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Search Results: 1 - 10 of 215838 matches for " Marie L.;Elabbadi "
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Basic biochemical investigations as rationale for the design of original antimalarial drugs. An example of phospholipid metabolism
Vial, Henri J.;Angelin, Marie L.;Elabbadi, Nourredine;Calas, Michele;Cordinas, Gerard;Giral, Louis;
Memórias do Instituto Oswaldo Cruz , 1992, DOI: 10.1590/S0074-02761992000700042
Abstract: the future of antimalarial chemotherapy is particulary alarming in view of the spread of parasite cross-resistances to drugs that are not even structurally related. only the availability of new pharmacological models will make it possible to select molecules with novel mechanisms of action, thus delaving resistance and allowing the development of new chemotherapeutic strategies. we reached this objective in mice. our approach is hunged on fundamental and applied research begun in 1980 to investigate to phospholipid (pl) metabolism of intraerythrocytic plasmodium. this metabolism is abundant, specific and indispensable for the production of plasmodium membranes. any drug to interfere with this metabolism blocks parasitic development. the most effective interference yet found involves blockage of the choline transporter, which supplies plasmodium with choline for the synthesis of phosphatidylcholine, its major pl, this is a limiting step in the pathway. the drug sensitivity thereshold is much lower for the parasite, which is more dependent on this metabolism than host cells. the compounds show in vitro activity against p. falciparum at 1 to 10 nm. they show a very low toxicity against a lymphblastoid cell line, demonstrating a total abscence of correlation between growth inhibition of parasites and lymphoblastoid cells. they show antimalarial activity in vivo, in the p. berghei or p. chabaudi/mouse system, at doses 20-to 100-fold lower than their in acute toxicity limit. the bioavailability of a radiolabeled form of the product seemed to be advantageous (slow blood clearance and no significant concentration in tissues). lastly, the compounds are inexpensive to produce. they are stable and water-soluble.
Infected erythrocyte choline carrier inhibitors: exploring some potentialities inside Plasmodium phospholipid metabolism for eventual resistance acquisition
Vial, Henri J.;Ancelin, Marie L.;Elabbadi, Noureddine;Orcel,lène;Yeo, Hye-Jeong;Gumila, Catherine;
Memórias do Instituto Oswaldo Cruz , 1994, DOI: 10.1590/S0074-02761994000600021
Abstract: we have developed a model for designing antimalarial drugs based on interference with an essential metabolism developed by plasmodium during its intraerythrocytic cycle, phospholipid (pl) metabolism. the most promising drug interference is choline transporter blockage, which provides plasmodium with a supply of precursor for synthesis of phosphatidylcholine (pc), the major pl of infected erythrocytes. choline entry is a limiting step in this metabolic pathway and occurs by a facilitated-diffusion system involving an asymmetric carrier operating according to a cyclic model. choline transport in the erythrocytes is not sodium dependent nor stereospecific as demonstrated using stereoisomers of α and beta methylcholine. these last two characteristics along with distinct effects of nitrogen substitution on transport rate demonstrate that choline transport in the infected erythrocyte possesses characteristics quite distinct from that of the nervous system. this indicates a possible discrimination between the antimalarial activity (inhibition of choline transport in the infected erythrocyte) and a possible toxic effect through inhibition of choline entry in synaptosomes. apart from the de novo pathway of choline, pc can be synthesized by n-methylation from phosphatidylethanolamine (pe). there is a de novo pathway for pe biosynthesis from ethanolamine in infected cells but phosphatidylserine (ps) decarboxylation also occurs. in addition, pe can be directly and abundantly synthesized from serine decarboxylation into ethanolamine, a pathway which is absent from the host. the variety of the pathways that exist for the biosynthesis of one given pl led us to investigate whether an equilibrium can occur between all pl metabolic pathways. indeed, if alternative (compensative) pathway(s) can operate after blockage of the de novo pc biosynthesis pathway this would indicate a potential mechanism for resistance acquisition. up until now, there is no evidence of such a compensative pro
Anti-tumor properties of blackseed (Nigella sativa L.) extracts
Ait Mbarek, L.;Ait Mouse, H.;Elabbadi, N.;Bensalah, M.;Gamouh, A.;Aboufatima, R.;Benharref, A.;Chait, A.;Kamal, M.;Dalal, A.;Zyad, A.;
Brazilian Journal of Medical and Biological Research , 2007, DOI: 10.1590/S0100-879X2006005000108
Abstract: the objective of the present study was to evaluate the in vitro and in vivo anti-cancer effect of nigella sativa l. seed extracts. the essential oil (ic50 = 0.6%, v/v) and ethyl acetate (ic50 = 0.75%) extracts were more cytotoxic against the p815 cell line than the butanol extract (ic50 = 2%). similar results were obtained with the vero cell line. although all extracts had a comparable cytotoxic effect against the ico1 cell line, with ic50 values ranging from 0.2 to 0.26% (v/v), tests on the bsr cell line revealed a high cytotoxic effect of the ethyl acetate extract (ic50 = 0.2%) compared to the essential oil (ic50 = 1.2%). these data show that the cytotoxicity of each extract depends on the tumor cell type. in vivo, using the dba2/p815 (h2d) mouse model, our results clearly showed that the injection of the essential oil into the tumor site significantly inhibited solid tumor development. indeed, on the 30th day of treatment, the tumor volume of the control animals was 2.5 ± 0.6 cm3, whereas the tumor volumes of the essential oil-treated animals were 0.22 ± 0.1 and 0.16 ± 0.1 cm3 when the animals were injected with 30 μl (28.5 mg)/mouse and 50 μl (47.5 mg)/mouse per 48 h (six times), respectively. interestingly, the administration of the essential oil into the tumor site inhibited the incidence of liver metastasis development and improved mouse survival.
Following the Leader: Examining Leadership Characteristics, Alcohol Use, and Hooking Up among College Students  [PDF]
Rose Marie Ward, Judith L. Weiner
Open Journal of Leadership (OJL) , 2012, DOI: 10.4236/ojl.2012.12002
Abstract: Although it is generally assumed that leadership traits are linked to positive outcomes, it is unclear how they might be related to less desirable health behaviors. In a sample of 623 undergraduate students, a series of structural equation models examined the relationship between transformational leadership traits and risky health behaviors (i.e., alcohol consumption and hooking up). The models fit the data well and indicated that higher levels of transformational leadership traits were related to higher levels of alcohol consumption and risky sexual behaviors. It seems that those students who endorse higher transformational leadership characteristics are also embracing negative health behaviors.
Reactions to a Female Perpetrator of Neglect and Financial Elder Abuse  [PDF]
Nerina J. Caltabiano, Marie L. Caltabiano
Psychology (PSYCH) , 2016, DOI: 10.4236/psych.2016.76080
Abstract:

There is a paucity of Australian research on elder abuse perpetrated by carers. Knowing how individuals would respond to an elder abuse scenario can inform prevention and intervention strategies. The objective of this study was to determine how undergraduate university students enrolled in caring profession degrees respond to an elder abuse scenario. The design of the study involved a paper-and-pencil survey using an elder abuse scenario. Thirty-two undergraduate volunteer students enrolled in a regional university participated in the study. Confronted with the scenario, students would offer the elder physical support such as house cleaning, they would recommend that the elder access government welfare agencies, and consider moving to elder accommodation. They would recommend that the carer get a job, clean the house and call tradespeople. Students enrolled in caring profession degrees, irrespective of gender, were prepared to take actions to improve the welfare of the abuse victim.

The 2001 Gairdner Foundation Awards
Marie L. Cappello
University of Toronto Medical Journal , 2001, DOI: 10.5015/utmj.v79i1.941
Abstract:
Interview with Dr. Donna E. Stewart, Lillian Love Chair in Women's Health
Marie L. Cappello
University of Toronto Medical Journal , 2002, DOI: 10.5015/utmj.v79i3.868
Abstract:
An Interview with Dr. Henry Friesen, 2001 Wightman Award Winner
Marie L. Cappello
University of Toronto Medical Journal , 2001, DOI: 10.5015/utmj.v79i1.942
Abstract:
Book Review: Lisa Lau and Ana Cristina Mendes (Eds.). Re-Orientalism and South Asian Identity Politics: The oriental Other within. New York: Routledge. 2011.
Ann Marie L. Davis
Journal of International and Global Studies , 2012,
Abstract:
TNFR1 Deficiency Protects Mice from Colitis-Associated Colorectal Cancer Coupled with a Decreased Level of Oxidative Damage in the Colon: Implications for Anti-TNF Therapy of Unremitting Colitis  [PDF]
Rose Marie Stillie, Heidi L. Sapp, Andrew W. Stadnyk
Journal of Cancer Therapy (JCT) , 2012, DOI: 10.4236/jct.2012.326119
Abstract: It has long been appreciated that there is a direct relationship between the intensity and duration of inflammatory bowel diseases (IBD) and increasing intestinal cancer risk but which elements of the inflammatory response are responsible have not been identified. Anti-TNF drugs have been successful at treating IBD but considering the presumed anti-tumor activity of TNF, it is important to understand whether the treatment impacts on the patients’ intestinal cancer risk. We modeled this relationship by “treating mice lacking TNF receptors with a colon cancer causing combination of azoxymethane followed by repeated dextran sulphate sodium exposures (AOM + DSS regime). TNF receptor type1 gene deficient (TNFR1-/-) and TNFR2-/- mice experienced similar clinical illnesses and colonic inflammation as C57BL/6 wildtype controls during the AOM + DSS regime. Despite the inflammation, TNFR1-/- mice developed significantly fewer colon tumors than the other strains. The reduced tumor incidence was a product of the combined lack of receptor expression on hematopoietic and nonhematopoietic cells, shown using bone marrow cell chimeras of wildtype and TNFR1-/- mice. As oxidative damage is a potent contributing factor to tumorigenesis and inflammatory leukocytes make copious amounts of reactive oxygen radicals, we measured oxidative damage in the animals’ colons. TNFR1-/- mice showed less damage compared to the other strains. We subsequently examined mice deficient in their leukocyte NADPH oxidative pathway (Nox2-/-) for their cancer incidence using the AOM + DSS regime. Nox2-/- mice became inflamed but had fewer tumors than wildtype mice. We conclude that TNF promotes colon cancer including through promoting oxidative processes utilizing TNFR1 in leukocytes. Moreover, the C57BL/6 strain can be used to dissociate mechanisms of colon inflammation from tumorigenic processes. We interpret our results to mean that IBD patients on TNF antagonist therapies will potentially benefit with reduced colon cancer risk even if they do not respond with reduced inflammation.
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