Chromo-polarizability and pipi final state interaction

The chromo-polarizability of a quarkonium state is a measure of the amplitude of the $E1$-$E1$ chromo-electric interaction of the quarkonium with soft gluon fields and can be measured in the heavy quarkonium decays. Based on the chiral unitary approach, formulas with modification caused by the $S$ wave $\pi\pi$ final state interaction (FSI) for measuring the chromo-polarizabilities are given. It is shown that the effect of the $S$ wave $\pi\pi$ FSI is very important in extracting chromo-polarizabilities from the experimental data. The resultant values with the FSI are reduced to about 1/3 of those determined without the FSI. The consequences of the FSI correction in the $J/\psi$-nucleon scattering near the threshold are also discussed. The estimated lower bound of the total cross section is reduced from about 17 mb to 2.9 mb, which agrees with the experimental data point and is compatible with the previously estimated values in the literature. In order to understand the interaction of heavy quarkonia with light hadrons at low energies better and to obtain the chromo-polarizabilities of quarkonia accurately, more data should be accumulated. This can be done in the $J/\psi \to \pi^+\pi^-l^+l^-$ decay at BES-III and CLEO-c and in the $\Upsilon \to \pi^+\pi^-l^+l^-$ decay at B factories.Comment: 5 pages, 3 figures, ReVTeX4. Version accepted for publication in Phys. Rev.

Src-homology 2 domain-containing tyrosine phosphatase 2 promotes oral cancer invasion and metastasis

BACKGROUND: Tumor invasion and metastasis represent a major unsolved problem in cancer pathogenesis. Recent studies have indicated the involvement of Src-homology 2 domain-containing tyrosine phosphatase 2 (SHP2) in multiple malignancies; however, the role of SHP2 in oral cancer progression has yet to be elucidated. We propose that SHP2 is involved in the progression of oral cancer toward metastasis. METHODS: SHP2 expression was evaluated in paired oral cancer tissues by using immunohistochemical staining and real-time reverse transcription polymerase chain reaction. Isogenic highly invasive oral cancer cell lines from their respective low invasive parental lines were established using a Boyden chamber assay, and changes in the hallmarks of the epithelial-mesenchymal transition (EMT) were assessed to evaluate SHP2 function. SHP2 activity in oral cancer cells was reduced using si-RNA knockdown or enforced expression of a catalytically deficient mutant to analyze migratory and invasive ability in vitro and metastasis toward the lung in mice in vivo. RESULTS: We observed the significant upregulation of SHP2 in oral cancer tissues and cell lines. Following SHP2 knockdown, the oral cancer cells markedly attenuated migratory and invasion ability. We observed similar results in phosphatase-dead SHP2 C459S mutant expressing cells. Enhanced invasiveness was associated with significant upregulation of E-cadherin, vimentin, Snail/Twist1, and matrix metalloproteinase-2 in the highly invasive clones. In addition, we determined that SHP2 activity is required for the downregulation of phosphorylated ERK1/2, which modulates the downstream effectors, Snail and Twist1 at a transcript level. In lung tissue sections of mice, we observed that HSC3 tumors with SHP2 deletion exhibited significantly reduced metastatic capacity, compared with tumors administered control si-RNA. CONCLUSIONS: Our data suggest that SHP2 promotes the invasion and metastasis of oral cancer cells. These results provide a rationale for further investigating the effects of small-molecule SHP2 inhibitors on the progression of oral cancer, and indicate a previously unrecognized SHP2-ERK1/2-Snail/Twist1 pathway that is likely to play a crucial role in oral cancer invasion and metastasis

Persistent termini of 2004- and 2005-like ruptures of the Sunda megathrust

To gain insight into the longevity of subduction zone segmentation, we use coral microatolls to examine an 1100-year record of large earthquakes across the boundary of the great 2004 and 2005 Sunda megathrust ruptures. Simeulue, a 100-km-long island off the west coast of northern Sumatra, Indonesia, straddles this boundary: northern Simeulue was uplifted in the 2004 earthquake, whereas southern Simeulue rose in 2005. Northern Simeulue corals reveal that predecessors of the 2004 earthquake occurred in the 10th century AD, in AD 1394 ± 2, and in AD 1450 ± 3. Corals from southern Simeulue indicate that none of the major uplifts inferred on northern Simeulue in the past 1100 years extended to southern Simeulue. The two largest uplifts recognized at a south-central Simeulue site—around AD 1422 and in 2005—involved little or no uplift of northern Simeulue. The distribution of uplift and strong shaking during a historical earthquake in 1861 suggests the 1861 rupture area was also restricted to south of central Simeulue, as in 2005. The strikingly different histories of the two adjacent patches demonstrate that this boundary has persisted as an impediment to rupture through at least seven earthquakes in the past 1100 years. This implies that the rupture lengths, and hence sizes, of at least some future great earthquakes and tsunamis can be forecast. These microatolls also provide insight into megathrust behavior between earthquakes, revealing sudden and substantial changes in interseismic strain accumulation rates