184 research outputs found
Size Effects in Carbon Nanotubes
The inter-shell spacing of multi-walled carbon nanotubes was determined by
analyzing the high resolution transmission electron microscopy images of these
nanotubes. For the nanotubes that were studied, the inter-shell spacing
is found to range from 0.34 to 0.39 nm, increasing with
decreasing tube diameter. A model based on the results from real space image
analysis is used to explain the variation in inter-shell spacings obtained from
reciprocal space periodicity analysis. The increase in inter-shell spacing with
decreased nanotube diameter is attributed to the high curvature, resulting in
an increased repulsive force, associated with the decreased diameter of the
nanotube shells.Comment: 4 pages. RevTeX. 4 figure
Quantum Cryptography
Quantum cryptography could well be the first application of quantum mechanics
at the individual quanta level. The very fast progress in both theory and
experiments over the recent years are reviewed, with emphasis on open questions
and technological issues.Comment: 55 pages, 32 figures; to appear in Reviews of Modern Physic
Superconductivity in Fullerides
Experimental studies of superconductivity properties of fullerides are
briefly reviewed. Theoretical calculations of the electron-phonon coupling, in
particular for the intramolecular phonons, are discussed extensively. The
calculations are compared with coupling constants deduced from a number of
different experimental techniques. It is discussed why the A_3 C_60 are not
Mott-Hubbard insulators, in spite of the large Coulomb interaction. Estimates
of the Coulomb pseudopotential , describing the effect of the Coulomb
repulsion on the superconductivity, as well as possible electronic mechanisms
for the superconductivity are reviewed. The calculation of various properties
within the Migdal-Eliashberg theory and attempts to go beyond this theory are
described.Comment: 33 pages, latex2e, revtex using rmp style, 15 figures, submitted to
Review of Modern Physics, more information at
http://radix2.mpi-stuttgart.mpg.de/fullerene/fullerene.htm
Quantum Communication
Quantum communication, and indeed quantum information in general, has changed
the way we think about quantum physics. In 1984 and 1991, the first protocol
for quantum cryptography and the first application of quantum non-locality,
respectively, attracted a diverse field of researchers in theoretical and
experimental physics, mathematics and computer science. Since then we have seen
a fundamental shift in how we understand information when it is encoded in
quantum systems. We review the current state of research and future directions
in this new field of science with special emphasis on quantum key distribution
and quantum networks.Comment: Submitted version, 8 pg (2 cols) 5 fig
Toward the Assessment of Food Toxicity for Celiac Patients: Characterization of Monoclonal Antibodies to a Main Immunogenic Gluten Peptide
13 pages, 8 figures.-- PMID: 18509534 [PubMed].-- PMCID: PMC2386552.[Background and Aims] Celiac disease is a permanent intolerance to gluten prolamins from wheat, barley, rye and, in some patients, oats. Partially digested gluten peptides produced in the digestive tract cause inflammation of the small intestine. High throughput, immune-based assays using monoclonal antibodies specific for these immunotoxic peptides would facilitate their detection in food and enable monitoring of their enzymatic detoxification. Two monoclonal antibodies, G12 and A1, were developed against a highly immunotoxic 33-mer peptide. The potential of each antibody for quantifying food toxicity for celiac patients was studied.[Methods] Epitope preferences of G12 and A1 antibodies were determined by ELISA with gluten-derived peptide variants of recombinant, synthetic or enzymatic origin.[Results] The recognition sequences of G12 and A1 antibodies were hexameric and heptameric epitopes, respectively. Although G12 affinity for the 33-mer was superior to A1, the sensitivity for gluten detection was higher for A1. This observation correlated to the higher number of A1 epitopes found in prolamins than G12 epitopes. Activation of T cell from gluten digested by glutenases decreased equivalently to the detection of intact peptides by A1 antibody. Peptide recognition of A1 included gliadin peptides involved in the both the adaptive and innate immunological response in celiac disease.[Conclusions] The sensitivity and epitope preferences of the A1 antibody resulted to be useful to detect gluten relevant peptides to infer the potential toxicity of food for celiac patients as well as to monitor peptide modifications by transglutaminase 2 or glutenases.This work was supported by the Asociación de Celiacos de Madrid (to Carolina Sousa), by the CTA (Corporación Tecnológica de Andalucía) and IDEA (Agencia de Innovación y Desarrollo de Andalucía) (to Angel Cebolla) and by grants BFU2007-64999 from Plan Nacional de Investigación científica, Desarrollo e Innovación tecnológica (Miniterio de Educación y Ciencia) and RICET-RD06/0021-0014, Spain (to Manuel C. López). Belén Morón was supported by a fellowship from Consejo Andaluz de Colegios Oficiales de Farmacéuticos.Peer reviewe
Parallels between Pathogens and Gluten Peptides in Celiac Sprue
Pathogens are exogenous agents capable of causing disease in susceptible organisms. In celiac sprue, a disease triggered by partially hydrolyzed gluten peptides in the small intestine, the offending immunotoxins cannot replicate, but otherwise have many hallmarks of classical pathogens. First, dietary gluten and its peptide metabolites are ubiquitous components of the modern diet, yet only a small, genetically susceptible fraction of the human population contracts celiac sprue. Second, immunotoxic gluten peptides have certain unusual structural features that allow them to survive the harsh proteolytic conditions of the gastrointestinal tract and thereby interact extensively with the mucosal lining of the small intestine. Third, they invade across epithelial barriers intact to access the underlying gut-associated lymphoid tissue. Fourth, they possess recognition sequences for selective modification by an endogenous enzyme, transglutaminase 2, allowing for in situ activation to a more immunotoxic form via host subversion. Fifth, they precipitate a T cell–mediated immune reaction comprising both innate and adaptive responses that causes chronic inflammation of the small intestine. Sixth, complete elimination of immunotoxic gluten peptides from the celiac diet results in remission, whereas reintroduction of gluten in the diet causes relapse. Therefore, in analogy with antibiotics, orally administered proteases that reduce the host's exposure to the immunotoxin by accelerating gluten peptide destruction have considerable therapeutic potential. Last but not least, notwithstanding the power of in vitro methods to reconstitute the essence of the immune response to gluten in a celiac patient, animal models for the disease, while elusive, are likely to yield fundamentally new systems-level insights
De Novo Truncating Mutations in WASF1 Cause Intellectual Disability with Seizures.
Next-generation sequencing has been invaluable in the elucidation of the genetic etiology of many subtypes of intellectual disability in recent years. Here, using exome sequencing and whole-genome sequencing, we identified three de novo truncating mutations in WAS protein family member 1 (WASF1) in five unrelated individuals with moderate to profound intellectual disability with autistic features and seizures. WASF1, also known as WAVE1, is part of the WAVE complex and acts as a mediator between Rac-GTPase and actin to induce actin polymerization. The three mutations connected by Matchmaker Exchange were c.1516C>T (p.Arg506Ter), which occurs in three unrelated individuals, c.1558C>T (p.Gln520Ter), and c.1482delinsGCCAGG (p.Ile494MetfsTer23). All three variants are predicted to partially or fully disrupt the C-terminal actin-binding WCA domain. Functional studies using fibroblast cells from two affected individuals with the c.1516C>T mutation showed a truncated WASF1 and a defect in actin remodeling. This study provides evidence that de novo heterozygous mutations in WASF1 cause a rare form of intellectual disability
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