17,489 research outputs found
The Strategies for Simple One-Point Ko Situation of Computer Go
No full text[[abstract]]Ko plays a very important role in Go, but most computer Go programs still cannot handle ko fights so far. Utilizing the principle of Minimax procedure, we obtain the best strategies for the simple one-point ko situation, enabling computer Go programs to gain maximum or loss minimum profit when dealing with the simple one-point ko situation. We also discuss in detail the strategies for using ko threats during the process of the ko fight.
Branching fraction and CP asymmetry of the decays B+→K0Sπ+ and B+→K0SK+
No full textAn analysis of B+ → K0
Sπ+ and B+ → K0
S K+ decays is performed with the LHCb experiment. The pp
collision data used correspond to integrated luminosities of 1 fb−1 and 2 fb−1 collected at centre-ofmass
energies of
√
s = 7 TeV and
√
s = 8 TeV, respectively. The ratio of branching fractions and the
direct CP asymmetries are measured to be B(B+ → K0
S K+
)/B(B+ → K0
Sπ+
) = 0.064 ± 0.009 (stat.) ±
0.004 (syst.), ACP(B+ → K0
Sπ+
) = −0.022 ± 0.025 (stat.) ± 0.010 (syst.) and ACP(B+ → K0
S K+
) =
−0.21 ± 0.14 (stat.) ± 0.01 (syst.). The data sample taken at
√
s = 7 TeV is used to search for
B+
c
→ K0
S K+ decays and results in the upper limit ( fc · B(B+
c
→ K0
S K+
))/( fu · B(B+ → K0
Sπ+
)) <
5.8 × 10−2 at 90% confidence level, where fc and fu denote the hadronisation fractions of a ¯b
quark
into a B+
c or a B+ meson, respectively
CCHFV infection of TNFA-R DBL KO mouse livers.
No full textA. Representative H&E staining of TNFA-R DBL KO mice on day 10 showing mitotic figures (arrows), indicative of liver recovery/regenerative response. B. Representative liver section from a day 10 infected TNF-R DBL KO mouse were stained with anti-CLEC4F (red) and anti-CCHFV N protein (green) antibodies. Cell nuclei were stained with DAPI (TIF)</p
Deletion of A<sub>2A</sub>R immunoreactivity in glutamatergic terminals of forebrain-A<sub>2A</sub>R KO and GABAergic terminals of both forebrain A<sub>2A</sub>R - and striatum-A<sub>2A</sub>R KO mice.
No full text<p>Detection and quantification of the percentage of GABAergic terminals (<b>A</b>, vGAT-positive) and glutamatergic terminals (<b>B</b>, vGluT1-positive) and from forebrain-selective-A<sub>2A</sub>R KO (fb-KO) or striatum-selective-A<sub>2A</sub>R KO (st-KO) mice and their wild type (WT) littermates (control) that are endowed with A<sub>2A</sub>R immunoreactivity. The bar graphs represent the percentage of vGluT1- or vGAT-immunopositive terminals that are also endowed with A<sub>2A</sub>R immunoreactivity (mean ± SEM, 3 fields per mouse, n = 4-6 animal per group). * p<0.05 <i>vs</i> corresponding WT littermates, using an unpaired Student’s <i>t</i> test. On the left side of each bar graph are shown representative immunocytochemistry photographs displaying the superimposed immunoreactivities of vGluT1 or vGAT (green) and of A<sub>2A</sub>R (red).</p
Cocaine-induced phosphorylation of striatal DARPP-32 at Thr-34 and Thr-75 are oppositely affected in striatum-A<sub>2A</sub>R KO and forebrain-A<sub>2A</sub>R KO mice.
No full text<p>Western blot analysis of phosphorylated (p-Thr-34 and p-Thr-75) and total DARPP-32. Representative Western blots of striatal protein extracts from fb-A<sub>2A</sub>R KO and fb-WT (<b>A</b> and <b>E</b>), st-A<sub>2A</sub>R KO or st-WT mice (<b>C</b> and <b>F</b>). The levels of DARPP-32 phosphorylation (normalized with total DARPP-32 level) are shown as mean ± SEM and presented as percentage of the value for saline-treated WT mice, for p-Thr-34 DARPP-32 levels in <i>fb</i>-A<sub>2A</sub>R KO (n = 4, <b>B</b>) and <i>st-</i>A<sub>2A</sub>R KO (n = 6, <b>D</b>) and p-Thr-75 DARPP-32 levels in <i>fb</i>-A<sub>2A</sub>R KO (n = 4, <b>F</b>) and <i>st-</i>A<sub>2A</sub>R KO (n = 6, <b>H</b>). # p<0.05 comparing cocaine with saline treatment within same genotype, two-way ANOVA and a <i>post hoc</i> Bonferroni test; * p<0.05 comparing fb-A<sub>2A</sub>R KO or st-A<sub>2A</sub>R KO with their corresponding WT littermates with same treatment, two-way ANOVA <i>post hoc</i> Bonferroni test.</p
MM activity and glucose metabolism in IL-1-KO mice during R+G+.
No full text<p>(A) IL-1-KO-MMs were easily fatigued in the R+G+ condition. WT and IL-1-KO mice (n = 12) were subjected to R+G+, and the MM activity was measured. Typical examples of plastic plates gnawed on during R+G+ by WT or IL-1-KO mice are shown on the right. Experimental values are given as the mean ± SE. *<i>P</i> < 0.05 compared to WT at the same time-points. (B) Effects of R+G+ on blood glucose. There was no difference in blood glucose levels between WT and IL-1-KO mice during R+G+ behavior. WT and IL-1-KO mice (n = 4–5) were subjected to R+G+, and blood was taken from the tail vein for blood glucose measurement. (C) Glycogen stores in IL-1-KO-MMs were strongly depleted during R+G+. WT and IL-1-KO mice (n = 12–16) were subjected to 1 h of R+G+ behavior or of R+G-, and MM glycogen content was measured. MMs from R-G- (i.e., resting, unrestrained) mice were also analyzed as a control. (D) Glucose uptake by IL-1-KO MMs (Left) was less than by WT MMs during R+G+, but not by the quadriceps femoris muscles (QFM, Right). WT and IL-1-KO mice (n = 10–12) were intraperitoneally injected with <sup>14</sup>C-2DG after 1 h of R+G+ activity, and 30 min later skeletal muscles were removed and glucose uptake was measured. Experimental values are given as the mean ± SE. *<i>P</i> < 0.05, **<i>P</i> < 0.01.</p
MAPs in CCK<sub>B</sub>R<sup>-/-</sup> mice and CCK<sub>B</sub>R<sup>+/+</sup> littermates.
No full text<p>MAPs were measured from the aorta, via the left carotid artery, under pentobarbital anesthesia. WT and KO indicate CCK<sub>B</sub>R<sup>+/+</sup> littermates (n = 19) and CCK<sub>B</sub>R<sup>-/-</sup> mice (n = 21) on normal salt diet, respectively; WT+HS and KO+HS indicate CCK<sub>B</sub>R<sup>+/+</sup> littermates (n = 11) and CCK<sub>B</sub>R<sup>-/-</sup> mice (n = 8) on high salt diet, respectively. *P<0.05 vs WT, #P<0.05 vs KO, &P<0.05 vs WT+HS, one-way factorial ANOVA.</p
Cocaine-induced psychomotor activity and striatal c-Fos expression were attenuated in forebrain-A<sub>2A</sub>R KO but enhanced in striatal-A<sub>2A</sub>R KO mice.
No full text<p>Ambulation was recorded for 180 min after injection of a single dose of cocaine (25 mg/kg, i.p.) or vehicle in fb-A<sub>2A</sub>R KO (n = 12, <b>A</b>) and in st-A<sub>2A</sub>R KO (n = 9, <b>B</b>) mice and their WT littermates (n = 8–12). The arrow indicates the time of injection and the data are mean ± SEM; *p<0.05, comparing fb-A<sub>2A</sub>R KO and st-A<sub>2A</sub>R KO groups to their corresponding WT group using two-way ANOVA and a <i>post hoc</i> Bonferroni test. (<b>C</b>) Cocaine-induced c-Fos expression in the striatum of fb-A<sub>2A</sub>R KO (n = 12) and st-A<sub>2A</sub>R KO (n = 9) and their corresponding WT littermates (n = 8–12) <sup>#</sup> p<0.05, comparing to corresponding wild-types with cocaine treatment, two-way ANOVA <i>post hoc</i> Bonferroni test. (<b>D</b>) Representative co-immunostaining of c-Fos with dynorphin. Black arrows indicate neurons co-stained with dynorphin and c-Fos; white arrow heads indicate neurons stained with dynorphin only (greyish brown) and black arrow heads indicate neurons stained with c-Fos (reddish brown). Scale bar = 25 µm.</p
SV2A/B KO neurons are resistant to TeNT.
No full text<p>(A) Mouse spinal cord neurons with the following genotypes: WT, SV2B KO [SV2A (+/+) SV2B (−/−)], and SV2A/B KO [SV2A (−/−) SV2B (−/−)], were exposed to HCR/T (50 nM). HCR/T fluorescence in SV2A/B KO neurons was dramatically reduced as compared to WT and SV2B KO. (B) Quantification of HCR/T binding: fluorescence was reduced by 30% and 50% for SV2B KO and SV2A/B KO neurons, respectively. Error bars represent SD, WT n = 9, SV2B KO n = 11, SV2A/B KO n = 12, ***p≤0.001. (C) SV2B KO and SV2A/B KO cultures were exposed to TeNT (20 nM) and BoNT/A (10 nM). Cell lysates were subjected to immunoblot analysis and probed for syb II, SV2, SNAP-25, and actin. Syb II in SV2A/B KO neurons was largely protected from TeNT action until resensitized through lentiviral expression of SV2A or SV2B; arrow indicates the BoNT/A cleaved form of SNAP-25. (D) SV2B KO and SV2A/B KO spinal cord neurons from were assayed for susceptibility to TeNT. Syb II was cleaved by 5 nM TeNT in SV2B KO neurons, while syb II was protected from TeNT in SV2A/B KO neurons. SV2A/B KO neurons could be resensitized to TeNT, upon lentiviral expression of SV2A. (E) Three putative glycosylation sites in SV2A were removed by creating N to Q mutants (residues 498, 548 and 573) and were expressed in SV2A/B KO neurons along with WT SV2A. Syb II was cleaved by TeNT in neurons reinfected with WT SV2A as well as the three mutants. (F) WT and SV2B KO mice were injected with the indicated amounts of TeNT and their time-to-death was recorded. SV2B KO mice were more than five-times more resistant to TeNT as compared to their WT counterparts. (G) WT and SV2A/B KO neurons were cultured and treated with BoNT/F at the indicated concentrations. Cell lysates were probed for syb II and syp by immunoblot analysis. WT and SV2A/B KO neurons exhibited similar sensitivities to BoNT/F.</p
LTP facilitation by R-96544 is impaired in the ACC of <i>Fmr1</i> KO mice.
No full text<p>(<b>A</b>) The pairing training produced a significant, long-lasting potentiation of synaptic responses in WT mice (n = 13 slices/5 mice); LTP was lost in ACC pyramidal neurons of <i>Fmr1</i> KO mice (n = 11 slices/6 mice). (<b>B</b>) R-96544 paired with training facilitated LTP induction in WT mice (n = 11 slices/5 mice); R-96544 failed to facilitate LTP induction in <i>Fmr1</i> KO mice (n = 12 slices/5 mice). (<b>C</b>) Ketanserin facilitated LTP induction in <i>Fmr1</i> WT mice (n = 12 slices/5 mice); Ketanserin failed to facilitate LTP induction in <i>Fmr1</i> KO mice (n = 12 slices/5 mice). (<b>D</b>) LTP was blocked in the presence of AP-5 (7 slices/3 mice) and BAPTA (n = 9 slices/4 mice) in the pipette solution in WT mice. (<b>E</b>) Summary of the effects of R-96544, ketanserin, AP-5, and BAPTA on LTP in the WT mice. **<i>P</i><0.01 compared to baseline control; <sup>& </sup><i>P</i><0.05 compared to saline control of LTP. (<b>F</b>) Summary of the effects of R-96544 and ketanserin on LTP in the <i>Fmr1</i> KO mice.</p
- …
