Relevant bibliographies by topics / RHDV

Academic literature on the topic 'RHDV'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "RHDV"

1

Fitzner, Andrzej, and Wiesław Niedbalski. "Diversity of RHD virus: epidemiological, diagnostic and immunological importance." Medycyna Weterynaryjna 73, no. 12 (2017): 811–18. http://dx.doi.org/10.21521/mw.5815.

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Rabbit haemorrhagic disease (RHD) was first recognized in China in 1984. In Europe, the disease appeared in 1986 in Italy, and in the following years RHD was observed in many other European countries, including Poland in 1988. The disease is caused by RHD virus (RHDV), classified as a representative of the Lagovirus genus within the Caliciviridae family. Lagoviruses include the non-pathogenic rabbit calicivirus (RCV) and the European brown hare syndrome virus (EBHSV). There are three basic variants (subtypes) of pathogenic RHD viruses: classic (RHDV) and antigenic subtypes RHDVa and RHDV2 (RHDVb), distinguished on the basis of epidemiological characteristics, infectious properties and antigenic and genetic modifications. Phylogenetic analysis of RHDV revealed the presence of five genogroups (G1-G5) with similar time of isolation, regardless of the place of occurrence. RHDVa strains are genetically more variable than RHDV, and all RHDVa strains belong to genogroup G6. RHDV2 was diagnosed for the first time in 2010 in domestic and wild rabbits in France, and later in the Iberian Peninsula, and it was called RHDVb. Like the previously identified variants of the RHD virus, RHDV2 spreads to other regions of the world, and in 2011-2016 it was diagnosed in many European countries, North America, Africa and Australia. Strains of RHD2 form a separate, uniform phylogenetic group and are more similar to the non-pathogenic rabbit calicivirus than to pathogenic RHDV and RHDVa. Infections with different variants of RHD viruses are a serious epidemiological, diagnostic and immunological problem. Advanced antigenic changes in RHD viruses limit the usefulness of standard RHD vaccines in controlling the disease....
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Reemers, Sylvia, Leon Peeters, Joyce van Schijndel, Beth Bruton, David Sutton, Leo van der Waart, and Saskia van de Zande. "Novel Trivalent Vectored Vaccine for Control of Myxomatosis and Disease Caused by Classical and a New Genotype of Rabbit Haemorrhagic Disease Virus." Vaccines 8, no. 3 (August 5, 2020): 441. http://dx.doi.org/10.3390/vaccines8030441.

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Myxoma virus (MV) and rabbit haemorrhagic disease virus (RHDV) are the major causes of lethal viral diseases in the European rabbit. In 2010, a new RHDV genotype (RHDV2) emerged in the field that had limited cross-protection with the classical RHDV (RHDV1). For optimal protection of rabbits and preventing spread of disease, a vaccine providing protection against all three key viruses would be ideal. Therefore, a novel trivalent myxoma vectored RHDV vaccine (Nobivac Myxo-RHD PLUS) was developed similar to the existing bivalent myxoma vectored RHDV vaccine Nobivac Myxo-RHD. The new vaccine contains the Myxo-RHDV1 strain already included in Nobivac Myxo-RHD and a similarly produced Myxo-RHDV2 strain. This paper describes several key safety and efficacy studies conducted for European licensing purposes. Nobivac Myxo-RHD PLUS showed to be safe for use in rabbits from five weeks of age onwards, including pregnant rabbits, and did not spread from vaccinated rabbits to in-contact controls. Furthermore, protection to RHDV1 and RHDV2 was demonstrated by challenge, while the serological response to MV was similar to that after vaccination with Nobivac Myxo-RHD. Therefore, routine vaccination with Nobivac Myxo-RHD PLUS can prevent the kept rabbit population from these major viral diseases.
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Abade dos Santos, Fábio A., Carolina Magro, Carina L. Carvalho, Pedro Ruivo, Margarida D. Duarte, and Maria C. Peleteiro. "A Potential Atypical Case of Rabbit Haemorrhagic Disease in a Dwarf Rabbit." Animals 11, no. 1 (December 28, 2020): 40. http://dx.doi.org/10.3390/ani11010040.

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Rabbit haemorrhagic disease (RHD) is a highly contagious infectious disease of European wild and domestic rabbits. Rabbit haemorrhagic disease virus (RHDV, GI.1) emerged in 1986 in Europe, rapidly spreading all over the world. Several genotypes of RHDV have been recognised over time, but in 2010, a new virus (RHDV2/RHDVb, GI.2) emerged and progressively replaced the previous RHDV strains, due to the lack of cross-immunity conferred between RHDV and RHDV2. RHDV2 has a high mutation rate, similarly to the other calivirus and recombines with strains of RHDV and non-pathogenic calicivirus (GI.4), ensuring the continuous emergence of new field strains. Although this poses a threat to the already endangered European rabbit species, the available vaccines against RHDV2 and the compliance of biosafety measures seem to be controlling the infection in the rabbit industry Pet rabbits, especially when kept indoor, are considered at lower risk of infections, although RHDV2 and myxoma virus (MYXV) constitute a permanent threat due to transmission via insects. Vaccination against these viruses is therefore recommended every 6 months (myxomatosis) or annually (rabbit haemorrhagic disease). The combined immunization for myxomatosis and RHDV through a commercially available bivalent vaccine with RHDV antigen has been extensively used (Nobivac® Myxo-RHD, MSD, Kenilworth, NJ, USA). This vaccine however does not confer proper protection against the RHDV2, thus the need for a rabbit clinical vaccination protocol update. Here we report a clinical case of hepatitis and alteration of coagulation in a pet rabbit that had been vaccinated with the commercially available bivalent vaccine against RHDV and tested positive to RHDV2 after death. The animal developed a prolonged and atypical disease, compatible with RHD. The virus was identified to be an RHDV2 recombinant strain, with the structural backbone of RHDV2 (GI.2) and the non-structural genes of non-pathogenic-A1 strains (RCV-A1, GI.4). Although confirmation of the etiological agent was only made after death, the clinical signs and analytic data were very suggestive of RHD.
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Capucci, Lorenzo, Patrizia Cavadini, and Antonio Lavazza. "Viral haemorrhagic disease: RHDV type 2 ten years later." World Rabbit Science 30, no. 1 (March 31, 2022): 1–11. http://dx.doi.org/10.4995/wrs.2022.16505.

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Until the early 1980s, it was totally unknown that lagomorphs were the hosts of several caliciviruses, which were included in the genus Lagovirus by the International Committee on Taxonomy of Viruses (ICTV) in 2000. In those years, two new diseases appeared, with very similar clinical and pathological profiles and associated high mortality rates: rabbit haemorrhagic disease (RHD) in rabbits and European Brown Hare Syndrome (EBHS) in European brown hares. It took a few years to ascertain that both diseases, actually acute and fatal forms of hepatitis, were caused by two genetically related caliciviruses, but they were finally classified by ICTV into two distinct viral species on the basis of their molecular characterisation and epidemiological data: RHDV in rabbit and EBHSV in brown hare. RHD has had a devastating effect on rabbit farms, causing great economic damage, especially in China, where RHD was first noticed around 1982, and in Europe. RHD has also severely affected wild rabbit populations, whose drastic decline has caused serious ecological imbalances in territories such as Spain, where rabbits are a central link in the wildlife food chain. Since the early 1990s, with the increased availability on the market of RHDV vaccines effective in protecting rabbits from RHD, the impact of the disease on rabbit farms has been significantly reduced. In the following years, also considering that RHDV is an endemic virus that cannot be eradicated, farmers learned how to manage the continuous use of RHDV vaccine in relation to the epidemiological situation, the type of breeding farm and the costs of vaccination prophylaxis. Although precarious, management of the RHD risk for rabbit farmers reached an acceptable equilibrium, which was, however, completely upset starting from 2010 by the emergence of another lagovirus also causing RHD. The genome of the newly emerged virus shows limited differences from that of RHDV, but the phenotypic traits of the two viruses are distinctive in at least three main respects: 1) The antigenic profile of the virus (the “face” of the virus recognised by the antibodies) is largely different from that of RHDV. 2) Newborn rabbits only a couple of weeks old die of RHD when infected with the new virus, while RHDV infections run asymptomatic until 7-8 wk of age. 3) The new virus, which started in Europe, has spread over the years to several continents, affecting wild and/or domestic rabbit populations. During this worldwide distribution, the new virus infected several lagomorph species and was shown to cause RHD in most of them. Considering these marked differences and the fact that the new virus is not a variant of RHDV, we proposed the name RHDV type 2 (RHDV2). All these main distinctive traits that differentiate RHDV from RHDV2 have the following consequences in practice: 1) The antigenic difference between RHDV and RHDV2 (their ‘faces’) is so great that we need “new” specific vaccines to control RHDV2 (i.e. RHDV2 is a new serotype). 2) In the event of an RHDV2 infection in suckling rabbits, the presence of maternal antibodies to RHDV2 in the blood is the only way to prevent RHD. In contrast, newborns are naturally resistant to RHD if infected with RHDV and therefore, in terms of protection, the presence of maternal antibodies is useless. 3) When RHD outbreaks occur in territories where rabbits live in sympatry with populations of other lagomorphs, viral contamination in the environment reaches sufficiently high levels to facilitate the transmission of RHDV2 to other lagomorphs, including those with a lower susceptibility to infection than the rabbit. Taken together, these phenotypic traits characteristic of RHDV2 are the reason for its rapid spread across the territory and the concomitant disappearance of RHDV. Probably the most striking example of the epidemiological consequences related to the peculiar features of RHDV2 is its rapid spread in the USA and Mexico, where it is now practically endemic. There, despite repeated isolated outbreaks of RHD caused by RHDV from 2000 onwards in small rabbit farms, RHDV has never been able to become endemic.
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Magouz, A. F., E. A. Elsayed, and A. Y. Metwally. "Detection and characterisation of rabbit haemorrhagic disease virus strains circulating in Egypt." BULGARIAN JOURNAL OF VETERINARY MEDICINE 22, no. 4 (2019): 409–18. http://dx.doi.org/10.15547/bjvm.2085.

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Rabbit haemorrhagic disease (RHD) is a highly virulent viral disease of Oryctolagus cuniculus which threatens the rabbit population in Egypt and worldwide. The etiological agent is the rabbit haemorrhagic disease virus (RHDV), a member of the family Caliciviridae. The aim of this study was to identify the possible evolutionary changes of the currently circulating RHDV in Egypt. Twenty suspected cases were collected from outbreaks that occurred in non-vaccinated rabbit flocks during 2015 and 2016. Liver homogenate samples were investigated for detection and identification of circulating RHDV using haemagglutination (HA) and reverse transcriptase polymerase chain reaction. Further characterisation of selected five viral strains was performed by nucleotide sequencing of VP60 gene. All twenty tested samples were haemagglutinin positive and VP60 gene was amplified. Based on nucleotide sequence analysis, four isolates were identified as classical RHDV strains, while one isolate was assigned as RHDVa variant strain but with the same HA pattern. The new RHDVb variant was not identified.
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Saidi, Aissa, and Abdelouahed Aboutaib. "Confirmation of the Rabbit Hemorrhagic Disease Virus Type 2 (GI.2) Circulation in North Africa." Acta Veterinaria 72, no. 4 (December 1, 2022): 433–41. http://dx.doi.org/10.2478/acve-2022-0035.

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Abstract Rabbit hemorrhagic disease (RHD) is a highly contagious viral disease that causes fatal acute hepatitis in domestic and wild lagomorphs. It has taken on major economic importance in countries like Morocco. In addition to the classical virus (RHDV), a novel emerged genotype (RHDV2) is circulating, especially in the north shore of the Mediterranean basin since 2010. Many small animal farmers reported clinical cases from several rabbitries in Agadir (Morocco) despite systematic vaccination against the RHDV. The main objective was to characterize the current RHDV strains circulating in the studied area to help to choose an adequate vaccine. For that, we extracted viral RNA from rabbit livers, carried out the PCR analyses, and we sequenced the viral structural capsid protein (VP60) of the RHDV. The phylogenetic analysis results allowed us to state that the novel genotype (RHDV2) is circulating in the studied geographical area, and to characterize the isolated sequences. As a conclusion, we recommend updating RHD epidemiological relating data and reviewing the vaccine protocols by both targeting RHDV (GI.1) and RHDV2 (GI.2) in any future preventive program.
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ABD EL-GHANY, WAFAA A. "A Review on Rabbit Hemorrhagic Disease with a Special Reference to Egyptian Situation." Journal of the Hellenic Veterinary Medical Society 71, no. 3 (October 15, 2020): 2243. http://dx.doi.org/10.12681/jhvms.25065.

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Rabbit hemorrhagic disease (RHD) is considered as one of the most important viral diseases that affects and threatens rabbit’s flocks. This disease has affected rabbits since mid-1980. Two epidemics of RHD had been discovered; the first was in mid-1980 and known as classical RHD virus (RHDV), while the second was in 2011 and described as variant virus (RHDVb/RHDV2). Domestic and wild rabbits are susceptible to RHD. All ages can be affected, but adults are more susceptible to young kitten. RHD is presented in three forms; per-acute, acute and subacute or chronic form. Mortality rate is usually high especially in per-acute and acute stages and it is associated with disseminated intravascular coagulopathy and necrotic hepatitis. The main lesions have been observed in the liver, lungs and spleen. Diagnosis of RHD is based on the clinical picture and detection of RHDV or specific antibodies. The prevention and control strategies depend mainly on using of preventive inactivated vaccine together with adoptionof hygienic measures. However, there is no specific treatment of RHDV infection. So, this review article puts a spot light on RHD regarding the epidemiology, the clinical and laboratory diagnosis as well as the prevention and control strategies with a special reference to Egyptian situation.
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Rosell, Joan M., L. Fernando de la Fuente, Francisco Parra, Kevin P. Dalton, J. Ignacio Badiola Sáiz, Ana Pérez de Rozas, Juan J. Badiola Díez, et al. "Myxomatosis and Rabbit Haemorrhagic Disease: A 30-Year Study of the Occurrence on Commercial Farms in Spain." Animals 9, no. 10 (October 10, 2019): 780. http://dx.doi.org/10.3390/ani9100780.

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In this retrospective study, we describe the relative occurrence of clinical myxomatosis, and rabbit haemorrhagic disease (RHD), on 1714 commercial farms visited in Spain, between 1988 and 2018. We determined the annual prevalence based on 817 visits to 394 farms affected by myxomatosis. Myxomatosis was more prevalent from August to March, being lowest in June (3%) and highest in September (8.9%). With regard to RHD, we assessed 253 visits to 156 affected farms. We analyzed mean annual and monthly incidence. Two important RHD epidemics occurred; the first in 1988–1989 due to RHDV GI.1 (also known as RHDV), and the second from 2011 to 2013 due to RHDV GI.2 (RHDV2 or RHDVb). These epidemics occurred at times when effective vaccination had not been carried out. Relative monthly incidence in 2011–2018 was higher from April to August (p < 0.001). The results we obtained from 1404 necropsies on 102 farms did not clearly relate serosanguinous nasal discharge in rabbits with disease caused by GI.2 infection. We also assessed vaccination schedules used on 200 doe farms visited from the end of 2014 to 2018; 95.5% vaccinated against myxomatosis and 97.5% against RHD. Both diseases remain prevalent; however, effective vaccination has produced a steady decline in myxomatosis and RHDV GI.1 and GI.2 on-farm detection. The maintenance of high hygienic standards will be needed to continue and improve this control. However, further studies are required to investigate the causes of sustained virus presence and vaccine breaks.
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Fitzner, Andrzej. "Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak." Bulletin of the Veterinary Institute in Pulawy 58, no. 2 (June 1, 2014): 177–86. http://dx.doi.org/10.2478/bvip-2014-0027.

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Abstract The field outbreak of RHD that occurred late summer 2012 on a small-scale rabbit-rearing operation in Poland and the usefulness of techniques for RHD virus diagnosis are described. During the epizootic, the overall mortality rate of rabbits older than two months was 77%. Eight liver specimens collected from dead unvaccinated rabbits (aged 3-5 months) underwent virological examinations. RHDV specific antigen was detected in two out of eight liver homogenates by haemagglutination (HA) test and ELISA, one of the two being negative in HA assay. However the presence of genetic material of RHD virus was confirmed by RT-PCR and real-time RT-PCR in all liver samples tested. Based on antigen reactivity in ELISA and sequencing of PCR amplicons of the VP60 gene, the RHDVa subtype strain was identified as the cause of infection. The partial genome sequence of a field isolate (STR 2012), comprising the C-terminus of the polymerase gene and the full capsid protein gene, revealed 91% nucleotide homology to reference FRG89 RHDV isolate and 97% to strain Triptis representing the RHDVa variant. Serological evidence of an RHD outbreak in the STR rabbit-rearing operation was confirmed in a serum sample collected from an unvaccinated surviving rabbit. A cross-reactivity examination of RHDV positive serum revealed a decrease in HI titre against the STR 2012 field antigen, and a decrease in the RHDVa control antigen as compared to classic RHDV.
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Hall, Robyn N., Tegan King, Tiffany W. O’Connor, Andrew J. Read, Sylvia Vrankovic, Melissa Piper, and Tanja Strive. "Passive Immunisation against RHDV2 Induces Protection against Disease but Not Infection." Vaccines 9, no. 10 (October 18, 2021): 1197. http://dx.doi.org/10.3390/vaccines9101197.

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Rabbit haemorrhagic disease virus 2 (RHDV2) is a lagovirus in the family Caliciviridae. The closely related Rabbit haemorrhagic disease virus (RHDV, termed RHDV1 throughout this manuscript for clarity) has been used extensively as a biocontrol agent in Australia since the mid-1990s to manage wild rabbit populations, a major economic and environmental pest species. Releasing RHDV1 into populations with a high proportion of rabbits less than 8–10 weeks of age leads to non-lethal infection in many of these young animals, with subsequent seroconversion and long-term immunity against reinfection. In contrast, RHDV2 causes lethal disease even in young rabbits, potentially offering substantial benefits for rabbit management programs over RHDV1. However, it is not clear how acquired resistance from maternal antibodies may influence immunity after RHDV2 infection. In this study, we assessed serological responses after RHDV2 challenge in young rabbits of three different ages (5-, 7-, or 9-weeks-old) that were passively immunised with either high- (titre of 2560 by RHDV IgG ELISA; 2.41 mg/mL total protein) or low- (titre of 160–640 by RHDV IgG ELISA; 1.41 mg/mL total protein) dose RHDV2 IgG to simulate maternal antibodies. All rabbits treated with a high dose and 75% of those treated with a low dose of RHDV2 IgG survived virus challenge. Surviving animals developed robust lagovirus-specific IgA, IgM, and IgG responses within 10 days post infection. These findings demonstrate that the protection against RHDV2 conferred by passive immunisation is not sterilising. Correspondingly, this suggests that the presence of maternal antibodies in wild rabbit populations may impede the effectiveness of RHDV2 as a biocontrol.
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Dissertations / Theses on the topic "RHDV"

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Marsh, Maija. "The effect of behaviour in disease transmission : Understanding RHDV Dynamics in Austrlian rabbit populations." Thesis, University of York, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520028.

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Fages, Marie-Philippe Bertagnoli Stéphane. "Identification d'un nouveau variant apathogène du virus de la maladie hémorragique virale du lapin (RHDV)." [S.l.] : [s.n.], 2007. http://oatao.univ-toulouse.fr/1755/1/debouch_1755.pdf.

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Joubert, Pascale. "Etude des mécanismes de maturation de la polyprotéine du virus de la maladie hémorragique du lapin (RHDV)." Tours, 2000. http://www.theses.fr/2000TOUR4009.

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Le rabbit haemorrhagic disease virus (RHDV) est responsable d'hépatites fulminantes et peut tuer 90% d'une population de lapins en moins de 48h. Le RHDV est un calicivirus du genre lagovirus. Non enveloppé, il présente un ARN simple brin de polarité positive de 7,5 KB pour génome. Cet ARN génomique possède 2 ORF : l'ORF1 codant pour une polyprotéine de 257 KDA et l'ORF2 codant pour la protéine structurale VP10. Cette polyprotéine présente 6 protéines non structurales dont l'hélicase, la protéase et l'ARN polymérase et 2 protéines structurales, la VPG et la protéine de capside. La protéase, apparentée au groupe des chymotrypsine-like cystéine protéases, semble être la seule protéine virale impliquée dans le processus de maturation. Les études réalisées jusqu'alors ont permis de montrer que le processus de maturation se déroulait en au moins 2 étapes et conduisait à la libération de 8 protéines impliquant 7 sites de clivage protéolytique. Trois sites spécifiquement clivés par la protéase avaient été décrits auparavant par différents auteurs : EG (718-719), EG (1108-1109) et EG (1767-1768) et, aussi, un 4ème site suspecté, le site ET (1251-1252). Le virus RHDV ne se multipliant pas en culture cellulaire, nous avons développé une technique basée sur l'utilisation du gène de la luciférase comme gène rapporteur. Cette technique originale a permis de confirmer les 3 sites EG déjà décrits, d'identifier le quatrième responsable de la maturation primiaire, le site EG (143-144) et 2 sites faiblement clivés EG (339-340) et EG (776-777). Ces 6 sites de clivage s'intègrent parfaitement dans le modèle de maturation proposé par König et al. (1998). Ce travail de thèse permet de comparer pour la première fois l'activité protéolytique de la protéase courte (1109-1251) avec celle du précurseur P72 (protéase-polymérase). La protéase courte est capable d'une activité protéolytique trans et cis au niveau de 4 sites cités précédemment. Cependant, le précurseur P72 présente la meilleure efficacité de clivage et semble responsable de la maturation complète de la polyprotéine du RHDV
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Müller, Claudia [Verfasser], and Gerd [Akademischer Betreuer] Sutter. "A new RHDV-2 vaccine based on recombinant baculovirus : generation and characterization of induced immunity in rabbits / Claudia Müller ; Betreuer: Gerd Sutter." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1158496206/34.

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Guillon, Patrice. "Antigènes tissulaires de groupe sanguin ABH acteurs de la protection innée antivirale : exemples des Calicivirus (NV et RHDV) et du Coronavirus SRAS-CoV." Nantes, 2008. https://archive.bu.univ-nantes.fr/pollux/show/show?id=d7627fae-7b41-4797-ad78-963bffc5f6c7.

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Les antigènes tissulaires de groupe sanguin sont des motifs glycanniques présents sur les cellules épithéliales ou dans les sécrétions et également trouvés sur les érythrocytes de certains primates. Leur synthèse nécessite l’action de glycosyltransférases codées par les gènes Fut1, Fut2, Sec1 ou Abo. Ils servent de ligands à diverses souches de Calicivirus du genre norovirus responsables de gastro-entérites chez l’homme, le polymorphisme aux loci FUT2 et ABO contrôlant la sensibilité à ces virus. Dans ce travail nous montrons que le lait maternel contient des molécules de type mucine qui inhibent la fixation de la souche NV. L’inhibition est dépendante de la présence d’un allèle FUT2 permettant la synthèse de glycannes α1,2fucosylés. Un autre Calicivirus, le RHDV, responsable de la maladie hémorragique du lapin (RHD), se fixe sur un glycanne α1,2fucosylé. Nous avons observé qu’il existe des lapins sauvages présentant un déficit d’expression de ce ligand dont la fréquence dans les populations est augmentée à la suite d’épidémies de RHD. Un allèle du gène Sec1 a pu être associé à la survie des animaux, suggérant une sélection par le virus. La protéine d’enveloppe du Coronavirus du SRAS lui permet de se fixer sur son récepteur cellulaire et peut porter des antigènes ABH. Des anticorps anti-A du plasma de sujets O inhibent la fixation de cette protéine sur son récepteur lorsqu’elle est synthétisée dans des cellules A, expliquant la plus grande sensibilité des individus A (ou B) au SRAS. Ainsi les antigènes de groupes sanguins tissulaires pourraient contribuer à la protection innée antivirale par des mécanismes complémentaires, expliquant leur maintien au cours de l’évolution
Histo-blood group antigens are glycan motifs present on mammalian epithelial surfaces and in secretion. They are also found on erythrocytes from apes. Their synthesis requires glycosyltransferases encoded by the Futi, Fut2, Seel and Abo genes. They are ligands for various Calicivirus strains of the norovirus genus which cause gastroenteritis in humans and polymorphisms at the FUT2 and ABO loci control sensitivity to these viruses. In this work, we show that maternal milk contains mucin-type molecules that inhibit NV strain binding to its α1,2fucosylated ligand. The inhibition depends upon a FUT2 allele that allows α1,2fucosylation. Another Calicivirus, RHDV, responsible for the rabbit hemorrhagic disease, binds to an α1,2fucosylated ligand. We observed that there exist wild rabbits presenting a deficit of expression of the ligand. Their frequency is increased following RHD outbreaks. Moreover, a Seel allele has been associated with the survival of animals, suggesting a selection by the virus. The enveloppe protein of the SARS Coronavirus allows binding to its cellular receptor and may carry ABH antigens. We show that natural antibodies from the plasma of 0 individuals inhibit attachment of this protein to its receptor when it is synthesized in A cells. This may explain the higher sensitivity of A (or B) individuals to SARS. Overall, the results are discussed to suggest that histo-blood group antigens could contribute to innate antivirus protection by various complementary mechanisms, which could explain why they have been maintained throughout mammalian evolution
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Müller, Alexandra. "Virus-host adatation and co-evolution of myxoma virus (MV) and rabbit haemorrhagic disease virus (RHDV) in their natural host, the wild rabbit (oryctolagus cuniculus)." Doctoral thesis, Instituto de Ciências Biomédicas Abel Salazar, 2009. http://hdl.handle.net/10216/45396.

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Müller, Alexandra. "Virus-host adatation and co-evolution of myxoma virus (MV) and rabbit haemorrhagic disease virus (RHDV) in their natural host, the wild rabbit (oryctolagus cuniculus)." Tese, Instituto de Ciências Biomédicas Abel Salazar, 2009. http://hdl.handle.net/10216/45396.

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Le, Gall Ghislaine. "Calicivirus des lagomorphes : détermination de la séquence nucléotidique de l'EBHSV (european brown hare syndrome virus) : épidémiologie moléculaire des virus EBHSV et RHDV(rabbit haemorrhagic disease virus)." Brest, 1997. http://www.theses.fr/1997BRES3103.

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Laurent, Sylvie. "Étude de la protéine de capside des calicivirus des lagomorphes RHDV (Rabbit Haemorrhagic Disease Virus) et EBHSV (European Brown Hare Syndrome Virus) : antigénicité, vaccination et assemblage." Compiègne, 1997. http://www.theses.fr/1997COMP1029.

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Les virus RHDV (Rabbit Haemorrhagic Disease Virus) et EBHSV (European Brown Hare Syndrome Virus) ont été décrits pour la première fois sur le continent européen au début des années 1980. Ces deux virus, responsables d'hépatites nécrosantes, sont capables de tuer 90% d'une population de lapins ou de lièvres en moins 48h. Ils ont été affiliés récemment à la famille des Caliciviridae. Les calicivirus possèdent un génome à ARN simple brin de polarité positive et sont composés d'une simple capside constituée d'une unique protéine structurale de 60KDa. Les protéines de capside de RHDV et EBHSV ont été exprimées dans le système baculovirus/cellules d'insecte. Les protéines de capside recombinantes produites en quantité massive ont été retrouvées dans le surnageant de culture sous la forme de pseudo-particules, présentant les mêmes caractéristiques morphologiques et antigéniques que les virions infectieux. Les particules recombinantes de RHDV utilisées dans des tests de vaccination ont conféré une protection équivalente à celle démontrée par les vaccins actuellement commercialisés. L'étude de la séroconversion des lapins vaccinés a mis en évidence le rôle clef de la réponse humorale dans la protection contre la maladie. Ces résultats ont conduit à l'élaboration d'un vaccin recombinant actuellement en cours de développement industriel. L'utilisation des particules recombinantes de RHDV et de EBHSV lors d'études comparatives, réalisées à l'aide de plusieurs anticorps monoclonaux anti-RHDV et anti-EBHSV, ont permis de caractériser les réactions antigéniques croisées entre les deux virus. Ces résultats couplés à ceux de tests de protection croisée ont permis de classer ces deux virus dans deux sérotypes du même sérogroupe au sein de la famille des Caliciviridae. Plusieurs données concernant l'assemblage des calicivirus, obtenues par l'analyse des particules recombinantes en conditions non dénaturantes, ainsi que par l'analyse des séquences peptidiques, sont discutées.
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Rodrigues, Artemis Socorro do Nascimento. "Caracterização molecular dos antigenos RhD, (RhD fraco e RhD parcial) e sua aplicação na pratica transfusional." [s.n.], 2005. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310418.

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Orientador: Lilian Maria de Castilho
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-04T11:27:19Z (GMT). No. of bitstreams: 1 Rodrigues_ArtemisSocorrodoNascimento_D.pdf: 9543028 bytes, checksum: 5774a3716484ea2212070f20c266a89f (MD5) Previous issue date: 2005
Resumo: Considerando a imunogenicidade e importância clínica do antígeno RhD bem como o grande número de variantes RhD identificadas, estudos que possam esclarecer sua expressão e mecanismos moleculares envolvidos são importantes para a padronização de técnicas moleculares e sorológicas em diferentes populações. Assim foram nossos objetivos: padronizar técnicas moleculares para realização da genotipagem RHD fraco e determinar sua ocorrência na população brasileira; associar os tipos de RhD fracos encontrados com os haplótipos Rh presentes; e avaliar a aplicação da determinação do antígeno RhD na prática transfusional. Estudamos 503 amostras de DNA de doadores voluntários de sangue fenotipados como RhD ftaco. Destas amostras de DNA estudadas, 415 (82,5%) foram caracterizadas como RhD ftaco, 65 (12,9%) como RhD parcial, 15 (3%) apresentaram associações de RhD parcial e RhD ftaco e 8 (1,6%) foram RhD normal. I Os antígenos RhD fraco tipos 1, 3 e 4 foram os mais fteqüentes em nossa população. Como estes três tipos de RhD fraco não apresentam risco de aloimunização anti-D, pacientes assim classificadospodem ser transfundidos com sangue RhD-positivo. Nossos resultados demonstraram que 12,~A>das amostras fenotipadas como RhD fraco eram na verdade RhD parcial. Os antígenos RhD parciais encontrados em nosso estudo foram D~ DHMi e DVI. Quarenta (7,9%) amostras de DNA foram caracterizadas como D~ 16 (3,2%) como DHMi e 9 (1,8%) como DVI. A caracterização dos antígenos RhD parciais que reagem sorologicamente como RhD ftaco, tais como D DHMi e RhD categoria VI pode ser de grande auxilio na prevenção da aloimunização anti-D em pacientes politransfundidos e gestantes. A freqüência dos antígenos RhD parciais D~ DHMi e DVI encontrada em nossas amostras sugere um elevado risco de aloimunização ao antígeno RhD em pacientes fenotipados como RhD ftaco. - Das 503 amostras estudadas, 15 apresentaram mutações responsáveis pela expressão do antígeno RhD fraco e ao mesmo tempo mutações características de antígenos RhD parciais, ou seja, estas amostras possuíam os antígenos RhD fraco e RhD parcial associados. Estudamos quatro amostras de DNA de pacientes fenotipados como RhD :fraco que apresentavam anti-D. Nosso estudo demonstrou que a aloimunização anti-D nestes pacientes estava relacionada à presença de um antígeno RhD parcial e não a um antígeno RhD :fraco como diagnosticado sorologicamente. Duas amostras foram classificadascomo RhD parcial DAR, 1 como RhD parcial DHMi e 1 como DVI. Os resuhados demonstraram que os tipos de RhD fraco 1, 2, 3 e 4 que foram detectados à TA ou à 3'te e apresentaram grau de aglutinação superior a 1+ na AGH podem ser considerados como RhD positivo, pois não foram associados ao antígeno RhD parcial. Apesar deste trabalho ter sido o único que relacionou os tipos de RhD ftaco com o grau de aglutinação, a literatura revela que ainda não foi demonstrada aloimunização anti-D em pacientes portadores dos antígenos RhD fraco tipos 1,2 e 3. De acordo com os nossos resultados pode-se concluir que: 1. A transfusão com sangue RhD-positivo pode ser recomendada para todos os pacientes que apresentam os tipos do antígeno RhD :ftaco 1, 3 e 4 identificados por técnicas moleculares e para aqueles que apresentarem grau de aglutinação superior a 1+ na fenotipagem RhD. 2. A utilização de métodos de fenotipagem mais sensíveis em combinação com reagentes anti-D de alta afinidade é recomendada na detecção de antígenos RhD ftaco com baixa densidade antigênica em doadores de sangue; 3. Há necessidade da utilização de dois anti-soros monoc1onais (IgM e IgG) na determinação do antígeno RhD :ftacoem pacientes; 4. As genotipagens RHD, RHD ftaco e RHD parcial devem ser rea1i73dasquando os resuhados sorológicos não forem claros ou quando o paciente for politransfundido. 5. A biologia molecular associada à hemaglutinação pode aumentar consideravelmente a segurança transfusional pela mellior caracterização dos antígenos RhD em nossa população
Abstract: The purpose of this study was to characterize by molecular studies theRhD antigens (weak D and partial D) in Brazilian blood donors. DNA samples ftom 503 blood donors phenotyped as weak D were tested by two different sequence-specific primers (pCR-SSP) assays to determine the presence or absence of RHD gene (PCR-SSP intron 4 and exon 10) and to detect the common weak D types. Ofthe 503 weak D samples studied, 415 (82,5%) were identified as weak D, 65 (12,9%) as partial D, 15 (3%) showed association ofweak D and partial D and 8 (1,6%) were normal D. Weak D types 1, 3 and 4 contributed more than 85% of alI molecular weak D types. For these 3 types, D-positive transfusion can be considered safe because no immunization events have been documented yet. These findings show for the first time the frequency of weak D types in Brazilians. Molecular analysis showed that 12,9% of the weak D phenotype samples studied carried a partia! D alIele. The partial Ds found in our study were DAR, DVI and DHMi. Forty (7,9%) DNA samples were characterized as DAR, 16 (3,8%) as DHMi and 9 (1,8%) as DVI. The characterization of the partia! D antigens DAR, DHMi and DVI may avoid alIoimmunization in patients phenotyped as weak D. Fiffeteen patients showed mutations to weak D and partia! D showing that these samples had the weak D and partia! D antigens associated. We also studied 4 DNA samples of patients phenotyped as weak D who had developed anti-D. Our study showed that anti-D alIoimmunization in these patients was associated with the presence of partia! D antigens. Two samples were classified as partia!, D DAR, 1 as DHMi and 1 was DVI.AlI the weak D types identified in our study were associated with the intensity of agglutination obtained at room temperature (RT), 3'fC and AGH. The sensitivity of detecting weak D depends on the anti-D reagent and on the exact conditions of the methods. Our results showed that the weak D types 1, 2, 3 and 4 were frequently detected at RT and 3'fC and therefore could be considered as D-positive for transfusion. According to our results we could recommend the use ofmonoclonal anti-DIgM with high avidity to detect weak D antigen with low antigen density in blood donors and two monoclonals, one IgM and one IgG in combination with AGT to detect the weak D antigen in patients
Doutorado
Ciencias Basicas
Doutor em Clínica Médica
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Books on the topic "RHDV"

1

Matheson, Kimberly. Functional characterization of the RHD promoter. Ottawa: National Library of Canada, 2002.

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García Martínez, Constantino Antonio, Abraham Otero Quintana, Xosé A. Vila, María José Lado Touriño, Leandro Rodríguez-Liñares, Jesús María Rodríguez Presedo, and Arturo José Méndez Penín. Heart Rate Variability Analysis with the R package RHRV. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65355-6.

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PHELPS. STUDYING DIVERSE LIVES RHD V3#4. Lawrence Erlbaum, 2007.

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Constantino Antonio Antonio García García Martínez, Abraham Otero Quintana, Xosé A. Vila, María José Lado Touriño, Leandro Rodríguez-Liñares, Jesús María Rodríguez Presedo, and Arturo José Méndez Penín. Heart Rate Variability Analysis with the R package RHRV. Springer, 2017.

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Heloisa Nascimento Beserra, Ana. NOÇÕES BÁSICAS DE ALOIMUNIZAÇÃO RhD Na gestação. EDITORA CRV, 2015. http://dx.doi.org/10.24824/978854440633.5.

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Roy, Kevin M. Second Chances As Transformative Stories Rhd V3 2&3. Taylor & Francis Group, 2015.

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Roy, Kevin M. Second Chances As Transformative Stories Rhd V3 2&3. Taylor & Francis Group, 2015.

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Roy, Kevin M. Second Chances As Transformative Stories Rhd V3 2&3. Taylor & Francis Group, 2015.

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Roy, Kevin M. Second Chances As Transformative Stories Rhd V3 2&3. Taylor & Francis Group, 2015.

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Antonucci, Toni C. Immigration Adaptation and Well Being Across Rhd V2#4. Taylor & Francis Group, 2016.

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Book chapters on the topic "RHDV"

1

Lavazza, Antonio, and Lorenzo Capucci. "How Many Caliciviruses are there in Rabbits? A Review on RHDV and Correlated Viruses." In Lagomorph Biology, 263–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-72446-9_18.

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Poisson, Jessica. "RhD Compatibility." In Transfusion Management of the Obstetrical Patient, 103–6. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77140-3_12.

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Kato, Shoji, and Jun Fukue. "Astrophysical RHD Flows." In Astronomy and Astrophysics Library, 445–76. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-4174-2_22.

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Clausen, Frederik Banch, Klaus Rieneck, Grethe Risum Krog, Birgitte Suhr Bundgaard, and Morten Hanefeld Dziegiel. "Noninvasive Antenatal Screening for Fetal RHD in RhD Negative Women to Guide Targeted Anti-D Prophylaxis." In Prenatal Diagnosis, 347–59. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8889-1_23.

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García Martínez, Constantino Antonio, Abraham Otero Quintana, Xosé A. Vila, María José Lado Touriño, Leandro Rodríguez-Liñares, Jesús María Rodríguez Presedo, and Arturo José Méndez Penín. "Introduction to Heart Rate Variability." In Heart Rate Variability Analysis with the R package RHRV, 1–14. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65355-6_1.

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García Martínez, Constantino Antonio, Abraham Otero Quintana, Xosé A. Vila, María José Lado Touriño, Leandro Rodríguez-Liñares, Jesús María Rodríguez Presedo, and Arturo José Méndez Penín. "Loading, Plotting, and Filtering RR Intervals." In Heart Rate Variability Analysis with the R package RHRV, 15–28. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65355-6_2.

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García Martínez, Constantino Antonio, Abraham Otero Quintana, Xosé A. Vila, María José Lado Touriño, Leandro Rodríguez-Liñares, Jesús María Rodríguez Presedo, and Arturo José Méndez Penín. "Time-Domain Analysis." In Heart Rate Variability Analysis with the R package RHRV, 29–36. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65355-6_3.

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García Martínez, Constantino Antonio, Abraham Otero Quintana, Xosé A. Vila, María José Lado Touriño, Leandro Rodríguez-Liñares, Jesús María Rodríguez Presedo, and Arturo José Méndez Penín. "Frequency Domain Analysis." In Heart Rate Variability Analysis with the R package RHRV, 37–68. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65355-6_4.

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García Martínez, Constantino Antonio, Abraham Otero Quintana, Xosé A. Vila, María José Lado Touriño, Leandro Rodríguez-Liñares, Jesús María Rodríguez Presedo, and Arturo José Méndez Penín. "Nonlinear and Fractal Analysis." In Heart Rate Variability Analysis with the R package RHRV, 69–116. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65355-6_5.

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García Martínez, Constantino Antonio, Abraham Otero Quintana, Xosé A. Vila, María José Lado Touriño, Leandro Rodríguez-Liñares, Jesús María Rodríguez Presedo, and Arturo José Méndez Penín. "Comparing HRV Variability Across Different Segments of a Recording." In Heart Rate Variability Analysis with the R package RHRV, 117–32. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65355-6_6.

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Conference papers on the topic "RHDV"

1

Guo, Zhen, Yuan Wang, Qian Yu, Jie Xiao, Kaiyu Liu, Ying Wang, Auguste Commeyras, and Yi Li. "Notice of Retraction: Construction of Recombinant Rabbit Hemorrhagic Disease Virus (RHDV) Vaccine Using Myxoma Virus (MV) as a Vector." In 2011 5th International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2011. http://dx.doi.org/10.1109/icbbe.2011.5781650.

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Clark, R. P., and C. P. Brown. "Selection of Descent and Ascent Method for the WHOI RHOV." In SNAME Maritime Convention. SNAME, 2008. http://dx.doi.org/10.5957/smc-2008-014.

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A deep submergence vehicle operated by the Woods Hole Oceanographic Institution (WHOI), Alvin has made more than 4,200 deep-ocean dives since 1964. Lockheed Martin Corp. was contracted in 2007 by WHOI with funding provided by the National Science Foundation to design a Replacement Human Occupied Vehicle (RHOV) which would take advantage of recent technological advances to provide expanded depth capability. This paper discusses the criteria, evaluation, and selection of the method of descent and ascent, a high-level naval architecture trade which drives the general arrangement of the entire vehicle. Constrained by vehicle performance requirements, exploration of the system design parameters through dynamic simulation and CFD modeling allows for design optimization. Considering the transient features of ascent and descent such as dynamic ballast pumping and variation in fluid and vehicle density driven by hydrostatic pressure, the preferred method of vertical travel for the RHOV is a level vehicle at zero angle of pitch with velocity orthogonal to the free surface.
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Manjula, M., M. Sundareswari, D. S. Jayalakshmi, and E. Viswanathan. "Theoretical investigation on improving the ductility of Rh3V by ternary addition." In NANOFORUM 2014. AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4918026.

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Soranna, Francesco, Yi-Chih Chow, Oguz Uzol, and Joseph Katz. "Flow Structure and Turbulence in the Tip Region of a Turbomachine Rotor Blade." In ASME Turbo Expo 2007: Power for Land, Sea, and Air. ASMEDC, 2007. http://dx.doi.org/10.1115/gt2007-27590.

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The flow structure and turbulence in the tip region of a rotor blade operating downstream of a row of Inlet Guide Vanes (IGVs) are investigated experimentally in a refractive index matched facility that provides unobstructed view of the entire flow field. Stereo-PIV measurements are performed in closely spaced radial planes near the blade tip in a region extending from (slightly upstream of) the blade trailing edge to about 40% of the chord downstream of it. The data enable calculations of all the components of the phase-averaged velocity and vorticity vectors, as well as the strain rate, Reynolds stress, and turbulent diffusion tensors. Each rotor blade is confined between two tip-leakage vortices, a right hand vortex (RHV), generated by the subject blade and propagating along its right hand side, and a left hand vortex (LHV), generated by the previous blade in the same row and propagating along the left hand side of the subject blade. In addition, a trailing edge vortex (TEV) lays underneath the LHV and is subject to intense shearing/deformation by the LHV. RHV-induced radial gradients of radial phase-averaged velocity cause negative turbulence production, P, along the RHV-axis, and formation of a region of low P in the gap between the RHV and the blade suction surface. Trends of turbulent kinetic energy k and P within the RHV do not agree due to the effects of advection by the phase-averaged flow. To the left of the blade, shearing of the TEV by the LHV enhances turbulence production in the region between the two vortices and the rotor wake. Trends of turbulent kinetic energy and its production rate are in good agreement and peaks of k and P occur at the same location. As the TEV migrates away from the LHV, shearing effects become weaker and the dominant contributors to production are terms containing vortex-induced radial gradients of axial and radial velocities. Turbulent diffusion is a minor contributor to the evolution of turbulent kinetic energy in the tip region. It is also shown that the tip-leakage flow/vortex deteriorates the rotor blade performance, causing a ∼66% increase in shaft power input (per unit mass flow-rate) in the tip region in comparison with midspan.
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Shahzad, Mian M., Ligegowda S. Mangala, Jeong W. Lee, Koji Matsuo, Maya P. Nair, Hee D. Han, Edna M. Mora, et al. "Abstract 5517: Targeting anticancer therapeutics: A role for reconstituted high density lipoprotein (rHDL)." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5517.

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Yang, Jing, Taariq Salie, Carlos R. Ramírez Medina, Simon Frain, Nophar Geifman, Anthony Whetton, Mark Engel, and Bernard Keavney. "47 Data independent acquisition mass spectrometry in severe rheumatic heart disease (rhd) identifies a proteomic signature showing ongoing inflammation and effectively classifying rhd cases." In British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.47.

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Yang, Jing, Taariq Salie, Carlos R. Ramírez Medina, Simon Frain, Nophar Geifman, Anthony Whetton, Mark Engel, and Bernard Keavney. "47 Data independent acquisition mass spectrometry in severe rheumatic heart disease (rhd) identifies a proteomic signature showing ongoing inflammation and effectively classifying rhd cases." In British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.47.

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YANG, Zexiao, Yadong LIU, Zhengqun MENG, Bo WANG, Xueping YAO, Yin WANG, Yi GENG, and Yan LI. "Preliminary Study on The SYBR Green I RT- qPCR for Rabbit Hemorrhagic Disease Virus 2 (RHDV2) Detection." In International Conference on Biological Engineering and Pharmacy 2016 (BEP 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/bep-16.2017.9.

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Rikken, Maarten, Daan Tjepkema, Rupert Gibson, and David Gration. "Refurbishment of orthotropic steel decks with steel plates." In IABSE Congress, Ghent 2021: Structural Engineering for Future Societal Needs. Zurich, Switzerland: International Association for Bridge and Structural Engineering (IABSE), 2021. http://dx.doi.org/10.2749/ghent.2021.1496.

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<p>A common problem in steel bridges is fatigue of orthotropic decks due to heavy traffic demands. Whilst replacing the asphalt with a high strength concrete overlay can solve this problem, it imposes significant additional self-weight. This additional self-weight often requires strengthening of the superstructure which in turn can result in long execution times with associated hindrance and costs. As no existing method addressed these issues Arup engineers developed an innovative solution for Rijkswaterstaat (RWS), the Dutch Highways Authority. The new solution consists of bolting steel plates to the orthotropic steel deck, stiffening it for fatigue. Arup and RHDHV work in a joint venture, the Managing Contractor, on the renovation of steel bridges for and with RWS.</p>
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Rikken, Maarten, Daan Tjepkema, Rupert Gibson, and David Gration. "Refurbishment of orthotropic steel decks with steel plates." In IABSE Congress, Ghent 2021: Structural Engineering for Future Societal Needs. Zurich, Switzerland: International Association for Bridge and Structural Engineering (IABSE), 2021. http://dx.doi.org/10.2749/ghent.2021.1496.

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<p>A common problem in steel bridges is fatigue of orthotropic decks due to heavy traffic demands. Whilst replacing the asphalt with a high strength concrete overlay can solve this problem, it imposes significant additional self-weight. This additional self-weight often requires strengthening of the superstructure which in turn can result in long execution times with associated hindrance and costs. As no existing method addressed these issues Arup engineers developed an innovative solution for Rijkswaterstaat (RWS), the Dutch Highways Authority. The new solution consists of bolting steel plates to the orthotropic steel deck, stiffening it for fatigue. Arup and RHDHV work in a joint venture, the Managing Contractor, on the renovation of steel bridges for and with RWS.</p>
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Reports on the topic "RHDV"

1

Anninos, P. Kull ALE: I. Unstructured Mesh Advection, Interface Capturing, and Multiphase 2T RHD with Material Interfaces. Office of Scientific and Technical Information (OSTI), February 2002. http://dx.doi.org/10.2172/15006516.

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