9 research outputs found
Abeilles et composante ligneuse
International audienceEspÚce mutualiste [1] et polylectique [2], l'abeille domestique est impliquée dans le processus de pollinisation de nombreuses plantes à fleurs sauvages et cultivées. En contrepartie, elle profite de la floraison de ces plantes pour l'acquisition de ressources polliniques et nectarifÚres [3]. Elle interagit avec une multitude de composantes paysagÚres et d'espÚces floristiques [4]. Pourtant, on constate depuis une vingtaine d'années une forte diminution des populations d'abeilles domestiques et sauvages [5]. Celle-ci reste encore inexpliquée sur bien des aspects
La composante ligneuse : un Ă©lĂ©ment clĂ© pour lâapport de ressources alimentaires aux colonies dâabeilles domestiques (Apis mellifera L.) en contexte paysager agricole
EspĂšce mutualiste et polylectique, lâabeille domestique est impliquĂ©e dans le processus de pollinisation de nombreuses plantes Ă fleurs sauvages et cultivĂ©es. En contrepartie, elle profite de la floraison de ces plantes pour lâacquisition de ressources polliniques et nectarifĂšres (Pouvreau, 2004). Elle interagit avec une multitude de composantes paysagĂšres et dâespĂšces floristiques (Odoux et al., 2012). Pourtant, on constate depuis une vingtaine dâannĂ©es une forte diminution des populations dâabeilles domestiques et sauvages (Potts et al., 2010). Celle-ci reste encore inexpliquĂ©e sur bien des aspects. Lâampleur ainsi que le nombre de pays touchĂ©s par ce phĂ©nomĂšne inquiĂštent (ibid.). Outre les difficultĂ©s concernant lâalimentation et le poids Ă©conomique du service rendu par la pollinisation (Gallai et al., 2009), câest un large pan du fonctionnement gĂ©nĂ©ral des Ă©cosystĂšmes qui semble fragilisĂ©. Les Ă©tudes les plus rĂ©centes ne permettent que dâaugurer une synergie entre plusieurs causes (Van Engelsdorp, et Meixner, 2010 ; Di Prisco et al., 2013). Parmi elles, lâorganisation du paysage (composition et structure) nâest pas immĂ©diatement suspectĂ©e comme Ă©lĂ©ment central et nâapparaĂźt pas comme facteur aussi dĂ©terminant que le varroa, les maladies parasitaires ou de maniĂšre plus prĂ©gnante, lâutilisation des pesticides et fongicides en agriculture (graines enrobĂ©es, pratiques dâĂ©pandage, etc.). En effet, comme lâindique lâĂ©tude bibliomĂ©trique de Requier (2013), rĂ©alisĂ©e Ă partir de 1538 publications parues entre 1975 et 2013, les causes de dĂ©pĂ©rissement et ou de mortalitĂ© des colonies dâabeilles domestiques les plus analysĂ©es portent Ă plus de 61 % sur les effets liĂ©s aux parasites et pathogĂšnes (Fig.1). 31 % seulement interrogent les rĂ©percussions liĂ©es aux stress environnementaux. Parmi elles seules 44 % Ă©tudient les impacts liĂ©s Ă la structure et Ă la composition du paysage (pertes dâhabitats et ressources trophiques). Moins encore questionnent le rĂŽle de la composante ligneuse (bois, bosquets, haies, arbres isolĂ©s, etc.), rare Ă©lĂ©ment pĂ©renne du paysage, pour lâapport de ressources trophiques aux colonies
An insight into the use of cationic peptides for plasmid DNA delivery in cells.
International audienceIn this work, we contribute an insight into the ability of cationic peptides for the delivery of plasmid DNA in cells. Although most peptides used for cellular transfection are cationic, not all of them possess this potential. Using plasmid DNA bearing reporter genes and cells of the breast cancer MDA-MB 435 line, we show at first that only peptides in an α-helical structure can give high levels whereas peptides with a ÎČ-strand structure cannot. Amphipathic peptides rich in lysine, namely L10K5 or L13K6, adopting both an α-helical structure are able to be used for this task. Subsequently, we show that protamine, equally rich in basic arginine, but not having an α-helical structure, cannot alone efficiently deliver DNA. However, it improved the transfection level by cationic liposomes, undoubtedly by a condensing effect. This enhancement in transfection by protamine was not observed using the peptide L13K6 and this peptide did not behave as protamine to enhance the transfection level of cationic liposomes
Aponecrotic, antiangiogenic and antiproliferative effects of a novel dextran derivative on breast cancer growth in vitro and in vivo
International audience1 Since the sodium phenylacetate (NaPa) was reported to enhance the inhibitory effect of carboxymethyl benzylamide dextran (CMDB) on the breast cancer growth, we performed the esterification of CMDB with NaPa to obtain a new drug carrying the characteristics of these two components. A new molecule, phenylacetate carboxymethyl benzylamide dextran, was named NaPaC. We investigated in vitro and in vivo the effects of NaPaC on MCFâ7ras cell growth as well as its apoptotic and antiangiogenic effects in comparison to NaPa and CMDB. In addition, we assessed in vitro the antiproliferative effects of these drugs on other breast cancer cells, including MDAâMBâ231, MDAâMBâ435 and MCFâ7. In vitro , NaPaC inhibited MCFâ7ras cell proliferation by 40% at concentration lower than that of CMDB and NaPa (12âÎŒ M vs 73âÎŒ M and 10âm M ). IC 50 s were 6 and 28âÎŒ M for NaPaC and CMDB, respectively. The similar results were obtained for three other breast cancer cell lines. NaPaC reduced the DNA replication and induced cell recruitment in G 0 /G 1 phase more efficiently than its components. Moreover, it induced a cell death at concentration 1000âfold lower than NaPa. In vivo , CMDB (150âmgâkg â1 ) and NaPa (40âmgâkg â1 ) inhibited the MCFâ7ras tumour growth by 37 and 57%, respectively, whereas NaPaC (15âmgâkg â1 ) decreased tumour growth by 66% without toxicity. NaPa or CMDB reduced the microvessel number in tumour by 50% after 7 weeks of treatment. NaPaC had the same effect after only 2 weeks. After 7 weeks, it generated a large necrosis area without detectable microvessels. In vitro , NaPaC inhibited human endothelial cell proliferation more efficiently than CMDB or NaPa. NaPaC interacts with vascular endothelial growth factor as observed by affinity electrophoresis. NaPaC acts like NaPa and CMDB but in more potent manner than components used separately. Its antiproliferative, aponecrotic and antiâangiogenic actions make it a good candidate for a new antiâcancer drug. British Journal of Pharmacology (2002) 135 , 1859â1871; doi: 10.1038/sj.bjp.070464
In vitro and in vivo study of Tc-99m-MIBI encapsulated in PEG-liposomes: A promising radiotracer for tumour imaging
Encapsulation of technetium-99m sestamibi (Tc-99m-MIBI) in polyethyleneglycol-liposomes (Tc-99m-MIBI-PEG-liposomes) could extend the duration of its circulation in blood and alter its biodistribution, enabling its concentration in tumours to be increased. An original method to encapsulate Tc-99m-MIBI in PEG-liposomes is described. The Tc-99m-MIBI-PEG-liposomes were compared with free Tc-99m-MIBI with respect to (a) tumour availability (b) ability to distinguish between chemotherapy-sensitive and -resistant cells and (c) uptake ratio in tumour imaging. PEG-liposomal systems composed of distearoylphosphatidylcholine/cholesterol/PEG(2000)-distearoyl phosphatidylethanolamine and lissamine-rhodamine B-labelled liposomes were used. The encapsulation of 99mTc-MIBI in liposomes was achieved using the K+ diffusion potential method. We compared the uptake of free versus encapsulated Tc-99m-MIBI by sensitive and resistant erythroleukaemia (K562) and breast tumour (MCF-7ras) cells. To assess the internalisation of these liposomes into cells, rhodamine B-labelled PEG-liposomes were used and visualised by fluorescence microscopy. Biodistribution and imaging characteristics of encapsulated and free radiotracer were determined in rats and tumour-bearing nude mice. The efficiency of Tc-99m-MIBI encapsulation in PEG-liposomes was 50+/-5%. Use of Tc-99m-MIBI-PEG-liposomes did not impair the ability of this tracer to distinguish between chemotherapy-sensitive and -resistant tumour cells; the percentage of radio-activity accumulated in the sensitive K562 cells was 1.24+/-0.04%, as compared with 0.41+/-0.04% in the resistant K562 cells. One hour post injection in rats, PEG-liposomes showed a ten times higher activity in blood than free Tc-99m-MIBI, whereas activity of free Tc-99m-MIBI in kidneys and bladder was markedly higher than that of encapsulated Tc-99m-MIBI, indicating faster clearance of the free radiotracer. In the (MCF7-ras)-bearing nude mice, PEG-liposome uptake in tumour was two times that of free Tc-99m-MIBI. Summarising, the Tc-99m-MIBI-PEG-liposomes demonstrated a longer blood circulation time, enabled distinction between chemotherapy-sensitive and -resistant cells and improved tumour to background contrast in in vivo imaging. Tc-99m-MIBI-PEG-liposomes therefore show promising potential for tumour imaging
Base experimentale de carbonisation de Saint-Martin de Londres: essais comparatifs de six systemes de carbonisation artisanale
SIGLECNRS RP 400 (746) / INIST-CNRS - Institut de l'Information Scientifique et TechniqueFRFranc
Aponecrotic, antiangiogenic and antiproliferative effects of a novel dextran derivative on breast cancer growth in vitro and in vivo
1. 1 Since the sodium phenylacetate (NaPa) was reported to enhance the inhibitory effect of carboxymethyl benzylamide dextran (CMDB) on the breast cancer growth, we performed the esterification of CMDB with NaPa to obtain a new drug carrying the characteristics of these two components. A new molecule, phenylacetate carboxymethyl benzylamide dextran, was named NaPaC. 2. We investigated in vitro and in vivo the effects of NaPaC on MCF-7ras cell growth as well as its apoptotic and antiangiogenic effects in comparison to NaPa and CMDB. In addition, we assessed in vitro the antiproliferative effects of these drugs on other breast cancer cells, including MDA-MB-231, MDA-MB-435 and MCF-7. 3. In vitro, NaPaC inhibited MCF-7ras cell proliferation by 40% at concentration lower than that of CMDB and NaPa (12âÎŒM vs 73âÎŒM and 10âmM). IC(50)s were 6 and 28âÎŒM for NaPaC and CMDB, respectively. The similar results were obtained for three other breast cancer cell lines. NaPaC reduced the DNA replication and induced cell recruitment in G(0)/G(1) phase more efficiently than its components. Moreover, it induced a cell death at concentration 1000-fold lower than NaPa. 4. In vivo, CMDB (150âmgâkg(â1)) and NaPa (40âmgâkg(â1)) inhibited the MCF-7ras tumour growth by 37 and 57%, respectively, whereas NaPaC (15âmgâkg(â1)) decreased tumour growth by 66% without toxicity. 5. NaPa or CMDB reduced the microvessel number in tumour by 50% after 7 weeks of treatment. NaPaC had the same effect after only 2 weeks. After 7 weeks, it generated a large necrosis area without detectable microvessels. In vitro, NaPaC inhibited human endothelial cell proliferation more efficiently than CMDB or NaPa. NaPaC interacts with vascular endothelial growth factor as observed by affinity electrophoresis. 6. NaPaC acts like NaPa and CMDB but in more potent manner than components used separately. Its antiproliferative, aponecrotic and anti-angiogenic actions make it a good candidate for a new anti-cancer drug