226 research outputs found
Search for {\eta}'(958)-nucleus bound states by (p,d) reaction at GSI and FAIR
The mass of the {\eta}' meson is theoretically expected to be reduced at
finite density, which indicates the existence of {\eta}'-nucleus bound states.
To investigate these states, we perform missing-mass spectroscopy for the (p,
d) reaction near the {\eta}' production threshold. The overview of the
experimental situation is given and the current status is discussed.Comment: 6 pages, 3 figures; talk at II Symposium on applied nuclear physics
and innovative technologies, September 24th - 27th, 2014, Jagiellonian
University, Krak\'ow Poland; to appear in Acta Physica Polonica
Spectroscopy of -nucleus bound states at GSI and FAIR --- very preliminary results and future prospects ---
The possible existence of \eta'-nucleus bound states has been put forward
through theoretical and experimental studies. It is strongly related to the
\eta' mass at finite density, which is expected to be reduced because of the
interplay between the anomaly and partial restoration of chiral
symmetry. The investigation of the C(p,d) reaction at GSI and FAIR, as well as
an overview of the experimental program at GSI and future plans at FAIR are
discussed.Comment: 7 pages, 3 figures; talk at the International Conference on Exotic
Atoms and Related Topics (EXA2014), Vienna, Austria, 15-19 September 2014. in
Hyperfine Interactions (2015
Observation of Lambda H-4 hyperhydrogen by decay-pion spectroscopy in electron scattering
At the Mainz Microtron MAMI, the first high-resolution pion spectroscopy from
decays of strange systems was performed by electron scattering off a Be-9
target in order to study the ground-state masses of Lambda-hypernuclei.
Positively charged kaons were detected by a short-orbit spectrometer with a
broad momentum acceptance at zero degree forward angles with respect to the
beam, efficiently tagging the production of strangeness in the target nucleus.
In coincidence, negatively charged decay-pions were detected by two independent
high-resolution spectrometers. About 10^3 pionic weak decays of hyperfragments
and hyperons were observed. The pion momentum distribution shows a
monochromatic peak at p_pi ~ 133 MeV/c, corresponding to the unique signature
for the two-body decay of hyperhydrogen Lambda H-4 -> He-4 + pi-, stopped
inside the target. Its binding energy was determined to be B_Lambda = 2.12 +-
0.01 (stat.) +- 0.09 (syst.) MeV with respect to the H-3 + Lambda mass
Genotoxic agents promote the nuclear accumulation of annexin A2: role of annexin A2 in mitigating DNA damage
Annexin A2 is an abundant cellular protein that is mainly localized in the cytoplasm and plasma membrane, however a small population has been found in the nucleus, suggesting a nuclear function for the protein. Annexin A2 possesses a nuclear export sequence (NES) and inhibition of the NES is sufficient to cause nuclear accumulation. Here we show that annexin A2 accumulates in the nucleus in response to genotoxic agents including gamma-radiation, UV radiation, etoposide and chromium VI and that this event is mediated by the nuclear export sequence of annexin A2. Nuclear accumulation of annexin A2 is blocked by the antioxidant agent N-acetyl cysteine (NAC) and stimulated by hydrogen peroxide (H2O2), suggesting that this is a reactive oxygen species dependent event. In response to genotoxic agents, cells depleted of annexin A2 show enhanced phospho-histone H2AX and p53 levels, increased numbers of p53-binding protein 1 nuclear foci and increased levels of nuclear 8-oxo-2'-deoxyguanine, suggesting that annexin A2 plays a role in protecting DNA from damage. This is the first report showing the nuclear translocation of annexin A2 in response to genotoxic agents and its role in mitigating DNA damage.Natural Sciences and Engineering Research Council of Canada (NSERC); European Union [PCOFUND-GA-2009-246542]; Foundation for Science and Technology of Portugal; Beatrice Hunter Cancer Research Institute; Terry Fox Foundationinfo:eu-repo/semantics/publishedVersio
Exclusive electroproduction of K+ Lambda and K+ Sigma^0 final states at Q^2 = 0.030-0.055 (GeV/c)^2
Cross section measurements of the exclusive p(e,e'K+)Lambda,Sigma^0
electroproduction reactions have been performed at the Mainz Microtron MAMI in
the A1 spectrometer facility using for the first time the Kaos spectrometer for
kaon detection. These processes were studied in a kinematical region not
covered by any previous experiment. The nucleon was probed in its third
resonance region with virtual photons of low four-momenta, Q^2= 0.030-0.055
(GeV/c)^2. The MAMI data indicate a smooth transition in Q^2 from
photoproduction to electroproduction cross sections. Comparison with
predictions of effective Lagrangian models based on the isobar approach reveal
that strong longitudinal couplings of the virtual photon to the N* resonances
can be excluded from these models.Comment: 16 pages, 7 figure
TP53-binding protein variants and breast cancer risk: a case-control study
INTRODUCTION: The TP53-binding protein (53BP1) has been shown to influence TP53-mediated transcriptional activation, thus playing a pivotal role in DNA damage signalling. Genetic aberrations in TP53 and in ATM and CHEK2 predispose to cancer. We have therefore examined the effects of 53BP1 single nucleotide polymorphisms (D353E, G412S, and K1136Q) and the novel 53BP1 6bp deletion (1347_1352delTATCCC) on breast cancer risk. METHODS: Allelic discrimination was performed to investigate the frequencies of 53BP1 D353E, G412S, and K1136Q and of 1347_1352delTATCCC in 353 patients with breast cancer and 960 control individuals. RESULTS: No significant association of 53BP1 D353E, G412S, or K1136Q with breast cancer risk was detected. 53BP1 1347_1352delTATCCC, leading to the loss of an isoleucine and a proline residue, showed a nonsignificant inverse association with breast cancer risk (odds ratio = 0.61, 95% confidence interval = 0.22 to 1.68, P = 0.34). CONCLUSION: The lack of association casts doubt on the putative effects of D353E, G412S, and K1136Q on breast cancer risk. Investigating a larger study cohort might elucidate the influence of the 6bp deletion 1347_1352delTATCCC. Studying the functional effect and the impact of this variant on the risk of other cancers may be revealing
Dysregulation of Gene Expression in the Artificial Human Trisomy Cells of Chromosome 8 Associated with Transformed Cell Phenotypes
A change in chromosome number, known as aneuploidy, is a common characteristic of cancer. Aneuploidy disrupts gene expression in human cancer cells and immortalized human epithelial cells, but not in normal human cells. However, the relationship between aneuploidy and cancer remains unclear. To study the effects of aneuploidy in normal human cells, we generated artificial cells of human primary fibroblast having three chromosome 8 (trisomy 8 cells) by using microcell-mediated chromosome transfer technique. In addition to decreased proliferation, the trisomy 8 cells lost contact inhibition and reproliferated after exhibiting senescence-like characteristics that are typical of transformed cells. Furthermore, the trisomy 8 cells exhibited chromosome instability, and the overall gene expression profile based on microarray analyses was significantly different from that of diploid human primary fibroblasts. Our data suggest that aneuploidy, even a single chromosome gain, can be introduced into normal human cells and causes, in some cases, a partial cancer phenotype due to a disruption in overall gene expression
The Role of p300 Histone Acetyltransferase in UV-Induced Histone Modifications and MMP-1 Gene Transcription
Matrix metalloproteinase (MMP)-1 promotes ultraviolet (UV)-triggered long-term detrimental effects such as cancer formation and premature skin aging. Although histone modifications may play a crucial role in the transcriptional regulation of MMP-1, the relationship between UV-induced histone modification and MMP-1 expression is not completely understood. Here, we identify regulators of histone acetylation that may link UV-mediated DNA damage and MMP-1 induction by UV in cultured human dermal fibroblasts (HDFs) in vitro. UV irradiation of HDFs induced MMP-1 expression and increased the level of phosphorylation of H2AX (γ-H2AX), p53 and the acetylation of histone H3 (acetyl-H3). Total histone deacetylase (HDAC) enzymatic activity was decreased by UV irradiation, while histone acetyltransferase (HAT) activity was increased. Suppression of p300 histone acetyltransferase (p300HAT) activity by the p300HAT inhibitor anacardic acid (AA) or by down-regulation of p300 by siRNA prevented UV-induced MMP-1 expression and inhibited UV-enhanced γ-H2AX, p53 level, and acetyl-H3. Using chromatin immunoprecipitation assays, we observed that γ-H2AX, p53, acetyl-H3, p300 and c-Jun were consistently recruited by UV to a distinct region (−2067/−1768) adjacent to the p300 binding site (−1858/−1845) in the MMP-1 promoter. In addition, these recruitments of γ-H2AX, p53, acetyl-H3, p300 and c-Jun to the p300-2 site were significantly abrogated by post-treatment with AA. Furthermore, overexpression of p300 increased the basal and UV-induced MMP-1 promoter activity. Our results suggest that p300HAT plays a critical role in the transcriptional regulation of MMP-1 by UV
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