98我很怕ML。很怕怀孕了能ml吗,怎么回事dsqrk

EMBO J. 1996 August 1; 15(15): .
PMCID: PMC452120The HeLa 200 kDa U5 snRNP-specific protein and its homologue in Saccharomyces cerevisiae are members of the DEXH-box protein family of putative RNA helicases., , , , , and
This article has been
other articles in PMC.The primary structure of the 200 kDa protein of purified HeLa U5 snRNPs (U5-200kD) was characterized by cloning and sequencing of its cDNA. In order to confirm that U5-200kD is distinct from U5-220kD we demonstrate by protein sequencing that the human U5-specific 220 kDa protein is homologous to the yeast U5-specific protein Prp8p. A 246 kDa protein (Snu246p) homologous to U5-200kD was identified in Saccharomyces cerevisiae. Both proteins contain two conserved domains characteristic of the DEXH-box protein family of putative RNA helicases and RNA-stimulated ATPases. Antibodies raised against fusion proteins produced from fragments of the cloned mammalian cDNA interact specifically with the HeLa U5-200kD protein on Western blots and co-immunoprecipitate U5 snRNA and to a lesser extent U4 and U6 snRNAs from HeLa snRNPs. Similarly, U4, U5 and U6 snRNAs can be co-immunoprecipitated from yeast splicing extracts containing an HA-tagged derivative of Snu246p with HA-tag specific antibodies. U5-200kD and Snu246p are thus the first putative RNA helicases shown to be intrinsic components of snRNPs. Disruption of the SNU246 gene in yeast is lethal and leads to a splicing defect in vivo, indicating that the protein is essential for splicing. Anti-U5-200kD antibodies specifically block the second step of mammalian splicing in vitro, demonstrating for the first time that a DEXH-box protein is involved in mammalian splicing. We propose that U5-200kD and Snu246p promote one or more conformational changes in the dynamic network of RNA-RNA interactions in the spliceosome.Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the
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[]Articles from The EMBO Journal are provided here courtesy of The European Molecular Biology Organization
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Non-local kinetic and macroscopic models for self-organised animal
aggregations
Abstract: The last two decades have seen a surge in kinetic and macroscopic models
derived to investigate the multi-scale aspects of self-organised biological
aggregations. Because the individual-level details incorporated into the
kinetic models (e.g., individual speeds and turning rates) make them somewhat
difficult to investigate, one is interested in transforming these models into
simpler macroscopic models, by using various scaling techniques that are
imposed by the biological assumptions of the models. Here, we consider three
scaling approaches (parabolic, hydrodynamic and grazing collision limits) that
can be used to reduce a class of non-local 1D and 2D models for biological
aggregations to simpler models existent in the literature. Next, we investigate
how some of the spatio-temporal patterns exhibited by the original kinetic
models are preserved via these scalings. To this end, we focus on the parabolic
scaling for non-local 1D models and apply asymptotic preserving numerical
methods, which allow us to analyse changes in the patterns as the scaling
coefficient $\epsilon$ is varied from $\epsilon=1$ (for 1D transport models) to
$\epsilon=0$ (for 1D parabolic models). We show that some patterns (describing
stationary aggregations) are preserved in the limit $\epsilon\to 0$, while
other patterns (describing moving aggregations) are lost in this limit. To
understand the loss of these patterns, we construct bifurcation diagrams.
Populations and Evolution (q-bio.PE); Analysis of PDEs (math.AP)
MSC&classes:
35Q92, 35A99
[q-bio.PE]
[q-bio.PE] for this version)
Submission history
From: Franca Hoffmann []
[v1] Tue, 8 Jul :16 GMT
(3006kb,D)CONSUMPTION AND CHILDREN on JSTOR
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CONSUMPTION AND CHIL...
CONSUMPTION AND CHILDREN
Martin Browning and Mette Ejrnaes
The Review of Economics and Statistics
Vol. 91, No. 1 (February 2009), pp. 93-111
Published by:
Stable URL: http://www.jstor.org/stable/
Page Count: 19
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Consumption by couples rises sharply in the beginning and the causes of the early rise are hotly contested. Among the suggestions are rule of thumb behavior, demographics, liquidity constraints, the precautionary motive, and nonseparabilities between consumption and labor supply. We develop two tests of the extreme hypothesis that only changes in family structure matter. We estimate effects of the numbers and ages of children on consumption. These estimates allow us to rationalize all of the increase in consumption without recourse to any of the causal mechanisms. Our estimates can be interpreted either as giving upper bounds on the effects of children or as evidence that the other causes are not important.
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