/mL. PRACTICAL APPLICATIONS The use of essential oil and organic extracts of Erigeron ramosus (Walt.) B.S.P. as antibacterial agents will be suitable for applications on the food industry as natural preservatives or flavoring to control foodborne pathogens. They can be used as growth inhibitors of Listeria monocytogenes, Staphylococcus aureus, Bacillus subtilis, Escherichia coli, Enterobacter aerogenes and Pseudomonas aeruginosa, some important foodborne pathogens and spoiling bacteria. The main reason for their suitability is their natural origin, which consumers find comforting and which is beneficial for the environment, and the very low risk that pathogens will develop resistance to the mixture of components that make up the oil and extracts with their apparent diversity of antibacterial mechanisms. These beneficial characteristics could increase food safety and shelf life. [source] Factors Affecting the Hydroxycinnamate Decarboxylase/Vinylphenol Reductase Activity of Dekkera/Brettanomyces: Application for Dekkera/Brettanomyces Control in Red Wine MakingJOURNAL OF FOOD SCIENCE, Issue 1 2009S. Benito ABSTRACT:, The growth of Dekkera/Brettanomyces yeasts during the ageing of red wines,which can seriously reduce the quality of the final product,is difficult to control. The present study examines the hydroxycinnamate decarboxylase/vinylphenol reductase activity of different strains of Dekkera bruxellensis and Dekkera anomala under a range of growth-limiting conditions with the aim of finding solutions to this problem. The yeasts were cultured in in-house growth media containing different quantities of growth inhibitors such as ethanol, SO2, ascorbic acid, benzoic acid and nicostatin, different sugar contents, and at different pHs and temperatures. The reduction of p -coumaric acid and the formation of 4-ethylphenol were periodically monitored by HPLC-PDA. The results of this study allow the optimization of differential media for detecting/culturing these yeasts, and suggest possible ways of controlling these organisms in wineries. [source] Tamoxifen attenuates inflammatory-mediated damage and improves functional outcome after spinal cord injury in ratsJOURNAL OF NEUROCHEMISTRY, Issue 6 2009Dai-Shi Tian Abstract Tamoxifen has been found to be neuroprotective in both transient and permanent experimental ischemic stroke. However, it remains unknown whether this agent shows a similar beneficial effect after spinal cord injury (SCI), and what are its underlying mechanisms. In this study, we investigated the efficacy of tamoxifen treatment in attenuating SCI-induced pathology. Blood,spinal cord barrier (BSCB) permeability, tissue edema formation, microglial activation, neuronal cell death and myelin loss were determined in rats subjected to spinal cord contusion. The results showed that tamoxifen, administered at 30 min post-injury, significantly decreased interleukin-1, (IL-1,) production induced by microglial activation, alleviated the amount of Evans blue leakage and edema formation. In addition, tamoxifen treatment clearly reduced the number of apoptotic neurons post-SCI. The myelin loss and the increase in production of myelin-associated axonal growth inhibitors were also found to be significantly attenuated at day 3 post-injury. Furthermore, rats treated with tamoxifen scored much higher on the locomotor rating scale after SCI than did vehicle-treated rats, suggesting improved functional outcome after SCI. Together, these results demonstrate that tamoxifen provides neuroprotective effects for treatment of SCI-related pathology and disability, and is therefore a potential neuroprotectant for human spinal cord injury therapy. [source] Temperature Dependences of Leakage Currents of ZnO Varistors Doped with Rare-Earth OxidesJOURNAL OF THE AMERICAN CERAMIC SOCIETY, Issue 8 2010Jun Hu Rare-earth oxides are doped into ZnO varistors as grain growth inhibitors for increasing the varistors' voltage gradients. However, their leakage currents become large and their nonlinear coefficients decrease at the same time. The reasonable explanation for such a phenomenon has not yet been available. In this paper, the temperature dependences of varistor samples' leakage currents are investigated, which reveal that the increased leakage currents of ZnO varistors with Y2O3 doping are mainly due to the bypass paths through the intergranular materials at grain corners. [source] Isolation and identification of a potent allelopathic substance in rice root exudatesPHYSIOLOGIA PLANTARUM, Issue 3 2002Hisashi Kato-Noguchi A search for growth inhibitors in rice root exudates was undertaken in order to clarify the allelopathic system in rice (Oryza sativa L.). Rice seedlings inhibited the growth of cress (Lepidium sativum L.) and lettuce (Lactuca sativa L.) seedlings when the cress and lettuce were grown with rice seedlings. The putative compound causing the inhibitory effect of rice seedlings was isolated from their culture solution, and the chemical structure of the inhibitor was determined by spectral data as momilactone B. Momilactone B inhibited the growth of cress and lettuce seedlings at concentrations greater than 3 and 30 µM, respectively. The concentration of momilactone B was 3.4 and 1.1 nmol per seedling in the culture solutions of husked and non-husked rice seedlings, respectively. These results suggest that rice seedlings may release momilactone B into the environment and the stress caused by the husk-treatment may increase the amount of momilactone B released. Thus, momilactone B may play an important role in rice allelopathy. [source] | |||||||||||||||||||||||||||||||