179 research outputs found
Humoral immune response to different routes of myxomatosis vaccine application
[EN] The aim of our study was to monitor the dynamics of the serological response to different application routes of live attenuated myxomatosis vaccine. The study included 42 Californian breed rabbits, aged 3 mo, of both sexes. They were separated into 7 groups: 6 experimental and 1 control. All experimental groups were vaccinated on day 0 with a single dose of myxomatosis vaccine (min 103.3 tissue culture infective dose 50 [TCID50], max 105.8 TCID50). Three of the groups were injected with monovalent attenuated myxomatosis vaccine using different types of application: intradermal (i.d.), intramuscular (i.m.) and subcutaneous (s.c.). The other 3 groups were injected with bivalent attenuated vaccine against myxomatosis and rabbit haemorrhagic disease; again the routes of administration were i.d., i.m. and s.c.. There were no clinical signs or serious side effects after vaccination. The serological response was evaluated on days 7, 15 and 30 with a monoclonal antibody based-competition enzyme-linked immunosorbent assay (cELISA). More rapid and potent humoral response was detected in groups with i.d. inoculation in comparison to i.m. and s.c. routes. Vaccination with monovalent vaccine against myxomatosis induced higher antibody titre in comparison to bivalent vaccine. Our study showed that the vaccine application route and the type of vaccine used influence the speed and intensity of antibody response.Manev, I.; Genova, K.; Lavazza, A.; Capucci, L. (2018). Humoral immune response to different routes of myxomatosis vaccine application. World Rabbit Science. 26(2):149-154. doi:10.4995/wrs.2018.7021SWORD149154262Alfonso M., Pagès-Manté A. 2003. Serological response to Myxomatosis vaccination by different inoculation systems on farm rabbits. World Rabbit Sci. 2003, 11: 145-156. https://doi.org/10.4995/wrs.2003.504Barcena J., Morales M., Vázquez B., Boga J., Parra F., Lucientes J., Pagès-Manté A., Sánchez-Vizcaino J., Blasco R., Torres J. 2000. Horizontal Transmissible Protection against Myxomatosis and Rabbit Hemorrhagic Disease by Using a Recombinant Myxoma Virus. J. Virol., 74, 1114-1123.Bertagnoli S., Gelfi J., Gall G., Boilletot E., Vautherot J., Rasschaert D., Laurent S., Petit F., Boucraut-Baralon C., Milon A. 1996. Protection against myxomatosis and rabbit viral hemorrhagic disease with recombinant myxoma viruses expressing rabbit hemorrhagic disease virus capsid protein. J. Virol., 70: 5061-5066.Best S., Kerr P. 2000. Coevolution of Host and Virus: The Pathogenesis of Virulent and Attenuated Strains of Myxoma Virus in Resistant and Susceptible European Rabbits. Virology, 267, 36-48. https://doi.org/10.1006/viro.1999.0104Bhanuprakash V., Hosamani M., Venkatesan G., Balamurugan V., Yogisharadhya R., Singh R. 2012. Animal poxvirus vaccines: a comprehensive review Expert Rev. Vaccines, 11, 1355-1374. https://doi.org/10.1586/erv.12.116Calvete C., Estrada R., Lucientes J., Osacar J., Villafuerte R., 2004. Effects of vaccination against viral haemorrhagic disease (VHD) and myxomatosis on long-term mortality rates of European wild rabbits. Vet. Rec., 155: 388-392.Dalton K., Nicieza I., Gullón J., Inza M., Petralanda M., Arroita Z., Parra F. 2012. Analysis of Myxomatosis outbreaks on Spanish rabbit farms. In Proc.: 10th World Rabbit Congress, September 3 - 6, 2012, Sharm El- Sheikh, Egypt, 1203-1207.Dalton K., Nicieza I., de Llano D., Gullón J., Inza M., Petralanda M., Arroita Z., Parra F. 2015. Vaccine breaks: Outbreaks of myxomatosis on Spanish commercial rabbit farms. Vet. Microbiol., 178, 208-216. https://doi.org/10.1016/j.vetmic.2015.05.008Dan M., Baraitareanu S., Danes D., 2014. Serosurveillance of Myxomatosis by Competitive ELISA. Bulletin UASVM Veterinary Medicine. 71, 266-267.Day M., Fenner F., Woodroofe G., McIntyre G.A. 1956. Further studies on the mechanism of mosquito transmission of Myxomatosis in the European rabbit. J. Hyg. Cambridge, 54:258-283.Farsang A., Makranszki L., Dobos-Kovacs M., Virag G., Fabian K., Barna T., Kuclsar G., Kucsera L., Vetesi F. 2003. Occurrence of atypical myxomatosis in central Europe: clinical and virological examinations. Acta Vet. Hung., 51, 493-501. https://doi.org/10.1556/AVet.51.2003.4.7Fenner F., Ratcliffe F. 1965. Myxomatosis. Cambridge University Press, Cambridge, England. Ferreira C., RamÃrez E., Castro F., Ferreras P., Alves P., Redpath S., Villafuerte R. 2009. Field experimental vaccination campaigns against myxomatosis and their effectiveness in the wild. Vaccine, 27: 6998-7002. https://doi.org/10.1016/j.vaccine.2009.09.075Jeklova E., Leva L., Matiasovic J., Kovarcik K., Kudlackova H., Nevorankova Z., Psikal I., Faldyna M. 2007. Characterisation of immunosuppression in rabbits after infection with myxoma virus, Vet. Microbiol., 129: 117-130. https://doi.org/10.1016/j.vetmic.2007.11.039Kerr P.J. 1997. An ELISA for Epidemiological Studies of Myxomatosis: Persistance of Antibodies to Myxoma Virus in European Rabbits (Oryctolagus cuniculus). Wildlife Res., 24: 53-65.https://doi.org/10.1071/WR96058Kerr P.J. 2012. Myxomatosis in Australia and Europe: A model for emerging infectious diseases. Antivir. Res., 93: 387-415. https://doi.org/10.1016/j.antiviral.2012.01.009Kim, Y.C., Jarrahian, C., Zehrung, D., Mitragotri, S., Prausnitz , M.R. 2012. Delivery Systems for Intradermal Vaccination. Curr. Top. Microbiol., 351: 77-112. https://doi.org/10.1007/82_2011_123King A., Adams M., Carstens E., Lefkowitz E. 2012. Virus Taxonomy. Classification and Nomenclature of Viruses. Ninth Report of the International Committee on Taxonomy of Viruses, 291-309.Lavazza A., Graziani M., Tranquillo V.M., Botti G., Palotta C., Cerioli M., Capucci L. 2004. Serorological evaluation of the immunity induced in commercial rabbits by vaccination for Myxomatosis and RHD, In Proc.: 8th World Rabbit Congress, September 7-10, 2004, Puebla, Mexico, 569-575.Le Normand B., Chatellier S., Devaud I., Delvecchio A., Lavazza A., Capucci L. 2015. Evaluation de l'immunité humorale consécutive à la vaccination avec Dervaximyxo SG33 chez des lapines reproductrices vaccinées à différents stades du cycle productif. 16e Journées de la Recherche Cunicole. Le Mans, France. 17-20.Lemiere S. 2000. Combined vaccination against myxomatosis and VHD: an innovative approach, In: 7th World Rabbit Congress, Valencia, 4-7th July, Spain, World Rabbit Sci., 8 suppl 1. Vol. B:289-297.Levin C., Perrin H., Combadiere B. 2015. Tailored immunity by skin antigen-presenting cells. Hum. Vacc. Immunother., 11: 27-36. https://doi.org/10.4161/hv.34299Marlier D. 2010. Vaccination strategies against myxomavirus infections: are we really doing the best? Tijdschr Diergeneesk., 135: 194-198.Marlier D., Mainil J., Boucraut-Baralon C., Linden A., Vindevogel H. 2000. The efficacy of two vaccination schemes against expérimental infection with a virulent amyxomatous or a virulent nodular myxoma virus strain. J. Comp. Path. Vol. 122, 115-122. https://doi.org/10.1053/jcpa.1999.0346Marshall I., Regnery C. 1960. Myxomatosis in a California brush rabbit (Sylvilagus bachmani). Nature, 188: 73-74. http://doi.org/10.1038/188073b0Morimoto M. 2009. General Physiology of Rabbits. In: Houdebine LM., Fan J. (eds) Rabbit Biotechnology. Springer, Dordrecht. OIE. 2014. Myxomatosis. Chapter 2.6.1. (NB: Version adopted in May 2014). Manual of Diagnostic Tests and Vaccines for Terrestrial Animals http://www.oie.int/fileadmin/Home/fr/Health_standards/tahm/2.06.01_MYXO.pdf Accessed June 2018.Panchanathan V., Chaudhri G., Karupiah G. 2008. Correlates of protective immunity in poxvirus infection: where does antibody stand? Immunol. Cell Biol., 86, 80-86. https://doi.org/10.1038/sj.icb.7100118Rouco C, Moreno S, Santoro S. 2016. A case of low success of blind vaccination campaigns against myxomatosis and rabbit haemorrhagic disease on survival of adult European wild rabbits. Prev. Vet. Med., 133: 108-113. https://doi.org/10.1016/j.prevetmed.2016.09.013Spibey N., McCabe V., Greenwood N., Jack S., Sutton D., van der Waart L. 2012. Novel bivalent vectored vaccine for control of myxomatosis and rabbit haemorrhagic disease. Vet. Rec., 170: 309. http://dx.doi.org/10.1136/vr.10036
Heart failure hospitalization prediction in remote patient management systems
Healthcare systems are shifting from patient care in hospitals to monitored care at home. It is expected to improve the quality of care without exploding the costs. Remote patient management (RPM) systems offer a great potential in monitoring patients with chronic diseases, like heart failure or diabetes. Patient modeling in RPM systems opens opportunities in two broad directions: personalizing information services, and alerting medical personnel about the changing conditions of a patient. In this study we focus on heart failure hospitalization (HFH) prediction, which is a particular problem of patient modeling for alerting. We formulate a short term HFH prediction problem and show how to address it with a data mining approach. We emphasize challenges related to the heterogeneity, different types and periodicity of the data available in RPM systems. We present an experimental study on HFH prediction using, which results lay a foundation for further studies and implementation of alerting and personalization services in RPM systems
Heart failure hospitalization prediction in remote patient management systems
Healthcare systems are shifting from patient care in hospitals to monitored care at home. It is expected to improve the quality of care without exploding the costs. Remote patient management (RPM) systems offer a great potential in monitoring patients with chronic diseases, like heart failure or diabetes. Patient modeling in RPM systems opens opportunities in two broad directions: personalizing information services, and alerting medical personnel about the changing conditions of a patient. In this study we focus on heart failure hospitalization (HFH) prediction, which is a particular problem of patient modeling for alerting. We formulate a short term HFH prediction problem and show how to address it with a data mining approach. We emphasize challenges related to the heterogeneity, different types and periodicity of the data available in RPM systems. We present an experimental study on HFH prediction using, which results lay a foundation for further studies and implementation of alerting and personalization services in RPM systems
Understanding communication networks in the emergency department
<p>Abstract</p> <p>Background</p> <p>Emergency departments (EDs) are high pressure health care settings involving complex interactions between staff members in providing and organising patient care. Without good communication and cooperation amongst members of the ED team, quality of care is at risk. This study examined the problem-solving, medication advice-seeking and socialising networks of staff working in an Australian hospital ED.</p> <p>Methods</p> <p>A social network survey (Response Rate = 94%) was administered to all ED staff (n = 109) including doctors, nurses, allied health professionals, administrative staff and ward assistants. Analysis of the network characteristics was carried out by applying measures of density (the extent participants are concentrated), connectedness (how related they are), isolates (how segregated), degree centrality (who has most connections measured in two ways, in-degree, the number of ties directed to an individual and out-degree, the number of ties directed from an individual), betweenness centrality (who is important or powerful), degree of separation (how many ties lie between people) and reciprocity (how bi-directional are interactions).</p> <p>Results</p> <p>In all three networks, individuals were more closely connected to colleagues from within their respective professional groups. The problem-solving network was the most densely connected network, followed by the medication advice network, and the loosely connected socialising network. ED staff relied on each other for help to solve work-related problems, but some senior doctors, some junior doctors and a senior nurse were important sources of medication advice for their ED colleagues.</p> <p>Conclusions</p> <p>Network analyses provide useful ways to assess social structures in clinical settings by allowing us to understand how ED staff relate within their social and professional structures. This can provide insights of potential benefit to ED staff, their leaders, policymakers and researchers.</p
Identification of a novel Drosophila gene, beltless, using injectable embryonic and adult RNA interference (RNAi)
BACKGROUND: RNA interference (RNAi) is a process triggered by a double-stranded RNA that leads to targeted down-regulation/silencing of gene expression and can be used for functional genomics; i.e. loss-of-function studies. Here we report on the use of RNAi in the identification of a developmentally important novel Drosophila (fruit fly) gene (corresponding to a putative gene CG5652/GM06434), that we named beltless based on an embryonic loss-of-function phenotype. RESULTS: Beltless mRNA is expressed in all developmental stages except in 0–6 h embryos. In situ RT-PCR localized beltless mRNA in the ventral cord and brain of late stage embryos and in the nervous system, ovaries, and the accessory glands of adult flies. RNAi was induced by injection of short (22 bp) beltless double-stranded RNAs into embryos or into adult flies. Embryonic RNAi altered cuticular phenotypes ranging from partially-formed to missing denticle belts (thus beltless) of the abdominal segments A2–A4. Embryonic beltless RNAi was lethal. Adult RNAi resulted in the shrinkage of the ovaries by half and reduced the number of eggs laid. We also examined Df(1)RK4 flies in which deletion removes 16 genes, including beltless. In some embryos, we observed cuticular abnormalities similar to our findings with beltless RNAi. After differentiating Df(1)RK4 embryos into those with visible denticle belts and those missing denticle belts, we assayed the presence of beltless mRNA; no beltless mRNA was detectable in embryos with missing denticle belts. CONCLUSIONS: We have identified a developmentally important novel Drosophila gene, beltless, which has been characterized in loss-of-function studies using RNA interference. The putative beltless protein shares homologies with the C. elegans nose resistant to fluoxetine (NRF) NRF-6 gene, as well as with several uncharacterized C. elegans and Drosophila melanogaster genes, some with prominent acyltransferase domains. Future studies should elucidate the role and mechanism of action of beltless during Drosophila development and in adults, including in the adult nervous system
Differential effects of lead and zinc on inhibitory avoidance learning in mice
We studied the effects of chronic intoxication with the heavy metals lead (Pb2+) and zinc (Zn2+) on memory formation in mice. Animals were intoxicated through drinking water during the pre- and postnatal periods and then tested in the step-through inhibitory avoidance memory task. Chronic postnatal intoxication with Pb2+ did not change the step-through latency values recorded during the 4 weeks of the test (ANOVA, P>0.05). In contrast, mice intoxicated during the prenatal period showed significantly reduced latency values when compared to the control group (day 1: q = 4.62, P<0.05; day 7: q = 4.42, P<0.05; day 14: q = 5.65, P<0.05; day 21: q = 3.96, P<0.05, and day 28: q = 6.09, P<0.05). Although chronic postnatal intoxication with Zn2+ did not alter a memory retention test performed 24 h after training, we noticed a gradual decrease in latency at subsequent 4-week intervals (F = 3.07, P<0.05), an effect that was not observed in the control or in the Pb2+-treated groups. These results suggest an impairment of memory formation by Pb2+ when the animals are exposed during the critical period of neurogenesis, while Zn2+ appears to facilitate learning extinction
Melatonin Promotes Oligodendroglial Maturation of Injured White Matter in Neonatal Rats
OBJECTIVE:To investigate the effects of melatonin treatment in a rat model of white matter damage (WMD) in the developing brain. Additionally, we aim to delineate the cellular mechanisms of melatonin effect on the oligodendroglial cell lineage. METHODS:A unilateral ligation of the uterine artery in pregnant rat at the embryonic day 17 induces fetal hypoxia and subsequent growth restriction (GR) in neonatal pups. GR and control pups received a daily intra-peritoneal injection of melatonin from birth to post-natal day (P) 3. RESULTS:Melatonin administration was associated with a dramatic decrease in microglial activation and astroglial reaction compared to untreated GR pups. At P14, melatonin prevented white matter myelination defects with an increased number of mature oligodendrocytes (APC-immunoreactive) in treated GR pups. Conversely, melatonin was not found to be associated with an increased density of total oligodendrocytes (Olig2-immunoreactive), suggesting that melatonin is able to promote oligodendrocyte maturation but not proliferation. These effects appear to be melatonin-receptor dependent and were reproduced in vitro. INTERPRETATION:These data suggest that melatonin has a strong protective effect on developing damaged white matter through decreased microglial activation and oligodendroglial maturation leading to a normalization of the myelination process. Consequently, melatonin should be a considered as an effective neuroprotective candidate not only in perinatal brain damage but also in inflammatory and demyelinating diseases observed in adults
Evaluating genetic markers and neurobiochemical analytes for fluoxetine response using a panel of mouse inbred strains
RationaleIdentification of biomarkers that establish diagnosis or treatment response is critical to the advancement of research and management of patients with depression.ObjectiveOur goal was to identify biomarkers that can potentially assess fluoxetine response and risk to poor treatment outcome.MethodsWe measured behavior, gene expression, and the levels of 36 neurobiochemical analytes across a panel of genetically diverse mouse inbred lines after chronic treatment with water or fluoxetine.ResultsGlyoxylase 1 (GLO1) and guanine nucleotide-binding protein 1 (GNB1) mostly account for baseline anxiety-like and depressive-like behavior, indicating a common biological link between depression and anxiety. Fluoxetine-induced biochemical alterations discriminated positive responders, while baseline neurobiochemical differences differentiated negative responders (p < 0.006). Results show that glial fibrillary acidic protein, S100 beta protein, GLO1, and histone deacetylase 5 contributed most to fluoxetine response. These proteins are linked within a cellular growth/proliferation pathway, suggesting the involvement of cellular genesis in fluoxetine response. Furthermore, a candidate genetic locus that associates with baseline depressive-like behavior contains a gene that encodes for cellular proliferation/adhesion molecule (Cadm1), supporting a genetic basis for the role of neuro/gliogenesis in depression.ConclusionWe provided a comprehensive analysis of behavioral, neurobiochemical, and transcriptome data across 30 mouse inbred strains that has not been accomplished before. We identified biomarkers that influence fluoxetine response, which, altogether, implicate the importance of cellular genesis in fluoxetine treatment. More broadly, this approach can be used to assess a wide range of drug response phenotypes that are challenging to address in human samples.Electronic supplementary materialThe online version of this article (doi:10.1007/s00213-011-2574-z) contains supplementary material, which is available to authorized users
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