The Mechanism for Primordial Germ-Cell Migration Is Conserved between Japanese Eel and Zebrafish

Primordial germ cells (PGCs) are segregated and specified from somatic cells during early development. These cells arise elsewhere and have to migrate across the embryo to reach developing gonadal precursors. Several molecules associated with PGC migration (i.e. dead-end, nanos1, and cxcr4) are highly conserved across phylum boundaries. However, since cell migration is a complicated process that is regulated spatially and temporally by multiple adaptors and signal effectors, the process is unlikely to be explained by these known genes only. Indeed, it has been shown that there are variations in PGC migration pattern during development among teleost species. However, it is still unclear whether the actual mechanism of PGC migration is conserved among species. In this study, we studied the migration of PGCs in Japanese eel (Anguilla japonica) embryos and tested the migration mechanism between Japanese eel and zebrafish (Danio rerio) for conservation, by transplanting eel PGCs into zebrafish embryos. The experiments showed that eel PGCs can migrate toward the gonadal region of zebrafish embryos along with endogenous PGCs, even though the migration patterns, behaviors, and settlements of PGCs are somewhat different between these species. Our results demonstrate that the migration mechanism of PGCs during embryonic development is highly conserved between these two distantly related species (belonging to different teleost orders)

Search for the Θ+\Theta^{+} pentaquark via the π−p→K−X\pi^-p\to K^-X reaction at 1.92 GeV/cc

The $\Theta^+$ pentaquark baryon was searched for via the $\pi^-p\to K^-X$ reaction in a missing-mass resolution of 1.4 MeV/$c^2$(FWHM) at J-PARC. $\pi^-$ meson beams were incident on the liquid hydrogen target with the beam momentum of 1.92 GeV/$c$. No peak structure corresponding to the $\Theta^+$ mass was observed. The upper limit of the production cross section averaged over the scattering angle of 2$^{\circ}$ to 15$^{\circ}$ in the laboratory frame was obtained to be 0.26 $\mu$b/sr in the mass region of 1.51$-$1.55 GeV/$c^2$.The upper limit of the $\Theta^+$ decay width using the effective Lagrangian approach was obtained to be 0.72 MeV/$c^2$ and 3.1 MeV/$c^2$ for $J^P_{\Theta}=1/2^+$ and $J^P_{\Theta}=1/2^-$, respectively.Comment: 5 pages, 3 figures, 1 tabl

The CrebA/Creb3-like transcription factors are major and direct regulators of secretory capacity

CrebA up-regulates expression of both the general protein machinery required in all cells for secretion and genes encoding cell type–specific secreted components

Toll-like receptor signaling adapter proteins govern spread of neuropathic pain and recovery following nerve injury in male mice.

BackgroundSpinal Toll-like receptors (TLRs) and signaling intermediaries have been implicated in persistent pain states. We examined the roles of two major TLR signaling pathways and selected TLRs in a mononeuropathic allodynia.MethodsL5 spinal nerve ligation (SNL) was performed in wild type (WT, C57BL/6) male and female mice and in male Tlr2-/-Tlr3-/-, Tlr4-/-, Tlr5-/-, Myd88-/-, Triflps2, Myd88/Triflps2, Tnf-/-, and Ifnar1-/- mice. We also examined L5 ligation in Tlr4-/- female mice. We examined tactile allodynia using von Frey hairs. Iba-1 (microglia) and GFAP (astrocytes) were assessed in spinal cords by immunostaining. Tactile thresholds were analyzed by 1- and 2-way ANOVA and the Bonferroni post hoc test was used.ResultsIn WT male and female mice, SNL lesions resulted in a persistent and robust ipsilateral, tactile allodynia. In males with TLR2, 3, 4, or 5 deficiencies, tactile allodynia was significantly, but incompletely, reversed (approximately 50%) as compared to WT. This effect was not seen in female Tlr4-/- mice. Increases in ipsilateral lumbar Iba-1 and GFAP were seen in mutant and WT mice. Mice deficient in MyD88, or MyD88 and TRIF, showed an approximately 50% reduction in withdrawal thresholds and reduced ipsilateral Iba-1. In contrast, TRIF and interferon receptor null mice developed a profound ipsilateral and contralateral tactile allodynia. In lumbar sections of the spinal cords, we observed a greater increase in Iba-1 immunoreactivity in the TRIF-signaling deficient mice as compared to WT, but no significant increase in GFAP. Removing MyD88 abrogated the contralateral allodynia in the TRIF signaling-deficient mice. Conversely, IFNβ, released downstream to TRIF signaling, administered intrathecally, temporarily reversed the tactile allodynia.ConclusionsThese observations suggest a critical role for the MyD88 pathway in initiating neuropathic pain, but a distinct role for the TRIF pathway and interferon in regulating neuropathic pain phenotypes in male mice

Measurement and comparison of individual external doses of high-school students living in Japan, France, Poland and Belarus -- the "D-shuttle" project --

Twelve high schools in Japan (of which six are in Fukushima Prefecture), four in France, eight in Poland and two in Belarus cooperated in the measurement and comparison of individual external doses in 2014. In total 216 high-school students and teachers participated in the study. Each participant wore an electronic personal dosimeter "D-shuttle" for two weeks, and kept a journal of his/her whereabouts and activities. The distributions of annual external doses estimated for each region overlap with each other, demonstrating that the personal external individual doses in locations where residence is currently allowed in Fukushima Prefecture and in Belarus are well within the range of estimated annual doses due to the background radiation level of other regions/countries

Measurements of the masses and widths of the Σc(2455)0/++\Sigma_{c}(2455)^{0/++} and Σc(2520)0/++\Sigma_{c}(2520)^{0/++} baryons

We present measurements of the masses and decay widths of the baryonic states $\Sigma_{c}(2455)^{0/++}$ and $\Sigma_{c}(2520)^{0/++}$ using a data sample corresponding to an integrated luminosity of 711 fb$^{-1}$ collected with the Belle detector at the KEKB $e^{+}e^{-}$ asymmetric-energy collider operating at the $\Upsilon(4S)$ resonance. We report the mass differences with respect to the $\Lambda_{c}^{+}$ baryon $M(\Sigma_{c}(2455)^{0})-M(\Lambda_{c}^{+}) = 167.29\pm0.01\pm0.02$ MeV/$c^{2}$, $M(\Sigma_{c}(2455)^{++})-M(\Lambda_{c}^{+}) = 167.51\pm0.01\pm0.02$ MeV/$c^{2}$, $M(\Sigma_{c}(2520)^{0})-M(\Lambda_{c}^{+}) = 231.98\pm0.11\pm0.04$ MeV/$c^{2}$, $M(\Sigma_{c}(2520)^{++})-M(\Lambda_{c}^{+}) = 231.99\pm0.10\pm0.02$ MeV/$c^{2}$, and the decay widths $\Gamma(\Sigma_{c}(2455)^{0}) = 1.76\pm0.04^{+0.09}_{-0.21}$ MeV/$c^{2}$, $\Gamma(\Sigma_{c}(2455)^{++}) = 1.84\pm0.04^{+0.07}_{-0.20}$ MeV/$c^{2}$, $\Gamma(\Sigma_{c}(2520)^{0}) = 15.41\pm0.41^{+0.20}_{-0.32}$ MeV/$c^{2}$, $\Gamma(\Sigma_{c}(2520)^{++}) = 14.77\pm0.25^{+0.18}_{-0.30}$ MeV/$c^{2}$, where the first uncertainties are statistical and the second are systematic. The isospin mass splittings are measured to be $M(\Sigma_{c}(2455)^{++})-M(\Sigma_{c}(2455)^{0})=0.22\pm0.01\pm0.01$ MeV/$c^{2}$ and $M(\Sigma_{c}(2520)^{++})-M(\Sigma_{c}(2520)^{0})=0.01\pm0.15\pm0.03$ MeV/$c^{2}$. These results are the most precise to date.Comment: 13 pages, 4 figures, Submitted to PRD(RC

Search for CP Violation in the Decay D+→KS0K+D^+\rightarrow K^0_S K^+

We search for CP violation in the decay $D^+\rightarrow K^0_S K^+$ using a data sample with an integrated luminosity of 977 fb$^{-1}$ collected with the Belle detector at the KEKB $e^+e^-$ asymmetric-energy collider. No CP violation has been observed and the CP asymmetry in $D^+\rightarrow K^0_S K^+$ decay is measured to be $(-0.25\pm0.28\pm0.14)$, which is the most sensitive measurement to date. After subtracting CP violation due to $K^0-\bar{K}^0$ mixing, the CP asymmetry in $D^+\rightarrow\bar{K}^0 K^+$ decay is found to be $(+0.08\pm0.28\pm0.14)$.Comment: 15 pages, 4 figures, 1 table. Published in JHE