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See detailAntiamoebic and Antiplasmodial Activities of Alkaloids Isolated from Strychnos usambarensis
Wright, Colin; Bray, Dorothy; O'Neill, Melanie et al

in Planta Medica (1991), 57

Seven alkaloids isolated from Strychnos usambarensis have been assessed for in vitro activities against Entamoeba histolytica and Plasmodium falciparum and for in vivo activity against Plasmodium berghei ... [more ▼]

Seven alkaloids isolated from Strychnos usambarensis have been assessed for in vitro activities against Entamoeba histolytica and Plasmodium falciparum and for in vivo activity against Plasmodium berghei in mice. Strychnopentamine and 3'-4'-dihydrousambarensine were highly active against P. falciparum in vitro, but were inactve and non-toxic against P.berghei in vivo.Usambarensine, usambarine and 18,19-dihydrousambarine were highly active against E. histolytica in vitro, but were less active against P. falciparum in vitro. Nb-methylusambarensine was less active against both protozoa than was usambarensine, and akagerine possessed little antiprotozoal activity.Structure-activity relationships are discussed in the context of the reported cytotoxic and pharmacological properties of those alkaloids. [less ▲]

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See detailThe antiangiogenic 16K prolactin disturbs functional tumor neovascularization by affecting vessel maturation
Nguyen, Ngoc-Quynh-Nhu ULg; Castermans, Karolien; Berndt, Sarah et al

Poster (2011, May)

16K hPRL, the antiangiogenic 16-kDa N-terminal fragment of human prolactin was shown to prevent tumor growth and metastasis by modifying tumor vessel morphology. Here we investigated the effect of 16K ... [more ▼]

16K hPRL, the antiangiogenic 16-kDa N-terminal fragment of human prolactin was shown to prevent tumor growth and metastasis by modifying tumor vessel morphology. Here we investigated the effect of 16K hPRL on tumor vessel maturation and on the related signaling pathways. We show that 16K hPRL treatment leads, in a murine B16-F10 tumor model, to a dysfunctional tumor vasculature with reduced pericyte coverage, and disruption of the PDGF-B/PDGFR-B, Ang/Tie2, and Delta/Notch pathways. In an aortic ring assay, 16K hPRL impairs endothelial cell and pericyte outgrowth from the vascular ring. In addition, 16K hPRL prevents pericyte migration to endothelial cells. This event was independent of a direct inhibitory effect of 16K hPRL on pericyte viability, proliferation, or migration. In endothelial cell-pericyte cocultures, we found 16K hPRL to disturb Notch signaling, this being the first time such an effect is observed with an endogenous antiangiogenic agent. These findings provide new insights into the mechanisms of 16K hPRL action and highlight its potential for use in anticancer therapy. [less ▲]

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See detailThe Antiangiogenic 16K Prolactin Impairs Functional Tumor Neovascularization by Inhibiting Vessel Maturation
Nguyen, Ngoc-Quynh-Nhu ULg; Castermans, Karolien; Berndt, Sarah et al

in PLoS ONE (2011), 6(11), 27318-27318

Background: Angiogenesis, the formation of new blood vessels from existing vasculature, plays an essential role in tumor growth, invasion, and metastasis. 16K hPRL, the antiangiogenic 16-kDa N-terminal ... [more ▼]

Background: Angiogenesis, the formation of new blood vessels from existing vasculature, plays an essential role in tumor growth, invasion, and metastasis. 16K hPRL, the antiangiogenic 16-kDa N-terminal fragment of human prolactin was shown to prevent tumor growth and metastasis by modifying tumor vessel morphology. Methodology/Principal Findings: Here we investigated the effect of 16K hPRL on tumor vessel maturation and on the related signaling pathways. We show that 16K hPRL treatment leads, in a murine B16-F10 tumor model, to a dysfunctional tumor vasculature with reduced pericyte coverage, and disruption of the PDGF-B/PDGFR-B, Ang/Tie2, and Delta/Notch pathways. In an aortic ring assay, 16K hPRL impairs endothelial cell and pericyte outgrowth from the vascular ring. In addition, 16K hPRL prevents pericyte migration to endothelial cells. This event was independent of a direct inhibitory effect of 16K hPRL on pericyte viability, proliferation, or migration. In endothelial cell-pericyte cocultures, we found 16K hPRL to disturb Notch signaling. Conclusions/Significance: Taken together, our data show that 16K hPRL impairs functional tumor neovascularization by inhibiting vessel maturation and for the first time that an endogenous antiangiogenic agent disturbs Notch signaling. These findings provide new insights into the mechanisms of 16K hPRL action and highlight its potential for use in anticancer therapy. [less ▲]

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See detailThe antiangiogenic factor 16K human prolactin induces caspase-dependent apoptosis by a mechanism that requires activation of nuclear factor-kappa B
Tabruyn, Sébastien ULg; Sorlet, C. M.; Rentier-Delrue, Françoise ULg et al

in Molecular Endocrinology (2003), 17(9), 1815-1823

We have previously shown that the 16-kDa N-terminal fragment of human prolactin (16K hPRL) has antiangiogenic properties, including the ability to induce apoptosis in vascular endothelial cells. Here, we ... [more ▼]

We have previously shown that the 16-kDa N-terminal fragment of human prolactin (16K hPRL) has antiangiogenic properties, including the ability to induce apoptosis in vascular endothelial cells. Here, we examined whether the nuclear factor-kappaB (NF-kappaB) signaling pathway was involved in mediating the apoptotic action of 16K hPRL in bovine adrenal cortex capillary endothelial cells. In a dose-dependent manner, treatment with 16K hPRL induced inhibitor kappaB-alpha degradation permitting translocation of NF-kappaB to the nucleus and reporter gene activation. Inhibition of NF-kappaB activation by overexpression of a nondegradable inhibitor kappaB-alpha mutant or treatment with NF-kappaB inhibitors blocked 16K hPRL-induced apoptosis. Treatment with 16K hPRL activated the initiator caspases-8 and -9 and the effector caspase-3, all of which were essential for stimulation of DNA fragmentation. This activation of the caspase cascade by 16K hPRL was also NF-kappaB dependent. These findings support the conclusion that NF-kappaB signaling plays a central role in 16K hPRL-induced apoptosis in vascular endothelial cells. [less ▲]

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See detailThe antiangiogenic factor 16K PRL induces programmed cell death in endothelial cells by caspase activation
Martini, J. F.; Piot, C.; Humeau, L. M. et al

in Molecular Endocrinology (2000), 14(10), 1536-49

We asked whether the antiangiogenic action of 16K human PRL (hPRL), in addition to blocking mitogen-induced vascular endothelial cell proliferation, involved activation of programmed cell death. Treatment ... [more ▼]

We asked whether the antiangiogenic action of 16K human PRL (hPRL), in addition to blocking mitogen-induced vascular endothelial cell proliferation, involved activation of programmed cell death. Treatment with recombinant 16K hPRL increased DNA fragmentation in cultured bovine brain capillary endothelial (BBE) and human umbilical vein endothelial (HUVE) cells in a time- and dose-dependent fashion, independent of the serum concentration. The activation of apoptosis by 16K hPRL was specific for endothelial cells, and the activity of the peptide could be inhibited by heat denaturation, trypsin digestion, and immunoneutralization, but not by treatment with the endotoxin blocker, polymyxin-B. 16K hPRL-induced apoptosis was correlated with the rapid activation of caspases 1 and 3 and was blocked by pharmacological inhibition of caspase activity. Caspase activation was followed by inactivation of two caspase substrates, poly(ADP-ribose) polymerase (PARP) and the inhibitor of caspase-activated deoxyribonuclease (DNase) (ICAD). Furthermore, 16K hPRL increased the conversion of Bcl-X to its proapoptotic form, suggesting that the Bcl-2 protein family may also be involved in 16K hPRL-induced apoptosis. These findings support the hypothesis that the antiangiogenic action of 16K hPRL includes the activation of programmed cell death of vascular endothelial cells. [less ▲]

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See detailThe antiangiogenic factor, 16-kDa human prolactin, induces endothelial cell cycle arrest by acting at both the G(0)-G(1) and the G(2)-M phases
Tabruyn, Sébastien ULg; Nguyen, Ngoc-Quynh-Nhu ULg; Cornet, Anne ULg et al

in Molecular Endocrinology (2005), 19(7), 1932-1942

The 16-kDa N-terminal fragment of human prolactin (16K hPRL) is a potent antiangiogenic factor that has been shown to prevent tumor growth in a xenograph mouse model. In this paper we first demonstrate ... [more ▼]

The 16-kDa N-terminal fragment of human prolactin (16K hPRL) is a potent antiangiogenic factor that has been shown to prevent tumor growth in a xenograph mouse model. In this paper we first demonstrate that 16K hPRL inhibits serum-induced DNA synthesis in adult bovine aortic endothelial cells. This inhibition is associated with cell cycle arrest at both the G(0)-G(1) and the G(2)-M phase. Western blot analysis revealed that 16K hPRL strongly decreases levels of cyclin D1 and cyclin B1, but not cyclin E. The effect on cyclin D1 is at least partially transcriptional, because treatment with 16K hPRL both reduces the cyclin D1 mRNA level and down-regulates cyclin D1 promoter activity. This regulation may be due to inhibition of the MAPK pathway, but it is independent of the glycogen synthase kinase-3 beta pathway. Lastly, 16K hPRL induces the expression of negative cell cycle regulators, the cyclin-dependent kinase inhibitors p21(cip1) and p27(kip1). In summary, 16K hPRL inhibits serum-induced proliferation of endothelial cells through combined effects on positive and negative regulators of cell cycle progression. [less ▲]

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See detailAntiangiogenic liposomal gene therapy with 16K human prolactin efficiently reduces tumor growth.
Kinet, Virginie ULg; Nguyen, Ngoc-Quynh-Nhu ULg; Sabatel, Céline ULg et al

in Cancer Letters (2009), 284(2), 222-228

Human 16K PRL (16K hPRL) is a potent inhibitor of angiogenesis both in vitro and in vivo. It has been shown to prevent tumor growth in three xenograft mouse models. Here we have used a gene transfer ... [more ▼]

Human 16K PRL (16K hPRL) is a potent inhibitor of angiogenesis both in vitro and in vivo. It has been shown to prevent tumor growth in three xenograft mouse models. Here we have used a gene transfer method based on cationic liposomes to produce 16K hPRL and demonstrate that 16K hPRL inhibits tumor growth in a subcutaneous B16F10 mouse melanoma model. Computer-assisted image analysis shows that 16K hPRL treatment results in the reduction of tumor vessel length and width, leading to a 57% reduction in average vessel size. We thus show, for the first time, that administration of the 16K hPRL gene complexed to cationic liposomes is effective to maintain antiangiogenic activities of 16K hPRL level. [less ▲]

Detailed reference viewed: 100 (36 ULg)
See detailAntiangiogenic peptides
Martial, Joseph ULg; Struman, Ingrid ULg; Nguyen, Ngoc-Quynh-Nhu ULg et al

Patent (2007)

The present invention refers to antiangiogenic peptides, especially to tilted peptides having antiangiogenic properties and peptides from the prolactin/growth hormone familiy having antiangiogenic ... [more ▼]

The present invention refers to antiangiogenic peptides, especially to tilted peptides having antiangiogenic properties and peptides from the prolactin/growth hormone familiy having antiangiogenic properties. [less ▲]

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See detailAntiangiogenic peptides
Martial, Joseph ULg; Struman, Ingrid ULg; Nguyen, Ngoc-Quynh-Nhu ULg et al

Patent (2008)

The present invention refers to a pharmaceutical composition comprising an isolated antiangiogenic peptide or a recombinant protein comprising the antiangiogenic peptide, wherein the peptide is between 11 ... [more ▼]

The present invention refers to a pharmaceutical composition comprising an isolated antiangiogenic peptide or a recombinant protein comprising the antiangiogenic peptide, wherein the peptide is between 11 and 40 amino acids in length and having antiangiogenic activity, the peptide comprising the amino acid sequence: X1-X2-X3-X4-X5-X6-X7-X8-X9-X10-X11-X12-X13-X14, wherein X1 is any amino acid residue comptabile with forming a helix; X2 is an amino acid redisue of : Leu, Ile, Val; X3 is an amino acid residue of: Arg, Lys, His, Ser, Thr; X4 is an amino acid residue of: Ile, Leu, Val; X5 is any amino acid residue compatible with forming a helix; X6 is an amino acid residue of: Leu, Ile, Val; X7 is an amino acid residue of: Leu, Ile, Val, Ser, Thr; X8 is any amino acid residue compatible with forming a helix; X9 is any amino acid residue compatible with forming a helix; X10 is an amino acid residue of: Gln, Glu, Asp, Arg, His, Lys, Asn; X11 is an amino acid residue of: Ser, Thr; X12 is an amino acid residue of: Trp, Tyr, Phe; X13 is an animo acid residue of Leu, Ile, Val, Asn, Gln; X14 is an amino acid residue of: Glu, Gln, Asp, Asn. [less ▲]

Detailed reference viewed: 62 (16 ULg)
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See detailAntiapoptotic effect of GM-CSF activated STAT5 signaling pathway in chronic mastitis-affected cows : possible involvement in persistent accumulation of neutrophils in milk
Boutet, Philippe ULg; Bureau, Fabrice ULg; Gillet, Laurent ULg et al

in Congress COST Action 844: “Apoptosis and programmed cell death : molecular mechanisms and applications in Biotechnology and Agriculture” (2004)

Detailed reference viewed: 26 (7 ULg)
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See detailAntibacterial activity of 5-acylaminothiazole derivatives, synthetic drugs related to β-lactam antibiotics
Pirotte, Bernard ULg; Delarge, Jacques; Coyette, Jacques ULg et al

in Journal of Antibiotics (The) (1991), 44

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See detailAntibacterial activity of poly(vinyl alcohol)-b-poly(acrylonitrile) based micelles loaded with silver nanoparticles
Bryaskova, Rayna; Pencheva, Daniela; Kyulavska, Mariya et al

in Journal of Colloid & Interface Science (2010), 344(2), 424-448

A new amphiphilic poly(vinyl alcohol)-b-poly(acrylonitrile) (PVOH-b-PAN) copolymer obtained by selective hydrolysis of well-defined poly(vinyl acetate)-b-poly(acrylonitrile) copolymer synthesized by ... [more ▼]

A new amphiphilic poly(vinyl alcohol)-b-poly(acrylonitrile) (PVOH-b-PAN) copolymer obtained by selective hydrolysis of well-defined poly(vinyl acetate)-b-poly(acrylonitrile) copolymer synthesized by cobalt mediated radical polymerization was used for the preparation of PVOH-b-PAN based micelles with embedded silver nanoparticles. The successful formation of silver loaded micelles has been confirmed by UV–vis, DLS and TEM analysis and their antibacterial activity against Escherichia coli (E. coli), Staphylococcus aureus (S. aureus), Pseudomonas aeruginosa (P. aeruginosa) and spore solution of Bacillus subtilis (B. subtilis) has been studied. PVOH-b-PAN based micelles with embedded silver nanoparticles showed a strong bactericidal effect against E. coli, S. aureus and P. aeruginosa and the minimum bactericidal concentration for each system (MBC) has been determined. [less ▲]

Detailed reference viewed: 129 (7 ULg)
See detailAntibacterial coatings of copolymers based on poly(ionic liquids)
Weiss-Maurin, Mathilde ULg; Detrembleur, Christophe ULg; Taton, Daniel

Conference (2015, March 16)

Detailed reference viewed: 8 (3 ULg)
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See detailAntibacterial polyelectrolyte micelles for coating stainless steel
Falentin, Céline ULg; Faure, Emilie ULg; Svaldo Lanero, Tiziana ULg et al

in Langmuir (2012), 28(18), 7233-7241

In this study, we report on the original synthesis and characterization of novel antimicrobial coatings for stainless steel by alternating the deposition of aqueous solutions of positively charged ... [more ▼]

In this study, we report on the original synthesis and characterization of novel antimicrobial coatings for stainless steel by alternating the deposition of aqueous solutions of positively charged polyelectrolytes micelles doped with silver based nanoparticles with a polyanion. The micelles are formed by electrostatic interaction between two oppositely charged polymers, a polycation bearing 3,4-dihydroxyphenylalanine units (DOPA, a major component of natural adhesives) and a polyanion (poly(styrene sulfonate), PSS) without using any block copolymer. DOPA units are exploited for their well-known ability to anchor to stainless steel and to form and stabilize biocidal silver nanoparticles (Ag0). The chlorine counter-anion of the polycation forms and stabilizes biocidal silver chloride nanoparticles (AgCl). We demonstrate that two layers of micelles (alternated by PSS) doped by silver particles are enough to impart to the surface a strong antibacterial activity against Gram-negative E. coli. Moreover, micelles that are reservoirs of biocidal Ag+ can be easily reactivated after depletion. This novel water-based approach is convenient, simple and attractive for industrial applications. [less ▲]

Detailed reference viewed: 165 (16 ULg)
See detailL'antibiorésistance chez l'animal et ses conséquences
Mainil, Jacques ULg

Scientific conference (1999, May)

Detailed reference viewed: 16 (0 ULg)