Performance of a micro-TPC for a time-resolved neutron PSD

We report on the performance of a micro-TPC with a micro pixel chamber($\mu$-PIC) readout for a time-resolved neutron position-sensitive detector(PSD). Three-dimensional tracks and the Bragg curves of protons with energies of around 1 MeV were clearly detected by the micro-TPC. More than 95% of gamma-rays of 511 keV were found to be discriminated by simple analysis. Simulation studies showed that the total track length of proton and triton emitted from the $\rm {}^{3}He$(n,p(573 keV))$\rm {}^{3}H(191 keV)$ reaction is about 1.2 cm, and that both particles have large energy losses ($\rm > 200 keV/cm$) in 1 atm Ar+$\rm C_{2}H_{6}(10$+${}^{3}$He($< 1$). These values suit the current performance of the micro-TPC, and we conclude that a time-resolved neutron PSD with spatial resolution of sub-millimeters shall be developed as an application of the micro-TPC.Comment: 13 pages, 10 figures, to appear in NIM

Spectroscopy and Thermoluminescence of LuAlO3:Ce

The present status of the LuAlO3:Ce scintillator is reviewed. Scintillation mechanism of this material is based on capture by Ce3+ of holes and then electrons from their respective bands. Results of spectroscopic and thermoluminescence experiments are presented to support this model

Search for the lightest scalar top quark in events with two leptons in p-pbar collisions at sqrt(s) = 1.96 TeV

Data collected by the D0 detector at a p-pbar center-of-mass energy of 1.96 TeV at the Fermilab Tevatron Collider have been used to search for pair production of the lightest supersymmetric partner of the top quark decaying into $b \ell \tilde{\nu}$. The search is performed in the $\ell\ell' = e\mu$ and $\mu \mu$ final states. No evidence for this process has been found in data samples of approximately 400 pb^-1. The domain in the [$M(\tilde{t}_1),M(\tilde{\nu})$] plane excluded at the 95% C.L. is substantially extended by this search.Comment: 9 pages, 11 figures. Selection-cut layouts slightly different than in PL

Integral analysis of p53 and its value as prognostic factor in sporadic colon cancer

Molecular tumour pathology - and tumour genetic

Increased frequency of 20q gain and copy-neutral loss of heterozygosity in mismatch repair proficient familial colorectal carcinomas

Many hereditary nonpolyposis colorectal cancers (CRCs) cannot be explained by Lynch syndrome. Other high penetrance genetic risk factors are likely to play a role in these mismatch repair (MMR)-proficient CRC families. Because genomic profiles of CRC tend to vary with CRC susceptibility syndromes, our aim is to analyze the genomic profile of MMR-proficient familial CRC to obtain insight into the biological basis of MMR-proficient familial CRC. We studied 30 MMR-proficient familial colorectal carcinomas, from 15 families, for genomic aberrations, including gains, physical losses, and copy-neutral loss of heterozygosity LOH (cnLOH) using SNP array comparative genomic hybridization. In addition, we performed somatic mutation analysis for KRAS, BRAF, PIK3CA and GNAS. The frequency of 20q gain (77%) is remarkably increased when compared with sporadic CRC, suggesting that 20q gain is involved in tumor progression of familial CRC. There is also a significant increase in the frequency of cnLOH and, as a consequence, a reduced frequency of physical loss compared with sporadic CRC. The most frequent aberrations observed included gains of 7p, 7q, 8q, 13q, 20p and 20q as well as physical losses of 17p, 18p and 18q. Most of these changes are also observed in sporadic CRC. Mutations in KRAS were identified in 37% of the MMR-proficient CRCs, and mutations in BRAF were identified in 16%. No mutations were identified in PIK3CA or chromosome 20 candidate gene GNAS. We show that the patterns of chromosomal instability of MMR-proficient familial CRC are clearly distinct from those from sporadic CRC. Both the increased gain on chromosome 20 and the increased levels of cnLOH suggest the presence of yet undiscovered germline defects that can, in part, underlie the cancer risk in these families.Molecular tumour pathology - and tumour genetic