Constructing a virtual Tower of Babel: a case study in cross-cultural collaboration across three continents

The collaboration project described in this paper revolves around the construction of a virtual Tower of Babel in a 3D Collaborative Virtual Environment (3D CVE). It involved students across three cooperating institutions, on three different continents in different time zones. It addresses the increasing need for students to engage in international collaboration, as much of today's Information and Communication Technology work demands it. This requires cross-cultural understandings with one's co-collaborators, yet there are few opportunities for this to occur in a pedagogical setting. Therefore, this paper discusses a pedagogically-oriented case study of the use of a 3D CVE as a multi-cultural classroom, describing and discussing different phases in the cross-cultural collaborative process

Characteristics of LPG-diesel dual fuelled engine operated with rapeseed methyl ester and gas-to-liquid diesel fuels

AbstractA Liquefied Petroleum Gas (LPG)-diesel dual fuelled combustion experimental study was carried out to understand the impact of the properties of the direct injection diesel fuels, such as rapeseed methyl ester (RME) and gas-to-liquid (GTL), on combustion characteristics, engine performance and emissions. The experimental results showed that up to 60% of liquid fuel replacement by LPG was reached while keeping engine combustion variability within the acceptable range and obtaining clear benefits in the soot-NOx trade-off. However, the amount of LPG was limited by adverse effects in engine thermal efficiency, HC and CO emissions. LPG–RME showed a good alternative to LPG-diesel dual fuelling, as better engine combustion variability, HC, CO and soot behaviour was obtained when compared to the other liquid fuels, mainly due to its fuel oxygen content. On the other hand, NOx emissions were the highest, but these can be balanced by the application of EGR. LPG–GTL dual fuelling resulted in the highest NOx emissions benefit over a wide range of engine operating conditions. The high cetane number and the absence of aromatic of GTL are the main parameters for the more favourable soot-NOx trade-off compared to LPG–ULSD (ultra low sulphur diesel) dual fuelling

Possible origins of macroscopic left-right asymmetry in organisms

I consider the microscopic mechanisms by which a particular left-right (L/R) asymmetry is generated at the organism level from the microscopic handedness of cytoskeletal molecules. In light of a fundamental symmetry principle, the typical pattern-formation mechanisms of diffusion plus regulation cannot implement the "right-hand rule"; at the microscopic level, the cell's cytoskeleton of chiral filaments seems always to be involved, usually in collective states driven by polymerization forces or molecular motors. It seems particularly easy for handedness to emerge in a shear or rotation in the background of an effectively two-dimensional system, such as the cell membrane or a layer of cells, as this requires no pre-existing axis apart from the layer normal. I detail a scenario involving actin/myosin layers in snails and in C. elegans, and also one about the microtubule layer in plant cells. I also survey the other examples that I am aware of, such as the emergence of handedness such as the emergence of handedness in neurons, in eukaryote cell motility, and in non-flagellated bacteria.Comment: 42 pages, 6 figures, resubmitted to J. Stat. Phys. special issue. Major rewrite, rearranged sections/subsections, new Fig 3 + 6, new physics in Sec 2.4 and 3.4.1, added Sec 5 and subsections of Sec

The Zinc Finger Protein A20 Inhibits TNF-induced NF-κB–dependent Gene Expression by Interfering with an RIP- or TRAF2-mediated Transactivation Signal and Directly Binds to a Novel NF-κB–inhibiting Protein ABIN

The zinc finger protein A20 is a tumor necrosis factor (TNF)– and interleukin 1 (IL-1)-inducible protein that negatively regulates nuclear factor-kappa B (NF-κB)–dependent gene expression. However, the molecular mechanism by which A20 exerts this effect is still unclear. We show that A20 does not inhibit TNF- induced nuclear translocation and DNA binding of NF-κB, although it completely prevents the TNF- induced activation of an NF-κB–dependent reporter gene, as well as TNF-induced IL-6 and granulocyte macrophage–colony stimulating factor gene expression. Moreover, NF-κB activation induced by overexpression of the TNF receptor–associated proteins TNF receptor–associated death domain protein (TRADD), receptor interacting protein (RIP), and TNF recep- tor–associated factor 2 (TRAF2) was also inhibited by expression of A20, whereas NF-κB activation induced by overexpression of NF-κB–inducing kinase (NIK) or the human T cell leukemia virus type 1 (HTLV-1) Tax was unaffected. These results demonstrate that A20 inhibits NF-κB–dependent gene expression by interfering with a novel TNF-induced and RIP- or TRAF2-mediated pathway that is different from the NIK–IκB kinase pathway and that is specifically involved in the transactivation of NF-κB. Via yeast two-hybrid screening, we found that A20 binds to a novel protein, ABIN, which mimics the NF-κB inhibiting effects of A20 upon overexpression, suggesting that the effect of A20 is mediated by its interaction with this NF-κB inhibiting protein, ABIN

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

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

The Alvarez impact theory of mass extinction; limits to its applicability and the „great expectations syndrome”

For the past three decades, the Alvarez impact theory of mass extinction, causally related to catastrophic meteorite impacts, has been recurrently applied to multiple extinction boundaries. However, these multidisciplinary research efforts across the globe have been largely unsuccessful to date, with one outstanding exception: the Cretaceous-Paleogene boundary. The unicausal impact scenario as a leading explanation, when applied to the complex fossil record, has resulted in force-fitting of data and interpretations ("great expectations syndrome". The misunderstandings can be grouped at three successive levels of the testing process, and involve the unreflective application of the impact paradigm: (i) factual misidentification, i.e., an erroneous or indefinite recognition of the extraterrestrial record in sedimentological, physical and geochemical contexts, (ii) correlative misinterpretation of the adequately documented impact signals due to their incorrect dating, and (iii) causal overestimation when the proved impact characteristics are doubtful as a sufficient trigger of a contemporaneous global cosmic catastrophe. Examples of uncritical belief in the simple cause-effect scenario for the Frasnian-Famennian, Permian-Triassic, and Triassic-Jurassic (and the Eifelian-Givetian and Paleocene-Eocene as well) global events include mostly item-1 pitfalls (factual misidentification), with Ir enrichments and shocked minerals frequently misidentified. Therefore, these mass extinctions are still at the first test level, and only the F-F extinction is potentially seen in the context of item-2, the interpretative step, because of the possible causative link with the Siljan Ring crater (53 km in diameter). The erratically recognized cratering signature is often marked by large timing and size uncertainties, and item-3, the advanced causal inference, is in fact limited to clustered impacts that clearly predate major mass extinctions. The multi-impact lag-time pattern is particularly clear in the Late Triassic, when the largest (100 km diameter) Manicouagan crater was possibly concurrent with the end-Carnian extinction (or with the late Norian tetrapod turnover on an alternative time scale). The relatively small crater sizes and cratonic (crystalline rock basement) setting of these two craters further suggest the strongly insufficient extraterrestrial trigger of worldwide environmental traumas. However, to discuss the kill potential of impact events in a more robust fashion, their location and timing, vulnerability factors, especially target geology and palaeogeography in the context of associated climate-active volatile fluxes, should to be rigorously assessed. The current lack of conclusive impact evidence synchronous with most mass extinctions may still be somewhat misleading due to the predicted large set of undiscovered craters, particularly in light of the obscured record of oceanic impact events

The σ\sigma pole in J/ψ→ωπ+π−J/\psi \to \omega \pi^+ \pi^-

Using a sample of 58 million $J/\psi$ events recorded in the BESII detector, the decay $J/\psi \to \omega \pi^+ \pi^-$ is studied. There are conspicuous $\omega f_2(1270)$ and $b_1(1235)\pi$ signals. At low $\pi \pi$ mass, a large broad peak due to the $\sigma$ is observed, and its pole position is determined to be $(541 \pm 39)$ - $i$ $(252 \pm 42)$ MeV from the mean of six analyses. The errors are dominated by the systematic errors.Comment: 15 pages, 6 figures, submitted to PL

2-Aminophenoxazine-3-one and 2-amino-4,4α-dihydro-4α,7-dimethyl-3H-phenoxazine-3-one cause cellular apoptosis by reducing higher intracellular pH in cancer cells

We examined intracellular pH (pHi) of ten cancer cell lines derived from different organs and two normal cell lines including human embryonic lung fibroblast cells (HEL) and human umbilical vein endothelial cells (HUVEC) in vitro, and found that pHi of most of these cancer cells was evidently higher (pH 7.5 to 7.7) than that of normal cells (7.32 and 7.44 for HEL and HUVEC, respectively) and that of primary leukemic cells and erythrocytes hitherto reported (≤7.2). Higher pHi in these cancer cells could be related to the Warburg effect in cancer cells with enhanced glycolytic metabolism. Since reversal of the Warburg effect may perturb intracellular homeostasis in cancer cells, we looked for compounds that cause extensive reduction of pHi, a major regulator of the glycolytic pathway and its associated metabolic pathway. We found that phenoxazine compounds, 2-aminophenoxazine-3-one (Phx-3) and 2-amino-4,4α-dihydro-4α,7-dimethyl-3H-phenoxazine-3-one (Phx-1) caused a rapid and drastic dose-dependent decrease of pHi in ten different cancer cells within 30 min, though the extent of the decrease of pHi was significantly larger for Phx-3 (ΔpHi = 0.6 pH units or more for 100 µM Phx-3) than for Phx-1 (ΔpHi = 0.1 pH units or more for 100 µM Phx-1). This rapid and drastic decrease of pHi in a variety of cancer cells caused by Phx-3 and Phx-1 possibly perturbed their intracellular homeostasis, and extensively affected the subsequent cell death, because these phenoxazines exerted dose-dependent proapoptotic and cytotoxic effects on these cells during 72 h incubation, confirming a causal relationship between ΔpHi and cytotoxic effects due to Phx-3 and Phx-1. Phx-3 and Phx-1 also reduced pHi of normal cells including HEL and HUVEC, although they exerted less proapoptotic and cytotoxic effects on these cells than on cancer cells. Drugs such as Phx-3 and Phx-1 that reduce pHi and thereby induce cellular apoptosis might serve as benevolent anticancer drugs