Chiral charge-density-waves

We discovered the chirality of charge density waves (CDW) in 1T-TiSe$_2$ by using scanning tunnelling microscopy (STM) and optical ellipsometry. We found that the CDW intensity becomes $I{a_1}:I{a_2}:I{a_3} = 1:0.7 \pm 0.1:0.5 \pm 0.1$, where $Ia_i$ (i =1, 2, 3) is the amplitude of the tunnelling current contributed by the CDWs. There were two states, in which the three intensity peaks of the CDW decrease \textit{clockwise} and \textit{anticlockwise} when we index each nesting vector in order of intensity in the Fourier transformation of the STM images. The chirality in CDW results in the three-fold symmetry breaking. Macroscopically, two-fold symmetry was indeed observed in optical measurement. We propose the new generalized CDW chirality H_{CDW} \equiv {\boldmath q_1} \cdot ({\boldmath q_2}\times {\boldmath q_3}), where {\boldmath q_i} are the nesting vectors, which is independent of the symmetry of components. The nonzero $H_{CDW}$ - the triple-{\boldmath q} vectors do not exist in an identical plane in the reciprocal space - should induce a real-space chirality in CDW system.Comment: 12 pages, 4 figure

CANGAROO-III Observation of TeV Gamma Rays from the vicinity of PSR B1 706-44

Observation by the CANGAROO-III stereoscopic system of the Imaging Cherenkov Telescope has detected extended emission of TeV gamma rays in the vicinity of the pulsar PSR B1706$-$44. The strength of the signal observed as gamma-ray-like events varies when we apply different ways of emulating background events. The reason for such uncertainties is argued in relevance to gamma-rays embedded in the "off-source data", that is, unknown sources and diffuse emission in the Galactic plane, namely, the existence of a complex structure of TeV gamma-ray emission around PSR B1706$-$44.Comment: 10 pages, 13 figures, to be published in Ap

CANGAROO-III observation of TeV gamma rays from the unidentified gamma-ray source HESS J1614-518

We report the detection, with the CANGAROO-III imaging atmospheric Cherenkov telescope array, of a very high energy gamma-ray signal from the unidentified gamma-ray source HESS J1614-518, which was discovered in the H.E.S.S. Galactic plane survey. Diffuse gamma-ray emission was detected above 760 GeV at the 8.9 sigma level during an effective exposure of 54 hr from 2008 May to August. The spectrum can be represented by a power-law: 8.2+-2.2_{stat}+-2.5_{sys}x10^{-12}x (E/1TeV)^{-Gamma} cm^{-2} s^{-1} TeV^{-1} with a photon index Gamma of 2.4+-0.3_{stat}+-0.2_{sys}, which is compatible with that of the H.E.S.S. observations. By combining our result with multi-wavelength data, we discuss the possible counterparts for HESS J1614-518 and consider radiation mechanisms based on hadronic and leptonic processes for a supernova remnant, stellar winds from massive stars, and a pulsar wind nebula. Although a leptonic origin from a pulsar wind nebula driven by an unknown pulsar remains possible, hadronic-origin emission from an unknown supernova remnant is preferred.Comment: 9 pages, 7 figures, accepted for publication in Ap

Increased production of viral proteins by a 3'-LTR-deleted infectious clone of human T-cell leukemia virus type 1

We previously reported that a full-length provirus of HTLV-1 was directly constructed from the HTLV-1-transformed cell line MT-2 using overlapping polymerase chain reaction (PCR) and cloned into a plasmid vector (pFL-MT2). 293T cells transfected with pFL-MT2 alone did not produce virus particles because there was no expression of the viral transactivator protein Tax, whereas cells transfected with pFL-MT2 plus a Tax expression vector produced virus-like particles. In the process of constructing the HTLV-1 provirus by overlapping PCR, we also constructed an incomplete molecular clone, in which the 3' long terminal repeat (LTR) was replaced with the endogenous human gene, which resulted in the expression of a tax gene shorter by 43 bp. This incomplete molecular clone alone expressed Tax and produced the viral protein in transfected cells. Various clones were then constructed with different lengths of the 3' LTR and lacking the reverse-direction TATA box. The clones contained over 113 bp of the 3' LTR, with no reverse-direction TATA box, which might express the full-length tax gene, and did not produce the viral antigen. These results suggest that Tax in which the C-terminal portion is deleted is more strongly expressed than the wild-type protein and has transcriptional activity

Surgery for recurrent inflammatory pseudotumor of the lung

<p>Abstract</p> <p>Background</p> <p>Cases of recurrent inflammatory pseudotumor have only rarely been reported. The treatment for recurrent pseudotumor is surgery. Patients not eligible for surgery require different treatment, and the optimal type of the treatment is controversial.</p> <p>Case Presentation</p> <p>A 54-year-old woman was noted to have an abnormal shadow in the right middle lung field on chest X-ray. Computed tomography of the chest revealed an infiltrative lesion in the right segment 4 and a nodule in the right segment 8. She underwent right middle lobectomy and partial resection of the right segment 8. Histopathology revealed non-atypical lymphocytes and plasma cells infiltrates, leading to the diagnosis of the lymphoplasmacytic type of inflammatory pseudotumor. During postoperative follow-up, chest computed tomography revealed a nodular lesion in the left segment 3 and an infiltrative lesion in the right segment 2. Left segment 3 segmentectomy and right segment 2 wedge resection were performed. The histopathological findings were similar to those of the first surgical specimen, leading to the diagnosis of recurrent lymphoplasmacytic type of inflammatory pseudotumor.</p> <p>Conclusion</p> <p>Surgical cases of recurrent inflammatory pseudotumor of the lung have been reported only very rarely. We believe that surgery is the best treatment for recurrent inflammatory pseudotumor of the lung when patients are eligible.</p

Reconstitution of Mdm2-Dependent Post-Translational Modifications of p53 in Yeast

p53 mediates cell cycle arrest or apoptosis in response to DNA damage. Its activity is subject to a tight regulation involving a multitude of post-translational modifications. The plethora of functional protein interactions of p53 at present precludes a clear understanding of regulatory principles in the p53 signaling network. To circumvent this complexity, we studied here the minimal requirements for functionally relevant p53 post-translational modifications by expressing human p53 together with its best characterized modifier Mdm2 in budding yeast. We find that expression of the human p53-Mdm2 module in yeast is sufficient to faithfully recapitulate key aspects of p53 regulation in higher eukaryotes, such as Mdm2-dependent targeting of p53 for degradation, sumoylation at lysine 386 and further regulation of this process by p14ARF. Interestingly, sumoylation is necessary for the recruitment of p53-Mdm2 complexes to yeast nuclear bodies morphologically akin to human PML bodies. These results suggest a novel role for Mdm2 as well as for p53 sumoylation in the recruitment of p53 to nuclear bodies. The reductionist yeast model that was established and validated in this study will now allow to incrementally study simplified parts of the intricate p53 network, thus helping elucidate the core mechanisms of p53 regulation as well as test novel strategies to counteract p53 malfunctions

Attentional Set-Shifting Deficit in Parkinson’s Disease Is Associated with Prefrontal Dysfunction: An FDG-PET Study

The attentional set-shifting deficit that has been observed in Parkinson’s disease (PD) has long been considered neuropsychological evidence of the involvement of meso-prefrontal and prefrontal-striatal circuits in cognitive flexibility. However, recent studies have suggested that non-dopaminergic, posterior cortical pathologies may also contribute to this deficit. Although several neuroimaging studies have addressed this issue, the results of these studies were confounded by the use of tasks that required other cognitive processes in addition to set-shifting, such as rule learning and working memory. In this study, we attempted to identify the neural correlates of the attentional set-shifting deficit in PD using a compound letter task and 18F-fluoro-deoxy-glucose (FDG) positron emission tomography during rest. Shift cost, which is a measure of attentional set-shifting ability, was significantly correlated with hypometabolism in the right dorsolateral prefrontal cortex, including the putative human frontal eye field. Our results provide direct evidence that dysfunction in the dorsolateral prefrontal cortex makes a primary contribution to the attentional set-shifting deficit that has been observed in PD patients

Epigenetic inactivation of TCF2 in ovarian cancer and various cancer cell lines

Transcription factor 2 gene (TCF2) encodes hepatocyte nuclear factor 1β (HNF1β), a transcription factor associated with development and metabolism. Mutation of TCF2 has been observed in renal cell cancer, and by screening aberrantly methylated genes, we have now identified TCF2 as a target for epigenetic inactivation in ovarian cancer. TCF2 was methylated in 53% of ovarian cancer cell lines and 26% of primary ovarian cancers, resulting in loss of the gene's expression. TCF2 expression was restored by treating cells with a methyltransferase inhibitor, 5-aza-2′deoxycitidine (5-aza-dC). In addition, chromatin immunoprecipitation showed deacetylation of histone H3 in methylated cells and, when combined with 5-aza-dC, the histone deacetylase inhibitor trichostatin A synergistically induced TCF2 expression. Epigenetic inactivation of TCF2 was also seen in colorectal, gastric and pancreatic cell lines, suggesting general involvement of epigenetic inactivation of TCF2 in tumorigenesis. Restoration of TCF2 expression induced expression of HNF4α, a transcriptional target of HNF1β, indicating that epigenetic silencing of TCF2 leads to alteration of the hepatocyte nuclear factor network in tumours. These results suggest that TCF2 is involved in the development of ovarian cancers and may represent a useful target for their detection and treatment

First detection of the growing humps at the rapidly rising stage of dwarf novae AL Com and WZ Sge

We report on time-series photometric observations in the earliest stages of superoutbursts of the extreme dwarf novae, AL Com and WZ Sge, which started on 2001 May after the 6 years quiescence and on 2001 July after the 23 years quiescence, respectively. We detected growth of ``early superhumps'' during the each rising stage. Our observations reject the mass transfer instability for the trigger of the superoutburst of WZ Sge stars, and show the existence of some relations between the ``early superhumps'' and the spiral structure, which give a hint of the origin of the ``early superhumps.''Comment: 4 pages, 4 figures, A&A macro in latex format, accepted to A&A letter