677 research outputs found
On the Non-existence of 3-Dimensional Tiling in the Lee Metric
AbstractWe prove that there does not exist a tiling with Lee spheres of radius at least 2 in the 3-dimensional Euclidean space. In particular, this result verifies a conjecture of Golomb and Welch forn=3
On the structure of non-full-rank perfect codes
The Krotov combining construction of perfect 1-error-correcting binary codes
from 2000 and a theorem of Heden saying that every non-full-rank perfect
1-error-correcting binary code can be constructed by this combining
construction is generalized to the -ary case. Simply, every non-full-rank
perfect code is the union of a well-defined family of -components
, where belongs to an "outer" perfect code , and these
components are at distance three from each other. Components from distinct
codes can thus freely be combined to obtain new perfect codes. The Phelps
general product construction of perfect binary code from 1984 is generalized to
obtain -components, and new lower bounds on the number of perfect
1-error-correcting -ary codes are presented.Comment: 8 page
Molecular diagnostic and genetic characterization of highly pathogenic viruses: application during Crimean–Congo haemorrhagic fever virus outbreaks in Eastern Europe and the Middle East
AbstractSeveral haemorrhagic fevers are caused by highly pathogenic viruses that must be handled in Biosafety level 4 (BSL–4) containment. These zoonotic infections have an important impact on public health and the development of a rapid and differential diagnosis in case of outbreak in risk areas represents a critical priority. We have demonstrated the potential of a DNA resequencing microarray (PathogenID v2.0) for this purpose. The microarray was first validated in vitro using supernatants of cells infected with prototype strains from five different families of BSL-4 viruses (e.g. families Arenaviridae, Bunyaviridae, Filoviridae, Flaviviridae and Paramyxoviridae). RNA was amplified based on isothermal amplification by Phi29 polymerase before hybridization. We were able to detect and characterize Nipah virus and Crimean–Congo haemorrhagic fever virus (CCHFV) in the brains of experimentally infected animals. CCHFV was finally used as a paradigm for epidemics because of recent outbreaks in Turkey, Kosovo and Iran. Viral variants present in human sera were characterized by BLASTN analysis. Sensitivity was estimated to be 105–106 PFU/mL of hybridized cDNA. Detection specificity was limited to viral sequences having ˜13–14% of global divergence with the tiled sequence, or stretches of ˜20 identical nucleotides. These results highlight the benefits of using the PathogenID v2.0 resequencing microarray to characterize geographical variants in the follow-up of haemorrhagic fever epidemics; to manage patients and protect communities; and in cases of bioterrorism
Syntaxin 8 regulates platelet dense granule secretion, aggregation, and thrombus stability.
Platelet secretion not only drives thrombosis and hemostasis, but also mediates a variety of other physiological and pathological processes. The ubiquitous SNARE machinery and a number of accessory proteins have been implicated in regulating secretion in platelet. Although several platelet SNAREs have been identified, further members of the SNARE family may be needed to fine-tune platelet secretion. In this study we identified expression of the t-SNARE syntaxin 8 (STX8) (Qc SNARE) in mouse and human platelets. In mouse studies, whereas STX8 was not essential for α-granule or lysosome secretion, Stx8(-/-) platelets showed a significant defect in dense granule secretion in response to thrombin and CRP. This was most pronounced at intermediate concentrations of agonists. They also showed an aggregation defect that could be rescued with exogenous ADP and increased embolization in Stx8(-/-) mice in vivo consistent with an important autocrine and paracrine role for ADP in aggregation and thrombus stabilization. STX8 therefore specifically contributes to dense granule secretion and represents another member of a growing family of genes that play distinct roles in regulating granule release from platelets and thus platelet function in thrombosis and hemostasis
Myosin5a tail associates directly with Rab3A-containing compartments in neurons
Author Posting. © The Author(s), 2011. This is the author's version of the work. It is posted here by permission of American Society for Biochemistry and Molecular Biology. The definitive version was published in Journal of Biological Chemistry, 286 (2011): 14352-14361, doi:10.1074/jbc.M110.187286.Myosin-Va (Myo5a) is a motor protein
associated with synaptic vesicles (SVs) but the
mechanism by which it interacts has not yet
been identified. A potential class of binding
partners are Rab GTPases and Rab3A is known
to associate with SVs and is involved in SV
trafficking. We performed experiments to
determine whether Rab3A interacts with
Myo5a and whether it is required for transport
of neuronal vesicles. In vitro motility assays
performed with axoplasm from the squid giant
axon showed a requirement for a Rab GTPase
in Myo5a-dependent vesicle transport.
Furthermore, mouse recombinant Myo5a tail
revealed that it associated with Rab3A in rat
brain synaptosomal preparations in vitro and
the association was confirmed by
immunofluorescence imaging of primary
neurons isolated from the frontal cortex of
mouse brains. Synaptosomal Rab3A was
retained on recombinant GST-tagged Myo5a
tail affinity columns in a GTP-dependent
manner. Finally, the direct interaction of
Myo5a and Rab3A was determined by
sedimentation v e l o c i t y analytical
ultracentrifugation using recombinant mouse
Myo5a tail and human Rab3A. When both
proteins were incubated in the presence of 1
mM GTPγS, Myo5a tail and Rab3A formed a
complex and a direct interaction was observed.
Further analysis revealed that GTP-bound
Rab3A interacts with both the monomeric and
dimeric species of the Myo5a tail. However, the
interaction between Myo5a tail and nucleotidefree
Rab3A did not occur. Thus, our results
show that Myo5a and Rab3A are direct binding
partners and interact on SVs and that the
Myo5a/Rab3A complex is involved in transport
of neuronal vesicles
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