A new stripe rust resistance gene transferred from Thinopyrum intermedium to hexaploid wheat (Triticum aestivum)

Wheat stripe rust (Puccinia striiforis f. sp. tritici) races CYR31 and CYR32, prevalent in China, are virulent to many wheat stripe rust resistance genes (Yr genes). To expand the availability of effective resistance to CYR31 and CYR32, stripe rust resistance was transferred from intermediate wheatgrass (Thinopyrum intermedium) to common wheat (Triticum aestivum). The susceptible wheat cultivar CM107 was crossed with amphiploid TAI7047, derived from the wide cross Taiyuan768/Thinopyrum intermedium//76(64). Two wheat lines originating from the cross, YU24 and YU25, were resistant to CYR31 and CYR32. Pedigree analysis showed that the resistance to stripe rust in YU24 and YU25 originated from intermediate wheatgrass. Genetic analyses indicated that the resistance to stripe rust is controlled by a single dominant gene. Allelic tests determined that the resistance gene(s) in YU24 and YU25 are identical. The new gene has temporarily been designated as YrYU25. SSR and RAPD analyses showed that YrYU25 was introduced by cryptic translocation into common wheat.Les races CYR31 et CYR32 de la rouille jaune du blé (Puccinia striiforis f. sp. tritici), très répandues en Chine, sont virulentes pour plusieurs gènes de résistance à cette maladie (gènes Yr). Afin d'accroître la disponibilité d'une résistance efficace aux races CYR31 et CYR32, la résistance à la rouille jaune du blé a été transférée de l'agropyre intermédiaire (Thinopyrum intermedium) au blé tendre (Triticum aestivum). CM107, un cultivar de blé sensible, a été croisé avec l'amphiploïde AI7047 dérivé du croisement éloigné Taiyuan768/Thinopyrum intermedium//76(64). Deux lignées de blé provenant de ce croisement, soit YU24 et YU25, étaient résistantes aux races CYR31 et CYR32. Une analyse généalogique a démontré que la résistance à la rouille jaune du blé chez les lignées YU24 et YU25 provenait de l'agropyre intermédiaire. Des analyses génétiques ont indiqué que cette résistance était contrôlée par un seul gène dominant. Des tests d'allélisme ont révélé que le(s) gène(s) de résistance dans les lignées YU24 et YU25 étaient identiques. Le nouveau gène a temporairement été nommé YrYU25. Des analyses SSR et RAPD ont démontré que le gène YrYU25 avait été introduit dans le blé tendre par translocation cryptique

Anatomical Asymmetry in Goiter: A Demonstration by Three-dimensional Power Doppler Ultrasound

The aim of the present study was to examine the anatomical differences in volumetric and intraparenchymal vascular parameters between the two thyroid lobes of patients with goiter, using three-dimensional power Doppler ultrasound. A total of 89 outpatients with goiter, including 55 with autoimmune thyroid disease (ATD) and 34 with simple goiter (SG), were evaluated by three-dimensional power Doppler ultrasound. Volumetric and intraparenchymal vascular indices including vascularization index, flow index and vascular flow index of each lobe were measured using the Virtual Organ Computer-Aided Analysis system. In all patients with goiter, the volume and vascular indices (vascularization index, flow index and vascular flow index) of the right thyroid lobe were significantly greater than those of the left lobe (p < 0.05). Differences in vascular indices were present in SG but not in ATD. ATD was associated with a larger thyroid volume and higher vascular indices compared with those of SG (p < 0.001), but there were no significant differences in volumetry and vascular indices between euthyroid ATD and SG. In conclusion, the right thyroid lobe was found to be significantly larger and more vascular than the left lobe in subjects with goiter, as measured by three-dimensional power Doppler ultrasound. In addition, ATD was associated with a higher thyroid volume and vascular indices compared with those of SG

Physics perspectives of heavy-ion collisions at very high energy

Heavy-ion collisions at very high colliding energies are expected to produce a quark-gluon plasma (QGP) at the highest temperature obtainable in a laboratory setting. Experimental studies of these reactions can provide an unprecedented range of information on properties of the QGP at high temperatures. We report theoretical investigations of the physics perspectives of heavy-ion collisions at a future high-energy collider. These include initial parton production, collective expansion of the dense medium, jet quenching, heavy-quark transport, dissociation and regeneration of quarkonia, photon and dilepton production. We illustrate the potential of future experimental studies of the initial particle production and formation of QGP at the highest temperature to provide constraints on properties of strongly interaction matter.Comment: 35 pages in Latex, 29 figure

Silibinin Inhibits ICAM-1 Expression via Regulation of N-Linked and O-Linked Glycosylation in ARPE-19 Cells

To evaluate the effects of silibinin on intercellular adhesion molecule-1 (ICAM-1) expression, we used ARPE-19 cells as a model in which tumor necrosis factor (TNF-) and interferon (IFN-) enhanced ICAM-1 expression. This upregulation was inhibited by silibinin. In an adherence assay using ARPE-19 and THP-1 cells, silibinin inhibited the cell adhesion function of ICAM-1. The inhibitory effects of silibinin on ICAM-1 expression were mediated via the blockage of nuclear translocation of p65 proteins in TNF-and phosphorylation of STAT1 in IFN--stimulated cells. In addition, silibinin altered the degree of N-linked glycosylation posttranslationally in ARPE-19 cells by significantly enhancing MGAT3 gene expression. Silibinin can increase the O-GlcNAc levels of glycoproteins in ARPE-19 cells. In a reporter gene assay, PUGNAc, which can also increase O-GlcNAc levels, inhibited NF-B reporter activity in TNF--induced ARPE-19 cells and this process was augmented by silibinin treatment. Overexpression of OGT gene was associated with reduced TNF--induced ICAM-1 levels, which is consistent with that induced by silibinin treatment. Taken together, silibinin inhibits ICAM-1 expression and its function through altered O-linked glycosylation in NF-B and STAT1 signaling pathways and decreases the N-linked glycosylation of ICAM-1 transmembrane protein in proinflammatory cytokinestimulated ARPE-19 cells

Protection of chicken against very virulent IBDV provided by in ovo priming with DNA vaccine and boosting with killed vaccine and the adjuvant effects of plasmid-encoded chicken interleukin-2 and interferon-γ

The aim of this study was to examine the efficacy of in ovo prime-boost vaccination against infectious bursal disease virus (IBDV) using a DNA vaccine to prime in ovo followed by a killed-vaccine boost post hatching. In addition, the adjuvant effects of plasmid-encoded chicken interleukin-2 and chicken interferon-γ were tested in conjunction with the vaccine. A plasmid DNA vaccine (pcDNA-VP243) encoding the VP2, VP4, and VP3 proteins of the very virulent IBDV (vvIBDV) SH/92 strain was injected into the amniotic sac alone or in combination with a plasmid encoding chicken IL-2 (ChIL-2) or chicken IFN-γ (ChIFN-γ) at embryonation day 18, followed by an intramuscular injection of a commercial killed IBD vaccine at 1 week of age. The chickens were orally challenged with the vvIBDV SH/92 strain at 3 weeks of age and observed for 10 days. In ovo DNA immunization followed by a killed-vaccine boost provided significantly better immunity than the other options. No mortality was observed in this group after a challenge with the vvIBDV. The prime-boost strategy was moderately effective against bursal damage, which was measured by the bursa weight/body weight ratio, the presence of IBDV RNA, and the bursal lesion score. In ovo DNA vaccination with no boost did not provide sufficient immunity, and the addition of ChIL-2 or ChIFN-γ did not enhance protective immunity. In the ConA-induced lymphocyte proliferation assay of peripheral blood lymphocyte collected 10 days post-challenge, there was greater proliferation responses in the DNA vaccine plus boost and DNA vaccine with ChIL-2 plus boost groups compared to the other groups. These findings suggest that priming with DNA vaccine and boosting with killed vaccine is an effective strategy for protecting chickens against vvIBDV