129 research outputs found

    Stock assessment and population dynamics of Senegal Jack, Caranx senegallus Cuvier, 1833, from industrial fishery of Cote d’Ivoire (West Africa)

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    Monthly data of C. senegallus length composition, was recorded from the continental shelf of CĂŽte d’Ivoire from March 2016 to February 2018. The population parameters such as length-frequency distribution, length-weight relationship, growth, mortality, exploitation ratio and length at first capture of this species were investigated to get information for effective management of this fish, by applying Beverton and Holt (1957), virtual population analysis (VPA), using the FISAT Tool II. The lengthfrequency distribution of 804 samples showed polymodal distribution. The folk length ranged from 16.10 to 47.00 cm with a mean equal to 25.68 ± 0.23 cm. The statistical analysis shows that the combined sexes (“b” = 2.9793), and male (“b” = 3.0199) growth is isometric. However, female (“b” = 2.9489) growth is negative allometric. The estimated growth parameters were: FL ∞ = 51.45 cm, K = 0.46 year-1 and t0 = -0.31 year-1. The length at first capture was 19.04 cm (FL). The current exploitation rate (E = 0.33), was lower than the optimum level (E = 0.36). VPA indicate that the fish which die by natural mortality are higher than those which die by fishing mortality. These results show that the current stock of C. senegallus is not overexploited. Keywords: Carangidae, Caranx senegallus, Stock, Population parameters, Fishery   English Title: Gestion des stocks et dynamique des populations du carangue du sĂ©nĂ©gal, caranx Senegallus Cuvier, 1833, de la pĂȘche industrielle de cĂŽte d’ivoire (Afrique de l’ouest) Les donnĂ©es mensuelles sur la composition en taille de C. senegallus, ont Ă©tĂ© enregistrĂ©es sur le plateau continental de la CĂŽte d’Ivoire entre mars 2016 et fĂ©vrier 2018. Les paramĂštres de population tels que la distribution des frĂ©quences de taille, la relation longueur-poids, la croissance, la mortalitĂ©, le taux d’exploitation et la taille de premiĂšre capture de cette espĂšce ont Ă©tĂ© Ă©tudiĂ©s pour obtenir des informations permettant une gestion efficace du stock de ce poisson, par la mĂ©thode de Beverton et Holt (1957) et l’analyse de population virtuelle, grĂące au logiciel FISAT II. La distribution des frĂ©quences de taille de 804 individus a montrĂ© une distribution polymodale. La longueur Ă  la fourche variait de 16,10 Ă  47,00 cm avec une moyenne Ă©gale Ă  25,68 ± 0,23 cm. L’analyse statistique montre que la croissance des sexes combinĂ©e (“b” = 2,9793) et des mĂąles (“b” =  3,0199) est isomĂ©trique. Tandis que, la croissance des femelles (“b” = 2,9489) est allomĂ©trique nĂ©gative. Les paramĂštres de croissance estimĂ©s ont  Ă©tĂ© les suivants : FL ∞ = 51,45 cm, K = 0,46 an-1 et t0 = - 0,31 an-1. La longueur Ă  la premiĂšre capture a Ă©tĂ© de 19,04 cm (FL). Le taux d’exploitation  actuel (E = 0,33), Ă©tait infĂ©rieur au niveau optimal (E = 0,36). L’Analyse des Populations Virtuelles indique que les poissons qui meurent par mortalitĂ© naturelle sont plus Ă©levĂ©s que ceux qui meurent par mortalitĂ© par pĂȘche. Ces rĂ©sultats montrent que le stock actuel de C. senegallus n’est pas  surexploitĂ©. Mots clĂ©s : Carangidae, Caranx senegallus, Stock, ParamĂštres des populations, PĂȘcheri

    Adoptive immunotherapy with Cl-IB-MECA-treated CD8+T cells reduces melanoma growth in mice

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    Cl-IB-MECA is a selective A3 adenosine receptor agonist, which plays a crucial role in limiting tumor progression. In mice, Cl-IB-MECA administration enhances the anti-tumor T cell-mediated response. However, little is known about the activity of Cl-IB-MECA on CD8+ T cells. The aim of this study was to investigate the effect of ex vivo Cl-IB-MECA treatment of CD8+ T cells, adoptively transferred in melanoma-bearing mice. Adoptive transfer of Cl-IB-MECA-treated CD8+ T cells or a single administration of Cl-IB-MECA (20 ng/mouse) inhibited tumor growth compared with the control group and significantly improved mouse survival. This was associated with the release of Th1-type cytokines and a greater influx of mature Langerin+ dendritic cells (LCs) into the tumor microenvironment. CD8+ T cells treated with Cl-IB-MECA released TNF-α which plays a critical role in the therapeutic efficacy of these cells when injected to mice. Indeed, neutralization of TNF-α by a specific monoclonal Ab significantly blocked the anti-tumor activity of Cl-IB-MECA-treated T cells. This was due to the reduction in levels of cytotoxic cytokines and the presence of fewer LCs. In conclusion, these studies reveal that ex vivo treatment with Cl-IB-MECA improves CD8+ T cell adoptive immunotherapy for melanoma in a TNF-α-dependent manner

    Inhibition of CD73 improves B cell-mediated anti-tumor immunity in a mouse model of melanoma.

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    CD73 is a cell surface enzyme that suppresses T cell-mediated immune responses by producing extracellular adenosine. Growing evidence suggests that targeting CD73 in cancer may be useful for an effective therapeutic outcome. In this study, we demonstrate that administration of a specific CD73 inhibitor, adenosine 5'-(α,ÎČ-methylene)diphosphate (APCP), to melanoma-bearing mice induced a significant tumor regression by promoting the release of Th1- and Th17-associated cytokines in the tumor microenvironment. CD8+ T cells were increased in melanoma tissue of APCP-treated mice. Accordingly, in nude mice APCP failed to reduce tumor growth. Importantly, we observed that after APCP administration, the presence of B cells in the melanoma tissue was greater than that observed in control mice. This was associated with production of IgG2b within the melanoma. Depletion of CD20+ B cells partially blocked the anti-tumor effect of APCP and significantly reduced the production of IgG2b induced by APCP, implying a critical role for B cells in the anti-tumor activity of APCP. Our results also suggest that APCP could influence B cell activity to produce IgG through IL-17A, which significantly increased in the tumor tissue of APCP-treated mice. In support of this, we found that in melanoma-bearing mice receiving anti-IL-17A mAb, the anti-tumor effect of APCP was ablated. This correlated with a reduced capacity of APCP-treated mice to mount an effective immune response against melanoma, as neutralization of this cytokine significantly affected both the CD8+ T cell- and B cell-mediated responses. In conclusion, we demonstrate that both T cells and B cells play a pivotal role in the APCP-induced anti-tumor immune response

    In vitro and in vivo evaluation of In-111-DTPAGlu-G-CCK8 for cholecystokinin-B receptor imaging

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    Regulatory peptides and their analogs are being extensively investigated as radiopharmaceuticals for cancer imaging and therapy. Receptors of the cholecystokinin family have been shown to be overexpressed in different types of neuroendocrine tumors. The purposes of this study were to evaluate the cholecystokinin octapeptide amide (CCK8) peptide tagged with a diethylenetriaminepentaacetic acid derivative (DTPAGlu) and to test whether a 111In-labeled conjugate (111In-DTPAGlu-G-CCK8, a derivative containing the chelating agent DTPAGlu bound through a glycine linker at the N-terminal end of the bioactive peptide CCK8) is suitable for cholecystokinin-B receptor (CCKBR) imaging. Methods: CCK8 was synthesized by solidphase techniques and covalently coupled to DTPAGlu through a glycine linker at its amino terminus. The compound was labeled with 111In. The radiochemical purity and stability of the compound were assessed by chromatographic methods. NIH-3T3 and A431 cells overexpressing CCKBR were used to characterize the in vitro properties of the compound. Nude mice bearing control and CCKBR-overexpressing A431 xenografts were used as an in vivo model. Results: DTPAGlu-G-CCK8 showed rapid and efficient labeling with 111In. The radiolabeled conjugate showed specific binding to both cell lines overexpressing CCKBR. Binding was saturable, with a dissociation constant of 20 nmol/L in both cell systems. Both cell lines showed internalization of the ligand after interaction with the receptor. Biodistribution studies showed rapid localization of 111In-DTPAGlu- G-CCK8 on CCKBR-overexpressing A431 xenografts that was severalfold higher than that on control tumors at all time points tested. Unbound activity showed rapid clearance of over 80% through the kidneys by 30 min after injection. The labeled peptide conjugate was very stable in serum but showed a rapid breakdown after injection. Incubation with kidney homogenates suggested that most breakdown occurred in the kidneys, favoring the clearance of unbound activity. Conclusion: Our findings indicate that the in vitro and in vivo characteristics of 111In-DTPAGlu-G-CCK8 are favorable for CCKBR imaging, as thepeptide shows high-affinity binding to the receptor, is internalized in CCKBR-expressing cells, and shows avid uptake in CCKBR-overexpressing xenografts, with rapid clearance of unbound radioactivity through the kidneys. Furthermore, the ease of synthesis, high labeling efficiency, and chemical stability of DTPAGlu make this chelating moiety an ideal candidate for widespread use in peptide radiolabeling for nuclear medicine applications

    The [Tc(N)(PNP)]2+ metal fragment labeled cholecystokinin-8 (CCK8) peptide for CCK-2 receptors imaging: in vitroand in vivo studies

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    The radiolabeling of the natural octapeptide CCK8, derivatized with a cysteine residue (Cys-Gly-CCK8), by using the metal fragment [99mTc(N)(PNP3)]2+ (PNP3 = N,N-bis(dimethoxypropylphosphinoethyl)methoxyethylamine) is reported. The [99mTc(N)(NS-Cys-Gly-CCK8)(PNP3)]+ complex was obtained according to two methods (one-step or two-step procedure) that gave the desired compound in high yield. The complex is stable in aqueous solution and in phosphate buffer. In vitro challenge experiments with an excess of cysteine and glutathione indicate that no transchelation reactions occur, confirming the high thermodynamic stability and kinetic inertness of this compound. Stability studies carried out in human and mouse serum, as well as in mouse liver homogenates, show that the radiolabeled compound remains intact for prolonged incubation at 37 degrees C. Binding properties give Kd (19.0 +/- 4.6 nmol/l) and Bmax (approximately 10(6) sites/cell) values in A431 cells overexpressing the CCK2-R. In vivo evaluation of the compound shows rapid and specific targeting to CCK2-R, a fourfold higher accumulation compared to nonreceptor expressing tumors

    POZ-, AT-hook-, and Zinc Finger-containing Protein (PATZ) Interacts with Human Oncogene B Cell Lymphoma 6 (BCL6) and Is Required for Its Negative Autoregulation.

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    The PATZ1 gene encoding a POZ/AT-hook/Kruppel zinc finger (PATZ) transcription factor, is considered a cancer-related gene because of its loss or misexpression in human neoplasias. As for other POZ/domain and Kruppel zinc finger (POK) family members, the transcriptional activity of PATZ is due to the POZ-mediated oligomer formation, suggesting that it might be not a typical transactivator but an architectural transcription factor, thus functioning either as activator or as repressor depending on the presence of proteins able to interact with it. Therefore, to better elucidate PATZ function, we searched for its molecular partners. By yeast two-hybrid screenings, we found a specific interaction between PATZ and BCL6, a human oncogene that plays a key role in germinal center (GC) derived neoplasias. We demonstrate that PATZ and BCL6 interact in germinal center-derived B lymphoma cells, through the POZ domain of PATZ. Moreover, we show that PATZ is able to bind the BCL6 regulatory region, where BCL6 itself acts as a negative regulator, and to contribute to negatively modulate its activity. Consistently, disruption of one or both Patz1 alleles in mice causes focal expansion of thymus B cells, in which BCL6 is up-regulated. This phenotype was almost completely rescued by crossing Patz1(+/-) with Bcl6(+/-) mice, indicating a key role for Bcl6 expression in its development. Finally, a significant number of Patz1 knock-out mice (both heterozygous and homozygous) also develop BCL6-expressing lymphomas. Therefore, the disruption of one or both Patz1 alleles may favor lymphomagenesis by activating the BCL6 pathway
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