Effect of entanglement on the decay dynamics of a pair of H(2p) atoms due to spontaneous emission

We have measured the coincidence time spectra of two Lyman-α photons emitted by a pair of H(2p) atoms in the photodissociation of H2 at the incident photon energy of 33.66 eV and at the hydrogen gas pressures of 0.40 and 0.02 Pa. The decay time constant at 0.02 Pa is approximately half the lifetime of a single H(2p) atom, 1.60 ns, while the decay time constant at 0.40 Pa is in agreement with the lifetime of a single H(2p) atom. It turns out that the decay faster than the lifetime of a single H(2p) atom originates from the entanglement in the pair of H(2p) atoms. We have demonstrated an effect of entanglement on atomic decayThe experiment was carried out under the approval of Photon Factory Program Advisory Committee for Proposal No. 2008G107. This work was partially supported by Grants- in-Aid for Scientific Research (C) (No. 19550011 and No. 22550008) from the Japan Society for the Promotion of Science. T.T. wishes to acknowledge the financial support by a Sasakawa Scientific Research Grant from the Japan Science Society, T.O. that of the Matsuo Foundation and Reimei Research Promotion Project of the Japan Atomic Energy Agency, and N.K. that of Research Foundation for Opto-Science and Technology. The authors are grateful to Dr. Kouichi Hosaka of the Department of Chemistry, Tokyo Institute of Technology, Dr. Atsushi Ichimura of the Institute of Space and Astronautical Science, JAXA, and Dr. James Harries of JAEA/SPring-8 for their fruitful discussions

Radiation-Induced Degradation Mechanism of X-ray SOI Pixel Sensors with Pinned Depleted Diode Structure

The X-ray Silicon-On-Insulator (SOI) pixel sensor named XRPIX has been developed for the future X-ray astronomical satellite FORCE. XRPIX is capable of a wide-band X-ray imaging spectroscopy from below 1 keV to a few tens of keV with a good timing resolution of a few tens of $\mu$s. However, it had a major issue with its radiation tolerance to the total ionizing dose (TID) effect because of its thick buried oxide layer due to the SOI structure. Although new device structures introducing pinned depleted diodes dramatically improved radiation tolerance, it remained unknown how radiation effects degrade the sensor performance. Thus, this paper reports the results of a study of the degradation mechanism of XRPIX due to radiation using device simulations. In particular, mechanisms of increases in dark current and readout noise are investigated by simulation, taking into account the positive charge accumulation in the oxide layer and the increase in the surface recombination velocity at the interface between the sensor layer and the oxide layer. As a result, it is found that the depletion of the buried p-well at the interface increases the dark current, and that the increase in the sense-node capacitance increases the readout noise.Comment: 7 pages, 10 figures, accepted for publication in IEEE-TN

Seropositivity of a blood recipient from a donor with positive adult T-cell leukemia-associated antigens.

A blood recipient, aged 66, was found to have positive adult T-cell leukemia-associated antigens (ATLA), approximately half a year after a transfusion. The donor's ATLA-antibody titer was 1: 640. Routine screening of blood donors for ATLA antibody was proposed.</p

Adult T-cell leukemia occurring in mother and son.

We report two cases of adult T-cell leukemia in which the disease developed in a mother, aged 62 years, and her son, aged 41 years, less than four months apart. Both mother and son showed abnormal karyotypes and high titers of adult T-cell leukemia-associated antibody.</p

Comparative study of fission product release of homogeneous and heterogeneous high-burn up MOX fuel by Knudsen Effusion Mass Spectrometry supported by EPMA, SEM/TEM and thermal diffusivity investigations

publishedVersio

Analysis of the anti-tumor mechanism of BRD4 inhibition in hepatocellular carcinoma

Bromodomain and extra terminal (BET) family proteins, which include BRD4, are readers of histone acetyl-lysines and key regulators of gene transcription. BRD4 inhibitors exert anti-tumor effects in various cancers, including hepatocellular carcinoma (HCC). We investigated the mechanism underlying the antitumor effects of BRD4 inhibition in HCC. We first tested the effects of the BRD4 inhibitor JQ1 in a series of 9 HCC cell lines and found that it strongly suppressed HCC cell proliferation by inducing cell cycle arrest and apoptosis. Gene expression microarray analysis revealed that JQ1 also induced marked changes in the gene expression profiles of HCC cells, and genes associated with cell cycle and apoptosis were significantly enriched among the affected genes. Notably, a number of cancer-related genes, including BCAT1, DDR1, GDF15, FANCD2, SENP1 and TYRO3, were strongly suppressed by JQ1 in HCC cells. We also confirmed BRD4 bound within the promoter regions of these genes, which suggests they are targets of BRD4 in HCC cells. JQ1 thus appears to exert its anti-tumor effects in HCC by suppressing multiple BRD4 target genes

Growth modes of InN (000-1) on GaN buffer layers on sapphire

In this work, using atomic force microscopy and scanning tunneling microscopy, we study the surface morphologies of epitaxial InN films grown by plasma-assisted molecular beam epitaxy with intervening GaN buffer layers on sapphire substrates. On smooth GaN buffer layers, nucleation and evolution of three-dimensional InN islands at various coverages and growth temperatures are investigated. The shapes of the InN islands are observed to be predominantly mesa-like with large flat (000-1) tops, which suggests a possible role of indium as a surfactant. Rough GaN buffer layers composed of dense small GaN islands are found to significantly improve uniform InN wetting of the substrates, on which atomically smooth InN films are obtained that show the characteristics of step-flow growth. Scanning tunneling microscopy imaging reveals the defect-mediated surface morphology of smooth InN films, including surface terminations of screw dislocations and a high density of shallow surface pits with depths less than 0.3 nm. The mechanisms of the three-dimensional island size and shape evolution and formation of defects on smooth surfaces are considered

Recurrent advanced colonic cancer occurring 11 years after initial endoscopic piecemeal resection: a case report

<p>Abstract</p> <p>Background</p> <p>The high frequency of local recurrence occurring after endoscopic piecemeal resection (EPMR) for large colorectal tumors is a serious problem. However, almost all of these cases of local recurrence can be detected within 1 year and cured by additional endoscopic resection. We report a rare case of recurrent advanced colonic cancer diagnosed 11 years after initial EPMR treatment.</p> <p>Case presentation</p> <p>A 65-year-old male was diagnosed with a sigmoid colon lesion following a routine health check-up. Total colonoscopy revealed a 12 mm type 0-Is lesion in the sigmoid colon, which was diagnosed as an adenoma or intramucosal cancer and treated by EPMR in 1996. The post-resection defect was closed completely using metallic endoclips to avoid delayed bleeding. In 2007, at the third follow up, colonoscopy revealed a 20 mm submucosal tumor (SMT) like recurrence at the site of the previous EPMR. The recurrent lesion was treated by laparoscopic assisted sigmoidectomy with lymph node dissection.</p> <p>Conclusion</p> <p>When it is difficult to evaluate the depth and margins of resected tumors following EPMR, it is important that the defect is not closed in order to avoid tumor implantation, missing residual lesions and to enable earlier detection of recurrence. It is crucial that the optimal follow-up protocol for EPMR cases is clarified, particularly how often and for how long they should be followed.</p

Periostin is essential for cardiac healingafter acute myocardial infarction

Acute myocardial infarction (AMI) is a common and lethal heart disease, and the recruitment of fibroblastic cells to the infarct region is essential for the cardiac healing process. Although stiffness of the extracellular matrix in the infarct myocardium is associated with cardiac healing, the molecular mechanism of cardiac healing is not fully understood. We show that periostin, which is a matricellular protein, is important for the cardiac healing process after AMI. The expression of periostin protein was abundant in the infarct border of human and mouse hearts with AMI. We generated periostin−/− mice and found no morphologically abnormal cardiomyocyte phenotypes; however, after AMI, cardiac healing was impaired in these mice, resulting in cardiac rupture as a consequence of reduced myocardial stiffness caused by a reduced number of α smooth muscle actin–positive cells, impaired collagen fibril formation, and decreased phosphorylation of FAK. These phenotypes were rescued by gene transfer of a spliced form of periostin. Moreover, the inhibition of FAK or αv-integrin, which blocked the periostin-promoted cell migration, revealed that αv-integrin, FAK, and Akt are involved in periostin signaling. Our novel findings show the effects of periostin on recruitment of activated fibroblasts through FAK-integrin signaling and on their collagen fibril formation specific to healing after AMI