TWO AND THREE-DIMENSIONAL ASSESSMENTS OF LOWER-LIMB KINEMATICS IN UNDERWATER FLY KICK

The purpose of this study was to compare sagittal plane lower limb kinematics of underwater fly kick measured using two and three-dimensional methods. Eight male participants (average FINA points score 801±138) completed underwater fly kick trials, recorded using a six camera Qualisys underwater system. Each trial was analysed using both two and three-dimensional methods. Lower-limb angles were significantly underestimated using two-dimensional methods, particularly at the hip where flexion and range of motion reduced by 13.73 degrees and 15.91 degrees respectively. The ankle and hip produce a large amount motion in the transverse and frontal planes. The results of two-dimensional analyses of underwater fly kick should be interpreted with caution due reductions in measured angles, and exclusion of out-of-plane kinematic information

Analysis of the white--light flickering of the Intermediate Polar V709 Cas with wavelets and Hurst analysis

We characterize the flickering observed in the optical lightcurve of the Intermediate Polar system V709 Cas by determining its position in the alpha-Sigma as in the Fritz and Bruch (1998) classification scheme. Sigma represents the strength of flickering at a given timescale, while alpha describes the energy distribution of the flickering at different time scales. Here alpha is independently obtained with both the wavelets and the Hurst R/S analysis. The flickering shows self-similarity in the time scale ranging from tens of minutes down to 10 seconds with stochastic persistent memory in time. alpha and Sigma appear anticorrelated. In the alpha-Sigma diagram V709 Cas falls in the region of magnetic systems. Since V709 Cas shows the spin period of the magnetic WD only in the X-ray but not in the optical, we conclude that this method can be used to characterize CV subtypes especially when their classification is uncertain.Comment: 6 figure

Primary T-cells from human CD4/CCR5-transgenic rats support all early steps of HIV-1 replication including integration, but display impaired viral gene expression

<p>Abstract</p> <p>Background</p> <p><it>In vivo </it>studies on HIV-1 pathogenesis and testing of antiviral strategies have been hampered by the lack of an immunocompetent small animal model that is highly susceptible to HIV-1 infection. Since native rodents are non-permissive, we developed transgenic rats that selectively express the HIV-1 receptor complex, hCD4 and hCCR5, on relevant target cells. These animals display a transient low-level plasma viremia after HIV-1_YU-2infection, demonstrating HIV-1 susceptibility <it>in vivo</it>. However, unlike macrophages, primary CD4 T-cells from double-transgenic animals fail to support viral spread <it>ex vivo</it>. To identify quantitative limitations or absolute blocks in this rodent species, we quantitatively assessed the efficiency of key steps in the early phase of the viral replication cycle in a side-by-side comparison in infected cell lines and primary T-cells from hCD4/hCCR5-transgenic rats and human donors.</p> <p>Results</p> <p>Levels of virus entry, HIV-1 cDNA synthesis, nuclear import, and integration into the host genome were shown to be remarkably similar in cell lines and, where technically accessible, in primary T-cells from both species. In contrast, a profound impairment at the level of early HIV gene expression was disclosed at the single-cell level in primary rat T-cells and most other rat-derived cells. Macrophages were a notable exception, possibly reflecting the unique transcriptional milieu in this evolutionarily conserved target cell of all lentiviruses. Importantly, transient trans-complementation by <it>ex vivo </it>nucleofection with the Tat-interacting protein Cyclin T1 of human origin markedly elevated HIV gene expression in primary rat T-cells.</p> <p>Conclusion</p> <p>This is the first study that has quantitatively determined the efficiency of consecutive steps in the HIV-1 replication cycle in infected primary HIV target cells from a candidate transgenic small animal and compared it to human cells. Unlike cells derived from mice or rabbits, rat cells complete all of the early steps in the HIV-1 replication cycle, including provirus integration <it>in vivo</it>, with high efficiency. A deficiency in gene expression was disclosed at the single cell level and could be counteracted by the human pTEFb transcription complex factor Cyclin T1. Collectively, these results provide the basis for the advancement of this transgenic rat model through strategies aimed at boosting HIV-1 gene expression in primary rat CD4 T-cells, including human Cyclin T1 transgenesis.</p

Human cyclin T1 expression ameliorates a T-cell-specific transcriptional limitation for HIV in transgenic rats, but is not sufficient for a spreading infection of prototypic R5 HIV-1 strains ex vivo

<p>Abstract</p> <p>Background</p> <p>Cells derived from native rodents have limits at distinct steps of HIV replication. Rat primary CD4 T-cells, but not macrophages, display a profound transcriptional deficit that is ameliorated by transient trans-complementation with the human Tat-interacting protein Cyclin T1 (hCycT1).</p> <p>Results</p> <p>Here, we generated transgenic rats that selectively express hCycT1 in CD4 T-cells and macrophages. hCycT1 expression in rat T-cells boosted early HIV gene expression to levels approaching those in infected primary human T-cells. hCycT1 expression was necessary, but not sufficient, to enhance HIV transcription in T-cells from individual transgenic animals, indicating that endogenous cellular factors are critical co-regulators of HIV gene expression in rats. T-cells from hCD4/hCCR5/hCycT1-transgenic rats did not support productive infection of prototypic wild-type R5 HIV-1 strains <it>ex vivo</it>, suggesting one or more significant limitation in the late phase of the replication cycle in this primary rodent cell type. Remarkably, we identify a replication-competent HIV-1 GFP reporter strain (R7/3 YU-2 Env) that displays characteristics of a spreading, primarily cell-to-cell-mediated infection in primary T-cells from hCD4/hCCR5-transgenic rats. Moreover, the replication of this recombinant HIV-1 strain was significantly enhanced by hCycT1 transgenesis. The viral determinants of this so far unique replicative ability are currently unknown.</p> <p>Conclusion</p> <p>Thus, hCycT1 expression is beneficial to <it>de novo </it>HIV infection in a transgenic rat model, but additional genetic manipulations of the host or virus are required to achieve full permissivity.</p