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Abstract: Asthma is children''s foremost chronic disease. If the medicinal progress is unambiguous, therapeutic education as well as rehabilitation efforts are integral parts of asthmatic children''s global care. Initiated and proposed by the Association asthme et allergies, a protocol that defines place, dates, purposes and means, received the agreement of the French ministry for Youth and Sports. Thirteen children (eight boys, five girls, with an average age of eleven) who suffer from persistent asthma, from moderate to severe and/or exercise-induced asthma, were selected by two Parisian hospitals. The children spent fourteen days on vacation in Ardèche (altitude, 1400m) during the month of July and were supervised by a medical and an animation team. Motivating children to engage in sports activities and strengthening therapeutic education trained in asthma''s schools (écoles de l’asthme) were the dual purpose of the stay. An educational diagnosis and an evaluation of the knowledge of each child were realized at the beginning and at the end of the stay. A flexible program was set up and combined outdoor games, role-playing, educational workshops on breathing, techniques of inhalation and measurement of breath… associated with tests and coupled with physical or sportive activities practiced individually or collectively. Climatic conditions did not provoke any asthma attack or intercurrent affection. The questionnaire dispensed at the end of the stay reveals the children''s global satisfaction. In terms of health, preliminary results are promising, particularly regarding their aerobic capacity and physical performances. A medium-term evaluation is in progress, but consequences of this experience – shared by children coming from different social milieus and in a less polluted environment – seem to confirm the interest for promoting educational and sportive stays supervised by health professionals specialized in therapeutic education and spent in specific places which correspond to the standards of allergens’ eviction. [Copyright &y& Elsevier]

The ChickRH6 radiation hybrid panel has been used to construct consensus chromosome radiation hybrid (RH) maps of the chicken genome. Markers genotyped were either from throughout the genome or targeted to specific chromosomes and a large proportion (one third) of data was the result of collaborative efforts. Altogether, 2,531 markers were genotyped, allowing the construction of RH reference maps for 20 chromosomes and linkage groups for four other chromosomes. Amongst the markers, 581 belong to the framework maps, while 1,721 are on the comprehensive maps. Around 800 markers still have to be assigned to linkage groups. Our attempt to assign the supercontigs from the chrun (virtual chromosome containing all the genome sequence that could not be attributed to a chromosome) as well as EST (Expressed Sequence Tag) contigs that do not have a BLAST hit in the genome assembly led to the construction of new maps for microchromosomes either absent or for which very little data is present in the genome assembly. RH data is presented through our ChickRH webserver (http://chickrh.toulouse.inra.fr/), which is a mapping tool as well as the official repository RH database for genotypes. It also displays the RH reference maps and comparison charts with the sequence thus highlighting the possible discrepancies. Future improvements of the RH maps include complete coverage of the sequence assigned to chromosomes, further mapping of the chrun and mapping of EST contigs absent from the assembly. This will help finish the mapping of the smallest gene-rich microchromosomes. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Characterizes the localization microsatellite loci in chickens using reference maps. Denaturation of amplified fragments using acrylamide gel; Segregation of chicken reference backrosses.

Examines the integration of chicken cytogenetic and genetic maps. Isolation of polymorphic markers from bacterial artificial chromosome and P1-derived artificial chromosome clones; Occurrence of potentially polymorphic (CA)n repeats; Development of a single strand conformational polymorphism.

Thermochemolysis of seven nucleobases—adenine, thymine, uracil, cytosine, guanine, xanthine, and hypoxanthine—in tetramethylammonium hydroxide (TMAH) was studied individually by pyrolysis gas chromatography mass spectrometry in the frame of the Mars surface exploration. The analyses were performed under conditions relevant to the Sample Analysis at Mars (SAM) instrument of the Mars Curiosity Rover and the Mars Organic Molecule Analyzer (MOMA) instrument of the ExoMars Rover. The thermochemolysis products of each nucleobase were identified and the reaction mechanisms studied. The thermochemolysis temperature was optimized and the limit of detection and quantification of each nucleobase were also investigated. Results indicate that 600°C is the optimal thermochemolysis temperature for all seven nucleobases. The methylated products trimethyl-adenine, 1, 3-dimethyl-thymine, 1, 3-dimethyl-uracil, trimethyl-cytosine, 1, 3, 7-trimethyl-xanthine (caffeine), and dimethyl-hypoxanthine, respectively, are the most stable forms of adenine, thymine, uracil, cytosine, guanine, and xanthine, and hypoxanthine in TMAH solutions. The limits of detection for adenine, thymine, and uracil were 0.075 nmol; the limits of detection for guanine, cytosine, and hypoxanthine were higher, at 0.40, 0.55, and 0.75 nmol, respectively. These experiments allowed to well constrain the analytical capabilities of the thermochemolysis experiments that will be performed on Mars to detect nucleobases. Image 1 • Seven nucleobases were detected by GC-MS under conditions relevant to in situ operating instruments on Mars: SAM and MOMA. • The TMAH thermochemolysis products coming from seven nucleobases were determined. • The LOD and LOQ values of seven nucleobases in TMAH were determined after GC-MS analysis. • Results of the nucleobases thermochemolysis will help to identify those compounds on Mars with SAM and MOMA. [ABSTRACT FROM AUTHOR]

Presents the use of radiation hybrid panel in developing a gene map of the chicken. Radiation hybrid clones; Principle of mapping markers on a chromosome with a radiation hybrid panel.

Molecular markers such as microsatellites, provide genetic signposts for navigating genomes. In general, genetic markers that are monomorphic or non-informative in mapping populations typically remain unmapped and as such are less likely to be included in future studies. The use of hybrid cell panels and in silico mapping via whole genome sequences allow for positional mapping of non-segregating markers. This study utilizes the INRA ChickRH6 whole-genome radiation hybrid panel and chicken whole-genome shotgun sequence to map microsatellite markers from the turkey (Meleagris gallopavo). Thirty-three of the 41 markers typed on the RH panel had significant linkage to at least one other marker and 83 of 100 sequences returned significant BLAST similarities. Positioning of these markers provides additional sequence tagged sites in the turkey genome and increases the potential use of these markers for future genetic studies. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

We have constructed a radiation hybrid (RH) map of chicken chromosome (GGA) 15. This map can be used as a resource to efficiently map genes to this chromosome. The map has been developed using a 6000 rad chicken–hamster whole-genome radiation hybrid panel (ChickRH6). In total, six microsatellite loci, 18 sequence tagged sites (STSs) from BAC end sequences and 11 genes were typed on the panel. The initial framework map comprised eight markers, and an additional 23 markers were then added to generate the final map. The total map length was 334 centiRay6000 (cR6000). The estimated retention frequency for the data set was 18%. Using an estimated physical length of 21 Mb, the ratio between cR6000 and physical distance over GGA15 was estimated to be 0.063 Mb/cR6000. The present map increases the marker density and the marker resolution on GGA15 and enables fast mapping of new chicken genes homologous to genes from human chromosomes 12 and 22. [ABSTRACT FROM AUTHOR]

The effects of maternal nutrition on offspring phenotypes have been mainly documented over the past years in mammals, and are now studied in poultry as well. In the present study, we investigated the effects of a reduced level of dietary Methionine (Met) on laying performances of common laying ducks and their impacts on the phenotype of their mule ducklings. A total of 60 female laying ducks were divided into 2 dietary treatments at 10 wk of age. The restricted group received Met-restricted diets (R group) containing 0.25% of Met whereas the control group received control diets (C group) containing 0.40% of Met that meets Met requirements. The restriction was applied during the growing and laying periods, from 10 to 51 wk of age and a particular focus was put on female breeder traits that might be affected by the Met restriction. Plasma parameters of hepatic and lipid metabolisms were recorded in ducklings. Total weight (P  < 0.001), albumen weight (P  < 0.001) and albumen percentage of dry matter (P  < 0.01) were decreased for eggs laid by female breeders from the R group. Both male and female ducklings from the R group of female breeders showed a reduced BW at hatching (P  < 0.001) and a tendency to an increased proportional liver weight (P  = 0.07). Finally, the maternal low dietary Met level modified plasma parameters in newborn ducklings regardless of sex: alkaline phosphatase (ALP) and alanine transaminase (ALT) activities were reduced (P  = 0.07 and P  = 0.002, respectively), levels of glucose (P  = 0.03) and triglycerides (P  = 0.01) were higher whereas level of free fatty acids decreased (P  = 0.01). It was concluded that feeding female laying ducks with a restricted dietary Met content during the growing and laying periods has a negative effect on egg weight and composition. The ducklings that were restricted in nutrients during their early development, have a reduced BW, and altered lipid and hepatic metabolisms. [ABSTRACT FROM AUTHOR]

Radiation hybrid mapping has emerged in the end of the 1990s as a successful and complementary approach to map genomes, essentially because of its ability to bridge the gaps between genetic and clone-based physical maps, but also using comparative mapping approaches, between ‘gene-rich’ and ‘gene-poor’ maps. Since its early development in human, radiation hybrid mapping played a pivotal role in the process of mapping animal genomes, especially mammalian ones. We review here all the different steps involved in radiation hybrid mapping from the constitution of panels to the construction of maps. A description of its contribution to whole genome maps with a special emphasis on domestic animals will also be presented. Finally, current applications of radiation hybrid mapping in the context of whole genome assemblies will be described. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Focuses on the cloning of cDNA encoding the nuclear form of chicken sterol response element binding protein-2, chromosomal localization and tissue expression of chicken SREBP-1 and -2 genes. Chicken whole genome radiation hybrid panel; DNA polymorphism and chromosomal localization od SREBP genes.

Studies the molecular genetic linkage map of the chicken genome. Assignment of linkage groups to identified microchromosome pairs with bacterial artificial chromosome clones; Correlations between macrochromosomes in chicken, turkey, quail and duck.

The satiety hormone leptin has a key role in the control of energy homeostasis in mammals. Leptin is produced almost exclusively by the adipose tissue and signals the amount of fat stores primarily to the hypothalamus, but also to peripheral tissues. Recently, we identified the long sought leptin (SEROUSSI et al., 2016), in the "dark side of the chicken genome", meaning extremely GC-rich regions that have been difficult to sequence and assemble. Expression profiling of the avian leptins showed a different pattern compared to mammals, surprisingly with no expression in the adipose tissue. Nevertheless, we found that leptin and leptin receptor (LEPR) genes are expressed in tissues that are implicated in the response to leptin signalling in mammals, and their expression pointed to an autocrine/paracrine instead of endocrine mode of action. Therefore, the role of avian leptins may be relevant to the control of reproduction, stress response and metabolism, but in a different way than in mammals, as it is not the signal of the adipose tissue. Following the success of the identification of chicken leptin and realizing its presence in RNA-seq data rather than genomic assemblies, we asked if other missing genes in chicken could be identified using the RNA-seq approach. Extensive RNA-seq analysis of visceral fat, hypothalamus and pituitary, followed by transcript assembly and bioinformatic analysis led to the identification of 191 novel genes in chickens (BORNELOV et al., 2017), all with very high GC content (~70%). These included the tumour necrosis factor (TNF, also known as TNF-alpha) and nephrin (NPHS1), which were long sought after in the chicken genome. Interestingly, 25 of our novel genes were mapped to the chicken genome in the most recent genome assembly Galgal5. This mapping showed that about 70% of the genes were mapped to chicken microchromosomes, which are known to be GC-rich. The same proportion of genes were mapped in gene blocks demonstrating that the indication that missing genes arranged in gene clusters in other vertebrates cannot be taken as an indication for their evolutionary loss. Altogether, these findings suggest that other missing genes in chickens may be positioned in GC-rich gene clusters in the chicken genome. Among our novel chicken genes, we found five genes belonging to the leptin synteny group in vertebrates: RBM28, SND1, LRRC4, and FLNC. We used this identification to map the chicken leptin gene and its syntenic genes to chicken chromosome 1p (SEROUSSI et al., 2017), thus providing the final proof for the correct identification of the chicken leptin gene. [ABSTRACT FROM AUTHOR]