Stratégies d’adaptation à la réduction des services écosystémiques : cas des potentialités de substitution de trois espèces forestières dans le Sud-Ouest du Burkina Faso

Les conséquences de la perte de biodiversité sont entre autres la baisse des services écosystémiques, avec des incidences graves sur la santé des populations, leur alimentation, voire leur habitat. Dans ce contexte, les populations locales ont tendance à adopter des stratégies d’adaptation qu’il importe d’identifier et d’en analyser la durabilité. L’objectif de cette l’étude était de déterminer les substituts de trois plantes (Crateva adansonii D.C., Sarcocephalus latifolius (Smith) Buce et Burkea africana Hook.) à haute valeur sociale et culturelle dans le Sud-Ouest du Burkina Faso. Il s’agit de fournir des informations à même d’orienter les mesures de conservation et d’anticipation des effets de la déforestation. Une enquête a été conduite auprès de 253 personnes de neuf localités appartenant à trois groupes ethniques. Les résultats ont montré que les populations ont identifié seize substituts pour C. adansonii, vingt-deux pour S. latifoliius et seize pour B. africana. La plupart des substituts sont des espèces locales ou exotiques, et très peu de produits manufacturés. Il est donc possible, plutôt que d’interdire sans proposition de rechange à l’exploitation des espèces menacées, d’inverser la tendance en accompagnant les populations à utiliser les diverses potentialités de substitution des espèces. Ceci est un axe de conservation efficace des ressources végétales.Mots clés : Crateva adansonii D.C, Sarcocephalus latifoliius (Smith) Buce, Burkea africana Hook.,biodiversité, conservatio

Targeting BTK for the treatment of FLT3-ITD mutated acute myeloid leukemia

Approximately 20% of patients with acute myeloid leukaemia (AML) have a mutation in FMS-like-tyrosine-kinase-3 (FLT3). FLT3 is a trans-membrane receptor with a tyrosine kinase domain which, when activated, initiates a cascade of phosphorylated proteins including the SRC family of kinases. Recently our group and others have shown that pharmacologic inhibition and genetic knockdown of Bruton's tyrosine kinase (BTK) blocks AML blast proliferation, leukaemic cell adhesion to bone marrow stromal cells as well as migration of AML blasts. The anti-proliferative effects of BTK inhibition in human AML are mediated via inhibition of downstream NF-κB pro-survival signalling however the upstream drivers of BTK activation in human AML have yet to be fully characterised. Here we place the FLT3-ITD upstream of BTK in AML and show that the BTK inhibitor ibrutinib inhibits the survival and proliferation of FLT3-ITD primary AML blasts and AML cell lines. Furthermore ibrutinib inhibits the activation of downstream kinases including MAPK, AKT and STAT5. In addition we show that BTK RNAi inhibits proliferation of FLT3-ITD AML cells. Finally we report that ibrutinib reverses the cyto-protective role of BMSC on FLT3-ITD AML survival. These results argue for the evaluation of ibrutinib in patients with FLT3-ITD mutated AML

Rhizobial inoculation, alone or coinoculated with Azospirillum brasilense, promotes growth of wetland rice

Rhizobia and associative bacteria promote growth in rice plants (Oryza sativa L.) through a series of mechanisms, but most studies on inoculation have been performed based on inoculation with these bacteria in a separate or singular manner. The objective of this study was to assess the efficiency of single/isolated inoculation and inoculation combined with symbiotic rhizobia from forage legume and with Azospirillum brasilense on promoting growth and the root colonization process in wetland rice. Two rhizobia among four isolates from a greenhouse and a laboratory experiment were selected that efficiently promoted seed germination and rice plant growth in a sterilized substrate and in soil. The two most efficient isolates (UFRGS Vp16 and UFRGS Lc348) were inoculated alone or in combination with a commercial product containing A. brasilense in two field experiments using two wetland rice cultivars over two growing seasons. In the field experiments, these isolates coinoculated with A. brasilense promoted larger increases in the agronomic variables of wetland rice compared to the control without inoculation. Confocal laser microscopy confirmed the presence of inoculated bacteria tagged with gfp (UFRGS Vp16, UFRGS Lc348, and A. brasilense) colonizing the root surface of the rice seedlings, mainly in the root hairs and lateral roots

Complete mitochondrial genomes and nuclear ribosomal RNA operons of two species of Diplostomum (Platyhelminthes: Trematoda): a molecular resource for taxonomy and molecular epidemiology of important fish pathogens

© 2015 Brabec et al. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http:// creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. The attached file is the published version of the article

Upregulation of hepatic bile acid synthesis via fibroblast growth factor 19 is defective in gallstone disease but functional in overweight individuals

Background: Fibroblast growth factor 19 (FGF19) is an enteric hormone regulating bile acid de novo synthesis by sensing ileal bile acid flux. However, the role of FGF19 in cholelithiasis has not yet been elucidated and therefore is investigated in the present study. Methods: Total mRNA and protein were isolated from ileal biopsies and used for tissue expression analysis. FGF19, 7α-hydroxycholesterol (7α-OH-Chol), 27-hydroxycholesterol (27-OH-Chol), and different bile acids were determined in the blood samples. Results: FGF19 serum levels did not differ between gallstone carriers and controls but were significantly decreased in the overweight individuals (−32%, p = 0.0002), irrespective of gallstone status (normalweight to overweight controls −29%, p = 0.0017; normalweight to overweight gallstone carriers −44%, p = 0.0338), and correlated inversely with bodyweight (p < 0.0001, ρ = −0.3317). Compared to non-overweight controls, apical sodium-dependent bile acid transporter expression was significantly diminished in the non-overweight gallstone carriers (−42%, PmRNA = 0.0393; −52%, pprotein = 0.0169) as well as in the overweight controls (−24%, PmRNA = 0.0148; −43%, pprotein = 0.0017). FGF19 expression varied widely and was similar in all groups. A significant negative correlation was noted between 7α-OH-Chol, 27-OH-Chol, and FGF19 serum levels (p < 0.01; ρ7α-OH-Chol = −0.2155; ρ27-OH-Chol = −0.2144) in obesity. Conclusion: Upregulation of hepatic bile acid synthesis via FGF 19 is defective in gallstone disease but functional in overweight individuals

Differential Regulation of Protrusion and Polarity by PI(3)K during Neutrophil Motility in Live Zebrafish

Cell polarity is crucial for directed migration. Here we show that phosphoinositide 3-kinase (PI(3)K) mediates neutrophil migration in vivo by differentially regulating cell protrusion and polarity. The dynamics of PI(3)K products PI(3,4,5)P3-PI(3,4)P2 during neutrophil migration were visualized in living zebrafish, revealing that PI(3)K activation at the leading edge is critical for neutrophil motility in intact tissues. A genetically encoded photoactivatable Rac was used to demonstrate that localized activation of Rac is sufficient to direct migration with precise temporal and spatial control in vivo. Similar stimulation of PI(3)K-inhibited cells did not direct migration. Localized Rac activation rescued membrane protrusion but not anteroposterior polarization of F-actin dynamics of PI(3)K-inhibited cells. Uncoupling Rac-mediated protrusion and polarization suggests a paradigm of two-tiered PI(3)K-mediated regulation of cell motility. This work provides new insight into how cell signaling at the front and back of the cell is coordinated during polarized cell migration in intact tissues within a multicellular organism

HNPCC: Six new pathogenic mutations

BACKGROUND: Hereditary non-polyposis colorectal cancer (HNPCC) is an autosomal dominant disease with a high risk for colorectal and endometrial cancer caused by germline mutations in DNA mismatch-repair genes (MMR). HNPCC accounts for approximately 2 to 5% of all colorectal cancers. Here we present 6 novel mutations in the DNA mismatch-repair genes MLH1, MSH2 and MSH6. METHODS: Patients with clinical diagnosis of HNPCC were counselled. Tumor specimen were analysed for microsatellite instability and immunohistochemistry for MLH1, MSH2 and MSH6 protein was performed. If one of these proteins was not detectable in the tumor mutation analysis of the corresponding gene was carried out. RESULTS: We identified 6 frameshift mutations (2 in MLH1, 3 in MSH2, 1 in MSH6) resulting in a premature stop: two mutations in MLH1 (c.2198_2199insAACA [p.N733fsX745], c.2076_2077delTG [p.G693fsX702]), three mutations in MSH2 (c.810_811delGT [p.C271fsX282], c.763_766delAGTGinsTT [p.F255fsX282], c.873_876delGACT [p.L292fsX298]) and one mutation in MSH6 (c.1421_1422dupTG [p.C475fsX480]). All six tumors tested for microsatellite instability showed high levels of microsatellite instability (MSI-H). CONCLUSIONS: HNPCC in families with MSH6 germline mutations may show an age of onset that is comparable to this of patients with MLH1 and MSH2 mutations