Molecular detection of Torque teno virus in different breeds of swine

<p>Abstract</p> <p>Background</p> <p>Torque teno virus (TTV), of the <it>Anelloviridae </it>family, <it>Iotatorquevirus </it>genus, is a non-enveloped, single-stranded, and negative sense DNA (ssDNA) virus infecting human and many domestic animals including swines. Very little information is known about the investigations of TTV prevalence in different swine breeds so far.</p> <p>Methods</p> <p>In this study, 208 serum samples collected from seven swine breeds (<it>Rongchang pig</it>, <it>Chenghua pig</it>, <it>Zibet pig</it>, <it>Wild boar</it>, <it>Duroc</it>, <it>Landrace</it>, <it>Large Yorkshire</it>) from two independent farms were detected to determine the prevalence of two swine TTV genogroups, TTV1 and TTV 2, by nested polymerase chain reaction methods, and to analyse prevalence difference among these breeds.</p> <p>Results</p> <p>The results showed that the prevalence of TTV in the seven breeds was 92%-100%. No significant difference (p > 0.05) in TTV infection was observed between different breeds. Interestingly, significantly higher prevalence for TTV1 in <it>Rongchang </it>boars (90%) and for TTV2 in <it>Rongchang </it>sows (95%) were detected, while co-infection rate (43.8%) was lower than other breeds. Sequence analysis showed that the homology of TTV1 and TTV2 were over 90.9% and 86.4% in these breeds, respectively.</p> <p>Conclusions</p> <p>The results indicated that TTV was widely distributed in the seven swine breeds. The prevalence of both TTV genogroups associated with swine breeds and genders. This study also respented the first description of swine TTV prevalence in different swine breeds. It was vitally necessary to further study swine TTV pathogenicity.</p

Effect of annealing in O2 or N2 on the aging of Fe0.5Mn1.84Ni0.66O4 NTC-ceramics

Fe0.5Mn1.84Ni0.66O4 NTC ceramic thermistors were annealed in nitrogen or oxygen atmosphere at 600 °C. The change of the electrical properties of the thermistors with time was reduced sharply by annealing in N2, whereas it was enhanced upon annealing in O2. N2-annealed samples exhibited a less degree of redistribution of cations in the lattice as compared with O2-annealed samples. The aging of the electrical properties is believed to result from the cation redistribution which in turn is favoured by the presence of cation vacancies. And the improved aging behaviour of the N2-annealed thermistor is explained by the reduction of the concentration of the cation vacancy upon annealing under lower oxygen partial pressure and the suppression of cation redistribution

hCLP46 Increases Smad3 Protein Stability Via Inhibiting its Ubiquitin-Proteasomal Degradation

hCLP46 (human CAP10-like protein 46 kDa) was initially isolated and identified from human acute myeloid leukemia transformed from myelodysplastic syndrome (MDS-AML) CD34+ cells (Teng et al., 2006) and we demonstrated previously that hCLP46 is abnormally expressed in many hematopoietic malignancies (Wang et al., 2010). Studies fromits Drosophila homolog, Rumi, suggested that Notch is a potential target of hCLP46 (Acar et al., 2008). We also found that overexpression of hCLP46 enhances Notch activation and regulates cell proliferation in a cell type-dependent manner (Ma et al., 2011; Chu et al., 2013). However, hCLP46−/− embryos show more severe phenotypes compared to those displayed by other global regulators of canonical Notch signaling, suggesting that hCLP46 is likely to have additional important targets during mammalian development (Fernandez- Valdivia et al., 2011). Based on the crosstalk between Notch and the transforming growth factor-β (TGF-β) signaling, we proposed that hCLP46 might be involved in TGF-β signal regulation, but the detail mechanism remains unclear

Advance in mechanism of plant leaf colour mutation

As a common mutation trait in plants, leaf colour mutation is related to the degree of chlorophyll and anthocyanin changes and the destruction of chloroplast structure. This study summarizes the latest research progress in leaf colour mutation mechanism, including the metabolic basis of plant leaf colour mutation, leaf colour mutation caused by gene mutation in the chlorophyll metabolism pathway, leaf colour mutation caused by blocked chloroplast development, leaf colour mutation controlled by key transcription factors and non-coding RNAs, leaf colour mutation caused by environmental factors, and leaf colour mutation due to the involvement of the mevalonate pathway. These results will lay a theoretical foundation for leaf colour development, leaf colour improvement, and molecular breeding for leaf colour among tree species