Several models combined with ultrasound techniques to predict breast muscle weight in broilers.

The weight of breast muscle (WBM) is a highly monitored indicator in broiler breeding that can be obtained after slaughtering. Currently, due to the lack of accurate in vivo phenotypes for both genomic and phenotypic selection, genetic gains in WBM fall short of initial expectations. In this study, 1,006 market-age (42 d) broilers from 3 generations over 2 yr were randomly selected, and the breast width (BW), fossil bone length (FBL), breast muscle thickness (BMT), and live weight (LW) were measured exactly in vivo. Eight models, including multiple linear regression (MLR), ridge regression (RR), least absolute shrinkage and selection operator (LASSO), and elastic net (EN), were fitted to explore the best regression relationships between breast muscle weight and these indicators. Support vector machine (SVM) methods with both linear kernels and radial kernels were used to fit the models, while 2 decision tree-based machine learning algorithms, random forest (RF), and extreme gradient boosting (XGBoost), were used to establish the prediction model. The predictive effects of different combinations of independent variables were compared, leading to the conclusion that the EN model achieves the best predictive power when all 4 live features are used as inputs and is slightly better than the other models (R2 = 0.7696). This method could be applied in practical production and breeding work, leading to substantial cost savings and enhancements in the breeding process.

Dominant changes in the breast muscle lipid profiles of broiler chickens with wooden breast syndrome revealed by lipidomics analyses.

BACKGROUND: Chicken is the most consumed meat worldwide and the industry has been facing challenging myopathies. Wooden breast (WB), which is often accompanied by white striping (WS), is a serious myopathy adversely affecting meat quality of breast muscles. The underlying lipid metabolic mechanism of WB affected broilers is not fully understood. RESULTS: A total of 150 chickens of a white-feathered, fast-growing pure line were raised and used for the selection of WB, WB + WS and control chickens. The lipids of the breast muscle, liver, and serum from different chickens were extracted and measured using ultra performance liquid chromatography (UPLC) plus Q-Exactive Orbitrap tandem mass spectrometry. In the breast, 560 lipid molecules were identified. Compared to controls, 225/225 of 560 lipid molecules (40.2%) were identified with differential abundance (DA), including 92/100 significantly increased neutral lipids and 107/98 decreased phospholipids in the WB/WB + WS groups, respectively. The content of monounsaturated fatty acids (MUFA) was significantly higher, and the polyunsaturated fatty acids (PUFA) and saturated fatty acids (SFA) were significantly lower in the affected breasts. In the liver, 434 lipid molecules were identified, and 39/61 DA lipid molecules (6.7%/14.1%) were detected in the WB and WB + WS groups, respectively. In the serum, a total of 529 lipid molecules were identified and 4/44 DA lipid molecules (0.8%/8.3%) were detected in WB and WB + WS group, respectively. Compared to controls, the content of MUFAs in the serum and breast of the WB + WS group were both significantly increased, and the content of SFAs in two tissues were both significantly decreased. Only five lipid molecules were consistently increased in both liver and serum in WB + WS group. CONCLUSIONS: We have found for the first time that the dominant lipid profile alterations occurred in the affected breast muscle. The relative abundance of 40.2% of lipid molecules were changed and is characteristic of increased neutral lipids and decreased phospholipids in the affected breasts. Minor changes of lipid profiles in the liver and serum of the affected groups were founded. Comprehensive analysis of body lipid metabolism indicated that the abnormal lipid profile of WB breast may be independent of the liver metabolism.

Identification of Candidate Genes for Meat Color of Chicken by Combing Selection Signature Analyses and Differentially Expressed Genes.

Meat color, an important index of chicken quality, is highly related to heme pigment, glycolysis, and intramuscular fat metabolisms. The objective of this study is to obtain candidate genes associated with meat color in chickens based on the comparison of fast-growing, white-feathered chickens (Line B) and slow-growing, yellow-feathered chickens (Jingxing Yellow), which have significant differences in meat color. The differentially expressed genes (DEGs) between Line B and Jingxing Yellow were identified in beast muscle. The fixation index (FST) method was used to detect signatures of positive selection between the two breeds. Screening of 1109 genes by the FST and 1317 candidate DEGs identified by RNA-seq. After gene ontology analysis along with the Kyoto Encyclopedia of Genes and Genomes, 16 genes associated with glycolysis, fatty acid metabolism, protein metabolism, and heme content were identified as candidate genes that regulate the color of chicken breast meat, especially TBXAS1 (redness), GDPD5 (yellowness), SLC2A6 (lightness), and MMP27 (lightness). These findings should be helpful for further elucidating the molecular mechanisms and developing molecular markers to facilitate the selection of chicken meat color.

Integrated metabolomics and lipidomics evaluate the alterations of flavor precursors in chicken breast muscle with white striping symptom.

White striping (WS) is the most common myopathy in the broiler chicken industry. To reveal flavor changes of WS meat objectively, flavor precursors of WS breast muscle were evaluated systematically with integrated metabolomics and lipidomics. The results showed that WS could be distinguished from normal controls by E-nose, and four volatile compounds (o-xylene, benzene, 1,3-dimethyl, 2-heptanone and 6-methyl and Acetic acid and ethyl ester) were detected as decreased compounds by gas chromatography-mass spectrometry. Lipidomic analysis showed that WS breast fillets featured increased neutral lipid (83.8%) and decreased phospholipid molecules (33.2%). Targeted metabolomic analysis indicated that 16 hydrophilic metabolites were altered. Thereinto, some water-soluble flavor precursors, such as adenosine monophosphate, GDP-fucose and L-arginine increased significantly, but fructose 1,6-bisphosphate and L-histidine significantly decreased in the WS group. These results provided a systematic evaluation of the flavor precursors profile in the WS meat of broiler chickens.

Serum Creatine Kinase as a Biomarker to Predict Wooden Breast in vivo for Chicken Breeding.

The present study aimed to find a blood marker for the prediction of wooden breast (WB) in live broiler to assist the genetic selection of fast-growing chickens. The experiments were carried out with two chicken flocks: 250 male broilers in flock 1 and 100 male and female broilers in flock 2. Both flocks were slaughtered and measured. The breast filets were assessed by combining subjective scoring and compression force at 28 (flock 1 only) and 42 days of age. The enzyme activity in serum and breast tissue (flock 1 only) of normal and affected groups was tested. The results showed that the compression force was significantly different between the normal and affected groups at 28 and 42 days of age (P < 0.001), and it increased significantly with rising WB and WS scores. The serum creatine kinase (CK) value increased significantly with rising compression force at 42 days of age (P < 0.001). The serum CK positively correlated with compression force (r = 0.608; P < 0.001) and the linear regression equation (serum CK = 0.9960∗compression force + 1.884) was established for the line studied. The association between serum CK and compression force is consistent between flocks 1 and 2. In conclusion, our study confirmed that compression force could be the quantitative indicator to differentiate breast filets and found that serum CK could be a candidate biomarker to predict WB in live broilers and assist genetic selection in broiler breeding.

Phylogenetic and molecular characterization of H9N2 influenza isolates from chickens in Northern China from 2007-2009.

The repeated transmission to pigs and humans, and the long-term endemicity in terrestrial poultry of H9N2 viruses in China lend urgency to the study of their ecology and pathogenicity. In the present paper, we reported an H9N2 virus sublineage isolated from chickens in northern China from 2007 to 2009 has high lethality for mice. Phylogenetic analysis of the full genome indicated that six representative H9N2 isolates shared high homology to each other, and they clustered in the same sublineage with other H9N2 viruses isolated recently in northern China. The isolates were double-reassortant viruses containing M genes similar to A/Quail/Hong Kong/G1/97 (H9N2) and the other seven gene segments from A/Chicken/Shanghai/F/98 (H9N2). These six isolates were capable of replicating in the lungs of infected chickens without producing observable clinical signs of disease or death. However, they were highly lethal to mice with mortality rates as high as 100% (14/14) without prior adaptation. The affected mice exhibited severe respiratory syndromes and diffuse lung injury. The H9N2 viruses could be detected in multiple organs of the infected mice, including hearts, livers, spleens, lungs and kidneys. Our findings demonstrated that H9N2 viruses isolated from the chickens in northern China have established a stable sublineage with enhanced pathogenicity to mice, suggesting that urgent attention will need to be paid to the transmission of H9N2 viruses from chickens to mammals.

Acute respiratory distress syndrome induced by H9N2 virus in mice.

H9N2 avian influenza viruses have repeatedly caused infections in swine and humans in some countries. The purpose of the present study was to evaluate the pulmonary pathology caused by H9N2 viral infection in mice. Six- to eight-week-old BALB/c mice were infected intranasally with 1 x 10(4) MID(50) of A/Chicken/Hebei/4/2008(H9N2) virus. Clinical signs, pathological changes and viral replication in lungs, arterial blood gas, and cytokines in bronchoalveolar lavage fluid (BALF) were observed at different time points after infection. A control group was infected intranasally with noninfectious allantoic fluid. H9N2-infected mice exhibited severe respiratory syndrome, with a mortality rate of 60%. Gross observations showed that infected lungs were highly edematous. Major histopathological changes in infected lungs included diffuse pneumonia and alveolar damage, with neutrophil-dominant inflammatory cellular infiltration, interstitial and alveolar edema, hemorrhage, and severe bronchiolitis/peribronchiolitis. In addition, H9N2 viral infection resulted in severe progressive hypoxemia, lymphopenia, and a significant increase in neutrophils, tumor necrosis factor-alpha and interleukin-6 in BALF. The features described above satisfy the criteria for acute respiratory distress syndrome (ARDS). Our data show that H9N2 viral infection resulted in ARDS in mice, and this may facilitate studies of the pathogenesis of future potential H9N2 disease in humans.