DAMA/LIBRA results and perspectives

The DAMA/LIBRA experiment, running at the Gran Sasso National Laboratory of the I.N.F.N. in Italy, has a sensitive mass of about 250 kg highly radiopure NaI(Tl). It is mainly devoted to the investigation of Dark Matter (DM) particles in the Galactic halo by exploiting the model independent DM annual modulation signature. The present DAMA/LIBRA experiment and the former DAMA/NaI one (the first generation experiment having an exposed mass of about 100 kg) have released so far results corresponding to a total exposure of 1.17 ton yr over 13 annual cycles. They provide a model independent evidence of the presence of DM particles in the galactic halo at 8.9 sigma C.L.. A short summary of the obtained results is presented and future perspectives of the experiment mentioned.Comment: 12 pages, Proceed. of the 15th Bled Workshop "What Comes Beyond Standard Models" (December 2012), Vol. 13, No.

High-sensitivity fiber-tip pressure sensor with graphene diaphragm

Author name used in this publication: Ji Yan Dai2011-2012 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Frequency Shift of Carbon-Nanotube-Based Mass Sensor Using Nonlocal Elasticity Theory

The frequency equation of carbon-nanotube-based cantilever sensor with an attached mass is derived analytically using nonlocal elasticity theory. According to the equation, the relationship between the frequency shift of the sensor and the attached mass can be obtained. When the nonlocal effect is not taken into account, the variation of frequency shift with the attached mass on the sensor is compared with the previous study. According to this study, the result shows that the frequency shift of the sensor increases with increasing the attached mass. When the attached mass is small compared with that of the sensor, the nonlocal effect is obvious and increasing nonlocal parameter decreases the frequency shift of the sensor. In addition, when the location of the attached mass is closer to the free end, the frequency shift is more significant and that makes the sensor reveal more sensitive. When the attached mass is small, a high sensitivity is obtained

Self-Organized Ni Nanocrystal Embedded in BaTiO3 Epitaxial Film

Ni nanocrystals (NCs) were embedded in BaTiO3 epitaxial films using the laser molecular beam epitaxy. The processes involving the self-organization of Ni NCs and the epitaxial growth of BaTiO3 were discussed. With the in situ monitoring of reflection high-energy electron diffraction, the nanocomposite films were engineered controllably by the fine alternation of the self-organization of Ni NCs and the epitaxial growth of BaTiO3. The transmission electron microscopy and the X-ray diffraction characterization confirmed that the composite film consists of the Ni NCs layers alternating with the (001)/(100)-oriented epitaxial BaTiO3 separation layers

NF-κB p65 Subunit Is Modulated by Latent Transforming Growth Factor-β Binding Protein 2 (LTBP2) in Nasopharyngeal Carcinoma HONE1 and HK1 Cells

NF-kappa B is a well-characterized transcription factor, widely known as a key player in tumor-derived inflammation and cancer development. Herein, we present the functional and molecular relevance of the canonical NF-kappa B p65 subunit in nasopharyngeal carcinoma (NPC). Loss-and gain-of-function approaches were utilized to reveal the functional characteristics of p65 in propagating tumor growth, tumor-associated angiogenesis, and epithelial-to-mesenchymal transition in NPC cells. Extracellular inflammatory stimuli are critical factors that trigger the NF-kappa B p65 signaling; hence, we investigated the components of the tumor microenvironment that might potentially influence the p65 signaling pathway. This led to the identification of an extracellular matrix (ECM) protein that was previously reported as a candidate tumor suppressor in NPC. Our studies on the Latent Transforming Growth Factor-beta Binding Protein 2 (LTBP2) protein provides substantial evidence that it can modulate the p65 transcriptional activity. Re-expression of LTBP2 elicits tumor suppressive effects that parallel the inactivation of p65 in NPC cells. LTBP2 was able to reduce phosphorylation of p65 at Serine 536, inhibit nuclear localization of active phosphorylated p65, and impair the p65 DNA-binding ability. This results in a consequential down-regulation of p65-related gene expression. Therefore, the data suggest that the overall up-regulation of p65 expression and the loss of this candidate ECM tumor suppressor are milestone events contributing to NPC development.published_or_final_versio

Nuclear Localization of DNAJB6 is Associated with Survival of Patients with Esophageal Cancer and Reduces AKT Signaling and Proliferation of Cancer Cells

Abstract BACKGROUND & AIMS: The DnaJ (Hsp40) homolog, subfamily B, member 6 (DNAJB6) is part of a family of proteins that regulate chaperone activities. One of its isoforms, DNAJB6a, contains a nuclear localization signal and regulates β-catenin signaling during breast cancer development. We investigated the role of DNAJB6 in pathogenesis of esophageal squamous cell carcinoma (ESCC). METHODS: We performed immunohistochemical analyses of primary ESCC samples and lymph node metastases from a cohort of 160 patients, who underwent esophagectomy with no pre-operative chemo-radiotherapy at Hong Kong Queen Mary Hospital. Data were collected on patient outcomes over a median time of 12.1±2.9 months. Retrospective survival association analyses were performed. Wild-type and mutant forms of DNAJB6a were overexpressed in cancer cell lines (KYSE510, KYSE 30TSI, KYSE140, and KYSE70TS), which were analyzed in proliferation and immunoblot assays, or injected subcutaneously into nude mice. Levels of DNAJB6 were knocked down in ESCC cell lines (KYSE450 and T.Tn), immortalized normal esophageal epithelial cell lines (NE3 and NE083), and other cells with short hairpin RNAs or by genome engineering. Bimolecular fluorescence complementation was used to study interactions between proteins in living cells. RESULTS: In primary ESCC samples, patients whose tumors had high nuclear levels of DNAJB6 had longer overall survival times (19.2±1.8 months; 95% confidence interval [CI], 15.6-22.8 months) than patients whose tumors had low nuclear levels of DNAJB6 (12.6±1.4 months; 95% CI, 9.8-15.4 months; P=.004, by log rank test). Based on Cox regression analysis, patients whose tumors had high nuclear levels of DNAJB6 had a lower risk of death than those with low levels (hazard ratio=0.562; 95% CI, 0.379-0.834; P=.004). Based on log rank analysis and Cox regression analysis, the combination of nuclear level of DNAJB6 and the presence of lymph node metastases at diagnosis could be used to stratify patients into groups with good or bad outcomes (P<.0005 for both analyses). There was a negative association between the nuclear level of DNAJB6 and the presence of lymph node metastases (P=.022; Pearson χ2 test). Cancer cell lines that overexpressed DNAJB6a formed tumors more slowly in nude mice than control cells or cells that expressed a mutant form of DNAJB6a that did not localize to the nucleus. DNAJB6 knockdown in cancer cell lines promoted their growth as xenograft tumors in mice. A motif of histidine, proline, and aspartic acid (HPD) in the J domain of DNAJB6a was required for its tumor suppressive effects and signaling via AKT1. Loss of DNAJB6a resulted in upregulation of AKT signaling in cancer cell lines and immortalized esophageal epithelial cells. Expression of a constitutively active form of AKT1 restored proliferation to tumor cells that overexpressed DNAJB6a, and DNAJB6a formed a complex with AKT1 in living cells. Expression of DNAJB6a reduced the sensitivity of ESCC to AKT inhibitors; the expression level of DNAJB6a affected AKT signaling in multiple cancer cell lines. CONCLUSIONS: Nuclear localization of DNAJB6 is associated with longer survival times of patients with ESCC. DNAJB6a reduces AKT signaling, and DNAJB6 expression in cancer cells reduces their proliferation and growth of xenograft tumors in mice. DNAJB6a might be developed as biomarker for progression of ESCC.postprin

Resonances in J/ψ→ϕπ+π−J/\psi \to \phi \pi ^+\pi ^- and ϕK+K−\phi K^+K^-

A partial wave analysis is presented of $J/\psi \to \phi \pi ^+\pi ^-$ and $\phi K^+K^-$ from a sample of 58M $J/\psi$ events in the BES II detector. The $f_0(980)$ is observed clearly in both sets of data, and parameters of the Flatt\' e formula are determined accurately: $M = 965 \pm 8$ (stat) $\pm 6$ (syst) MeV/c$^2$, $g_1 = 165 \pm 10 \pm 15$ MeV/c$^2$, $g_2/g_1 = 4.21 \pm 0.25 \pm 0.21$. The $\phi \pi \pi$ data also exhibit a strong $\pi \pi$ peak centred at $M = 1335$ MeV/c$^2$. It may be fitted with $f_2(1270)$ and a dominant $0^+$ signal made from $f_0(1370)$ interfering with a smaller $f_0(1500)$ component. There is evidence that the $f_0(1370)$ signal is resonant, from interference with $f_2(1270)$. There is also a state in $\pi \pi$ with $M = 1790 ^{+40}_{-30}$ MeV/c$^2$ and $\Gamma = 270 ^{+60}_{-30}$ MeV/c$^2$; spin 0 is preferred over spin 2. This state, $f_0(1790)$, is distinct from $f_0(1710)$. The $\phi K\bar K$ data contain a strong peak due to $f_2'(1525)$. A shoulder on its upper side may be fitted by interference between $f_0(1500)$ and $f_0(1710)$.Comment: 17 pages, 6 figures, 1 table. Submitted to Phys. Lett.

Measurement of the Branching Fraction of J/psi --> pi+ pi- pi0

Using 58 million J/psi and 14 million psi' decays obtained by the BESII experiment, the branching fraction of J/psi --> pi+ pi- pi0 is determined. The result is (2.10+/-0.12)X10^{-2}, which is significantly higher than previous measurements.Comment: 9 pages, 8 figures, RevTex

Search for K_S K_L in psi'' decays

K_S K_L from psi'' decays is searched for using the psi'' data collected by BESII at BEPC, the upper limit of the branching fraction is determined to be B(psi''--> K_S K_L) < 2.1\times 10^{-4} at 90% C. L. The measurement is compared with the prediction of the S- and D-wave mixing model of the charmonia, based on the measurements of the branching fractions of J/psi-->K_S K_L and psi'-->K_S K_L.Comment: 5 pages, 1 figur

First Measurements of eta_c Decaying into K^+K^-2(pi^+pi^-) and 3(pi^+pi^-)

The decays of eta_c to K^+K^-2(pi^+pi^-) and 3(pi^+pi^-) are observed for the first time using a sample of 5.8X10^7 J/\psi events collected by the BESII detector. The product branching fractions are determined to be B(J/\psi-->gamma eta_c)*B(eta_c-->K^+K^-pi^+pi^-pi^+pi^-)=(1.21+-0.32+- 0.23)X10^{-4}$,B(J/\psi-->gamma eta_c)*B(eta_c-->K^{*0}\bar{K}^{*0}pi^+pi^-)= (1.29+-0.43+-0.32)X10^{-4}$, and (J/\psi-->gamma eta_c)* B(eta_c-->pi^+pi^-pi^+pi^-pi^+pi^-)= (2.59+-0.32+-0.48)X10^{-4}. The upper limit for eta_c-->phi pi^+pi^-pi^+pi^- is also obtained as B(J/\psi-->gamma eta_c)*B(eta_c--> phi pi^+pi^-pi^+pi^-)< 6.03 X10^{-5} at the 90% confidence level.Comment: 11 pages, 4 figure