Distribution and composition of macrobenthic communities along a Victoria-Land Transect (Ross Sea, Antarctica)

The Victoria-Land Transect project onboard the Italian research vessel ‘‘Italica’’ in February 2004, was a large-scale attempt to obtain benthic samples of smaller macrozoobenthic specimens systematically along a latitudinal and a depth transect along the Victoria- Land coast. Data presented from this survey are based on Rauschert dredge samples, which were taken at four areas at depth ranging from 84 to 515 m. A cluster analysis based on relative numbers of abundance was performed and demonstrated a change in community structure depending on the location along the latitudinal transect. A change in community structure with depth was not recorded. Dominant taxa of the Ross Sea fauna along the Victoria-Land coast were the Arthropoda (65.7%), followed by Annelida (20.7%), Mollusca (9.6%) and Echinodermata (2.5%). Total number of abundance decreased with depth with an exception at Cape Russell, whereas a trend in biomass was not documented. Abundance and biomass proportions of major taxa changed gradually along the latitudinal transect

Non-fatal injuries in three Central and Eastern European urban population samples: the HAPIEE study

Background: Despite high mortality from injuries and accidents, data on rates and distribution of non-fatal injuries in Central and Eastern European populations are scarce. Methods: Cross-sectional study of random population samples of 45–69-year-old men and women (n = 28 600) from Novosibirsk (Russia), Krakow (Poland) and six Czech towns, participating in the Health, Alcohol and Psychosocial factors In Eastern Europe (HAPIEE) study. Participants provided information on non-fatal injuries in the past 12 months, socio-economic characteristics, alcohol consumption and other covariates. Results: The period prevalence of non-fatal injuries in the last year among Czech, Russian and Polish men was 12.5, 9.4 and 5.3%, respectively; among women, the respective proportions were 9.9, 9.8 and 6.4%. Injury prevalence declined with age in men and increased with age in women. Higher injury prevalence was associated with being unmarried, material deprivation, higher drinking frequency and problem drinking. In the pooled data, the adjusted odds ratio (OR) for the highest versus lowest material deprivation category was 1.57 [95% confidence interval (CI) 1.38–1.79]; for problem drinking, the OR was 1.44 (95% CI 1.23–1.69). Alcohol did not mediate the link between socio-economic status and injury. Conclusion: Non-fatal injuries were associated with material deprivation, other socio-economic characteristics and with alcohol. These results not only underscore the universality of the inequality phenomenon, but also suggest that the mediating role of alcohol in social differentials in non-fatal injury remains an unresolved issue

Alcohol as a Risk Factor for Type 2 Diabetes: A systematic review and meta-analysis

OBJECTIVE - To clarify the dose-response relationship between alcohol consumption and type 2 diabetes.RESEARCH DESIGN AND METHODS - A systematic computer-assisted and hand search was conducted to identify relevant articles with longitudinal design and quantitative measurement of alcohol consumption. Adjustment was made for the sick-quitter effect. We used fractional polynomials in a meta-regression to determine the dose-response relationships by sex and end point using lifetime abstainers as the reference group.RESULTS - The search revealed 20 cohort studies that met our inclusion criteria. A U-shaped relationship was found for both sexes. Compared with lifetime abstainers, the relative risk (RR) for type 2 diabetes among men was most protective when consuming 22 g/day alcohol (RR 0.87 [95% CI 0.76-1.00]) and became deleterious at just over 60 g/day alcohol (1.01 [0.71-1.44]). Among women, consumption of 24 g/day alcohol was most protective (0.60 [0.52-0.69]) and became deleterious at about 50 g/day alcohol (1.02 [0.83-1.26]).CONCLUSIONS - Our analysis confirms previous research findings that moderate alcohol consumption is protective for type 2 diabetes in men and women

Systems analysis of cancer cell heterogeneity in caspase-dependent apoptosis subsequent to mitochondrial outer membrane permeabilization.

Deregulation of apoptosis is a hallmark of carcinogenesis. We here combine live cell imaging and systems modeling to investigate caspase-dependent apoptosis execution subsequent to mitochondrial outer membrane permeabilization (MOMP) in several cancer cell lines. We demonstrate that, although most cell lines that underwent MOMP also showed robust and fast activation of executioner caspases and apoptosis, the colorectal cancer cell lines LoVo and HCT-116 Smac(-/-), similar to X-linked inhibitor of apoptosis protein (XIAP)-overexpressing HeLa (HeLa XIAP(Adv)) cells, only showed delayed and often no caspase activation, suggesting apoptosis impairment subsequent to MOMP. Employing APOPTO-CELL, a recently established model of apoptosis subsequent to MOMP, this impairment could be understood by studying the systemic interaction of five proteins that are present in the apoptosis pathway subsequent to MOMP. Using APOPTO-CELL as a tool to study detailed molecular mechanisms during apoptosis execution in individual cell lines, we demonstrate that caspase-9 was the most important regulator in DLD-1, HCT-116, and HeLa cells and identified additional cell line-specific co-regulators. Developing and applying a computational workflow for parameter screening, systems modeling identified that apoptosis execution kinetics are more robust against changes in reaction kinetics in HCT-116 and HeLa than in DLD-1 cells. Our systems modeling study is the first to draw attention to the variability in cell specific protein levels and reaction rates and to the emergent effects of such variability on the efficiency of apoptosis execution and on apoptosis impairment subsequent to MOMP

Influence of nuclear structure on sub-barrier hindrance in Ni+Ni fusion

Fusion-evaporation cross sections for $^{64}$Ni+$^{64}$Ni have been measured down to the 10 nb level. For fusion between two open-shell nuclei, this is the first observation of a maximum in the $S$-factor, which signals a strong sub-barrier hindrance. A comparison with the $^{58}$Ni+$^{58}$Ni, $^{58}$Ni+$^{60}$Ni, and $^{58}$Ni+$^{64}$Ni systems indicates a strong dependence of the energy where the hindrance occurs on the stiffness of the interacting nuclei.Comment: Submitted to Phys. Rev. Lett. 4 pages, 3 figure

The endothelial glycocalyx prefers albumin for evoking shear stress-induced, nitric oxide-mediated coronary dilatation

Background: Shear stress induces coronary dilatation via production of nitric oxide ( NO). This should involve the endothelial glycocalyx ( EG). A greater effect was expected of albumin versus hydroxyethyl starch ( HES) perfusion, because albumin seals coronary leaks more effectively than HES in an EG-dependent way. Methods: Isolated hearts ( guinea pigs) were perfused at constant pressure with Krebs-Henseleit buffer augmented with 1/3 volume 5% human albumin or 6% HES ( 200/0.5 or 450/0.7). Coronary flow was also determined after EG digestion ( heparinase) and with nitro-L-arginine ( NO-L-Ag). Results: Coronary flow ( 9.50 +/- 1.09, 5.10 +/- 0.49, 4.87 +/- 1.19 and 4.15 +/- 0.09 ml/ min/ g for `albumin', `HES 200', `HES 450' and `control', respectively, n = 5-6) did not correlate with perfusate viscosity ( 0.83, 1.02, 1.24 and 0.77 cP, respectively). NO-L-Ag and heparinase diminished dilatation by albumin, but not additively. Alone NO-L-Ag suppressed coronary flow during infusion of HES 450. Electron microscopy revealed a coronary EG of 300 nm, reduced to 20 nm after heparinase. Cultured endothelial cells possessed an EG of 20 nm to begin with. Conclusions: Albumin induces greater endothelial shear stress than HES, despite lower viscosity, provided the EG contains negative groups. HES 450 causes some NO-mediated dilatation via even a rudimentary EG. Cultured endothelial cells express only a rudimentary glycocalyx, limiting their usefulness as a model system. Copyright (c) 2007 S. Karger AG, Basel

Role of break-up processes in fusion enhancement of drip-line nuclei at energies below the Coulomb barrier

We carry out realistic coupled-channels calculations for $^{11}$Be + $^{208}$Pb reaction in order to discuss the effects of break-up of the projectile nucleus on sub-barrier fusion. We discretize in energy the particle continuum states, which are associated with the break-up process, and construct the coupling form factors to these states on a microscopic basis. The incoming boundary condition is employed in solving coupled-channels equations, which enables us to define the flux for complete fusion inside the Coulomb barrier. It is shown that complete fusion cross sections are significantly enhanced due to the couplings to the continuum states compared with the no coupling case at energies below the Coulomb barrier, while they are hindered at above barrier energies.Comment: RevTex, 3 pages, 5 figure

Reaction mechanisms in 24Mg+12C and 32S+24Mg

The occurence of "exotic" shapes in light N=Z alpha-like nuclei is investigated for 24Mg+12C and 32S+24Mg. Various approaches of superdeformed and hyperdeformed bands associated with quasimolecular resonant structures with low spin are presented. For both reactions, exclusive data were collected with the Binary Reaction Spectrometer in coincidence with EUROBALL IV installed at the VIVITRON Tandem facility of Strasbourg. Specific structures with large deformation were selectively populated in binary reactions and their associated $\gamma$-decays studied. The analysis of the binary and ternary reaction channels is discussed.Comment: 7 pages, 4 figures, Paper presented at the Fusion08 International Conference on New Aspects of Heavy Ion Collisions Near the Coulomb Barrier, Chicago. Proceedings to be published by AIP Conference Proceedings Illinois, USA, September 22-26, 200

Diffusion is capable of translating anisotropic apoptosis initiation into a homogeneous execution of cell death

<p>Abstract</p> <p>Background</p> <p>Apoptosis is an essential cell death process throughout the entire life span of all metazoans and its deregulation in humans has been implicated in many proliferative and degenerative diseases. Mitochondrial outer membrane permeabilisation (MOMP) and activation of effector caspases are key processes during apoptosis signalling. MOMP can be subject to spatial coordination in human cancer cells, resulting in intracellular waves of cytochrome-c release. To investigate the consequences of these spatial anisotropies in mitochondrial permeabilisation on subsequent effector caspase activation, we devised a mathematical reaction-diffusion model building on a set of partial differential equations.</p> <p>Results</p> <p>Reaction-diffusion modelling suggested that even if strong spatial anisotropies existed during mitochondrial cytochrome c release, these would be eliminated by free diffusion of the cytosolic proteins that instantiate the apoptosis execution network. Experimentally, rapid sampling of mitochondrial permeabilisation and effector caspase activity in individual HeLa cervical cancer cells confirmed predictions of the reaction-diffusion model and demonstrated that the signalling network of apoptosis execution could efficiently translate spatial anisotropies in mitochondrial permeabilisation into a homogeneous effector caspase response throughout the cytosol. Further systems modelling suggested that a more than 10,000-fold impaired diffusivity would be required to maintain spatial anisotropies as observed during mitochondrial permeabilisation until the time effector caspases become activated.</p> <p>Conclusions</p> <p>Multi-protein diffusion efficiently contributes to eliminating spatial asynchronies which are present during the initiation of apoptosis execution and thereby ensures homogeneous apoptosis execution throughout the entire cell body. For previously reported biological scenarios in which effector caspase activity was shown to be targeted selectively to specific subcellular regions additional mechanisms must exist that limit or spatially coordinate caspase activation and/or protect diffusing soluble caspase substrates from unwanted proteolysis.</p

\u3ci\u3ePseudomonas syringae\u3c/i\u3e Hrp type III secretion system and effector proteins

Pseudomonas syringae is a member of an important group of Gram-negative bacterial pathogens of plants and animals that depend on a type III secretion system to inject virulence effector proteins into host cells. In P. syringae, hrpyhrc genes encode the Hrp (type III secretion) system, and avirulence (avr) and Hrpdependent outer protein (hop) genes encode effector proteins. The hrpyhrc genes of P. syringae pv syringae 61, P. syringae pv syringae B728a, and P. syringae pv tomato DC3000 are flanked by an exchangeable effector locus and a conserved effector locus in a tripartite mosaic Hrp pathogenicity island (Pai) that is linked to a tRNALeu gene found also in Pseudomonas aeruginosa but without linkage to Hrp system genes. Cosmid pHIR11 carries a portion of the strain 61 Hrp pathogenicity island that is sufficient to direct Escherichia coli and Pseudomonas fluorescens to inject HopPsyA into tobacco cells, thereby eliciting a hypersensitive response normally triggered only by plant pathogens. Large deletions in strain DC3000 revealed that the conserved effector locus is essential for pathogenicity but the exchangeable effector locus has only a minor role in growth in tomato. P. syringae secretes HopPsyA and AvrPto in culture in a Hrp-dependent manner at pH and temperature conditions associated with pathogenesis. AvrPto is also secreted by Yersinia enterocolitica. The secretion of AvrPto depends on the first 15 codons, which are also sufficient to direct the secretion of an Npt reporter from Y. enterocolitica, indicating that a universal targeting signal is recognized by the type III secretion systems of both plant and animal pathogens