The reaction of ground-state cyano radicals, CN(X(2)Σ(+)), with the simplest polyene, 1,3-butadiene (C4H6(X(1)Ag)), is investigated to explore probable routes and feasibility to form pyridine at ultralow temperatures. The isomerization and dissociation channels for each of the seven initial collision complexes are characterized by utilizing the unrestricted B3LYP/cc-pVTZ and the CCSD(T)/cc-pVTZ calculations. With facilitation of RRKM rate constants, through ab initio paths composed of 7 collision complexes, 331 intermediates, 62 hydrogen atom, 71 hydrogen molecule, and 3 hydrogen cyanide dissociated products, the most probable paths at collision energies up to 10 kcal/mol, and thus the reaction mechanism, are determined. Subsequently, the corresponding rate equations are solved that the concentration evolutions of collision complexes, intermediates, and products versus time are obtained. As a result, the final products and yields are determined. The low-energy routes for the formation of most thermodynamically stable product, pyridine, are identified. This study, however, predicts that seven collision complexes would produce predominately 1-cyano-1,3-butadiene, CH2CHCHCHCN (p2) plus atomic hydrogen via the collision complex c1(CH2CHCHCH2CN) and intermediate i2(CH2CHCH2CHCN), with a very minor amount of pyridine. Our scheme also effectively excludes the presence of 2-cyano-1,3-butadiene, which has energy near-degenerate to 1-cyano-1,3-butadiene, as supported by experimental findings.

Avian leukosis is an immunosuppressive neoplastic disease caused by avian leukosis viruses (ALV), which causes tremendous economic losses in the worldwide poultry industry. The susceptibility or resistance of chicken cells to subgroup A ALV and subgroup B, D, and E ALV are determined by the receptor genes tumor virus locus A (tva) and tumor virus locus B (tvb), respectively. Four genetic resistant loci (tva(r1), tva(r2), tva(r3), and tva(r4)) in tva receptor gene and a genetic resistant locus tvb(r) in the tvb receptor gene have been identified in inbred lines of White Leghorn. To evaluate the genetic resistance to subgroup A, B, D, and E ALV, genetic variations within resistant loci in tva and tvb genes were screened in Chinese local chicken breeds and commercial broiler lines. Here, the heterozygote tva(s1/r1) and the resistant genotype tva(r2/r2), tva(r3/r3), and tva(r4/r4) were detected in Chinese chickens by direct sequencing. The heterozygote tva(s1/r1) was detected in Huiyang Bearded chicken (HYBC), Rizhaoma chicken, and commercial broiler line 13 to 15 (CB13 to CB15), with the frequencies at 0.08, 0.18, 0.17, 0.25, and 0.15, respectively. The resistant genotype tva(r2/r2) was detected in Jiningbairi chicken (JNBRC), HYBC, and CB15, with the frequencies at 0.03, 0.08, and 0.06, respectively, whereas tva(r3/r3) and tva(r4/r4) were detected in 19 and 17 of the 25 Chinese chickens tested, with the average frequencies at 0.13 and 0.20, respectively. Furthermore, the resistant genotype tvb(r/r) was detected in JNBRC, CB07, CB12, CB14, and CB15 by pyrosequencing assay, with the frequencies at 0.03, 0.03, 0.11, 0.09, and 0.15, respectively. These results demonstrated that the potential for genetic improvement of resistance to subgroup A, B, D, and E ALV were great both in Chinese local chickens and commercial broilers. This study provides valuable insight into the selective breeding for chickens genetically resistant to ALV.