Design and performance of the muon monitor for the T2K neutrino oscillation experiment

This article describes the design and performance of the muon monitor for the T2K (Tokaito-Kamioka) long baseline neutrino oscillation experiment. The muon monitor consists of two types of detector arrays: ionization chambers and silicon PIN photodiodes. It measures the intensity and profile of muons produced, along with neutrinos, in the decay of pions. The measurement is sensitive to the intensity and direction of the neutrino beam. The linearity and stability of the detectors were measured in beam tests to be within 2.4% and 1.5%, respectively. Based on the test results, the precision of the beam direction measured by the muon monitor is expected to be 0.25 mrad.Comment: 22 page

Secondary Beam Monitors for the NuMI Facility at FNAL

The Neutrinos at the Main Injector (NuMI) facility is a conventional neutrino beam which produces muon neutrinos by focusing a beam of mesons into a long evacuated decay volume. We have built four arrays of ionization chambers to monitor the position and intensity of the hadron and muon beams associated with neutrino production at locations downstream of the decay volume. This article describes the chambers' construction, calibration, and commissioning in the beam.Comment: Accepted for publication in Nucl. Instr. Meth.

Determination of the high-twist contribution to the structure function xF3νNxF^{\nu N}_3

We extract the high-twist contribution to the neutrino-nucleon structure function $xF_3^{(\nu+\bar{\nu})N}$ from the analysis of the data collected by the IHEP-JINR Neutrino Detector in the runs with the focused neutrino beams at the IHEP 70 GeV proton synchrotron. The analysis is performed within the infrared renormalon (IRR) model of high twists in order to extract the normalization parameter of the model. From the NLO QCD fit to our data we obtained the value of the IRR model normalization parameter $\Lambda^2_{3}=0.69\pm0.37~({\rm exp})\pm0.16~({\rm theor})~{\rm GeV}^2$. We also obtained $\Lambda^2_{3}=0.36\pm0.22~({\rm exp})\pm0.12~({\rm theor})~{\rm GeV}^2$ from a similar fit to the CCFR data. The average of both results is $\Lambda^2_{3}=0.44\pm0.19~({\rm exp})~{\rm GeV}^2$.Comment: preprint IHEP-01-18, 7 pages, LATEX, 1 figure (EPS

Association of the HTR2A T102C SNP with Weight Gain and Changes in Biochemical Markers in Patients Receiving Antipsychotics

The purpose of our research was to study the association of the HTR2A T102C (rs6313) SNP with anthropometric and biochemical markers in patients treated with typical and atypical antipsychotics in monotherapy mode. Materials and methods: One hundred and seventeen white inpatients (95 men and 22 women) with F2 disorders (ICD-10, 1995) were enrolled in the study. All patients were divided into two groups by the antipsychotic class with which they were treated (Group 1 included 40 patients treated with typical antipsychotics; Group 2 included 77 patients treated with atypical antipsychotics) and two subgroups by weight change criteria during the study (Subgroup 1 included patients with weight change >6%; Subgroup 2 included patients with weight change <6%). The following examinations were performed: physical examination, anthropometric measurements (BMI. WC, TC), clinical examination, blood test (ALT, AST, FPG, VLDL-C, LDL-C, HDL-C, total cholesterol, triglycerides, total protein, albumin, creatinine, uric acid, carbamide), and genotyping for the HTR2A T102C (rs6313) SNP. Results: There were no statistically significant differences in the distribution of genotypes of the HTR2A T102C (rs6313) SNP between Group 1 and Group 2 (P>0.05). Kruskal-Wallis one-way analysis of variance between subgroups showed statistically significant differences between carbamide levels in the second visit in Group 2 (P=0.02). A Dunn post hoc test with Bonferroni adjustment showed statistically significant differences between TT and CT genotypes of the HTR2A T102C SNP: carbamide level was greater in TT carriers (P=0.02). The strength of associations and risks between alleles of the HTR2A T102C SNP and antipsychotic-induced weight change were as follows: ORC=0.49; CIC [0.25; 0.95]; RRC=0.58 CIC [0.35; 0.97]; ORT=2.03; CIT [1.05; 3.94]; RRT=1.7 CIT [1.02; 2.81]. Conclusion: Our results of the pilot pharmacogenetic studies show an association of the T allele carriage of the HTR2A T102C SNP with risk of antipsychotic-induced weight gain. The continuation of this study and an increase in the sample size will allow establishing valid pharmacogenetic markers for the risk of antipsychotic-induced weight gain

Genetic selection system allowing monitoring of myofibrillogenesis in living cardiomyocytes derived from mouse embryonic stem cells

Embryonic stem (ES) cell-derived cardiomyocytes recapitulate cardiomyogenesis in vitro and are a potential source of cells for cardiac repair. However, this requires enrichment of mixed populations of differentiating ES cells into cardiomyocytes. Toward this goal, we have generated bicistronic vectors that express both the blasticidin S deaminase (bsd) gene and a fusion protein consisting of either myosin light chain (MLC)-3f or human a-actinin 2A and enhanced green fluorescent protein (EGFP) under the transcriptional control of the a-cardiac myosin heavy chain (a-MHC) promoter. Insertion of the DNase I-hypersensitive site (HS)-2 element from the b-globin locus control region, which has been shown to reduce transgene silencing in other cell systems, upstream of the transgene promoter enhanced MLC3f-EGFP gene expression levels in mouse ES cell lines. The a-MHC-a- actinin-EGFP, but not the a-MHC-MLC3f-EGFP, construct resulted in the correct incorporation of the newly synthesized fusion protein at the Z-band of the sarcomeres in ES cellderived cardiomyocytes. Exposure of embryoid bodies to blasticidin S selected for a relatively pure population of cardiomyocytes within 3 days. Myofibrillogenesis could be monitored by fluorescence microscopy in living cells due to sarcomeric epitope tagging. Therefore, this genetic system permits the rapid selection of a relatively pure population of developing cardiomyocytes from a heterogeneous population of differentiating ES cells, simultaneously allowing monitoring of early myofibrillogenesis in the selected myocytes

N-cadherin is essential for retinoic acid-mediated cardiomyogenic differentiation in mouse embryonic stem cells.

Contraction forces developed by cardiomyocytes are transmitted across the plasma membrane through end-to-end connections between the myocytes, called intercalated disks, which enable the coordinated contraction of heart muscle. A component of the intercalated disk, the adherens junction, consists of the cell adhesion molecule, N-cadherin. Embryos lacking N-cadherin die at mid-gestation from cardiovascular abnormalities. We have evaluated the role of N-cadherin in cardiomyogenesis using N-cadherin-null mouse embryonic stem (ES) cells grown as embryoid bodies (EBs) in vitro. Myofibrillogenesis, the spatial orientation of myofibers, and intercellular contacts including desmosomes were normal in N-cadherin-null ES cell-derived cardiomyocytes. The effect of retinoic acid (RA), a stage and dose-dependent cardiogenic factor, was assessed in differentiating ES cells. all-trans (at) RA increased the number of ES cell-derived cardiomyocytes by approximately 3-fold (at 3 x 10(-9) M) in wt EBs. However, this effect was lost in N-cadherin-null EBs. In the presence of supplemented at-RA, the emergence of spontaneously beating cardiomyocytes appeared to be delayed and slightly less efficient in N-cadherin-null compared with wt and heterozygous EBs (frequencies of EBs with beating activity at 5 days: 54+/-18% vs. 96+/-0.5%, and 93+/-7%, respectively; peak frequencies of EBs with beating activity: 83+/-8% vs. 96+/-0.5% and 100%, respectively). In conclusion, cardiomyoyctes differentiating from N-cadherin-null ES cells in vitro show normal myofibrillogenesis and intercellular contacts, but impaired responses to early cardiogenic effects mediated by at-RA. These results suggest that N-cadherin may be essential for RA-induced cardiomyogenesis in mouse ES cells in vitro

Genetic selection system allowing monitoring of myofibrillogenesis in living cardiomyocytes derived from mouse embryonic stem cells

Embryonic stem (ES) cell-derived cardiomyocytes recapitulate cardiomyogenesis in vitro and are a potential source of cells for cardiac repair. However, this requires enrichment of mixed populations of differentiating ES cells into cardiomyocytes. Toward this goal, we have generated bicistronic vectors that express both the blasticidin S deaminase (bsd) gene and a fusion protein consisting of either myosin light chain (MLC)-3f or human alpha-actinin 2A and enhanced green fluorescent protein (EGFP) under the transcriptional control of the alpha-cardiac myosin heavy chain (alpha-MHC) promoter. Insertion of the DNase I-hypersensitive site (HS)-2 element from the beta-globin locus control region, which has been shown to reduce transgene silencing in other cell systems, upstream of the transgene promoter enhanced MLC3f-EGFP gene expression levels in mouse ES cell lines. The alpha-MHC-alpha-actinin-EGFP, but not the alpha-MHC-MLC3f-EGFP, construct resulted in the correct incorporation of the newly synthesized fusion protein at the Z-band of the sarcomeres in ES cell-derived cardiomyocytes. Exposure of embryoid bodies to blasticidin S selected for a relatively pure population of cardiomyocytes within 3 days. Myofibrillogenesis could be monitored by fluorescence microscopy in living cells due to sarcomeric epitope tagging. Therefore, this genetic system permits the rapid selection of a relatively pure population of developing cardiomyocytes from a heterogeneous population of differentiating ES cells, simultaneously allowing monitoring of early myofibrillogenesis in the selected myocyte

Characteristics of opioid regulation of gastric and duodenal afferent reactions at early stages of acute damage

[No abstract available

Characteristics of opioid regulation of gastric and duodenal afferent reactions at early stages of acute damage

[No abstract available