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A prototype system based on a combination of 4π sensitive gamma imaging and simultaneous localization and mapping (SLAM) was developed to find unknown radiation source(s) rapidly. The system consisted of a spherical visible camera, a three-dimensional light detection and ranging, a CdTe pixel array detector for 4π gamma imaging, a portable battery, and a control laptop personal computer; these were mounted on an unmanned vehicle. In a search area of 16 × 16 m2 with a height of 3 m, the prototype system successfully demonstrated the finding of a 137Cs point source with an activity of 0.67 MBq in the surrounding thin walls. [ABSTRACT FROM AUTHOR]

Sit-to-stand motion is an important daily activity, and disability of motion can significantly reduce quality of life. Therefore, it is important to understand the mechanism of sit-to-stand motion in order to prevent such scenarios. The sit-to-stand motion was found to be generated by four muscle groups, through muscle synergy. However, it is unclear how muscle synergy can be controlled. Human sit-to-stand motion may be planned based on body condition before motion. In this study, we aimed to clarify the relationship between body condition and muscle activity during the sit-to-stand motion. Accordingly, we measured the muscle activity when knee movability was disturbed as a condition of body change. We also measured the muscle activity during normal sit-to-stand motion and sit-to-stand motion with disturbed knee movability using surface electromyography. Subsequently, we extracted the muscle synergy from the measured muscle activity and compared the activity levels of muscle synergy. The results revealed that muscle activity contributing to forward bending increased and that contributing to the rise of the hip and stabilization decreased when knee movability was disturbed. These results suggest that humans compensate for disturbed knee movability with forward momentum and bending motion. Moreover, this implies that humans adjust their motion to various environments or body conditions by adjusting the level of forward bending activity. [ABSTRACT FROM AUTHOR]

Smad proteins transduce signals downstream of transforming growth factor-β (TGF-β) and are one of the factors that regulate the expression of genes related to diseases affecting the skin. In the present study, we identified MAB21L4, also known as male abnormal 21 like 4 or C2orf54 , as the most up-regulated targets of TGF-β and Smad3 in differentiated human progenitor epidermal keratinocytes using chromatin immunoprecipitation sequencing (ChIP-seq) and RNA sequencing (RNA-seq). We found that TGF-β induced expression of the barrier protein involucrin (encoded by the IVL gene). Transcriptional activity of the IVL promoter induced by TGF-β was inhibited by MAB21L4 siRNAs. Further analysis revealed that MAB21L4 siRNAs also down-regulated the expression of several target genes of TGF-β. MAB21L4 protein was located mainly in the cytosol, where it was physically bound to Smad3 and a transcriptional corepressor c-Ski. siRNAs for MAB21L4 did not inhibit the binding of Smad3 to their target genomic regions but down-regulated the acetylation of histone H3 lys 27 (H3K27ac), an active histone mark, near the Smad3 binding regions. These findings suggest that TGF-β-induced MAB21L4 up-regulates the gene expression induced by TGF-β, possibly through the inhibition of c-Ski via physical interaction in the cytosol. [ABSTRACT FROM AUTHOR]

The activation of RIG‐I‐like receptor (RLR) signaling in cancer cells is widely recognized as a critical cancer therapy method. The expected mechanism of RLR ligand‐mediated cancer therapy involves the promotion of cancer cell death and strong induction of interferon (IFN)‐β that affects the tumor microenvironment. We have recently shown that activation of RLR signaling in triple‐negative breast cancer cells (TNBC) attenuates transforming growth factor‐β (TGF‐β) signaling, which partly contributes to the promotion of cancer cell pyroptosis. However, the consequences of suppression of TGF‐β signaling by RLR ligands with respect to IFN‐β‐mediated tumor suppression are not well characterized. This study showed that transfection of a typical RLR ligand polyI:C in cancer cells produces significant levels of IFN‐β, which inhibits the growth of the surrounding cancer cells. In addition, IFN‐β‐induced cell cycle arrest in surrounding cancer cells was inhibited by the expression of constitutively active Smad3. Constitutively active Smad3 suppresses IFN‐β expression through the alleviation of IFN regulatory factor 3 binding to the canonical target genes, as suggested by ChIP sequencing analysis. Based on these findings, a new facet of the protumorigenic function of TGF‐β that suppresses IFN‐β expression is suggested when RLR‐mediated cancer treatment is used in TNBC. [ABSTRACT FROM AUTHOR]