Relationship between autistic traits and letter-recognition under attention to face-likeness: study using a henohenomoheji-type compound stimulus.

This study aimed to clarify the relationship between autistic traits and letter information processing, specifically, the components of faces when attention is paid to face-like information. We created a new "henohenomoheji-type compound stimulus," in which letters are placed in positions in such a way as to resemble a face. In Experiment 1, we examined the relationship between autistic traits and the participants' performance in a letter-recognition task in which a henohenomoheji-type compound stimulus was used. The results showed a significant moderate negative correlation between Autism-Spectrum Quotient-Japanese Version (AQ-J) scores and letter-recognition sensitivity when the compound stimuli were arranged like a face. The letter-detection task was employed in Experiment 2 to examine how autistic traits affect tasks' performance with a lower cognitive load than in Experiment 1. We found no correlation between AQ-J scores and letter-detection sensitivity with or without face-like features. These results suggest that paying attention to faces reduces the participants' performance in letter recognition, which represents a higher cognitive load in individuals with higher autistic traits. A major implication of this study is that the henohenomoheji-type compound stimuli can be applied to several cognitive tasks, such as cognitive processing in individuals with autistic traits.

First observation of ultrafast intramolecular proton transfer rate between electronic ground states in solution.

Despite the importance of ultrafast (time scale exceeding 10(-11) s) intramolecular proton transfer (PT) events between electronic ground states in solution, experimental determination of the rates of such reactions has not yet been accomplished because of the limitations of the utilized methods. The objective of this study was to evaluate the PT rates of intramolecular O···H···O hydrogen-bonded systems in solution through the (1)H spin-lattice relaxation times of the hydroxyl protons, induced by the (1)H-(17)O dipolar interactions (T(1dd)(OH)), taking into account the contribution of the OH reorientational motion to T(1dd)(OH). Solutions of the benzoic acid dimer (BA dimer), 1-benzoyl-6-hydroxy-6-phenylfulvene (Fulvene), and dibenzoylmethane (DBM) were chosen as test systems. For Fulvene in CCl(4), the PT time, τ(PT), was deduced to be 7 × 10(-11) s. In the case of the BA dimer in CCl(4), the τ(PT) value was considerably greater than the OH reorientational correlation time, τ(R(OH)) = 4.3 × 10(-11) s. In contrast, the experimental results for DBM in CCl(4) indicated that the proton is located about midway between the two oxygen atoms, that is, the PT potential energy surface is a single well or a double well with a PT barrier near or below the zero-point energy.

CARD11 mutation and HBZ expression induce lymphoproliferative disease and adult T-cell leukemia/lymphoma.

Adult T-cell leukemia/lymphoma (ATL) is caused by human T-cell leukemia virus type 1 (HTLV-1). In addition to HTLV-1 bZIP factor (HBZ), a leukemogenic antisense transcript of HTLV-1, abnormalities of genes involved in TCR-NF-κB signaling, such as CARD11, are detected in about 90% of patients. Utilizing mice expressing CD4+ T cell-specific CARD11(E626K) and/or CD4+ T cell-specific HBZ, namely CARD11(E626K)CD4-Cre mice, HBZ transgenic (Tg) mice, and CARD11(E626K)CD4-Cre;HBZ Tg double transgenic mice, we clarify these genes' pathogenetic effects. CARD11(E626K)CD4-Cre and HBZ Tg mice exhibit lymphocytic invasion to many organs, including the lungs, and double transgenic mice develop lymphoproliferative disease and increase CD4+ T cells in vivo. CARD11(E626K) and HBZ cooperatively activate the non-canonical NF-κB pathway, IRF4 targets, BATF3/IRF4/HBZ transcriptional network, MYC targets, and E2F targets. Most KEGG and HALLMARK gene sets enriched in acute-type ATL are also enriched in double transgenic mice, indicating that these genes cooperatively contribute to ATL development.