Re-calibration of SDF/SXDS Photometric Catalogs of Suprime-Cam with SDSS Data Release 8

We present photometric recalibration of the Subaru Deep Field (SDF) and Subaru/XMM-Newton Deep Survey (SXDS). Recently, Yamanoi et al. (2012) suggested the existence of a discrepancy between the SDF and SXDS catalogs. We have used the Sloan Digital Sky Survey (SDSS) Data Release 8 (DR8) catalog and compared stars in common between SDF/SXDS and SDSS. We confirmed that there exists a 0.12 mag offset in B-band between the SDF and SXDS catalogs. Moreover, we found that significant zero point offsets in i-band (~ 0.10 mag) and z-band (~ 0.14 mag) need to be introduced to the SDF/SXDS catalogs to make it consistent with the SDSS catalog. We report the measured zero point offsets of five filter bands of SDF/SXDS catalogs. We studied the potential cause of these offsets, but the origins are yet to be understood.Comment: 36 pages, 19 figures(128 EPS files), PASJ accepte

Consistent map building in petrochemical complexes for firefighter robots using SLAM based on GPS and LIDAR

The objective of this study was to achieve simultaneous localization and mapping (SLAM) of firefighter robots for petrochemical complexes. Consistency of the SLAM map is important because human operators compare the map with aerial images and identify target positions on the map. The global positioning system (GPS) enables increased consistency. Therefore, this paper describes two Rao-Blackwellized particle filters (RBPFs) based on GPS and light detection and ranging (LIDAR) as SLAM solutions. Fast-SLAM 1.0 and Fast-SLAM 2.0 were used in grid maps for RBPFs in this study. We herein propose the use of Fast-SLAM to combine GPS and LIDAR. The difference between the original Fast-SLAM and the proposed method is the use of the log-likelihood function of GPS; the proposed combination method is implemented using a probabilistic mathematics formulation. The proposed methods were evaluated using sensor data measured in a real petrochemical complex in Japan ranging in size from 550–380 m. RTK-GPS data was used for the GPS measurement and had an availability of 56%. Our results showed that Fast-SLAM 2.0 based on GPS and LIDAR in a dense grid map produced the best results. There was significant improvement in alignment to aerial data, and the mean square root error was 0.65 m. To evaluate the mapping consistency, accurate 3D point cloud data measured by Faro Focus 3D (± 3 mm) was used as the ground truth. Building sizes were compared; the minimum mean errors were 0.17 and 0.08 m for the oil refinery and management building area and the area of a sparse building layout with large oil tanks, respectively. Consequently, a consistent map, which was also consistent with an aerial map (from Google Maps), was built by Fast-SLAM 1.0 and 2.0 based on GPS and LIDAR. Our method reproduced map consistency results for ten runs with a variance of ± 0.3 m. Our method reproduced map consistency results with a global accuracy of 0.52 m in a low RTK-Fix-GPS environment, which was a factory with a building layout similar to petrochemical complexes with 20.9% of RTK-Fix-GPS data availability

Bacterial Lipopolysaccharide Plus Interferon-γ Elicit a Very Fast Inhibition of a Ca2+-dependent Nitric-oxide Synthase Activity in Human Astrocytoma Cells

Abstract Previous results indicate that induction of inducible nitric-oxide synthase (iNOS) expression may be kept suppressed by the endogenous NO level as produced by a constitutive NOS (cNOS) enzyme. In cell types possessing both cNOS and iNOS, this may represent an evident paradox. Here, we report that lipopolysaccharide and interferon-γ, which are able to strongly induce iNOS in astrocytoma cells, can rapidly inhibit the NO production generated by the constitutive NOS isoform, thus obtaining the best conditions for iNOS induction and resolving the apparent paradox. In fact, a 30-min treatment of T67 cells with the combination of lipopolysaccharide plus interferon-γ (MIX) strongly inhibits the cNOS activity, as determined by measuring [3H]citrulline production. In addition, the effect of MIX is also observed by measuring nitrite, the stable breakdown product of NO: a 30-min pretreatment of T67 cells with MIX is able to reduce significantly the N-methyl-D-aspartate-induced nitrite production. Finally, using reverse transcriptase-polymerase chain reaction, we have observed that a 30-min treatment of T67 cells with MIX does not affect expression of mRNA coding for the neuronal NOS-I isoform. These results suggest the novel concept of a possible role of a cNOS isoform in astrocytes as a control function on iNOS induction

Rapid inactivation of NOS-I by lipopolysaccharide plus interferon-gamma-induced tyrosine phosphorylation.

Human astrocytoma T67 cells constitutively express a neuronal NO synthase (NOS-I) and, following administration of lipopolysaccharide (LPS) plus interferon-gamma (IFNgamma), an inducible NOS isoform (NOS-II). Previous results indicated that a treatment of T67 cells with the combination of LPS plus IFNgamma, by affecting NOS-I activity, also inhibited NO production in a very short time. Here, we report that under basal conditions, a NOS-I protein of about 150 kDa was weakly and partially tyrosine-phosphorylated, as verified by immunoprecipitation and Western blotting. Furthermore, LPS plus IFNgamma increased the tyrosine phosphorylation of NOS-I, with a concomitant inhibition of its enzyme activity. The same effect was observed in the presence of vanadate, an inhibitor of phosphotyrosine-specific phosphatases. On the contrary, genistein, an inhibitor of protein-tyrosine kinases, reduced tyrosine phosphorylation of NOS-I, enhancing its enzyme activity. Finally, using reverse transcriptase-polymerase chain reaction, we have observed that a suboptimal induction of NOS-II mRNA expression in T67 cells was enhanced by vanadate (or L-NAME) and inhibited by genistein. Because exogenous NO has been found to suppress NOS-II expression, the decrease of NO production that we have obtained from the inactivation of NOS-I by LPS/IFNgamma-induced tyrosine phosphorylation provides the best conditions for NOS-II expression in human astrocytoma T67 cells

The Stimulation of Inducible Nitric-oxide Synthase by the Prion Protein Fragment 106–126 in Human Microglia Is Tumor Necrosis Factor-α-dependent and Involves p38 Mitogen-activated Protein Kinase

A synthetic peptide consisting of amino acid residues 106-126 of the human prion protein (PrP-(106--126)) has been previously demonstrated to be neurotoxic and to induce microglial activation. The present study investigated the expression of the inducible form of the nitric-oxide synthase (NOS-II) in human microglial cells treated with PrP-(106--126). Using reverse transcriptase-polymerase chain reaction, we found that PrP-(106--126) induces NOS-II gene expression after 24 h of treatment and that this effect is accompanied by a peak of nuclear factor kappa B (NF-kappa B) binding at 30 min as evaluated by electrophoretic mobility shift assay. Since our previous data demonstrated tumor necrosis factor-alpha (TNF-alpha) to be a potent inducer of NOS-II in these cells, we analyzed the expression of this cytokine in PrP-(106--126)-treated microglia. PrP-(106--126) caused the release of TNF-alpha as detected by enzyme-linked immunosorbent assay, and a blocking antibody, anti-TNF-alpha, abolished NOS-II induction elicited by this peptide. Moreover, PrP-(106-126) activates p38 mitogen-activated protein kinase, and the inhibition of this pathway determines the ablation of NF-kappa B binding induced by this fragment peptide

Induction of Nitric Oxide Synthase mRNA Expression SUPPRESSION BY EXOGENOUS NITRIC OXIDE

The reactive nitrogen species, nitric oxide (NO), plays an important role in the pathogenesis of neurodegenerative diseases. The suppression of NO production may be fundamental for survival of neurons. Here, we report that pretreatment of human ramified microglial cells with nearly physiological levels of exogenous NO prevents lipopolysaccharide (LPS)/tumor necrosis factor alpha (TNF alpha)-inducible NO synthesis, because by affecting NF-kappa B activation it inhibits inducible Ca(2+)-independent NO synthase isoform (iNOS) mRNA expression. Using reverse transcriptase polymerase chain reaction, we have found that both NO donor sodium nitroprusside (SNP) and authentic NO solution are able to inhibit LPS/TNF alpha-inducible iNOS gene expression; this effect was reversed by reduced hemoglobin, a trapping agent for NO. The early presence of SNP during LPS/TNF alpha induction is essential for inhibition of iNOS mRNA expression. Furthermore, SNP is capable of inhibiting LPS/TNF alpha-inducible nitrite release, as determined by Griess reaction. Finally, using electrophoretic mobility shift assay, we have shown that SNP inhibits LPS/TNF alpha-elicited NF-kappa B activation. This suggests that inhibition of iNOS gene expression by exogenous NO may be ascribed to a decreased NF-kappa B availability

Consistent map building in petrochemical complexes for frefghter robots using SLAM based on GPS and LIDAR

The objective of this study was to achieve simultaneous localization and mapping (SLAM) of frefghter robots for petrochemical complexes. Consistency of the SLAM map is important because human operators compare the map with aerial images and identify target positions on the map. The global positioning system (GPS) enables increased consistency. Therefore, this paper describes two Rao-Blackwellized particle flters (RBPFs) based on GPS and light detection and ranging (LIDAR) as SLAM solutions. Fast-SLAM 1.0 and Fast-SLAM 2.0 were used in grid maps for RBPFs in this study. We herein propose the use of Fast-SLAM to combine GPS and LIDAR. The diference between the original FastSLAM and the proposed method is the use of the log-likelihood function of GPS; the proposed combination method is implemented using a probabilistic mathematics formulation. The proposed methods were evaluated using sensor data measured in a real petrochemical complex in Japan ranging in size from 550–380 m. RTK-GPS data was used for the GPS measurement and had an availability of 56%. Our results showed that Fast-SLAM 2.0 based on GPS and LIDAR in a dense grid map produced the best results. There was signifcant improvement in alignment to aerial data, and the mean square root error was 0.65 m. To evaluate the mapping consistency, accurate 3D point cloud data measured by Faro Focus 3D (± 3 mm) was used as the ground truth. Building sizes were compared; the minimum mean errors were 0.17 and 0.08 m for the oil refnery and management building area and the area of a sparse building layout with large oil tanks, respectively. Consequently, a consistent map, which was also consistent with an aerial map (from Google Maps), was built by Fast-SLAM 1.0 and 2.0 based on GPS and LIDAR. Our method reproduced map consistency results for ten runs with a variance of ± 0.3 m. Our method reproduced map consistency results with a global accuracy of 0.52 m in a low RTK-Fix-GPS environment, which was a factory with a building layout similar to petrochemical complexes with 20.9% of RTK-Fix-GPS data availability

Antitumor effects of α-bisabolol against pancreatic cancer.

In the present study, we investigated whether α-bisabolol, a sesquiterpene alcohol present in essential oils derived from a variety of plants, has antitumor effects against pancreatic cancer. α-Bisabolol induced a decrease in cell proliferation and viability in pancreatic cancer cell lines (KLM1, KP4, Panc1, MIA Paca2), but not in pancreatic epithelial cells (ACBRI515). α-Bisabolol treatment induced apoptosis and suppressed Akt activation in pancreatic cancer cell lines. Furthermore, α-bisabolol treatment induced the overexpression of early growth response-1 (EGR1), whereas EGR1 siRNA decreased the α-bisabolol-induced cell death of KLM1 cells. Tumor growth in both subcutaneous and peritoneal xenograft nude mouse models was significantly inhibited by intragastric administration of 1000 mg/kg of α-bisabolol, once a week for three weeks. The results indicate that α-bisabolol could be a novel therapeutic option for the treatment of pancreatic cancer

Pro-apoptotic activity of α-bisabolol in preclinical models of primary human acute leukemia cells

<p>Abstract</p> <p>Background</p> <p>We previously demonstrated that the plant-derived agent α-bisabolol enters cells <it>via </it>lipid rafts, binds to the pro-apoptotic Bcl-2 family protein BID, and may induce apoptosis. Here we studied the activity of α-bisabolol in acute leukemia cells.</p> <p>Methods</p> <p>We tested <it>ex vivo </it>blasts from 42 acute leukemias (14 Philadelphia-negative and 14 Philadelphia-positive B acute lymphoid leukemias, Ph^-/Ph⁺B-ALL; 14 acute myeloid leukemias, AML) for their sensitivity to α-bisabolol in 24-hour dose-response assays. Concentrations and time were chosen based on CD34⁺, CD33⁺my and normal peripheral blood cell sensitivity to increasing α-bisabolol concentrations for up to 120 hours.</p> <p>Results</p> <p>A clustering analysis of the sensitivity over 24 hours identified three clusters. Cluster 1 (14 ± 5 μM α-bisabolol IC₅₀) included mainly Ph^-B-ALL cells. AML cells were split into cluster 2 and 3 (45 ± 7 and 65 ± 5 μM IC₅₀). Ph⁺B-ALL cells were scattered, but mainly grouped into cluster 2. All leukemias, including 3 imatinib-resistant cases, were eventually responsive, but a subset of B-ALL cells was fairly sensitive to low α-bisabolol concentrations. α-bisabolol acted as a pro-apoptotic agent <it>via </it>a direct damage to mitochondrial integrity, which was responsible for the decrease in NADH-supported state 3 respiration and the disruption of the mitochondrial membrane potential.</p> <p>Conclusion</p> <p>Our study provides the first evidence that α-bisabolol is a pro-apoptotic agent for primary human acute leukemia cells.</p