26. Sitzung des FAO/WHO-Codex-Alimentarius-Komitees für Fische und Fischerzeugnisse

Die 26. Sitzung des Codex-Alimentarius-Komitees für Fische und Fischerzeugnisse fand vom 13. bis 17.Oktober 2003 in Aales und, Norwegen, statt. Die Tagung wurde von 130 Delegierten und Beobachtern aus 47 Mitgliedsstaaten und 5 internationalen Organisationen besucht. Die größten Delegationen stellten Deutschland(7), Thailand (7), Japan (8), USA (11) und Norwegen als Gastgeber (14). Die deutsche Delegation wurde von Dr. Markus Brill (BMVEL) geleitet. Weitere Mitgliederwaren Prof. Jörg Oehlenschläger (BFAFi, Sprecher), Dr. Kristina Ravelhofer-Rotheneder (BMVEL), Dr. Reinhard Schubring (BFAFi), Dr. Mathias Keller (Bundesmarktverband der deutschen Fischindustrie und des Fischgroßhandels e.V.), Petra Weigl (Pickenpack-Hussmann und Hahn Seafood GmbH) und Dr. Ralf Peter Pund (BfR). Die Sitzung, die von Janne Johnson, Staatssekretärin im norwegischen Fischereiministerium, eröffnet wurde, leitete Dr. Bjørn Rothe Knudtsen, Regionaldirektor des norwegischen Direktorats für Fischerei und Aquakultur, Trondheim.

Glycocalyx production in teleosts [Translation from: Verhandlungen der Deutschen Zoologischen Gesellschaft, p.286, 1970]

Shielding the organism against harmful effects from the environment is one of the most important tasks of the outer covering of all animals. The epidermis of primarily aquatic organisms and the epithelia of organs which are exposed to water, such as the digestive or the urinary system, possess a film of glycoproteins and mucopolysaccharides, the glycocalyx. This short paper examines the relationship of the mucus cells with the glycocalyx.

Analysis of defect-related localized emission processes in InGaN/GaN-based LEDs

This paper reports an extensive analysis of the defect-related localized emission processes occurring in InGaN/GaN-based light-emitting diodes (LEDs) at low reverse- and forward-bias conditions. The analysis is based on combined electrical characterization and spectrally and spatially resolved electroluminescence (EL) measurements. Results of this analysis show that: (i) under reverse bias, LEDs can emit a weak luminescence signal, which is directly proportional to the injected reverse current. Reverse-bias emission is localized in submicrometer-size spots; the intensity of the signal is strongly correlated to the threading dislocation (TD) density, since TDs are preferential paths for leakage current conduction. (ii) Under low forward-bias conditions, the intensity of the EL signal is not uniform over the device area. Spectrally resolved EL analysis of green LEDs identifies the presence of localized spots emitting at 600 nm (i.e., in the yellow spectral region), whose origin is ascribed to localized tunneling occurring between the quantum wells and the barrier layers of the diodes, with subsequent defect-assisted radiative recombination. The role of defects in determining yellow luminescence is confirmed by the high activation energy of the thermal quenching of yellow emission (Ea =0.64&eV). © 2012 IEEE.

Kelvin-Helmholtz-like instabilities in turbulent flows over complex surfaces

Riblets are small surface protrusions aligned with the flow direction, which confer an anisotropic roughness to the surface [6]. We have recently reported that the transitional-roughness effect in riblets, which limits their performance, is due to a Kelvin–Helmholtz-like instability of the overlying mean flow [7]. According to our DNSs, the instability sets on as the Reynolds number based on the roughness size of the riblets increases, and coherent, elongated spanwise vortices begin to develop immediately above the riblet tips, causing the degradation of the drag-reduction effect. This is a very novel concept, since prior studies had proposed that the degradation was due to the interaction of riblets with the flow as independent units, either to the lodging of quasi-streamwise vortices in the surface grooves [2] or to the shedding of secondary streamwise vorticity at the riblet peaks [9]. We have proposed an approximate inviscid analysis for the instability, in which the presence of riblets is modelled through an average boundary condition for an overlying, spanwise-independent mean flow. This simplification lacks the accuracy of an exact analysis [4], but in turn applies to riblet surfaces in general. Our analysis succeeds in predicting the riblet size for the onset of the instability, while qualitatively reproducing the wavelengths and shapes of the spanwise structures observed in the DNSs. The analysis also connects the observations with the Kelvin–Helmholtz instability of mixing layers. The fundamental riblet length scale for the onset of the instability is a ‘penetration length,’ which reflects how easily the perturbation flow moves through the riblet grooves. This result is in excellent agreement with the available experimental evidence, and has enabled the identification of the key geometric parameters to delay the breakdown. Although the appearance of elongated spanwise vortices was unexpected in the case of riblets, similar phenomena had already been observed over other rough [3], porous [1] and permeable [11] surfaces, as well as over plant [5,14] and urban [12] canopies, both in the transitional and in the fully-rough regimes. However, the theoretical analyses that support the connection of these observations with the Kelvin–Helmholtz instability are somewhat scarce [7, 11, 13]. It has been recently proposed that Kelvin–Helmholtz-like instabilities are a dominant feature common to “obstructed” shear flows [8]. It is interesting that the instability does not require an inflection point to develop, as is often claimed in the literature. The Kelvin-Helmholtz rollers are rather triggered by the apparent wall-normal-transpiration ability of the flow at the plane immediately above the obstructing elements [7,11]. Although both conditions are generally complementary, if wall-normal transpiration is not present the spanwise vortices may not develop, even if an inflection point exists within the roughness [10]. REFERENCES [1] Breugem, W. P., Boersma, B. J. & Uittenbogaard, R. E. 2006 J. Fluid Mech. 562, 35–72. [2] Choi, H., Moin, P. & Kim, J. 1993 J. Fluid Mech. 255, 503–539. [3] Coceal, O., Dobre, A., Thomas, T. G. & Belcher, S. E. 2007 J. Fluid Mech. 589, 375–409. [4] Ehrenstein, U. 2009 Phys. Fluids 8, 3194–3196. [5] Finnigan, J. 2000 Ann. Rev. Fluid Mech. 32, 519–571. [6] Garcia-Mayoral, R. & Jimenez, J. 2011 Phil. Trans. R. Soc. A 369, 1412–1427. [7] Garcia-Mayoral, R. & Jimenez, J. 2011 J. Fluid Mech. doi: 10.1017/jfm.2011.114. [8] Ghisalberti, M. 2009 J. Fluid Mech. 641, 51–61. [9] Goldstein, D. B. & Tuan, T. C. 1998 J. Fluid Mech. 363, 115–151. [10] Hahn, S., Je, J. & Choi, H. 2002 J. Fluid Mech. 450, 259–285. [11] Jimenez, J., Uhlman, M., Pinelli, A. & G., K. 2001 J. Fluid Mech. 442, 89–117. [12] Letzel, M. O., Krane, M. & Raasch, S. 2008 Atmos. Environ. 42, 8770–8784. [13] Py, C., de Langre, E. & Moulia, B. 2006 J. Fluid Mech. 568, 425–449. [14] Raupach, M. R., Finnigan, J. & Brunet, Y. 1996 Boundary-Layer Meteorol. 78, 351–382.

U19/Eaf2 Binds to and Stabilizes von Hippel-Lindau Protein

Studies have firmly established a key regulatory role for the tumor suppressor pVHL in the regulation of the vascular system and normal spermatogenesis. Here, we report that knockout of the newly identified tumor suppressor U19/Eaf2 also caused vascular system abnormalities and aspermatogenesis, suggesting a potential link between U19/Eaf2 and pVHL. Coimmunoprecipitation and in vitro binding assays showed an association between U19/Eaf2 and pVHL, whereas deletion mutagenesis revealed the requirement of the NH2 terminus of U19/Eaf2 and both the alpha and beta domains of pVHL for this binding. U19/Eaf2 stabilizes pVHL, as shown by protein stability and pulse-chase studies. Testes and mouse embryonic fibroblasts (MEF) derived from U19/Eaf2 knockout mice expressed reduced levels of pVHL, indicating that full in vivo expression of pVHL indeed requires U19/Eaf2. As expected, U19/Eaf2 knockout MEF cells exhibited an increased level and activity of hypoxia-inducible factor 1 alpha (HIF1 alpha), a protein typically regulated via a pVHL-mediated degradation pathway. Furthermore, angiogenesis in a Matrigel plug assay was significantly increased in U19/Eaf2 knockout mice. The above observations argue that U19/Eaf2 can modulate HIF1 alpha and angiogenesis, possibly via direct binding and stabilization of pVHL. [Cancer Res 2009;69(6):2599-606]

U19/Eaf2 knockout causes lung adenocarcinoma, B-cell lymphoma, hepatocellular carcinoma and prostatic intraepithelial neoplasia

Upregulated gene 19 (U19)/ELL-associated factor 2 (Eaf2) is a potential human tumor suppressor that exhibits frequent allelic loss and downregulation in high-grade prostate cancer. U19/Eaf2, along with its homolog Eaf1, has been reported to regulate transcriptional elongation via interaction with the eleven-nineteen lysine-rich leukemia (ELL) family of proteins. To further explore the tumor-suppressive effects of U19/Eaf2, we constructed and characterized a murine U19/Eaf2-knockout model. Homozygous or heterozygous deletion of U19/Eaf2 resulted in high rates of lung adenocarcinoma, B-cell lymphoma, hepato cellular carcinoma and prostate intraepithelial neoplasia. Within the mouse prostate, U19/Eaf2 defficiency enhanced cell proliferation and increased epithelial cell size. The knockout mice also exhibited cardiac cell hypertrophy. These data indicate a role for U19/Eaf2 in growth suppression and cell size control as well as argue for U19/Eaf2 as a novel tumor suppressor in multiple mouse tissues. The U19/Eaf2 knockout mouse also provides a unique animal model for three important cancers: lung adenocarcinoma, B-cell lymphoma and hepatocellular carcinoma.

Coherence loss and recovery of an electron spin coupled inhomogeneously to a one-dimensional interacting spin bath: An adaptive time-dependent density-matrix renormalization group study

Coherence evolution and echo effect of an electron spin, which is coupled inhomogeneously to an interacting one-dimensional finite spin bath via hyperfine-type interaction, are studied using the adaptive time-dependent density-matrix renormalization group method. It is found that the interplay of the coupling inhomogeneity and the transverse intrabath interactions results in two qualitatively different coherence evolutions, namely, a coherence-preserving evolution characterized by periodic oscillation and a complete decoherence evolution. Correspondingly, the echo effects induced by an electron-spin flip at time tau exhibit stable recoherence pulse sequence for the periodic evolution and a single peak at root 2 tau for the decoherence evolution, respectively. With the diagonal intrabath interaction included, the specific feature of the periodic regime is kept, while the root 2 tau-type echo effect in the decoherence regime is significantly affected. To render the experimental verifications possible, the Hahn echo envelope as a function of tau is calculated, which eliminates the inhomogeneous broadening effect and serves for the identification of the different status of the dynamic coherence evolution, periodic versus decoherence.

Intra-habitat heterogeneity of microbial food web structure under the regime of eutrophication and sediment resuspension in the large subtropical shallow Lake Taihu, China

Planktonic microbial community structure and classical food web were investigated in the large shallow eutrophic Lake Taihu (2338 km(2), mean depth 1.9 m) located in subtropical Southeast China. The water column of the lake was sampled biweekly at two sites located 22 km apart over a period of twelve month. Site 1 is under the regime of heavy eutrophication while Site 2 is governed by wind-driven sediment resuspension. Within-lake comparison indicates that phosphorus enrichment resulted in increased abundance of microbial components. However, the coupling between total phosphorus and abundance of microbial components was different between the two sites. Much stronger coupling was observed at Site 1 than at Site 2. The weak coupling at Site 2 was mainly caused by strong sediment resuspension, which limited growth of phytoplankton and, consequently, growth of bacterioplankton and other microbial components. High percentages of attached bacteria, which were strongly correlated with the biomass of phytoplankton, especially Microcystis spp., were found at Site 1 during summer and early autumn, but no such correlation was observed at Site 2. This potentially leads to differences in carbon flow through microbial food web at different locations. Overall, significant heterogeneity of microbial food web structure between the two sites was observed. Site-specific differences in nutrient enrichment (i.e. nitrogen and phosphorus) and sediment resuspension were identified as driving forces of the observed intra-habitat differences in food web structure.

Christian missions and a new world culture

http://www.archive.org/details/christianmission027881mbp

Wonders in the western isles, being a narrative of the commencement and progress of mission work in western Polynesia.

http://www.archive.org/details/wondersofwestern00murruoft

Polymeric and monomeric IgA response in serum and milk after parenteral cholera and oral typhoid vaccination

SCOPUS: ar.j

MYC activity mitigates response to rapamycin in prostate cancer through eukaryotic initiation factor 4E-binding protein 1-mediated inhibition of autophagy.

Loss of PTEN and activation of phosphoinositide 3-kinase are commonly observed in advanced prostate cancer. Inhibition of mammalian target of rapamycin (mTOR), a downstream target of phosphoinositide 3-kinase signaling, results in cell cycle arrest and apoptosis in multiple in vitro and in vivo models of prostate cancer. However, single-agent use of mTOR inhibition has limited clinical success, and the identification of molecular events mitigating tumor response to mTOR inhibition remains a critical question. Here, using genetically engineered human prostate epithelial cells (PrEC), we show that MYC, a frequent target of genetic gain in prostate cancers, abrogates sensitivity to rapamycin by decreasing rapamycin-induced cytostasis and autophagy. Analysis of MYC and the mTOR pathway in human prostate tumors and PrEC showed selective increased expression of eukaryotic initiation factor 4E-binding protein 1 (4EBP1) with gain in MYC copy number or forced MYC expression, respectively. We have also found that MYC binds to regulatory regions of the 4EBP1 gene. Suppression of 4EBP1 expression resulted in resensitization of MYC-expressing PrEC to rapamycin and increased autophagy. Taken together, our findings suggest that MYC expression abrogates sensitivity to rapamycin through increased expression of 4EBP1 and reduced autophagy.