A comparative study of MEA and DEA for post-combustion CO2 capture with different process configurations

This paper presented a comparative study of monoethanolamine (MEA) and diethanolamine (DEA) for post-combustion CO2 capture (PCC) process with different process configurations to study the interaction effect between solvent and process. The steady state process model of the conventional MEA-based PCC process was developed in Pro/II® and was validated with the experimental data. Then ten different process configurations were simulated for both MEA and DEA. Their performances in energy consumption were compared in terms of reboiler duty and total equivalent work. The results show that DEA generally has better thermal performances than MEA for all these ten process configurations. Seven process configurations provide 0.38%–4.61% total energy saving compared with the conventional PCC process for MEA, and other two configurations are not favourable. For DEA, except one configuration, other process configurations have 0.27%–4.50% total energy saving. This work also analyzed the sensitivities of three key parameters (amine concentration, stripper pressure and lean solvent loading) in conventional process and five process modifications to show optimization strategy

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

Growth rings show limited evidence for ungulates' potential to suppress shrubs across the Arctic

Global warming has pronounced effects on tundra vegetation, and rising mean temperatures increase plant growth potential across the Arctic biome. Herbivores may counteract the warming impacts by reducing plant growth, but the strength of this effect may depend on prevailing regional climatic conditions. To study how ungulates interact with temperature to influence growth of tundra shrubs across the Arctic tundra biome, we assembled dendroecological data from 20 sites, comprising 1153 individual shrubs and 223 63 annual growth rings. Evidence for ungulates suppressing shrub radial growth was only observed at intermediate summer temperatures (6.5 degrees C-9 degrees C), and even at these temperatures the effect was not strong. Multiple factors, including forage preferences and landscape use by the ungulates, and favourable climatic conditions enabling effective compensatory growth of shrubs, may weaken the effects of ungulates on shrubs, possibly explaining the weakness of observed ungulate effects. Earlier local studies have shown that ungulates may counteract the impacts of warming on tundra shrub growth, but we demonstrate that ungulates' potential to suppress shrub radial growth is not always evident, and may be limited to certain climatic conditions

Systematic meta-review of supported self-management for asthma: a healthcare perspective

BACKGROUND: Supported self-management has been recommended by asthma guidelines for three decades; improving current suboptimal implementation will require commitment from professionals, patients and healthcare organisations. The Practical Systematic Review of Self-Management Support (PRISMS) meta-review and Reducing Care Utilisation through Self-management Interventions (RECURSIVE) health economic review were commissioned to provide a systematic overview of supported self-management to inform implementation. We sought to investigate if supported asthma self-management reduces use of healthcare resources and improves asthma control; for which target groups it works; and which components and contextual factors contribute to effectiveness. Finally, we investigated the costs to healthcare services of providing supported self-management. METHODS: We undertook a meta-review (systematic overview) of systematic reviews updated with randomised controlled trials (RCTs) published since the review search dates, and health economic meta-analysis of RCTs. Twelve electronic databases were searched in 2012 (updated in 2015; pre-publication update January 2017) for systematic reviews reporting RCTs (and update RCTs) evaluating supported asthma self-management. We assessed the quality of included studies and undertook a meta-analysis and narrative synthesis. RESULTS: A total of 27 systematic reviews (n = 244 RCTs) and 13 update RCTs revealed that supported self-management can reduce hospitalisations, accident and emergency attendances and unscheduled consultations, and improve markers of control and quality of life for people with asthma across a range of cultural, demographic and healthcare settings. Core components are patient education, provision of an action plan and regular professional review. Self-management is most effective when delivered in the context of proactive long-term condition management. The total cost (n = 24 RCTs) of providing self-management support is offset by a reduction in hospitalisations and accident and emergency visits (standard mean difference 0.13, 95% confidence interval -0.09 to 0.34). CONCLUSIONS: Evidence from a total of 270 RCTs confirms that supported self-management for asthma can reduce unscheduled care and improve asthma control, can be delivered effectively for diverse demographic and cultural groups, is applicable in a broad range of clinical settings, and does not significantly increase total healthcare costs. Informed by this comprehensive synthesis of the literature, clinicians, patient-interest groups, policy-makers and providers of healthcare services should prioritise provision of supported self-management for people with asthma as a core component of routine care. SYSTEMATIC REVIEW REGISTRATION: RECURSIVE: PROSPERO CRD42012002694 ; PRISMS: PROSPERO does not register meta-reviews

Growth rings show limited evidence for ungulates’ potential to suppress shrubs across the Arctic

Global warming has pronounced effects on tundra vegetation, and rising mean temperatures increase plant growth potential across the Arctic biome. Herbivores may counteract the warming impacts by reducing plant growth, but the strength of this effect may depend on prevailing regional climatic conditions. To study how ungulates interact with temperature to influence growth of tundra shrubs across the Arctic tundra biome, we assembled dendroecological data from 20 sites, comprising 1153 individual shrubs and 223 63 annual growth rings. Evidence for ungulates suppressing shrub radial growth was only observed at intermediate summer temperatures (6.5 ◦C–9 ◦C), and even at these temperatures the effect was not strong. Multiple factors, including forage preferences and landscape use by the ungulates, and favourable climatic conditions enabling effective compensatory growth of shrubs, may weaken the effects of ungulates on shrubs, possibly explaining the weakness of observed ungulate effects. Earlier local studies have shown that ungulates may counteract the impacts of warming on tundra shrub growth, but we demonstrate that ungulates’ potential to suppress shrub radial growth is not always evident, and may be limited to certain climatic conditions.Research Council of Norwayhttp://iopscience.iop.org/1748-9326dm2022Mammal Research InstituteZoology and Entomolog