The Composition of Cosmic Rays at the Knee

The observation of a small change in spectral slope, or 'knee' in the fluxes of cosmic rays near energies 10^15 eV has caused much speculation since its discovery over 40 years ago. The origin of this feature remains unknown. A small workshop to review some modern experimental measurements of this region was held at the Adler Planetarium in Chicago, USA in June 2000. This paper summarizes the results presented at this workshop and the discussion of their interpretation in the context of hadronic models of atmospheric airshowers.Comment: 36 pages, 10 figure

A study of charged kappa in J/ψ→K±Ksπ∓π0J/\psi \to K^{\pm} K_s \pi^{\mp} \pi^0

Based on $58 \times 10^6$ $J/\psi$ events collected by BESII, the decay $J/\psi \to K^{\pm} K_s \pi^{\mp} \pi^0$ is studied. In the invariant mass spectrum recoiling against the charged $K^*(892)^{\pm}$, the charged $\kappa$ particle is found as a low mass enhancement. If a Breit-Wigner function of constant width is used to parameterize the kappa, its pole locates at $(849 \pm 77 ^{+18}_{-14}) -i (256 \pm 40 ^{+46}_{-22})$ MeV/$c^2$. Also in this channel, the decay $J/\psi \to K^*(892)^+ K^*(892)^-$ is observed for the first time. Its branching ratio is $(1.00 \pm 0.19 ^{+0.11}_{-0.32}) \times 10^{-3}$.Comment: 14 pages, 4 figure

Evidence for kappa Meson Production in J/psi -> bar{K}^*(892)^0K^+pi^- Process

Based on 58 million BESII J/psi events, the bar{K}^*(892)^0K^+pi^- channel in K^+K^-pi^+pi^- is studied. A clear low mass enhancement in the invariant mass spectrum of K^+pi^- is observed. The low mass enhancement does not come from background of other J/psi decay channels, nor from phase space. Two independent partial wave analyses have been performed. Both analyses favor that the low mass enhancement is the kappa, an isospinor scalar resonant state. The average mass and width of the kappa in the two analyses are 878 +- 23^{+64}_{-55} MeV/c^2 and 499 +- 52^{+55}_{-87} MeV/c^2, respectively, corresponding to a pole at (841 +- 30^{+81}_{-73}) - i(309 +- 45^{+48}_{-72}) MeV/c^2.Comment: 17 pages, 5 figure

Epstein-Barr virus: clinical and epidemiological revisits and genetic basis of oncogenesis

Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancie

Cytokine genotype suggests a role for inflammation in nucleoside analog-associated sensory neuropathy (NRTI-SN) and predicts an individual's NRTI-SN risk

Nucleoside analog-associated sensory neuropathy (NRTI-SN) attributed to stavudine, didanosine, or zalcitabine (the dNRTIs) and distal sensory polyneuropathy (DSP) attributed to HIV are clinically indistinguishable. As inflammatory cytokines are involved in DSP, we addressed a role for inflammation in NRTI-SN by determining the alleles of immune-related genes carried by patients with and without NRTI-SN. Demographic details associated with risk of various neuropathies were included in the analysis. Alleles of 14 polymorphisms in 10 genes were determined in Australian HIV patients with definite NRTI-SN (symptom onset 6 months on dNRTIs, n = 20), patients with late onset NRTI-SN (neuropathy onset after >6 months of dNRTIs, n = 19), and HIV-negative controls. Carriage of TNFA-1031*2 was highest in NRTI-SN patients, suggesting potentiation of NRTI-SN. Carriage of IL12B (3′ UTR)*2 was higher in NRTI-SN-resistant patients than controls or NRTI-SN patients, suggesting a protective role. BAT1 (intron 10)*2 was more common in NRTI-SN than resistant patients, but neither group differed from controls. This marks the conserved HLA-A1, B8, DR3 haplotype. Of the demographic details considered, increasing height was associated with NRTI-SN risk. A model including cytokine genotype and height predicted NRTI-SN status (p < 0.0001, R 2 = 0.54). Late onset NRTI-SN patients clustered genetically with NRTI-SN-resistant patients, so these patients may be genetically "protected." In addition to patient height, cytokine genotype influenced NRTI-SN risk following dNRTI exposure, suggesting inflammation contributes to NRTI-SN