The inhibition of motor contagion induced by action observation.

In sports, success and failure are believed to be contagious. Yet it is unclear what might cause contagion. This study investigated whether motor contagion is associated with the active observation of the kinematic actions of others. In Experiment 1, six skilled hammer throwers threw a hammer after watching a video of a model throwing toward the left, center, or right. The video included two types of action kinematics which resulted in throw directions that were either easy or difficult to predict based on the model's kinematics. In Experiment 2, the athletes threw hammers after watching the same stimuli as Experiment 1, but while engaging in one of two types of focus (self-focus or non-self-focus) to determine whether motor contagion could be diminished. Results demonstrated that the direction of each participant's throw was more influenced by the videos that contained easy action kinematics, supporting a critical role for the meaningfulness of the link between an action and its outcome in producing motor contagion. Motion analysis revealed that motor contagion was not likely to be a result of the observer imitating the model's action kinematics. The contagion observed in Experiment 1 disappeared when participants engaged in self-focus. These results suggest that motor contagion is influenced by the predictability of an action outcome when observing an action, and that motor contagion can be inhibited through self-focus when observing

Example of time course of EMG signals in vastus lateralis muscle of front leg.

<p>Monophasic and biphasic EMG activation of vastus lateralis muscle of front leg of one participant in response to unchanged and decreased velocity conditions, respectively. Target start time was 0 s.</p

Outline of elapsed time from moment that target started to move until impact in response to unchanged and decreased velocity.

<p>Data are shown as means and SD. Target start (■), Onset of EMG activation (●), time to peak EMG amplitude in response to unchanged condition and monophasic EMG pattern in decreased velocity condition (▲), time to peak EMG amplitude of first (△) and second (□) peaks in response to biphasic EMG pattern in decreased velocity condition, impact time (×).</p

Relationship between ATE and probability.

<p>Relationship between absolute temporal error (ATE) in response to decreased velocity condition and probability that biphasic EMG pattern will appear in response to this condition.</p

Schematic diagram of relationships between absolute temporal error (ATE) and electromyographic (EMG) characteristics.

<p>Relationships: +, positive, <i>p</i> < 0.05; ++, positive, <i>p</i> < 0.01; --, negative, <i>p</i> < 0.01; -, negative, <i>p</i> < 0.05.</p

Inter-subject correlations (r) between parameters (n = 11).

<p>ATE, absolute temporal error; U, unchanged condition; DV, decreased velocity; Latency, latency time from onset of EMG activation to time to peak; Max, Peak EMG amplitude; Onset, onset of EMG activation from target start; Prob, probability that biphasic EMG will appear in response to decreased velocity; TP, time to peak from target start.</p><p>*<i>p</i> < 0.05</p><p>^†<i>p</i> < 0.01.</p><p>Inter-subject correlations (r) between parameters (n = 11).</p

Synthesis of a Vpr-Binding Derivative for Use as a Novel HIV-1 Inhibitor

<div><p>The emergence of multidrug-resistant viruses compromises the efficacy of anti-human immunodeficiency virus type 1 (HIV-1) therapy and limits treatment options. Therefore, new targets that can be used to develop novel antiviral agents need to be identified. We previously identified a potential parent compound, hematoxylin, which suppresses the nuclear import of HIV-1 via the Vpr-importin α interaction and inhibits HIV-1 replication in a Vpr-dependent manner by blocking nuclear import of the pre-integration complex. However, it was unstable. Here, we synthesized a stable derivative of hematoxylin that bound specifically and stably to Vpr and inhibited HIV-1 replication in macrophages. Furthermore, like hematoxylin, the derivative inhibited nuclear import of Vpr in an <i>in vitro</i> nuclear import assay, but had no effect on Vpr-induced G2/M phase cell cycle arrest or caspase activity. Interestingly, this derivative bound strongly to amino acid residues 54–74 within the C-terminal α-helical domain (αH3) of Vpr. These residues are highly conserved among different HIV strains, indicating that this region is a potential target for drug-resistant HIV-1 infection. Thus, we succeeded in developing a stable hematoxylin derivative that bound directly to Vpr, suggesting that specific inhibitors of the interaction between cells and viral accessory proteins may provide a new strategy for the treatment of HIV-1 infection.</p></div

Analysis of the conserved regions within Vpr using the Wu-Kabat method.

<p>In total, 2,004 Vpr sequences were obtained from the HIV sequence database and used to calculate the Wu-Kabat index for each amino acid residue (a). The four Vpr regions were α Helix 1 domain (αH1, residues 17 to 33), α Helix 2 domain (αH2, residues 38 to 50), α Helix 3 domain (αH3, residues 54 to 74), and the non-Helix region (residues 1 to 16, residues 34 to 37, residues 51 to 53, and residues 75 to 96). These four regions plus the whole Vpr region (residues 1 to 96) were used to estimate the average Wu-Kabat index value (b).</p

Purification of recombinant Vpr protein and binding analysis by SPR.

<p>(a) SDS-PAGE analysis of purified recombinant proteins. COS-7 cells were transfected with mammalian pCAGGS vectors encoding FLAG-mRFP (mRFP) or FLAG-mRFP-Vpr (mRFP-Vpr) and then purified on ANTI-FLAG M2 agarose beads. Proteins were separated on reducing 15% SDS-PAGE and stained with Coomassie brilliant blue. (b) SPR to determine the binding of the derivative to Vpr. The derivative was coupled to PGS and incubated with mRFP or mRFP-Vpr. DMSO was used as a negative control.</p