The Xi(2230) Meson and The Pomeron Trajectory

We examine the possibility that the xi(2230) meson is a member of the Pomeron trajectory. A method of connecting the xi --> p pbar decay width and the pp cross sections through the Pomeron residue function is presented. We have used a relativistic, singularity-free form factor to make the analytic continuation of the residue function between crossed channels. We predict that if the xi(2230) meson is a Pomeron, then it should have a xi --> p pbar decay width of about 2 MeV.Comment: 9 page

Eigenmodes of Decay and Discrete Fragmentation Processes

Linear rate equations are used to describe the cascading decay of an initial heavy cluster into fragments. This representation is based upon a triangular matrix of transition rates. We expand the state vector of mass multiplicities, which describes the process, into the biorthonormal basis of eigenmodes provided by the triangular matrix. When the transition rates have a scaling property in terms of mass ratios at binary fragmentation vertices, we obtain solvable models with explicit mathematical properties for the eigenmodes. A suitable continuous limit provides an interpolation between the solvable models. It gives a general relationship between the decay products and the elementary transition rates.Comment: 6 pages, plain TEX, 2 figures available from the author

Pomeron and Reggeized Glueball/Sigma

It has long been believed that the Pomeron, which has been successful in phenomenological fits to high energy scattering data, is associated with gluonic exchange. By determining the Regge-nucleon vertex in terms of previously determined glueball-quark coupling we show that the Pomeron might be related to the Regge trajectory defined by a light scalar glueball/sigma system and a tensor glueball, which involves complicated nonperturbative QCD. We predict a tensor glueball at 2.8 GeV.Comment: tex file and two eps files with figure

Impact of flood disasters on Taiwan in the last quarter century

Copyright © Springer 2006. The final publication is available at Springer via http://dx.doi.org/10.1007/s11069-005-4667-7The increasing natural disasters, especially floods during the last quarter century, are raising the economic losses in Taiwan. The most severe hazard in Taiwan is flooding induced by typhoons and storms in summer and autumn. By comparing the rivers around the world, the ones in Taiwan have the steepest slopes, the largest discharge per unit drainage area, and the shortest time of concentrations. Rapid urbanization without proper land uses managements usually worsen the flood problems. Consequently, flood hazards mitigation has become the most essential task for Taiwan to deal with. Although the government keeps improving flood defense structures, the flood damage grows continuously. In this article, possible flood mitigation strategies are identified for coping with complex environmental and social decisions with flood risk involved.National Science and Technology Center for Disaster ReductionNational Science Council, RO

Longitudinal Transitions Of Baryon Resonances in Constituent Quark Model

A longitudinal transition operator that satisfies the gauge invariance requirement is introduced in constituent quark model. The corresponding longitudinal transitions between the nucleon and baryon resonances are calculated. We show that the study of the longitudinal coupling plays an important role in understanding the structure of baryons.Comment: 13 pages with 5 figures in ps. file can be obtained from autho

Anesthetic Propofol Reduces Endotoxic Inflammation by Inhibiting Reactive Oxygen Species-regulated Akt/IKKβ/NF-κB Signaling

BACKGROUND: Anesthetic propofol has immunomodulatory effects, particularly in the area of anti-inflammation. Bacterial endotoxin lipopolysaccharide (LPS) induces inflammation through toll-like receptor (TLR) 4 signaling. We investigated the molecular actions of propofol against LPS/TLR4-induced inflammatory activation in murine RAW264.7 macrophages. METHODOLOGY/PRINCIPAL FINDINGS: Non-cytotoxic levels of propofol reduced LPS-induced inducible nitric oxide synthase (iNOS) and NO as determined by western blotting and the Griess reaction, respectively. Propofol also reduced the production of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-10 as detected by enzyme-linked immunosorbent assays. Western blot analysis showed propofol inhibited LPS-induced activation and phosphorylation of IKKβ (Ser180) and nuclear factor (NF)-κB (Ser536); the subsequent nuclear translocation of NF-κB p65 was also reduced. Additionally, propofol inhibited LPS-induced Akt activation and phosphorylation (Ser473) partly by reducing reactive oxygen species (ROS) generation; inter-regulation that ROS regulated Akt followed by NF-κB activation was found to be crucial for LPS-induced inflammatory responses in macrophages. An in vivo study using C57BL/6 mice also demonstrated the anti-inflammatory properties against LPS in peritoneal macrophages. CONCLUSIONS/SIGNIFICANCE: These results suggest that propofol reduces LPS-induced inflammatory responses in macrophages by inhibiting the interconnected ROS/Akt/IKKβ/NF-κB signaling pathways

Heart Rate-Corrected QT Interval Helps Predict Mortality after Intentional Organophosphate Poisoning

INTRODUCTION: In this study, we investigated the outcomes for patients with intentional organophosphate poisoning. Previous reports indicate that in contrast to normal heart rate-corrected QT intervals (QTc), QTc prolongation might be indicative of a poor prognosis for patients exposed to organophosphates. METHODS: We analyzed the records of 118 patients who were referred to Chang Gung Memorial Hospital for management of organophosphate poisoning between 2000 and 2011. Patients were grouped according to their initial QTc interval, i.e., normal (<0.44 s) or prolonged (>0.44 s). Demographic, clinical, laboratory, and mortality data were obtained for analysis. RESULTS: The incidence of hypotension in patients with prolonged QTc intervals was higher than that in the patients with normal QTc intervals (P = 0.019). By the end of the study, 18 of 118 (15.2%) patients had died, including 3 of 75 (4.0%) patients with normal QTc intervals and 15 of 43 (34.9%) patients with prolonged QTc intervals. Using multivariate-Cox-regression analysis, we found that hypotension (OR = 10.930, 95% CI = 2.961-40.345, P = 0.000), respiratory failure (OR = 4.867, 95% CI = 1.062-22.301, P = 0.042), coma (OR = 3.482, 95% CI = 1.184-10.238, P = 0.023), and QTc prolongation (OR = 7.459, 95% CI = 2.053-27.099, P = 0.002) were significant risk factors for mortality. Furthermore, it was revealed that non-survivors not only had longer QTc interval (503.00±41.56 versus 432.71±51.21 ms, P = 0.002), but also suffered higher incidences of hypotension (83.3 versus 12.0%, P = 0.000), shortness of breath (64 versus 94.4%, P = 0.010), bronchorrhea (55 versus 94.4%, P = 0.002), bronchospasm (50.0 versus 94.4%, P = 0.000), respiratory failure (94.4 versus 43.0%, P = 0.000) and coma (66.7 versus 11.0%, P = 0.000) than survivors. Finally, Kaplan-Meier analysis demonstrated that cumulative mortality was higher among patients with prolonged QTc intervals than among those with normal QTc intervals (Log-rank test, Chi-square test = 20.36, P<0.001). CONCLUSIONS: QTc interval helps predict mortality after intentional organophosphate poisoning

Insulin resistance and hyperinsulinaemia in the development and progression of cancer

Experimental, epidemiological and clinical evidence implicates insulin resistance and its accompanying hyperinsulinaemia in the development of cancer, but the relative importance of these disturbances in cancer remains unclear. There are, however, theoretical mechanisms by which hyperinsulinaemia could amplify such growth-promoting effects as insulin may have, as well as the growth-promoting effects of other, more potent, growth factors. Hyperinsulinaemia may also induce other changes, particularly in the IGF (insulin-like growth factor) system, that could promote cell proliferation and survival. Several factors can independently modify both cancer risk and insulin resistance, including subclinical inflammation and obesity. The possibility that some of the effects of hyperinsulinaemia might then augment pro-carcinogenic changes associated with disturbances in these factors emphasizes how, rather than being a single causative factor, insulin resistance may be most usefully viewed as one strand in a network of interacting disturbances that promote the development and progression of cancer