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Cannibalism is known to be a significant source of natural mortality of young North-east Arctic (NEA) cod. Cannibalism data, starting from 1984, have been used in NEA cod stock assessments since 1995, which has led to inconsistency in the cod abundance time series from 1946 to the present. To address this inconsistency, this study estimates the cannibalism-induced mortality (M2) of NEA cod at age 3–5 for the period 1946–1983. Combined qualitative and quantitative cod stomach content data for 1984–2010 were used to make the M2 estimations for age groups 3–5 (ICES 2014), then different factors including SSB were used to examine which covariates explained variability in M2 and thus make predictions for 1946–1983. The level of cannibalism was estimated to be high in the 1950s – early1960s. VPA-based assessment was run using these estimated M2 values. As a result, numbers of cod eaten by their conspecifics in the historical period and new increased recruitment estimates at age 3 were computed. The main factors affecting cannibalism appeared to be young cod abundance, total stock biomass (TSB) of large cod, and capelin total stock biomass (which represents an alternative prey). The problems involved in using the new recruitment time series in fishery management are discussed. The methodology presented here represents a generic approach to extending predation mortalities back in time to improve historical stock estimates. 相似文献
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Jan-Paul Flacke Sanjeev Kumar Sawa Kostin H. Peter Reusch Yury Ladilov 《Apoptosis : an international journal on programmed cell death》2009,14(1):90-96
To analyze the underlying cellular mechanisms of adaptation to ischemia-induced apoptosis through short acidic pretreatment,
i.e. acidic preconditioning (APC), Wistar rat coronary endothelial cells (EC) were exposed for 40 min to acidosis (pH 6.4)
followed by a 14 h recovery period (pH 7.4) and finally treated for 2 h with simulated in vitro ischemia (glucose-free anoxia
at pH 6.4). APC led to a transient activation of p38 and Akt kinases, but not of JNK and ERK1/2 kinases, which was accompanied
by significant reduction of the apoptotic cell number, caspase-12/-3 cleavage and Bcl-xL overexpression. These effects of
APC were completely abolished by prevention of Akt- or p38-phosphorylation during APC. Furthermore, knock-down of Bcl-xL by
siRNA-transfection also abolished the anti-apoptotic effect of APC. Therefore, APC leads to protection of EC against ischemic
apoptosis by activation of Akt and p38 followed by overexpression of Bcl-xL, which is a key anti-apoptotic mechanism of APC. 相似文献
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Vadim I. Nazarov Mikhail V. Pogorelyy Ekaterina A. Komech Ivan V. Zvyagin Dmitry A. Bolotin Mikhail Shugay Dmitry M. Chudakov Yury B. Lebedev Ilgar Z. Mamedov 《BMC bioinformatics》2015,16(1)
Background
The Immunoglobulins (IG) and the T cell receptors (TR) play the key role in antigen recognition during the adaptive immune response. Recent progress in next-generation sequencing technologies has provided an opportunity for the deep T cell receptor repertoire profiling. However, a specialised software is required for the rational analysis of massive data generated by next-generation sequencing.Results
Here we introduce tcR, a new R package, representing a platform for the advanced analysis of T cell receptor repertoires, which includes diversity measures, shared T cell receptor sequences identification, gene usage statistics computation and other widely used methods. The tool has proven its utility in recent research studies.Conclusions
tcR is an R package for the advanced analysis of T cell receptor repertoires after primary TR sequences extraction from raw sequencing reads. The stable version can be directly installed from The Comprehensive R Archive Network (http://cran.r-project.org/mirrors.html). The source code and development version are available at tcR GitHub (http://imminfo.github.io/tcr/) along with the full documentation and typical usage examples. 相似文献8.
Flexible Electronics: Natural Fiber Welded Electrode Yarns for Knittable Textile Supercapacitors (Adv. Energy Mater. 4/2015) 下载免费PDF全文
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Alexander Belyy Irina Tabakova Alexander E. Lang Thomas Jank Yury Belyi Klaus Aktories 《PloS one》2015,10(12)
Clostridium perfringens iota toxin is a binary toxin composed of the enzymatically active component Ia and receptor binding component Ib. Ia is an ADP-ribosyltransferase, which modifies Arg177 of actin. The previously determined crystal structure of the actin-Ia complex suggested involvement of Asp179 of actin in the ADP-ribosylation reaction. To gain more insights into the structural requirements of actin to serve as a substrate for toxin-catalyzed ADP-ribosylation, we engineered Saccharomyces cerevisiae strains, in which wild type actin was replaced by actin variants with substitutions in residues located on the Ia-actin interface. Expression of the actin mutant Arg177Lys resulted in complete resistance towards Ia. Actin mutation of Asp179 did not change Ia-induced ADP-ribosylation and growth inhibition of S. cerevisiae. By contrast, substitution of Glu270 of actin inhibited the toxic action of Ia and the ADP-ribosylation of actin. In vitro transcribed/translated human β-actin confirmed the crucial role of Glu270 in ADP-ribosylation of actin by Ia. 相似文献