I=2I=2 ππ\pi\pi potential in the HAL QCD method with all-to-all propagators

In this paper, we perform the first application of the hybrid method (exact low modes plus stochastically estimated high modes) for all-to-all propagators to the HAL QCD method. We calculate the HAL QCD potentials in the $I=2$ $\pi\pi$ scattering in order to see how statistical fluctuations of the potential behave under the hybrid method. All of the calculations are performed with the 2+1 flavor gauge configurations on $16^3 \times 32$ lattice at the lattice spacing $a \approx 0.12$ fm and $m_{\pi} \approx 870$ MeV. It is revealed that statistical errors for the potential are enhanced by stochastic noises introduced by the hybrid method, which, however, are shown to be reduced by increasing the level of dilutions, in particular, that of space dilutions. From systematic studies, we obtain a guiding principle for a choice of dilution types/levels and a number of eigenvectors to reduce noise contaminations to the potential while keeping numerical costs reasonable. We also confirm that we can obtain the scattering phase shifts for the $I=2$ $\pi\pi$ system by the hybrid method within a reasonable numerical cost, which are consistent with the result obtained with the conventional method. The knowledge we obtain in this study will become useful to investigate hadron resonances which require quark annihilation diagrams such as the $\rho$ meson by the HAL QCD potential with the hybrid method.Comment: 20 pages, 10 figures, published version in PTE

Structural Changes in Amorphous Pd_<80>Si_<20> by Neutron Irradiation(Metallurgy)

Amorphous Pd_Si_ was irradiated with fast neutrons ( neutrons/cm^2. X-ray scattering intensities were measured before and after the irradiation with monochromatic Cu-Kα_1 rays. Scattered intensities for s>0.4A^ (s=2sinθ/λ) proved unaffected, while intensities were found remarkably enhanced for s>0.4A^ after the irradiation, i.e., in the small-angle region and the leading edge of the first halo . The results are discussed in relation to the structural anomalies in amorphous solids

The determination of glial fibrillary acidic protein for the diagnosis and histogenetic study of central nervous system tumors: a study of 152 cases.

Glial fibrillary acidic protein (GFAP) was purified from human spinal cord and cerebral white matter. GFAP was localized by an immuno-peroxidase method in normal adult and fetal human brains, rat brains, and 152 central nervous system (CNS) tumors. GFAP was found in reactive and normal astrocytes, immature cells of fetal brain at the 18th to 21st gestational weeks, and normal rat astrocytes. This GFAP staining was quite specific for glial tumors, including astrocytomas, glioblastomas, astroblastomas, and ependymomas. GFAP-positive cells were also found in oligodendrogliomas and choroid plexus papillomas, and they were interpreted as being astroglial or ependymal differentiations. Stromal cells in cerebellar hemangioblastomas were negative. However, engulfed astrocytes were found at the periphery of such tumors and often adjacent to the proliferate blood vessels. In meningiomas, neurinomas, metastatic carcinomas, pituitary adenomas and other non-glial tumors, GFAP-positive cells were not identified.</p

Coupled channel approach to strangeness S = -2 baryon-bayron interactions in Lattice QCD

The baryon-baryon interactions with strangeness S = -2 with the flavor SU(3) breaking are calculated for the first time by using the HAL QCD method extended to coupled channel system in lattice QCD. The potential matrices are extracted from the Nambu-Bethe-Salpeter wave functions obtained by the 2+1 flavor gauge configurations of CP-PACS/JLQCD Collaborations with a physical volume of 1.93 fm cubed and with m_pi/m_K = 0.96, 0.90, 0.86. The spatial structure and the quark mass dependence of the potential matrix in the baryon basis and in the SU(3) basis are investigated.Comment: 17 pages, 15 figure

The Role of PPARs in Cancer

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that belong to the nuclear hormone receptor superfamily. PPARα is mainly expressed in the liver, where it activates fatty acid catabolism. PPARα activators have been used to treat dyslipidemia, causing a reduction in plasma triglyceride and elevation of high-density lipoprotein cholesterol. PPARδ is expressed ubiquitously and is implicated in fatty acid oxidation and keratinocyte differentiation. PPARδ activators have been proposed for the treatment of metabolic disease. PPARγ2 is expressed exclusively in adipose tissue and plays a pivotal role in adipocyte differentiation. PPARγ is involved in glucose metabolism through the improvement of insulin sensitivity and represents a potential therapeutic target of type 2 diabetes. Thus PPARs are molecular targets for the development of drugs treating metabolic syndrome. However, PPARs also play a role in the regulation of cancer cell growth. Here, we review the function of PPARs in tumor growth