Diversity in insect seed parasite guilds at large geographical scale: the roles of host specificity and spatial distance

[Aim]: Host specificity within plant-feeding insects constitutes a fascinating example of natural selection that promotes inter-specific niche segregation. If specificity is strong, composition of local plant parasitic insect guilds is largely dependent on the presence and prevalence of the preferred hosts. Alternatively, if it is weak or absent, historic and stochastic demographic processes may drive the structuring of insect communities. We assessed whether the species composition of acorn feeding insects (Curculio spp. guilds) and their genetic variation change geographically according to the local host community. [Location]: An 800 km transect across California, USA. [Methods]: We used DNA taxonomy to detect potential Curculio cryptic speciation and assessed intra-specific genetic structure among sampling sites. We monitored larval performance on different hosts, by measuring the weight of each larva upon emerging from the acorn. Our phylogenetic and spatial analyses disentangled host specificity and geographical effects on Curculio community composition and genetic structure. [Results]: DNA taxonomy revealed no specialized cryptic species. Californian Curculio spp. were sister taxa that did not segregate among Quercus species or, at a deeper taxonomic level, between red and white oaks. Curculio species turnover and intra-specific genetic differentiation increased with geographical distance among localities irrespective of local oak species composition. Moreover, larval performance did not differ among oak species or acorn sizes when controlling for the effect of the locality. [Main conclusions]: Historical processes have contributed to the structuring of acorn weevil communities across California. Trophic niche overlapped among species, indicating that ecologically similar species can co-exist. Acorn crop inter-annual variability and unpredictability in mixed oak forests may have selected against narrow specialization, and facilitated co-existence by means of an inter-specific time partitioning of the resources. Wide-scale geographical records of parasitic insects and their host plants are necessary to understand the processes underlying species diversity.This work was financed by the projects: CONSOLIDER-MONTES CSD2008-00040 MICINN, PII1C09-0256-9052JCCM and ESF, AGL2014-54739-R (MINECO), PPII-2014-01-PJCCM ESF and CGL2008-00095 ⁄ BOS (MICINN). A.M.was funded by a Juan de la Cierva contract and R.B. by acontract of the Atracción de Talento Investigador Programme (Gobierno de Extremadura TA13032). J.O. wasfunded by Severo Ochoa (SEV-2012-0262) and Ramón y Cajal (RYC-2013-12501) research fellowships.Peer reviewe

A digital-based integrated methodology for the preventive conservation of cultural heritage: the experience of HeritageCare project

A sustainable conservation strategy for cultural heritage protection is not feasible without a systematic documentation, registration and management of the information. The adoption of integrated inspection protocols and regular tracking processes, based on standardized procedures and uniform criteria, are the basis to successfully replace actual curative strategies with proactive conservation approaches. The opportunities brought by the digital tools can offer tremendous advantages in this regard. This paper explores the leading role that digitization is assuming in the context of heritage conservation through the experience of the HeritageCare project - Monitoring and preventive conservation of historic and cultural heritage" (SOE1/P5/P0258). The project has developed a digital-based integrated methodology aimed at providing enhanced tools and services to properly document cultural heritage buildings and engage directly owners in the conservation process of their legacy. The structured digital workflow on which the HeritageCare protocol relies is described in detail, encompassing different levels of information. Finally, the full application of the protocol is presented with reference to one of the most emblematic case studies of the project, the Ducal Palace of Guimaraes, Portugal.- This work was partly financed by FEDER funds through the Competitiveness Factors Operational Programme (COMPETE) and by national funds through the Foundation for Science and Technology (FCT) within the scope of project POCI-01-0145-FEDER-007633

Down-Regulation of hsa-miR-10a in Chronic Myeloid Leukemia CD34+ Cells Increases USF2-Mediated Cell Growth

MicroRNAs (miRNA) are small noncoding, single-stranded RNAs that inhibit gene expression at a posttranscriptional level, whose abnormal expression has been described in different tumors. The aim of our study was to identify miRNAs potentially implicated in chronic myeloid leukemia (CML). We detected an abnormal miRNA expression profile in mononuclear and CD34+ cells from patients with CML compared with healthy controls. Of 157 miRNAs tested, hsa-miR-10a, hsa-miR-150, and hsa-miR-151 were down-regulated, whereas hsa-miR-96 was up-regulated in CML cells. Down-regulation of hsa-miR-10a was not dependent on BCR-ABL1 activity and contributed to the increased cell growth of CML cells. We identified the upstream stimulatory factor 2 (USF2) as a potential target of hsa-miR-10a and showed that overexpression of USF2 also increases cell growth. The clinical relevance of these findings was shown in a group of 85 newly diagnosed patients with CML in which expression of hsa-miR-10a was down-regulated in 71% of the patients, whereas expression of USF2 was up-regulated in 60% of the CML patients, with overexpression of USF2 being significantly associated with decreased expression of hsa-miR-10a (P = 0.004). Our results indicate that down-regulation of hsa-miR-10a may increase USF2 and contribute to the increase in cell proliferation of CML implicating a miRNA in the abnormal behavior of CML

Relapse of unusual localization of classic seminoma with post-chemotherapy transformation

Germ cell tumor is the most common cancer among males in the 20–39 year-old age range, representing 21% of invasive cancer diagnose. The vast majority of testicular tumors in this age range are germ cell tumors. There are two types of malignant tumors, the pure seminoma cell and non-seminomatous germinal cell tumors (NGCT). We present the case of a patient who underwent a testicular tumor surgery, classic seminoma stage I, receiving two cycles of adjuvant carboplatin chemotherapy. During the follow up, an elevation on the alpha-fetoprotein level was observed, thus the final diagnosis was adenopatic recurrence of the Yolk Sac tumor.-----------------------------------------------------------------Cite this article as: Urena MD, Legeren M, Galvez F, Villaescusa A, Aparicio J, Jurado JM, Blancas I, Sanchez MJ, Romera AL, Martinez AP, Quiñonez E, Dulcey I, Puche JL. Relapse of unusual localization of classic seminoma with post-chemotherapy transformation. Int J Cancer Ther Oncol 2014; 2(1):02016.DOI: http://dx.doi.org/10.14319/ijcto.0201.

The Prevalence of Anti-Hexokinase-1 and Anti-Kelch-Like 12 Peptide Antibodies in Patients With Primary Biliary Cholangitis Is Similar in Europe and North America: A Large International, Multi-Center Study

Primary biliary cholangitis (PBC), formerly known as primary biliary cirrhosis, is present worldwide. Autoantibodies, in particular anti-mitochondrial antibodies (AMA) detected by indirect immunofluorescence assays or newer solid phase immunoassays can detect most, but not all individuals with PBC. Detection of antibodies to the anti-nuclear antigens sp100 and gp210 can identify additional PBC patients, but some seronegative patients remain, often resulting in delayed diagnosis and treatment. Antibodies to kelch-like 12 (KLHL12) and hexokinase 1 (HK-1) were recently identified as new biomarkers for PBC and notably identify patients who are negative for conventional autoantibodies. To become globally adopted, it is important to validate these new biomarkers in different geographic areas. In the present study we evaluated the prevalence of anti-KLHL12 (measured by a KLHL12-derived peptide referred to as KL-p) and anti-HK-1 antibodies by ELISA at five sites within Europe and North America and demonstrated the presence of these antibodies in patients with PBC in all geographies

Pathogenic Mouse Hepatitis Virus or Poly(I:C) Induce IL-33 in Hepatocytes in Murine Models of Hepatitis.

International audienceThe IL-33/ST2 axis is known to be involved in liver pathologies. Although, the IL-33 levels increased in sera of viral hepatitis patients in human, the cellular sources of IL-33 in viral hepatitis remained obscure. Therefore, we aimed to investigate the expression of IL-33 in murine fulminant hepatitis induced by a Toll like receptor (TLR3) viral mimetic, poly(I:C) or by pathogenic mouse hepatitis virus (L2-MHV3). The administration of poly(I:C) plus D-galactosamine (D-GalN) in mice led to acute liver injury associated with the induction of IL-33 expression in liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells (VEC), while the administration of poly(I:C) alone led to hepatocyte specific IL-33 expression in addition to vascular IL-33 expression. The hepatocyte-specific IL-33 expression was down-regulated in NK-depleted poly(I:C) treated mice suggesting a partial regulation of IL-33 by NK cells. The CD1d KO (NKT deficient) mice showed hepatoprotection against poly(I:C)-induced hepatitis in association with increased number of IL-33 expressing hepatocytes in CD1d KO mice than WT controls. These results suggest that hepatocyte-specific IL-33 expression in poly(I:C) induced liver injury was partially dependent of NK cells and with limited role of NKT cells. In parallel, the L2-MHV3 infection in mice induced fulminant hepatitis associated with up-regulated IL-33 expression as well as pro-inflammatory cytokine microenvironment in liver. The LSEC and VEC expressed inducible expression of IL-33 following L2-MHV3 infection but the hepatocyte-specific IL-33 expression was only evident between 24 to 32h of post infection. In conclusion, the alarmin cytokine IL-33 was over-expressed during fulminant hepatitis in mice with LSEC, VEC and hepatocytes as potential sources of IL-33