2,424 research outputs found
Mesoscale modeling of the rheology of pressure sensitive adhesives through inclusion of transient forces
For optimal application, pressure-sensitive adhesives must have rheological
properties in between those of a viscoplastic solid and those of a viscoelastic
liquid. Such adhesives can be produced by emulsion polymerisation, resulting in
latex particles which are dispersed in water and contain long-chain acrylic
polymers. When the emulsion is dried, the latex particles coalesce and an
adhesive film is formed. The rheological properties of the dried samples are
believed to be dominated by the interface regions between the original latex
particles, but the relation between rheology and latex particle properties is
poorly understood. In this paper we show that it is possible to describe the
bulk rheology of a pressure-sensitive adhesive by means of a mesoscale
simulation model. To reach experimental time and length scales, each latex
particle is represented by just one simulated particle. The model is subjected
to oscillatory shear flow and extensional flow. Simple order of magnitude
estimates of the model parameters already lead to semi-quantitative agreement
with experimental results. We show that inclusion of transient forces in the
model, i.e. forces with memory of previous configurations, is essential to
correctly predict the linear and nonlinear properties.Comment: 29 pages, 8 figure
A 16-channel Digital TDC Chip with internal buffering and selective readout for the DIRC Cherenkov counter of the BABAR experiment
A 16-channel digital TDC chip has been built for the DIRC Cherenkov counter
of the BaBar experiment at the SLAC B-factory (Stanford, USA). The binning is
0.5 ns, the conversion time 32 ns and the full-scale 32 mus. The data driven
architecture integrates channel buffering and selective readout of data falling
within a programmable time window. The time measuring scale is constantly
locked to the phase of the (external) clock. The linearity is better than 80 ps
rms. The dead time loss is less than 0.1% for incoherent random input at a rate
of 100 khz on each channel. At such a rate the power dissipation is less than
100 mw. The die size is 36 mm2.Comment: Latex, 18 pages, 13 figures (14 .eps files), submitted to NIM
Analyzing powers in inclusive pion production at high energy and the nucleon spin structure
Analyzing powers in inclusive pion production in high energy transversely
polarized proton-proton collisions are studied theoretically in the framework
of the quark recombination model. Calculations by assuming the SU(6)
spin-flavor symmetry for the nucleon structure disagree with the experiments.
We solve this difficulty by taking into account the %We overcome this
difficulty by taking into account the realistic spin distribution functions of
the nucleon, which differs from the SU(6) expectation at large , %but
coincides with a perturbative QCD constraint on the ratio of the unpolarized
valence distributions, as . We also discuss the kaon spin
asymmetry and find in the polarized proton-proton
collisions at large .Comment: 13 pages, 4 figures, late
Thrombospondin modulates melanoma--platelet interactions and melanoma tumour cell growth in vivo.
In this study we have investigated the role of thrombospondin (TSP) as a possible ligand playing a key role in human M3Da. melanoma cell interaction with platelets and in tumour growth. TSP is secreted (80 +/- 6 ng TSP 10(-6) cells) and bound to the surface of M3Da. cells via receptors different from CD36, as shown by biosynthetic labelling and immunofluorescence studies. The levels of TSP binding to M3Da. cells evaluated by binding studies, using an anti-TSP monoclonal antibody (MAb) (LYP8), shows 367,000 +/- 58,000 (mean +/- s.d.) LYP8 binding sites per cell with a dissociation constant (Kd) of 67 nM. TSP binding to M3Da. cells shows 400,000 +/- 50,000 TSP binding sites per cell with a Kd of 10 nM. The capacity of anti-TSP MAb (LYP8) to inhibit M3Da.-platelet interactions was followed on an aggregometer and evaluated by electron microscopy studies. The biological role of TSP binding to M3Da. cells was investigated by implanting subcutaneously the M3Da. cell line in nude mice and following the size and time of in vivo tumour growth. Reducing the availability or the functional level of TSP by using an anti-TSP MAb (LYP8) resulted in a significant decrease in platelet aggregates interacting with M3Da. melanoma cells. Using an enzyme-linked immunosorbent assay, purified alpha nu beta 3 was shown to bind TSP. Moreover, LYP8-coated M3Da. cells showed a reduced capacity to form tumours in vivo. M3Da. cells were observed to attach and spread on human platelet TSP-coated plastic wells. This attachment by M3Da. cells was inhibited in a similar way by LYP8 and an anti-alpha nu beta 3 MAb (LYP18). The results obtained in this study show that TSP secreted and bound to the surface of a human melanoma cell line (M3Da.) acts as a link between aggregated platelets and the M3Da. cell surface. Moreover, these results shows that TSP can modulate tumour growth in vivo. Reagents such as MAbs directed against TSP and peptides derived from TSP could not only be used as a new therapeutic approach in the control of tumour metastasis of melanoma, but may also contribute to elucidation of the role of TSP in cancer biology
Clinical update: Heparin-induced thrombocytopenia: An update for the COVID-19 era
The increased use of heparin during the current COVID-19 pandemic has highlighted the risk of a rare but potentially serious complication of heparin therapy, viz. heparin-induced thrombocytopenia (HIT). This is a short review on the pharmacology of heparin and its derivatives, and the pathophysiology of HIT. Guidance on laboratory testing for and clinical management of HIT is presented in accordance with international guidelines. There are important similarities and differences between HIT and the new entity of vaccine-induced immune thrombotic thrombocytopenia, also known as thrombosis with thrombocytopenia syndrome, which clinicians need to be aware of
Analytic curves in algebraic varieties over number fields
We establish algebraicity criteria for formal germs of curves in algebraic
varieties over number fields and apply them to derive a rationality criterion
for formal germs of functions, which extends the classical rationality theorems
of Borel-Dwork and P\'olya-Bertrandias valid over the projective line to
arbitrary algebraic curves over a number field.
The formulation and the proof of these criteria involve some basic notions in
Arakelov geometry, combined with complex and rigid analytic geometry (notably,
potential theory over complex and -adic curves). We also discuss geometric
analogues, pertaining to the algebraic geometry of projective surfaces, of
these arithmetic criteria.Comment: 55 pages. To appear in "Algebra, Arithmetic, and Geometry: In Honor
of Y.i. Manin", Y. Tschinkel & Yu. Manin editors, Birkh\"auser, 200
Ranking ligand affinity for the DNA minor groove by experiment and simulation
The structural and thermodynamic basis for the strength and selectivity of the interactions of minor-groove binders (MGBs) with DNA is not fully understood. In 2003 we reported the first example of a thiazole containing MGB that bound in a phase shifted pattern that spanned 6 base-pairs rather than the usual 4 (for tricyclic distamycin-like compounds). Since then, using DNA footprinting, nuclear magnetic resonance spectroscopy, isothermal titration calorimetry and molecular dynamics, we have established that the flanking bases around the central 4 being read by the ligand have subtle effects on recognition. We have investigated the effect of these flanking sequences on binding and the reasons for the differences and established a computational method to rank ligand affinity against varying DNA sequences
Randomness Increases Order in Biological Evolution
n this text, we revisit part of the analysis of anti-entropy in Bailly and Longo (2009} and develop further theoretical reflections. In particular, we analyze how randomness, an essential component of biological variability, is associated to the growth of biological organization, both in ontogenesis and in evolution. This approach, in particular, focuses on the role of global entropy production and provides a tool for a mathematical understanding of some fundamental observations by Gould on the increasing phenotypic complexity along evolution. Lastly, we analyze the situation in terms of theoretical symmetries, in order to further specify the biological meaning of anti-entropy as well as its strong link with randomness
Gln-tRNAGln synthesis in a dynamic transamidosome from Helicobacter pylori, where GluRS2 hydrolyzes excess Glu-tRNAGln
In many bacteria and archaea, an ancestral pathway is used where asparagine and glutamine are formed from their acidic precursors while covalently linked to tRNAAsn and tRNAGln, respectively. Stable complexes formed by the enzymes of these indirect tRNA aminoacylation pathways are found in several thermophilic organisms, and are called transamidosomes. We describe here a transamidosome forming Gln-tRNAGln in Helicobacter pylori, an ε-proteobacterium pathogenic for humans; this transamidosome displays novel properties that may be characteristic of mesophilic organisms. This ternary complex containing the non-canonical GluRS2 specific for Glu-tRNAGln formation, the tRNA-dependent amidotransferase GatCAB and tRNAGln was characterized by dynamic light scattering. Moreover, we observed by interferometry a weak interaction between GluRS2 and GatCAB (KD = 40 ± 5 µM). The kinetics of Glu-tRNAGln and Gln-tRNAGln formation indicate that conformational shifts inside the transamidosome allow the tRNAGln acceptor stem to interact alternately with GluRS2 and GatCAB despite their common identity elements. The integrity of this dynamic transamidosome depends on a critical concentration of tRNAGln, above which it dissociates into separate GatCAB/tRNAGln and GluRS2/tRNAGln complexes. Ester bond protection assays show that both enzymes display a good affinity for tRNAGln regardless of its aminoacylation state, and support a mechanism where GluRS2 can hydrolyze excess Glu-tRNAGln, ensuring faithful decoding of Gln codons
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