EPICURE : A Partitioning and CoDesign Framework For Reconfigurable Computing

This paper presents a new global design methodology capable to bridge the gap between an abstract specification level and a heterogeneous reconfigurable architecture level. The Epicure contribution is the result of a joint study on abstraction/refinement methods and a smart reconfigurable architecture within the formal Esterel design tools suite. The original points of this work are : i) a generic HW/SW interface model, ii) a specification methodology that handles the control, includes efficient verification and HW/SW synthesis capabilities, iii) a method for parallelism exploration based on abstract resources/performance estimation expressed in terms of area/delay tradeoffs, iv) a HW/SW partitioning approach that refines the specification into explicit HW configurations and the associated SW control. The Epicure framework shows how a cooperation of complementary methodologies and CAD tools associated with a relevant architecture can significantly improve the designer productivity, especially in the context of reconfigurable architectures

Radio Resource Management in NB-IoT Systems:Empowered by Interference Prediction and Flexible Duplexing

NB-IoT is a promising cellular technology for enabling low cost, low power, long-range connectivity to IoT devices. With the bandwidth requirement of 180 kHz, it provides the flexibility to deploy within the existing LTE band. However, this raises serious concerns about the performance of the technology due to severe interference from multi-tier 5G HetNets. Furthermore, as NB-IoT is based on HD-FDD, the symmetric allocation of spectrum band between the downlink and uplink results in underutilization of resources, particularly in the case of asymmetric traffic distribution. Therefore, an innovative RRM strategy needs to be devised to improve spectrum efficiency and device connectivity. This article presents the detailed design challenges that need to be addressed for the RRM of NB-IoT and proposes a novel framework to devise an efficient resource allocation scheme by exploiting cooperative interference prediction and flexible duplexing techniques

Dendritic Cells Cause Bone Lesions in a New Mouse Model of Histiocytosis.

Langerhans cell histiocytosis (LCH) is a rare disease caused by the clonal accumulation of dendritic Langerhans cells, which is often accompanied by osteolytic lesions. It has been reported that osteoclast-like cells play a major role in the pathogenic bone destruction seen in patients with LCH and these cells are postulated to originate from the fusion of DCs. However, due to the lack of reliable animal models the pathogenesis of LCH is still poorly understood. In this study, we have established a mouse model of histiocytosis- recapitulating human disease for osteolytic lesions seen in LCH patients. At 12 weeks after birth, severe bone lesions were observed in our multisystem histiocytosis (Mushi) model, when CD8α conventional dendritic cells (DCs) are transformed (MuTuDC) and accumulate. Most importantly, our study demonstrates that bone loss in LCH can be accounted for the transdifferentiation of MuTuDCs into functional osteoclasts both in vivo and in vitro. Moreover, we have shown that injected MuTuDCs reverse the osteopetrotic phenotype of oc/oc mice in vivo. In conclusion, our results support a crucial role of DCs in bone lesions in histiocytosis patients. Furthermore, our new model of LCH based on adoptive transfer of MuTuDC lines, leading to bone lesions within 1-2 weeks, will be an important tool for investigating the pathophysiology of this disease and ultimately for evaluating the potential of anti-resorptive drugs for the treatment of bone lesions

First Report of Root and Collar Rot Caused by Fusarium tricinctum and Fusarium avenaceum on Carrot in France

In 2017, carrot (Daucus carota L.) seed production represented around 22% of the area devoted to the production of vegetable fine seeds. Since 2015, symptoms of root and collar rot have been observed in carrot seed parcels located in the Central Region, one of the most important production zone in France. Diseased plants became dried prematurely, compromising seed development. Depending on the year and the climatic conditions, the disease in a same field can be considered as epidemic (rate losses between 30 to 100% of plants in 2016) or can impact plants more sporadically (less than 10% in 2017 and 2018). Sixteen diseased carrot samples (Nantaise type) were collected from five fields of seed production in the Central Region: two fields in 2016 and 2017, one field in 2018. Seven fungal isolates, obtained from lesions, were grown on Potato Dextrose Agar (PDA) medium and incubated for one week at 20°C in darkness. From the colony top, fluffy mycelium pigmented in pink, red, purple or orange was observed, with a red color at the reverse. To induce sporulation, isolates were grown on Synthetischer Nährstoffarmer Agar (SNA) medium during three weeks at 24°C in near-UV radiations under a 12h-photoperiod. Four isolates (FT001, FT003, FT007, FT017) developed orange sporodochia with lunar or crescent-shaped macroconidia (40.3 ± 0.8 × 5.9 ± 0.1 µm; n=90) and lime or pear-shaped microconidia (10.7 ± 0.2 × 7.7 ± 0.2 µm; n=60), as described in Fusarium tricinctum (Leslie and Summerell 2006). Three isolates (FA001, FA002, FA006) developed orange sporodochia with sickle-shaped macroconidia (50.5 ± 1.1 × 5.0 ± 0.1 µm; n= 60), but no microconidia, as observed in Fusarium avenaceum (Leslie and Summerell 2006). To confirm the identification, DNA was extracted from the mycelium of the seven isolates and molecular markers (ATP citrate lyase, ACL1; RNA polymerase II, RPB2) were used for PCR amplification (Gräfenhan et al. 2011; O’Donnell et al. 2013). The ACL1 sequences from the seven field isolates (GenBank Accession numbers MK183788-MK183791; MK181528-MK181530) were 99-100% identical with the ACL1 sequence of a reference F. tricinctum isolate (query coverages 99-100%; E-values of 0.0) and a reference F. avenaceum isolate (query coverages 98-99%; E-values of 0.0) [respectively DAOM 235630 isolate, GenBank Acc. No. JX397813 and BBA64135 isolate, GenBank Acc. No. JX397768, Niessen et al. 2012]. Using RPB2, sequences from field isolates (GenBank Acc. No. MK183109-MK183115) were 98.5-99.9% identical with the RPB2 sequence of a reference F. tricinctum isolate (query coverages 96-100%; E-values of 0.0) and a reference F. avenaceum isolate (query coverages 95-100%; E-values of 0.0) [respectively MRC 1895 isolate, GenBank Acc. No. MH582113 and MRC 1413 isolate, GenBank Acc. No. MH582082, O’Donnell et al. 2018]. To confirm pathogenicity, FT001 and FA002 were inoculated on collars of 10-weeks old carrot plants in the greenhouse. Forty plants per isolate and 40 control plants were used. Ten microliters of a conidial suspension (105 conidia.mL-1) - or sterile water for the controls - were deposited at the collar, previously wounded using a scalpel blade. Necrotic lesions developed at 20 dpi (FT001) and at 30 dpi (FA002). Fusarium tricinctum and F. avenaceum were re-isolated from the lesions and identified by sequencing using ACL1 and RPB2 markers. No isolation of Fusarium was obtained from the controls. To our knowledge, this is the first report of F. tricinctum and F. avenaceum in carrot in France

Rabbit haemorrhagic disease: experimental study of a recent highly pathogenic GI.2/RHDV2/b strain and evaluation of vaccine efficacy

[EN] In 2010, a variant of the rabbit haemorrhagic disease virus (RHDV) belonging to a new GI.2 genotype was identified in France and rapidly spread worldwide. Due to antigenic difference, new vaccines including G1.2 strains have been developed to confer adequate protection. An increase in the pathogenicity of the circulating strains was recently reported. The objective of this experimental study was to characterise the infection with a highly pathogenic GI.2/RHDV2/b isolate (2017) and assess the efficacy of Filavac VHD K C+V vaccine (Filavie) against this strain. Four and 10-wk-old specific pathogen-free rabbits were inoculated with a recommended dose of vaccine. After 7 d, controls and vaccinated rabbits were challenged and clinically monitored for 14 d. All animals were necropsied and blood, organs and urine were sampled for quantitative reverse transcription polymerase chain reaction (RT-qPCR) analysis. In adult groups, regular nasal and rectal swabbing were performed, and faeces were collected after death to monitor RNA shedding. In control groups, the challenge strain induced acute RHD between 31 and 72 h post-inoculation, with a mortality rate of 100% for kits and 89% for adult rabbits. Except for a shorter mean time to death in kits, similar clinical signs and lesions were observed between age groups. The vaccination significantly prevented all mortality, clinical signs, detection of viral RNA in serum and gross lesions in kits and adult rabbits. In adult groups, we also demonstrated that vaccine significantly protected from detectable RNA shedding via naso-conjunctival and rectal routes. Two weeks after challenge, RNA copies were not detected by PCR in the liver, spleen, lungs, kidneys, faeces and urine of vaccinated adult rabbits. The findings for kits were similar, except that very low levels of RNA were present in the liver and spleen of a few rabbits. These data show that immunisation prevented any significant viral multiplication and/or allowed a rapid clearance. We concluded that, despite the quick evolution of GI.2/RHDV2/b strains, the protection conferred by the vaccine remains adequate. In the context of coexistence of both GI.1 and GI.2 genotypes in some countries, with the circulation of multiples recombinant viruses, the vaccination should be based on the association of strains from both genotypes.Le Minor, O.; Boucher, S.; Joudou, L.; Mellet, R.; Sourice, M.; Le Moullec, T.; Nicolier, A.... (2019). Rabbit haemorrhagic disease: experimental study of a recent highly pathogenic GI.2/RHDV2/b strain and evaluation of vaccine efficacy. World Rabbit Science. 27(3):143-156. https://doi.org/10.4995/wrs.2019.11082SWORD143156273Abrantes J., van der Loo W., Le Pendu J., Esteves P.J. 2012. Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review. Vet. Res., 43: 12. https://doi.org/10.1186/1297-9716-43-12Abrantes J., Lopes A.M., Dalton K.P., Melo P., Correia J.J., Ramada M., Alves P.C., Parra F., Esteves P.J. 2013. New variant of rabbit hemorrhagic disease virus, Portugal, 2012-2013. Emerg. Infect. Dis., 19: 1900-1902. https://doi.org/10.3201/eid1911.130908Calvete C., Sarto P., Calvo A.J., Monroy F., Calvo J.H. 2014. Letter - Could the new rabbit haemorrhagic disease virus variant (RHDVb) be fully replacing classical RHD strains in the Iberian Peninsula?. World Rabbit Sci., 22: 91-91. https://doi.org/10.4995/wrs.2014.1715Calvete C, Mendoza M, Alcaraz A, Sarto M.P., Jiménez-de-Bagüéss M.P., Calvo A.J., Monroy F., Calvo J.H., 2018. Rabbit haemorrhagic disease: Cross-protection and comparative pathogenicity of GI.2/RHDV2/b and GI.1b/RHDV lagoviruses in a challenge trial. Vet. Microbiol., 219: 87-95. https://doi.org/10.1016/j.vetmic.2018.04.018Capucci L., Cavadini P., Schiavitto M., Lombardi G., Lavazza A. 2017. Increased pathogenicity in rabbit haemorrhagic disease virus type 2 (RHDV2). Vet. Rec., 180: 426. https://doi.org/10.1136/vr.104132Carvalho C.L., Duarte E.L., Monteiro M., Botelho A., Albuquerque T., Fevereiro M., Henriques A.M., Barros SS., Duarte MD. 2017. Challenges in the rabbit haemorrhagic disease 2 (RHDV2) molecular diagnosis of vaccinated rabbits. Vet. Microbiol. 198: 43-50. https://doi.org/10.1016/j.vetmic.2016.12.006Dalton K.P., Balseiro A., Juste R.A., Podadera A., Nicieza I., Del Llano D., González R., Martin Alonso J.M., Prieto J.M., Parra F., Casais R. 2018. Clinical course and pathogenicity of variant rabbit haemorrhagic disease virus in experimentally infected adult and kit rabbits: Significance towards control and spread. Vet. Microbiol., 220: 24-32. https://doi.org/10.1016/j.vetmic.2018.04.033Dalton K.P., Nicieza I., Abrantes J., Esteves P.J., Parra F., 2014. Spread of new variant RHDV in domestic rabbits on the Iberian Peninsula. Vet. Microbiol., 169: 67-73. https://doi.org/10.1016/j.vetmic.2013.12.015Dalton K.P., Nicieza I., Balseiro A., Muguerza M.A., Rosell J.M., Casais R., Álvarez Á.L., Parra F. 2012. Variant rabbit hemorrhagic disease virus in young rabbits, Spain. Emerg. Infect. Dis., 18: 2009-2012. https://doi.org/10.3201/eid1812.120341Duarte M., Henriques M., Barros S.C., Fagulha T., Ramos F., Luís T., Fevereiro M., Benevides S., Flor L., Barros S.V., Bernardo S. 2015. Detection of RHDV variant 2 in the Azores. Vet. Rec.,176: 130. https://doi.org/10.1136/vr.h497Forrester N.L., Boag B., Moss S.R., Turner S.L., Trout R.C., White P.J., Hudson P.J., Gould E.A., 2003. Long-term survival of New Zealand rabbit haemorrhagic disease virus RNA in wild rabbits, revealed by RT-PCR and phylogenetic analysis. J. Gen.Virol., 84: 3079-3086. https://doi.org/10.1099/vir.0.19213-0Gall A., Schirrmeier H. 2006. Persistence of rabbit haemorrhagic disease virus genome in vaccinated rabbits after experimental infection. J. Vet. Med. B. Infect. Dis. Vet. Public Health, 53: 358-362. https://doi.org/10.1111/j.1439-0450.2006.00986.xGall A., Hoffmann B., Teifke J.P., Lange B., Schirrmeier H., 2007. Persistence of viral RNA in rabbits which overcome an experimental RHDV infection detected by a highly sensitive multiplex real-time RT-PCR. Vet. Microbiol.,120: 17-32. https://doi.org/10.1016/j.vetmic.2006.10.006Hall R.N., Mahar J.E., Haboury S., Stevens V., Holmes E.C., Strive T. 2015. Emerging Rabbit Hemorrhagic Disease Virus 2 (RHDVb), Australia. Emerg. Infect. Dis., 21: 2276-2278. https://doi.org/10.3201/eid2112.151210Le Gall G., Boilletot E., Morisse J.P. 1992. Viral haemorrhagic disease of rabbit: purification and characterization of a strain isolated in France. Ann. Rech. Vet., 23: 381-387.Le Gall-Reculé G., Zwingelstein F., Boucher S., Le Normand B., Plassiart G., Portejoie Y., Decors A., Bertagnoli S., Guérin J.L., Marchandeau S. 2011. Detection of a new variant of rabbit haemorrhagic disease virus in France. Vet. Rec., 168: 137-138. https://doi.org/10.1136/vr.d697Le Gall-Reculé G., Lavazza A., Marchandeau S., Bertagnoli S., Zwingelstein F., Cavadini, P., Martinelli N., Lombardi G., Guérin J.L., Lemaitre E., Decors A., Boucher S., Le Normand B., Capucci L. 2013. Emergence of a new lagovirus related to Rabbit Haemorrhagic Disease Virus. Vet. Res., 44: 81. https://doi.org/10.1186/1297-9716-44-81Le Gall-Reculé G., Lemaitre E., Bertagnoli S., Hubert C., Top S., Decors A., Marchandeau S., Guitton J.S., 2017. Large-scale lagovirus disease outbreaks in European brown hares (Lepus europaeus) in France caused by RHDV2 strains spatially shared with rabbits (Oryctolagus cuniculus). Vet. Res., 48: 70. https://doi.org/10.1186/s13567-017-0473-yLe Minor O., Beilvert F., Le Moullec T., Djadour D., Martineau J. 2013. Evaluation de l'efficacité d'un nouveau vaccin contre le virus variant de la maladie hémorragique virale du lapin (VHD).15èmes Journées de la Recherche Cunicole, 19-20 novembre, Le Mans, France.Le Minor O., Joudou L., Le Moullec T., Beilvert F. 2017. Innocuité et efficacité de la vaccination à 2 et 3 semaines d'âge contre le virus RHDV2 de la maladie hémorragique virale du lapin (VHD).17èmes Journées de la Recherche Cunicole, 22-13 novembre, Le Mans, France.Le Pendu J., Abrantes J., Bertagnoli S., Guitton J.S., Le Gall-Reculé G., Lopes A.M., Marchandeau S., Alda F., Almeida T., Célio A.P., Bárcena J., Burmakina G., Blanco E., Calvete C., Cavadini P., Cooke B., Dalton K., Delibes Mateos M., Deptula W., Eden J.S., Wang F., Ferreira C.C., Ferreira P., Foronda P., Gonçalves D., Gavier-Widén D., Hall R., Hukowska-Szematowicz B., Kerr P., Kovaliski J., et al. 2017. Proposal for a unified classification system and nomenclature of lagoviruses. J. Gen. Virol., 98:1658-1666. https://doi.org/10.1099/jgv.0.000840Lopes A.M., Correia J., Abrantes J., Melo P., Ramada M., Magalhães M.J., Alves P.C., Esteves P.J. 2015. Is the new variant RHDV replacing genogroup 1 in Portuguese wild rabbit populations? Viruses, 7: 27-36. https://doi.org/10.3390/v7010027Mahar J.E., Hall R.N., Peacock D., Kovaliski J., Piper M., Mourant R., Huang N., Campbell S., Gu X., Read A., Urakova N., Cox T., Holmes E.C., Strive T. 2018. Rabbit haemorrhagic disease virus 2 (GI.2) is replacing endemic strains of RHDV in the Australian landscape within 18 months of its arrival. J. Virol., https://doi.org/10.1128/JVI.01374-17Martin-Alonso A., Martin-Carrillo N., Garcia-livia K., Valladares B., Foronda P. 2016. Emerging rabbit haemorrhagic disease virus 2 (RHDV2) at the gates of the African continent. Infect. Genet. Evol., 44: 46-50. https://doi.org/10.1016/j.meegid.2016.06.034Morin H., Le Minor O., Beilvert F., Le Moullec T. 2015. Durée d'immunité conférée par un vaccin vis-à-vis des calicivirus classique et variant de la maladie virale hémorragique. 16èmes Journées de la Recherche Cunicole, 18-19 novembre, Le mans, France.Neimanis A., Larsson Pettersson U., Huang N., Gavier‑Widén D.,Strive T. 2018. Elucidation of the pathology and tissue distribution of Lagovirus europaeus GI.2/RHDV2 (rabbit haemorrhagic disease virus 2) in young and adult rabbits (Oryctolagus cuniculus). Vet. Res., 49: 46. https://doi.org/10.1186/s13567-018-0540-zOIE, 2017. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2017. Chapter 2.6.2. Rabbit Haemorrhagic disease. Available at: (Accessed 8 February 2018): http://www.oie.int/fileadmin/Home/fr/Health_standards/tahm/3.06.02_RHD.pdfOIE, 2016. Rabbit Haemorrhagic disease, Canada-immediate notification report. Available at: http://www.oie.int/wahis_2/public/wahid.php/Reviewreport/Review?page_refer=MapFullEventReport&reportid=20799.Puggioni G., Cavadini P., Maestrale C., Scivoli R., Botti G., Ligios C., Le Gall- Recule G., Lavazza A., Capucci L. 2013. The new French 2010 Rabbit Hemorrhagic Disease Virus causes an RHD-like disease in the Sardinian Cape hare (Lepus capensis mediterraneus). Vet. Res., 44: 96.https://doi.org/10.1186/1297-9716-44-96Read A.J., Kirkland P.D. 2017. Efficacy of a commercial vaccine against different strains of rabbit haemorrhagic disease virus. Aust. Vet. J., 95: 223-226. https://doi.org/10.1111/avj.12600Silvério D., Lopes A.M., Melo-Ferreira J., Magalhães M.J., Monterroso P., Serronha A., Maio E., Alves P.C., Esteves P.J., Abrantes J. 2018. Insights into the evolution of the new variant rabbit haemorrhagic disease virus (GI.2) and the identification of novel recombinant strains. Transbound. Emerg. Dis., 65: 983-992. https://doi.org/10.1111/tbed.12830Shien, J.H., Shieh, H.K., Lee, L.H. 2000. Experimental infections of rabbits with rabbit haemorrhagic disease virus monitored by polymerase chain reaction. Res. Vet. Sci., 68, 255-259. https://doi.org/10.1053/rvsc.1999.0372Spikey N., McCabe V.J., Greenwood N.M., Jack S.C., Sutton D., van der Waart L. 2012. Novel bivalent vectored vaccine for control of myxomatosis and rabbit haemorrhagic disease. Vet. Rec., 170: 309. https://doi.org/10.1136/vr.100366Strive T., Wright J., Kovaliski J., Botti G., Capucci L. 2010. The non-pathogenic Australian lagovirus RCV-A1 causes a prolonged infection and elicits partial crossprotection to rabbit haemorrhagic disease virus. Virology, 398, 125-134. https://doi.org/10.1016/j.virol.2009.11.045Westcott D.G., Frossard J.P., Everest D., Dastjerdi A., Duff J.P., Choudhury B. 2014. Incursion of RHDV2- like variant in Great Britain. Vet. Rec., 174: 333-333. https://doi.org/10.1136/vr.g234

Annual ring growth of a widespread high arctic shrub reflects past fluctuations in community-level plant biomass

Norges Forskningsråd. Grant Numbers: 223257, 244647, 246054, 276080Peer reviewedPostprin

A first assessment of the genetic diversity of Mycobacterium tuberculosis complex in Cambodia

<p>Abstract</p> <p>Background</p> <p>Cambodia is among the 22 high-burden TB countries, and has one of the highest rates of TB in South-East Asia. This study aimed to describe the genetic diversity among clinical <it>Mycobacterium tuberculosis </it>complex (MTC) isolates collected in Cambodia and to relate these findings to genetic diversity data from neighboring countries.</p> <p>Methods</p> <p>We characterized by 24 VNTR loci genotyping and spoligotyping 105 <it>Mycobacterium tuberculosis </it>clinical isolates collected between 2007 and 2008 in the region of Phnom-Penh, Cambodia, enriched in multidrug-resistant (MDR) isolates (n = 33).</p> <p>Results</p> <p>Classical spoligotyping confirmed that the East-African Indian (EAI) lineage is highly prevalent in this area (60%-68% respectively in whole sample and among non-MDR isolates). Beijing lineage is also largely represented (30% in whole sample, 21% among non-MDR isolates, OR = 4.51, CI_95%[1.77, 11.51]) whereas CAS lineage was absent. The 24 loci MIRU-VNTR typing scheme distinguished 90 patterns with only 13 multi-isolates clusters covering 28 isolates. The clustering of EAI strains could be achieved with only 8 VNTR combined with spoligotyping, which could serve as a performing, easy and cheap genotyping standard for this family. Extended spoligotyping suggested relatedness of some unclassified "T1 ancestors" or "Manu" isolates with modern strains and provided finer resolution.</p> <p>Conclusions</p> <p>The genetic diversity of MTC in Cambodia is driven by the EAI and the Beijing families. We validate the usefulness of the extended spoligotyping format in combination with 8 VNTR for EAI isolates in this region.</p

A Molecular Epidemiological and Genetic Diversity Study of Tuberculosis in Ibadan, Nnewi and Abuja, Nigeria

Background Nigeria has the tenth highest burden of tuberculosis (TB) among the 22 TB high-burden countries in the world. This study describes the biodiversity and epidemiology of drug-susceptible and drug-resistant TB in Ibadan, Nnewi and Abuja, using 409 DNAs extracted from culture positive TB isolates. Methodology/Principal Findings DNAs extracted from clinical isolates of Mycobacterium tuberculosis complex were studied by spoligotyping and 24 VNTR typing. The Cameroon clade (CAM) was predominant followed by the M. africanum (West African 1) and T (mainly T2) clades. By using a smooth definition of clusters, 32 likely epi-linked clusters related to the Cameroon genotype family and 15 likely epi-linked clusters related to other “modern” genotypes were detected. Eight clusters concerned M. africanum West African 1. The recent transmission rate of TB was 38%. This large study shows that the recent transmission of TB in Nigeria is high, without major regional differences, with MDR-TB clusters. Improvement in the TB control programme is imperative to address the TB control problem in Nigeria