9 research outputs found

    Abeilles et composante ligneuse

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    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 l’apport de ressources alimentaires aux colonies d’abeilles domestiques (Apis mellifera L.) en contexte paysager agricole

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    EspĂšce mutualiste et polylectique, l’abeille 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 l’acquisition de ressources polliniques et nectarifĂšres (Pouvreau, 2004). Elle interagit avec une multitude de composantes paysagĂšres et d’espĂšces floristiques (Odoux et al., 2012). Pourtant, on constate depuis une vingtaine d’annĂ©es une forte diminution des populations d’abeilles domestiques et sauvages (Potts et al., 2010). Celle-ci reste encore inexpliquĂ©e sur bien des aspects. L’ampleur ainsi que le nombre de pays touchĂ©s par ce phĂ©nomĂšne inquiĂštent (ibid.). Outre les difficultĂ©s concernant l’alimentation et le poids Ă©conomique du service rendu par la pollinisation (Gallai et al., 2009), c’est un large pan du fonctionnement gĂ©nĂ©ral des Ă©cosystĂšmes qui semble fragilisĂ©. Les Ă©tudes les plus rĂ©centes ne permettent que d’augurer une synergie entre plusieurs causes (Van Engelsdorp, et Meixner, 2010 ; Di Prisco et al., 2013). Parmi elles, l’organisation du paysage (composition et structure) n’est pas immĂ©diatement suspectĂ©e comme Ă©lĂ©ment central et n’apparaĂźt pas comme facteur aussi dĂ©terminant que le varroa, les maladies parasitaires ou de maniĂšre plus prĂ©gnante, l’utilisation des pesticides et fongicides en agriculture (graines enrobĂ©es, pratiques d’épandage, etc.). En effet, comme l’indique l’étude 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 d’abeilles 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 d’habitats 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 l’apport de ressources trophiques aux colonies

    An insight into the use of cationic peptides for plasmid DNA delivery in cells.

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    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

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    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 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. In vitro , NaPaC inhibited MCF‐7ras cell proliferation by 40% at concentration lower than that of CMDB and NaPa (12 Ό M vs 73 Ό M and 10 m M ). IC 50 s were 6 and 28 Ό 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 1000‐fold lower than NaPa. In vivo , CMDB (150 mg kg −1 ) and NaPa (40 mg kg −1 ) inhibited the MCF‐7ras tumour growth by 37 and 57%, respectively, whereas NaPaC (15 mg kg −1 ) 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 anti‐angiogenic actions make it a good candidate for a new anti‐cancer drug. British Journal of Pharmacology (2002) 135 , 1859–1871; 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

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    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

    Aponecrotic, antiangiogenic and antiproliferative effects of a novel dextran derivative on breast cancer growth in vitro and in vivo

    No full text
    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 (12 ΌM vs 73 ΌM and 10 mM). IC(50)s were 6 and 28 ΌM 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 (150 mg kg(−1)) and NaPa (40 mg kg(−1)) inhibited the MCF-7ras tumour growth by 37 and 57%, respectively, whereas NaPaC (15 mg kg(−1)) 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
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